Objective To study the method and outcome for intercondylar comminuted fractures of the humerus through open reduction and internal fixation with AO reconstructive plate. Methods From March 1997 to September 2000, 31 cases of intercondylar comminuted fracture of humerus were reviewed, which involved 24 males and 7 females with an average age of 37.4 years (range, 18-67 years). The fracture was located on left side in 17 and on right side in 14. According to AO/ASIF classification, there were C1 in 11, C2 in 12, and C3 in 8, among them, 9 cases were open fractures including of Cusstilo and Aderson typeⅠin 5 and Ⅱ in 4. Posterior trans-olecranon osteotomy with open reduction and internal fixation by AO reconstructive plate or plus 1/3 tube plate were performed in all the cases within 48 hours after injury. The osteotomy was "V" shape at 2 cm to proximal end of ulna. All the patients began the passive motion exercise within 24-48 h, and active training at one week postoperatively. X-ray was taken in 1, 3, 6 and 12 months after operation to observe the bony union. 5 cases with ulnar nerve injury underwent nerve exploration and anterior transposition. Results All the cases were followed up 1-3.4 years (average, 1.5 years), the fractures healed well, and the elbow function recovered satisfactorily. According to the Cassebaum scoring system, 11 were assessed as excellent 11, good 14 and fair 6, and the excellent-good rate was 80.6%. The complications included 1 infection, 1 heterotopic ossification and 2 injuries of the radial nerve, which recovered with dressings, antibiotics and neural nutrients. Conclusion The technique of AO reconstruction plating for the intercondylar comminuted fractures of the humerus through trans-olecranon approach offers many advantages, such as sufficient exposure, anatomical reduction, stable fixation, earlier exercise and satisfactory elbow function.

Tetrandrine (Tet) is a bibenzylisoquinoline alkaloid isolated from Stephania tetrandra S Morr. Lots of studies demonstrated that Tet could: ① act as a calcium antagonist via blocking plasma membrane voltage- or receptor-operating calcium channels, inhibiting extracellular calcium entry and intracellular calcium mobilization, so it could prevent hepatocytes, cardiomyocytes, pancreas cells and neurocytes from toxic or ischemia-reperfusion injuries. However, in HL-60 and leukamia T cells, Tet promoted calcium releasing from mitochondria or/and microsomes and induced these cells death. ② down-regulate T cell protein kinase C signal transduction pathway, inhibit T cell proliferation, interleukin-2 secretion and expression of the T cell activation antigen. It could also interrupted integrity of macrophages, reduced neutrophiles and macrophages respiratory-bursting and proinflammatory cytokines secretion through minimizing nuclear transcription factor kappa B DNA binding activity. ③ induce tumor cells apoptosis. ④ down-regulate P glucoprotein activity and reverse tumor cells multidrug resistance. ⑤ also inhibit platelet-derived growth factor induced hepaticstellate cells and human lung fibroblast proliferation, down-regulete type Ⅰ and type Ⅲ collagen secretion. In this article, we also reviewed the therapeutic effects of Tet on hepatic fibrosis, pulmonary fibrosis, portal hypertension, pulmonary hypertension, anti-inflammation and anti-tumors.

Purpose:T0 study the mechanism and the potentiality of calciumchannel blocker to prevent organal fibrogenisis. Materials and Mehods:The effects ofnifedipine(Nif)and nicardipine (Nic)on proliferation of human lung fibroblasts(HLF)and synthesis of coliagen and hyaluronic acid(HA)were determined by means of MTT,measuring the incorporation of 3H-proline and radioimmunoassay, respectively.Results: both Nif and Nic supressed HLF proliferation and collagen synthesis,as wellas decreased the production of HA in a concentration-dependent manner at l0-40?mol/L. In addition,there were no significant toxic actions on HLF. Conclusion: Nifand Nic might be hopeful antifibrotic drugs.

Objective Recently, a series of studies demonstrated that activation of local renin angiotensin system (RAS) may be related to tissue fibrosis, but the role of RAS in hepatic fibrogenesis has not been evaluated. The present study was designed: (1) to assess the effect of angiotensin converting enzyme (ACE) inhibitor and angiotensin Ⅱ type 1 (AT1) receptor antagonist in preventing hepatic fibrosis induced by CCl 4 administration in rats; (2) to investigate whether or not there are expression of AT1 receptors on hepatic stellate cells. Methods Study was conducted in male Sprague Dawley rats. Except for control group, three treated groups, either enalapril (10 mg/kg), losartan (10 mg/kg) or a combination of enalapril and losartan were given to the fibrotic rats (daily gavage), and saline vehicle was given to the control rats. After 6 weeks, liver fibrosis was assessed directly by hepatic morphometric analysis, which have been considered the gold standard for the quantitative measurement of fibrosis. The expression of AT1 receptors and ? smooth muscle actin (? SMA) in liver tissue were detected by immunohistochemical techniques. Results Compared to the rats of control groups, either enalapril or losartan, or a combination of two drugs can limit the expansion of the interstitium ( P 0.05). Expression of AT1 receptors was found in abundance in hepatic fibrotic interstitium of fibrotic rats, whereas only limited in vasculature in rats of control group to a very slight degree. Conclusions The present results demonstrated that: (1) activation of RAS is related to hepatic fibrosis induced by CCl 4; (2) angiotensin converting enzyme inhibitor and AT1 blocker might slow the propression of hepatic fibrosis; (3) activated hepatic stellate cell expresses AT1 receptors.

AIM:To evaluate the negative regulatory effects of somatostatin(SST) and octreotide(OCT) on the extracellular matrixes(ECM) metabolism in rat hepatic stellate cells(HSCs).METHODS:HSCs were treated with different concentrations of SST or OCT.The mRNA levels of collage type I,III and the intracellular expression of collagen,matrix metalloproteinase-1(MMP-1),tissue inhibitor of metalloproteinase-1(TIMP-1) in activated HSCs were assessed by in situ hybridization(ISH),[3H]-proline incorporation and immunocytochemistry,respectively.In addition,levels of hyaluronic acid(HA),laminin(LM),and procollagen type III(PCIII) in the culture supernatant of HSCs were also detected by enzyme-linked immunosorbent assay.RESULTS:Both SST(10-7 mol/L-10-6 mol/L) and OCT(10-7 mol/L-10-5 mol/L) markedly down-regulated the transcription of collagen type I,III,and the production of collagen,HA,LM,PCIII in HSCs in a dose-dependent manner.Furthermore,HSCs treated with SST(10-6 mol/L) and OCT(10-6 mol/L-10-5 mol/L) significantly reduced TIMP-1 level,which resulted in an elevated ratio of MMP-1/TIMP-1.CONCLUSION:SST and its analogy inhibit the synthesis of ECM and enhance its degradation both at transcriptional and translational levels.

Objective To analyze the clinical presentation of functional dyspepsia in Chinese ado lescents.Methods A stratified,randomized study by cluster sampling was employed,which recruited 51 956 students from high and primary schools in six provinces and two cities.All students were requested to fill in a questionnaire.Functional dyspepsia was diagnosed according to Rome Ⅱ criteria.Results Among 51 956 students,10 174 were diagnosed as functional dyspepsia(accounted for 19.58%).Heart burn,hiccup and air swallowing to terminate hiccup were major symptoms of functional dyspepsia.The upper abdominal distention,epigastric pain,anorexia and insomnia were common in boys than girls with no significance(P＞0.05).The belching,early satiety,fatigue and anxiety were significantly higher in girls than boys.Conclusions Functional dyspepsia is a common disorder among the adolescents.Educa-tion and psychotherapy are important in the treatment of students with functional dyspepsia.

OBJECTIVETo assess whether Angiotensin II (Ang II) and carbon tetrachloride (CCl(4)) used in combination could accelerate the process of fibrosis and whether Ang II play a role in exagerating hepatic fibrosis in rats.

METHODSAng II was injected into the abdominal cavity of Sprague-Dawley (SD) rats together with subcutaneous injection of CCl(4). Rats were killed after 14 and 28 d. Blood serum and liver specimen were collected. The extent of fibrosis in the stained liver tissue sections was determined with the KS 400 Image Analysis System.

RESULTSRats receiving Ang II and CCl(4) for 28 d showed extensive liver fibrosis. Along with the increase of hepatic fibrosis, the serum concentration of Ang II went up gradually.

CONCLUSIONSA combination of Ang II and CCl(4) would accelerate the process of hepatic fibrosis. Ang II probably took part in the occurrence of heparic fibrosis.

Alanine Transaminase ; blood ; Angiotensin II ; blood ; toxicity ; Animals ; Aspartate Aminotransferases ; blood ; Carbon Tetrachloride ; toxicity ; Liver Cirrhosis, Experimental ; chemically induced ; Male ; Rats ; Rats, Sprague-Dawley ; Renin-Angiotensin System ; physiology

OBJECTIVETo examine the expression changes of activin beta A, beta C, beta E and follistatin mRNA in the development of rat hepatic fibrosis induced by carbon tetrachloride (CCl(4)).

METHODSHepatic fibrosis was induced in rats by subcutaneous injections of 40% carbon tetrachloride oily solution for a period of 1 to 7 weeks. After carbon tetrachloride injection of 1, 2, 3, 4, 5, 6, and 7 weeks, the 6-12 rats were killed every time. The kinetics of activin beta A, beta C, beta E and follistatin mRNA expression were assessed by the semi-quantity RT-PCR.

RESULTSActivin beta A, beta C, beta E and follistatin mRNA could be detected in normal rat livers. After CCl(4) injection for 2 or 3 weeks, beta A mRNA was transiently decreased and became undetectable, then increased gradually. After CCl injection for 6 and 7 weeks, beta A mRNA level was significantly higher than controls (P<0.01). beta C mRNA could be detected after CCl(4) injection for 1 to 4 weeks and was significantly increased after 5 weeks over controls (P<0.05). beta E mRNA could not be detected after CCl(4) injection for 1 to 5 weeks, but significantly increased after CCl(4) injection for 6 or 7 weeks compared with controls (P<0.01). Except for normal rat liver, no follistatin mRNA was detected in rats after CCl(4) injection.

CONCLUSIONSActivins and follistatin have different expression changes in the development of hepatic fibrosis and the imbalance of activins and follistatin expression may involve in the formation of hepatic fibrosis.

Activins ; genetics ; Animals ; Carbon Tetrachloride ; Follistatin ; Gene Expression ; Inhibin-beta Subunits ; genetics ; Liver Cirrhosis, Experimental ; chemically induced ; genetics ; pathology ; Male ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction