Diagnostic Performance of Intestinal in Colorectal Cancer: A Meta-Analysis / 中华医学杂志(英文版)

<p><b>Background</b>Increasing evidence has supported the link of intestinal Fusobacterium nucleatum infection to colorectal cancer (CRC). However, the value of F. nucleatum as a biomarker in CRC detection has not been fully defined. In order to reduce the random error and bias of individual research, this meta-analysis aimed to evaluate the diagnostic performance of intestinal F. nucleatum in CRC patients and provide evidence-based data to clinical practice.</p><p><b>Methods</b>An article search was performed from PubMed, Embase, Cochrane Library, and Web of Science databases up to December 2017, using the following key words: "Fusobacterium nucleatum", "Fusobacterium spp.", "Fn", "colorectal cancer(s)", "colorectal carcinoma(s)", "colorectal neoplasm(s)", and "colorectal tumor(s)". Articles on relationships between F. nucleatum and CRC were selected according to the preestablished inclusion and exclusion criteria. This meta-analysis was performed using STATA 12.0 software, which included mapping of forest plots, heterogeneity tests, meta-regression, subgroup analysis, sensitivity analysis, and publication bias. The sensitivity, specificity, positive likelihood ratio (LR), negative LR, diagnostic odds ratio (DOR), and their corresponding 95% confidence interval (CI) of each eligible study were summarized.</p><p><b>Results</b>Finally, data for 1198 participants (629 CRC and 569 healthy controls) in 10 controlled studies from seven articles were included. The summary receiver operator characteristic curve was mapped. The diagnostic performance of intestinal F. nucleatum infection on CRC was as follows: the area under the curve: 0.86 (95% CI: 0.83-0.89), the pooled sensitivity: 0.81 (95% CI: 0.64-0.91), specificity: 0.77 (95% CI: 0.59-0.89), and DOR: 14.00 (95% CI: 9.00-22.00).</p><p><b>Conclusion</b>Intestinal F. nucleatum is a valuable marker for CRC diagnosis.</p>

Novel syngeneic liver hapten protein compounds play different roles in pathogenesis of autoimmune hepatitis in the C57BL/6 mouse.

BACKGROUND/AIMS: The autoimmune hepatitis (AIH) model in C57BL/6 mice with syngeneic hapten S100 and adjuvant injected intraperitoneally has been designed to elucidate the pathogenesis of AIH. Three separate hapten peak proteins, peak I, peak II and peak III, could be derived from S100, but little is understood their roles on the development of AIH. This study aims to learn more about these roles on pathogenesis of AIH. METHODOLOGY: Novel AIH C57BL/6 mouse models were developed by weekly immunization by intraperitoneal injection with syngeneic S100 liver proteins and the three separated hapten peak proteins emulsified covalently in complete Freund's adjuvant (CFA) for 4 weeks and sacrificed for liver histopathological study. Additionally, TNF-α and INF-γ in culture supernatants of spleen lymphocytes of healthy C57BL/6 mice cultured together with S100 plus CFA for 48 hours were detected, and the T-lymphocytes proliferative response after stimulation with crude S100, peak I, II or III proteins were also assessed. RESULTS: Data showed that hepatitis induced by CFA+S100 was accompanied with more severe inflammation characterized by diffusely distributed liver necrosis and enhanced lymphocyte infiltration in portal tracts, while hepatitis induced by peak I+CFA was characterized by mass lymphocyte infiltration, occasional isolated liver necrosis and many acidophilic bodies, which was more similar to autoimmune hepatitis; hepatitis induced by peak II+CFA was characterized by massive liver necrosis and mild lymphocyte infiltration; hepatitis induced by peak III+CFA was characterized by mild inflammation with isolated acidophilic bodies or dotted hepatocellular necrosis. TNF-α, INF-γ from culture supernatants were increased, and T-lymphocyte proliferative response stimulated with peak I protein significantly increased compared with those stimulated with crude S100, peak II or III proteins. CONCLUSIONS: Syngenic S100 liver protein and its three separated hapten proteins have different roles in the pathogenesis of AIH, and peak I protein may be important in its development.

Effect of peroxisome proliferator-activated receptors-gamma and co-activator-1alpha genetic polymorphisms on plasma adiponectin levels and susceptibility of non-alcoholic fatty liver disease in Chinese people.

BACKGROUND/AIMS: Peroxisome proliferator-activated receptors-gamma (PPAR-gamma) and its co-activator-1alpha (PGC-1alpha) are involved in the regulation of lipid and glucose metabolisms. This study aimed to investigate the genetic polymorphisms of PPAR-gamma and PGC-1alpha in Chinese people and their influence on plasma adiponectin levels and non-alcoholic fatty liver disease (NAFLD) susceptibility. METHODS: Ninety-six patients with NAFLD and 96 healthy controls were included. The single nucleotide polymorphisms (SNPs) of C161T PPAR-gammaand Gly482Ser PGC-1alpha genes were analysed by polymerase chain reaction and restriction fragment length polymorphism. RESULT: The CC, CT and TT genotypic distributions of the NAFLD group were significantly different from those of controls (55.2, 39.6, 5.2 vs. 74.0, 25.0, 1.0%; P=0.015). The allelic frequencies of C and T were also different between the two groups (P=0.004). As for the PGC-1alpha gene, there was no difference of the genotypic and allelic frequencies between the two groups (P>0.05). In NAFLD patients, the plasma adiponectin concentrations were lower in the PPAR-gamma CT/TT genotypes compared with those in the CC genotype group (3.0+/-0.6 vs. 4.3+/-0.9, P=0.02). Multivariate logistic regression analysis showed that CT/TT genotypes of PPAR-gamma, TG, waist hip ratio, hypoadiponectinaemia and homoeostasis model assessment (HOMA)-IR were the risk factors for NAFLD. CONCLUSION: SNPs in the PPAR-gamma, but not PGC-1alpha, gene are associated with NAFLD susceptibility possibly through the adiponectin pathway.

Treatment of congenital hypertrophic pyloric stenosis with endoscopic pyloromyotomy / 中华儿科杂志

<p><b>OBJECTIVE</b>To evaluate the effect of the treatment of congenital hypertrophic pyloric stenosis (CHPS) with endoscopic pyloromyotomy.</p><p><b>METHOD</b>Nine consecutive infants (7 boys, 2 girls; age range 26 - 70 days; weight range 2.65 - 6.10 kg), with a diagnosis of CHPS according to typical clinical manifestations, transabdominal ultrasound (US), gastroenterography and gastroscope. All the cases had accompanying malnutrition, anaemia, metabolic alkalosis, and some were complicated with congenital heart disease. In gastroscope operating room, all the patients were given pentobarbital and midazolam intravenously. A gastroscope with an outer diameter of 5.9 mm was passed through mouth, stomach, pylorus to the descending segment of duodenum. Under gastroscopy, two incisions were made along the anterior and posterior wall of pylorus from the duodenal bulb to the antrum by using endoscopic electrosurgical needle knife and an arch sphincter sarcosome. Incisions were deepened by 2 to 3 procedures until the longitudinal muscle was exposed, about 2 to 4 mm according to transabdominal US performed before operation. The incision depth was 2 - 3 mm if pylorus wall was 4 - 6 mm in thickness; or 3 - 4 mm when the wall was thicker than 6 mm.</p><p><b>RESULT</b>The endoscope was easily passed through the pylorus to the duodenum post-operation. The transabdominal US and gastroenterography showed that liquid easily flew through pylorus. All patients were able to have regular feeding about 2 to 10 hours after the operation. Vomiting in all patients was significantly decreased in frequency and amount, and in 8 infants vomiting stopped within 1 week, in one case it did not stop until 1 month after the treatment. Some cases showed slight adverse reaction, no perforation or massive haemorrhage in stomach or intestines occurred in any of the patients during and post-operation. Eight infants were doing well at follow-up (range 2 to 9 months). One girl had recurred vomiting at normal feeding after a period of 1 month postoperation without vomiting. This case was cured by second endoscopic pyloromyotomy.</p><p><b>CONCLUSIONS</b>Endoscopic pyloromyotomy is effective, safe, simple, and offers several advantages: no need for open-abdomen surgery, feeding can be initiated rapidly.</p>

Association of hepatic lipase gene promoter polymorphism -514C/T with nonalcoholic fatty liver disease / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study the prevalence of the hepatic lipase gene (LIPC) promoter polymorphism (at position -514) in patients with nonalcoholic fatty liver disease (NAFLD), and its relationship with the susceptibility to NAFLD.</p><p><b>METHODS</b>Genotype of LIPC promoter was detected with PCR-RFLP in 106 patients with NAFLD. Body mass index, waist-to-hip ratio (WHR), blood pressure, CHOL, HDL, LDL, TG, FPG and FINS of the patients were measured. Index of insulin resistance was determined using the homeostasis model assessment (HOMA) method. One hundred six healthy subjects matched for age and sex served as controls.</p><p><b>RESULTS</b>The frequency of CC genotype and C allele in the NAFLD group were significantly higher than those in the control group (31.1% vs 26.4%, 62.7% vs 54.2%, P<0.05). Compared with TT genotype, both CC genotype and CT genotypes had higher relative risk of NAFLD (OR: 3.73, 95% CI: 1.31, 10.63; OR: 3.60, 95% CI: 1.35, 9.60). At the same time, the non-carriers of T allele in -514 had higher WHR than the T carriers (0.877+/-0.06 vs 0.848+/-0.06, t=2.072, P<0.05)). Logistic regression analysis showed that T substitution in LIPC-514 position (OR: 1.28, 95% CI 0.10-0.74) had a lower susceptibility to NAFLD.</p><p><b>CONCLUSION</b>The LIPC-514C/T polymorphism is associated with WHR, and the T substitution of LIPC-514 may lower the susceptibility to NAFLD.</p>

The relationship between insulin resistance and adiponectin gene expression in nonalcoholic fatty liver disease / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the relationship between insulin resistance (IR) and adiponectin gene expression in patients with nonalcoholic fatty liver disease (NAFLD).</p><p><b>METHODS</b>Subcutaneous (SC) and omental (OM) adipose tissues were obtained from 21 NAFLD patients with obesity (n=10) and nonobesity (n=11) and also from 24 subjects (without NAFLD) with obesity (n=11) and nonobesity (n=13) who served as controls. Adiponectin mRNA expression levels in subcutaneous and omental adipose tissues were measured using SYBR Green I quantitative real-time PCR. The levels of plasma adiponectin and insulin were measured with ELISA. IR was estimated using the homeostasis assessment (HOMA).</p><p><b>RESULTS</b>The scores of HOMA-IR levels of the NAFLD patients and the controls with obesity and nonobesity were: 3.0+/-0.8, 2.8+/-0.9, 2.0+/-0.6, 1.2+/-0.5 respectively. The relative mRNA expression of adiponectin and blood adiponectin levels in NAFLD patients differed significantly from those of the controls. The HOMA-IR negatively correlated with the adiponectin mRNA expression levels of adipose tissues (r = -0.5) and blood adiponectin; it positively correlated with body mass index (r = 0.4), waist-hip-ratio (r = 0.4) and serum triglyceride (r = 0.3), but did not correlate with serum total cholesterol (r = 0.2).</p><p><b>CONCLUSION</b>IR of NAFLD patients was linked to low adiponectin gene expression in their adipose tissues. This finding suggests that low adiponectin gene expression may play a role in the pathogenesis of insulin resistance and NAFLD.</p>

Relationship between leptin gene of adipose tissues and nonalcoholic fatty liver disease / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate leptin mRNA expressions in subcutaneous (SC) and omental (OM) adipose tissues of patients with nonalcoholic fatty liver disease (NAFLD), and their relationships with insulin resistance (IR), blood leptin, blood triglyceride, total blood cholesterol, blood glucose, body weight index and waist-hip ratio.</p><p><b>METHODS</b>SC and OM adipose tissues were obtained from 10 obese and 11 nonobese NAFLD patients and from 11 obese and 13 nonobese patients without NAFLD, who served as controls. Leptin mRNA expression levels in the subcutaneous and omental adipose tissues were measured using SYBR Green I quantitative real-time PCR. IR was estimated using homeostasis assessment (HOMA). The levels of plasma leptin and insulin were measured using ELISA.</p><p><b>RESULTS</b>The relative mRNA expression of leptin, HOMA-IR and blood leptin levels in NAFLD differed significantly from those of the controls (P < 0.05). The leptin/GAPDH ratio of the obese and nonobese NAFLD and control cases were 1.32 +/- 0.12, 0.99 +/- 0.05, 1.10 +/- 0.09, 0.87 +/- 0.13 respectively. The expression levels of SC and OM adipose leptin mRNA in NAFLD patients were positively correlated with HOMA-IR (r=0.72, P < 0.05), blood leptin (r=0.69, P < 0.05), blood triglyceride (r=0.32, P < 0.05), body weight index (r=0.57, P < 0.05) and waist-hip ratio (r=0.50, P <0.05).</p><p><b>CONCLUSION</b>The primary reason for high levels of blood leptin is high leptin mRNA expression in adipose tissues; in both obese and nonobese patients with NAFLD; high levels of blood leptin and the leptin mRNA expression in adipose tissues and IR exist. These findings suggest that leptin resistance exists in patients with NAFLD and leptin resistance is positively correlated with NAFLD, the same as in insulin resistance.</p>

An epidemiological survey of subclinical hepatic encephalopathy / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the prevalence and correlative factors of subclinical hepatic encephalopathy (SHE) in patients with cirrhosis in China by using psychometric tests with big sample size.</p><p><b>METHODS</b>409 patients with cirrhosis and 416 patients with chronic hepatitis were investigated for the prevalence of SHE. In prevalence study questionnaire, psychometric tests (NCT and DST), laboratory data were used to estimate their liver function.</p><p><b>RESULTS</b>According to age, the patients were divided into 5 groups (including<35, 35 to 44, 45 to 54, 55 to 64 and >65 groups). There was highly statistical significance on the results of NCT and DST, between the cirrhosis patients and the controls (t> or =4.108, P<0.01). The prevalence of SHE in cirrhosis patients was 51.3%. Highly statistical significance was found (chi 2=23.910, P<0.01) among the Child-Pugh A, B, C groups (39.9%, 55.2% and 71.8%). According to age, gender, smoking, etiology and education, no statistical significance was found. Logistic regression showed that there was a close relationship between the SHE prevalence and the Child-Pugh score only, and no relationship had been found between the SHE prevalence and other factors including age, gender, smoking, etiology and education.</p><p><b>CONCLUSION</b>The SHE prevalence in hepatic cirrhosis patients is 51.3%, and the Child-Pugh score may be an important risk factor</p>

The effect of anal electrical stimulation on anal sphincter pressure in conscious dogs / 中华消化杂志

Objective To investigate the effects and mechanisms of anal electrical stimulation (AES) with long pulses on anal sphincter pressure (ASP) in conscious dogs.Methods Nine healthy female hound dogs were used for the study,composed of 4 randomized sessions including AES with vari- ous stimulation parameters,20-min sustained AES to assess anal sphincter fatigue,atropine or phentolamine were used to block corresponding receptor.ASP was measured with manometry and the contractile area under the contraction curve.AES was performed via a pair of ring electrodes attached to the manometric catheter.The stimulation parameters in all sessions but the first session included a frequency of 20 ppm,width of 200 ms and amplitude of 3 mA.Results ASP was 55.7?6.0 at baseline and increased by 37% to 76.4?6.5 during AES (P