Humans ; Occupational Health ; Polymorphism, Single Nucleotide

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

Objective To share our experiences on integrated services in providing fetal diagnosis and postnatal treatment for congenital diaphragmatic hernia(CDH).Methods A retrospective analysis was conducted on 25 pregnancies diagnosed as CDH by both prenatal ultrasound and MRI in Maternal and Children Hospital of Guangdong Province from January 2012 to January 2014.All of the subjects received integral medical management including prenatal management (prenatal diagnosis and consultation), perinatal management (prenatal care and delivery) and neonatal treatment.Results Among the 25 CDH fetuses, 11 were mild, nine were moderate, and five were severe.One severe case, who was diagnosed at 26 gestational weeks, was aborted on demand of the mother.The other 24 cases continued their pregnancy and all delivered after 35 weeks including 13 cesarean sections (one due to twin pregnancy and 12 due to maternal demand) and 11 vaginal birth.The mean gestational age when CDH was diagnosed was (24.5 ± 3.5) weeks, and the 24 women delivered at an average of (37.5 ± 1.4) gestational weeks.The eleven mild cases accepted mask oxygenation.For those 13 moderate or severe CDH cases, all received dexamethasone to promote fetal lung maturity at 32 gestational weeks, seven were intubated before clamp the cord, and the other six did after.These 13 babies accepted high-frequency oscillation ventilation, with a median duration of 58 hours, and some of them treated with inhaled nitric oxide on requirement with a median duration of 52 hours.Except two cases died before operation, the rest 22 cases underwent neonatal surgery.One moderate case died at 48 hours after surgery due to pulmonary hypertension and respiratory failure.Another one severe case withdrew treatment at two months old.The other 20 infants recovered fully.Conclusions Integrated management including prenatal diagnosis and postnatal treatment, provides an effective and streamlined mode for diagnosis and treatment of CDH.Therefore,it might minimize potential medical risks.

Objective To investigate the safety, feasibility and results of laparoscopic assisted distal radical gastrectomy for gastric cancer. Methods Twenty-three cases of gastric cancer were subjected to laparoscopic assisted distal radical gastrectomy, D_(1+α)/D_(1+β) lymphadenectomy on 3 cases and D_2 lymphadenectomy on 20 cases. All cases received Billroth I reconstruction. Results Laparoscopic assisted distal radical gastrectomy was carried out in all cases successfully. The mean operative time was (205 ±38 )min, mean blood loss was (105 ± 66) ml and mean number of lymph nodes dissected was 19.7 ± 6.2 each case. The mean postoperative time of recovery of bowel function was (3.5 ±1.2) d,mean postoperative time of liquid intake was (4.9 ±0.9) d and mean hospitalization was (10.2 ± 2.7) d. No postoperative death or anastomotic fistula was found. Postoperative upper gastrointestinal bleeding occurred in 1 case and was cured by conservative treatment. Follow-up for 1-12 months revealed no recurrence or metastasis. Conclusions Laparoscopic assisted distal radical gastrectomy is a safe and feasible procedure with satisfactory short-term outcomes.Moreover,the short-term outcomes may be improved if the patients are treated under the notion of fast track surgery.

Objective To explore the regulatory effects of hyd ro gen sulfide (H 2S) on hypoxic pulmonary hypertension and pulmonary vascular rem odeling in rats. Methods Twenty-four rats were divided into 3 groups: control group(n=8), hypoxia group(n=8), and hypoxia +NaHS group( n=8). After 21 days of hypoxia, the mean pulmonary artery pressure (mPAP) wa s measured. The weight ratio of right ventricle. left ventricle +septum (R/L+S r atio) was measured. The microstructure and ultrastrcture changes in pulmonary sm all arteries were examined. The contents of proliferating cell nuclear antigen (PCNA) and Bc l-2 protein expressions were detected by immunohistochemical assay.Resu lts Compared with rats in the control group, the mPAP increased by 45.6 % (P

Humans ; Manipulation, Orthopedic ; methods ; Medicine, Chinese Traditional ; methods ; Models, Theoretical

AIMTo study upon to serum deprivation if delta-opioid receptor activation has direct effect on cultured impaired cardiomyocytes survival.

METHODSMyocardial cells of neonatal rats were cultured in vitro. The cell viability was determined with crystal violet staining uptake. The percentage of S + G2 + M in cell cycle was determined by flow cytometry. Apoptosis rates were determined by flow cytometry (FCM). The expression of Caspase-3 were investigated by Western blotting.

RESULTSMyocardial cells of neonatal rats were cultured of serum-free in vitro, apoptotic index was significantly increased, the expression of Caspase-3 was significantly increased, free-serum induced apoptosis in cardiac myocytes after 48 h. At concentrations of 10 nmol x L(-1) - 10 micromol x L(-1), a delta opoid receptor agonist [D-Ala2, D-Leu5]-enkephalin DADLE promoted the myocardial cells survival, in a concentration-dependent manner. The optimal response was achieved at 0.1 micromol x L(-1), which increase survival index of cardiac myocyte, percentage of S + G2 + M in cell cycle, decrease apoptotic index of cardiac myocyte, and the expression activate caspase-3. Delta-opioid receptor antagonist naltrindole at 10 micromol x L(-1) inhibited the promoting effects of DADLE, which decrease survival index of cardiac myocyte, and percentage of S + G2 + M in cell cycle, increase apoptotic index of cardiac myocyte and the expression of Caspase-3.

CONCLUSIONThe protective of delta-opioid receptor activation can promote survival in cultured impaired myocardial cells.

Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Cell Survival ; drug effects ; Cells, Cultured ; Culture Media, Serum-Free ; Enkephalin, Leucine-2-Alanine ; pharmacology ; Female ; Male ; Myocytes, Cardiac ; cytology ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, delta ; agonists

OBJECTIVEIntravenous anesthetics, such as propofol, are widely used in general anesthesia. Neurodegeneration and neurocognitive impairment after exposure to propofol in neonatal rats have raised concerns regarding the safety of pediatric anesthesia. We examined the effects of neonatal propofol exposure on brain cell viability, as well as expression of hippocampal survivin and Caspase-3 mRNA and protein.

METHODSOne hundred male Sprague-Dawley rats aged 7 d that were weighed 10-15 g were randomly divided into 4 groups (n = 25 each group). Group A: the rats were injected with no drugs. Group B: the rats were intraperitoneally injected with 50 mg/kg propofol. Group C: the rats were first intraperitoneally injected with 50 mg/kg propofol and another 50 mg/kg propofol was used when the dynamic response of rats appeared again. Group D: the rats were first intraperitoneally injected with 50 mg/kg propofol and another 50 mg/kg propofol was used three times once the dynamic response of rats appeared. To study the effects of propofol exposure on respiratory and metabolic function, arterial blood was aspirated from the left ventricle of neonatal rats 2 h after discontinuation of propofol. pH, PaO(2), PaCO(2), HCO(3)(-), BE and SaO(2) were detected by blood gas analyzer. Moreover, to examine the effects of propofol exposure on short-term cellular viability, the ultrastructure of neurons was observed by transmission electron microscope and Fluoro-Jade B (FJB) staining was performed to examine neuronal degeneration in hippocampal CA1 region of neonatal rats. Survivin and Caspase-3 mRNA and protein expression in hippocampus were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blotting 2 h after discontinuation of propofol.

RESULTSThe time of anesthesia maintaince in newborn rats was the longest in Group D and the time of anesthesia maintaince in Group C was longer than that in Group B. Two hours after discontinuation of propofol, pH, PaO(2), PaCO(2), HCO(3)(-), BE and SaO(2) of arterial blood in rats were not significantly different among groups A, B, C and D (P > 0.05). The structure of hippocampal neurons was normal in Group A and Group B while 100 mg/kg propofol resulted in nuclear blebbing and 200 mg/kg propofol led to nuclear fragmentation, chromatin condensation and apoptotic bodies. Cellular degeneration, as measured by Fluoro-Jade B staining, significantly increased in hippocampal CA1 region in the anesthesia groups compared with littermates in the no anesthesia group. FJB-positive stained degenerative neurons in groups B, C and D were (2.5 ± 1.3), (7.1 ± 2.3) and (9.4 ± 2.6), which were different from that in Group A (0.6 ± 0.3) (P < 0.05). Moreover, the number of FJB-positive neurons was the highest in Group D, that in Group C was more than that in Group B. At the same time point, apoptosis was measured by expression of Caspase-3 and Survivin mRNA and protein in hippocampus of rats. Caspase-3 mRNA in groups A, B and C was (0.78 ± 0.12), (0.84 ± 0.17) and (0.89 ± 0.19), while Caspase-3 protein in groups A, B and C was (0.22 ± 0.05), (0.26 ± 0.07) and (0.21 ± 0.06). Survivin mRNA in groups A, B and C was (0.56 ± 0.12), (0.58 ± 0.15) and (0.53 ± 0.16), while Survivin protein in these 3 groups was (0.24 ± 0.07), (0.21 ± 0.05) and (0.23 ± 0.06). Compared with that in Group A, Caspase-3 and Survivin mRNA and protein were not significantly different among Group B and Group C (P > 0.05). However, Caspase-3 mRNA and protein in Group D were (1.21 ± 0.14) and (0.42 ± 0.12), which were higher than that in the other 3 groups (P < 0.05). Survivin mRNA and protein in Group D were lower than that in the other 3 groups (P < 0.05).

CONCLUSIONSA high dose of propofol exposure may destroy the structure of neurons, induce neurodegeneration, increase Caspase-3 activity and inhibit survivin expression in hippocampus of newborn rats in vivo.

Anesthetics, Intravenous ; administration & dosage ; pharmacology ; Animals ; Animals, Newborn ; Blood Gas Analysis ; Caspase 3 ; genetics ; metabolism ; Dose-Response Relationship, Drug ; Gene Expression Regulation ; drug effects ; Hippocampus ; drug effects ; metabolism ; Injections, Intraperitoneal ; Male ; Microtubule-Associated Proteins ; genetics ; metabolism ; Neurons ; metabolism ; pathology ; Propofol ; administration & dosage ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley

Animals ; Escherichia coli ; genetics ; metabolism ; Female ; Hepatitis B Core Antigens ; biosynthesis ; genetics ; immunology ; Hepatitis B Surface Antigens ; biosynthesis ; genetics ; immunology ; Hepatitis B Vaccines ; immunology ; Male ; Mice ; Mice, Inbred BALB C ; Protein Precursors ; biosynthesis ; genetics ; immunology ; Recombinant Fusion Proteins ; biosynthesis ; genetics ; immunology ; Vaccines, Synthetic ; immunology

OBJECTIVETo observe the dynamic change in expression of protease-activated receptor 2 (PAR2) during onset and progression of liver fibrosis by using a rat model.

METHODSA cholestatic liver fibrosis model was established in Sprague-Dawley rats (aged 8-9 weeks, body weight 350 - 400 g) by bile duct ligation surgery. Rats receiving a sham operation and unoperated rats served as the negative and normal control groups, respectively. At baseline (pre-surgery) and post-surgery weeks 2, 4, 6, and 8, five rats from each group were sacrificed for whole liver resection. The protein and mRNA expressions of PAR2 and collagen I/III were detected by western blotting and RT-PCR, respectively. Between-group differences were assessed by analysis of variance testing.

RESULTSAt post-surgery week 2, the liver fibrosis group showed higher expression of PAR2 mRNA and protein than either control group. The expression levels of PAR2 continued to rise over time in the liver fibrosis group (peaking at week 8), and were significantly higher than those detected in the control groups (weeks 4-6: P less than 0.05; week 8, P less than 0.05). A similar trend was observed for the expression of collagen I/III.

CONCLUSIONDynamic expression of PAR2 observed in a cholestatic liver fibrosis rat model may indicate a role for this factor in the formation of liver fibrosis.

Animals ; Collagen Type I ; metabolism ; Collagen Type III ; metabolism ; Disease Models, Animal ; Liver ; metabolism ; pathology ; Liver Cirrhosis, Biliary ; metabolism ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Receptor, PAR-2 ; metabolism