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Background Prevention of Alzheimer's disease (AD) with Vitamin D (VD) supplementation has been studied widely, but the results in the literature are very conflicting. The study question Can VD supplementation really prevent AD? Study design The literature was searched from PubMed, Cochrane library, Web of Science, and EMBASE to identify relevant randomized clinical trials (RCTs). The titles and abstracts were evaluated independently by 2 of the authors. Results Nine RCTs with 2345 participants were included. In the meta-analysis, we found no significant difference in the Mini-Mental State Examination, verbal fluency, verbal memory, visual ability, and attention scores between the VD intervention group and comparison group [standardized mean difference (SMD) = -0.05, 95% confidence interval (CI) = -0.51 to 0.41; SMD = -0.01, 95% CI = -0.13 to 0.11; SMD = 0.12, 95% CI = -0.45 to 0.69; SMD = 0.42, 95% CI = -0.15 to 1.00; and SMD = 0.01, 95% CI = -0.24 to 0.27, respectively]. In subgroup analysis, we found that the intervention with only VD or plus calcium, follow-up duration, and baseline 25(OH)D levels did not explain the cause for high heterogeneity. Conclusions Overall, the current evidence did not support the beneficial effect of VD supplement to prevent AD. High quality RCTs and further studies are needed to clarify the effects of VD supplementation on preventing AD.

Signal transducer and activator of transcription 1 (STAT1) is a transcription factor that mediates cellular responses to interferons (IFNs) and other cytokines and growth factors in diverse cell types. STAT1 gain-of-function (GOF) mutations result in an unexpectedly wide range of clinical features. It remains unclear why STAT1 GOF mutations result in such a broad spectrum of phenotypes. We analyzed the clinical, molecular, and phenotypic characteristics of nine Chinese patients with STAT1 GOF mutations. This study enrolled nine patients with STAT1 GOF mutations including five novel mutations. We discuss the molecular and phenotypic characterization such as unique Penicillium marneffei lymphadenitis. Patients with STAT1 GOF mutations had defects in both innate and adaptive immunity, including impaired T cell receptor (TCR) diversity; reduced numbers of naive and effector memory CD4+ T cells, memory B cells, and NK cells; and defects in the production of IL-17A and IFN-γ. In addition, experiments with primary immune cells revealed that enhanced STAT1 phosphorylation resulted from not only lower rates of STAT1 dephosphorylation but also increased total STAT1 expression. Our report provides the first comprehensive overview of the molecular genetics, clinical heterogeneity, and underlying immunological abnormalities of patients with STAT1 GOF mutations in China. In further study, to find the relationship between different STAT1 GOF mutations and clinical phenotype as well as the mechanism of increased total STAT1 expression will be needed.

This study aimed to investigate the prognostic factors of patients after liver cancer surgery and evaluate the predictive power of nomogram. Liver cancer patients with the history of surgery in the Surveillance, Epidemiology, and End Results database between 2000 and 2016 were preliminary retrieved. Patients were divided into the survival group (n = 2120, survival ≥5 years) and the death group (n = 2615, survival

Different opinions exist on the relationship between the C-reactive protein-to-albumin ratio (CAR) and the prognosis of colon cancer. This study is aimed at evaluating the relationship between CAR and prognosis of stage II–III colon cancer and establishing a clinical prognosis model. Patients were randomised to a training set (566 cases) and validation set (110 cases). The relationship between CAR and clinicopathological variables was calculated, and the Kaplan-Meier method was used to analyse the overall survival (OS) rate of colon cancer. In the training set, colon cancer independent risk factors were included in the prognosis model and then tested in the validation set. The accuracy and discrimination of the model were assessed using the C-index and calibration curves. Compared with patients with low CAR, patients with high CAR showed significantly poorer survival (P=0.020). In the multivariate analysis, CAR, carcinoembryonic antigen (CEA), lymph node metastasis, operation mode, and perineural invasion were identified as independent prognostic indicators and adopted to establish the prediction model. The C-index of the nomogram for predicting OS reached 0.751 in the training set and 0.719 in the validation set. The calibration curve exhibited good consistency. In the present study, the CAR may be an independent prognostic factor for stage II–III colon cancer, and the nomogram has a certain predictive value. However, further prospective large-sample research needs to be conducted to validate our findings.

The aim of this research was to explore whether IL-18 can be a serological marker for the diagnosis of systemic-onset juvenile idiopathic arthritis (sJIA). A total of 23 sJIA patients (13 males, median age 8.2), 20 acute lymphoblastic leukemia (ALL) patients, 18 patients with severe infections (SIF), 26 Kawasaki disease (KD) patients, 18 juvenile idiopathic arthritis (JIA) patients, and 25 healthy control patients were selected for this study. Enzyme-linked immunosorbent assays (ELISAs) were used to determine the serum concentrations of the S100A8, S100A9, and IL-6 proteins. The serum IL-18 levels were detected by a cytometric bead array (CBA). The serum IL-6 concentrations in various disease groups were significantly higher than that in the healthy control group. The IL-6 concentrations exhibited no significant difference between disease groups. The S100A8 level in the sJIA group was significantly higher than those of the ALL, JIA, and healthy control groups but showed no significant difference compared to the SIF and KD groups. The S100A9 serum concentration in the sJIA group was significantly higher than those in the ALL and healthy control groups and exhibited no significant difference from the SIF, KD, and JIA groups. The IL-18 level of the sJIA group was significantly higher than that of the other febrile disease groups. The IL-18 serum concentration may be used as a biological serum marker to distinguish sJIA from other febrile diseases.

To explore the relevance between nasal symptoms and laryngopharyngeal reflux disease in patients with allergic rhinitis.Thirty patients of laryngopharyngeal reflux disease were diagnosed in ENT outpatient department in our hospital. All patients have symptoms of sneeze, nasal discharge as chief complaint and they responded no effect for other normal treatment for nasal-sinusitis at least three months. Orally before meals, a dose of 5 mg Mosapride citrate each time, three times a day for 7 days. Orally before meals, a dose of 20 mg Esomeprazole each time, two times a. day for 2-3 months. Nasal spray, one spray of azelastine hydrochloride once, two times a day for 2 month.Laryngopharyngeal reflux symptom scores at four time points (the first visit, post treatment 15 days, 45 days, 75 days) were analyzed by repeated measures analysis of variance. There is a significant difference in four time points.Laryngopharyngeal reflux disease has a strong association with allergic rhinitis. Patients who has allergic rhinitis nasal symptoms as chief complaint must be exclude, the laryngopharyngeal reflux disease first.