Objective To evaluate the risk factors of pediatric indirect inguinal hernia. Methods A hospital-based case-control study was performed. One hundred and three indirect inguinal hernia cases with two -fold controls (206 cases) were enrolled. Parents were interviewed for their charateristics before and during conception. Unconditional logistic regression model was used for single factor and multivariate analysis to estimate odds ratios and their 95% confidence intervals by SAS 6.12 computer software. Results There were more males than females in the overall identified indirect inguinal hernia(Ratio=93.20%, P

Objective:To investigate the inhibitory effect of RXRγ and RARβ on the growth of human gastric carcinoma cell line SGC7901 treated by RXR agonist(9-cis-RA). Methods:The human gastric carcinoma cell line SGC7901 was treated with 9-cis-RA, and then the morphological changes were observed by H-E staining. The cell growth was detected by MTT assay. The apoptosis and the cell cycle progression were analyzed by flow cytometry. The expressions of RXRγ and RARβ were detected by immunocytochemistry staining and western-blot assay. Results: HE stain showed that the SGC7901 cells were sparser with the increasing concentration of 9-cis-RA. The growth of SGC7901 cell was inhibited by 9-cis-RA at the concentration of 20 μmol/L in time and dose depended manner. The apoptotic rate of the tumor cells increased after 72 hours at the concentration of 20 μmol/L 9-cis-RA and the tumor cells were arrested in G0/G1 phase. Immunocytochemistry and Western-blot assay showed that the expressions of RXRγ and RARβ increased after 72 hours, compared with those of negative control group. Conclusion: RXR agonist 9-cis-RA can inhibit the growth of SGC7901 cells via inducing cell apoptosis through upgrading the expressions of RXRγ and RARβ.

Objective To detect the expression of interlenkin-22 (IL-22) and relative CD4+ T cell subsets in patients with ulcerative colitis (UC),and to explore their roles in the pathogenesis of UC.Methods Thirty-five adult UC patients were enrolled in this study and 35 healthy subjects were taken as control.Plasma IL-22 level was quantified by ELISA.The percentages of Th1,Th17 and Th22 cells in peripheral blood were determined by flow cytometry.The relationships of these results and disease activity were analyzed.Results Plasma IL-22 levels in UC patients [ (354.12±104.22 ) pg/ml ]were significantly higher than that of healthy controls ( P＜0.05 ),and the levels increased significantly in severely active patients.The percentages of Th17 cells in UC patients [ (2.36±0.94) ％ ]were elevated compared to healthy controls ( P＜0.05 ),and the percentages increased significantly in moderately active and severely active patients.The percentages of Th22 cells in UC patients [ (2.27±0.87 ) ％ ]were elevated compared to healthy controls (P±0.05),and the percentages increased significantly in severely active patients.The percentage of Th1 cells was not significantly different between UC patients and normal controls.ConclusionOur resuits demonstrate elevated IL-22 correlated to Th17 and Th22 cells may play an important role in the immunopathogenesis of UC.

Objective To explore the effects of H2S on cerebral injury after cardiopulmonary resuscitation (CPR) and its mechanism.Methods Forty-five healthy Sprague-Dawley (SD) rats were randomly (random number) divided into shame-operated group ( group A,n =5 ),resuscitation group ( group B,further divided into four subgroups as per rats sacrificed 6 h,12 h,24 h,and 72 h after resuscitation,n =5),and NaHS pretreatment group ( group C,further divided into 4 subgroups as done in group B).The ratio of water content in brain tissue was calculated.The content of H2S in cerebral cortex of rats in all groups was determined by using universal microplate reader. Immunohistochemistry method was used to count the Nestin-positive cells. Results The content of H2S in hippocampus area of brain showed dramatic changes from rising up at first and then to lowering down to the minimum and finally returning to the original level in 72 h in B group.Compare to group B,brain water content was lesser ( P ＜0.05 or P ＜ 0.01 ) and the levels of Nestin in hippocampus increased in group C(P＜0.05 or P ＜0.01).The neurological deficit score (NDS) was improved (P ＜0.05 or P ＜0.01) and pathological changes in hippocampus of rat brain detected by using hemotoxylin - eosin staining were slighter in group C in comparison with group B.Conclusions Endogenous H2S may involve in the course of formation and progress of cerebral injury after CPR and small dose of NaHS (exogenous H2S) can improve NDS by decreasing cerebral edema and up-regulating Nestin level in hippocampus of brain,playing a protection role in cerebral injury after CPR.

Objective To summarize the safety and efficacy of low dose of hepatitis B immunoglobulin (HBIG) for prevention of de novo hepatitis B infection after renal transplantation.MethodsThe clinical data of 138 patients who received renal transplantation without hepatitis B infection between January 2007 and June 2010 were retrospectively studied (study group).All the patients in study group were given low dose of HBIG injection before transplantation.The HBsAb titer was monitored regularly after transplantation,and the dosage of HBIG adjusted according to the level of the HBsAb titer.HBIG was implied to all patients in the study group for more than one year.The clinical data of 196 patients who received renal transplantation without hepatitis B infection between January 2004 and December 2006 served as the control group.These 196 patients were not treated with HBIG.The incidence of de novo hepatitis B infection,and acute rejection of these two groups was analyzed.The one-year graft and patients survival rate was also investigated.Results During the follow- up period of 12 months,only one case in the study group had de novo hepatitis B infection (0.7％) 6 months after renal transplantation,while 11 cases (5.6％) in the control group had de novo hepatitis B infection,in which 2 cases were died from acute hepatic failure.The incidence of de novo hepatitis B infection had statistically difference between the two groups (P＜0.05).The incidence of acute rejection in the study and control groups was 13.8％ and 17.3％ respectively (P＞0.05).The one-year graft and patient survival rate in the study and control groups was 96.4％ and 97.8％,and 90.3％ and 91.8％ respectively (P＜0.05).ConclusionLow dose of HBIG is effective and safe for prevention of de novo hepatitis B infection after renal transplantation.

Although the essential oil of Xiangfu Siwu decoction (XFSWD) has strong pharmacological activity, its special physical and chemical properties restrict the clinical application and curative effect. In this paper, Xiangfu Siwu decoction essential oil (XFS-WO) was prepared by forming inclusion complex with β-cyclodextrin (β-CD). The present study is to investigate the effect of β-CD inclusion complex on the transport of major components of XFSWO using Caco-2 cell monolayer model, thus to research the effect of this formation on the absorption of drugs with low solubility and high permeability, which belong to class 2 in biopharmaceutics classification system. A sensitive and rapid UPLC-MS/MS method was developed for simultaneous quantification of senkyunolide A, 3-n-butylphthalide, Z-ligustilide, dehydrocostus lactone and α-cyperone, which are active compounds in XFSWO. The transport parameters were analyzed and compared in free oil and its β-CD inclusion complex. The result revealed that the formation of XFSWO/β-CD inclusion complex has significantly increased the transportation and absorption of major active ingredients than free oil. Accordingly, it can be speculated that cyclodextrin inclusion complex can improve bioavailability of poorly water-soluble drugs. Above all these mentioned researches, it provided foundation and basis for physiological disposition and pharmaceutical study of XFSWD.
Biological Transport ; Caco-2 Cells ; Drugs, Chinese Herbal ; analysis ; Humans ; Oils, Volatile ; analysis ; beta-Cyclodextrins ; pharmacology

Objective To explore the changes of mineral and bone metabolism before and after renal transplantation as well as the effect of preoperative parathyroid hormone (PTH) level on postoperative mineral and bone metabolism.Methods In this retrospective analysis,we recruited 82 cases of renal transplant recipients with normal renal function and receiving kidney transplantation in our hospital from January 2011 to January 2015.All of these patients had intact PTH (iPTH) level ＞300 pg/mL.We chose 26 cases of recipients whose preoperative iPTH was more than or equal to 800 pg/mL as very high PTH group,and 56 cases of recipients whose preoperative iPTH was between 301-799 pg/mL as high PTH group.We monitored and performed analysis of the total serum calcium (Ca),serum inorganic phosphorus (P),25-(hydroxyl) vitamin D3 (25 OHD),serum alkaline phosphatase (ALP),Beta C-terminal telopeptide (β-CTX),N-terminal/midregion (N-MID) pre-and 1 month,4 months,1 year,2 years,3 years post-kidney transplantation.Results Serum total calcium in the two groups was gradually increased,returned to normal range 1 month post-transplantation and reached the plateau 4 months post-transplantation.The incidence of hypercalcemia in very high PTH group was statistically significantly higher than in high PTH group.Serum phosphorus in the two groups showed a trend of gradual decline after renal transplantation,and returned to the normal range 1 month post-transplantation.The serum phosphorus level in very high PTH group reached the plateau 4 months post-transplantation,and that in high PTH group 1 month post-transplantation.Compared with high PTH group,very high PTH group has greater The incidence of long-term hypophosphatemia after renal transplantation was significantly higher in very high PTH group then in high PTH group.iPTH,ALP,β-CTX and N-MID in the two groups showed a downward trend after renal transplantation.At first month post-transplantation,iPTH,ALP,β-CTX and N-MID levels were reduced most significantly.The average levels of the three mentioned indicators in very high PTH group were higher than in high PTH group at every time point after surgery with the difference being significant during the early post-transplantation period.The anomalies of iPTH and β-CTX levels persisted to long term after transplantation in very high PTH group.25-OHD levels in these two groups showed rising trend after renal transplantation,reached the plateau 4 months posttransplantation,but failed to achieve the ideal reference level,and no significant difference was found between two groups at any time point monitored.Conclusion The anomalies of mineral and bone metabolism after renal transplantation could persist a long time.Conclusion hyperparathyroidism in the renal transplantation plays an important role in mineral and bone metabolism.Preoperative severe HPT could continue to post-transplantation period and increase the incidence of hyperphosphatemia and hypocalcemia long term after transplantation,which may aggravate bone turnover and this effect can last a long time after transplantation.

OBJECTIVETo explore the effects of ytterbium citrate on human liver carcinoma HepG2 cell line and the potential mechanisms.

METHODSThe HepG2 cells were cultured with DMEM medium and divided into different groups in the following media, in serum-free medium as control, different concentration (0.01 - 5.00 mmol/L) [YbCit(2)](3-)+serum-free medium as treatment group, MTT assay was used to measure the viability of the cells; 2.00 mmol/L [YbCit(2)](3-)+serum-free medium was used as treatment group, and Hoechst 33258 staining was used to detect apoptosis in HepG2 cells. Differential proteomic analysis, assay of intracellular H(2)O(2) levels and mitochondrial transmembrane potential were performed to study the effects of [YbCit(2)](3-) on HepG2 cells and the potential mechanisms.

RESULTSThe data showed that 72 h treatment of [YbCit(2)](3-) at 2.00 - 5.00 mmol/L significantly inhibited cell proliferation, and the IC(50) was (2.46 ± 0.23) mmol/L. After treatment with 2.00 mmol/L [YbCit(2)](3-) for 48 h and 72 h, Hoechst 33258 staining demonstrated that [YbCit(2)](3-) induced significantly increased apoptosis in HepG2 cells. After treatment with 2.00 mmol/L [YbCit(2)](3-) for 72 h, two dimensional gel electrophoresis and MALDI-TOF mass spectrometry analysis revealed 14 differentially expressed proteins between [YbCit(2)](3-)-treated cells and the control cells. These proteins mainly included cofilin1, peroxiredoxin6, S100 calcium-binding protein A6, and proteasome 26S non-ATPase subunit 13 isoform 3 and so on. These proteins played important roles in the processes of anti-apoptosis, oxidation reduction, cell proliferation and protein degradation. The mitochondrial membrane potential were investigated, the results showed the red and green fluorescence ratio was 2.45 ± 0.28 in the control group, 1.56 ± 0.23 in 24 h group, 1.16 ± 0.18 in 48 h group, compared with the control, the differences were significant (F = 23.97, P = 0.001). The results of H(2)O(2) detection showed the fluorescence intensity was 20.00 ± 2.08 in the control group, 40.00 ± 5.50 in 24 h group, and 48.00 ± 2.03 in 48 h group, compared with the control, the differences were significant (F = 48.40, P = 0.000). The results indicated a significant reduction in mitochondrial transmembrane potential and significant increase in H2O2 generation were observed in [YbCit(2)](3-)-treated cells.

CONCLUSIONThese results suggested that [YbCit(2)](3-) could induce apoptosis of HepG2 cells through the mechanisms involving oxidative stress and mitochondrial dysfunction.

Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Hep G2 Cells ; Humans ; Liver Neoplasms ; metabolism ; pathology ; Membrane Potential, Mitochondrial ; drug effects ; Oxidative Stress ; Proteome ; analysis ; Proteomics ; Ytterbium ; pharmacology

5-Aryl-4-cyano-1H-1, 2, 3-triazoles bearing a variety of substituting groups on 5-phenyl were synthesized. Their structures were established by MS, IR and 1H NMR spectra. The crystal structures of compounds 3f and 3m were determined by X-ray diffraction analysis. The active H of the triazole was on 1-N from the crystal structures. The compounds, designed as HER2 tyrosine kinase inhibitors, were screened for bioactivity of growth-inhibition of breast cancer MDA-MB-453 cells. The lowest IC50 value of inhibiting HER2 tyrosine kinase phosphorylation in breast cancer cells is 6.6 micromol x L(-1). The inhibiting-growth of breast cancer cells was enhanced from electron-drawing groups joining 5-phenyl on the triazole.
Breast Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Crystallization ; Crystallography, X-Ray ; Female ; Humans ; Phosphorylation ; Protein-Tyrosine Kinases ; antagonists & inhibitors ; metabolism ; Receptor, ErbB-2 ; antagonists & inhibitors ; metabolism ; Triazoles ; chemical synthesis ; chemistry ; pharmacology

OBJECTIVETo probe the effects of long-term oral administration of lanthanum nitrate [La(NO(3))(3)] on morphological change in the liver, aftereffect of deposited La in the liver and their mechanism in rats.

METHODSYoung Wistar rats were divided into two groups, one fed with 0.1, 0.2, 2.0, 10.0 and 20.0 mg/kg of La(NO(3))(3) for six months and the other for the control. Changes in ratio of liver to body weight were observed after exposure to La(NO(3))(3) at varied doses for six months and one month after six-month exposure, as well as morphology of the liver in the rats with routine histochemistry and transmission electron microscopy (TEM) technique. Content of La in the liver was measured with inductively coupled plasma-mass spectrometry (ICP-MS).

RESULTSRatio of liver to body weight was significantly higher in the male rats exposed to 20.0 mg/kg of lanthanum for six months than that in the control group. Ratio of liver to body weight restored to normal in the rats exposed to 20.0 mg/kg of La one month after six-month exposure. Infiltration of inflammatory cells in the portal region of the liver, small amount of fat drops in hepatocytic cytoplasm, increased density of mitochondria stroma, lysosome containing highly-electronic-density bodies and dense granules, normal nucleus and slightly deformed nucleus of hepatocytes could be found in the rats exposed to 20.0 mg/kg. Areas of the liver deposited with glycogen after six-month exposure to 20.0 mg/kg of La accounted for (26.1 +/- 1.5)% and (4.1 +/- 1.4)%, respectively for male and female rats, significantly lower than those in the control group [(31.3 +/- 1.4)% and (39.4 +/- 0.9)%, respectively], with a statistical significance and very statistical significance, respectively. There was a little infiltration of inflammatory cells in the portal region of the liver one month after six-month exposure to 20.0 mg/kg of La, and amount of the dense bodies was lower in the rats exposed to La for six months. Liver contents of La in the rats of all experimental groups were lower one month after six-month exposure than those in the rats exposed for six months.

CONCLUSIONSExposure to a dose of 20.0 mg/kg La(NO(3))(3) for a long term could damage the liver structure to certain extent, but lanthanum deposited in the liver could be eliminated from the body gradually.

Administration, Oral ; Animals ; Female ; Lanthanum ; toxicity ; Liver ; drug effects ; metabolism ; pathology ; Male ; Organ Size ; Rats ; Rats, Wistar