Prevalence and risk factors for left ventricular hypertrophy and left ventricular geometric abnormality in the patients with hypertension among Han Chinese / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Left ventricular hypertrophy (LVH) and geometric abnormality are associated with morbidity and mortality of cardiovascular disease and stroke. Hypertension is the major cause of LVH. Yet the prevalence and other risk factors of LVH and geometric abnormality in Chinese hypertensive population are unknown. The objective of this study was to investigate the prevalence and risk factors of LVH and geometric abnormality in community-based Chinese hypertensive population.</p><p><b>METHODS</b>The study was a community-based cross-sectional study, and comprised 4270 hypertension patients with integrated clinical and echocardiographic data. Left ventricular mass was measured by transthoracic echocardiography. LVH was diagnosed by using the criteria of over 49.2 g/m(2.7) for men and 46.7 g/m(2.7) for women. LV geometric patterns (normal, concentric remodeling, concentric or eccentric hypertrophy) were calculated according to LVH and relative wall thickness. Logistic regression model was used to determine the odds ratio (OR) and 95% confidence intervals (CI) of the risk factors of LVH.</p><p><b>RESULTS</b>The prevalence of LVH was 42.7% in 4270 hypertensive patients, with 37.4% in males and 45.4% in females, respectively. The prevalence of concentric remodeling, concentric or eccentric hypertrophy was 24.7%, 20.2%, and 22.6%, respectively. In Logistic regression model, female (OR 1.3, 95%CI 1.1 - 1.5, P < 0.01), age (OR 1.02, 95%CI 1.01 - 1.03, P < 0.01), body mass index (OR 1.2, 95%CI 1.15 - 1.20, P < 0.01), systolic blood pressure (OR 1.02, 95%CI 1.01 - 1.03, P < 0.01), and serum triglyceride (OR 1.10, 95% CI 1.00 - 1.20, P < 0.01) were risk factors of LVH. Female, age, body mass index, systolic blood pressure and serum triglyceride were also risk factors of left ventricular geometric abnormality.</p><p><b>CONCLUSIONS</b>The echocardiographic LVH is the major complication of patients with hypertension in rural area of China, especially for women. To effectively treat hypertension, weight loss and control of serum triglyceride may help to prevent LVH in hypertensive population.</p>

Relationship between p53 gene and chromosome 13q14 variations and prognosis in primary intestinal lymphoma / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Some research has shown that primary intestinal lymphoma with the same immunophenotype has different prognosis. It suggests that the prognosis of this disease is not determined by a single factor but may be related to genetic or chromosomal variations. The p53 gene is an important tumor suppressor gene, and 13q14 deletion is a common chromosomal abnormality of lymphocyte proliferation diseases. This study aimed to explore the role of the p53 gene and chromosome 13q14 variations in the assessment of prognosis in primary intestinal lymphoma.</p><p><b>METHODS</b>p53 gene and chromosome 13q14 expression in paraffin sections of 30 cases of primary intestinal lymphoma and 10 cases of lymph node reactive hyperplasia were ascertained using an improved FISH technique.</p><p><b>RESULTS</b>p53 gene deletion was found in 22.7% of patients with primary intestinal lymphoma at stage I-II and in 75.0% of patients at stage III-IV (x2=6.903, p<0.01). The 30 patients with primary intestinal lymphoma were pathologically classified into-mucosa-associated lymphoid tissue (MALT) (n=14) and non-MALT types (n=16). The MALT lymphoma group had significantly lower incidence of p53 gene deletion (14.3% vs 56.3%; x2=5.662, p<0.05). Average survival time in patients with p53 gene deletion was 13.41 months, being shorter than the patients with normal p53 gene (36.1 months) (t=2.637, p<0.05). 13q14 deletion was found in 40.0% of patients with primary intestinal lymphoma, but none of patients with lymph node reactive hyperplasia showed 13q14 deletion. 13q14 deletion was not significantly related to the pathological type and the clinical stage of primary intestinal lymphoma as well as the survival time. There was no significant correlation between p53 gene and 13q14 deletions.</p><p><b>CONCLUSIONS</b>There was a high incidence of p53 gene deletion in patients with non-MALT lymphoma or at stage III-IV. p53 gene deletion is related to a high tumor malignant degree and a poor prognosis, while-chromosome 13q14 variation is not associated with the prognosis in patients with primary intestinal lymphoma.</p>

Effect of FGF-2 on survivin and subcellular location of Smac in human small cell lung cancer cell NCI-H446 / 中南大学学报(医学版)

OBJECTIVE@#To investigate the effect of basic fibroblast growth factor (FGF-2)on survivin and subcellular location of Smac in human small cell lung cancer (SCLC) cell NCI-H446.@*METHODS@#Western blot was used to detect the expression of survivin protein induced by FGF-2. The release of Smac from mitochondria to cytoplasm affected by FGF-2 was observed by Western blot and immunofluorescence. Apoptosis of NCI-H446 cells was detected with flow cytometry and Hoechst 33258 staining.@*RESULTS@#The expression of survivin could be up-regulated in response to FGF-2 treatment in NCI-H446 cells, and the level of survivin expression is related to the concentration and time of FGF-2 treatment. FGF-2 could inhibit the release of Smac from the mitochondria to cytoplasm induced by serum starving. FGF-2 could inhibit the apoptosis induced by serum starving.@*CONCLUSION@#FGF-2 up-regulates the expression of survivin protein in NCI-H446 cells, and blocks the release of Smac from mitochondria cytoplasm. Survivin and Smac might play important roles in the apoptosis inhibited by FGF-2.

Construction of 2-dimensional tumor microvascular architecture phenotype in non-small cell lung cancer / 中南大学学报(医学版)

OBJECTIVE@#To construct a technological platform of 2-dimensional tumor microvascular architecture phenotype (2D-TAMP) expression.@*METHODS@#Thirty samples of non-small cell lung cancer (NSCLC) were collected after surgery. The corresponding sections of tumor tissue specimens to the slice of CT perfusion imaging were selected. Immunohistochemical staining,Gomori methenamine silver stain, and electron microscope observation were performed to build a technological platform of 2D-TMAP expression by detecting the morphology and the integrity of basement membrane of microvasculature, microvascular density, various microvascular subtype, the degree of the maturity and lumenization of microvasculature, and the characteristics of immunogenetics of microvasculature.@*RESULTS@#The technological platform of 2D-TMAP expression was constructed successfully. There was heterogeneity in 2D-TMAP expression of non-small cell lung cancer. The microvascular of NSCLC had certain characteristics.@*CONCLUSION@#2D-TMAP is a key technology that can be used to observe the overall state of micro-environment in tumor growth.

Polymorphisms of angiotensin-converting enzyme 2 gene associated with magnitude of left ventricular hypertrophy in male patients with hypertrophic cardiomyopathy / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Even carrying an identical gene mutation, inter- and intra-family variations have been noticed worldwide in the presence and the severity of left ventricular hypertrophy and sudden death in patients with hypertrophic cardiomyopathy (HCM). Modifier genes may contribute to the diversity. Angiotensin-converting enzyme 2 (ACE2) gene has been established to be associated with parameters of left ventricular hypertrophy in community based male subjects. The objective of the present study was to investigate the association of ACE2 gene polymorphisms with the phenotype of HCM.</p><p><b>METHODS</b>A total of 261 consecutive HCM patients and 609 healthy controls were enrolled into this study. The polymorphism of rs2106809 and rs6632677 were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and confirmed by sequencing. Logistic regression model and multivariate analysis were used to determine the odds ratio (OR) and 95% confidence intervals (CI) of variations of ACE2 for HCM.</p><p><b>RESULTS</b>The T allele of rs2106809 and C allele of rs6632677 conferred increasing risk for HCM (OR 1.34, 95% CI 1.01 - 1.77, P = 0.04; OR 1.11, 95% CI 1.03 - 1.21, P = 0.002, respectively), and the 2 single nucleotide polymorphisms (SNPs) were in strong linkage disequilibrium (LD), the TC haplotype was independently associated with a higher OR for HCM (OR = 1.59, 95% CI 1.21 - 1.87) after adjusted for conventional risk factors. And the risk alleles were associated with thicker interventricular septal thickness of HCM ((20.0 +/- 6.3) mm vs (17.9 +/- 5.5) mm, P = 0.03 and (21.3 +/- 5.9) mm vs (17.9 +/- 5.8) mm, P = 0.04, respectively). No association was found between the two polymorphisms with female patients with HCM.</p><p><b>CONCLUSION</b>Minor alleles of ACE2 gene might be the genetic modifier for the magnitude of left ventricular hypertrophy in male patients with HCM.</p>

A two-year animal experimental study on the pathological effects of Helicobacter pylori on liver tissues / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To observe whether H. pylori administered orally in mice could arrive in their livers after a long-term infection, leading to active inflammation and even causing HCC as an independent etiological factor.</p><p><b>METHODS</b>Twenty C57BL/6 mice were orally administered H. pylori SS1 and kept for 24 months (experimental group) along with 13 mice which served as blank controls (control group). H. pylori colonization and pathologic consequences were studied in the livers and gastric tissues of the mice. The bacterial DNA extracted from liver tissues was examined by nested PCR for H. pylori 16S rRNA genes. 16S rRNA PCR amplicons were sequenced and compared with sequencing results of 16S rRNA PCR amplicons of the bacteria cultured from gastric mucosa and compared with that of the inoculated H. pylori SS1.</p><p><b>RESULTS</b>Of the 20 mice in the experimental group, H. pylori was found in the gastric mucosa of 12, and in 11 of them pathological gastric lesions were found, including one with gastric lymphoma. H. pylori were found in the livers of 7 mice. Liver lesions, one with mild inflammation, 3 with inflammation and fibrosis, 2 with inflammation, fibrosis and hepatocyte hyperplasia with atypia were found in 6 of them. No liver lesions were found in the mice of the control group. In the mice of the experimental group no liver lesions were found in those mice with no H. pylori in their gastric mucosae. Sequencing results of 16S rRNA PCR products of the liver showed 100% homogeneity with the cultured H. pylori from gastric mucosa and the administered H. pylori SS1.</p><p><b>CONCLUSION</b>Two years after oral administration of H. pylori to C57BL/6 mice, gastric mucosal lesions and liver lesions, including inflammation, cirrhosis and hepatocyte hyperplasia with atypia were found in those animals.</p>

Clinical features of dilated cardiomyopathy-like hypertrophic cardiomyopathy caused by a 13261 G > A mutation in cardiac myosin-binding protein C gene / 中华心血管病杂志

<p><b>OBJECTIVE</b>To study the disease-causing gene mutation in Chinese patients with hypertrophic cardiomyopathy (HCM) and to analyze the genotype and phenotype correlation.</p><p><b>METHODS</b>One family (n = 27) affected with HCM were chosen for the study. The full encoding exons and flanking sequences of beta-myosin heavy chain gene (MYH7) and cardiac myosin-binding protein C gene (MYBPC3) were amplified with PCR and the products were sequenced. The clinical data including symptom, physical, echocardiography and electrocardiography examinations were collected.</p><p><b>RESULTS</b>We identified a 13261 G > A mutation, which causes a missense mutation (G758D) in exon 23 of MYBPC3 in 9 family members. One mutation carrier suffered from dilated cardiomyopathy (DCM) with asymmetric interventricular septal hypertrophy (14 mm). Another mutation carrier was diagnosed as HCM.</p><p><b>CONCLUSIONS</b>The 13261 G > A mutation is associated with a DCM-like HCM and HCM phenotype in this Chinese family affected with HCM.</p>

Effects of a novel familial dilated cardiomyopathy associated LMNA gene mutation E82K on cell cycle of HEK293 cells / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effect of a novel LMNA gene mutation E82K found in a Chinese family with dilated cardiomyopathy on cell cycle of HEK293 cells.</p><p><b>METHODS</b>(1) Human wild type full-length LMNA gene cDNA was subcloned into eukaryotic expression vector pTracer-CMV and point mutation was introduced into the cDNA. LMNA gene wild type and mutant E82K LMNA gene were transfected into HEK293 cells respectively and stable cell lines resistant to antibiotic were obtained 4 weeks later. (2) Cell cycle changes were analyzed by flow cytometry in HEK293 cells transfected with wild type and mutant E82K LMNA gene and empty vector in the presence of 0.8 mmol/L H(2)O(2).</p><p><b>RESULTS</b>Cell circle was arrested at G0/G1 phase in the cells transfected with mutated E82K LMNA gene and at G2/M phase in other cell groups in the presence of H(2)O(2).</p><p><b>CONCLUSION</b>Cell circle was arrested at G0/G1 phase in the cells transfected with E82K LMNA gene in the presence of H(2)O(2) in HEK293 cells.</p>

Expression of Ang2 and Tie2 and their relation with the angiogenesis of hepatocellular carcinoma in rats / 中南大学学报(医学版)

OBJECTIVE@#To investigate the relationship between the expression of Ang2, Tie2 and the angiogenesis of hepatocellular carcinoma in rats.@*METHODS@#Thirty-eight healthy male rats were randomly divided into 3 groups: 5 rats in the control group; 25 rats in the experimental group were equally divided into 5-day, 10-day, 15-day, 20-day, and 25-day groups; the other 8 rats were used as the supplement of the experimental group. An allogenic transplanted rat model of CBRH-7919 hepatocellular carcinoma in situ was established by immunosuppression. The expressions of Ang2 and Tie2 were detected by immunohistochemical staining in cancerous tissues of different developmental stages and liver tissues of the control group. At the same time, microvessel density was determined by anti-CD31 immunohistochemical staining.@*RESULTS@#CBRH-7919 hepatocellular carcinoma models were successfully set up in 24 rats. The expression level of Ang2 and Tie2 in cancerous tissues was much higher than that of liver tissues of the control group (P <0.05). The overexpression of Ang2 was pristine and continuous in different developmental stages. The expressions of Ang2 and Tie2 positively correlated with microvessal density in hepatocellular carcinoma (P<0.05).@*CONCLUSION@#The up-regulation of Ang2 and Tie2 may play important roles in the angiogenesis of hepatocellular carcinoma. Ang2 may participate in the start of angiogenesis of hepatocellular carcinoma.

Experimental study on the pathological effect of Helicobacter pylori on liver tissues / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To observe whether H. pylori inoculated by oral route could arrive in livers and cause liver inflammation as an independent etiological factor.</p><p><b>METHODS</b>C57BL/6 mice were orally inoculated with H. pylori SS1 strains and fed for 8 months. H. pylori colonization and pathologic consequences were studied in the liver and gallbladder tissues of the mice; the blood, liver tissue and gastric mucosa were obtained and cultured for H. pylori growth; The bacterial DNA extracted from the liver, bile and blood was examined by nested PCR for H. pylori genes. 16S rRNA PCR amplicons were sequenced and compared with the sequencing results of 16S rRNA PCR amplicons of the bacteria cultured from gastric mucosa and the inoculated H. pylori SS1.</p><p><b>RESULTS</b>The bacterial DNA extracted from the liver, bile and blood of the infected mice was detected for H. pylori genes by nested PCR. Six of the 15 samples were positive (40%) in the liver, 6 of 10 samples in the bile (60%), and 2 of 10 samples in the blood (20%). Sequencing results of 16S rRNA PCR products of the livers showed 100% homogeneity when compared with the cultured H. pylori from gastric mucosa and inoculated H. pylori SS1. H. pylori was found in 4 liver tissues of the 15 infected mice (26.7%) and 6 in the gallbladders (40%). Infiltrations of lymphocyte cells along hepatic sinusoids and a lower degree infiltration around interlobular arteries and veins were observed; ballooning degeneration was also observed in some hepatocytes.</p><p><b>CONCLUSION</b>H. pylori inoculated by oral route could arrive in the liver and cause inflammation as an independent etiological factor. The routes which the microorganisms took to reach the livers may involve hematogenous and/or biliary system dissemination.</p>