In the study, the inhibitory effect of epigallocatechin gallate (EGCG) on Calcium oxalate nephrolithiasis and its possible mechanism were investigated. The rat Calcium oxalate nephrolithiasis model was induced through the combined oral administration of ethylene glycol and ammonium chloride, which was intervened with EGCG. Rat blood samples were collected to detect blood creatinine (Cr), blood urea nitrogen (BUN) and blood calcium. Rat urine samples were collected to observe and compare 24-hour urine volume, oxalic acid (Ox) and calcium in urine. Renal samples were collected to prepare tissue slices and observe the pathological changes in Calcium oxalate nephrolithiasis. The expression of osteopontin (OPN) in renal tissues was evaluated by Real-time PCR and Western blot. According to the results, compared with normal rats, rats in the nephrolithiasis model showed significant increases in Cr, BUN, urine Calcium, urine Ox and renal OPN expression (P < 0.05), but obvious decrease in 24-hour urine volume (P < 0.05); Compared with rats with nephrolithiasis, those processed with EGCG revealed remarkable declines in Cr, BUN, urine Calcium and urine Ox (P < 0.05), with significant rise in 24-hour urine volume (P < 0.05) in a concentration-dependent manner. Additionally, compared with the control group, nephrolithiasis rats showed significant pathological changes in Calcium oxalate calculus. After ECCG treatment, the renal pathological changes and OPN expression attenuated significantly in a concentration-dependent manner. The results showed that EGCG inhibits the formation of calcium oxalate nephrolithiasis in rats and shows a notable protective effect on renal functions.
Animals ; Blood Urea Nitrogen ; Calcium ; blood ; Calcium Oxalate ; metabolism ; Catechin ; administration & dosage ; analogs & derivatives ; Creatinine ; blood ; Disease Models, Animal ; Humans ; Kidney ; drug effects ; metabolism ; Male ; Nephrolithiasis ; blood ; drug therapy ; genetics ; Osteopontin ; genetics ; metabolism ; Rats ; Rats, Wistar

Humans ; Infant ; Lymphohistiocytosis, Hemophagocytic ; complications ; Male ; Mucocutaneous Lymph Node Syndrome ; complications

Objective To explore the diagnostic significance of CT and MRI in dermatofibrosarcoma protuberans.Methods Analyze the CT and MRI images of 16 cases which were confirmed as dermatofibrosarcoma protuberans by pathology.The medical imaging features of dermatofibrosarcoma protuberans were summarized.In the total 16 cases(including 6 male cases,10 female cases),15 cases had suffered from dermatofibrosarcoma protuberans for more than 1 year, 11 cases for more than 5 years, and 9 cases had history of recurrence.Results On MRI, the mass was slightly hypointense on T 1 WI, inhomogeneously hyperintense on T 2 WI with inhomogenous enhancement.The diameters of mass were less than 5 cm in 3 cases,and were more than 5cm in 13 cases.Fifteen cases had clear demarcation between the masses and their adjacent muscles , 7 cases had “suspension sign” in shapes, 10 cases had “sub-nodules outward” features at the edge of the tumors , 12 cases had “multinodular” features inside the tumor , and 8 tumors grew into the surrounding fat layer like roots.Conclusion Dermatofibrosarcoma protuberans can be diagnosed accurately based on the features displayed on CT and MRI.

Objective To detect the mutations of COL7A1 gene in three cases of dystrophic epidermolysis bullosa pruriginosa (DEBP). Methods Clinical data were collected from 3 patients with DEBP. Skin lesions were obtained from these patients and subjected to transmission electron microscopy. DNA was extracted from the peripheral blood of the 3 patients, their 16 relatives, and 150 unrelated normal human controls, and PCR was performed to amplify all the exons and flanking sequences of COL7A1 gene followed by sequencing.Results The patient 1 and 2 had family history, whereas the case 3 was sporadic. Transmission electron microscopy showed tissue cleavage beneath lamina densa in case 1 and slightly decreased anchoring fibrils in some areas of the lesions in case 1 and 3. Three heterozygous mutations of COL7A1 gene, i.e., c. G6734T, c.G6859A and c. G5318T, which leaded to three amino acid mutations, i.e., p. G2245V, p. G1773V and p. G2287R, were found in patient 1, 2 and 3 respectively. Of them, p. G2245V and p. G1773V were novel mutations. The mutations strictly cosegregated with the phenotype in the patients of family 1 and 2. No mutation was detected in the unaffected parents of patient 3 or the 150 unrelated healthy controls. Conclusions The p. G2245V, p. G2287Rand p. G1773V mutations of COL7A1 gene may be responsible for the phenotype of DEBP in the three cases,and of them, p. G2245V and p. G1773V have never been reported.

Carcinoma ; metabolism ; Cell Differentiation ; genetics ; Gallbladder Neoplasms ; genetics ; metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Kangai-1 Protein ; genetics ; metabolism ; NM23 Nucleoside Diphosphate Kinases ; genetics ; metabolism

Objective To investigate the effects of high-affinity tyrosine kinase receptors TrkB,TrkC and the low-affinity neurotrophin receptor p75 in spiral ganglion cell(SGC)of cisplatin-induced ototoxicity.Methods The 50 adult Wistar rats were divided randomly into 5 groups received intraperitoneal injection of cisplatin with vary dose.Control group was received equivalent volumes of saline.The group received l day intraperitoneal injection was cisplatin treated at a dose of 5 mg/kg and killed at next day.The group received 3 days was cisplatin treated for 3 days at sanle dose daily and then killed at next day.The group A received 5 days was cisplatin treated for 5 days and killed at next day.The group B received 5 days was cisplatin treated for 5 days and then were sacrificed after 7 davs.The change of mRNA level of neurotrophin receptors in cochlear tissue were examined bv RT-PCR.The expressing pattern of TrkB,TrkC,P75 in damaged cochlea were study by immunochemistry using antibodies against TrkB,TrkC,P75 protein.Results The research data showed the expression of Trk B,Trk C,D75 exhibited in SGC wag dynamic along with the administration lasting.The mRNA and protein level of Trk B(x±s)at day 1 and 3 after cisplatin treatment were 0.76±0.06,88.78±4.28,0.82±0.09 and 91.64±4.06,with significant difference among those and other groups(P＜0.05).The mRNA and protein level of TrkC at day 1 after cisplatin treatment were 0.80±0.05 and 89.55±2.76.with significant difference among that and other groups(P＜0.05).The mRNA and protein level of p75 at the control group and cisplatin treated groups were 0.64±0.04,55.16±3.10.0.77±0.04,78.46±3.86,1.01±0.09,105.02±6.61,1.18±0.09,111.10±6.08.0.51±0.04 and 42.74±5.20.with significant difference among the control group and cisplatin treated groups(P＜0.05).Conclusions The expression of Trk B increased to peak at day 1-3 after cisplatin treatment and decreased at day 5 early and following weeks.The expression of Trk C went up to peak at day l after cisplatin treatment and went down during subsequently time.P75 kept a trend of continuance increased during the drug treatment and decrease at drug stopped.The expression of Trk B.Trk C and P75 may be involved in cochlear insuh with cisplatin-induced.Trk B and Trk C may play an important role in the reparative process of cochlear,especially at early stage of the damage.P75 could promote SGC apoptosis in cisplatin-induced neuretoxicity.

Objective To observe spiral ganglion cell(SGC) death pattern caused by cisplatin and investigate pro-apoptotic protein BNIP3 involve ment in SGC death. Methods Cochlear SGC were isolated from the neonatal rats and cultured in vitro. A cochleas insult model were induced by treatment of 100 μmol/L cisplatin. Real-time PCR were used to determine expression of apoptosis related gene in neonatal rat cochlear cultures after cisplatin treatment. Western blotting was used to detect α-spectrin and indirectly determine caspase-3 activity. Double immunohischemical staining method was performed to indicated the localization and expression of BNIP3 and NF-200. Results Morphological finding showed that SGC were smaller, and neurofiber were blebbing and broken at treatment of cisplatin for 12 h. NF-200marker positive cell number decreased. The transcription level of BNIP3 in cisplatin treatment for 3 h,6 h and 12 h was higher than the control group(P ＜0. 05). Western blotting results showed that 120 000 of breakdown products of α-spectrin relative gray level were 0. 10 ±0. 05 in the control group, 0. 49 ±0. 09 and 0. 75 ±0. 08 in cisplatin treatment for 6 h and 12 h group. It increased significantly in the group of cisplatin treatment for 6 h and 12 h than the control group (q =8. 63 and 14. 61 ,P ＜0. 01 ). When compared between 6 h of cisplatin treatment and 12 h group, significant difference was detected (q = 5.98 ,P ＜ 0. 05 ). There was weak BNIP3 positive expression in cytoplasm of the control group. However, strongly BNIP3-positive labeled were seen in the nucleus of SGC and cytoplasm of some stromal cells around SGC after cisplatin treatment. Conclusions BNIP3 played an important role in cisplatin induced SGC death and followed independent signaling transduction pathway that differ from stromal cells around SGC. It may suggest that BNIP3 enter nucleus to bind DNA and up-regulate apoptotic gene expression to promote cells death.

Child ; Child, Preschool ; Female ; Flow Cytometry ; methods ; Humans ; Infant ; Male ; Thrombasthenia ; classification ; diagnosis

UNLABELLEDTo observe the efficacy of adefovir dipivoxil(ADV) in combination with Anluohuaxian capsule in the treatment of chronic hepatitis B (CHB) patients.

METHODS72 cases with CHB were randomly divided into two groups. 36 cases of treatment group were given ADV combined with Anluohuaxian capsule for 48 weeks. 36 cases of control group were given ADV. The levels of serum ALT, AST, Alb, TBil, HA, LN, CIV, HBV DNA and hepatic tissue were compared before and after being treated.

RESULTSAfter 48 weeks treatment,the liver function, serum fibrosis index and histology of treatment group and control group all have improved. After treatment, the two groups in the levels of ALT(t=0.746, P=0.342), AST (t=0.369, P=0.713), TBil (t=0.146, P=0.684), Alb(t=0.148, P=0.883), liver tissue inflammation mobility scoring (t=1.666, P=0.100) and HBV DNA negative rate (x2=0.141, P=0.708) were no evident difference.The level of HA, LN, CIV were significantly lower in treatment group(101.58+/-30.11, 147.89+/-41.72, 38.75+/-9.50) compared with control group(182.25+/-117.59, 181.50+/-56.96, 74.92+/-31.14) (P less than 0.05). After the treatment, the liver tissue fibrosis scoring was significantly lower in treatment group (10.61+/-2.37) compared with before the treatment (12.28+/-3.16) (P less than 0.05).There was no difference found between after the treatment (11.36+/-2.93) and before the treatment (12.17+/-3.01) in control group (P more than 0.05).

CONCLUSIONSThe results show that the treatment with ADV in combination with Anluohuaxian capsule can play promoting antifibrotic effect and significant improved liver histology of chronic hepatitis B patients.

Adenine ; analogs & derivatives ; therapeutic use ; Adult ; Antiviral Agents ; therapeutic use ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Hepatitis B, Chronic ; drug therapy ; pathology ; Humans ; Liver ; pathology ; Male ; Middle Aged ; Organophosphonates ; therapeutic use ; Phytotherapy ; Treatment Outcome

[ABSTRACT]AIM:ToinvestigatetheeffectofimmunosuppressantFK506onserumglucoseinratsandtoex-plore its mechanism .METHODS: Sprague-Dawley rats ( n =12 ) were randomly divided into drug group and normal group.The rats in drug group were intraperitoneally injected with FK 506 at dose of 1 mg· kg-1 · d-1 and the rats in nor-mal group received saline (1 mL· kg-1 · d-1 , ip) for 14 d.The fasting weight and fasting glucose were regularly meas-ured every 2 d.Visceral fat was isolated from the rats at the end of experiment .The mRNA expression of adiponectin , lep-tin, visfatin, resistin, retinol-binding protein 4 ( RBP4) and peroxisome proliferator-activated receptors γ( PPAR-γ) was determined by real-time fluorescence quantitative PCR .The protein expression of PPAR-γand adiponectin was measured by Western blotting .RESULTS:Compared with normal group , the concentration of fasting blood glucose in model group was significantly increased from the 10th day (P<0.05).At day 14, the fasting blood glucose of the model group increased from (5.10 ±0.62) mmol/L to (7.73 ±0.73) mmol/L.No significant change of blood glucose in normal group between the 10th day and the 14th day [from (4.66 ±0.32) mmol/L to (5.80 ±0.10) mmol/L] was observed.Compared with normal group , the mRNA expression of PPAR-γ, adiponectin and leptin in the adipose tissue of model group was signifi-cantly decreased ( P <0.01 ) , whereas the expression of visfatin , resistin and RBP4 was significantly increased ( P <0.05).Compared with normal group, the expression of PPAR-γand adiponectin in model group was decreased (P <0.01).CONCLUSION:FK506 may decrease the expression of PPAR-γto change the expression of adipocytokines and induce hyperglycemia in rats .