Glycemic control and its influencing factors in type 2 diabetes patients in Anhui, China.

Objective: To investigate the status of glycemic control and analyze its influencing factors in patients with type 2 diabetes (T2D) in Anhui, China. Methods: 1,715 T2D patients aged 18-75 years old were selected from 4 counties or districts in Anhui Province in 2018, using a convenience sampling method. All patients have undergone a questionnaire survey, physical examination, and a glycosylated hemoglobin (HbA1c) test. According to the 2022 American Diabetes Association criteria, HbA1c was used to evaluate the glycemic control status of patients, and HbA1c < 7.0% was defined as good glycemic control. The influencing factors of glycemic control were analyzed by multivariate unconditional logistic regression. Results: The prevalence of good glycemic control among people with T2D in the Anhui Province was low (22.97%). On univariate analysis, gender, education level, occupation, region, smoking, drinking, waist circumference and disease duration (all P < 0.05) were significantly associated with glycemic control. The factors associated with pool glycemic control were female gender [OR = 0.67, 95%CI (0.52, 0.86), P = 0.001], higher level of education [OR = 0.47, 95%CI (0.27, 0.83), P = 0.001], living in rural areas [OR = 1.77, 95%CI (1.39, 2.26), P < 0.001], central obesity [OR = 1.58, 95%CI (1.19, 2.09), P = 0.001] and longer duration of disease [OR = 2.66, 95%CI (1.91, 3.69), P < 0.001]. Conclusions: The prevalence of good glycemic control in people with T2D in Anhui Province was relatively low, and gender, region, education level, central obesity and course of the disease were influencing factors. The publicity and education on the importance of glycemic control should be further strengthened in T2D patients, and targeted intervention measures should be carried out for risk groups.

[Determination of forbidden and restricted pesticides in Angelicae Sinensis Radix].

The present study is to establish a method for simultaneous determination of 50 kinds of pesticides in Angelicae Sinensis Radix by using liquid chromatography tandem mass spectrometry. The forbidden,restricted and customary pesticides were picked out as detecting indexes according to the principals of risk management. The factors affecting the extraction,purification,and detection were optimized,and the final condition was established as follows: the samples were extracted with acetonitrile. The separation of target compounds were performed by liquid column,and quantitative analysis was carried out by LC-MS/MS with MRM model. The calibration curves were linear in the range of 1-100 µg·L~(-1) with correction coefficients of greater than 0. 990. The recoveries of more than 93. 9%pesticides were ranged from 60% to 140% at three spiked levels. The detecting indexes in the method cover most forbidden and restricted pesticides,which is meaningful for the safety supervision of the Angelicae Sinensis Radix. With the advantage of rapidness and accuracy,this method can be used for routine determination of multi-pesticides in Angelicae Sinensis Radix.

Specific OCT1 and ABCG2 polymorphisms are associated with Lamotrigine concentrations in Chinese patients with epilepsy.

PURPOSE: The pharmacokinetics of Lamotrigine (LTG) varies widely among patients with epilepsy. In this study, we are aiming to investigate the effects of OCT1, ABCG2, ABCC2 and HNF4α genetic polymorphisms on plasma LTG concentrations and therapeutic efficacy in Chinese patients with epilepsy. METHODS: The study cohort comprised 112 Han Chinese patients with epilepsy who were receiving LTG monotherapy. Blood samples were taken and LTG levels were measured. The polymorphisms of OCT1 rs2282143, rs628031, ABCG2 rs2231142, rs2231137, ABCC2 rs2273697 and HNF4α rs2071197, rs3212183 were determined. The therapeutic efficacy of LTG at the 1-year time-point was assessed. Data analysis was performed using IBM SPSS Statistics 22.0. RESULTS: There were significant associations between OCT1 rs628031, ABCG2 rs2231142 polymorphisms and normalized LTG concentrations in patients with epilepsy (P<0.05). On the other hand, polymorphisms of OCT1 rs2282143, ABCG2 rs2231137, ABCC2 rs2273697 and HNF4α rs2071197, rs3212183 exhibited no correlation with LTG concentrations. Additionally, no significant association existed between all the studied genotypes and LTG treatment response. CONCLUSIONS: These results suggested that the polymorphisms of OCT1 rs628031 and ABCG2 rs2231142 may affect LTG metabolism in Chinese patients with epilepsy. However, future studies are necessary to be investigated in a larger cohort of epileptic patients.

Subarachnoid Hemorrhage due to Spinal Cord Schwannoma Presenting Findings Mimicking Meningitis.

BACKGROUND: Subarachnoid hemorrhage (SAH) of spinal origin is uncommon in clinical practice, and spinal schwannomas associated with SAH are even more rarely reported. We report an unusual case of spinal SAH mimicking meningitis with normal brain computed tomography (CT)/magnetic resonance imaging (MRI) and negative CT angiography. Cerebrospinal fluid examination results were consistent with the manifestation of SAH. Spinal MRI performed subsequently showed an intradural extramedullary mass. The patient received surgery and was finally diagnosed with spinal cord schwannoma. METHOD: A retrospective chart review of the patient was performed. RESULTS: We describe a case of SAH due to spinal cord schwannoma. Our case highlights the importance of careful history taking and complete evaluation. CONCLUSION: We emphasize that spinal causes should always be ruled out in patients with angionegative SAH and that schwannoma should be considered in the differential diagnosis of SAH etiologies even though rare.

Neuro-Sweet disease with positive modified acid-fast staining of the cerebrospinal fluid: A case report.

Neuro-Sweet disease (NSD) is Sweet disease with central nervous system (CNS) involvement. To the best of our knowledge, the present case report is the first to describe NSD complicated by endogenous infection with Mycobacterium tuberculosis. The present case report describes a male patient who developed NSD-induced meningitis, which initially manifested as a fever, headache and neck stiffness. Painful erythematous plaques subsequently developed on his face, neck and upper trunk. Brain magnetic resonance imaging was performed and the results were normal, whereas modified acid-fast stain analysis of the cerebrospinal fluid (CSF) provided a positive result. The patient was thus diagnosed with viral meningitis and tuberculosis. However, subsequent skin biopsy results demonstrated neutrophilic infiltration into the dermis without vasculitis, and subsequent human leukocyte antigen typing was positive for Cw1 and negative for B51 and the patient was diagnosed with NSD. Following treatment with corticosteroids, and antiviral and anti-tuberculotic agents, the clinical symptoms were reduced and the previously abnormal findings in the CSF examinations and associated laboratory data were improved. The present case indicates that the diagnosis of NSD is not easily achieved, and early skin biopsy is vital to ensure a fast and effective diagnosis. In addition to systemic corticosteroids, comprehensive treatment is also recommended for patients with NSD complicated by additional complex medical problems.

TMPyP4-regulated cell proliferation and apoptosis through the Wnt/ß-catenin signaling pathway in SW480 cells.

BACKGROUND: The aim of this study was to investigate the potential effects of the 5, 10, 15, 20-tetrakis (1-methylpyridinium-4-yl) porphyrin (TMPyP4) on the proliferation and apoptosis of SW480 cells and the underlying mechanisms by which TMPyP4 exerted its actions. METHODS: After treated with different doses of TMPyP4, cell viability was determined by MTT method, the apoptosis was observed by flow cytometry (FCM) and the expression of Wnt, GSK-3ß, ß-catenin and cyclinD1 was measured by RT-PCR and Western blot analysis. RESULTS: The analysis revealed that TMPyP4 potently suppressed cell viability and induced the apoptosis of SW480 cells in a dose-dependent manner. In addition, the downregulation of Wnt, ß-catenin and cyclinD1 expression levels was detected in TMPyP4-treated SW480 cells. However, followed by the block of Wnt signaling pathway using siRNA methods, the effects of TMPyP4 on proliferation and apoptosis of SW480 cells were significantly reduced. CONCLUSION: It indicates that the TMPyP4-inhibited proliferation and -induced apoptosis in SW480 cells was accompanied by the suppression of Wnt/ß-catenin signaling pathway. Therefore, TMPyP4 may represent a potential therapeutic method for the treatment of colon carcinoma.

Association between bone marrow stromal cell antigen 1 gene polymorphisms and the susceptibility to Parkinson's disease: a meta-analysis.

A number of studies have investigated the association between Parkinson's disease (PD) and genetic polymorphisms of bone marrow stromal cell antigen 1 (BST-1). However, the results to date have been conflicting. In this study a meta-analysis was performed to assess the association between BST-1 polymorphisms and PD. Previous relevant studies were identified from Medline, Embase and Cochrane databases, among which the studies evaluating the association of BST-1 polymorphisms with risk of PD were used in the meta-analysis. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were determined for different genetic models using meta-analytic methods. Subgroup analysis was performed based on study designs and participant ethnicity, and sensitivity analysis was also performed. Eleven studies comprising 11,070 cases and 19,169 controls were included in this meta-analysis. ORs and 95% CIs were used to assess the strength of association. The rs4698412 variant (G→A) showed a significant summary OR of 1.12 (95% CI: 1.05-1.20; P=0.001) in an allelic model. This significant association was also observed in the subgroup analysis based on participants' ethnicity and study designs. The pooled OR of the rs11724635 variant (C→A) indicated a non-significant association with PD in a recessive model (OR, 1.16, 95% CI: 0.97-1.40; P=0.112), dominant model (OR, 1.10, 95% CI: 0.86-1.41; P=0.458) and allelic model (OR, 1.10, 95% CI: 0.95-1.27; P=0.224). Although the rs11931532 variant (T→C) did not show association with PD (OR, 0.99, 95% CI: 0.85-1.15; P=0.9), the pooled estimation of genome-wide association studies (GWAS) showed a significant connection with PD (OR, 1.19, 95% CI: 1.08-1.31; P=0.001). Sensitivity analysis supported these findings, and no evidence of publication bias was observed in the meta-analysis. Our studies suggested that the rs4698412 variant of BST-1 may increase the PD susceptibility.

Prevalence of hyperhomocysteinaemia and some of its major determinants in Shaanxi Province, China: a cross-sectional study.

The aim of the present study was to investigate the prevalence of hyperhomocysteinaemia (HHCY; total plasma homocysteine (tHcy) concentration >15 µmol/l) and its major determinants in healthy Chinese northerners. A descriptive and cross-sectional study was conducted in Shaanxi Province, China. The study sample included 2645 participants (1042 men and 1603 women) aged >20 years. Demographic characteristics and lifestyle factors were assessed via questionnaire interviews and physical examination. Plasma levels of homocysteine and folate and methylenetetrahydrofolate reductase (MTHFR) gene polymorphism were determined according to standard methods. The prevalence of HHCY was 67·7 % (81·4 % in men and 58·8 % in women). The geometric mean of tHcy concentration was 19·1 µmol/l. The OR of HHCY were 0·44 (95 % CI 0·34, 0·57) for women v. men; 1·95 (95 % CI 1·41, 2·70), 1·41 (95 % CI 1·05, 1·88) and 0·76 (95 % CI 0·64, 0·89) for participants with smoking and alcohol drinking cessation and improved physical activity levels, respectively; 0·25 (95 % CI 0·17, 0·38), 0·33 (95 % CI 0·22, 0·49) and 0·56 (95 % CI 0·36, 0·88) for participants with an education level of elementary school, secondary school and university v. illiterate, respectively; 1·41 (95 % CI 1·13, 1·75) and 3·05 (95 % CI 2·35, 3·97) for participants with CT and TT v. CC genotype at MTHFR 677C â†’ T polymorphism, respectively. These results demonstrate that the prevalence of HHCY is considerably high in Chinese northerners, especially in TT subjects, suggesting that implementation of tHcy-lowering strategies, such as lifestyle changes, is necessary.

Targeted knockdown of IQGAP1 inhibits the progression of esophageal squamous cell carcinoma in vitro and in vivo.

IQGAP1 is a scaffolding protein that can regulate several distinct signaling pathways. The accumulating evidence has demonstrated that IQGAP1 plays an important role in tumorigenesis and tumor progression. However, the function of IQGAP1 in esophageal squamous cell carcinoma (ESCC) has not been thoroughly investigated. In the present study, we showed that IQGAP1 was overexpressed in ESCC tumor tissues, and its overexpression was correlated with the invasion depth of ESCC. Importantly, by using RNA interference (RNAi) technology we successfully silenced IQGAP1 gene in two ESCC cell lines, EC9706 and KYSE150, and for the first time found that suppressing IQGAP1 expression not only obviously reduced the tumor cell growth, migration and invasion in vitro but also markedly inhibited the tumor growth, invasion, lymph node and lung metastasis in xenograft mice. Furthermore, Knockdown of IQGAP1 expression in ESCC cell lines led to a reversion of epithelial to mesenchymal transition (EMT) progress. These results suggest that IQGAP1 plays crucial roles in regulating ESCC occurrence and progression. IQGAP1 silencing may therefore develop into a promising novel anticancer therapy.

Overexpression of IQGAP1 in human pancreatic cancer.

BACKGROUND: Pancreatic cancer is a highly aggressive malignant tumor with the lowest survival rate. A better understanding of the molecular mechanisms which contribute to pancreatic cancer occurrence and progression will aid in the development of new approaches to the early diagnosis, prevention, and treatment of this deadly disease. The scaffold protein IQGAP1 shows elevated levels in a variety of cancer types. Currently, we investigated whether or not IQGAP1 is also overexpressed in pancreatic cancer. METHODS: IQGAP1 expression was examined in pancreatic cancer and normal tissues adjacent to cancerous tissues (adjacent tissues) by Western blotting and real-time RT-PCR as well as in paraffin sections of tissue microarray by immunohistochemistry. The correlations between IQGAP1 expression and various clinicopathological characteristics were analyzed. RESULTS: Western blotting and real-time RT-PCR revealed that the levels of IQGAP1 protein and mRNA expression in pancreatic cancer tissues were significantly increased compared with adjacent tissues. Immunohistochemistry analysis on tissue microarray showed that IQGAP1 protein expression was significantly higher in pancreatic cancer (80.0%, 48/60) compared with adjacent tissues (18.3%, 11/60) (P<0.001). Moreover, overexpression of IQGAP1 was shown to be associated with the grades of tumor differentiation (P<0.05). CONCLUSION: The overexpression of IQGAP1 may play an important role in pancreatic cancer occurrence and progression, and IQGAP1 may serve as a novel molecular target for the diagnosis and treatment of pancreatic cancer.

The disturbance of hippocampal CaMKII/PKA/PKC phosphorylation in early experimental diabetes mellitus.

BACKGROUND: Defining the impact of diabetes and related risk factors on brain cognitive function is critically important for patients with diabetes. AIMS: To investigate the alterations in hippocampal serine/threonine kinases signaling in the early phase of type 1 and type 2 diabetic rats. METHODS: Early experimental diabetes mellitus was induced in rats with streptozotocin or streptozotocin/high fat. Changes in the phosphorylation of proteins were determined by immunoblotting and immunohistochemistry. RESULTS: Our data showed a pronounced decrease in the phosphorylation of Ca(2+) /calmodulin-dependent protein kinase II (CaMKII) in the hippocampi of both type 1 and type 2 diabetic rats compared with age-matched control rats. Unexpectedly, we found a significant increase in the phosphorylation of synapsin I (Ser 603) and GluR1 (Ser 831) in the same experiment. In addition, aberrant changes in hippocampal protein kinase C (PKC) and protein kinase A (PKA) signaling in type 1 and type 2 diabetic rats were also found. Moreover, PP1α and PP2A protein levels were decreased in the hippocampus of type 1 diabetic rats, but significantly up-regulated in type 2 diabetic rats. CONCLUSIONS: The disturbance of CaMKII/PKA/PKC phosphorylation in the hippocampus is an early change that may be associated with the development and progression of diabetes-related cognitive dysfunction.

DCC is specifically required for the survival of retinal ganglion and displaced amacrine cells in the developing mouse retina.

Netrin-1 and DCC are well known for their roles in neurite growth, axonal guidance, and neuronal migration. Recently, a number of studies showed that DCC is involved in the induction of apoptosis, and this proapoptotic activity can be blocked in the presence of Netrin-1. However, here, we found that DCC is required for the survival of two types of neurons selectively in the developing mouse retina where DCC is abundantly expressed. Our results showed that the DCC(-/-) retina displayed a reduced ganglion cell layer with relatively normal neuroblastic layer. Immunostaining assays revealed that in DCC(-/-) mice, initial neurogenesis within retina was unchanged while the numbers of differentiated retinal ganglion cells and displaced amacrine cells in ganglion cell layer were greatly reduced due to increased apoptosis. By contrast, other neuronal types including horizontal cells, bipolar cells, amacrine cells, photoreceptors, and Müller cells appeared normal in DCC mutant retinas. Moreover, DCC(kanga) mice that lack the intracellular P3 domain of DCC receptor displayed the same defects as DCC(-/-) mice. Thus, our findings suggest that DCC is a key regulator for the survival of specific types of neurons during retinal development and that DCC-P3 domain is essential for this developing event.

A refined map of early gene expression in the dorsal rhombomere 1 of mouse embryos.

Rhombomere 1 (r1), a temporary structure in the early developing brain, is bounded rostrally by the isthmus organizer and caudally by the r2 domain. Many genes involved in r1 induction and patterning have been identified. However, our knowledge of a comprehensive map of r1 regionalization defined by these genes at early embryonic stages remains fragmentary. In the present study, we examined the expression of a variety of genes in the dorsal r1 of E9.0-E10.5 mouse embryos. The expression domains within ventricular zone of these genes examined allowed us to define four distinct regions along the anterior-posterior (A-P) axis of the dorsal r1: the Wnt1/Lmx1a/Gdf7/Msx1/Msx2-positive roof plate, Math1/Olig3/Msx1/Msx2-positive, upper rhombic lip, Mash1/Ngn1/Ngn2-positive intermediate domain, and Mash1/Ngn1/Ngn2-positive rostral domain. Moreover, we defined the distribution of several genes expressed in the mantle zone of the dorsal r1, including Lmx1b, Lhx2, Lhx9, Phox2a and Phox2b. Taken together, our gene expression data identify a refined subdivision of the dorsal r1 with four distinct domains along the A-P axis and a mantle zone at early embryonic stages.

Effect of temperature on iron leaching from bauxite residue by sulfuric acid.

Bauxite residue, as solid waste from alumina production, contains mainly hematite [Fe2O3]. Kinetic study of iron leaching of bauxite residue by diluted sulfuric acid at atmospheric pressure has been investigated. The results have been obtained as following: (i) Temperature play an important role in iron leaching from bauxite residue. Higher temperature is favor of Fe(III) leaching from bauxite residue. (ii) The leaching process is applicable to the intra-particle diffusion model and the apparent activation energy of model of leaching is found to be 17.32 kJ/mol.

[Mutation analysis of keratin 9 gene in a pedigree with epidermolytic palmoplantar keratoderma].

OBJECTIVE: To identify mutations of keratin 9 (KRT9) gene in a big Chinese family with epidermolytic palmoplantar keratoderma(EPPK) combined with knuckle-pad-like lesions and nail lesions. METHODS: Genomic DNA from peripheral blood of all available members in this family and 50 unrelated healthy individuals was used for amplification of the whole coding sequence and the intron-exon boundaries of KRT9 gene by PCR; The mutation was detected by direct sequence analysis and identified by restriction endonuclease Dde I. RESULTS: A mutation of AAT>AGT at codon 160 (N160S) was found in all patients but not in unaffected family members and 50 controls. CONCLUSION: The mutation of AAT>AGT at codon 160 (N160S) is the disease-causing mutation in this Chinese pedigree with EPPK.