IntroductionThere is growing attention towards the possible long-term effect of COVID-19 on neuropsychiatric disorders.MethodsWe tested the effect of a combined nutraceutical (Synaid) with known nootropic effects in 40 elderly patients with self-perceived cognitive decline after SARS-CoV-2 infection, treated at home or in hospital.ResultsAfter 3 months of treatment, Synaid significantly improved functional status, MMSE and the main psychological disorders associated with mild cognitive impairment, both in patients previously cared for at home and in hospital because of SARS-CoV-2 infection.ConclusionsSynaid was well tolerated and effective in improving cognitive function and psychosocial parameters after SARS-CoV-2 infection.

IntroductionDipeptidyl peptidase-4 (DPP-4) inhibitors have various cellular effects that are associated with vascular protection. Here, we examined whether vildagliptin protected endothelial function in diabetic rats and explored the involved mechanism.Material and methodsExperimental diabetic rats were obtained by feeding a high-fat diet and administering an intraperitoneal injection of streptozotocin. Rats were randomly divided into four groups: controls (CON), diabetes (DM), diabetes + low dose of vildagliptin (Lvil, 10 mg/kg/day), and diabetes + high dose of vildagliptin (Hvil, 20 mg/kg/day). The metabolic parameters, endothelial function, and whole miRNA expression were measured.ResultsAfter a 12-week treatment, vildagliptin-treated rats showed a significant reduction in blood glucose and blood lipid levels. Moreover, vildagliptin recovered aortic endothelial function in diabetic rats. We identified 31 miRNAs that were differentially expressed in the Hvil group compared with the diabetic group. Importantly, through miRNA target biological function and pathway analysis, we found that vildagliptin activated miR-190-5p to inhibit Ccl2 expression and inhibited miR-134-5p and miR-375-3p to increase Bdnf and Pdk1 expression in the aorta.ConclusionsOur present study indicates that vildagliptin can recover endothelial function in diabetic rats. Anti-inflammatory and anti-apoptosis mechanisms and endothelial moderation may be the intervention targets of vildagliptin to protect the cardiovascular system through miRNA regulation.

IntroductionTuberculous meningitis (TBM) is still a great challenge to global public health. As conventional diagnostic methods for TBM are unsatisfactory, interferon-γ release assays (IGRAs) have been introduced for TBM diagnosis tentatively. However, the role of IGRAs for diagnosing TBM remains unclear. Thus, we systematically evaluated the diagnostic performance of cerebrospinal fluid (CSF) and peripheral blood (PB) IGRAs in TBM to fill this blank.Material and methodsRelevant studies were systematically searched in both foreign and Chinese databases up to March 2018. Studies in which TBM diagnosis was based on microbiological or clinical criteria were included. The quality of the included studies was assessed through the Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2) tool. Main outcome measures, including sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR) and diagnostic odds ratio (DOR), were pooled statistically using random effects models. The potential heterogeneity was explored by threshold effect analysis, subgroup analyses and meta-regression. Funnel plots and Egger’s test were used to test the potential publication bias. Statistical analyses were performed using Stata and Meta-DiSc software.ResultsTwenty-six out of 656 publications were eligible for meta-analysis, including 1892 participants in total. The pooled estimates of PB IGRAs for TBM diagnosis are as follows: sensitivity: 0.81 (95% CI: 0.78–0.84); specificity: 0.76 (95% CI: 0.73–0.78); PLR: 4.23 (95% CI: 2.95–6.07); NLR: 0.24 (95% CI: 0.19–0.32) and DOR: 21.06 (11.91-37.24). The corresponding estimates for CSF IGRAs were obtained: sensitivity: 0.81 (95% CI: 0.76–0.85); specificity: 0.89 (95% CI: 0.86–0.92); PLR: 7.87 (95% CI: 4.98–12.46); NLR: 0.19 (95% CI: 0.13–0.29); and DOR: 47.74 (25.02–91.12).ConclusionsThe diagnostic performance of IGRAs is suboptimal. In terms of cost, turn-around time and accessibility, these assays are unsuitable for use as biomarkers for TBM diagnosis.

IntroductionSeveral published results have established variations in respect to plasma/serum macrophage migration inhibitory factor (MIF) levels and gene polymorphisms with systemic lupus erythematosus (SLE). This study gave a more concise estimation on the MIF levels for SLE patients and established the association between MIF polymorphisms and SLE.Material and methodsAll articles were searched from PubMed, Embase, Web of Science, Wan-Fang, Chinese Biological Medical Literature, and China National Knowledge Infrastructure up to 6th October 2017, with no language restriction. Pooled standard mean difference with 95% confidence interval was evaluated using random effect model. Thirteen articles were used for this meta-analysis, with 620 SLE patients and 779 healthy controls assessed for MIF levels, and 2,159 SLE patients and 2,574 healthy controls considered for MIF-173 C/G and MIF-794 CATT polymorphisms.ResultsThere was a significant higher MIF levels in SLE patients than in healthy controls (p = 0.004). The subgroup analysis showed Asians and ages < 30 had higher MIF levels in SLE patients than in healthy controls. It was evident that patients with systemic lupus erythematosus diseases activity index scores < 8 and ≥ 8, and disease duration for both year < 5 and ≥ 5 of SLE had higher MIF levels when compared to healthy controls. We found a significant association between SLE and MIF-173 C/G, but not MIF-794 CATT.ConclusionsThis study provided evidence of significant higher MIF levels in SLE patients and supported the association of MIF-173 C/G and SLE. However, we were not able to establish an association between MIF-794 CATT and SLE.

IntroductionMaternal glycemic state is positively correlated with fetal insulin secretion. Randomized control studies have shown that treatment during pregnancy inhibits to some degree this glycemic effect. Our study aimed to assess fetal pancreas size in a population of treated mothers with gestational diabetes.Material and methodsA cross-sectional, prospective observational study was conducted. Pregnant women at 19–36 weeks of gestation with pre-gestational diabetes receiving insulin therapy or with gestational diabetes receiving either insulin or oral hypoglycemic therapy were recruited. The fetal pancreas circumference was measured and compared to the normal reference range. The Z score of the difference between measured and normal predicted mean pancreas circumference, the regression analysis throughout pregnancy, and the correlation between estimated fetal weight centile and pancreas circumference were calculated.ResultsNinety-one women who had gestational diabetes and thirty-four women who had pre-gestational diabetes were included in the study. For both groups, fetal pancreas circumference correlated significantly with abdominal circumference, estimated fetal weight and gestational age. The mean Z score between the predicted pancreas circumference in the group of women diagnosed with gestational diabetes and the predicted pancreas circumference in a normal population peaked at around 24 weeks of gestation (1.1) and decreased gradually afterward to a value of zero at 37 weeks. The mean Z score between the predicted pancreas circumference in the group of women with pre-gestational diabetes and the predicted pancreas circumference in a normal population constantly decreased with duration of pregnancy. It was positive until the 25th week of gestation and then presented negative values towards the term.ConclusionsThe presented preliminary data suggest a possible correlation between glycemic control treatment, pancreas size, and gestational age.

IntroductionInfections after spinal surgery are sporadic and depend on the patient's condition and the type and extent of surgery. The incidence of surgical site infections in European centers ranges from 0% to 18%. The aim of the study was to determine the frequency of infections in patients after spinal surgery.Material and methodsThe analysis covered 6067 patients who underwent spinal surgery in the Department of Neuroorthopedics between 2015-2019, taking into account the number of microbiological tests and the number of detected infections, the number of surgical procedures and the rate of SSI infections, the number of readmissions and reoperations, and the use of antibiotics. The analysis was based on retrospective data of patients hospitalized in the analyzed period.ResultsThe number of operated patients remained at a similar level in the analyzed annual periods, from 1136 to 1269 patients, while the infection rate of the operated site ranged from 0,33% to 1,04%, and the percentage of infections was between 0,58% and 3,29 %. In turn, the analysis of reoperations performed due to infection of the operated site in 2018 and 2019 was 0,56% and 0,07%, respectively, which places the center in the leading position in the European ranking. During the analyzed five years, the use of antibiotics was reduced by 2/3.ConclusionsThe analysis of infections in patients after spinal surgery over a 5-year period showed that the SSI rate did not exceed 1,04%, which is comparable with data from recognized European centers. Infections caused by alarm pathogens have been detected occasionally.

IntroductionCarotid atherosclerosis (CAS) is one of the main causes of cerebral infarction in the ageing population. Long non-coding RNA small nucleolar RNA host gene 16 (lnc-SNHG16) could promote the development of atherosclerosis. However, the mechanism of lnc-SNHG16 in CAS remains vague.Material and methodsThe expression levels of lnc-SNHG16, microRNA-30c-5p (miR-30c-5p) and disintegrin and metalloproteinase 10 (ADAM10) were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability and migration were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) and transwell assays, severally. The levels of interleukin-6 (IL-6), IL-β and tumor necrosis factor-α (TNF-α) were assessed by enzyme-linked immunosorbent assay (ELISA). Protein levels of spinal muscular atrophy (SMA), calponin and ADAM10 were examined by western blot assay. The binding relationship between miR-30c-5p and lnc-SNHG16 or ADAM10 was predicted by Starbase, then verified by the dual-luciferase reporter assay.ResultsLnc-SNHG16 and ADAM10 were increased, and miR-30c-5p was decreased in CAS patient and oxidized low-density lipoprotein (ox-LDL)-treated human aortic smooth muscle cells (hASMCs). Lnc-SNHG16 silencing repressed cell viability, migration, inflammation, facilitated differentiation in ox-LDL-treated hASMCs. Moreover, mechanical analysis proved that lnc-SNHG16 improved ADAM10 expression by sponging miR-30c-5p.ConclusionsOur data indicated that lnc-SNHG16 could regulate the progression of ox-LDL induced CAS model by the miR-30c-5p/ADAM10 axis, implying a potential therapeutic strategy for CAS

The present study aimed to investigate the role of peptidase M20 domain containing 1 (PM20D1) in gestational diabetes mellitus (GDM). This observational study included 189 cases of GDM patients who came to our department between March 2018 and December 2019. Additionally, 100 healthy pregnant individuals who came to physical examination were included as healthy controls during the same period. Western blotting was used to determine the expression of PM20D1 at gestational age 24-28 weeks and gestational age 37-40 weeks. Serum inflammatory factors of C-reactive protein (CRP), interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, as well as leptin and adiponectin, were all measured by ELISA. The GDM related indices were also measured. The expression of PM20D1 was markedly decreased in GDM patients compared with the healthy controls. Patients in the third trimester of pregnancy (gestational age 37-40 weeks) showed significantly lower expression of PM20D1 than patients in the second trimester of pregnancy (gestational age 24-28 weeks). Serum levels of CRP, IL-1β, IL-6, TNF-α and leptin were remarkably higher and levels of adiponectin were markedly lower in GDM patients at both the second and third trimester of pregnancy. Also, levels of CRP, IL-1β, IL-6, TNF-α and leptin in GDM patients were the highest at the third trimester of pregnancy. Pearson's analysis showed that PM20D1 was negatively correlated with IL-1β, IL-6 and leptin and was positively correlated with adiponectin. At the second trimester of pregnancy, patients with lower expression of PM20D1 showed remarkably higher levels of HOMA-IR, fasting insulin, FBG, OGTT-1hPG, OGTT-2hPG, TG and LDL-C, and showed markedly lower levels of HDL-C. Down-regulated PM20D1 predicted poor pregnancy outcomes. Reduced PM20D1 was associated with patients' clinical outcomes and pregnancy outcomes in GDM.

IntroductionGlucocorticoids (GCs) are used in the treatment of numerous diseases, and long-term use of GCs causes bone loss. GC receptor activation decreases Bone Mineral Density (BMD) by inhibiting and stimulating osteoblasts and osteoclasts, respectively. GC receptor gene polymorphisms are also associated with increased susceptibility to GCs. The purpose of this study was to assess the relationship between osteoporosis and Glucocorticoid receptor gene (NR3C1) polymorphism in Turkish population.Material and methodsThe study group consisted of 232 unrelated patients with osteoporosis and 150 unrelated healthy controls. All participants, patients and healthy controls, were of Turkish origin, from the central region of Turkey. Genomic DNA was isolated from whole venous blood samples using a commercial DNA isolation kit. The NR3C1 BclI gene C/G polymorphism was analyzed by polymerase chain reaction.ResultsThe frequencies of CC, CG and GG genotypes in the patients were 34.5%, 48.3%, and 17.2% and in the controls were 48.0%, 42.0%, and 10.0%. A statistically significant difference was observed between patients and controls according to genotype frequencies (p=0.01). C and G allele frequencies of C/G polymorphism were 58.6% and 41.4% in patient group and 69.0% and 31.0% in control group (p=0.005).ConclusionsThe NR3C1 BclI gene C/G polymorphism could be one of the genetic factors causing osteoporosis.