Correlations of glucose metabolism, insulin resistance and inflammatory factors with symptom score of patients with benign prostatic hyperplasia.

OBJECTIVE: To investigate the effects of glucose metabolism, insulin resistance, and inflammatory factors on International Prostatic Symptom Score (IPSS) of patients with benign prostatic hyperplasia (BPH), to explore their correlations and evaluate the clinical significance. PATIENTS AND METHODS: 90 patients with BPH were selected and divided into normal blood glucose group and abnormal blood glucose group. The changes of indexes related to prostate function, prostate volume (PV), prostate-specific antigen (PSA), and IPSS in two groups were evaluated. The fasting blood glucose (FBS), fasting insulin (FINS), homeostasis model assessment of insulin resistance (HOMA-IR) index and inflammatory factors interleukin-8 (IL-8) and cyclooxygenase 2 (COX-2) levels in expressed prostatic secretion (EPS) were compared. The correlations of glucose metabolism, insulin resistance and inflammatory factors with IPSS were analyzed by Logistic regression. The changes of these indexes after treatment of BPH were observed. RESULTS: The FBS, FINS, HOMA-IR, and inflammatory factors IL-8 and COX-2 levels were significantly different between high IPSS group and low IPSS group of patients with BPH. Moreover, the PV and PSA were higher in high IPSS group than those in low IPSS group. The FBS, FINS and inflammatory factors IL-8 and COX-2 levels were positively correlated with IPSS (p<0.05). All the indexes above of BPH patients were decreased after treatment. CONCLUSIONS: The FBS, FINS, and inflammatory factors IL-8 and COX-2 levels are closely correlated with IPSS, which can reflect the severity and prognosis of BPH. It can effectively postpone the progression of BPH by lowering blood glucose, improving insulin resistance, and controlling the expressions of inflammatory factors in serum through a healthy lifestyle and clinical comprehensive treatment.

Autism-associated Dyrk1a truncation mutants impair neuronal dendritic and spine growth and interfere with postnatal cortical development.

Autism is a prevailing neurodevelopmental disorder with a large genetic/genomic component. Recently, the dual-specificity tyrosine-(Y)-phosphorylation-regulated kinase 1 A (DYRK1A) gene was implicated as a risk factor for autism spectrum disorder (ASD). We identified five DYRK1A variants in ASD patients and found that the dose of DYRK1A protein has a crucial role in various aspects of postnatal neural development. Dyrk1a loss of function and gain of function led to defects in dendritic growth, dendritic spine development and radial migration during cortical development. Importantly, two autism-associated truncations, R205X and E239X, were shown to be Dyrk1a loss-of-function mutants. Studies of the truncated Dyrk1a mutants may provide new insights into the role of Dyrk1a in brain development, as well as the role of Dyrk1a loss of function in the pathophysiology of autism.