Objective To discuss the complications following internal fixation of intra-articular calcaneal fractures and its prevention and treatment. Methods From January 1997 to July 2002, 59 sides of calcaneal fractures in 54 patients were treated with open reduction and Y-shaped plate fixation through lateral approach, most of them supplemented by autogenous bone grafting. According to Sanders classification, 20 sides were accounted for typeⅡ, 24 for type Ⅲ, 15 for type Ⅳ. During operation, lateral roentgenograms were made to assess Bler angle and Gissane angle, Broden view was made to evaluate congruency of the posterior facet. The wounds were drained underneath the lateral flap to prevent hematoma formation. Perioperative antibiotics were used routinely. All the cases were followed-up for an average of 17 months(range, 9 to 48 months). Results The clinical results were evaluated according to Maryland Foot Score, excellent results achieved in 30 cases, good in 21, fair in 6, poor in 2; excellent and good rate was 86.4%. Early complications were found in 4 cases(6.8%). Among them, 2 cases of wound necrosis were treated with suture after resection of necrotic tissue or covered with flap grafts, 1 case of wound infection recovered after dressing changes, 1 case of sural nerve injury recovered uncompletely without any special treatment. Late complications were found in 2 cases(3.4%) with obvious chronic pain, the patients were treated by subtalar arthrodesis and relieved from pain later. Conclusion The complications of internal fixation to fractures are related to anatomic features of calcaneus and their injury mechanism. Serious complications can be minimized in several ways as follows: optimal time for operation and preoperative design should be carefully considered, a full-thickness flap is recommended in avoidance of excessive distraction, bone grafting is needed to support intra-articular fracture fragments and to enhance the stability of internal fixation, the affected extremity should be immobilized by plaster and elevated, and perioperative use of antibiotics.The appropriate management should be taken in cases of complications.

Objective:To elucidate the signal transduction mechanism of the modulation of immune cells by estrogen,the effect of 17?-estradiol(E2)on the production of nitric oxide (NO)from spleen mononuclear cells(MNC)of rats and the expression of inductible NO synthase(iNOS) in estrogen receptor(ER) knockout mice were examined.Methods:Culture of the spleen MNC from normal,Freund's incomplete adjuvant(FIA)or myelin basic protein(MBP) immunized Lewis rats.Detection NO production in the supernatant of culture was determined by Griess reagent.The expression of iNOS in spleen sections were observed by immunofluorescence staining.Results:①E2 dose-dependently induce NO production in spleen MNC from normal rats,MNC from FIA or MBP immunized rats manifest in the same manner.iNOS INHIBITOR l-NAME or MAPK blocker could suppress the induction.②In vivo E2 enhanced iNOS expression in wild type mice(WT),but had no effect in ER ? knockout mice(EPKO).ER? knockout mice(BERKO)appear the same with wt.Conclusion:E2 could modulate the immune system via induction of NO,which involves both genomic and nongenomic mechanisms.

OBJECTIVE:To introduce a self-cure method for the cough caused by cold.METHODS:By placing control group and trial group,30 cases(control group)were assigned to receive Dextromethorphan Hydrobromide oral liquid and 32 cases(trial group)to employ self-cure method for cough caused by cold.And a self-cure method for the cough caused by cold was induced.RESULTS & CONCLUSION:The practice of self-cure method can speed up the self-cure of cough caused by cold and this method deserves to be popularized.

Autosomal recessive polycystic kidney disease (ARPKD) had a low incidence, and mainly in neonates or infants. It is caused by mutations of the polycystic kidney and hepatic disease 1 gene (PKHD1). The pathogenesis of ARPKD is still not clear. The principal of treatment is focused on the control of complications and slow down the progression. In this article, the research advances in the pathogenesis and treatment of ARPKD was reviewed.

Abstract Sepsis and related syndromes are the major cause of multiple organ failure and death in patients with critical illnesses.Neuroendocrine dysfunction has long been thought to be an important event in sepsis.In clinic,optimal management of the hormones could alleviate severe complications in sepsis.In this article,we review the dysfunction of neuroendocrine system as well as autonomic nervous system in sepsis,and summarize the respective therapy strategies.

Objective:To compare the differences of bond strength usi ng gold intermediate layer between Ni-Cr alloy and opaque porcelain(OP) baked at different temperatures. Methods:36 standard samples of Ni-Cr al loy and 36 of gold were prepared. The samples were divided into 4 groups with 9 in each. In group 1,OP was smeared to the surface of the samples and then baked at 950 ℃. In group 2,3 and 4 blendgold neu(a gold past) was put on the surface of the samples, then baked at 820 ℃,890 ℃ and 960 ℃ respectively. The samples were proccessed for further tests.The bond strength was tested by shear bond te st, and the electron probe was used to observe interfacial bond state and diffus ion of interfacial elements. Results:The bond strength(MPa) in g roup 1,2,3 and 4 was 19.66? 1.83,22.34?2.73,21.33?2.75 and 28.02?5.71 res pectively(group 1 vs group 4 P

Objective To explore the effects of fluvastatin on NF-?B activity and osteopontin(OPN) mRNA expression in albumin-induced renal tubular epithelial cells.Methods The renal tubular epithelial cells were cultured with 30 mg/ml fat free bovine serum albumin(BSA) as the control group.The renal tubular epithelial cells in the treatment group were cultured with different concentrations of fluvastatin for different hours.EMSA and RT-PCR were used to observe NF-?B activity and OPNmRNA expression.Results Fluvastatin can inhibit the NF-?B activity and OPNmRNA expression in a time and dose dependent manner.Conclusion Fluvastatin can inhibit NF-?B activity and OPNmRNA expression in albumin induced tubular epithelial cells.

Objective To explore the alternations of CD4 + T cell subsets and their cytokines and transcription factors in children with Henoch - Schonlein purpura(HSP). Methods Forty - one children were enrolled in this stud-y,including 41 in acute stage of HSP,35 cases of HSP in clinical remission stage and 30 healthy children as healthy control group. The percentages of helper T lymphocytes(Th)1,Th2,regulatory T cells(Treg)and Th17 subsets were determined by flow cytometry(FCM). The concentrations of plasma interferon - γ( INF - γ),interleukin( IL) - 4, transforming growth factor - β1(TGF - β1 )and IL - 17 were examined by ways of enzyme - linked immunosorbent assay(ELISA). The expressions of T - bet,GATA3,Foxp3 and ROR - γt mRNA in peripheral blood mononuclear cells were examined by means of reverse transcription - polymerase chain reaction(RT - PCR). Results (1)During the a-cute and recovery stage of HSP,compared with the control group,the percentages of Th2 and Th17 cell subsets,the le-vels of plasma IL - 4 and IL - 17,and the expressions of GATA3 and ROR - γt mRNA were significantly higher(all P ﹤ 0. 05). The percentages of Th1 and Treg cell subsets,the levels of plasma INF - γ and TGF - β1 and the expres-sions of T - bet and Foxp3 mRNA were lower(all P ﹤ 0. 05). The imbalances of Th1 / Th2 and Treg/ Th17 appeared during the acute stage of HSP.(2)During the recovery stage of HSP,the percentages of Th1,Th2,Th17 and Treg,and the ratio of Treg / Th17 were of no difference compared with those in acute stage( all P ﹥ 0. 05). The ratio of Th1 / Th2,and the expressions of T - bet and Foxp3 mRNA were increased(all P ﹤ 0. 05),while the levels of plasma IL - 4 and IL - 17,the expressions of GATA3 and ROR - γt mRNA were decreased(all P ﹤ 0. 05)compared with those in acute stage. In the recovery stage of HSP,the imbalances of Th1 / Th2 and Treg/ Th17 were still obvious .(3)There was a positive correlation in every 2 cytokines of Th1,INF - γ and T - bet. And the same correlation existed in Th2, IL - 4 and GATA3,in Treg,TGF - β1 and Foxp3,and in Th17,IL - 17 and ROR - γt(P ﹤ 0. 05). Conclusions The imbalance of Th1 / Th2 and Treg/ Th17 is critical in pathological mechanism of HSP. The disturbance of immune tole-rance induced by Treg cells is important in HSP.

AIM To investigate the effect of tamoxifen on the proliferation of the anterior pituitary cell of rats and its mechanism. METHODS Primary culture of the anterior pituitary cell of rats and 3H TdR incorporation method were applied. The changes of cell morphology were observed directly by electric microscope. RESULTS Tamoxifen could inhibit the proliferation of the anterior pituitary cell of rats. The inhibitory effect of tamoxifen (0 1 ?mol?L -1 ) could be reversed by estrogen.The classical apoptotic changes appeared in the cells after tamoxifen incubation for 48 h. CONCLUSION Tamoxifen can inhibit the proliferation of the anterior pituitary cell of rats and resultin the cell apoptosis.

Objective To investigate the relation between polymorphism of NOS3 G894T and susceptibility of cancer .Methods Literatures under the inclusion and exclusion criteria about relation between polymorphism of NOS 3 G894T and susceptibility of cancer were collected by computer -based retrieval and manual retrieval .The pools ORs with 95% CI were calculated to assess the association strength between polymorphism of NOS 3 G894T and cancer risk by Meta methods .Sensitivity and publication bias were evaluated .Results 19 literatures with 7679 cases of cancer and 8180 cases as control group were included .The pooled result indica-ted that no significant association between its polymorphism and cancer (ORT versus G=1 .030 ,95% CI=0 .964 -1 .101 ;ORTT versus GG=1 .056 ,95% CI=0 .895-1 .245 ;ORTG versus GG=1 .045 ,95% CI=0 .977-1 .119 ;ORTT/TG versus GG=1 .047 , 95% CI=0 .981-1 .117 ;ORTT versus TG/GG=1 .005 ,95% CI=0 .900-1 .123) .No significant association was observed in sub-group analysis based on ethnicity ,cancer type ,and source of control group .Conclusion There was no relationship between NOS3 G894T polymorphism and cancer susceptibility .