Objective:To investigate the diagnosis and treatment principles of multiple primary colorectal carcinoma(MPCC).Methods:A retrospective analysis was made on 63 patients with MPCC admitted from January 1993 to January 2007 in our hospital. Results:The incidence of MPCC was 2.1%(63/3 021) with 31 cases being synchronous carcinoma(SC) and 32 cases diagnosed as metachronous carcinoma(MC). Male to female ratio was 2.5:1.Most tumors were located in rectum and sigmoid colon.A total of 34 cases(54.0%) were diagnosed by fiberoptic colonoscopy before operation.The diagnosis rate of SC by fiberoptic colonoscopy before operation and during operative exploration were all 38.7%(12 cases). The diagnosis rate of MC by fiberoptic colonoscopy before operation and during operative exploration were 68.7%(22 cases) and 6.25%(2 cases) respectively.The overall 5-year survival rate of the patients in SC was 45%(9/20),the overall 5-year survival rate of the patients in MC after the first operation was 72.4%(21/29). Conclusion:Clinician should improve the recognition of MPCC.Patients with colorectal carcinoma should undergo routine fibercolonscopy and standard radical excision. Periodic follow-up for the high-risk group should be highlighted.

Endothelium, Vascular ; cytology ; Humans ; Mucocutaneous Lymph Node Syndrome ; complications ; pathology ; Neovascularization, Pathologic ; Stem Cells ; cytology

ObjectiveTo investigate the effect of hyperbric oxygen (HBO) on infarct volume and relevant mechanism after permanent focal cerebral ischemia in adult rats.MethodsRat model of focal cerebral ischemia induced by intraluminal filament occlusion of middle cerebral artery (MCA) was used. HBO(2.0 ATA) was applied to HBO group. Infarct volume, matrix metalloproteinase 2 (MMP-2) and MMP-9 were detected at 6h, 24h, 48h, 72h,120h and 10d after ischemia.ResultsThe infarct volume obviously decreased at 120h and 10d and expression of MMP-9 lowered at 48—120h in HBO groups. There was no significant change in MMP-2.Conclusion HBO can reduce infarct volume after cerebral ischemia, which may be related to downregulation of MMP-9 levels.

ObjectiveTo observe the clinical therapeutic effect of intra-articular injection with sodium hyaluronate (SH) on osteoarthritis of the ankle.Methods25 patients with osteoarthritis of the ankles (36 ankles) were treated with SH intra-articular injection 2 ml every week for 5 weeks. The degree of pain, swelling and functional disturbance of the ankles were observed to evaluate the effect.ResultsAfter treatment, the degree of pain, swelling and functional disturbance of the ankles improved (P<0.05～0.01). The total efficiency rate was 91.61%.ConclusionSodium hyaluronate injected intra-articular is an effective, ideal and safe treatment for osteoarthritis of the ankle.

BACKGROUND:The pain caused by osteoporosis and osteoporotic fracture is usually treated with non-steroidal anti-inflammatory drugs (NSAIDs) in clinic,which has been reported that dysfunction of liver and kidney will follow the use,but what has happened in the tissue of liver and kidney is not reported.OBJECTIVE:To study the effect of NSAIDs on the tissue of liver and kidney in osteoporotic fracture rats.DESIGN,TIME AND SETTING:Randomized controlled animal experiment.The experiment was completed in the Animal Experiment Center in Shanghai University of Traditional Chinese Medicine from August 2007 to February 2008.MATERIALS:A total of 24 female SD rats,8-month-old,weighing 300-320 g,were randomly divided into 3 groups,saline group,diclofenac sodium (fracture before medicine) group and diclofenac sodium (fracture after medicine) group,with 8 rats in each group.METHODS:The rats were housed for 3 months after ovariectomized to establish osteoporosis models.Rats in the saline group and diclofenac sodium (fracture before medicine) group were administrated saline and diclofenac sodium after transverse osteotomy at the middle shaft of bilateral femur respectively;in the diclofenac sodium (fracture after medicine) group were administrated 5 mg/(kg?d) diclofenac sodium for 3 weeks,then received transverse osteotomy at the middle shaft of bilateral femur.MAIN OUTCOME MEASURES:The histological observation of liver and kidney was performed at weeks 2,3,4 and 6 after fracture.RESULTS:In the diclofenac sodium (fracture before medicine) group,diclofenac sodium caused the inflammatory response at glomeruli,which exhibited expansion of tubular lumen,edema of epithelial cells,disappeared cell nuclei,degeneration and necrosis of renal tubule,cell debris and drugs crystals accumulated in the tubular lumen,congestion and inflammatory cell infiltration of renal interstitium.Administrating diclofenac sodium may cause the inflammatory response at portal area,indistinct structure of hepatic lobule,hepatic cells edema,steatosis and necrosis.Administrating diclofenac sodium before osteoporotic fracture also resulted in tissue lesions in kidney and liver,the damage would continue about 3 weeks.CONCLUSION:The diclofenac sodium cause histological lesions of kidney and liver in osteoporotic rats,especially in kidney.The histological lesions of kidney and liver are inreversible after administrating diclofenac sodium for a long time.

BACKGROUND: The pain caused by osteoporosis and osteoporotic fracture is usually treated with non-steroidal anti-inflammatory drugs (NSAIDs) in clinic, which has been reported that dysfunction of liver and kidney will follow the use, but what has happened in the tissue of liver and kidney is not reported. OBJECTIVE: To study the effect of NSAIDs on the tissue of liver and kidney in osteoporotic fracture rats. DESIGN, TIME AND SETTING: Randomized controlled animal experiment. The experiment was completed in the Animal Experiment Center in Shanghai University of Traditional Chinese Medicine from August 2007 to February 2008.MATERIALS: A total of 24 female SD rats, 8-month-old, weighing 300-320 g, were randomly divided into 3 groups, saline group,diclofenac sodium (fracture before medicine) group and diclofenac sodium (fracture after medicine) group, with 8 rats in each group.METHODS: The rats were housed for 3 months after ovariectomized to establish osteoporosis models. Rats in the saline group and diclofenac sodium (fracture before medicine) group were administrated saline and diclofenac sodium after transverse osteotomy at the middle shaft of bilateral femur respectively; in the diclofenac sodium (fracture after medicine) group were femur.MAIN OUTCOME MEASURES: The histological observation of liver and kidney was performed at weeks 2, 3, 4 and 6 after fracture.RESULTS: In the diclofenac sodium (fracture before medicine) group, diclofenec sodium caused the inflammatory response at glomeruli, which exhibited expansion of tubular lumen, edema of epithelial cells, disappeared cell nuclei, degeneration and necrosis of renal tubule, cell debris and drugs crystals accumulated in the tubular lumen, congestion and inflammatory cell infiltration of renal interstitium. Administrating diclofenac sodium may cause the inflammatory response at portal area, indistinct structure of hepatic Iobule, hepatic cells edema, steatosis and necrosis. Administrating diclofenac sodium before osteoporotic fracture also resulted in tissue lesions in kidney and liver, the damage would continue about 3 weeks.CONCLUSION: The diclofenac sodium cause histological lesions of kidney and liver in osteoporotic rats, especially in kidney. The histological lesions of kidney and liver are inreversible after administrating diclofenac sodium for a long time.

Humans ; Respiratory Tract Infections ; complications ; microbiology ; Silicotuberculosis ; complications ; microbiology ; Tuberculosis, Multidrug-Resistant ; complications ; microbiology

AIM: To examine whether lipoxin A_4 (LXA_4) induces apoptosis of rat renal interstitial fibroblasts and explore the mechanisms. METHODS: Rat renal interstitial fibroblasts (NRK-49F cells) were incubated in RPMI-1640 medium supplemented with 5% fetal calf serum and exposed to LXA_4 at the concentration of 10 nmol/L, 100 nmol/L or 1 ?mol/L for 24 hours. Prior to experiment, some cells were transfected with calpain 10 antisense oligodeoxynucleotide. Apoptosis of cells was recognized by double staining using fluorescent dye acridine orange and ethidium bromide, observed under laser scanning confocal microscopy and counted by flow cytometry following propidium iodide and annexin staining. Activity of caspase-3 was measured by colorimetric assay. The expression of calpain 10 mRNA was determined by RT-PCR. RESULTS: LXA_4 at the concentration of 100 nmol/L or 1 ?mol/L induced 9.83% or 33.82% apoptosis of cells, respectively. Treatment of cells with LXA_4 up-regulated the expression of calpain 10 mRNA and increased the activity of caspase-3. The transfection of the cells with calpain 10 antisense oligodeoxynucleotide inhibited the LXA_4-induced apoptosis, activity of caspase-3 and expression of calpain 10. CONCLUSION: LXA_4 at high concentration induceds apoptosis in rat renal interstitial fibroblasts via up-regulating of calpain 10 mRNA expression.

AIM: To find whether lipoxin A_4 (LXA_4) inhibits cell proliferation induced by TNF-? in rat mesangial cells, and to explore the molecular mechanisms of signal pathways of LXA_4 actions. METHODS: Cultured rat mesangial cells were growth-arrested and exposed to TNF-? with or without preincubation with LXA_4. Proliferation of mesangial cells was measured by MTT methods. Activities of STAT_3 were analyzed by electrophoretic mobility shift assay. Expression of cyclin E mRNA was assessed by RT-PCR. Cyclin E proteins were determined by Western blotting analysis. RESULTS: TNF-?-induced proliferation and increased mRNA and protein expression of cyclin E in mesangial cells were inhibited by LXA_4 in a dose-dependant manner. TNF-?-stimulation of the STAT_3-binding activities in mesangial cells was down-regulated by lipoxin A_4. CONCLUSION: Inhibitory effect of LXA_4 on TNF-?-induced mesangial cell proliferation is mediated by Jak_1/STAT_3 signal pathway.