Cell Line, Tumor ; Cell Proliferation ; drug effects ; Diterpenes, Kaurane ; pharmacology ; Humans ; Nasopharyngeal Neoplasms ; pathology

Purpose:To determine the efficacy of paclitaxel in human bladder cancer lines and to investigate the mechanism by which paclita xel induce apoptosis in human bladder cancer cells. Methods:BIU-87, 5637, T24 and EJ bladder cancer cell lines wer e cultured by techniques of cell culture in vitro. The cytotoxic activity an d apoptosis induction abilities of paclitaxel were analyzed by MTT and Annexin- V assay as well as DNA cytometry , respectively. The effects on the cell cycle w ere assessed by flow cytometry of propidium iodide. The expressions of Bcl-2, B ax, p53 and Caspase3 proteins were determined by flow cytometry immunofluorescen ce. Results:Paclitaxel dose-dependent inhibition of cell prolifera tion was seen.Paclitaxel induced G_2/M arrest (71.29% and 64.57%) which was maximal in 5637 and EJ cell lines. While paclitaxel at 1?g/ml concentration ex posure to 5637 12h, 14h and 48h respectively, the apoptosis rates of the respect ive times were 5.0%, 12.9%, 27.6%. The expression of genes p53 and Bcl-2 was no t influenced, whereas the expression of Bax and Caspase3 had increases time-dep endently after exposure to paclitaxel. The analysis of Annexin-V showed a drama tic dose-dependent increase of apoptosis. Conclusions:Paclitaxel inhibited bladder cancer cells prolifera tion and had more effect on those cells whose grade was lower and doubling time was longer. Paclitaxel could block G_2/M arrest, and induce apoptosis by th e path of Bcl-2/Bax in bladder cancer cell lines.

Objective To study the feasibility and indication of liver injury in children treated nonoperatively.Methods Ninteen(cases) with liver injury who underwent nonoperative management(NOM) were analyzed retrospectively.Patients with obvious trauma were reviewed.The main cause of trauma was due to traffic accident.Eleven cases(57.9%) had subcapsular hematoma and 8 cases(42.1%)had intrapararenchymatous hematoma.The treatment procedure included blood transfusion,hemostasis and monitoring the hemodynamic parameters.Results Seventeen cases(89.5%)were cured nonoperatively;2 cases underwent the operation later.Followed up for 10-24 months,patients were well recovered.Conclusions Most of cases with liver injury in children can be cured by NOM due to the physicalogical and anatomic features of children.During treatment,it is very important for the doctors to observe the vital signs closely,and(mana)-ge the combined injuries effectively and take regular imaging measurement.

ObjectiveTo investigate the mechanism of cerebral white matter damage in premature rats induced by intrauterine infection.Methods30 mature pregnant Wistar-Imamichi rats were divided into the experimental group (n=18) and control group (n=12). The rats of the experimental group were injected with lipopolysaccharide (LPS) 0.2 mg/kg in abdomen on 15th and 16th day after gestation. Those of the control group were injected with distilled water in equal volume. 45 premature rats born in the experimental group and 45 full-term rats born in the control group were tested with RIA for interleukin-6 (IL-6). The brain tissues of another 47 premature rats and 41 full-term rats were stained with HE method. Finally water content in brain tissue were tested in 50 premature rats and 50 full-term rats.ResultsIL-6 concentration of brain tissue of the premature rats in the experimental group was significantly higher than that in the control group ( P<0.01); and water content of the premature rats' brain was also higher than that of the full-term rats ( P<0.01). The edema of periventricular white matter, loose neuropil, decreased cell numbers, broaden intercellular space, and cell swelling and rupture were found in the brain tissue of the premature rats, no abnormal form and structure were found in the control group.ConclusionWhite matter damage of premature rats can be caused by endotoxin, and accompanied by IL-6 and water contents increasing.

Objective To investigate the effect of gastrodin on rat vascular smooth muscle cell (VSMC) migration induced by platelet-derived growth factor-BB (PDGF-BB) and its possible mechanisms.Methods Enzyme digestion method wasused to obtain rataorticVSMCs and be purified bypassage.Immunofluorescence staining was used to identify VSMC marker proteins.A PDGF-BB induced cell migration model was established.Transwell chamber assay was used to evaluate the effect of gastrodin on PDGF-BB induced VSMC migration.Western blots were performed to detect the phosphohorylation levels of c-jun N-terminal kinase (JNK).Results The purity of primary cultured VSMC was more than 99％.The VSMC migrated number in the PDGF-BB group was 85.2 ± 3.486 per field.It was significantly more than 42.5 ± 1.927 per field in the control group (t =9.981,P＜0.001),and gastrodin was enable to make PDGF-BB induced the number of VSMC migration significantly reduce to 71.3 ± 1.783 per filed (t=3.550,P =0.002).Western blots analysis showed that gastrodin inhibited PDGF-BB induced JNK phosphorylation (0.190 ± 0.015 vs.0.190 ± 0.015; t =14.548,P =0.000).Conclusions Gastrodin inhibits PDGF-BB induced VSMC migration,its mechanisms may be associated with the inhibition of the JNK signaling pathway activation.

Objective To investigate the adjuvant effect of dimo-thylidioctyl ammonium bromide (DDA) and/or DDA-BCG polysaccharide nucleic acid( BCG-PSN), which was combined with a Mycobacterium tuberculosis fusion protein AMM ( Ag 8 5 B - MPT64190-198 - Mtb8.4 ) to boost BCG primed immunization. Methods DDA with or without BCG PSN was mixed with the fusion protein AMM to construct the boosting vaccine. Mice were immunized with BCG and then boosted twice with AMM formulated with the adjuvant DDA with or without BCG-PSN. PBS or BCG vaccination without boosting was used as control. The humoral and cell-mediated immune responses were analyzed by ELISA and ELISPOT. Moreover, the protective efficacy of BCG prime-AMM subunit vaccine boosting against Mycobacterium tuberculosis infection was analyzed. Results With in vitro stimulation of Ag85B and PPD( purified protein derivative) antigen, the number of IFN-γ secreting cells from the mice boosted twice by AMM/DDA/BCG-PSN and AMM/DDA were higher than BCG and PBS group (P <0.05). The CFU in lungs of mice boosted with AMM/DDA/BCG-PSN was less than that of PBS group(P <0.05), while the CFU of AMM/DDA-boosted mice was less than that of BCG and PBS group(P < 0.05).However, fewer lesions were seen in lungs of mice immunized with BCG alone or BCG-prime-AMM/DDA/BCG-PSN boosting than the other groups. Conclusion DDA is an idea adjuvant for tuberculosis subunit vaccine;BCG-PSN might play a role in alleviating the immunity-mediated pathology.

Objective To determine the effect of iron deficiency on hemoglobin A2(HbA2) expression in patients with β-thalassemia.Methods The participants were recruited from the out-patient clinics of the Pediatrics Department and Obstetrics Department of Affiliated Hospital of Guilin Medical College and from some β-thalassemia major families.Blood samples from the participants were used for blood smear tests and hemoglobin electrophoresis and to analyze serum ferritin (SF),3 alpha-globin gene deletions,and 17 beta-globin point mutations.Results Of the 408 individuals,304 were assigned to group A (normal controls),26 to group B (iron deficiency),56 to group C (β-thalassemia),and 22 to group D (β-thalassemia combined with iron deficiency). The results for the comparison of the mean HbA2 values among pairs of groups were as follows: group A vs group B,q=5.074 7,P<0.05; group A vs group C,q=37.650 8,P<0.05; group A vs group D,q=16.043 0,P<0.05;group C vs group D,q=7.682 9,P<0.05; Group B vs group D,q=15.806 6,P<0.05. There were no significant correlation between SF and HbA2 in all 4 groups.Conclusions Iron deficiency decreased the HbA2 level in both controls and individuals with β-thalassemia. HbA2 levels decreased significantly in individuals with both β-thalassemia and iron deficiency as compared with β-thalassemia group alone. However,they remained significantly higher than both the control and iron-deficient groups. Therefore,the elevation of HbA2 could be used to diagnose β-thalassemia reliably even in the presence of iron deficiency.

OBJECTIVETo review the clinical features of the thoracolumbar fracture with ankylosing spondylitis (AS) in order to avoid delayed or missed diagnosis.

METHODSFive patients of thoracolumbar fracture with AS treated from April 2005 to June 2007 in our department were studied retrospectively, male 4 cases, female 1 case, the age from 26- to 72-years-old with an average of 44.8 years. Analysis including: case history, number of the ankylosed vertebras, characteristic of fracture, active state rheumatism.

RESULTSThe patients had the history of AS for average 22.6 years. The mean number of the ankylosed vertebras was 18.2. Of the 5 cases, 1 case encountered traffic accident, 1case was sprained, and 3 cases without trauma were diagnosed as stress fracture. Two cases were trans-vertebra fracture: the fracture line was through T6, T7, or L1 vertebral body respectively; 3 cases were through the disc space: 2 cases were through L1,2 disc space, 1 case was through L2,3. No compression fracture and neurological injury were found. The acute inflammatory index such as ESR and CRP in 4 cases didn't correlate with the degree of pain. The non-steroidal anti-inflammatory drugs (NSAIDs) hadn't significant effectiveness in relieving pain. The patients were diagnosed as 'relapse' of AS in other hospital, and had been misdiagnosed for average 1.51 months.

CONCLUSION1) the fracture is prevalent at the middle or late period of AS when extensive ankylosis has been existed at the thoracolumbar region; 2) the fracture is common at the lower thoracal spine and the upper lumbar spine, and the majority is the stress fracture; 3) the fracture line may be through the vertebral body, but more often through the disc space; 4) it is like an exacerbation of AS and therefore to be missed diagnosis; 5) when the back pain exacerbated suddenly in the middle or late period of AS, the degree of pain not correlating with acute inflammatory index, and the NSAIDs ineffective, the thoracolumbar fracture should be considered.

Aged ; Female ; Humans ; Lumbar Vertebrae ; injuries ; Male ; Middle Aged ; Retrospective Studies ; Spinal Fractures ; diagnosis ; drug therapy ; etiology ; Spondylitis, Ankylosing ; complications ; Thoracic Vertebrae ; injuries

Adolescent ; Anticoagulants ; therapeutic use ; Body Temperature ; Child ; Child, Preschool ; Critical Illness ; therapy ; Female ; Hemodynamics ; Hemofiltration ; Humans ; Infant ; Male

OBJECTIVETo observe the therapeutic effect of continuous blood purification (CBP) combined with hemoperfusion (HP) in children with hemolytic-uremic syndrome (HUS) and to investigate its possible mechanism.

METHODSEight children with HUS received CBP combined with HP on the basis of internal medicine treatment in the acute stage. Before and after treatment, serum levels of interleukin-6 (IL-6), IL-8 and tumor necrosis factor-α (TNF-α) were measured by chemiluminescence method, and levels of blood urea nitrogen (BUN), serum creatinine (SCr), alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatine kinase (CK), creatine kinase MB (CKMB), hemoglobin (Hb), platelet (PLT) and C-reactive protein (CRP) were measured. Eight healthy children undergoing physical examination were used as controls.

RESULTSThe 8 children with HUS all survived after CBP combined with HP and showed improved conditions. They had increased Hb and PLT levels and decreased serum levels of IL-6, IL-8, TNF-α, BUN, SCr, ALT, CK and CRP after treatment (P<0.05).

CONCLUSIONSCBP combined with HP can quickly remove pathogenic factors, continually eliminate inflammatory mediators and toxins, and reverse multiple organ dysfunction, and is one of effective methods for treating HUS in children.

Child ; Child, Preschool ; Female ; Hemofiltration ; Hemolytic-Uremic Syndrome ; therapy ; Hemoperfusion ; Humans ; Infant ; Male