摘要:目的:探討系統性紅斑狼瘡（SLE）肝損害的臨床特點、肝損害發生率與SLE的病情嚴重程度的關系。方法:對98例SLE的臨床資料進行分析,收集所有研究對象的臨床資料,對肝損害組(30例)的癥狀與體征、病情程度、肝功能指標、影像學檢查結果進行數據分析,并將其部分生化及免疫學指標與無肝損害組(68對照組)進行比較。結果:SLE患者中SLE肝損害的發生率為30.61%。肝損害組中,病情重度16例(53.33%),17例患者(56.67%)無明顯自覺癥狀,以ALT、AST輕中度升高為主。7例患者肝臟B超異常。肝損害組患者的白細胞值明顯低與無肝損害組(Plt;0.05)。而2組的血紅蛋白、血小板、CRP、ESR、抗核抗體、抗dsDNA抗體、IgG、補體3等比較差異均無統計學意義(P均gt;0.05)。11例患者接受腎上腺皮質激素(激素)、免疫抑制劑(環磷酰胺、甲氨蝶呤)等藥物治療,9例在出院時復查肝功能正常或好轉,另2例肝功能無明顯改善;19例患者在接受激素、免疫抑制劑治療的同時,給予護肝治療,15例出院復查肝功能正常或好轉,另4例無明顯改善。而對照組68例中病情重度8例(11.76%)。結論:肝臟是SLE常見累及的靶器官之一,SLE肝損害的臨床表現缺乏特異性,以輕至中度肝細胞損害多見,肝損害發生率與SLE病情嚴重程度成正相關、與SLE的近期預后無關、與長期預后有待進一步研究。Abstract: Objective: To discuss the relationship between the clinical characteristic, The incidence of liver damage and the severity of SLE. Methods: Carries on the mathematical analysis to 98 example SLE clinical material, the collection all object of study clinical material, to liver harm group (30 examples) the symptom and the symptom，Severity the liver function target， the phantom study inspection result carries on the mathematical analysis, and (68 control groups) carries on its part of biochemistry and the immunology target with the nonliver harm group the comparison.Results: In the SLE patient the SLE liver harms the formation rate is 30.61%.In liver harm group, severe illness in 16 cases (53.33%), 17 example patient (56.67%) not obvious subjective symptom, by ALT, AST light moderate ascension primarily.7 example patient liver B ultra exceptionally.The liver harm group patient’s white blood cell value is lower than the nonliver harm group obviously (Plt;0.05), but 2 groups of hemoglobins, the blood platelet, CRP, ESR, the antinuclear immune body, the antidsDNA immune body, IgG, the complement 3 and so on the comparison differences do not have statistics significance (Pgt;0.05). 11 example patients accept the adrenal cortex hormone (hormone), the immunity inhibitor (endoxan, armor ammonia pterin) and so on the medicine treatments, 9 examples when out of hospital reexamines the liver function normal or the change for the better, another 2 example liver function improves not obviously; 19 example patients while accept the hormone, immunity inhibitor treatment, gives protects the liver treatment, 15 example out of hospital reexamination liver function normal or change for the better, another 4 examples improve not obviously. While the control group, 68 cases of severe illness in 8 cases (11.76%).Conclusion: The liver is one of target organs which SLE implicates common, the SLE liver harm. the clinical manifestation lacks the specificity, by sees lightly to the moderate liver cell harm,The incidence of liver damage and SLE severity is positively correlated with shortterm prognosis of SLE has nothing to do with the longterm prognosis remains to be further studied.
OBJECTIVE: To determine the long-term results and possible complications of the posterior tibialis transfer in correction of the foot-drop in leprosy patients, and to compare the results by the circum-tibial and interosseous routes. METHODS: From January to October 2001, 37 cases (treated from October 1989 to October 1999) were followed up. Walking gait, active dorsiflexion and plantar flexion of the ankle joint, deformities of the feet, and patients’ satisfaction were recorded. RESULTS: Of 37 patients, 22 were treated by circum-tibial transfer, 15 by interosseous transfer. All patients’ Achilles tendons were lengthened. Excellent and good results were obtained in 30 cases (86%). The active dorsiflexion was better by interosseous route than by circum-tibial route. Out of 35 patients followed up for 2-11 years (4 years on average), 14 had talipes varus in 22 by circum-tibial transfer, 2 had talipes varus in 13 by interosseous transfer; there was significant difference between two routes (P lt; 0.05). The complications included drop-toe(5 cases), muscle atrophy (4 cases), tendon rupture (1 case) and tendon adhesion (1 case). CONCLUSION: Tibialis posterior transfer with elongation of tendo Achilles can obtain excellent results in treating foot-drop due to leprosy. Interosseous route is preferred and physiotherapy is emphasized pre- and postoperatively.
Objective To explore the effects of heat-inactivated Lactobacillus gasseri TMC0356 on liver lipid metabolism in rats with metabolic syndrome (MS) and its possible mechanism. Methods Sixty male Sprague-Dawley rats were selected. Rats were randomly divided into 5 groups, including control group, MS model group and three TMC0356 test groups (low-, medium- and high-dose groups). The rats in each group were fed with different diets for 7 days, and the liver was dissected and removed after 15 weeks. The mRNA and protein expression levels of peroxisome hyperbioactive receptor-α (PPAR-α), sterol regulatory element binding protein-1c (REBP-1c), fatty acid synthase (FAS) and carnitine lipoacyltransferase-1 (CPT-1) genes in liver were detected. Results There was no significant difference in the mRNA expression of PPAR-α, SREBP-1c or CPT-1 among the five groups (P>0.05). The mRNA expression of FAS in low-dose TMC0356 test group was lower than that in MS model group (P=0.011), medium-dose TMC0356 test group (P=0.042) and high-dose TMC0356 test group (P=0.009). There was no significant difference in the expression of FAS mRNA between other groups (P>0.05). There was no significant difference in the protein expression of PPAR-α, SREBP-1c or FAS among the five groups (P>0.05). The protein expression of CPT-1 in low-dose TMC0356 test group was higher than that in control group (P=0.033) and high-dose TMC0356 test group (P=0.043). There was no significant difference in the protein expression of CPT-1 between the other groups (P>0.05). Conclusion Heat-inactivated Lactobacillus gasseri TMC0356 may improve the symptoms of metabolic disorder in rats by suppressing appetite, improving insulin resistance, and downregulating the expression of key fat metabolism genes such as FAS and SREBP-1c.
ObjectiveTo investigate the distribution of uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1) gene polymorphisms in esophageal carcinoma (EC) patients, and their relationship with adverse effects (delayed diarrhea and neutropenia) of Irinotecan. MethodsForty-eight patients with esophageal squamous carcinoma who were admitted to Sichuan Provincial People's Hospital between January and October 2012 were recruited in the study. There were 37 male and 11 female patients with their age of 56 (25-38) years. Formalin-fixed, paraffin-embedded samples were collected from those EC patients and genomic DNA was extracted. UGT1A1 polymorphisms were detected by PCR and DNA sequencing. Three genetic loci were investigated including UGT1A1* 28 (TA6 > TA7), UGT1A1* 6 (211G > A) and UGT1A1* 93 (-3156G > A). Adverse effects (delayed diarrhea and neutropenia) of patients with different UGT1A1 polymorphisms after Irinotecan treatment were recorded. The relationship between UGT1A1 polymorphisms and Irinotecan-induced adverse effects was analyzed. ResultsUGT1A1 polymorphisms were detected in 10 out of 48 (20.8%) EC patients. UGT1A1* 93 (-3156G > A)polymorphisms were most common with the polymorphism rate of 16.7% (8/48), followed by GT1A1* 6 (211G > A) polymorphisms with the polymorphism rate of 4.2% (2/48). The incidences of grade 3~4 diarrhea and grade 3~4 neutropenia after Irinotecan treatment in the patients with UGT1A1 polymorphisms were 60.0% and 40.0% respectively, which were significantly higher than those of the patients with wild type UGT1A1 (21.1% and 15.8% respectively, P < 0.05). UGT1A1 polymorphism rates were 45.5% (5/11) in female patients and 13.5% (5/37) in male patients, which were significantly different (P < 0.05). ConclusionsIn EC patients, 2 polymorphism loci including UGT1A1* 93 (-3156G > A) and GT1A1* 6 (211G > A) can effectively predict adverse effects caused by Irinotecan treatment. UGT1A1 polymorphism rate of male patients is significantly lower than that of female patients.
ObjectiveTo establish a cell inflammation model induced by tumor necrosis factor-α (TNF-α) in human bronchus epithelial cells, and investigate the effects of glutathione S-transferase mu 5 (GSTM5) on the inflammation and oxidative stress. Methods16HBE cells were treated with TNF-α (10 ng/mL, 24 h) in the absence or presence of the constructed GSTM5 eukaryotic expression vector (1 μg/mL). The concentration of malondialdehyde (MDA) and total antioxidation capacity (T-AOC) were detected by colorimetric method. The survival rate of cells was assessed by the methyl thiazolyl tetrazolium (MTT) assay. The transcription level of NADPH oxidase-1 (NOX1), NOX2, NOX3, NOX4, NOX5, dual oxidase-1 (DUOX1) and DUOX2 were evaluated by RT-PCR. Western blot was performed to investigate the protein levels of NOX1 and NOX2. ResultsTNF-α simulation significantly increased the level of MDA in cells, and decreased the level of T-AOC and survival rate of 16HBE. When transfected with the GSTM5 eukaryotic expression vector, the concentration of MDA significantly decreased (P < 0.05), and the activation of T-AOC increased dramatically (P < 0.05). Consequently, the survival rate of 16HBE in the GSTM5 group improved (P < 0.05). The 16HBE cells transfected with the constructed GSTM5 eukaryotic expression vector had a lower transcription and protein levels of NOX1 and NOX2 (all P < 0.01). There were no significant changes in the mRNA expressions of NOX3, NOX4, NOX5, DUOX1 or DUOX2. ConclusionGSTM5 may down-regulate the transcription level of NOX1 and NOX2 to reduce the inflammation and oxidative stress induced by TNF-α.
OBJECTIVE In order to inquire the methods of thumb reconstruction by transferring the index finger with incomplete conditions of nerve or blood vessels. METHODS From April 1987 to October 1997, 6 cases were treated by 3 kinds of operative methods according to the damage type of thumb and complications injures of the rest of hand: 1. transferring the index finger with pedicle without proximal phalanx, 2. transferring the index finger with palmar nerve and blood vessels, and dorsal skin pedicle, 3. transferring the index finger with compound pedicle. RESULTS All 6 cases of thumb reconstruction were successful. Followed up 6 months to 2 years, the pinching and gribing functions in 6 cases were completely recovered, and the sensation were partly recovered. CONCLUSION The operative method of thumb reconstruction had following advantages: Simple operation, high survival rate and certain function recovery. It can enlarge the indications of thumb reconstruction.
Objective To introduce the research update of microencapsulation and its application in orthopedics. Methods Recent articlesconcerned were extensively reviewed. Results Drugs and cells modified by genecould be encapsulated in different materials and be implanted in vivo avoiding a host immune system rejection. It act as a continuous source of desired medicine for enhancement of bone healing, the treatment of bone tumor and bone infection, and the regeneration of bone and cartilage. Conclusion Microencapsulation can be used asa carrier for drugs and cells modified gene to treat related disease in orthopedics.
【Abstract】ObjectiveTo study the effect of transfection with antisense DNMT3b gene eukaryotic expression vector on the expression of DNMT3b gene in human cholangiocarcinoma cell line QBC-939. MethodsThe constructed antisense DNMT3b gene eukaryotic expression vector was transfected into the human cholangiocarcinoma cell line QBC-939 by using lipofectamine transfection reagents, and positive cell clones were obtained by using G418 selection after transfection. Whether the constructed recombinant vector was transfected into QBC-939 cells successfully was confirmed by amplifying the exogenous neoR gene with PCR method. The expression of DNMT3b gene mRNA and protein were detected by semi-quantitative RT-PCR and FCM methods respectively. ResultsFollowing the transfection of antisense DNMT3b gene eukaryotic expression vector, the mRNA level of DNMT3b gene in QBC-939 cells of human cholangiocarcinoma decreased from 0.956±0.053 to 0.209±0.023, and the protein level of DNMT3b gene also decreased from (75.38±3.22)% to (29.87±3.46)%. There were very significant differences on the expression levels of DNMT3b gene between non-tranfections group and the antisense DNMT3b gene eukaryotic expression vector transfection group (P＜0.01). ConclusionTransfection with antisense DNMT3b gene eukaryotic expression vector significantly reduces the expression level of DNMT3b gene in human cholangiocarcinoma cell line QBC-939, and this study may provide a valid tool and method to investigate the function of DNMT3b gene and its role in cholangiocarcinoma.
Objective To study the effect of adenovirus bone morphogenetic protein 2 gene(Ad-BMP-2) transfer inducing mesenchymal stem cells (MSCs) compounded with fibrin gel on repair of rabbit cartilage defect. Methods ①BMP-2 and collagen type Ⅱ in MSCs transferred by Ad-BMP-2 were examined by RT-PCR, aniline dyeing and immunohistochemical analysis in vitro. ②MSCs were cultured in fibrin gel for 9 days, and were examined with electron microscope. ③Fortytwo rabbits suffering from cartilage defect were divided into 3 groups:the defects were treated with Ad-BMP-2 transfer inducing MSCs compounded with fibrin in group A, with MSCs compounded with fibringel in group B and with no implants in group C as control. HE and aniline dyeing, immunohistochemical analysis and biomechanics study were carried out in the 4th, 8thand 12th weeks. Results ①The positive results were observed for BMP-2 and collagen type Ⅱ with RT-PCR on the 3rd day and 5th day respectively, being statisticallysignificant difference when compared with control group(P＜0.05). ②Ad-BMP-2 transfer inducing MSCs cultured in fibrin gel were positively stained by aniline dyeing and immunohistochemstry. ③The therapy effect of group A was better than that of the other two groups in histology, biochemistry and biomechanics, and the biomechanic and histological features of repaired cartilage were similar to those of the natural cartilage. Conclusion Ad-BMP-2 can induce the expressionof collagen type Ⅱ and mucopolysaccharide in MSCs by secreting BMP-2, and can reconstruct articular cartilage defects better when compounded with fibrin gel.
ObjectiveTo investigate the expression of miR-195 and the underlying molecular mechanisms of miR-195 regulating HMGB1 in diabetic retinopathy (DR). MethodsExtract 5 ml venous blood from DR patients, diabetes mellitus (DM) patients and normal subjects, then extract and perificate plasma total RNA. MicroRNA array and real time polymerase chain reaction (RT-PCR) was used to screen out miRNAs which were expressed with significant differences in the serum of patients with DR. Bioinformatics was employed to predict the miR-195 related to high mobility group box 1 (HMGB1) regulation. Next, miR-195 was down-regulated or up-regulated in umbilical vein endothelial cells through transfection of miR-195 inhibitor and miR-29b mimics respectively.Then we analyzed expression of HMGB1 mRNA and protein by RT-PCR and Western blot. ResultsMicroRNA array results showed the expression of miR-195 in DR group is decreased by 8.34 times and 11.47 times compared with DM group and the normal group. RT-PCR verification results conforms to the microRNA array results. Compared with the DM group (F=0.034, t=8.057) and the normal group (F=0.370, t=9.522), the expression of miR-195 in DR group were significantly reduced, the differences were statistically significant (P < 0.05). RT-PCR showed that the expression of HMGB1 mRNA was significantly decreased in up-regulation group, compared with blank (F=0.023, t=11.287) and negative control group (F=0.365, t=7.471), the difference was statistically significant (P < 0.05). The expression of HMGB1 mRNA was significantly increased in down-regulation group, compared with blank (F=0.053, t=10.871) and negative control group (F=0.492, t=6.883), the difference was statistically significant (P < 0.05). Western blot showed that the expression of HMGB1 protein was significantly decreased in up-regulation group, compared with blank (F=0.021, t=8.820) and negative control group (F=0.039, t=7.401), the difference was statistically significant (P < 0.05); and significantly increased in down-regulation group, compared with blank (F=0.186, t=10.092) and negative control group (F=0.017, t=12.923), the difference was statistically significant (P < 0.05). ConclusionMiR-195 can inhibit the expression of HMGB1, reduce the inflammation and angiogenesis, thereby delaying or inhibiting the occurrence and development of DR.