bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation, Function, and Dysregulation of Endocannabinoids in Models of Adipose and β-Pancreatic Cells and in Obesity and Hyperglycemia
Authors: Matias Isabel , Gonthier Marie-Paule , Orlando Pierangelo , Martiadis Vassilis , De Petrocellis Luciano , Cervino Cristina , Petrosino Stefania , Hoareau Laurence , Festy Franck , Pasquali Renato , Roche Regis , Maj Mario , Pagotto Uberto , Monteleone Palmiero , Di Marzo Vincenzo 
Published: May 2006

Abstract
Context: Cannabinoid CB1 receptor blockade decreases weight and hyperinsulinemia in obese animals and humans in a way greatly independent from food intake.
Objective: The objective of this study was to investigate the regulation and function of the endocannabinoid system in adipocytes and pancreatic β-cells.
Design, Setting, and Patients: Mouse 3T3-F442A adipocytes and rat insulinoma RIN-m5F β-cells, pancreas and fat from mice with diet-induced obesity, visceral and sc fat from patients with body mass index equal to or greater than 30 kg/m2, and serum from normoglycemic and type 2 diabetes patients were studied.
Main Outcome Measure: Endocannabinoid enzyme and adipocyte protein expression, and endocannabinoid and insulin levels were measured.
Results: Endocannabinoids are present in adipocytes with levels peaking before differentiation, and in RIN-m5F β-cells, where they are under the negative control of insulin. Chronic treatment of adipocytes with insulin is accompanied by permanently elevated endocannabinoid signaling, whereas culturing of RIN-m5F β-cells in high glucose transforms insulin down-regulation of endocannabinoid levels into up-regulation. Epididymal fat and pancreas from mice with diet-induced obesity contain higher endocannabinoid levels than lean mice. Patients with obesity or hyperglycemia caused by type 2 diabetes exhibit higher concentrations of endocannabinoids in visceral fat or serum, respectively, than the corresponding controls. CB1 receptor stimulation increases lipid droplets and decreases adiponectin expression in adipocytes, and it increases intracellular calcium and insulin release in RIN-m5F β-cells kept in high glucose.
Conclusions: Peripheral endocannabinoid overactivity might explain why CB1 blockers cause weight-loss independent reduction of lipogenesis, of hypoadiponectinemia, and of hyperinsulinemia in obese animals and humans.
Diabetes Reporting as a Cause of Death
Authors: McEwen Laura N. , Kim Catherine , Haan Mary , Ghosh Debashis , Lantz Paula M. , Mangione Carol M. , Safford Monika M. , Marrero David , Thompson Theodore J. , Herman William H. ,   the TRIAD Study Group*
Published: May 2006

OBJECTIVE—To determine the frequency of reporting of diabetes on death certificates of decedents with known diabetes, define factors associated with reporting of diabetes, and describe trends in reporting over time.
RESEARCH DESIGN AND METHODS—Data were obtained from 11,927 participants with diabetes who were enrolled in the Translating Research Into Action for Diabetes study, a multicenter prospective observational study of diabetes care in managed care. Data on decedents (n = 540) were obtained from the National Death Index. The primary dependent variable was the presence of ICD-10 codes for diabetes on the death certificate. Covariates included age at death, sex, race/ethnicity, education, income, duration of diabetes, type of diabetes, diabetes treatment, smoking status, and number of comorbidities.
RESULTS—Diabetes was recorded on 39% of death certificates and as the underlying cause of death for 10% of decedents with diabetes. Diabetes was significantly less likely to be reported on the death certificates of decedents with diabetes dying of cancer. Predictors of recording diabetes anywhere on the death certificate included longer duration of diabetes and insulin treatment. Longer duration of diabetes, insulin treatment, and fewer comorbidities were associated with recording of diabetes as the underlying cause of death.
CONCLUSIONS—Diabetes is much more likely to be reported on the death certificates of diabetic individuals who die of cardiovascular causes. Reporting of diabetes on death certificates has been stable over time. Death certificates underestimate the prevalence of diabetes among decedents and present a biased picture of the causes of death among people with diabetes.
Depression Treatment and Satisfaction in a Multicultural Sample of Type 1 and Type 2 Diabetic Patients
Authors: de Groot Mary , Pinkerman Brenda , Wagner Julie , Hockman Erin 
Published: May 2006

OBJECTIVE—To assess rates of depressive symptoms, depression treatment, and satisfaction in a multicultural sample of individuals with type 1 and type 2 diabetes.
RESEARCH DESIGN AND METHODS—This study was conducted with a cross-sectional community-based survey design.
RESULTS—The sample (n = 221) was predominantly female (60.3%), had type 2 diabetes (75%), and was middle class with a mean (±SD) age of 54 ± 12 years. A total of 53% were white. Depressive symptoms were assessed using the Center for Epidemiologic Studies Depression Scale (CESD) (mean 16.4 ± 11.3). Using conservative thresholds (CESD score ≥22), 25.3% of participants reported clinically significant depression. Rates of depression did not differ by ethnic group or diabetes type. The majority (76%) of depressed participants reported treatment (52% antidepressants, 63% mental health providers, 19% alternative healers, and 15% herbal remedies). African Americans were less likely to report any depression treatment, to receive antidepressant medications, or receive treatment from a mental health professional compared with whites. Participants with high depressive symptoms reported general satisfaction with depression treatment experiences.
CONCLUSIONS—High rates of depressive symptoms were observed across ethnic groups, yet significant differences in use of depression treatment existed across ethnic groups. Those seeking depression treatment reported satisfaction with a variety of depression treatment modalities. Increased depression screening and treatment may be beneficial for ethnically diverse patients with type 1 and type 2 diabetes.
Efficacy of Benfluorex in Combination With Sulfonylurea in Type 2 Diabetic Patients
Authors: Moulin Philippe , Andre Marie , Alawi Hasan , dos Santos Lelita C. , Khalid Abdul K. , Koev Dragomir , Moore Ray , Serban Viorel , Picandet Brigitte , Francillard Marie 
Published: May 2006

OBJECTIVE—The aim of this study was to demonstrate the superiority of benfluorex over placebo as an add-on therapy in type 2 diabetic patients in whom diabetes is insufficiently controlled by sulfonylurea monotherapy and who have a limitation for the use of metformin.
RESEARCH DESIGN AND METHODS—Type 2 diabetic patients with HbA1c (A1C) (7–10%) who were receiving the maximum tolerated sulfonylurea dose and had a contraindication to or poor tolerance of metformin were randomly assigned (double blind) to receive benfluorex 450 mg/day (n = 165) or placebo (n = 160) for 18 weeks. The main efficacy criterion was A1C, analyzed as the change from baseline to the end of treatment using ANCOVA with baseline and country as covariates. Secondary criteria were fasting plasma glucose (FPG), insulin resistance, and plasma lipid level.
RESULTS—Both groups were similar at baseline in the intention-to-treat population. A1C significantly decreased with benfluorex from 8.34 ± 0.83 to 7.52 ± 1.04% (P &lt; 0.001) and tended to increase with placebo from 8.33 ± 0.87 to 8.52 ± 1.36% (NS), resulting in a mean adjusted difference between groups of −1.01% (95% CI −1.26 to −0.76; P &lt; 0.001). The target A1C (≤7%) was achieved in 34% of patients receiving benfluorex versus 12% of patients receiving placebo. Significant between-group differences in favor of benfluorex were observed for mean FPG (−1.65 mmol/l) (P &lt; 0.001) and for homeostasis model assessment of insulin resistance. Overall tolerance was similar in both groups. Serious adverse events were more frequent in the benfluorex group, without evidence of causality relationship.
CONCLUSIONS—Benfluorex as an add-on therapy was superior to placebo in lowering A1C with a between-group difference of 1% in type 2 diabetic patients whose disease was insufficiently controlled with sulfonylurea alone and in whom metformin was contraindicated or not tolerated.
Peripheral Arterial Disease and Risk of Cardiac Death in Type 2 Diabetes
Authors: Norman Paul E. , Davis Wendy A. , Bruce David G. , Davis Timothy M.E. 
Published: May 2006

OBJECTIVE—The purpose of this study was to examine the natural history of peripheral arterial disease (PAD) complicating type 2 diabetes, in particular the influence of PAD on the risk of cardiac death and the adequacy of PAD risk factor management.
RESEARCH DESIGN AND METHODS—The Fremantle Diabetes Study (FDS) was a prospective community-based observational study of diabetic patients recruited between 1993 and 1996. The present sample comprised the 1,294 FDS type 2 diabetic patients and a subgroup of 531 of these who had valid data at baseline and five or more subsequent consecutive annual reviews. Assessments consisted of a range of clinical and biochemical variables including the ankle/brachial index (ABI). PAD was defined as an ABI ≤0.90 at two consecutive reviews or any PAD-related lower-extremity amputation.
RESULTS—The prevalence of PAD at study entry was 13.6% and the incidence of new PAD was 3.7 per 100 patient-years. Both prevalent and incident PAD was strongly and independently associated with increasing age, systolic blood pressure, total serum cholesterol, and especially smoking. Risk factor management improved but remained suboptimal during follow-up. An ABI of ≤0.90 was independently associated with an increased risk of cardiac death of 67%.
CONCLUSIONS—Measurement of the ABI is a simple means of identifying PAD in diabetic patients. PAD is common in diabetic patients and predicts cardiac death. These data further support the role of regular screening for PAD in diabetes so that intensive management of vascular risk factors can be pursued.
Stability of Body Weight in Type 2 Diabetes
Authors: Chaudhry Zoobia W. , Gannon Mary C. , Nuttall Frank Q. 
Published: May 2006

OBJECTIVE—There is a concern that an “epidemic of obesity” is occurring in Western societies. One consequence of obesity is that type 2 diabetes may develop. Presumably, a great increase in body weight would continue in people with diabetes and may be accelerated due to pharmacological treatment. In this retrospective study, we tested the hypothesis that the weight gain in a diabetic population is greater than that in the general population.
RESEARCH DESIGN AND METHODS—Data were obtained from the records of 205 adult men who have attended a diabetes clinic for ≥5 years. Their weight and glycohemoglobin at the last visit were compared with the initial visit data. The subjects were categorized according to treatment modalities. The mean follow-up was 9.4 years (range 5–23).
RESULTS—For the group as a whole, the mean increase in body weight was 0.23 ± 0.2 kg/year. BMI or initial age had little effect on the rate of weight gain. Treatment regimen used did have an effect on weight change. In subjects treated with insulin, with or without oral agents, body weight increased at a rate of 0.44 ± 0.1 kg/year. In subjects treated with metformin or metformin and a sulfonylurea, there was a mean loss in weight, i.e., −0.24 ± 0.09 kg/year, and with sulfonylureas alone weight increased by 0.42 ± 0.2 kg/year.
CONCLUSIONS—The men treated with insulin alone or insulin combined with oral agents gained weight at a rate comparable with that reported for the general population, i.e., the weight gain was not extraordinary. Metformin treatment resulted in a modest loss of weight.
Treatment Escalation and Rise in HbA1c Following Successful Initial Metformin Therapy
Authors: Nichols Gregory A. , Alexander Charles M. , Girman Cynthia J. , Kamal-Bahl Sachin J. , Brown Jonathan B. 
Published: May 2006

OBJECTIVE—To describe secondary failure of initial metformin therapy in patients who achieved initial HbA1c (A1C) &lt;8% and to identify predictors of failure.
RESEARCH DESIGN AND METHODS—We identified 1,288 patients who achieved A1C &lt;8% within 1 year of initiating metformin as their first-ever antihyperglycemic drug. Subjects were followed until they added/switched antihyperglycemics, they terminated health plan membership, or 31 December 2004. We defined secondary failure using two separate but overlapping approaches: 1) addition/switch to another antihyperglycemic drug or 2) first A1C measurement &gt;8.0% after at least 6 months on metformin.
RESULTS—The best A1C achieved within 1 year of metformin initiation was the most powerful predictor of avoiding secondary failure. Approximately 50% of subjects whose best A1C was 7–7.9% added/switched antihyperglycemic drugs within 36 months, whereas it took &gt;60 months for those in the 6–6.9% A1C category to reach a 50% failure rate. Those who achieved an A1C &lt;6% did not reach a 50% rate of adding/switching drugs until 84 months. For the alternative secondary failure outcome, about half of those whose best A1C was 7.0–7.9% reached an A1C &gt;8% within 24 months. Only ∼25% of subjects in the 6–6.9% category failed by 48 months, and &gt;80% of subjects in the &lt;6% category remained below 8% through 60 months.
CONCLUSIONS—Whether defined by adding/switching to another drug or by reaching an A1C of 8%, secondary failure is inversely associated with the reduction of A1C achieved within the 1st year of metformin monotherapy.
Long-Term Breast-Feeding in Women With Type 1 Diabetes
Authors: Stage Edna , Nørgård Hanne , Damm Peter , Mathiesen Elisabeth 
Published: May 2006

OBJECTIVE—Breast-feeding may be more difficult in women with diabetes because of neonatal morbidity and fluctuating maternal blood glucose values. The frequency of long-term breast-feeding and the possible predictors for successful breast-feeding were investigated.
RESEARCH DESIGN AND METHODS—One hundred two consecutive women with type 1 diabetes were interviewed about breast-feeding using a semistructured questionnaire 5 days and 4 months after delivery. Clinical data were collected from the medical records.
RESULTS—Five days after delivery, 86% of the women were breast-feeding. Four months after delivery, 55 (54%) women were exclusively, 14 (14%) were partly, and 33 (32%) were not breast-feeding compared with 50, 26, and 24% in the background population (NS). Mothers exclusively breast-feeding at 4 months were characterized by previous experience with breast-feeding, a higher educational level, and vaginal delivery and included a high proportion of nonsmokers, whereas there were no associations with diabetes-related parameters such as white classes, duration of diabetes, HbA1c, and insulin dose at conception. Breast-fed offspring had a significantly higher birth weight and gestational age and were less often receiving glucose intravenously compared with the remaining offspring. Independent predictors of exclusive breast-feeding at 4 months were previous experience with breast-feeding (odds ratio 6.3 [95% CI 2.4–17]) and higher educational level (7.1 [2.4–21]). Cessation of breast-feeding was mainly due to common nursing problems, such as perceived milk supply, and not related to maternal diabetes status.
CONCLUSIONS—The majority of the women with type 1 diabetes initiated breast-feeding, and the prevalence of breast-feeding at 4 months was comparable to that in the background population. Independent predictors of exclusive breast-feeding at 4 months were previous experience with breast-feeding and higher educational level.
Pentamethylcyclopentadienyl–Ruthenium Catalysts for Regio‐ and Enantioselective Allylation of Nucleophiles
Authors: Bruneau Christian , Renaud Jean‐Luc , Demerseman Bernard 
Published: May 2006

AbstractRuthenium(II) complexes containing the pentamethylcyclopentadienyl ligand efficiently perform the activation of allylic carbonates and halides to generate cationic and dicationic ruthenium(IV) complexes. This activation has been transferred as a key step to the catalytic allylation of nucleophiles. The structural and electronic properties of the allylic moieties lead to the regioselective formation of chiral products resulting from nucleophilic addition to their most substituted terminus. The catalytic activity of various Ru(Cp*) precatalysts in several allylic substitutions by C and O nucleophiles will be presented. The enantioselective version that has been demonstrated by using optically pure bisoxazoline ligands will also be discussed.
Triphenylphosphine Polymer‐Bound/Iodine Complex: A Suitable Reagent for the Preparation of O‐Isopropylidene Sugar Derivatives.
Authors: Pedatella Silvana , Guaragna Annalisa , D'Alonzo Daniele , De Nisco Mauro , Palumbo Giovanni 
Published: May 2006

AbstractChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract, please click on HTML or PDF.
Asymmetric Synthesis of Cryptofolione and Determination of Its Absolute Configuration.
Authors: Matsuoka Yuko , Aikawa Kohsuke , Irie Ryo , Katsuki Tsutomu 
Published: May 2006

AbstractChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract, please click on HTML or PDF.
Preliminary data on the presence of mycotoxins (ochratoxin A, citrinin and aflatoxin B1) in black table olives “Greek style” of Moroccan origin
Authors: El Adlouni Chakib , Tozlovanu Marianne , Naman Fatima , Faid Mohammed , Pfohl‐Leszkowicz Annie 
Published: May 2006

AbstractMany mould strains, in particular Aspergillus and/or Penicillium, are able to develop on olive and produce ochratoxin A (OTA) and/or citrinin (CIT) and/or aflatoxin B (AFB) after harvest, during drying and storage of olives. The development of fungi on olives is responsible for the reduction of nutritional quality of olive because they can disturb the synthesis of the fatty acids. OTA, CIT and AFB are particularly dangerous for health, inducing cancer of urinary tracts or liver carcinoma. In this study, ten olive samples bought at retailer and at supermarket in Morocco were analyzed for their OTA, CIT and AFB contents. These three mycotoxins were extracted simultaneously by a method based on solvent partition validated in‐house, then separated by HPLC coupled to a fluorescence detector. All olive samples contain OTA ranging from LOQ to 1.02 μg/kg. Respectively, 50 and 25% from retailer and supermarket samples were contaminated by more than 0.65 μg/kg. In addition, 80% of olive samples contained CIT above LOD, and 100% of olive tested contained AFB above 0.5 μg/kg. As simultaneous presence of these toxins increases toxic risks, it is thus essential to have a good control of the conservation of olives after harvest.
New therapeutic target for CNS injury? The role of retinoic acid signaling after nerve lesions
Authors: Mey Jörg 
Published: May 2006

AbstractExperiments with sciatic nerve lesions and spinal cord contusion injury demonstrate that the retinoic acid (RA) signaling cascade is activated by these traumatic events. In both cases the RA‐synthesizing enzyme is RALDH‐2. In the PNS, lesions cause RA‐induced gene transcription, intracellular translocation of retinoid receptors, and increased transcription of CRBP‐I, CRABP‐II, and retinoid receptors. The activation of RARβ appears to be responsible for neurotrophic and neuritogenic effects of RA on dorsal root ganglia and embryonic spinal cord. While the physiological role of RA in the injured nervous system is still under investigation three domains of functions are suggested: (1) neuroprotection and support of axonal growth, (2) modulation of the inflammatory reaction by microglia/macrophages, and (3) regulation of glial differentiation. Few studies have been performed to support nerve regeneration with RA signalsin vivo, but a large number of experiments with neuronal and glial cell cultures and spinal cord explants point to beneficial effects of RA, so that future therapeutic approaches will likely focus on the activation of RA signaling. © 2006 Wiley Periodicals, Inc. J Neurobiol 66: 757–779, 2006
Methods for detecting and identifying retinoids in tissue
Authors: Gundersen Thomas E. 
Published: May 2006

AbstractMethods for retinoid analysis in tissue include direct spectrophotometry or fluorometry and retinoid responsive reporter constructs in the form of cell reporter assays or transgenic reporter animals, but chromatographic methods dominate and posses several superior features in quantitative analysis. The multitude of extraction protocols used can coarsely be divided into manual liquid‐liquid extraction protocols and semi‐ or fully automated solid phase extraction‐based protocols. Liquid chromatographic separation in reversed phase dominates although normal phase is also used. Detection is mainly performed with UV detectors although electrochemical and fluorescence detection is also used. Mass spectrometry in combination with LC is more often used in retinoid analysis and is likely to dominate in the future. © 2006 Wiley Periodicals, Inc. J Neurobiol 66: 631–644, 2006
Retinoid signaling in inner ear development
Authors: Romand Raymond , Dollé Pascal , Hashino Eri 
Published: May 2006

AbstractThe inner ear originates from an embryonic ectodermal placode and rapidly develops into a three‐dimensional structure (the otocyst) through complex molecular and cellular interactions. Many genes and their products are involved in inner ear induction, organogenesis, and cell differentiation. Retinoic acid (RA) is an endogenous signaling molecule that may play a role during different phases of inner ear development, as shown from pathological observations. To gain insight into the function of RA during inner ear development, we have investigated the spatio‐temporal expression patterns of major components of RA signaling pathway, including cellular retinoic acid binding proteins (CRABPs), cellular retinoid binding proteins (CRBPs), retinaldehyde dehydrogenases (RALDHs), catabolic enzymes (CYP26s), and nuclear receptors (RARs). Although the CrbpI, CrabpI, and ‐II genes are specifically expressed in the inner ear throughout development, loss‐of‐function studies have revealed that these proteins are dispensable for inner development and function. Several Raldh and Cyp26 gene transcripts are expressed at embryological day (E) 9.0–9.5 in the otocyst and show mainly complementary distributions in the otic epithelium and mesenchyme during following stages. From Western blot, RT‐PCR, and in situ hybridization analysis, there is a low expression of Raldhs in the early otocyst at E9, while Cyp26s are strongly expressed. During the following days, there is an up‐regulation of Raldhs and a down‐regulation for Cyp26s. Specific RA receptor (Rar and Rxr) genes are expressed in the otocyst and during further development of the inner ear. At the otocyst stage, most of the components of the retinoid pathway are present, suggesting that the embryonic inner ear might act as an autocrine system, which is able to synthesize and metabolize RA necessary for its development. We propose a model in which two RA‐dependent pathways may control inner ear ontogenesis: one indirect with RA from somitic mesoderm acting to regulate gene expression within the hindbrain neuroepithelium, and another with RA acting directly on the otocyst. Current evidence suggests that RA may regulate several genes involved in mesenchyme‐epithelial interactions, thereby controlling inner ear morphogenesis. Our investigations suggest that RA signaling is a critical component not only of embryonic development, but also of postnatal maintenance of the inner ear. © 2006 Wiley Periodicals, Inc. J Neurobiol 66: 687–704, 2006