PMID- 29074629
OWN - NLM
STAT- MEDLINE
DCOM- 20171030
LR  - 20171219
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Linking)
VI  - 359
DP  - 2017 Oct 26
TI  - Obesity and gynaecological and obstetric conditions: umbrella review of the
      literature.
PG  - j4511
LID - 10.1136/bmj.j4511 [doi]
AB  - Objective To study the strength and validity of associations between adiposity
      and risk of any type of obstetric or gynaecological conditions.Design An umbrella
      review of meta-analyses.Data sources PubMed, Cochrane database of systematic
      reviews, manual screening of references for systematic reviews or meta-analyses
      of observational and interventional studies evaluating the association between
      adiposity and risk of any obstetrical or gynaecological outcome.Main outcomes
      Meta-analyses of cohort studies on associations between indices of adiposity and 
      obstetric and gynaecological outcomes.Data synthesis Evidence from observational 
      studies was graded into strong, highly suggestive, suggestive, or weak based on
      the significance of the random effects summary estimate and the largest study in 
      the included meta-analysis, the number of cases, heterogeneity between studies,
      95% prediction intervals, small study effects, excess significance bias, and
      sensitivity analysis with credibility ceilings. Interventional meta-analyses were
      assessed separately.Results 156 meta-analyses of observational studies were
      included, investigating associations between adiposity and risk of 84 obstetric
      or gynaecological outcomes. Of the 144 meta-analyses that included cohort
      studies, only 11 (8%) had strong evidence for eight outcomes: adiposity was
      associated with a higher risk of endometrial cancer, ovarian cancer, antenatal
      depression, total and emergency caesarean section, pre-eclampsia, fetal
      macrosomia, and low Apgar score. The summary effect estimates ranged from 1.21
      (95% confidence interval 1.13 to 1.29) for an association between a 0.1 unit
      increase in waist to hip ratio and risk endometrial cancer up to 4.14 (3.61 to
      4.75) for risk of pre-eclampsia for BMI >35 compared with <25. Only three out of 
      these eight outcomes were also assessed in meta-analyses of trials evaluating
      weight loss interventions. These interventions significantly reduced the risk of 
      caesarean section and pre-eclampsia, whereas there was no evidence of association
      with fetal macrosomia.Conclusions Although the associations between adiposity and
      obstetric and gynaecological outcomes have been extensively studied, only a
      minority were considered strong and without hints of bias.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not
      already granted under a licence) please go to
      http://group.bmj.com/group/rights-licensing/permissions.
FAU - Kalliala, Ilkka
AU  - Kalliala I
AD  - Department of Surgery and Cancer, IRDB, Faculty of Medicine, Imperial College,
      London W12 0NN, UK.
AD  - Department of Obstetrics and Gynaecology, University of Helsinki and Helsinki
      University Hospital, Haartmaninkatu 2, 00029 HUS, Finland.
FAU - Markozannes, Georgios
AU  - Markozannes G
AD  - Department of Hygiene and Epidemiology, University of Ioannina School of
      Medicine, 45110, Ioannina, Greece.
FAU - Gunter, Marc J
AU  - Gunter MJ
AD  - Section of Nutrition and Metabolism, International Agency for Research on Cancer 
      (IARC), Lyon, France.
FAU - Paraskevaidis, Evangelos
AU  - Paraskevaidis E
AD  - Department of Obstetrics and Gynaecology, University of Ioannina, 45500,
      Ioannina, Greece.
FAU - Gabra, Hani
AU  - Gabra H
AD  - Department of Surgery and Cancer, IRDB, Faculty of Medicine, Imperial College,
      London W12 0NN, UK.
AD  - Clinical Discovery Unit, Early Clinical Development, AstraZeneca, Cambridge, UK.
FAU - Mitra, Anita
AU  - Mitra A
AD  - Department of Surgery and Cancer, IRDB, Faculty of Medicine, Imperial College,
      London W12 0NN, UK.
AD  - West London Gynaecological Cancer Centre, Queen Charlotte's and
      Chelsea-Hammersmith Hospital, Imperial Healthcare NHS Trust, London W12 0HS, UK.
FAU - Terzidou, Vasso
AU  - Terzidou V
AD  - Department of Surgery and Cancer, IRDB, Faculty of Medicine, Imperial College,
      London W12 0NN, UK.
AD  - West London Gynaecological Cancer Centre, Queen Charlotte's and
      Chelsea-Hammersmith Hospital, Imperial Healthcare NHS Trust, London W12 0HS, UK.
FAU - Bennett, Phillip
AU  - Bennett P
AD  - Department of Surgery and Cancer, IRDB, Faculty of Medicine, Imperial College,
      London W12 0NN, UK.
AD  - West London Gynaecological Cancer Centre, Queen Charlotte's and
      Chelsea-Hammersmith Hospital, Imperial Healthcare NHS Trust, London W12 0HS, UK.
FAU - Martin-Hirsch, Pierre
AU  - Martin-Hirsch P
AD  - Department Gynaecologic Oncology, Lancashire Teaching Hospitals, Preston PR29HT, 
      UK.
AD  - Department of Biophysics, University of Lancaster, Lancaster, UK.
FAU - Tsilidis, Konstantinos K
AU  - Tsilidis KK
AD  - Department of Hygiene and Epidemiology, University of Ioannina School of
      Medicine, 45110, Ioannina, Greece.
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Imperial
      College London, London W2 1PG, UK.
FAU - Kyrgiou, Maria
AU  - Kyrgiou M
AD  - Department of Surgery and Cancer, IRDB, Faculty of Medicine, Imperial College,
      London W12 0NN, UK.
AD  - West London Gynaecological Cancer Centre, Queen Charlotte's and
      Chelsea-Hammersmith Hospital, Imperial Healthcare NHS Trust, London W12 0HS, UK.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Review
DEP - 20171026
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
SB  - AIM
SB  - IM
MH  - Apgar Score
MH  - Cesarean Section
MH  - Depression/complications
MH  - Endometrial Neoplasms/complications
MH  - Female
MH  - Fetal Macrosomia/complications
MH  - Genital Diseases, Female/*complications
MH  - Humans
MH  - Obesity/*complications
MH  - Ovarian Neoplasms/complications
MH  - Pre-Eclampsia
MH  - Pregnancy
MH  - *Pregnancy Complications/psychology
PMC - PMC5656976
COIS- Competing interests: All authors have completed the ICMJE uniform disclosure form
      at www.icmje.org/coi_disclosure.pdf and declare: no support from any organisation
      for the submitted work; no financial relationships with any organisations that
      might have an interest in the submitted work in the previous three years; no
      other relationships or activities that could appear to have influenced the
      submitted work.
EDAT- 2017/10/28 06:00
MHDA- 2017/10/31 06:00
CRDT- 2017/10/28 06:00
PHST- 2017/10/28 06:00 [entrez]
PHST- 2017/10/28 06:00 [pubmed]
PHST- 2017/10/31 06:00 [medline]
PST - epublish
SO  - BMJ. 2017 Oct 26;359:j4511.

id: 29066470 Error occurred: The following PMID is not available: 29066470

PMID- 29083501
OWN - NLM
STAT- MEDLINE
DCOM- 20180731
LR  - 20180815
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 35
IP  - 1
DP  - 2018 Jan
TI  - Pilot feasibility study examining a structured self-management diabetes education
      programme, DESMOND-ID, targeting HbA1c in adults with intellectual disabilities.
PG  - 137-146
LID - 10.1111/dme.13539 [doi]
AB  - AIM: To report on the outcomes of a pilot feasibility study of a structured
      self-management diabetes education programme targeting HbA1c . METHODS: We
      conducted a two-arm, individually randomized, pilot superiority trial for adults 
      with intellectual disability and Type 2 diabetes mellitus. A total of 66 adults
      with disabilities across the UK met the eligibility criteria. Of these, 39 agreed
      to participate and were randomly assigned to either the DESMOND-ID programme (n =
      19) or a control group (n = 20). The programme consisted of seven weekly
      educational sessions. The primary outcome was HbA1c level, and secondary outcomes
      included BMI, diabetes illness perceptions, severity of diabetes, quality of
      life, and attendance rates. RESULTS: This study found that the DESMOND-ID
      programme was feasible to deliver. With reasonable adjustments, the participants 
      could be recruited successfully, and could provide consent, complete the outcome 
      measures, be randomized to the groups and attend most of the sessions, with
      minimal loss to follow-up. The fixed-effects model, the interaction between
      occasion (time) and condition, showed statistically significant results (0.05
      level) for HbA1c ; however, the CI was large. CONCLUSION: This is the first
      published study to adapt and pilot a national structured self-management diabetes
      education programme for adults with intellectual disability. This study shows it 
      is possible to identify, recruit, consent and randomize adults with intellectual 
      disabilities to an intervention or control group. Internationally, the results of
      this pilot are promising, demonstrating that a multi-session education programme 
      is acceptable and feasible to deliver. Its effectiveness should be further tested
      in an adequately powered trial.
CI  - (c) 2017 Diabetes UK.
FAU - Taggart, L
AU  - Taggart L
AUID- ORCID: 0000-0002-0954-2127
AD  - Institute of Nursing and Health Research, Ulster University, Belfast, UK.
FAU - Truesdale, M
AU  - Truesdale M
AD  - Edinburgh Napier University, Edinburgh, UK.
FAU - Carey, M E
AU  - Carey ME
AD  - Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust,
      Leicester, UK.
FAU - Martin-Stacey, L
AU  - Martin-Stacey L
AD  - Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust,
      Leicester, UK.
FAU - Scott, J
AU  - Scott J
AD  - Northern Health and Social Care Trust, Coleraine, UK.
FAU - Bunting, B
AU  - Bunting B
AD  - Institute of Psychology, Ulster University, Derry, UK.
FAU - Coates, V
AU  - Coates V
AUID- ORCID: 0000-0002-8069-2961
AD  - Institute of Nursing and Health Research, Ulster University, Belfast, UK.
FAU - Brown, M
AU  - Brown M
AD  - Edinburgh Napier University, Edinburgh, UK.
FAU - Karatzias, T
AU  - Karatzias T
AD  - Edinburgh Napier University, Edinburgh, UK.
FAU - Northway, R
AU  - Northway R
AD  - University of South Wales, Cardiff, UK.
FAU - Clarke, J M
AU  - Clarke JM
AD  - MRC Hub for Trials Methodology Research, Queen's University Belfast, Belfast, UK.
LA  - eng
SI  - ISRCTN/ISRCTN93185560
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
DEP - 20171121
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (hemoglobin A1c protein, human)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Diabetes Mellitus, Type 2/complications/metabolism/*therapy
MH  - Education of Intellectually Disabled/methods
MH  - Feasibility Studies
MH  - Female
MH  - Glycated Hemoglobin A/metabolism
MH  - Humans
MH  - Intellectual Disability/*complications
MH  - Male
MH  - Middle Aged
MH  - Patient Compliance
MH  - Patient Education as Topic/*methods
MH  - Pilot Projects
MH  - Program Evaluation
MH  - Quality of Life
MH  - *Self Care
MH  - Self-Management/*education
MH  - Severity of Illness Index
MH  - Treatment Outcome
EDAT- 2017/10/31 06:00
MHDA- 2018/08/01 06:00
CRDT- 2017/10/31 06:00
PHST- 2017/10/25 00:00 [accepted]
PHST- 2017/10/31 06:00 [pubmed]
PHST- 2018/08/01 06:00 [medline]
PHST- 2017/10/31 06:00 [entrez]
AID - 10.1111/dme.13539 [doi]
PST - ppublish
SO  - Diabet Med. 2018 Jan;35(1):137-146. doi: 10.1111/dme.13539. Epub 2017 Nov 21.

PMID- 29083500
OWN - NLM
STAT- MEDLINE
DCOM- 20180731
LR  - 20180815
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 35
IP  - 1
DP  - 2018 Jan
TI  - Prognosis of the infected diabetic foot ulcer: a 12-month prospective
      observational study.
PG  - 78-88
LID - 10.1111/dme.13537 [doi]
AB  - AIMS: To determine clinical outcomes and explore prognostic factors related to
      ulcer healing in people with a clinically infected diabetic foot ulcer. METHODS: 
      This multicentre, prospective, observational study reviewed participants' data at
      12 months after culture of a diabetic foot ulcer requiring antibiotic therapy.
      From participants' notes, we obtained information on the incidence of wound
      healing, ulcer recurrence, lower extremity amputation, lower extremity
      revascularization and death. We estimated the cumulative incidence of healing at 
      6 and 12 months, adjusted for lower extremity amputation and death using a
      competing risk analysis, and explored the relationship between baseline factors
      and healing incidence. RESULTS: In the first year after culture of the index
      ulcer, 45/299 participants (15.1%) had died. The ulcer had healed in 136
      participants (45.5%), but recurred in 13 (9.6%). An ipsilateral lower extremity
      amputation was recorded in 52 (17.4%) and revascularization surgery in 18
      participants (6.0%). Participants with an ulcer present for ~2 months or more had
      a lower incidence of healing (hazard ratio 0.55, 95% CI 0.39 to 0.77), as did
      those with a PEDIS (perfusion, extent, depth, infection, sensation) perfusion
      grade of >/=2 (hazard ratio 0.37, 95% CI 0.25 to 0.55). Participants with a
      single ulcer on their index foot had a higher incidence of healing than those
      with multiple ulcers (hazard ratio 1.90, 95% CI 1.18 to 3.06). CONCLUSIONS:
      Clinical outcomes at 12 months for people with an infected diabetic foot ulcer
      are generally poor. Our data confirm the adverse prognostic effect of limb
      ischaemia, longer ulcer duration and the presence of multiple ulcers.
CI  - (c) 2017 The Authors. Diabetic Medicine published by John Wiley & Sons Ltd on
      behalf of Diabetes UK.
FAU - Ndosi, M
AU  - Ndosi M
AUID- ORCID: 0000-0002-7764-3173
AD  - Department of Nursing and Midwifery, University of the West of England, Bristol, 
      UK.
AD  - Academic Rheumatology Unit, University Hospitals Bristol NHS Foundation Trust,
      Bristol, UK.
FAU - Wright-Hughes, A
AU  - Wright-Hughes A
AD  - Clinical Trials Research Unit, University of Leeds, Leeds, UK.
FAU - Brown, S
AU  - Brown S
AD  - Clinical Trials Research Unit, University of Leeds, Leeds, UK.
FAU - Backhouse, M
AU  - Backhouse M
AD  - Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds,
      Leeds, UK.
FAU - Lipsky, B A
AU  - Lipsky BA
AD  - Division of Medical Sciences, University of Oxford, Oxford, UK.
FAU - Bhogal, M
AU  - Bhogal M
AD  - School of Biomedical Sciences, University of Leeds, Leeds, UK.
FAU - Reynolds, C
AU  - Reynolds C
AD  - Clinical Trials Research Unit, University of Leeds, Leeds, UK.
FAU - Vowden, P
AU  - Vowden P
AD  - Bradford Royal Infirmary, Bradford, UK.
FAU - Jude, E B
AU  - Jude EB
AD  - Tameside and Glossop Integrated Care NHS Foundation Trust, Ashton-Under-Lyne, UK.
AD  - University of Manchester, Manchester, UK.
FAU - Nixon, J
AU  - Nixon J
AD  - Clinical Trials Research Unit, University of Leeds, Leeds, UK.
FAU - Nelson, E A
AU  - Nelson EA
AD  - Schoool of Healthcare, University of Leeds, Leeds, UK.
LA  - eng
GR  - 09/75/01/Department of Health/United Kingdom
GR  - PDF-2013-06-055/Department of Health/United Kingdom
PT  - Journal Article
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20171120
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
SB  - IM
MH  - Age Factors
MH  - Aged
MH  - Amputation/*utilization
MH  - Diabetic Foot/complications/*therapy
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Mortality
MH  - Prognosis
MH  - Proportional Hazards Models
MH  - Prospective Studies
MH  - Recurrence
MH  - Time Factors
MH  - Vascular Surgical Procedures/*utilization
MH  - *Wound Healing
MH  - Wound Infection/complications/*therapy
PMC - PMC5765512
EDAT- 2017/10/31 06:00
MHDA- 2018/08/01 06:00
CRDT- 2017/10/31 06:00
PHST- 2017/10/25 00:00 [accepted]
PHST- 2017/10/31 06:00 [pubmed]
PHST- 2018/08/01 06:00 [medline]
PHST- 2017/10/31 06:00 [entrez]
AID - 10.1111/dme.13537 [doi]
PST - ppublish
SO  - Diabet Med. 2018 Jan;35(1):78-88. doi: 10.1111/dme.13537. Epub 2017 Nov 20.

PMID- 29078006
OWN - NLM
STAT- MEDLINE
DCOM- 20180731
LR  - 20180815
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 35
IP  - 1
DP  - 2018 Jan
TI  - Risk of prostate cancer across different racial/ethnic groups in men with
      diabetes: a retrospective cohort study.
PG  - 107-111
LID - 10.1111/dme.13536 [doi]
AB  - AIM: To examine the associations between prostate cancer, diabetes and
      race/ethnicity. METHODS: Using administrative data from British Columbia, Canada 
      for the period 1994 to 2012, we identified men aged >/=50 years with and without 
      diabetes. Validated surname algorithms identified men as Chinese, Indian or of
      other race/ethnicity. Multivariable Cox regression was used to estimate adjusted 
      risks of prostate cancer according to diabetes status and race/ethnicity.
      RESULTS: Our cohort of 160 566 men had a mean (sd) age of 64.7 (9.4) years and a 
      median of 9 years' follow-up. The incidence rates of prostate cancer among those 
      with and without diabetes were 177.4 (171.7-183.4) and 216.0 (209.7-222.5) per
      1000 person-years, respectively. The incidence among Chinese men was 120.9
      (109.2-133.1), among Indian men it was 144.1 (122.8-169.0) and in men of other
      ethnicity it was 204.8 (200.2-209.5). Diabetes was independently associated with 
      a lower risk of prostate cancer (adjusted hazard ratio 0.82, 95% CI 0.78-0.86),
      as was Chinese (adjusted hazard ratio 0.54, 95% CI 0.46,0.63) and Indian
      (adjusted hazard ratio 0.66, 95% CI 0.49,0.89) race/ethnicity; however, there was
      no statistically significant interaction between diabetes status and
      race/ethnicity (all P>0.1). CONCLUSION: Diabetes and Chinese and Indian
      race/ethnicity were each independently associated with a lower risk of prostate
      cancer.
CI  - (c) 2017 Diabetes UK.
FAU - Chen, C B
AU  - Chen CB
AUID- ORCID: 0000-0002-5862-8955
AD  - School of Public Health, University of Alberta, Edmonton, Alberta, Canada.
FAU - Eurich, D T
AU  - Eurich DT
AUID- ORCID: 0000-0003-2197-0463
AD  - School of Public Health, University of Alberta, Edmonton, Alberta, Canada.
FAU - Majumdar, S R
AU  - Majumdar SR
AD  - Department of Medicine, Faculty of Medicine and Dentistry, University of Alberta,
      Edmonton, Alberta, Canada.
FAU - Johnson, J A
AU  - Johnson JA
AUID- ORCID: 0000-0001-8290-2857
AD  - School of Public Health, University of Alberta, Edmonton, Alberta, Canada.
LA  - eng
PT  - Journal Article
DEP - 20171127
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
SB  - IM
MH  - Aged
MH  - Asian Continental Ancestry Group/*statistics & numerical data
MH  - British Columbia/epidemiology
MH  - Cohort Studies
MH  - Diabetes Mellitus/*epidemiology
MH  - Ethnic Groups/statistics & numerical data
MH  - European Continental Ancestry Group/*statistics & numerical data
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Proportional Hazards Models
MH  - Prostatic Neoplasms/epidemiology/*ethnology
MH  - Retrospective Studies
MH  - Risk Factors
EDAT- 2017/10/28 06:00
MHDA- 2018/08/01 06:00
CRDT- 2017/10/28 06:00
PHST- 2017/10/23 00:00 [accepted]
PHST- 2017/10/28 06:00 [pubmed]
PHST- 2018/08/01 06:00 [medline]
PHST- 2017/10/28 06:00 [entrez]
AID - 10.1111/dme.13536 [doi]
PST - ppublish
SO  - Diabet Med. 2018 Jan;35(1):107-111. doi: 10.1111/dme.13536. Epub 2017 Nov 27.

PMID- 29079703
OWN - NLM
STAT- MEDLINE
DCOM- 20180111
LR  - 20180512
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
VI  - 67
IP  - 1
DP  - 2018 Jan
TI  - Thioredoxin-1 Overexpression in the Ventromedial Nucleus of the Hypothalamus
      Preserves the Counterregulatory Response to Hypoglycemia During Type 1 Diabetes
      in Male Rats.
PG  - 120-130
LID - 10.2337/db17-0930 [doi]
AB  - We previously showed that the glutathione precursor, N-acetylcysteine (NAC),
      prevented hypoglycemia-associated autonomic failure (HAAF) and impaired
      activation of ventromedial hypothalamus (VMH) glucose-inhibited (GI) neurons by
      low glucose after recurrent hypoglycemia (RH) in nondiabetic rats. However, NAC
      does not normalize glucose sensing by VMH GI neurons when RH occurs during
      diabetes. We hypothesized that recruiting the thioredoxin (Trx) antioxidant
      defense system would prevent HAAF and normalize glucose sensing after RH in
      diabetes. To test this hypothesis, we overexpressed Trx-1 (cytosolic form of Trx)
      in the VMH of rats with streptozotocin (STZ)-induced type 1 diabetes. The
      counterregulatory response (CRR) to hypoglycemia in vivo and the activation of
      VMH GI neurons in low glucose using membrane potential sensitive dye in vitro was
      measured before and after RH. VMH Trx-1 overexpression normalized both the CRR
      and glucose sensing by VMH GI neurons in STZ rats. VMH Trx-1 overexpression also 
      lowered the insulin requirement to prevent severe hyperglycemia in STZ rats.
      However, like NAC, VMH Trx-1 overexpression did not prevent HAAF or normalize
      activation of VMH GI neurons by low glucose in STZ rats after RH. We conclude
      that preventing HAAF in type 1 diabetes may require the recruitment of both
      antioxidant systems.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Zhou, Chunxue
AU  - Zhou C
AD  - Department of Pharmacology, Physiology and Neurosciences, New Jersey Medical
      School, Rutgers University, Newark, NJ.
FAU - Routh, Vanessa H
AU  - Routh VH
AUID- ORCID: 0000-0003-3644-970X
AD  - Department of Pharmacology, Physiology and Neurosciences, New Jersey Medical
      School, Rutgers University, Newark, NJ routhvh@njms.rutgers.edu.
LA  - eng
GR  - R01 DK081538/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20171027
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Blood Glucose)
RN  - 52500-60-4 (Thioredoxins)
RN  - IY9XDZ35W2 (Glucose)
SB  - AIM
SB  - IM
MH  - Animals
MH  - Blood Glucose/metabolism
MH  - Diabetes Mellitus, Experimental/metabolism
MH  - Diabetes Mellitus, Type 1/genetics/*metabolism
MH  - Glucose/pharmacology
MH  - Hypoglycemia/*metabolism
MH  - Hypothalamus/*metabolism
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Real-Time Polymerase Chain Reaction
MH  - Thioredoxins/genetics/*metabolism
MH  - Ventromedial Hypothalamic Nucleus/drug effects/*metabolism
PMC - PMC5741147
EDAT- 2017/10/29 06:00
MHDA- 2018/01/13 06:00
CRDT- 2017/10/29 06:00
PMCR- 2019/01/01 00:00
PHST- 2017/08/09 00:00 [received]
PHST- 2017/10/23 00:00 [accepted]
PHST- 2019/01/01 00:00 [pmc-release]
PHST- 2017/10/29 06:00 [pubmed]
PHST- 2018/01/13 06:00 [medline]
PHST- 2017/10/29 06:00 [entrez]
AID - db17-0930 [pii]
AID - 10.2337/db17-0930 [doi]
PST - ppublish
SO  - Diabetes. 2018 Jan;67(1):120-130. doi: 10.2337/db17-0930. Epub 2017 Oct 27.

PMID- 29079702
OWN - NLM
STAT- MEDLINE
DCOM- 20180525
LR  - 20180525
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
VI  - 67
IP  - 3
DP  - 2018 Mar
TI  - Metallothionein Preserves Akt2 Activity and Cardiac Function via Inhibiting TRB3 
      in Diabetic Hearts.
PG  - 507-517
LID - 10.2337/db17-0219 [doi]
AB  - Cardiac insulin resistance is a key pathogenic factor for diabetic cardiomyopathy
      (DCM), but the mechanism remains largely unclear. We found that diabetic hearts
      exhibited decreased phosphorylation of total Akt and isoform Akt2 but not Akt1 in
      wild-type (WT) male FVB mice, which was accompanied by attenuation of Akt
      downstream glucose metabolic signal. All of these signal changes were not
      observed in metallothionein cardiac-specific transgenic (MT-TG) hearts.
      Furthermore, insulin-induced glucose metabolic signals were attenuated only in WT
      diabetic hearts. In addition, diabetic hearts exhibited increased Akt-negative
      regulator tribbles pseudokinase 3 (TRB3) expression only in WT mice, suggesting
      that MT may preserve Akt2 function via inhibiting TRB3. Moreover, MT prevented
      tert-butyl hydroperoxide (tBHP)-reduced insulin-stimulated Akt2 phosphorylation
      in MT-TG cardiomyocytes, which was abolished by specific silencing of Akt2.
      Specific silencing of TRB3 blocked tBHP inhibition of insulin-stimulated Akt2
      phosphorylation in WT cardiomyocytes, whereas overexpression of TRB3 in MT-TG
      cardiomyocytes and hearts abolished MT preservation of insulin-stimulated Akt2
      signals and MT prevention of DCM. Most importantly, supplementation of Zn to
      induce MT preserved cardiac Akt2 signals and prevented DCM. These results suggest
      that diabetes-inhibited cardiac Akt2 function via TRB3 upregulation leads to
      aberrant cardiac glucose metabolism. MT preservation of cardiac Akt2 function by 
      inhibition of TRB3 prevents DCM.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Gu, Junlian
AU  - Gu J
AD  - Chinese-American Research Institute for Diabetic Complications, School of
      Pharmaceutical Sciences and the First Affiliated Hospital at the Wenzhou Medical 
      University, Wenzhou, China.
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
FAU - Yan, Xiaoqing
AU  - Yan X
AD  - Chinese-American Research Institute for Diabetic Complications, School of
      Pharmaceutical Sciences and the First Affiliated Hospital at the Wenzhou Medical 
      University, Wenzhou, China.
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
FAU - Dai, Xiaozhen
AU  - Dai X
AD  - Chinese-American Research Institute for Diabetic Complications, School of
      Pharmaceutical Sciences and the First Affiliated Hospital at the Wenzhou Medical 
      University, Wenzhou, China.
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
AD  - School of Biomedicine, Chengdu Medical College, Chengdu, Sichuan, China.
FAU - Wang, Yuehui
AU  - Wang Y
AD  - Departments of Geriatrics, Cardiovascular Disorders and Cardiac Surgery, The
      First Hospital of Jilin University, Changchun, China.
FAU - Lin, Qian
AU  - Lin Q
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
AD  - Department of Pharmacology and Toxicology, University of Louisville, Louisville, 
      KY.
FAU - Xiao, Jian
AU  - Xiao J
AD  - Chinese-American Research Institute for Diabetic Complications, School of
      Pharmaceutical Sciences and the First Affiliated Hospital at the Wenzhou Medical 
      University, Wenzhou, China.
FAU - Zhou, Shanshan
AU  - Zhou S
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
AD  - Departments of Geriatrics, Cardiovascular Disorders and Cardiac Surgery, The
      First Hospital of Jilin University, Changchun, China.
FAU - Zhang, Jian
AU  - Zhang J
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
AD  - Departments of Geriatrics, Cardiovascular Disorders and Cardiac Surgery, The
      First Hospital of Jilin University, Changchun, China.
FAU - Wang, Kai
AU  - Wang K
AD  - Chinese-American Research Institute for Diabetic Complications, School of
      Pharmaceutical Sciences and the First Affiliated Hospital at the Wenzhou Medical 
      University, Wenzhou, China.
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
FAU - Zeng, Jun
AU  - Zeng J
AD  - Chinese-American Research Institute for Diabetic Complications, School of
      Pharmaceutical Sciences and the First Affiliated Hospital at the Wenzhou Medical 
      University, Wenzhou, China.
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
FAU - Xin, Ying
AU  - Xin Y
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
AD  - Key Laboratory of Pathobiology, Ministry of Education, Jilin University,
      Changchun, China.
FAU - Barati, Michelle T
AU  - Barati MT
AD  - Department of Medicine, University of Louisville, Louisville, KY.
FAU - Zhang, Chi
AU  - Zhang C
AD  - Chinese-American Research Institute for Diabetic Complications, School of
      Pharmaceutical Sciences and the First Affiliated Hospital at the Wenzhou Medical 
      University, Wenzhou, China.
FAU - Bai, Yang
AU  - Bai Y
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
AD  - Departments of Geriatrics, Cardiovascular Disorders and Cardiac Surgery, The
      First Hospital of Jilin University, Changchun, China.
FAU - Li, Yan
AU  - Li Y
AD  - Department of Surgery, University of Louisville, Louisville, KY.
FAU - Epstein, Paul N
AU  - Epstein PN
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
AD  - Department of Pharmacology and Toxicology, University of Louisville, Louisville, 
      KY.
AD  - Wendy L. Novak Diabetes Care Center, Louisville, KY.
FAU - Wintergerst, Kupper A
AU  - Wintergerst KA
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
AD  - Wendy L. Novak Diabetes Care Center, Louisville, KY.
AD  - Division of Endocrinology, Department of Pediatrics, University of Louisville,
      Louisville, KY.
FAU - Li, Xiaokun
AU  - Li X
AD  - Chinese-American Research Institute for Diabetic Complications, School of
      Pharmaceutical Sciences and the First Affiliated Hospital at the Wenzhou Medical 
      University, Wenzhou, China.
FAU - Tan, Yi
AU  - Tan Y
AUID- ORCID: 0000-0002-9798-6237
AD  - Chinese-American Research Institute for Diabetic Complications, School of
      Pharmaceutical Sciences and the First Affiliated Hospital at the Wenzhou Medical 
      University, Wenzhou, China yi.tan@louisville.edu.
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
AD  - Department of Pharmacology and Toxicology, University of Louisville, Louisville, 
      KY.
AD  - Wendy L. Novak Diabetes Care Center, Louisville, KY.
FAU - Cai, Lu
AU  - Cai L
AUID- ORCID: 0000-0003-3048-1135
AD  - Chinese-American Research Institute for Diabetic Complications, School of
      Pharmaceutical Sciences and the First Affiliated Hospital at the Wenzhou Medical 
      University, Wenzhou, China.
AD  - Children's Hospital Research Institute, Department of Pediatrics, University of
      Louisville, Louisville, KY.
AD  - Department of Pharmacology and Toxicology, University of Louisville, Louisville, 
      KY.
AD  - Wendy L. Novak Diabetes Care Center, Louisville, KY.
LA  - eng
GR  - R01 HL125877/HL/NHLBI NIH HHS/United States
GR  - UL1 TR000117/TR/NCATS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20171027
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Oxidants)
RN  - 0 (TRB3 protein, mouse)
RN  - 9038-94-2 (Metallothionein)
RN  - EC 2.7.11.1 (Akt2 protein, mouse)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - AIM
SB  - IM
MH  - Animals
MH  - Cell Cycle Proteins/antagonists & inhibitors/genetics/*metabolism
MH  - Cells, Cultured
MH  - Diabetes Mellitus, Type 1/drug therapy/*metabolism/pathology/physiopathology
MH  - Heart/drug effects/*physiopathology
MH  - Hypoglycemic Agents/pharmacology/therapeutic use
MH  - Insulin/pharmacology/therapeutic use
MH  - *Insulin Resistance
MH  - Lipopolysaccharides/toxicity
MH  - Male
MH  - Metallothionein/genetics/*metabolism
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Mice, Transgenic
MH  - Myocardium/enzymology/*metabolism/pathology
MH  - Myocytes, Cardiac/drug effects/metabolism/pathology
MH  - Organ Specificity
MH  - Oxidants/toxicity
MH  - Oxidative Stress/drug effects
MH  - Phosphorylation/drug effects
MH  - Protein Processing, Post-Translational/drug effects
MH  - Proto-Oncogene Proteins c-akt/antagonists & inhibitors/genetics/*metabolism
MH  - RNA Interference
PMC - PMC5828458
EDAT- 2017/10/29 06:00
MHDA- 2018/05/26 06:00
CRDT- 2017/10/29 06:00
PMCR- 2019/03/01 00:00
PHST- 2017/02/17 00:00 [received]
PHST- 2017/10/20 00:00 [accepted]
PHST- 2019/03/01 00:00 [pmc-release]
PHST- 2017/10/29 06:00 [pubmed]
PHST- 2018/05/26 06:00 [medline]
PHST- 2017/10/29 06:00 [entrez]
AID - db17-0219 [pii]
AID - 10.2337/db17-0219 [doi]
PST - ppublish
SO  - Diabetes. 2018 Mar;67(3):507-517. doi: 10.2337/db17-0219. Epub 2017 Oct 27.

PMID- 29074598
OWN - NLM
STAT- MEDLINE
DCOM- 20180111
LR  - 20180618
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
VI  - 67
IP  - 1
DP  - 2018 Jan
TI  - Deletion of the Akt/mTORC1 Repressor REDD1 Prevents Visual Dysfunction in a
      Rodent Model of Type 1 Diabetes.
PG  - 110-119
LID - 10.2337/db17-0728 [doi]
AB  - Diabetes-induced visual dysfunction is associated with significant neuroretinal
      cell death. The current study was designed to investigate the role of the Protein
      Regulated in Development and DNA Damage Response 1 (REDD1) in diabetes-induced
      retinal cell death and visual dysfunction. We recently demonstrated that REDD1
      protein expression was elevated in response to hyperglycemia in the retina of
      diabetic rodents. REDD1 is an important regulator of Akt and mammalian target of 
      rapamycin and as such plays a key role in neuronal function and survival. In R28 
      retinal cells in culture, hyperglycemic conditions enhanced REDD1 protein
      expression concomitant with caspase activation and cell death. By contrast, in
      REDD1-deficient R28 cells, neither hyperglycemic conditions nor the absence of
      insulin in culture medium were sufficient to promote cell death. In the retinas
      of streptozotocin-induced diabetic mice, retinal apoptosis was dramatically
      elevated compared with nondiabetic controls, whereas no difference was observed
      in diabetic and nondiabetic REDD1-deficient mice. Electroretinogram abnormalities
      observed in b-wave and oscillatory potentials of diabetic wild-type mice were
      also absent in REDD1-deficient mice. Moreover, diabetic wild-type mice exhibited 
      functional deficiencies in visual acuity and contrast sensitivity, whereas
      diabetic REDD1-deficient mice had no visual dysfunction. The results support a
      role for REDD1 in diabetes-induced retinal neurodegeneration.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Miller, William P
AU  - Miller WP
AD  - Department of Cellular and Molecular Physiology, Penn State College of Medicine, 
      Hershey, PA.
FAU - Yang, Chen
AU  - Yang C
AD  - Department of Cellular and Molecular Physiology, Penn State College of Medicine, 
      Hershey, PA.
FAU - Mihailescu, Maria L
AU  - Mihailescu ML
AD  - Department of Cellular and Molecular Physiology, Penn State College of Medicine, 
      Hershey, PA.
FAU - Moore, Joshua A
AU  - Moore JA
AD  - Department of Cellular and Molecular Physiology, Penn State College of Medicine, 
      Hershey, PA.
FAU - Dai, Weiwei
AU  - Dai W
AD  - Department of Cellular and Molecular Physiology, Penn State College of Medicine, 
      Hershey, PA.
FAU - Barber, Alistair J
AU  - Barber AJ
AD  - Department of Ophthalmology, Penn State College of Medicine, Hershey, PA.
FAU - Dennis, Michael D
AU  - Dennis MD
AUID- ORCID: 0000-0002-0645-6864
AD  - Department of Cellular and Molecular Physiology, Penn State College of Medicine, 
      Hershey, PA mdennis@psu.edu.
LA  - eng
GR  - K99 EY023612/EY/NEI NIH HHS/United States
GR  - R00 EY023612/EY/NEI NIH HHS/United States
GR  - MOP 86545/CIHR/Canada
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20171026
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Ddit4 protein, mouse)
RN  - 0 (Transcription Factors)
RN  - EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - AIM
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Cell Line
MH  - Diabetes Mellitus, Experimental/genetics/metabolism
MH  - Diabetes Mellitus, Type 1/genetics/*metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Male
MH  - Mechanistic Target of Rapamycin Complex 1/genetics/*metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Proto-Oncogene Proteins c-akt/genetics/*metabolism
MH  - Retina/metabolism/pathology
MH  - Transcription Factors/genetics/*metabolism
PMC - PMC5741149
EDAT- 2017/10/28 06:00
MHDA- 2018/01/13 06:00
CRDT- 2017/10/28 06:00
PMCR- 2019/01/01 00:00
PHST- 2017/06/22 00:00 [received]
PHST- 2017/10/20 00:00 [accepted]
PHST- 2019/01/01 00:00 [pmc-release]
PHST- 2017/10/28 06:00 [pubmed]
PHST- 2018/01/13 06:00 [medline]
PHST- 2017/10/28 06:00 [entrez]
AID - db17-0728 [pii]
AID - 10.2337/db17-0728 [doi]
PST - ppublish
SO  - Diabetes. 2018 Jan;67(1):110-119. doi: 10.2337/db17-0728. Epub 2017 Oct 26.

PMID- 29066600
OWN - NLM
STAT- MEDLINE
DCOM- 20180111
LR  - 20180512
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
VI  - 67
IP  - 1
DP  - 2018 Jan
TI  - Evidence That Differences in Fructosamine-3-Kinase Activity May Be Associated
      With the Glycation Gap in Human Diabetes.
PG  - 131-136
LID - 10.2337/db17-0441 [doi]
AB  - The phenomenon of a discrepancy between glycated hemoglobin levels and other
      indicators of average glycemia may be due to many factors but can be measured as 
      the glycation gap (GGap). This GGap is associated with differences in
      complications in patients with diabetes and may possibly be explained by
      dissimilarities in deglycation in turn leading to altered production of advanced 
      glycation end products (AGEs). We hypothesized that variations in the level of
      the deglycating enzyme fructosamine-3-kinase (FN3K) might be associated with the 
      GGap. We measured erythrocyte FN3K concentrations and enzyme activity in a
      population dichotomized for a large positive or negative GGap. FN3K protein was
      higher and we found a striking threefold greater activity (323%) at any given
      FN3K protein level in the erythrocytes of the negative-GGap group compared with
      the positive-GGap group. This was associated with lower AGE levels in the
      negative-GGap group (79%), lower proinflammatory adipokines
      (leptin-to-adiponectin ratio) (73%), and much lower prothrombotic PAI-1 levels
      (19%). We conclude that FN3K may play a key role in the GGap and thus diabetes
      complications such that FN3K may be a potential predictor of the risk of diabetes
      complications. Pharmacological modifications of its activity may provide a novel 
      approach to their prevention.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Dunmore, Simon J
AU  - Dunmore SJ
AUID- ORCID: 0000-0001-7227-5597
AD  - Diabetes Research Group, Academic Institute of Medicine, University of
      Wolverhampton, Wolverhampton, U.K. s.dunmore@wlv.ac.uk.
FAU - Al-Derawi, Amr S
AU  - Al-Derawi AS
AD  - Diabetes Research Group, Academic Institute of Medicine, University of
      Wolverhampton, Wolverhampton, U.K.
FAU - Nayak, Ananth U
AU  - Nayak AU
AD  - Department of Endocrinology and Diabetes, University Hospital of North Midlands
      NHS Trust, Stoke-on-Trent, U.K.
FAU - Narshi, Aruna
AU  - Narshi A
AD  - Diabetes Research Group, Academic Institute of Medicine, University of
      Wolverhampton, Wolverhampton, U.K.
FAU - Nevill, Alan M
AU  - Nevill AM
AD  - Faculty of Health, Education and Wellbeing, Institute of Sport, University of
      Wolverhampton, Walsall, U.K.
FAU - Hellwig, Anne
AU  - Hellwig A
AD  - Food Chemistry, Technische Universitat Dresden, Dresden, Germany.
FAU - Majebi, Andrew
AU  - Majebi A
AD  - Diabetes Research Group, Academic Institute of Medicine, University of
      Wolverhampton, Wolverhampton, U.K.
FAU - Kirkham, Paul
AU  - Kirkham P
AD  - Faculty of Science and Engineering, Department of Biomedical Science and
      Physiology, University of Wolverhampton, Wolverhampton, U.K.
FAU - Brown, James E
AU  - Brown JE
AD  - Aston Research Centre for Healthy Ageing, School of Life and Health Sciences,
      Aston University, Birmingham, U.K.
FAU - Singh, Baldev M
AU  - Singh BM
AD  - Diabetes Research Group, Academic Institute of Medicine, University of
      Wolverhampton, Wolverhampton, U.K.
AD  - Wolverhampton Diabetes Centre, New Cross Hospital, Royal Wolverhampton NHS Trust,
      Wolverhampton, U.K.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171024
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Adipokines)
RN  - 0 (Adiponectin)
RN  - 0 (Blood Glucose)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (Glycation End Products, Advanced)
RN  - 0 (Leptin)
RN  - 0 (Plasminogen Activator Inhibitor 1)
RN  - EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor))
RN  - EC 2.7.1.- (fructosamine-3-kinase)
SB  - AIM
SB  - IM
MH  - Adipokines/metabolism
MH  - Adiponectin/metabolism
MH  - Aged
MH  - Aged, 80 and over
MH  - Blood Glucose/metabolism
MH  - Diabetes Mellitus/*metabolism
MH  - Female
MH  - Glycated Hemoglobin A/metabolism
MH  - Glycation End Products, Advanced
MH  - Glycosylation
MH  - Humans
MH  - Leptin/metabolism
MH  - Male
MH  - Middle Aged
MH  - Phosphorylation
MH  - Phosphotransferases (Alcohol Group Acceptor)/genetics/*metabolism
MH  - Plasminogen Activator Inhibitor 1/metabolism
EDAT- 2017/10/27 06:00
MHDA- 2018/01/13 06:00
CRDT- 2017/10/26 06:00
PHST- 2017/04/13 00:00 [received]
PHST- 2017/10/17 00:00 [accepted]
PHST- 2017/10/27 06:00 [pubmed]
PHST- 2018/01/13 06:00 [medline]
PHST- 2017/10/26 06:00 [entrez]
AID - db17-0441 [pii]
AID - 10.2337/db17-0441 [doi]
PST - ppublish
SO  - Diabetes. 2018 Jan;67(1):131-136. doi: 10.2337/db17-0441. Epub 2017 Oct 24.

PMID- 29066598
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20180512
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
VI  - 67
IP  - 1
DP  - 2018 Jan
TI  - Erratum. Deletion of p66(Shc) Longevity Gene Protects Against Experimental
      Diabetic Glomerulopathy by Preventing Diabetes-Induced Oxidative Stress. Diabetes
      2006;55:1642-1650.
PG  - 165
LID - 10.2337/db18-er01a [doi]
FAU - Menini, Stefano
AU  - Menini S
FAU - Amadio, Lorena
AU  - Amadio L
FAU - Oddi, Giovanna
AU  - Oddi G
FAU - Ricci, Carlo
AU  - Ricci C
FAU - Pesce, Carlo
AU  - Pesce C
FAU - Pugliese, Francesco
AU  - Pugliese F
FAU - Giorgio, Marco
AU  - Giorgio M
FAU - Migliaccio, Enrica
AU  - Migliaccio E
FAU - Pelicci, PierGiuseppe
AU  - Pelicci P
FAU - Iacobini, Carla
AU  - Iacobini C
FAU - Pugliese, Giuseppe
AU  - Pugliese G
LA  - eng
PT  - Journal Article
PT  - Published Erratum
DEP - 20171024
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
EFR - Diabetes. 2006 Jun;55(6):1642-50. PMID: 16731826
PMC - PMC5741146
EDAT- 2017/10/27 06:00
MHDA- 2017/10/27 06:01
CRDT- 2017/10/26 06:00
PMCR- 2019/01/01 00:00
PHST- 2019/01/01 00:00 [pmc-release]
PHST- 2017/10/27 06:00 [pubmed]
PHST- 2017/10/27 06:01 [medline]
PHST- 2017/10/26 06:00 [entrez]
AID - db18-er01a [pii]
AID - 10.2337/db18-er01a [doi]
PST - ppublish
SO  - Diabetes. 2018 Jan;67(1):165. doi: 10.2337/db18-er01a. Epub 2017 Oct 24.

PMID- 29079715
OWN - NLM
STAT- MEDLINE
DCOM- 20180508
LR  - 20180519
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 41
IP  - 1
DP  - 2018 Jan
TI  - Changes in Albuminuria and the Risk of Major Clinical Outcomes in Diabetes:
      Results From ADVANCE-ON.
PG  - 163-170
LID - 10.2337/dc17-1467 [doi]
AB  - OBJECTIVE: To assess the association between 2-year changes in urine
      albumin-to-creatinine ratio (UACR) and the risk of clinical outcomes in type 2
      diabetes. RESEARCH DESIGN AND METHODS: We analyzed data from 8,766 participants
      in the Action in Diabetes and Vascular Disease: Preterax and Diamicron MR
      Controlled Evaluation Post-Trial Observational Study (ADVANCE-ON). Change in UACR
      was calculated from UACR measurements 2 years apart, classified into three
      groups: decrease in UACR of >/=30%, minor change, and increase in UACR of >/=30%.
      By analyzing changes from baseline UACR groups, categorized into thirds, we
      repeated these analyses accounting for regression to the mean (RtM). The primary 
      outcome was the composite of major macrovascular events, renal events, and
      all-cause mortality; secondary outcomes were these components. Cox regression
      models were used to estimate hazard ratios (HRs). RESULTS: Over a median
      follow-up of 7.7 years, 2,191 primary outcomes were observed. Increases in UACR
      over 2 years independently predicted a greater risk of the primary outcome (HR
      for >/=30% UACR increase vs. minor change: 1.26; 95% CI 1.13-1.41), whereas a
      decrease in UACR was not significantly associated with lower risk (HR 0.93; 95%
      CI 0.83-1.04). However, after allowing for RtM, the effect of "real" decrease in 
      UACR on the primary outcome was found to be significant (HR 0.84; 95% CI
      0.75-0.94), whereas the estimated effect on an increase was unchanged.
      CONCLUSIONS: Changes in UACR predicted changes in the risk of major clinical
      outcomes and mortality in type 2 diabetes, supporting the prognostic utility of
      monitoring albuminuria change over time.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Jun, Min
AU  - Jun M
AUID- ORCID: 0000-0003-1460-7535
AD  - The George Institute for Global Health, UNSW Sydney, Sydney, Australia.
FAU - Ohkuma, Toshiaki
AU  - Ohkuma T
AUID- ORCID: 0000-0001-5463-1631
AD  - The George Institute for Global Health, UNSW Sydney, Sydney, Australia.
FAU - Zoungas, Sophia
AU  - Zoungas S
AD  - The George Institute for Global Health, UNSW Sydney, Sydney, Australia.
AD  - School of Public Health and Preventive Medicine, Monash University, Melbourne,
      Australia.
FAU - Colagiuri, Stephen
AU  - Colagiuri S
AD  - Boden Institute of Obesity, Nutrition, Exercise and Eating Disorders, Sydney
      Medical School, University of Sydney, Sydney, Australia.
FAU - Mancia, Giuseppe
AU  - Mancia G
AD  - Istituto Auxologico Italiano, University of Milano-Bicocca, Milan, Italy.
FAU - Marre, Michel
AU  - Marre M
AD  - INSERM, UMR S1138, Centre de Recherche des Cordeliers, Paris, France.
AD  - Department of Diabetology, Endocrinology and Nutrition, Assistance
      Publique-Hopitaux de Paris, Bichat Hospital, DHU FIRE, Paris, France.
AD  - Universite Paris Diderot, Sorbonne Paris Cite, UFR de Medecine, Paris, France.
FAU - Matthews, David
AU  - Matthews D
AD  - Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford,
      Oxford, U.K.
FAU - Poulter, Neil
AU  - Poulter N
AD  - International Centre for Circulatory Health, Imperial College, London, U.K.
FAU - Williams, Bryan
AU  - Williams B
AD  - Institute of Cardiovascular Sciences, University College London (UCL) and
      National Institute of Health Research UCL Hospitals Biomedical Research Centre,
      London, U.K.
FAU - Rodgers, Anthony
AU  - Rodgers A
AD  - The George Institute for Global Health, UNSW Sydney, Sydney, Australia.
FAU - Perkovic, Vlado
AU  - Perkovic V
AD  - The George Institute for Global Health, UNSW Sydney, Sydney, Australia.
FAU - Chalmers, John
AU  - Chalmers J
AUID- ORCID: 0000-0002-9931-0580
AD  - The George Institute for Global Health, UNSW Sydney, Sydney, Australia
      chalmers@georgeinstitute.org.au.
FAU - Woodward, Mark
AU  - Woodward M
AD  - The George Institute for Global Health, UNSW Sydney, Sydney, Australia.
AD  - The George Institute for Global Health, University of Oxford, Oxford, U.K.
AD  - Department of Epidemiology, Johns Hopkins University, Baltimore, MD.
CN  - ADVANCE Collaborative Group
LA  - eng
PT  - Journal Article
PT  - Observational Study
PT  - Clinical Trial, Phase I
PT  - Research Support, Non-U.S. Gov't
DEP - 20171027
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - AYI8EX34EU (Creatinine)
SB  - IM
MH  - Aged
MH  - Albuminuria/*urine
MH  - Cardiovascular Diseases/*diagnosis/*urine
MH  - Cohort Studies
MH  - Creatinine/urine
MH  - Diabetes Mellitus, Type 2/*diagnosis/*urine
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Kidney
MH  - Male
MH  - Middle Aged
MH  - Prognosis
MH  - Proportional Hazards Models
MH  - Randomized Controlled Trials as Topic
MH  - Risk Factors
MH  - Urinalysis
EDAT- 2017/10/29 06:00
MHDA- 2018/05/09 06:00
CRDT- 2017/10/29 06:00
PHST- 2017/07/19 00:00 [received]
PHST- 2017/09/26 00:00 [accepted]
PHST- 2017/10/29 06:00 [pubmed]
PHST- 2018/05/09 06:00 [medline]
PHST- 2017/10/29 06:00 [entrez]
AID - dc17-1467 [pii]
AID - 10.2337/dc17-1467 [doi]
PST - ppublish
SO  - Diabetes Care. 2018 Jan;41(1):163-170. doi: 10.2337/dc17-1467. Epub 2017 Oct 27.

PMID- 29074816
OWN - NLM
STAT- MEDLINE
DCOM- 20180515
LR  - 20180519
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 41
IP  - 1
DP  - 2018 Jan
TI  - Prediction of Type 2 Diabetes by Hemoglobin A1c in Two Community-Based Cohorts.
PG  - 60-68
LID - 10.2337/dc17-0607 [doi]
AB  - OBJECTIVE: Hemoglobin A1c (HbA1c) can be used to assess type 2 diabetes (T2D)
      risk. We asked whether HbA1c was associated with T2D risk in four scenarios of
      clinical information availability: 1) HbA1c alone, 2) fasting laboratory tests,
      3) clinic data, and 4) fasting laboratory tests and clinic data. RESEARCH DESIGN 
      AND METHODS: We studied a prospective cohort of white (N = 11,244) and black (N =
      2,294) middle-aged participants without diabetes in the Framingham Heart Study
      and Atherosclerosis Risk in Communities study. Association of HbA1c with incident
      T2D (defined by medication use or fasting glucose [FG] >/=126 mg/dL) was
      evaluated in regression models adjusted for 1) age and sex (demographics); 2)
      demographics, FG, HDL, and triglycerides; 3) demographics, BMI, blood pressure,
      and T2D family history; or 4) all preceding covariates. We combined results from 
      cohort and race analyses by random-effects meta-analyses. Subsidiary analyses
      tested the association of HbA1c with developing T2D within 8 years or only after 
      8 years. RESULTS: Over 20 years, 3,315 individuals developed T2D. With adjustment
      for demographics, the odds of T2D increased fourfold for each percentage-unit
      increase in HbA1c. The odds ratio (OR) was 4.00 (95% CI 3.14, 5.10) for blacks
      and 4.73 (3.10, 7.21) for whites, resulting in a combined OR of 4.50 (3.35,
      6.03). After adjustment for fasting laboratory tests and clinic data, the
      combined OR was 2.68 (2.15, 3.34) over 20 years, 5.79 (2.51, 13.36) within 8
      years, and 2.23 (1.94, 2.57) after 8 years. CONCLUSIONS: HbA1c predicts T2D in
      different common scenarios and is useful for identifying individuals with
      elevated T2D risk in both the short- and long-term.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Leong, Aaron
AU  - Leong A
AUID- ORCID: 0000-0002-3248-9547
AD  - Division of General Internal Medicine, Massachusetts General Hospital, Boston,
      MA.
AD  - Harvard Medical School, Boston, MA.
FAU - Daya, Natalie
AU  - Daya N
AD  - Johns Hopkins Bloomberg School of Public Health, Baltimore, MD.
FAU - Porneala, Bianca
AU  - Porneala B
AD  - Division of General Internal Medicine, Massachusetts General Hospital, Boston,
      MA.
FAU - Devlin, James J
AU  - Devlin JJ
AD  - Quest Diagnostics, San Juan Capistrano, CA.
FAU - Shiffman, Dov
AU  - Shiffman D
AD  - Quest Diagnostics, San Juan Capistrano, CA.
FAU - McPhaul, Michael J
AU  - McPhaul MJ
AD  - Quest Diagnostics, San Juan Capistrano, CA.
FAU - Selvin, Elizabeth
AU  - Selvin E
AUID- ORCID: 0000-0001-6923-7151
AD  - Johns Hopkins Bloomberg School of Public Health, Baltimore, MD.
FAU - Meigs, James B
AU  - Meigs JB
AUID- ORCID: 0000-0002-2439-2657
AD  - Division of General Internal Medicine, Massachusetts General Hospital, Boston, MA
      jmeigs@mgh.harvard.edu.
AD  - Harvard Medical School, Boston, MA.
LA  - eng
GR  - HHSN268201100012C/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100009I/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100010C/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100008C/HL/NHLBI NIH HHS/United States
GR  - HHSN268201500001C/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100005G/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100008I/HL/NHLBI NIH HHS/United States
GR  - R01 DK089174/DK/NIDDK NIH HHS/United States
GR  - HHSN268201100007C/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100011I/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100011C/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100006C/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100005I/HL/NHLBI NIH HHS/United States
GR  - K24 DK106414/DK/NIDDK NIH HHS/United States
GR  - HHSN268201500001I/HL/NHLBI NIH HHS/United States
GR  - K24 DK080140/DK/NIDDK NIH HHS/United States
GR  - HHSN268201100009C/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100005C/HL/NHLBI NIH HHS/United States
GR  - N01HC25195/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100007I/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20171026
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - 0 (Blood Glucose)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (Triglycerides)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Adult
MH  - Blood Glucose/analysis
MH  - Blood Pressure
MH  - Body Mass Index
MH  - Cholesterol/blood
MH  - Diabetes Mellitus, Type 2/*blood/*diagnosis
MH  - Female
MH  - Follow-Up Studies
MH  - Glycated Hemoglobin A/*analysis
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Prospective Studies
MH  - Risk Factors
MH  - Triglycerides/blood
PMC - PMC5741154
EDAT- 2017/10/28 06:00
MHDA- 2018/05/16 06:00
CRDT- 2017/10/28 06:00
PMCR- 2019/01/01 00:00
PHST- 2017/03/26 00:00 [received]
PHST- 2017/09/23 00:00 [accepted]
PHST- 2019/01/01 00:00 [pmc-release]
PHST- 2017/10/28 06:00 [pubmed]
PHST- 2018/05/16 06:00 [medline]
PHST- 2017/10/28 06:00 [entrez]
AID - dc17-0607 [pii]
AID - 10.2337/dc17-0607 [doi]
PST - ppublish
SO  - Diabetes Care. 2018 Jan;41(1):60-68. doi: 10.2337/dc17-0607. Epub 2017 Oct 26.

PMID- 29074815
OWN - NLM
STAT- MEDLINE
DCOM- 20180508
LR  - 20180519
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 41
IP  - 1
DP  - 2018 Jan
TI  - Hyperbaric Oxygen Therapy in the Treatment of Ischemic Lower- Extremity Ulcers in
      Patients With Diabetes: Results of the DAMO2CLES Multicenter Randomized Clinical 
      Trial.
PG  - 112-119
LID - 10.2337/dc17-0654 [doi]
AB  - OBJECTIVE: Conflicting evidence exists on the effects of hyperbaric oxygen
      therapy (HBOT) in the treatment of chronic ischemic leg ulcers. The aim of this
      trial was to investigate whether additional HBOT would benefit patients with
      diabetes and ischemic leg ulcers. RESEARCH DESIGN AND METHODS: Patients with
      diabetes with an ischemic wound (n = 120) were randomized to standard care (SC)
      without or with HBOT (SC+HBOT). Primary outcomes were limb salvage and wound
      healing after 12 months, as well as time to wound healing. Other end points were 
      amputation-free survival (AFS) and mortality. RESULTS: Both groups contained 60
      patients. Limb salvage was achieved in 47 patients in the SC group vs. 53
      patients in the SC+HBOT group (risk difference [RD] 10% [95% CI -4 to 23]). After
      12 months, 28 index wounds were healed in the SC group vs. 30 in the SC+HBOT
      group (RD 3% [95% CI -14 to 21]). AFS was achieved in 41 patients in the SC group
      and 49 patients in the SC+HBOT group (RD 13% [95% CI -2 to 28]). In the SC+HBOT
      group, 21 patients (35%) were unable to complete the HBOT protocol as planned.
      Those who did had significantly fewer major amputations and higher AFS (RD for
      AFS 26% [95% CI 10-38]). CONCLUSIONS: Additional HBOT did not significantly
      improve complete wound healing or limb salvage in patients with diabetes and
      lower-limb ischemia.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Santema, Katrien T B
AU  - Santema KTB
AUID- ORCID: 0000-0002-3388-248X
AD  - Department of Surgery, Academic Medical Center, Amsterdam, the Netherlands.
FAU - Stoekenbroek, Robert M
AU  - Stoekenbroek RM
AD  - Department of Surgery, Academic Medical Center, Amsterdam, the Netherlands.
FAU - Koelemay, Mark J W
AU  - Koelemay MJW
AD  - Department of Surgery, Academic Medical Center, Amsterdam, the Netherlands.
FAU - Reekers, Jim A
AU  - Reekers JA
AD  - Department of Radiology, Academic Medical Center, Amsterdam, the Netherlands.
FAU - van Dortmont, Laura M C
AU  - van Dortmont LMC
AD  - Department of Surgery, Vlietland Hospital, Schiedam, the Netherlands.
FAU - Oomen, Arno
AU  - Oomen A
AD  - Department of Surgery, St. Anna Hospital, Geldrop, the Netherlands.
FAU - Smeets, Luuk
AU  - Smeets L
AD  - Department of Surgery, Rijnstate Hospital, Arnhem, the Netherlands.
FAU - Wever, Jan J
AU  - Wever JJ
AD  - Department of Surgery, Haga Hospital, Den Haag, the Netherlands.
FAU - Legemate, Dink A
AU  - Legemate DA
AD  - Department of Surgery, Academic Medical Center, Amsterdam, the Netherlands.
FAU - Ubbink, Dirk T
AU  - Ubbink DT
AD  - Department of Surgery, Academic Medical Center, Amsterdam, the Netherlands
      d.ubbink@amc.nl.
CN  - DAMO2CLES Study Group
LA  - eng
SI  - NTR/NTR3944
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
DEP - 20171026
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
SB  - IM
CIN - Diabetes Care. 2018 Apr;41(4):e60. PMID: 29559459
CIN - Diabetes Care. 2018 Apr;41(4):e61. PMID: 29559460
CIN - Diabetes Care. 2018 Apr;41(4):e62-e63. PMID: 29559461
CIN - Ann Transl Med. 2018 Jun;6(11):228. PMID: 30023391
MH  - Aged
MH  - Aged, 80 and over
MH  - Amputation
MH  - Body Mass Index
MH  - Diabetes Mellitus, Type 2/*therapy
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - *Hyperbaric Oxygenation
MH  - Ischemia/*therapy
MH  - *Limb Salvage
MH  - Male
MH  - Middle Aged
MH  - Sample Size
MH  - Treatment Outcome
MH  - Ulcer/*therapy
MH  - *Wound Healing
IR  - Reichart M
FIR - Reichart, M
IR  - Balm R
FIR - Balm, R
IR  - Bodegom ME
FIR - Bodegom, M E
IR  - van Wanroij JL
FIR - van Wanroij, J L
IR  - Ten Raa S
FIR - Ten Raa, S
IR  - Willems MC
FIR - Willems, M C
IR  - Klemm P
FIR - Klemm, P
IR  - de Valk FG
FIR - de Valk, F G
IR  - Wever JJ
FIR - Wever, J J
IR  - Hulst I
FIR - Hulst, I
IR  - de Mol van Otterloo JCA
FIR - de Mol van Otterloo, J C A
IR  - Lenselink EA
FIR - Lenselink, E A
IR  - Vos AWF
FIR - Vos, A W F
IR  - van Nieuwenhuizen RC
FIR - van Nieuwenhuizen, R C
IR  - Vahl AC
FIR - Vahl, A C
IR  - Smeets L
FIR - Smeets, L
IR  - Nio D
FIR - Nio, D
IR  - van den Heuvel JCH
FIR - van den Heuvel, J C H
IR  - Oomen A
FIR - Oomen, A
IR  - Swinkels J
FIR - Swinkels, J
IR  - Vriens PWHE
FIR - Vriens, P W H E
IR  - van Hees CPA
FIR - van Hees, C P A
IR  - van Brussel JP
FIR - van Brussel, J P
IR  - Koedam NA
FIR - Koedam, N A
IR  - Buijk S
FIR - Buijk, S
IR  - Lauwers P
FIR - Lauwers, P
IR  - van Dortmont LMC
FIR - van Dortmont, L M C
IR  - Nederhoed JH
FIR - Nederhoed, J H
IR  - Kievit JK
FIR - Kievit, J K
IR  - Wiersema AM
FIR - Wiersema, A M
IR  - Vierhout BP
FIR - Vierhout, B P
IR  - van Baal JG
FIR - van Baal, J G
IR  - van Hulst RA
FIR - van Hulst, R A
IR  - Groot R
FIR - Groot, R
IR  - Everts PAM
FIR - Everts, P A M
IR  - Raap RDB
FIR - Raap, R D Bol
IR  - Boonstra O
FIR - Boonstra, O
IR  - Monsieurs KG
FIR - Monsieurs, K G
IR  - Vellinga TPVR
FIR - Vellinga, T P van Rees
IR  - Zwinderman AH
FIR - Zwinderman, A H
IR  - Hamming JF
FIR - Hamming, J F
IR  - Peters EJG
FIR - Peters, E J G
EDAT- 2017/10/28 06:00
MHDA- 2018/05/09 06:00
CRDT- 2017/10/28 06:00
PHST- 2017/03/31 00:00 [received]
PHST- 2017/09/23 00:00 [accepted]
PHST- 2017/10/28 06:00 [pubmed]
PHST- 2018/05/09 06:00 [medline]
PHST- 2017/10/28 06:00 [entrez]
AID - dc17-0654 [pii]
AID - 10.2337/dc17-0654 [doi]
PST - ppublish
SO  - Diabetes Care. 2018 Jan;41(1):112-119. doi: 10.2337/dc17-0654. Epub 2017 Oct 26.

PMID- 29070577
OWN - NLM
STAT- MEDLINE
DCOM- 20180405
LR  - 20180426
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 40
IP  - 12
DP  - 2017 Dec
TI  - Improving the Clinical Value and Utility of CGM Systems: Issues and
      Recommendations: A Joint Statement of the European Association for the Study of
      Diabetes and the American Diabetes Association Diabetes Technology Working Group.
PG  - 1614-1621
LID - 10.2337/dci17-0043 [doi]
AB  - The first systems for continuous glucose monitoring (CGM) became available over
      15 years ago. Many then believed CGM would revolutionize the use of intensive
      insulin therapy in diabetes; however, progress toward that vision has been
      gradual. Although increasing, the proportion of individuals using CGM rather than
      conventional systems for self-monitoring of blood glucose on a daily basis is
      still low in most parts of the world. Barriers to uptake include cost,
      measurement reliability (particularly with earlier-generation systems), human
      factors issues, lack of a standardized format for displaying results, and
      uncertainty on how best to use CGM data to make therapeutic decisions. This
      Scientific Statement makes recommendations for systemic improvements in clinical 
      use and regulatory (pre- and postmarketing) handling of CGM devices. The aim is
      to improve safety and efficacy in order to support the advancement of the
      technology in achieving its potential to improve quality of life and health
      outcomes for more people with diabetes.
CI  - (c) 2017 by the American Diabetes Association and Springer-Verlag.
FAU - Petrie, John R
AU  - Petrie JR
AD  - Institute of Cardiovascular & Medical Sciences, University of Glasgow, Glasgow,
      U.K. john.petrie@glasgow.ac.uk.
FAU - Peters, Anne L
AU  - Peters AL
AD  - Keck School of Medicine of the University of Southern California, Los Angeles,
      CA.
FAU - Bergenstal, Richard M
AU  - Bergenstal RM
AD  - International Diabetes Center at Park Nicollet, Minneapolis, MN.
FAU - Holl, Reinhard W
AU  - Holl RW
AD  - Institute of Epidemiology and Medical Biometry, University of Ulm, Ulm, Germany.
FAU - Fleming, G Alexander
AU  - Fleming GA
AD  - Kinexum, Harpers Ferry, WV.
FAU - Heinemann, Lutz
AU  - Heinemann L
AD  - Science & Co, Dusseldorf, Germany.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20171025
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - 0 (Blood Glucose)
RN  - 0 (Insulin)
SB  - IM
MH  - Blood Glucose/metabolism
MH  - *Blood Glucose Self-Monitoring
MH  - Cost-Benefit Analysis
MH  - Diabetes Mellitus, Type 1/*drug therapy
MH  - Diabetes Mellitus, Type 2/*drug therapy
MH  - Europe
MH  - Humans
MH  - Insulin/therapeutic use
MH  - Insulin Infusion Systems
MH  - Meta-Analysis as Topic
MH  - Quality of Life
MH  - Randomized Controlled Trials as Topic
MH  - Reproducibility of Results
MH  - Societies, Medical
MH  - United States
EDAT- 2017/10/27 06:00
MHDA- 2018/04/06 06:00
CRDT- 2017/10/27 06:00
PHST- 2017/10/27 06:00 [pubmed]
PHST- 2018/04/06 06:00 [medline]
PHST- 2017/10/27 06:00 [entrez]
AID - dci17-0043 [pii]
AID - 10.2337/dci17-0043 [doi]
PST - ppublish
SO  - Diabetes Care. 2017 Dec;40(12):1614-1621. doi: 10.2337/dci17-0043. Epub 2017 Oct 
      25.

PMID- 29099931
OWN - NLM
STAT- MEDLINE
DCOM- 20180626
LR  - 20180626
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
VI  - 103
IP  - 1
DP  - 2018 Jan 1
TI  - Clinical Fractures Among Older Men With Diabetes Are Mediated by Diabetic
      Complications.
PG  - 281-287
LID - 10.1210/jc.2017-01593 [doi]
AB  - Introduction: Type 2 diabetes mellitus among older women has been associated with
      increased bone mineral density, but paradoxically with increased fracture risk.
      Findings among older men have varied, and potential mechanisms have not been
      fully elucidated. Methods: A retrospective study of male veterans 65 to 99 years 
      of age who received primary care in the Veterans Health Administration from 2000 
      to 2010, using administrative data from all 146 Veterans Health Administration
      medical centers linked to Centers for Medicare and Medicaid Services Medicare
      fee-for-service data. Potential mediating factors of the diabetes-associated risk
      were evaluated using negative binomial regression models with the outcomes of any
      clinical fracture and hip fracture. Results: Of 2,798,309 Veterans included in
      the cohort, 900,402 (32.3%) had a diagnosis of diabetes. After adjusting for age,
      race, ethnicity, body mass index, alcohol and tobacco use, rheumatoid arthritis, 
      and corticosteroid use, the risk of any clinical fracture associated with
      diabetes was 1.22 (95% confidence interval, 1.21 to 1.23) and that of hip
      fracture was 1.21 (95% confidence interval, 1.19 to 1.23). Significant mediating 
      factors included peripheral neuropathy, cardiovascular disease, and congestive
      heart failure, with 45.5% of the diabetes-associated fracture risk explained by
      these diagnoses. Conclusions: Older male Veterans with diabetes have a 22%
      increased risk of incident clinical fracture compared with those without. A
      significant portion of this risk is explained by diabetes-related comorbidities, 
      specifically peripheral neuropathy and congestive heart failure. Identification
      of these mediating factors suggests possible mechanisms, as well as potential
      interventions.
CI  - Copyright (c) 2017 Endocrine Society
FAU - Lee, Richard H
AU  - Lee RH
AD  - Duke University School of Medicine, Durham, North Carolina.
AD  - Durham Veterans Affairs Medical Center, Durham, North Carolina.
FAU - Sloane, Richard
AU  - Sloane R
AD  - Duke University School of Medicine, Durham, North Carolina.
AD  - Durham Veterans Affairs Medical Center, Durham, North Carolina.
FAU - Pieper, Carl
AU  - Pieper C
AD  - Duke University School of Medicine, Durham, North Carolina.
FAU - Lyles, Kenneth W
AU  - Lyles KW
AD  - Duke University School of Medicine, Durham, North Carolina.
AD  - Durham Veterans Affairs Medical Center, Durham, North Carolina.
FAU - Adler, Robert A
AU  - Adler RA
AD  - Hunter Holmes McGuire Veterans Affairs Medical Center, Richmond, Virginia.
AD  - Virginia Commonwealth University School of Medicine, Richmond, Virginia.
FAU - Van Houtven, Courtney
AU  - Van Houtven C
AD  - Duke University School of Medicine, Durham, North Carolina.
AD  - Durham Veterans Affairs Medical Center, Durham, North Carolina.
FAU - LaFleur, Joanne
AU  - LaFleur J
AD  - University of Utah, Salt Lake City, Utah.
AD  - Salt Lake City Veterans Affairs Medical Center, Salt Lake City, Utah.
FAU - Colon-Emeric, Cathleen
AU  - Colon-Emeric C
AD  - Duke University School of Medicine, Durham, North Carolina.
AD  - Durham Veterans Affairs Medical Center, Durham, North Carolina.
LA  - eng
GR  - K24 AG049077/AG/NIA NIH HHS/United States
GR  - P30 AG028716/AG/NIA NIH HHS/United States
GR  - R03 AG048119/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
SB  - AIM
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Bone Density
MH  - Cardiovascular Diseases/*etiology/pathology
MH  - Comorbidity
MH  - Diabetes Complications/*etiology/pathology
MH  - Diabetes Mellitus, Type 2/*complications/physiopathology
MH  - Diabetic Nephropathies/*etiology/pathology
MH  - Follow-Up Studies
MH  - Hip Fractures/*etiology/pathology
MH  - Humans
MH  - Male
MH  - Prognosis
MH  - Retrospective Studies
MH  - Risk Factors
MH  - United States
MH  - Veterans
PMC - PMC5761492
EDAT- 2017/11/04 06:00
MHDA- 2018/06/27 06:00
CRDT- 2017/11/04 06:00
PMCR- 2019/01/01 00:00
PHST- 2017/07/14 00:00 [received]
PHST- 2017/10/27 00:00 [accepted]
PHST- 2019/01/01 00:00 [pmc-release]
PHST- 2017/11/04 06:00 [pubmed]
PHST- 2018/06/27 06:00 [medline]
PHST- 2017/11/04 06:00 [entrez]
AID - 4584213 [pii]
AID - 10.1210/jc.2017-01593 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 2018 Jan 1;103(1):281-287. doi: 10.1210/jc.2017-01593.

PMID- 29095990
OWN - NLM
STAT- MEDLINE
DCOM- 20180525
LR  - 20180525
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
VI  - 103
IP  - 2
DP  - 2018 Feb 1
TI  - Reducing Cholesterol and Fat Intake Improves Glucose Tolerance by Enhancing beta 
      Cell Function in Nondiabetic Subjects.
PG  - 622-631
LID - 10.1210/jc.2017-02089 [doi]
AB  - Context: A diet low in cholesterol and fat is commonly recommended to prevent
      metabolic and cardiovascular diseases; however, its effect on glucose tolerance
      is largely unknown. Objective: We examined whether and by which mechanisms a
      chronic reduction of cholesterol and fat intake affects glucose tolerance in
      nondiabetic individuals, independently of weight changes. Design and
      Participants: In this crossover, randomized clinical trial, 30 healthy subjects, 
      including 15 with family history of type 2 diabetes (T2D) (T2D offspring),
      underwent a 75-g oral glucose tolerance test (OGTT) after two 14-day isocaloric
      high-cholesterol, high-fat (HChF) or low-cholesterol, and low-fat (LChF) diets.
      Main Outcome Measures: We evaluated changes in glucose tolerance, beta cell
      function, insulin clearance, and insulin sensitivity by modeling plasma glucose, 
      insulin, and C-peptide levels during the OGTT. Results: The shift from the HChF
      to the LChF diet was neutral on body weight but increased glucose tolerance (mean
      glucose -5%, P = 0.01) and three components of beta cell function: glucose
      sensitivity (+17%, P = 0.01), insulin secretion at fasting glucose (+20%, P =
      0.02), and potentiation (+19%, P = 0.03). The LChF diet improved insulin
      sensitivity (+7%, P = 0.048) only in T2D offspring, who tended to be more
      susceptible to the positive effect of the diet on glucose tolerance. Conclusions:
      A chronic and isocaloric decrease in dietary cholesterol and fat intake improves 
      glucose tolerance by diffusely ameliorating beta cell function in nondiabetic
      subjects. Individuals genetically predisposed to develop T2D tend to be more
      susceptible to the positive effect of this dietary intervention on glucose
      tolerance and insulin sensitivity.
CI  - Copyright (c) 2017 Endocrine Society
FAU - Trico, Domenico
AU  - Trico D
AD  - Department of Clinical and Experimental Medicine, University of Pisa, Pisa,
      Italy.
AD  - Institute of Life Sciences, Sant'Anna School of Advanced Studies, Pisa, Italy.
FAU - Trifiro, Silvia
AU  - Trifiro S
AD  - Department of Clinical and Experimental Medicine, University of Pisa, Pisa,
      Italy.
FAU - Mengozzi, Alessandro
AU  - Mengozzi A
AD  - Department of Clinical and Experimental Medicine, University of Pisa, Pisa,
      Italy.
FAU - Morgantini, Cecilia
AU  - Morgantini C
AD  - Department of Clinical and Experimental Medicine, University of Pisa, Pisa,
      Italy.
FAU - Baldi, Simona
AU  - Baldi S
AD  - Department of Clinical and Experimental Medicine, University of Pisa, Pisa,
      Italy.
FAU - Mari, Andrea
AU  - Mari A
AD  - Institute of Neuroscience, National Research Council, Padua, Italy.
FAU - Natali, Andrea
AU  - Natali A
AD  - Department of Clinical and Experimental Medicine, University of Pisa, Pisa,
      Italy.
LA  - eng
SI  - ClinicalTrials.gov/NCT02549144
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Blood Glucose)
RN  - 0 (Dietary Fats)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - AIM
SB  - IM
MH  - Adult
MH  - Blood Glucose/*metabolism
MH  - Child of Impaired Parents
MH  - Cholesterol/*administration & dosage
MH  - Cross-Over Studies
MH  - Diabetes Mellitus, Type 2
MH  - *Diet, Fat-Restricted
MH  - Dietary Fats/*administration & dosage
MH  - Female
MH  - Glucose Intolerance/*diet therapy/physiopathology/*prevention & control
MH  - Glucose Tolerance Test
MH  - Humans
MH  - Insulin Resistance
MH  - Insulin-Secreting Cells/*physiology
MH  - Male
MH  - Medical History Taking
MH  - Young Adult
EDAT- 2017/11/03 06:00
MHDA- 2018/05/26 06:00
CRDT- 2017/11/03 06:00
PHST- 2017/09/21 00:00 [received]
PHST- 2017/10/23 00:00 [accepted]
PHST- 2017/11/03 06:00 [pubmed]
PHST- 2018/05/26 06:00 [medline]
PHST- 2017/11/03 06:00 [entrez]
AID - 4583443 [pii]
AID - 10.1210/jc.2017-02089 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 2018 Feb 1;103(2):622-631. doi: 10.1210/jc.2017-02089.

PMID- 29092051
OWN - NLM
STAT- MEDLINE
DCOM- 20171214
LR  - 20180814
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
VI  - 102
IP  - 12
DP  - 2017 Dec 1
TI  - The Role of Age and Excess Body Mass Index in Progression to Type 1 Diabetes in
      At-Risk Adults.
PG  - 4596-4603
LID - 10.1210/jc.2017-01490 [doi]
AB  - Background: Given the global rise in both type 1 diabetes incidence and obesity, 
      the role of body mass index (BMI) on type 1 diabetes pathophysiology has gained
      great interest. Sustained excess BMI in pediatric participants of the TrialNet
      Pathway to Prevention (PTP) cohort increased risk for progression to type 1
      diabetes, but the effects of age and obesity in adults remain largely unknown.
      Objective: To determine the effect of age and sustained obesity on the risk for
      type 1 diabetes in adult participants in the TrialNet PTP cohort (i.e.,
      nondiabetic autoantibody-positive relatives of patients with type 1 diabetes).
      Research Design and Methods: Longitudinally accumulated BMI >25 kg/m2 was
      calculated to generate a cumulative excess BMI (ceBMI) for each participant, with
      ceBMI values >/=0 kg/m2 and >/=5 kg/m2 representing sustained overweight or obese
      status, respectively. Recursive partitioning analysis yielded sex- and
      age-specific thresholds for ceBMI that confer the greatest risk for type 1
      diabetes progression. Results: In this cohort of 665 adults (age 20 to 50 years; 
      median follow-up, 3.9 years), 49 participants developed type 1 diabetes. Age was 
      an independent protective factor for type 1 diabetes progression (hazard ratio,
      0.95; P = 0.008), with a threshold of >35 years that reduced risk for type 1
      diabetes. In men age >35 years and women age <35 years, sustained obesity (ceBMI 
      >/=5 kg/m2) increased the risk for type 1 diabetes. Conclusions: Age is an
      important factor for type 1 diabetes progression in adults and influences the
      impact of elevated BMI, indicating an interplay of excess weight, age, and sex in
      adult type 1 diabetes pathophysiology.
CI  - Copyright (c) 2017 Endocrine Society
FAU - Ferrara, Christine T
AU  - Ferrara CT
AD  - Department of Pediatric Endocrinology, University of California at San
      Francisco94143.
FAU - Geyer, Susan M
AU  - Geyer SM
AD  - Department of Informatics and Biostatistics, University of Southern Florida.
FAU - Evans-Molina, Carmella
AU  - Evans-Molina C
AD  - Department of Medicine, Indiana University School of Medicine.
FAU - Libman, Ingrid M
AU  - Libman IM
AD  - Department of Pediatric Endocrinology, Children's Hospital of Pittsburgh of UPMC.
FAU - Becker, Dorothy J
AU  - Becker DJ
AD  - Department of Pediatric Endocrinology, Children's Hospital of Pittsburgh of UPMC.
FAU - Wentworth, John M
AU  - Wentworth JM
AD  - Department of Medicine, Royal Melbourne Hospital, Australia.
FAU - Moran, Antoinette
AU  - Moran A
AD  - Department of Pediatric Endocrinology, University of Minnesota.
FAU - Gitelman, Stephen E
AU  - Gitelman SE
AD  - Department of Pediatric Endocrinology, University of California at San
      Francisco94143.
FAU - Redondo, Maria J
AU  - Redondo MJ
AD  - Section of Pediatric Endocrinology, Texas Children's Hospital.
CN  - Type 1 Diabetes TrialNet Study Group
LA  - eng
SI  - ClinicalTrials.gov/NCT00097292
GR  - U01 DK085476/DK/NIDDK NIH HHS/United States
GR  - U01 DK061010/DK/NIDDK NIH HHS/United States
GR  - U01 DK085466/DK/NIDDK NIH HHS/United States
GR  - U01 DK103153/DK/NIDDK NIH HHS/United States
GR  - U01 DK061058/DK/NIDDK NIH HHS/United States
GR  - U01 DK085505/DK/NIDDK NIH HHS/United States
GR  - U01 DK085453/DK/NIDDK NIH HHS/United States
GR  - I01 BX001733/BX/BLRD VA/United States
GR  - U01 DK085499/DK/NIDDK NIH HHS/United States
GR  - U01 DK085463/DK/NIDDK NIH HHS/United States
GR  - U01 DK103266/DK/NIDDK NIH HHS/United States
GR  - K12 DK094726/DK/NIDDK NIH HHS/United States
GR  - U01 DK107014/DK/NIDDK NIH HHS/United States
GR  - U01 DK061042/DK/NIDDK NIH HHS/United States
GR  - U01 DK061034/DK/NIDDK NIH HHS/United States
GR  - U01 DK085461/DK/NIDDK NIH HHS/United States
GR  - U01 DK085509/DK/NIDDK NIH HHS/United States
GR  - U01 DK103180/DK/NIDDK NIH HHS/United States
GR  - U01 DK085465/DK/NIDDK NIH HHS/United States
GR  - U01 DK085504/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Autoantibodies)
RN  - 0 (Insulin Antibodies)
SB  - AIM
SB  - IM
MH  - Adult
MH  - Aging/*pathology
MH  - Algorithms
MH  - Autoantibodies
MH  - Body Mass Index
MH  - Cohort Studies
MH  - Diabetes Mellitus, Type 1/*pathology
MH  - Disease Progression
MH  - Female
MH  - Humans
MH  - Insulin Antibodies/analysis
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Obesity/*pathology
MH  - Overweight/pathology
MH  - Risk Factors
MH  - Sex Characteristics
MH  - Socioeconomic Factors
MH  - Young Adult
PMC - PMC5718698
EDAT- 2017/11/02 06:00
MHDA- 2017/12/15 06:00
CRDT- 2017/11/02 06:00
PMCR- 2018/12/01 00:00
PHST- 2017/06/30 00:00 [received]
PHST- 2017/10/03 00:00 [accepted]
PHST- 2018/12/01 00:00 [pmc-release]
PHST- 2017/11/02 06:00 [pubmed]
PHST- 2017/12/15 06:00 [medline]
PHST- 2017/11/02 06:00 [entrez]
AID - 4349677 [pii]
AID - 10.1210/jc.2017-01490 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 2017 Dec 1;102(12):4596-4603. doi:
      10.1210/jc.2017-01490.

PMID- 29077935
OWN - NLM
STAT- MEDLINE
DCOM- 20180604
LR  - 20180604
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
VI  - 103
IP  - 2
DP  - 2018 Feb 1
TI  - Glycation Reduces the Stability of ApoAI and Increases HDL Dysfunction in
      Diet-Controlled Type 2 Diabetes.
PG  - 388-396
LID - 10.1210/jc.2017-01551 [doi]
AB  - Context: Hyperglycemia plays a key role in the pathogenesis of cardiovascular
      complications of diabetes. Type 2 diabetes mellitus (T2DM) is associated with
      high-density lipoprotein (HDL) dysfunction and increased degradation of
      apolipoprotein I (ApoAI). The mechanism(s) of these changes is largely unknown.
      Objective: To study the role of hyperglycemia-induced glycation on ApoAI kinetics
      and stability in patients with diet-controlled T2DM. Design: 2H2O-metabolic
      labeling approach was used to study ApoAI turnover in patients with
      diet-controlled T2DM [n = 9 (5 F); 59.3 +/- 8.5 years] and matched healthy
      controls [n = 8 (4 F); 50.7 +/- 11.6 years]. The effect of Amadori glycation on
      in vivo ApoAI stability and the antioxidant and cholesterol efflux properties of 
      HDL were assessed using a proteomics approach and in vitro assays. Results:
      Patients with T2DM had increased turnover of ApoAI and impaired cholesterol
      efflux and antioxidant properties of HDL. Glycated hemoglobin was negatively
      correlated with the half-life of ApoAI and cholesterol efflux function of HDL.
      Proteomics analysis identified several nonenzymatic early (Amadori) glycations of
      ApoAI at lysine sites. The kinetics analysis of glycated and native ApoAI
      peptides in patients with T2DM revealed that glycation resulted in a threefold
      shorter ApoAI half-life. Conclusions: The 2H2O method allowed the detection of
      early in vivo impairments in HDL metabolism and function that were related to
      hyperglycemia-induced glycation of ApoAI in T2DM.
CI  - Copyright (c) 2017 Endocrine Society
FAU - Kashyap, Sangeeta R
AU  - Kashyap SR
AD  - Department of Endocrinology and Metabolism, Cleveland Clinic, Cleveland, Ohio.
FAU - Osme, Abdullah
AU  - Osme A
AD  - Department of Pharmaceutical Sciences, Northeast Ohio Medical University,
      Rootstown, Ohio.
FAU - Ilchenko, Serguei
AU  - Ilchenko S
AD  - Department of Pharmaceutical Sciences, Northeast Ohio Medical University,
      Rootstown, Ohio.
FAU - Golizeh, Makan
AU  - Golizeh M
AD  - Department of Pharmaceutical Sciences, Northeast Ohio Medical University,
      Rootstown, Ohio.
FAU - Lee, Kwangwon
AU  - Lee K
AD  - Department of Pharmaceutical Sciences, Northeast Ohio Medical University,
      Rootstown, Ohio.
FAU - Wang, Shuhui
AU  - Wang S
AD  - Department of Cellular & Molecular Medicine, Cleveland Clinic, Cleveland, Ohio.
FAU - Bena, James
AU  - Bena J
AD  - Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, Ohio.
FAU - Previs, Stephen F
AU  - Previs SF
AD  - Merck Research Laboratories, Kenilworth, New Jersey.
FAU - Smith, Jonathan D
AU  - Smith JD
AD  - Department of Cellular & Molecular Medicine, Cleveland Clinic, Cleveland, Ohio.
FAU - Kasumov, Takhar
AU  - Kasumov T
AD  - Department of Pharmaceutical Sciences, Northeast Ohio Medical University,
      Rootstown, Ohio.
AD  - Department of Hepatology, Cleveland Clinic, Cleveland, Ohio.
LA  - eng
GR  - R01 GM112044/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Apolipoprotein A-I)
RN  - 0 (Lipoproteins, HDL)
SB  - AIM
SB  - IM
MH  - Adult
MH  - Aged
MH  - Animals
MH  - Apolipoprotein A-I/blood/*metabolism
MH  - Case-Control Studies
MH  - Cells, Cultured
MH  - Diabetes Mellitus, Type 2/complications/*diet therapy/metabolism
MH  - Diet
MH  - Dyslipidemias/complications/diet therapy/*metabolism
MH  - Female
MH  - Glycosylation
MH  - Humans
MH  - Hyperglycemia/complications/diet therapy/*metabolism
MH  - Lipoproteins, HDL/*metabolism
MH  - Male
MH  - Mice
MH  - Middle Aged
MH  - Protein Stability
PMC - PMC5800833
EDAT- 2017/10/28 06:00
MHDA- 2018/06/05 06:00
CRDT- 2017/10/28 06:00
PMCR- 2019/02/01 00:00
PHST- 2017/07/14 00:00 [received]
PHST- 2017/10/20 00:00 [accepted]
PHST- 2019/02/01 00:00 [pmc-release]
PHST- 2017/10/28 06:00 [pubmed]
PHST- 2018/06/05 06:00 [medline]
PHST- 2017/10/28 06:00 [entrez]
AID - 4565491 [pii]
AID - 10.1210/jc.2017-01551 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 2018 Feb 1;103(2):388-396. doi: 10.1210/jc.2017-01551.

PMID- 29082873
OWN - NLM
STAT- MEDLINE
DCOM- 20180917
LR  - 20180917
IS  - 1474-547X (Electronic)
IS  - 0140-6736 (Linking)
VI  - 390
IP  - 10105
DP  - 2017 Oct 21
TI  - Type 2 diabetes in youth is a disease of poverty.
PG  - 1829
LID - S0140-6736(17)32461-3 [pii]
LID - 10.1016/S0140-6736(17)32461-3 [doi]
FAU - McGavock, Jonathan
AU  - McGavock J
AD  - Department of Pediatrics and Child Health, Rady Faculty of Health Sciences,
      Children's Hospital Research Institute of Manitoba, University of Manitoba,
      Winnipeg, MB R3E 3P4, Canada. Electronic address: jmcgavock@chrim.ca.
FAU - Wicklow, Brandy
AU  - Wicklow B
AD  - Department of Pediatrics and Child Health, Rady Faculty of Health Sciences,
      Children's Hospital Research Institute of Manitoba, University of Manitoba,
      Winnipeg, MB R3E 3P4, Canada.
FAU - Dart, Allison B
AU  - Dart AB
AD  - Department of Pediatrics and Child Health, Rady Faculty of Health Sciences,
      Children's Hospital Research Institute of Manitoba, University of Manitoba,
      Winnipeg, MB R3E 3P4, Canada.
LA  - eng
PT  - Letter
PT  - Comment
DEP - 20171019
PL  - England
TA  - Lancet
JT  - Lancet (London, England)
JID - 2985213R
SB  - AIM
SB  - IM
CON - Lancet. 2017 Jun 3;389(10085):2252-2260. PMID: 28589895
MH  - Adolescent
MH  - *Diabetes Mellitus, Type 2
MH  - Humans
MH  - *Poverty
EDAT- 2017/10/31 06:00
MHDA- 2018/09/18 06:00
CRDT- 2017/10/31 06:00
PHST- 2017/08/15 00:00 [received]
PHST- 2017/09/05 00:00 [accepted]
PHST- 2017/10/31 06:00 [entrez]
PHST- 2017/10/31 06:00 [pubmed]
PHST- 2018/09/18 06:00 [medline]
AID - S0140-6736(17)32461-3 [pii]
AID - 10.1016/S0140-6736(17)32461-3 [doi]
PST - ppublish
SO  - Lancet. 2017 Oct 21;390(10105):1829. doi: 10.1016/S0140-6736(17)32461-3. Epub
      2017 Oct 19.

PMID- 29091568
OWN - NLM
STAT- MEDLINE
DCOM- 20171109
LR  - 20180504
IS  - 1533-4406 (Electronic)
IS  - 0028-4793 (Linking)
VI  - 377
IP  - 18
DP  - 2017 Nov 2
TI  - ACE Inhibitors and Statins in Adolescents with Type 1 Diabetes.
PG  - 1733-1745
LID - 10.1056/NEJMoa1703518 [doi]
AB  - BACKGROUND: Among adolescents with type 1 diabetes, rapid increases in albumin
      excretion during puberty precede the development of microalbuminuria and
      macroalbuminuria, long-term risk factors for renal and cardiovascular disease. We
      hypothesized that adolescents with high levels of albumin excretion might benefit
      from angiotensin-converting-enzyme (ACE) inhibitors and statins, drugs that have 
      not been fully evaluated in adolescents. METHODS: We screened 4407 adolescents
      with type 1 diabetes between the ages of 10 and 16 years of age and identified
      1287 with values in the upper third of the albumin-to-creatinine ratios; 443 were
      randomly assigned in a placebo-controlled trial of an ACE inhibitor and a statin 
      with the use of a 2-by-2 factorial design minimizing differences in baseline
      characteristics such as age, sex, and duration of diabetes. The primary outcome
      for both interventions was the change in albumin excretion, assessed according to
      the albumin-to-creatinine ratio calculated from three early-morning urine samples
      obtained every 6 months over 2 to 4 years, and expressed as the area under the
      curve. Key secondary outcomes included the development of microalbuminuria,
      progression of retinopathy, changes in the glomerular filtration rate, lipid
      levels, and measures of cardiovascular risk (carotid intima-media thickness and
      levels of high-sensitivity C-reactive protein and asymmetric dimethylarginine).
      RESULTS: The primary outcome was not affected by ACE inhibitor therapy, statin
      therapy, or the combination of the two. The use of an ACE inhibitor was
      associated with a lower incidence of microalbuminuria than the use of placebo; in
      the context of negative findings for the primary outcome and statistical analysis
      plan, this lower incidence was not considered significant (hazard ratio, 0.57;
      95% confidence interval, 0.35 to 0.94). Statin use resulted in significant
      reductions in total, low-density lipoprotein, and non-high-density lipoprotein
      cholesterol levels, in triglyceride levels, and in the ratio of apolipoprotein B 
      to apolipoprotein A1, whereas neither drug had significant effects on carotid
      intima-media thickness, other cardiovascular markers, the glomerular filtration
      rate, or progression of retinopathy. Overall adherence to the drug regimen was
      75%, and serious adverse events were similar across the groups. CONCLUSIONS: The 
      use of an ACE inhibitor and a statin did not change the albumin-to-creatinine
      ratio over time. (Funded by the Juvenile Diabetes Research Foundation and others;
      AdDIT ClinicalTrials.gov number, NCT01581476 .).
FAU - Marcovecchio, M Loredana
AU  - Marcovecchio ML
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Chiesa, Scott T
AU  - Chiesa ST
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Bond, Simon
AU  - Bond S
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Daneman, Denis
AU  - Daneman D
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Dawson, Sarah
AU  - Dawson S
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Donaghue, Kim C
AU  - Donaghue KC
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Jones, Timothy W
AU  - Jones TW
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Mahmud, Farid H
AU  - Mahmud FH
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Marshall, Sally M
AU  - Marshall SM
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Neil, H Andrew W
AU  - Neil HAW
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Dalton, R Neil
AU  - Dalton RN
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Deanfield, John
AU  - Deanfield J
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
FAU - Dunger, David B
AU  - Dunger DB
AD  - From the Department of Paediatrics (M.L.M., D.B.D.) and the Wellcome
      Trust-Medical Research Council Institute of Metabolic Science (D.B.D.),
      University of Cambridge, and the Cambridge Clinical Trials Unit, Cambridge
      University Hospitals NHS Foundation Trust, Addenbrooke's Hospital (S.B., S.D.),
      Cambridge, the National Centre for Cardiovascular Prevention and Outcomes,
      University College London (S.T.C., J.D.), and the WellChild Laboratory, Evelina
      London Children's Hospital, St. Thomas' Hospital (R.N.D.), London, the Institute 
      of Cellular Medicine (Diabetes), Faculty of Clinical Medical Sciences, Newcastle 
      University, Newcastle upon Tyne (S.M.M.), and the Oxford Centre for Diabetes,
      Endocrinology and Metabolism, University of Oxford, Oxford (H.A.W.N.) - all in
      the United Kingdom; the Department of Paediatrics, Hospital for Sick Children and
      University of Toronto, Toronto (D.D., F.H.M.); and the Institute of Endocrinology
      and Diabetes, Children's Hospital at Westmead and University of Sydney, Sydney
      (K.C.D.), and the Telethon Kids Institute, University of Western Australia, Perth
      (T.W.J.) - both in Australia.
CN  - AdDIT Study Group
LA  - eng
SI  - ClinicalTrials.gov/NCT01581476
SI  - ClinicalTrials.gov/NCT01581476
GR  - G0600717/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
PL  - United States
TA  - N Engl J Med
JT  - The New England journal of medicine
JID - 0255562
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Lipids)
RN  - AYI8EX34EU (Creatinine)
SB  - AIM
SB  - IM
CIN - N Engl J Med. 2018 Feb 08;378(6):579. PMID: 29419269
CIN - N Engl J Med. 2018 Feb 08;378(6):579. PMID: 29419270
CIN - N Engl J Med. 2018 Feb 08;378(6):580. PMID: 29419271
CIN - Ann Transl Med. 2018 May;6(10):193. PMID: 29951515
MH  - Adolescent
MH  - Albuminuria/etiology/*prevention & control
MH  - Angiotensin-Converting Enzyme Inhibitors/adverse effects/*therapeutic use
MH  - Area Under Curve
MH  - Child
MH  - Creatinine/*urine
MH  - Diabetes Mellitus, Type 1/blood/complications/*drug therapy/urine
MH  - Double-Blind Method
MH  - Drug Therapy, Combination
MH  - Female
MH  - Humans
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects/*therapeutic use
MH  - Lipids/blood
MH  - Male
MH  - Medication Adherence
IR  - Acerini C
FIR - Acerini, Carlo
IR  - Ackland F
FIR - Ackland, Francis
IR  - Smith A
FIR - Smith, Anne
IR  - Anand B
FIR - Anand, Binu
IR  - Barrett T
FIR - Barrett, Tim
IR  - Birrell V
FIR - Birrell, Virginia
IR  - Campbell F
FIR - Campbell, Fiona
IR  - Cheetham T
FIR - Cheetham, Tim
IR  - Cooper C
FIR - Cooper, Chris
IR  - Doughty I
FIR - Doughty, Ian
IR  - Dutta A
FIR - Dutta, Atanu
IR  - Edge J
FIR - Edge, Julie
IR  - Hamilton-Shield J
FIR - Hamilton-Shield, Julian
IR  - Gray A
FIR - Gray, Alastair
IR  - Mann N
FIR - Mann, Nick
IR  - Yaliwal C
FIR - Yaliwal, Chandan
IR  - Rayman G
FIR - Rayman, Gerry
IR  - Robinson M
FIR - Robinson, Mark
IR  - Russell-Taylor M
FIR - Russell-Taylor, Michelle
IR  - Sankar V
FIR - Sankar, Vengudi
IR  - Thalange N
FIR - Thalange, Nandu
IR  - Charakida M
FIR - Charakida, Marietta
IR  - Bergman P
FIR - Bergman, Phil
IR  - Rodda C
FIR - Rodda, Christine
IR  - Cameron F
FIR - Cameron, Fergus
IR  - Cotterill A
FIR - Cotterill, Andrew
IR  - Couper J
FIR - Couper, Jennifer
IR  - Davis E
FIR - Davis, Elizabeth
IR  - Craig M
FIR - Craig, Maria
IR  - King B
FIR - King, Bruce
IR  - Verge C
FIR - Verge, Charles
IR  - Benitez-Aguirre P
FIR - Benitez-Aguirre, Paul
IR  - Wong T
FIR - Wong, Tien
IR  - Cusumano J
FIR - Cusumano, Janine
IR  - Clarson C
FIR - Clarson, Cheril
IR  - Curtis J
FIR - Curtis, Jacqueline
IR  - Sochett E
FIR - Sochett, Etienne
IR  - Armitage J
FIR - Armitage, Jane
IR  - Bingley P
FIR - Bingley, Polly
IR  - Van't Hoff W
FIR - Van't Hoff, William
IR  - Baigent C
FIR - Baigent, Colin
IR  - Emberson J
FIR - Emberson, Jon
IR  - Flather M
FIR - Flather, Marcus
IR  - Bilous R
FIR - Bilous, Rudy
EDAT- 2017/11/02 06:00
MHDA- 2017/11/10 06:00
CRDT- 2017/11/02 06:00
PHST- 2017/11/02 06:00 [entrez]
PHST- 2017/11/02 06:00 [pubmed]
PHST- 2017/11/10 06:00 [medline]
AID - 10.1056/NEJMoa1703518 [doi]
PST - ppublish
SO  - N Engl J Med. 2017 Nov 2;377(18):1733-1745. doi: 10.1056/NEJMoa1703518.