Miracle-dz/UniFAR-FTUs huggingface dataset:
Gestational diabetes mellitus among Norwegian women with polycystic ovary syndrome: prevalence and risk factors according to the WHO and the modified IADPSG criteria.

OBJECTIVE The consequences of the recently proposed International Association of Diabetes in Pregnancy Study Group (IADPSG) criteria for gestational diabetes mellitus (GDM) in women with polycystic ovary syndrome (PCOS) are not known. We compared the prevalence rates and risk factors for GDM in PCOS women according to both the WHO and the modified IADPSG criteria. DESIGN Post hoc analyses from a randomized, multicenter study were used. METHODS Fasting and 2-h plasma glucose levels were measured using a 75 g oral glucose tolerance test. GDM was diagnosed according to both the WHO and the modified IADPSG criteria. RESULTS The prevalence rates of GDM according to the WHO and the modified IADPSG criteria were 9.2 and 15.0% at week 12, 18.7 and 18.7% at week 19, and 25.6 and 24.2% at week 32. Shorter stature and increased insulin levels were correlated with WHO-GDM, but not with modified IADPSG-GDM at weeks 12 and 19. Less weight gain in pregnancy predicted GDM according to both sets of criteria. GDM diagnosis was correlated with less maternal weight loss the first year post-partum. CONCLUSIONS No difference was found in the prevalence of GDM between the two sets of criteria used. Less weight gain in pregnancy was associated with GDM, independent of the diagnostic criteria used. Reduced weight loss the first year post-partum in women with GDM raises the question of whether GDM diagnosis per se or the fact that these women lose less weight after pregnancy predicts later diabetes mellitus.
Oxidative stress in chronic obstructive pulmonary disease alters ferroxidase activity of ceruloplasmin.

Aims: Oxidative stress is one of the major patho-physiologic hallmarks in the development of COPD. Ceruloplasmin, the major serum inhibitor of lipid peroxidation has been documented as a main extracellular antioxidant in serum and plays a role in preventing lung injury, and an abnormality in its oxidative inhibition could be involved in pathogenesis of COPD. This study aims to estimate levels of ceruloplasmin and its ferroxidase activity in COPD and compare with that in controls to explore their utility in COPD. Study Design: Comparison study. Place and Duration of Study: Department of Biochemistry, AFMC, Pune. Subjects for COPD were selected from the patients reporting with symptoms of COPD to respiratory OPD of Cardio Thoracic Centre, Pune, during Dec 2010 to Aug 2012. Methodology: Study comprised of two groups: Group I of 77 normal as controls (61 men, 16 women; age range 27-90 years) and Group II of 92 COPD patients (70 men, 22 Original Research Article British Journal of Medicine & Medical Research, 4(5): 1257-1268, 2014 1258 women; age range 45 97 years). Both the groups were further divided into smoker and nonsmoker groups. Ferroxidase activity of ceruloplasmin was estimated by indigenous patented kinetic method of Somani and Ambade while ceruloplasmin was estimated by immunotubidimetric method using commercially available kit. Results: Serum ceruloplasmin and ferroxidase activity were significantly higher in COPD patients as compared to normal controls. Mean ± SD in COPD versus controls respectively are ceruloplasmin: 45.84 ± 12.7 mg/dL versus 37 ± 9.7 mg/dL; ferroxidase: 1324.9 ± 278.53 IU/L versus 980.5 ± 202.3 IU/L, P 0.7) was found between ceruloplasmin and ferroxidase in controls, nonsmoker controls and smoker controls (r = 0.76, 0.71 and 0.79 respectively) while in COPD, COPD nonsmokers and COPD smokers, no correlation was found (r = 0.00, 0.29 and 0.09 respectively). Conclusion: There is alteration in the ferroxidase activity of ceruloplasmin in COPD. Future studies with quantification of carbonyl residues or other groups in ceruloplasmin molecule leading to altered oxidative or ferroxidase activity of ceruloplasmin may provide further evidence to support a role of oxidative stress in COPD.
Suboptimal effect of different vitamin D3 supplementations and doses adapted to baseline serum 25(OH)D on achieved 25(OH)D levels in patients with a recent fracture: a prospective observational study.

OBJECTIVE Guidelines on the need for dose adaptation of vitamin D3 supplementation according to baseline serum 25(OH)D are inconclusive. The effects of increasing doses of vitamin D3 at lower baseline serum 25(OH)D values on the serum 25(OH)D after 4.2 and 11 months were determined in an observational study. DESIGN A prospective observational study. METHODS Out of 1481 consecutive women and men with a recent clinical fracture, 707 had a baseline 25(OH)D level <50 nmol/l and were supplemented with increasing doses of vitamin D3 (400, 800, 1700, and ≥3500 IU/day) according to the lower baseline 25(OH)D. Final analysis was restricted to the 221 participants who had full follow-up data available for 11 months. RESULTS Serum 25(OH)D ≥50 nmol/l was achieved in 57-76% of patients after 4.2 months and in 73-79% after 11 months. These percentages were similar for all doses (P=0.06 and P=0.91 respectively). The mean achieved 25(OH)D was similar for all dose groups (56.1-64.0 nmol/l after 4.2 months and 60.2-76.3 nmol/l after 11 months). With multivariate analysis, the increase in 25(OH)D (17±32.0 after 4.2 months and 24.3±34.0 nmol/l after 11 months) was dependent on the baseline 25(OH)D (P<0.001), not on supplementation dose, season, age, BMI, or gender. CONCLUSIONS The increase in serum 25(OH)D was significantly larger with higher vitamin D3 supplementation doses. However, this dose-effect response was mainly explained by the baseline 25(OH)D, not the supplementation dose, with a greater magnitude of response at lower baseline 25(OH)D concentrations. In 21-27% of patients, serum 25(OH)D3 levels did not reach 50 nmol/l after 11 months, at any dose. Further studies are needed to identify possible causes of suboptimal response such as non-compliance, undiagnosed malabsorption syndromes, or variability in cholecalciferol content of the vitamin D supplements.
Metformin inhibits goitrogenous effects of type 2 diabetes.

OBJECTIVE Data on the association between type 2 diabetes mellitus (T2DM) and thyroid volume are sparse. An experimental study demonstrated an inhibitory effect of metformin on the growth of human thyroid cells. So far no study on humans has investigated potentially modulating effects of metformin on the association between T2DM and thyroid volume. Therefore, we investigated these effects in a population-based cohort study. DESIGN AND METHODS We used data from the Study of Health in Pomerania and included 2570 individuals for cross-sectional and 1088 individuals for longitudinal analyses. T2DM was defined by physician-diagnosed self-report or intake of antidiabetic medication. RESULTS In the cross-sectional data, females with T2DM treated with antidiabetic medication other than metformin had a larger thyroid volume (β=4.69; 95% CI 1.87 to 7.50) and a higher odds ratio (OR) for goiter (OR=1.71; 95% CI 1.05 to 2.79) than females without T2DM, whereas in males, no such association was detected. In females or males treated with metformin, T2DM was not associated with thyroid volume or goiter. In longitudinal analyses, incident T2DM not treated with metformin was significantly associated with a higher risk for incident goiter in the total population (incidence rate ratio (IRR)=1.70; 95% CI 1.10 to 2.91). Individuals with T2DM having changed from metformin to other antidiabetic agents during follow-up also had a higher risk for incident goiter than individuals without T2DM (IRR=2.71; 95% CI 1.74 to 4.20). CONCLUSIONS We demonstrate an inhibitory effect of metformin on prevalent and incident goiter. Anti-goitrogenous effects of metformin add to the general benefits of metformin treatment of T2DM.
Body iron stores and the risk of type 2 diabetes in middle-aged men.

OBJECTIVE We investigated the risk of type 2 diabetes mellitus (T2DM) over a wide range of body iron stores. METHODS Prospective cohort of 1613 men in the Kuopio Ischemic Heart Disease Risk Factor study, aged 42-60 years, free of T2DM and hereditary hemochromatosis at baseline in 1984-1989. Baseline serum ferritin (sF) and serum-soluble transferrin receptor (sTfR) concentrations were used to predict incident T2DM. T2DM was assessed by questionnaires, blood glucose measurements, and medication reimbursement register. RESULTS There were 331 cases of incident T2DM during the mean follow-up of 16.8 years (27,098 person-years). At baseline, subjects who later developed T2DM had average sF concentrations of 191 μg/l (S.D. 155) vs 151 μg/l (S.D. 119) among those who remained healthy, P<0.001. In a multivariate-adjusted logistic regression, each 100 μg/l increase in sF corresponded to an average of 14% increased (odds ratio=1.14, 95% CI 1.03-1.26, P=0.009) risk of developing T2DM. In a Cox regression, a markedly increased risk of developing T2DM was observed from the fourth sF quintile (185 μg/l, the median) upward (hazard ratio (HR) first vs fifth quintile=1.5, 95% CI 1.0-2.2, P-trend=0.05). In a corresponding Cox model in sTfR, the subjects in the third quintile (1840 μg/l, the median) had the least risk (HR=0.63, 95% CI 0.42-0.97, P=0.04). CONCLUSIONS Body iron within the sF reference range is not an important determinant of T2DM risk, whereas high normal and above is associated with markedly increased risk. Iron depletion toward iron deficiency as assessed by sTfR is not protective against T2DM. A rule of thumb safe range could be 30-200 μg/l of sF.
Somatic and psychological effects of low-dose aromatase inhibition in men with obesity-related hypogonadotropic hypotestosteronemia.

INTRODUCTION Reduced testosterone levels are frequently observed in obese men. Increased aromatase activity may be an etiological factor. OBJECTIVE In this study, we evaluate the clinical effects of aromatase inhibition in obesity-related hypogonadotropic hypotestosteronemia (OrHH). METHODS Double-blind, placebo-controlled, 6-month trial in 42 obese men with a BMI >35 kg/m(2), and a serum total testosterone <10 nmol/l. All patients started on one tablet of 2.5 mg/week, with subsequent dose escalation every month until a serum total testosterone of 20 nmol/l was reached. ENDPOINTS Psychological function, body composition, exercise capacity, and glucose, lipid, and bone metabolism. RESULTS Thirty-nine patients completed the study according to protocol. Letrozole decreased serum estradiol from 119.1±10.1 to 59.2±6.1 pmol/l (P<0.001), and increased serum LH from 3.3±0.3 to 8.8±0.9 U/l (P<0.0001) and serum total testosterone from 8.6±0.7 to 21.5±1.3 nmol/l (P<0.0001). Significant effects on the predefined endpoints were not observed. CONCLUSION Despite a marked rise in serum testosterone, low-dose aromatase inhibition had no somatic or psychological effects in men with OrHH.
Compressão medular em bovinos associada à vacinação contra febre aftosa

This paper reports the etiological, epidemiological, clinic, and pathological features of an outbreak of incoordination observed after vaccination against foot and mouth disease (FMD) in cattle in the states of Paraiba and Pernambuco. The signs of incoordination were observed approximately 45 days after vaccination that was applied in the toracic and lumbar region. A lump was found in the local of the vaccination.Twenty-four animals showed this signs, six in Paraiba and 18 in Pernambuco. Six animals died and four were euthanized. At necropsy exam were observed abscedative myositis with yellow irregular areas to multifocal coalescing a white liquid in the left muscle Longissimus lumborum (two animals) and yellowish firm mass compressing the spinal cord between vertebrae T11 and T12 (one animal) and L3 and L5 vertebrae (one animal). The myositis and the pyogranulomatous paquimeningitis were characterized by multifocal to coalescing areas showing clear spherical spaces of various sizes centrally located corresponding to the oil adjuvant of FMD vaccine removed by histologic processing. It has been determined the diagnosis of spinal cord compression secondary to vaccine granuloma.
Prostate volume and growth during testosterone replacement therapy is related to visceral obesity in Klinefelter syndrome.

OBJECTIVE Klinefelter syndrome (KS) is a chromosomal alteration characterized by increased risk of metabolic syndrome, mainly caused by visceral obesity. In the last years, obesity has been studied as a potential risk factor for prostate disease and recently a link has been demonstrated between visceral adiposity with prostate volume. The aim of this study was to analyze the relationship between obesity and prostate volume and growth during testosterone therapy in KS subjects. DESIGN AND METHODS We evaluated reproductive hormones, metabolic parameters, anthropometric measures, PSA, and prostate volume in 121 naïve non-mosaic KS patients and 60 age-matched healthy male controls. Fifty-six KS hypogonadic subjects were treated with testosterone-gel 2% and reevaluated after 18 months of treatment. RESULTS Prostate volume in KS was positively related to waist circumference (WC). The KS group with WC ≥94 cm had significantly higher prostate volume, BMI, insulin plasma levels, homeostasis model assessment index, total cholesterol, triglycerides, and glycemia with respect to the KS group with WC <94 cm. After testosterone replacement therapy, only hypogonadic KS men with WC ≥94 cm had a statistically significant increase in prostate volume. Furthermore, in untreated KS subjects, prostate volume showed a statistically significant increase after 18 months of follow-up only in subjects with WC ≥94 cm. CONCLUSIONS This study showed that visceral obesity, insulin resistance, and lipid and glucose metabolism alterations are associated with prostate volume and growth during testosterone replacement therapy in KS, independently from androgen or estrogen levels. These latter findings might provide the basis for a better management and follow-up of KS subjects.
Physical Activity, Blood Lipids, and Lipoproteins

Dyslipidemia is a major modifiable cardiovascular disease (CVD) risk factor. While pharmacological treatment has been a focal point of dyslipidemia management for several years, increasing physical activity is a safe, cost-effective treatment option that should also be recommended by health care practitioners. Moderate aerobic exercise consistently increases high-density lipoprotein cholesterol (HDL-C) and reduces triglycerides (TG), independent of changes in body weight. However, reductions in total and low-density lipoprotein cholesterol are reported less often following aerobic exercise. Therefore, clinicians should understand that aerobic exercise is not likely to be an effective treatment option for their management. Recent empirical evidence also indicates that aerobic exercise may be of benefit for treating emerging lipid and lipoprotein risk factors such as lipoprotein particle size and number and triglyceride-rich lipoproteins. Further work is needed to clarify the impact of aerobic exercise on apolipoproteins. Based on current evidence, prescribing aerobic exercise as a means of increasing HDL-C and lowering TG is usually an efficacious strategy for treating these aspects of dyslipidemia. These effects are likely to be accompanied by changes in emerging lipid and lipoprotein risk factors.
Global Synchronization of a New Chua's System

The problem of global synchronization control for a class of new Chua's system is studied in this paper. Several linear controllers are proposed to realize the global exponential synchronization of two Chua's systems. Decoupling feedback control method is used to make Chua's system global exponential synchronized. Global exponential synchronization with respect to (w.r.t) partial state variables is studied when one of the error variables is zero. Finally, an adaptive synchronization controller is designed to make the response and the driven systems synchronized. Moreover, the estimate errors of the uncertain parameters converge to zero since the persistent excitation condition holds. Additionally, numerical simulations show the effectiveness of the proposed controllers.
Procedimentos de um banco de ossos e a aplicabilidade dos enxertos por ele proporcionados

The authors demonstrate in this study the viability and functionality of a Bank of Bones and the experience of the use during the seventeen years of your creation. The objective of this study is to demonstrate the importance of the maintenance of a service of Bank of Bone, as well as to show your usefulness in the several types of orthopedical interventions. Being demonstrated, the protocol for the possible donors' obtaining, methods for retreat and storage of those bones, and your use in several orthopedical procedures.
Lack of influence of somatic mutations on steroid gradients during adrenal vein sampling in aldosterone-producing adenoma patients.

OBJECTIVE Adrenal vein sampling (AVS) is a technically demanding procedure required for the identification of suitable candidates for unilateral adrenalectomy in primary aldosteronism. Recently, somatic KCNJ5 K(+)-channel mutations in aldosterone-producing adenoma (APA) patients have been shown to influence steroid gradients during AVS. These and other recently identified genetic modifiers (ATP1A1 and ATP2B3) might affect the final diagnosis and treatment of the affected patients. DESIGN Fifty-nine patients with APAS who had undergone successful AVS (adrenal vein cortisol:peripheral cortisol ratio 2) and had undergone a mutation analysis of their tumor tissue were studied. the mutation status of the APAS was as follows: 19 KCNJ5 mutations, eight ATPase mutations (five ATP1A1 and three ATP2B3), and 32 patients with none of these mutations. METHODS The lateralization index (ratio of aldosterone:cortisol on the side of the adenoma to aldosterone to cortisol on the contralateral side) and the contralateral suppression index (ratio of aldosterone:cortisol on the contralateral side to aldosterone to cortisol in the periphery) were calculated for the KCNJ5-mutated, ATPase-mutated, and the KCNJ5/ATPase mutation-negative APA patients. RESULTS The lateralization indices of the ATPase mutation carriers had a median of 19.9 compared with a median of 16.0 in the KCNJ5 mutation carriers and that of 20.5 in the KCNJ5/ATPase mutation-negative patients. The contralateral suppression indices of the ATPase-mutated patients had a median of 0.1 compared with a median of 0.4 in the KCNJ5 mutation carriers and that of 0.2 in the KCNJ5/ATPase mutation-negative patients. The differences between the genetic groups were not statistically significant. CONCLUSIONS We did not find evidence for a clinically important impact of mutation status on steroid gradients during AVS.
Hyperthyroidism and psychiatric morbidity: evidence from a Danish nationwide register study.

OBJECTIVE Thyroid hormones are essential for the normal development of the fetal brain, while hyperthyroidism in adults is associated with mood symptoms and reduced quality of life. In this study, we aimed to investigate the association and temporal relationship between hyperthyroidism and psychiatric morbidity. DESIGN Register-based nationwide cohort study. METHOD Data on hyperthyroidism and psychiatric morbidity were obtained by record linkage of the Danish National Patient Registry and the Danish National Prescription Registry. A total of 2631 hyperthyroid individuals were identified and matched 1:4 with non-hyperthyroid controls and followed for a mean duration of 6 years (range 0-13). Logistic and Cox regression models were used to assess the risk of psychiatric morbidity before and after the diagnosis of hyperthyroidism respectively. RESULTS BEFORE THE DIAGNOSIS OF HYPERTHYROIDISM, SUCH INDIVIDUALS HAD AN INCREASED RISK OF BEING HOSPITALIZED WITH PSYCHIATRIC DIAGNOSES (ODDS RATIO (OR): 1.33; 95% CI: 0.98-1.80) and an increased risk of being treated with antipsychotics (OR: 1.17; 95% CI: 1.00-1.38), antidepressants (OR: 1.13; 95% CI: 1.01-1.27), or anxiolytics (OR: 1.28; 95% CI: 1.16-1.42). After the diagnosis of hyperthyroidism, there was a higher risk of being hospitalized with psychiatric diagnoses (hazard ratio (HR): 1.51; 95% CI: 1.11-2.05) and an increased risk of being treated with antipsychotics (HR: 1.46; 95% CI: 1.20-1.79), antidepressants (HR: 1.54; 95% CI: 1.36-1.74), or anxiolytics (HR: 1.47; 95% CI: 1.27-1.69). CONCLUSIONS Hyperthyroid individuals have an increased risk of being hospitalized with psychiatric diagnoses and being treated with antipsychotics, antidepressants, and anxiolytics, both before and after the diagnosis of hyperthyroidism.
Abnormal metabolic phenotype in middle-aged GH-deficient adults despite long-term recombinant human GH replacement.

BACKGROUND Adult GH deficiency (GHD) is associated with increased cardiovascular mortality. Recombinant human GH (rhGH) replacement has beneficial short-term metabolic effects. Although these positive effects sustain during longer follow-up, the prevalence of the metabolic syndrome (MS) remains increased in comparison with population data not adjusted for the higher mean BMI in GHD adults. OBJECTIVE To explore whether middle-aged patients with proposed physiological rhGH replacement have been normalized with respect to MS and its individual components in comparison with the general population, adjusted for age, sex, and BMI. METHODS One hundred and sixty-one GHD patients (aged 40-70 years) were studied before the start and after 5 years of rhGH replacement, and were compared with 1671 subjects (aged 45-66 years) from the general population (NEO Study). RESULTS MS PROPORTION IN GHD PATIENTS WAS 41.0% BEFORE THE START OF RHGH SUPPLETION, INCREASING TO 53.4% AFTER 5 YEARS (P=0.007). DESPITE CHRONIC RHGH REPLACEMENT, GHD PATIENTS HAD A 1.3-TIMES HIGHER MS PROPORTION THAN THE GENERAL POPULATION, INDEPENDENTLY OF AGE, SEX, AND BMI (95% CI 1.11.5, P=0.008). THE GHD POPULATION SHOWED A DIFFERENT METABOLIC PROFILE THAN THE GENERAL POPULATION WITH SIMILAR BMI: an increased risk of hypertriglyceridemia (adjusted prevalence ratio (PR) 2.0, 95% CI 1.7-2.3) and low HDL-C (adjusted PR 1.8, 95% CI 1.5-2.2), but less hyperglycemia (adjusted PR 0.5, 95% CI 0.4-0.7). CONCLUSIONS Despite 5 years of rhGH replacement, GHD patients still have a different metabolic profile and more frequently MS than the general population. These differences were independent of BMI, and resemble the unfavorable metabolic profile of untreated GHD patients, pointing to question the long-term benefits of rhGH replacement.