Objective To investigate the relationship of TCRCα-575A/G polymorphism with anti-neutrophil antibody(ANCA) associated vasculitis in Chinese Han population. Methods 86 cases of ANCA associated vasculi-tis in Chinese Han population and 196 healthy subjects were enrolled. TCRCα-575A/G was genotyped by PCR-re-striction fragment length polymorphism (PCR-RFLP) assay. Case-control study was performed. Results No signifi-cant difference was found in either genotype distribution(AA,AG,GG) or allele frequencies between 86 patients and healthy subjects(P>0.05);But significant differences between AA group, AG group, and GG group in systolic pres-sure[(127.47±24.18)、(124.11±25.21)、(148.92±19.23) mm Hg],diastolic pressure [(75.35±14.12)、 (74.50±13.01)、(85.46±9.40) mm Hg],red blood cell count[(3.41±1.01)×109/L、(3.46±1.04)× 109/L、(2.68±0.67)×109/L] and hemoglobin [(90.45±20.69)、(100.66±29.80)、(77.61±15.81) g/L (P<0.05 for each) were found. The patients in GG group had higher blood pressure and more severe anaemia;By following the patients about (16.0±36.8) months,no statistics significance was found between groups with and without chronic renal failure in distributions and genetypes of TCRCα-575A/G (P>0.05 ). Conclusions In Chi-nese Han population,TCRCα-575A/G polymorphism might not be related to genetic susceptibility and chronic renal failure of ANCA associated vaseulitis;but G allele might be associated with more serious anaemia and hypertension.

Objective To investigate the association between TGFβ1-509 C/T gene polymorphism with primary ANCA associated vasculitis (AAV) in Chinese Han population . Methods The blood DNA and clinical data of 88 patients were collected, TGFβ1-509 C/T genotypes were determined by PCR-RFLP, 107 healthy individuals were tested as controL Clinical and pathological data of the patients with different genotype were compared. Results No significant difference was found in neither genotype distributions nor allele frequencies between the patients and the control (P > 0. 05). Significant difference was found in uria protien level of the three groups of patients with different genotypes(P <0.05) ,but not in blood pressure, serum urea nitrogen or creatinine, vasculitic damage index, birminghan vasculitis activity score (P > 0. 05 ). Significant difference was found in med-heavier glomerular mesangial proliferation of the three groups ( P < 0.05 ) , but not in lighter glomerular mesangial proliferation, glomerular sclerosis, crescent formation and tubule-interstitial fibrosis and atrophy. Conclusions In Chinese Han population, TGFβ1-509 C/T polymorphism might have no relationship to susceptibility of primary AAV, but might relate to uria protein and med-heavier degree of mesenterium proliferation.

Objective To investigate the relationship between TGFβ1-509 C/T, TCRCα-575 A/G SNPs and primary AAV using a transmission disequilibrium theory based pedigree analysis Methods Genotypes of 264 individuals from 88 AAV families include patients, their parents, brothers and sisters were determined by PCR-RFLP and direct sequencing. Transmission disequilibrium test(TDT) and HRR were employed for the data analysis to observe the transmission disequilibrium of TGF31-509 C/T and TCRCα -575 A/G polymorphisms. Results No transmission disequilibrium from heterozygous parents onto the patients was found in the trios analyzed by TDT for either TGFβ1-509 C/T (observed C/T = 36/28, expected C/T =33. 5/30. 5, x2 =0.51, P＞0.05) or TCRCo-575 A/G ( observed A/G = 29/39, expected A/G = 33.5/34. 5, x2 = 1. 59, P ＞ 0. 05 ). The genotype-based HRR and haplotype-based HRR showed there was no increased risk of AAV in the observed trios for either -509 C/T polymorphism of TGFβ1 (transmitted genotype CC/CT/TT =12/20/6, allele C/T = 44/32; nontransmitted genotype CC/CT/TT = 10/19/9,allele C/T =39/37, genotype-based HRR x2 =0.81, P ＞0. 05, haplotype-based HRR x2 =0. 66, P＞0. 05,HRR = 1.30) or -575 A/G polymorphism of TCRCα ( transmitted genotype AA/AG/GG = 9/18/12, allel A/G = 36/42; nontransmitted genotype AA/AG/GG = 15/15/9, allel A/G = 35/33, genotype-based HRR x2=2. 20, P ＞0. 05. Haplotype-based HRR x2 =0. 41, P ＞0. 05, HRR =0. 81 ). The deviation of HRR coefficient was not excessive(1.00). Conclusion TGFβ1-509 C/T and TCRCo-575 A/G polymorphism may not be associated with the genetic susceptibility of primary AAV in Guangxi Han population.

OBJECTIVE: The aim of the study was to compare transcatheter arterial chemoembolization (TACE) plus ¹³¹I-labelled metuximab with TACE alone for hepatocellular carcinoma (HCC). MATERIALS AND METHODS: A comprehensive search was conducted in PubMed, Embase, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, and Chinese BioMedical Literature Database with published date from the earliest to February 29th, 2016. No language restrictions were applied, but only prospective randomized controlled trials (RCTs) or non-RCTs were eligible for a full-text review. The primary outcome was the overall survival (OS) and effective rate (the rate of partial atrophy or complete clearance of the tumor lesion). The odds ratios (ORs) were combined using either the fixed-effects model or random-effects model. RESULTS: Eight trials (3 RCTs and 5 non-RCTs) were included, involving a total of 1121 patients. Patients receiving combined therapy of TACE plus ¹³¹I-labelled metuximab showed significant improvement in effective rate {OR = 4.00, (95% confidence interval [CI]: 2.40–6.66), p < 0.001}, 1-year OS (OR = 2.03 [95% CI: 1.55–2.67], p < 0.001) and 2-year OS (OR = 2.57 [95% CI: 1.41–4.66], p = 0.002]. CONCLUSION: TACE plus ¹³¹I-labelled metuximab is more beneficial for treating advanced HCCs than TACE alone in terms of tumor response and OS. Large, multi-center, and blinded randomized trials are required to confirm these findings.
Asian Continental Ancestry Group ; Atrophy ; Carcinoma, Hepatocellular* ; Humans ; Odds Ratio ; Prospective Studies ; Radioimmunotherapy

OBJECTIVE: To observe changes of the length of sarcomere of rat when restiffening. METHODS: We measured the length of sarcomere of quadriceps in 40 rats in different condition by scanning electron microscope. RESULTS: The length of sarcomere of rigor mortis without destroy is obviously shorter than that of restiffening. CONCLUSION The length of sarcomere is negatively correlative to the intensity of rigor mortis. Measuring the length of sarcomere can determine the intensity of rigor mortis and provide evidence for estimation of time since death.
Animals ; Female ; Male ; Microscopy, Electron ; Postmortem Changes ; Rats ; Rats, Wistar ; Rigor Mortis/pathology* ; Sarcomeres/ultrastructure* ; Time Factors

Background To test the hypothesis that chronic administration of angiotensin-(1-7) [Ang-(1-7)] attenuates cardiac hypertrophy in rats in vivo. Methods Coarctation of the suprarenal abdominal aorta was performed in 41 8-week-old male Sprague Dawley rats. Twenty-four hours after the operation, osmotic minipumps were surgically implanted subcutaneously in the rats, which were randomly divided into 3 groups, including a sham-operation group (n=15) receiving infusion with normal saline, a suprarenal aortic coarctation group (n=12), and a suprarenal aortic coarctation group (n=14) with Ang-(1-7) treatment at the dose of 25 μg.kg-1 .h-1. Four weeks later, the systolic and diastolic blood pressures were measured and the left ventricular mass index (LVMI, mg/g) was calculated from the ratio of left ventricular weight to body weight. The concentrations of Ang Ⅱ in the plasma and myocardium were measured by radioimmunoassay, and myocardial interstitial collagen volume fraction (ICVF) was determined by quantitative morphometry of the sections with Picrosirius red staining using an automated image analyzer. Results Suprarenal abdominal aortic coarctation induced a significant increase in carotid artery systolic and diastolic blood pressure, heart weight, LVMI, ICVF, and the concentration of Ang Ⅱ in the myocardium (P＜0.01). Chronic administration of Ang-(1-7) attenuated the increase in the heart weight, LVMI, ICVF and left ventricular diastolic end pressure (LVEDP) caused by suprarenal abdominal aortic coarctation (P＜0.05). Ang-(1-7) also increased the formerly decreased maximum left ventricular pressure reduction rate (-dP/dtmax) (P＜0.05), but had no effect on blood pressure and the concentration of Ang Ⅱ in the myocardium. No difference was noted in plasma concentration of Ang Ⅱ between the 3 groups. Conclusions Ang-(1-7) attenuates cardiac hypertrophy and fibrosis and preserved the impaired left ventricular function induced by left ventricular pressure-overload in rats. These effects are not associated with the changes in the concentrations of AngⅡin the left ventricular myocardium and plasma.

Background To test the hypothesis that chronic administration of angiotensin-(1-7) [Ang-(1-7)] attenuates cardiac hypertrophy in rats in vivo. Methods Coarctation of the suprarenal abdominal aorta was performed in 41 8-week-old male Sprague Dawley rats. Twenty-four hours after the operation, osmotic minipumps were surgically implanted subcutaneously in the rats, which were randomly divided into 3 groups, including a sham-operation group (n=15) receiving infusion with normal saline, a suprarenal aortic coarctation group (n=12), and a suprarenal aortic coarctation group (n=14) with Ang-(1-7) treatment at the dose of 25 μg.kg-1 .h-1. Four weeks later, the systolic and diastolic blood pressures were measured and the left ventricular mass index (LVMI, mg/g) was calculated from the ratio of left ventricular weight to body weight. The concentrations of Ang Ⅱ in the plasma and myocardium were measured by radioimmunoassay, and myocardial interstitial collagen volume fraction (ICVF) was determined by quantitative morphometry of the sections with Picrosirius red staining using an automated image analyzer. Results Suprarenal abdominal aortic coarctation induced a significant increase in carotid artery systolic and diastolic blood pressure, heart weight, LVMI, ICVF, and the concentration of Ang Ⅱ in the myocardium (P＜0.01). Chronic administration of Ang-(1-7) attenuated the increase in the heart weight, LVMI, ICVF and left ventricular diastolic end pressure (LVEDP) caused by suprarenal abdominal aortic coarctation (P＜0.05). Ang-(1-7) also increased the formerly decreased maximum left ventricular pressure reduction rate (-dP/dtmax) (P＜0.05), but had no effect on blood pressure and the concentration of Ang Ⅱ in the myocardium. No difference was noted in plasma concentration of Ang Ⅱ between the 3 groups. Conclusions Ang-(1-7) attenuates cardiac hypertrophy and fibrosis and preserved the impaired left ventricular function induced by left ventricular pressure-overload in rats. These effects are not associated with the changes in the concentrations of AngⅡin the left ventricular myocardium and plasma.

OBJECTIVETo investigate the protective effect of reactive oxygen species (ROS) scavenger, N-acetyl-L-cysteine (NAC), against H9c2 cardiomyocytes from injuries induced by chemical hypoxia.

METHODSH9c2 cells were treated with cobalt chloride (CoCl2), a chemical hypoxia-mimetic agent, to establish the chemical hypoxia-induced cardiomyocyte injury model. NAC was added into the cell medium 60 min prior to CoCl2 exposure. The cell viability was evaluated using cell counter kit (CCK-8), and the intercellular ROS level was measured by 2', 7'- dichlorfluorescein-diacetate (DCFH-DA) staining and photofluorography. Mitochondrial membrane potential (MMP) of the cells was observed by Rhodamine123 (Rh123) staining and photofluorography, and the ratio of GSSG/ (GSSG+GSH) was calculated according to detection results of the GSSG kit.

RESULTSExposure of H9c2 cardiomyocytes to 600 micromol/L CoCl2 for 36 h resulted in significantly reduced cell viability. Pretreatment with NAC at the concentrations ranging from 500 to 2000 micromol/L 60 min before CoCl2 exposure dose-dependently inhibited CoCl2-induced H9c2 cell injuries, and obviously increased the cell viability. NAC at 2000 micromol/L obviously inhibited the oxidative stress induced by CoCl2, decreased the ratio of GSSG/(GSSG+GSH), increased ROS level, and antagonized CoCl2-induced inhibition on MMP.

CONCLUSIONNAC offers obvious protective effect on H9c2 cardiomyocytes against injuries induced by chemical hypoxia by decreasing in the ratio of GSSG/(GSSG+GSH) and ROS level and ameliorating MMP.

Animals ; Cell Hypoxia ; drug effects ; Cells, Cultured ; Embryo, Mammalian ; Free Radical Scavengers ; pharmacology ; Myocytes, Cardiac ; drug effects ; metabolism ; pathology ; Oxidative Stress ; drug effects ; Rats ; Reactive Oxygen Species ; metabolism

OBJECTIVETo determine the optimal position of hypoglossal nerve in hypoglossal-facial nerve anastomosis and the eligibility of hypoglossal-facial nerve anastomosis with the cervical loop.

METHODSThe cervical course and adjacent structures of the hypoglossal nerve were observed on 21 adult cadavers. The hypoglossal nerve and facial nerve were taken from 3 fresh specimens, and the number of the fasciculus and the cross-sectional area of the nerve were measured.

RESULTSThe facial nerve trunk were monofascicular with a cross-sectional area of 5.1-/+0.2 (range 4.6-5.7) mm(2). The number of the fasciculus and the cross-sectional areas of the nerve trunk and the fasciculus were 1.6-/+0.8 (range 1-4) mm(2) , 7.5-/+0.7 mm(2) (range 6.8-8.0) mm(2), and 4.7-/+0.6 (4.1-5.5) mm(2), respectively, at the proximal segment of the hypoglossal nerve, 3.6-/+0.5 (1-5) mm(2) , 5.6-/+0.5 (4.9-6.1) mm(2) , and 1.6-/+0.4 (0.9-2.2) mm(2) at the distal segment, and 2.4-/+0.8 (1-3) mm(2), 1.1-/+0.7 (0.6-2.2) mm(2), and 0.5-/+0.3 (0.3-1.2) mm(2) at the cervical loop.

CONCLUSIONThe cervical loop is inadequate for facial nerve anastomosis and the proximal segment is large enough to allow partial harvesting of the hypoglossal nerve for neurotisation of the facial nerve.

Anastomosis, Surgical ; methods ; Cadaver ; Facial Nerve ; anatomy & histology ; surgery ; Humans ; Hypoglossal Nerve ; anatomy & histology ; surgery ; Nerve Transfer ; methods

BACKGROUNDAlthough dopamine transporter (DAT) is essential for addiction, the effect of additive drugs on DAT function is still controversial, especially for opiates. We investigated the functional changes of dopamine transporter in striatum of rhesus monkeys during acute morphine injection and its abstinence.

METHODSFour rhesus monkeys, 6 to 9 years old, two male and two female, were examined for 12 days. Single photon emission computed tomography (SPECT) was performed with (99)T(cm)-TRODAT-1 as the radiopharmaceutical dopamine transporter agent during different stages of acute morphine injection and its abstinence. The ratios of SPECT signal between striatum and cerebellum (ST/CB) were calculated.

RESULTSThe ST/CB ratio declined significantly on the first day of morphine injection and continued declining with more morphine injections. After abstinence, the ratio increased with time, but was still significantly lower on the 5th day of abstinence than the normal level.

CONCLUSIONSIn rhesus monkey, acute morphine injection has both rapid and lasting effects on DAT by downregulating its function. The decline was partially reversible following morphine abstinence. The results suggest that striatum is one effective target of morphine and that the DAT function in striatum is one indicator for morphine addiction.

Acute Disease ; Animals ; Cerebellum ; metabolism ; Corpus Striatum ; drug effects ; metabolism ; Dopamine Plasma Membrane Transport Proteins ; analysis ; physiology ; Female ; Macaca mulatta ; Male ; Morphine Dependence ; physiopathology ; Organotechnetium Compounds ; Tomography, Emission-Computed, Single-Photon ; Tropanes