Maternal Neudesin Levels in Pregnant Women with Gestational Diabetes Mellitus.

BACKGROUND: Our aim was to investigate the changes in neudesin levels in pregnant women with GDM and the relationship between neudesin and metabolic parameters. METHODS: Forty pregnant women diagnosed with GDM and forty age- and gestational week-matched control subjects were included in the study. Demographic data were obtained from records. Maternal lipid profiles, glucose levels, fasting insulin, HbA1C, and HOMA-IR results were compared between the groups. Correlation tests were performed to evaluate the relationship between neudesin and clinical and laboratory diagnostic parameters. p < 0.05 were interpreted as statistically significant. RESULTS: The human serum neudesin levels were significantly lower in the GDM group compared with the controls. The correlation tests showed statistically negative and weak correlations between the neudesin levels and the maternal age, 50 g OGCT, 100 g OGTT 3 hours, and HbA1C. The optimum neudesin cutoff value for a diagnosis of GDM disease is 6.94 ng/dL, with a sensitivity of 65.9% and a specificity of 63.2%. CONCLUSIONS: This study has shown that lower neudesin levels may occur as a reflection of changes in glucose metabolism during intrauterine life.

Benign transient hyperphosphatasemia in the pediatric population: a single center cohort study.

OBJECTIVES: Alkaline phosphatase (ALP) can be increased in a benign condition known as benign-transient hyperphosphatasemia (BTH). We aimed to evaluate the demographic, and clinical characteristics of infants and children with BTH. METHODS: In our retrospective study, infants and children diagnosed with BTH between September 2019 and September 2023 were included. RESULTS: Of 249 children with elevated ALP levels, 95 (38.1 %) had BTH. The mean age at diagnosis of children with BTH was 2.4 ± 1.3 years (min 0.6 - max 6.2 years). ALP mean value was 2,587 ± 1252 U/L (min 972 - max 5757 U/L). ALP value was an average 7.4 ± 3.6 times higher than the corresponding upper limit of normal. The second measurement was made after an average of 13.2 ± 6 days, and a statistically significant difference was detected compared to the first value, with a decrease of 61 ± 23 % in the ALP value (p<0.001). ALP value returned to normal in an average of 44 ± 29.2 days. Elevated ALP was detected during infection in 49 (51.6 %) children. When the sample was divided into those under 2 years of age and aged 2 and over, no statistical difference was observed in ALP levels in the time it took for ALP levels to return to the normal range (p=0.480). CONCLUSIONS: BTH should be kept in mind if high serum ALP is detected in children without clinical or laboratory suspicion of bone or liver disease. In the follow up detecting a significant decrease trend compared to the first value may be guiding for BTH.

Progranulin and tumor necrosis factor-alpha in lean polycystic ovary syndrome patients.

OBJECTIVE: In this study, levels of progranulin (PGRN) and tumor necrosis factor-alpha (TNF-α) were measured to detect the presence of inflammation in lean polycystic ovary (PCOS) patients. METHODS: 40 lean PCOS patients were assessed by Rotterdam criteria. Forty healthy women with regular menstrual cycles and without biochemical and clinical hyperandrogenism were involved in our study. Blood samples were taken from the patient and control groups for the measurement of progranulin (PGRN), tumor necrosis factor-alpha (TNF-α), lipid parameters, glucose, insulin, and other hormones. RESULTS: Serum PGRN and TNF-α levels were significantly higher in patients with lean PCOS, compared with the control group (p = .037, p = .041). PGRN levels were positively correlated with TNF-α levels in lean PCOS patients. CONCLUSION: PGRN is known as a ligand for the TNF-α receptor. PGRN level increase in lean PCOS patients may be due to inhibiting the inflammatory effects of TNF-α. To observe the PGRN and TNF-α connection in obesity, further study is needed in obese PCOS patients and obese control groups.

Association of Glial Cell-Line Derived Neurotrophic Factor and Nerve Growth Factor with Duration of Untreated Psychosis and Clinical Symptoms in Drug-Naive Schizophrenia.

Background: The neurodevelopmental hypothesis is one of the most-emphasized hypotheses in the etiology of schizophrenia. Nerve growth factor (NGF) and glial cell-line derived neurotropic factor (GDNF) are neurotrophic factors that provide growth, differentiation, and survival in nerve cells in the development process. In this study, we aimed to compare the GDNF and NGF levels of schizophrenia patients with healthy controls and to analyze the relationship between the Positive and Negative Syndrome Scale (PANSS) scores, serum GDNF and NGF levels and the duration of untreated psychosis (DUP) of the patients. Methods: The study involved 45 patients with a diagnosis of schizophrenia, who had never used any antipsychotic drug, and 45 age- and sex-matched healthy participants. The participants filled a sociodemographic data form. The PANSS was applied to evaluate the clinical conditions. Before the initiation of the treatment, serum samples were collected from the patients. Results: The difference between the GDNF and NGF levels of the patient group and control group was statistically significant. The serum GDNF and NGF levels in schizophrenia patients were lower than healthy controls. No correlation was found between the DUP and serum GDNF and NGF levels. There was a positive correlation between general psychopathology and negative scores of PANSS and the DUP of patients. Conclusion: GDNF and NGF levels seem to be indicators of schizophrenia and its progress; nevertheless, we still do not have sufficient information about these neurotrophic factors. The results of our study indicate that the neurodevelopmental changes occurring at the early stages of the illness prominently affect the progress of disease, highlighting the importance of treatment in the early stages of disease.

Default mode network connectivity is linked to cognitive functioning and CSF Aß1-42 levels in Alzheimer's disease.

BACKGROUND: Changes in the default mode network (DMN) activity are early features of Alzheimer's disease (AD) and may be linked to AD-specific Aß pathology. METHODS: Cognitive profiles; DMN connectivity alterations; and cerebrospinal fluid (CSF) amyloid beta (Aß)1-42, total tau, phosphorylated tau 181, and α-synuclein levels were studied in 21 patients with AD and 10 controls. RESULTS: DMN activity is altered in AD. Posterior cingulate cortex (PCC) functional connectivity with other parts of DMN was related to cognitive function scores. The reduction of connectivity of the dorsal PCC with the retrosplenial cortex on the right side was closely related to decreased CSF Aß1-42 levels in patients with AD. CONCLUSIONS: The dorsal PCC and retrosplenial cortex may have special importance in the pathogenesis and cognitive findings of AD.

Tamoxifen citrate: a glimmer of hope for silicosis.

BACKGROUND: Inhalation of crystalline silica nanoparticles causes pulmonary damage resulting in progressive lung fibrosis. Currently, there is no effective treatment for silicosis. Tamoxifen citrate is a selective estrogen receptor modulator, which is one of the adjuvant treatment choices for breast cancer. It is also known with its inhibitory effect on the production of transforming growth factor-beta (TGF-ß) and studied for the anti-fibrotic effect in some fibrotic diseases. The aim of the study was to determine the effect of tamoxifen citrate on the prevention of pulmonary fibrosis and the treatment of silicosis. METHODS: A total of 100 adult female Wistar Albino rats (200-250 g) were used in this study. The rats were divided into five groups including 20 rats in each. Rats were exposed to silica for 84 d in all groups. In group 1, rats were sacrificed on the day 84 without receiving treatment. In group 2, rats received 1 mg/kg tamoxifen (tmx1 + 1), from the first day of the study for the whole 114 d of the study. In group 3, (tmx10 + 10) rats were given 10 mg/kg tamoxifen from the first day of the study for the whole 114 d of the study. In group 4 (tmx1), rats were started 1 mg/kg of tamoxifen on day 84 and were given until day 114. In group 5 (tmx10), rats were fed with 10 mg/kg tamoxifen starting from day 84 to day 114. All rats except group 1 were sacrificed on 114 day of the study. Lung inflammation and fibrosis scores, serum TGF ß levels, lung smooth muscle antigen and tissue transforming growth factor ß (t-TGF-ß) antibody staining levels, and number of silicotic rats were compared between groups. RESULTS: Silicosis was caused successfully in all rats in group 1. There were six silicotic rats in group 3 and it was the lowest number of all groups. Plasma TGF-ß levels and fibrosis score were significantly lower in all groups when compared with the control group. Tamoxifen could have preventive or treating effects in silicosis and found that lung fibrosis score was significantly lower in rats treated with tamoxifen. CONCLUSIONS: Tamoxifen treatment after and/or before induction of silicosis decreased lung fibrosis score with blood TGF-ß levels. We hope that this study may introduce a new indication as prophylactic use of tamoxifen in high-risk groups for silicosis and for treatment of silicosis.