Elderly population is hospitalized more frequently than young people, and they suffer from more severe diseases that are difficult to diagnose and treat. The present study aimed to investigate the factors affecting mortality in elderly patients hospitalized for nonmalignant reasons. Demographic data, reason for hospitalization, comorbidities, duration of hospital stay, and results of routine blood testing at the time of first hospitalization were obtained from the hospital records of the patients, who were over 65 years of age and hospitalized primarily for nonmalignant reasons. The mean age of 1012 patients included in the study was 77.8 ± 7.6. The most common reason for hospitalization was diabetes mellitus (18.3%). Of the patients, 90.3% had at least a single comorbidity. Whilst 927 (91.6%) of the hospitalized patients were discharged, 85 (8.4%) died. Comparison of the characteristics of the discharged and dead groups revealed that the dead group was older and had higher rates of poor general status and comorbidity. Differences were observed between the discharged and dead groups in most of the laboratory parameters. Hypoalbuminemia, hypertriglyceridemia, hypopotassemia, hypernatremia, hyperuricemia, and high TSH level were the predictors of mortality. In order to meet the health necessities of the elderly population, it is necessary to well define the patient profiles and to identify the risk factors.

In the last decade, studies were first done to determine the frequency of Gsalpha and later thyrotropin receptor (TSHR) mutations in benign autonomously functioning thyroid nodules (AFTN). Different frequencies ranging from 0% to 38% for GSp mutations and from 20% to 86% for TSHR mutations were found. There were only some limited case reports related to TSHR genetic alterations in malignant AFTN. Their role in autonomously functioning thyroid carcinomas is not well established. We present a patient who had thyroidectomy for toxic multinodular goiter and a papillary carcinoma was demonstrated histopathologically. Genomic DNA was isolated from two solid areas in the hot nodule and peripheral leukocytes of the patient. After amplifying the related regions, TSHR and GSalpha genes were analyzed by single-strand conformation polymorphism (SSCP) analysis. The precise localization of the mutations was identified by automatic DNA sequence analysis. An activating mutation of the TSHR gene (Leu 512 Arg) was found in the autonomously functioning papillary carcinoma. It is believed that this mutation causes constitutive activation of the cyclic adenosine monophosphate (cAMP) signal transduction pathway and thereby causes thyrotoxicosis and a hot thyroid nodule in an autonomously functioning papillary carcinoma.

In this study, we concluded that fasting during Ramadan did not worsen the glycemic control of patients with type 2 diabetes.

Chronic myeloid leukemia (CML) is one of the etiologic causes of sudden hearing loss and vertigo. However, deafness in association with vestibular symptoms rarely occurs in CML as the first sign. In this article, a 50-year-old male with CML whose first signs and symptoms were unilateral sudden hearing loss and tinnitus in the right ear, vertigo and nausea was presented. Aetiopathogenetic mechanisms, clinical and radiological aspects and therapeutic options for CML with deafness and vertigo were discussed reviewing the literature.

Background Lipid profiles in the blood are altered in human cocaine users, suggesting that cocaine-exposure can induce lipid remodeling. Methods Cocaine-induced locomotor sensitization in rats was followed by shotgun lipidomics using electrospray ionization-mass spectrometry (ESI-MS) and determined changes in brain tissues. To determine if any lipidomic changes were also reflected in the blood, we performed principal component analysis (PCA) of lipidomic spectra isolated from cocaine-treated animals. Alterations in the abundance of phospholipid species were correlated with behavioral changes in the magnitude of either the initial response to drug or locomotor sensitization. Results Behavioral sensitization altered the relative abundance of several phospholipid species in the hippocampus and cerebellum, measured one week following the final exposure to cocaine. In contrast, relatively few effects on phospholipids in either the dorsal or the ventral striatum were observed. PCA analysis demonstrated that cocaine altered the relative abundance of several glycerophospholipid species as compared to saline-injected controls. Subsequent MS/MS analysis identified some of these lipids as phosphatidylethanolamines, phosphatidylserines and phosphatidylcholines. The relative abundance of some of these phospholipid species were well correlated (R2 of 0.7 or higher) with either the initial response to cocaine or locomotor sensitization. Conclusion Taken together, these data demonstrate that a cocaine-conditioning experience results in the remodeling of specific phospholipids in rat brain tissue in a region-specific manner and also alters the intensities and types of phospholipid species in rat blood. These results further suggest that such changes may serve as biomarkers to assess the neuroadaptations occurring following repeated exposure to cocaine.

Infections are still major factors in crush syndrome-related deaths.

Polycystic ovary syndrome (PCOS) is one of the most common causes of female infertility. It affects nearly 5-10% of young women. It is characterized by the presence of hirsutism, acne, anovulation, hyperandrogenism, polycystic ovaries, and infertility [1]. Many mechanisms have been reported to be responsible for the pathophysiology of PCOS. The condition is thought to be determined by complex interactions between the hypothalamic-pituitary-ovarian or hypothalamic-pituitary-adrenal axis functions and metabolic disorders, such as obesity, insulin resistance (IR), and compensatory hyperinsulinemia [2]. PCOS increases the prevalence of hyperglycemia, hypertension, and dyslipidemia [3], increasing thus the risk of developing cardiovascular diseases [4].Nesfatin-1 (N1) is derived from nucleobindin 2 (NUCB2), which is encoded by the NUCB2 gene. It is a newly identified peptide that has 82 amino acids [5]. It is released from several tissues including forebrain, hindbrain, brainstem, spinal cord, adipose tissues [6]. It has an anorexigenic effect and plays an important role in hypothalamic pathways such as regulating food intake, energy homeostasis, water intake, and body temperature [7,8]. In addition, it exerts cardiovascular and hypertensive effects [9]. It is closely related to glucose, insulin metabolism, and IR [5,10]. Several studies have demonstrated N1 to be associated with body mass index (BMI), IR, inflammatory stimulation in diabetes, hypertension, and PCOS [9][10][11]. It may also affect the control of the reproduction system, e.g. puberty onset and gonadotropin secretion [12]. ABSTRACTObesity, insulin resistance (IR), inflammation, and hyperandrogenism may lead to polycystic ovary syndrome (PCOS) and hypertension. Nesfatin-1 (N1) may be related to IR, obesity, and hypertension. Furthermore, a vitamin D (VD) deficiency is associated with hypertension and PCOS. We aimed to investigate N1 and VD levels in PCOS that have an effect on systolic and diastolic blood pressure (BP) and heart rate (HR). This study included 54 patients with PCOS and 48 age-body mass index (BMI)-matched healthy controls. PCOS was diagnosed according to clinical practice guidelines. Ferriman-Gallwey scores (FGS) were calculated, while N1, VD, and other hormonal and biochemical parameters were measured for all subjects. Systolic and diastolic BP was measured as well. HR was calculated using an electrocardiogram. The levels of N1 (p < 0.001), high-sensitivity C-reactive protein (hs-CRP) (p = 0.036), homeostasis model assessment as an index of insulin resistance (HOMA-IR) (p < 0.001), systolic (p < 0.001) and diastolic (p < 0.001) BP and HR (p < 0.001) in the PCOS group were significantly higher than in the control group. However, the VD levels of the PCOS group were lower than the control group (p = 0.004). N1 had a strong positive correlation with BMI, HOMA-IR, hs-CRP, luteinizing hormone, systolic and diastolic BP, and HR. VD levels were negatively correlated with HOMA-IR and luteinizing hormone. Elevated N1 and decreased VD levels may...

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