Objective To investigate association between postural changes of blood pressure and carotid atherosclerosis in the elderly.Methods Standardized questionnaires,physical examination and biochemical blood tests were performed to acquire clinical characteristics of the participants.Presences of carotid plaques were identified by carotid ultrasound examination.Orthostatic hypotension (OH) and orthostatic hypertension (OHT) were defined according to the international consensus.Multivariable logistic regression analysis was performed to analyze the associations of carotid plaques with OH and OHT.Results 377 old people were finally included,of which 101 had OH and 33 had OHT.After full adjustment for possible confounders,old people with carotid plaques had significantly increased risk for OH as compared with those without carotid plaques (OR=2.27,95％ CI:1.32-3.90,P=0.003).Participants with bilateral carotid plaques were associated with significantly increased risk for OH (OR=3.45,95％CI:1.74 6.84,P=0.001),while the association between unilateral carotid plaques and OH was not significant (OR=1.71,95％ CI:0.88-3.32,P=0.112).No significant association was identified between carotid plaques (bilateral or unilateral) and OHT.Conclusions Presence of carotid plaques,particularly bilateral plaques,may be an independent risk factor for OH.

Objective To investigate the relationship between rapists and related allele genes based on the analysis of 15 short tandem repeats (STRs) loci genetic polymorphism. Methods The method of Genome-wide scan was being used. Buccal swab samples of 129 rapists and 156 random populations were collected and PCR compound amplification was carried out with the aid of AmpFISTR Identifiler system. Then the products were subjected to electrophoresis and gene detection with AB13100 type gene analysis system so as to calculate and compare the alleles of 15 STRs gene frequency in the two groups. Results All the 15 STRs loci allele gene frequency in rapists and random population was found to coincide with Hardy-Weinberg law(P>0. 05). Allele 28 of D21S11 (rapists: 1.55% ,control group:5. 13%) ,allele22 of FGA(rapists:24.03% ,control group:16.99%),allele23 of FGA(rapists: 17.05% ,control group:26.28%) ,allele 10 of TH01(rapists:1.16% ,control group:4.17%) ,allele 8 of TPOX(rapists:55.77% ,control group:63.77%),allele 12 of TPOX(rapists:4.26% ,control group: 1.28%) were different between the two groups (P< 0.05) .while it is no differ significantly in other STRs loci allele gene(P >0.05). Conclusion Allele 28 of D21 S11,allele 22 and 23 of FGA, allele 10 of TH01, allele 8 and 12 of TPOX may be associated with the violent crime of rape. It is suggested that there are existing sensitive or resistance genes about the violent crime of rape in chromosome 2,4,11,21.

In this study, a rapid and sensitive analytical method was developed for the determination of 10 major compounds (procyanidin B1, catechin, procyanidin B2, rutin, isoquercitrin, kaempferol-3-O-rutinoside, astragalin, quercitrin, quercetin, and kaempferol) in Tetrastigma hemsleyanum by using ultra-performance liquid chromatography coupled with triple-quadrupole tandem mass spectrometry (UPLC-MS/MS) in multiple-reaction monitoring (MRM) mode. UPLC-MS/MS assay with negative ion mode was performed on a Waters CORTECS C18 (2.1 mm x 100 mm, 1.6 μm) with the mobile phase consisting of acetonitrile (A) and 0.1% aqueous formic acid (B) in gradient elution at a flow rate of 0.25 mL · min(-1) and the column temperature was set at 45 °C. Under the optimized chromatographic conditions, good separation for 10 target compounds were obtained including chiral isomer procyanidins B1 and B2 were completely separated within 8.5 min. Satisfactory linearity was achieved with wide linear range and fine determination coefficient (r > 0.996 6), the overall recoveries were ranged from 95.44%-110.40% with the RSD ranging from 2.37%-8.69%. It is the first report about simultaneous analysis of 10 major flavonoids components in Tetrastigma hemsleyanum by using UPLC-MS/MS method, which affords highly sensitive, specific, speedy and efficient method for quality control of Tetrastigma hemsleyanum

AIM:MicroRNAs ( miRNAs) were recognized to play significant roles in cardiac hypertrophy .But, it remains unknown whether cyclin/Rb pathway is modulated by miRNAs during cardiac hypertrophy .This study investigates the potential roles of microRNA-1 (miR-1) and microRNA-16 (miR-16) in modulating cyclin/Rb pathway during cardiomyocyte hypertrophy .METHODS:An animal model of hypertrophy was established in a rat with abdominal aortic constriction (AAC).In addition, a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocyte .RESULTS:miR-1 and-16 expression were markedly de-creased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats .Overexpression of miR-1 and -16 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes .Expression of cyclins D1, D2 and E1, CDK6 and phosphorylated pRb was increased in hypertrophic myocardium and hypertrophic cardiomyocytes , but could be reversed by enforced expression of miR-1 and -16.CDK6 was validated to be modulated post-transcriptionally by miR-1, and cyclins D1, D2 and E1 were further validated to be modulated post-transcriptionally by miR-16.CONCLUSION: Attenuations of miR-1 and -16 provoke cardiomyocyte hypertrophy via derepressing the cyclins D1, D2, E1 and CDK6, and activating cyclin/Rb pathway.

AIM:To investigate the effect of miR-214 on cardiomyocyte hypertrophy and the expression of the potential target genes . METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular car-diomyocytes (NMVCs).Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Wes-tern blotting, respectively.RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-in-duced hypertrophic cardiomyocytes .Dual luciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly in-creased in the hypertrophic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hy-pertrophy-related genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .

AIM:To investigate the effect of microRNA-214 ( miR-214) on cardiomyocyte hypertrophy and the expression of the potential target genes .METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular cardiomyocytes ( NMVCs) .Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Western blot , respectively .RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-induced hypertrophic cardiomyocytes .Dual lu-ciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly increased in the hypertro-phic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hypertrophy-re-lated genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .

Objective:To investigate the expression level of C-type lectin domain family 4 member G ( CLEC4 G) in liver disease tissues and its correlation with the clinicopathological characteristics of hepatocellular carcinoma (HCC) patients. Methods:The cancer tissue and the corresponding adjacent tissues (at least 2 cm from the edge of the cancer tissue), cut in surgeries from January to December in 2019, of 40 HCC patients in Zhuzhou Central Hospital, as well as 10 normal liver tissue samples (seen as far away as possible from the edge of the cancer tissue with naked eyes) and 10 liver cirrhosis samples were analyzed retrospectively. The tumor genome atlas (TCGA) database was used to screen the HCC transcriptome data sets, and bioinformatics methods were used to make expression heat maps and box maps which can help analyze the difference of CLEC4 G in cancer and adjacent tissues. The mRNA expression level of CLEC4 G was detected by conducting real-time fluorescence quantitative PCR (qRT-PCR), and the protein expression level of CLEC4G was detected by immunohistochemistry (IHC). The measurement data were expressed as mean±standard deviation ( Mean± SD). Group t test was used for inter-group comparison. The counting information was expressed as a percentage (%). The χ2 test was adopted to analyze the correlation between CLEC4 G expression level and the clinicopathological features of patients. Results:The expression level of CLEC4 G in cancer tissues was significantly decreased in heat map compared with that in adjacent tissues. In the box figure, the relative expression of CLEC4 G mRNA in the cancer tissues was (82.5±18.9) and (3 354.4±296.2) in paracancer tissues, with statistically significant difference ( P<0.001). Respectively, qRT-PCR and IHC showed that mRNA of CLEC4 G were abundant in normal liver tissues (3 301.3±286.4), while they were very little in liver cancer tissues (63.6±32.9), significantly decreasing in liver cirrhosis (1 742.6±208.7) and paracancer tissues (1 553.2±249.9), with statistically significant difference ( P<0.001). Moreover, low CLEC4 G expression level was associated with tumor vascular metastasis in HCC patients. Conclusions:CLEC4 G is highly expressed in normal liver tissue, but with the progression of malignant liver disease, it is significantly decreased with little expression in HCC tissue. It can be expected to be a good marker for the pathological diagnosis of HCC.

Objective:To explore the efficacy of breaking blood expelling stasis method accelerates hematoma resolution after intracerebral hemorrhage (ICH) and its potential mechanism.Methods:63 ICH patients confirmed by computer tomography (CT) scan from August 2019 to February 2020 were selected as the research objects and randomly divided into control group ( n=29, routine treatment plus placebo) and observation group ( n=34, routine treatment plus breaking blood expelling stasis granules). The changes of neurological function and hematoma volume were observed before and after treatment. At the same time, the ICH rat model was constructed to observe the changes of neurobehavior and hematoma volume after the intervention of breaking blood expelling stasis granules. The expressions of peroxidase proliferator-activated-receptor γ(PPARγ), CD11b and CD36 in the surrounding tissues of hematoma were detected by Western blot on the third day after the intervention. Results:After two weeks of treatment, the National Institutes of Health Stroke Scale (NIHSS) score and hematoma volume of the two groups decreased (all P<0.05), and the NIHSS score and hematoma volume of the observation group were significantly lower than those of the control group (all P<0.05). In addition, the changes of NIHSS score and hematoma volume in the observation group before and after treatment were significantly greater than those in the control group ( P<0.01). In animal experiments, the hematoma volume in the breaking blood expelling stasis group on the 14th day after ICH was significantly smaller than that in the ICH group [(9.8±4.9)mm 3 vs (17.6±6.4)mm 3,P<0.05], and the reduction of hematoma in the breaking blood expelling stasis group on the 7th and 14th day was significantly larger than that in the ICH group [(4.6±2.9)mm 3 vs (-2.1±1.6)mm 3, (14.3±3.8)mm 3 vs (4.2±2.8)mm 3, all P<0.01]. The percentage of right turn on 3rd, 7th and 14th day and the modified Neurological Severity Score (mNSS) on 7th and 14th day in the breaking blood expelling stasis group were lower than those in the ICH group (all P<0.05). Western blot analysis showed that the expressions of CD11b, CD36 and PPARγ in the breaking blood expelling stasis group on the third day after ICH were significantly higher than those in the ICH group (CD11b: 0.78±0.12 vs 0.49±0.11, P<0.05; CD36: 1.16±0.16 vs 0.80±0.11, P<0.05; PPARγ: 0.78±0.11 vs 0.37±0.10, P<0.01). Conclusions:Breaking blood expelling stasis can effectively accelerate intracerebral hematoma clearance and improve neurological outcome after ICH, and the mechanism maybe probably mediated by activating PPARγ and enhanced CD36, CD11b upregulation on microglia/macrophages, which resulting in facilitating erythrocyte endogenous phagocytosis.

Objective To analyze the clinical features and risk factors of delayed intracranial hemorrhage (DICH) after ventriculoperitoneal shunt (VPS) in patients with communicating hydrocephalus.Methods One hundred and seventy-six patients with ventriculoperitoneal shunt due to communicating hydrocephalus secondary to craniocerebral trauma,hypertensive intracerebral hemorrhage,brain tumor or intracranial aneurysm rupture hemorrhage,admitted to our hospital from January 2012 to August 2018,were selected in our study;these patients were divided into DICH group and non-DICH group according to whether or not DICH occurred.The clinical features,including incidence,time and location of DICH,were analyzed.The differences of age,gender,length of stay,concomitant diseases,previous operation history,incidences of subdural effusion and puncture canal edema after ventriculoperitoneal shunt,and history of down-regulating shunt valve within 2 weeks between the two groups were compared by univariate analysis.The independent risk factors for DICH were further assessed using multivariable Logistic regression.Results Among 176 patients,23 (13.07％) had DICH;2-11 d after surgery,DICH appeared,manifesting as subdural,ventriculoventricular end canal and/or hemorrhage in one or more areas of the ventricle.There were significant differences in incidence of subdural effusion and history of down-regulating shunt valve within 2 weeks between the two groups (P＜0.05).Multivariate Logistic regression analysis showed that subdural effusion after surgery and down-regulation of shunt valve pressure within 2 weeks after ventriculoperitoneal shunt were independent risk factors for DICH (OR=4.516,95％CI:1.555-13.110,P=0.006;OR=5.352,95％CI:1.987-14.414,P=0.001).Conclusion High incidence of DICH mighty be noted within two weeks of ventriculoperitoneal shunt;subdural effusion and pressure reduction of shunt valve within 2 weeks are independent risk factors for DICH,which needs close monitoring and clinical intervention.

Episodic ataxia (EA) is a group of disorders characterized by recurrent spells of vertigo, truncal ataxia, and dysarthria. Episodic ataxia type 2 (EA2), the most common subtype of EA, is an autosomal dominant disease caused by mutation of the CACNA1A gene. EA2 has been rarely reported in the Chinese population. Here we present an EA2 family admitted to Xiangya Hospital in October 2018. The proband was a 22-year-old male who complained of recurrent spells of vertigo, slurred speech, and incoordination for 4 years. Brain magnetic resonance imaging (MRI) showed cerebellar atrophy. He had neuropsychological development disorder in childhood, and cognitive assessment in adulthood showed cognitive impairment. The proband's mother and grandmother had a similar history. Peripheral blood samples from the proband and family members were collected, and genomic DNA was isolated. Whole exome sequencing of the proband detected a heterozygous frameshift mutation c.2042_2043del (p.Q681Rfs*100) of CACNA1A gene. This mutation was verified in the proband and 2 family members using Sanger sequencing. One family member carrying this mutation was free of symptoms and signs, suggesting an incomplete penetrance of the mutation. We reported a variant c.2042_2043del of CACNA1A gene as the pathogenic mutation in a Chinese EA2 family for the first time. This case enriched the clinical spectrum of CACNA1A related EA2, and contributed to the understanding of clinical and genetic characteristics of EA2 to reduce misdiagnosis.
Adult ; Ataxia ; Calcium Channels/genetics* ; Humans ; Male ; Mutation ; Nystagmus, Pathologic ; Pedigree ; Vertigo ; Young Adult