Objective To detect genetic alterations in pleomorphic xanthoastrocytoma (PXA), and to investigate the mechanism of development of this neoplasm. Methods Three patients with PXA were studied. Comparative genomic hybridization (CGH) was performed to study chromosomal imbalances in PXA. Using immunohistochemical analysis, the expression of EGFR was detected in PXA. Results Using CGH analysis, genetic imbalance was detected on at least one chromosome for each case. One patient revealed multiple genetic alterations, including gains of 2p14-pter, 4p15-pter, 7p21-qter, 11q24-qter, 12 and 15q14-qter,as well as losses of 8p11.2-pter, 9p11-p23, 10p12-pter, and 13q14-qter. This patient experienced tumor recurrence and died one year later. Gain on Chromosome 7 and loss on Chromosome 8p were demonstrated in 2 of the 3 patients. Immunohistochemically, no EGFR positive reaction was found in all cases. Conclusion Detection of genetic alterations is very important in understanding the pathogenesis of PXA.

Objective To investigate the clinicopathologic features,diagnosis,differential diagnosis and treatment of sclerosing angiomatoid nodular transformation(SANT). Methods The clinical data,pathologic characteristics,immunophenotype and postoperative follow-up of SANT were analysed. Results There were no specific findings in the clinical manifestations of the 4 cases of SANT.Grossly,the cut surface of the masses was gray-white and vague nodularity was observed.Microscopically,it was characterized by the multinodular angiomatoid appearance in a fibrosclerotic stroma.The nodules were composed of slit-like,sinusoid-like vascular spaces and were interspersed with a population of spindly or ovoid cells.It was revealed by immunohistochemistry that the expression of CD34 in some vessels' endothelial cells was positive,and CD8 was negative.While in another vessels' endothelial cells,CD8 was positive and CD34 was negative.The expression of SMA,Actin,Vimentin,Collage IV and CD68 was positive in all of the 4 cases,while that of CD21,Desmin and NSE was negative.No relapse or metastasis was found during the follow-up.Conclusion SANT is a rarely encountered benign lesion of the spleen,which should be distinguished from the malignant tumor of the spleen.The diagnosis counts on the pathologic and immunohistochemical findings.It could be cured by splenectomy with a favourable prognosis.

Objective To investigate the regulatory effects of tuberculin on growth and apoptosis of liver cancer and lung cancer cell lines. Methods HePG2(liver cancer) and A549(lung cancer) cell lines were treated with TB supernatant(TB-SN) with different concentrations. Cell viability was detected by using LIVE/DEAD Viability/Cytotoxicity cell kits including specific fluorescence primer,and cell apoptosis was detected by Vybrant apoptosis assay. Results After treatment with 5% TB-SN for 5 d,cell apoptosis was significantly increased in HePG2 and A549 cell lines.Cell growth of HePG2 and A549 cell lines was inhibited after treatment with TB-SN. Conclusion Tuberculin can induce cell apoptosis and inhibit cell growth of liver cancer and lung cancer cell lines.

BACKGROUND: Experimental autoimmune encephalomyelitis has become the most classical animal model for multiple sclerosis. However, the experimental autoimmune encephalomyelitis model of China presented one-way course of disease. By using proteolipid protein 139-151 and proteolipid protein 178-191, relapse remitting experimental autoimmune encephalomyelitis models may be induced in SJL/J mice which were susceptible to immune, which have similar clinical situation, course and histologicallterations to multiple sclerosis.OBJECTIVE: To establish the relapse remitting experimental autoimmune encephalomyelitis mouse model induced by proteolipid protein, which has similar clinical situation, course and histological alterations to multiple sclerosis.DESIGN: Completely randomized controlled study.SETTING: The centre of Neuro-information, and Neurological Institute,General Hospital of Chinese PLA.MATERIALS: The study was carried out at the Laboratory of Neuro-pathology, General Hospital of Chinese PLA, from February to June 2004.Sixty female SJL/J mice with 8-12 weeks old were selected and randomly divided into proteolipid protein 139-151 group and proteolipid protein-178-191 group with 30 in each.INTERVENTIONS: After injected with proteolipid protein-139-151 or proteolipid protein-178-191, the models of relapse remitting experimental autoimmune encephalomyelitis were induced, and the body weight and neurological signs of each female SJL/J mouse were viewed. The tissue morphological changes of models were observed with hematoxylin and eosin and uxol fast blue stain.MAIN OUTCOME MEASURES: The neurological symptoms and signs,features of relapse and remitting and the perivascular inflammatory cell infiltration, demyelinated lesion of the model of experimental autoimmune encephalomyelitis mouse induced by two proteolipid protein peptides.RESULTS: All 60 mice entered the final analysis. ① Significant neurological symptoms, signs and features of relapse and remitting was manifested in the model of experimental autoimmune encephalomyelitis mouse induced by two proteolipid protein peptides. Obvious phenomena of perivascular inflammatory cuffing, satellitism, predominant perivascular inflammatory cell infiltration and demyelinated lesion were found in spinal and cerebral tissue. ②Changes of body mass: Before immunity, the body mass of mice in two groups was( 17. 84 ± 2.59) g and (17. 88 ± 0.52) g respectively. Onset of relapse of the mice in proteolipid protein-178-191 group was earlier and faster, their body mass had no distinctive change after immunization and the mean body mass was(23.52 ± 2.37) g till the 60th day. Meanwhile, Onset of relapse of the mice in proteolipid protein-139-151 group was later and slower. After the immunity, the body mass of mice was little decrease, and the body mass was (16. 70 ±0.46) g on the 60th day. ③ Neural functional scores: The highest functional scores in the two groups were not different(3.86 ± 1.10vs 3.71 ±1.05, t=0.49, P=0.628).CONCLUSION: The two different antigenic peptides of proteolipid protein can all cause the autoimmune response of central nervous system. Both models have the same characters of relapse and remitting and the severity has no significant difference. But compared with proteolipid protein 139- 151 group,onset and recover of the experimental autoimmune encephalomyelitis of the mice in proteolipid protein 178-191 group were earlier, as well as weight variance was larger, which maybe due to the different structure of two peptides.

Objective To explore the mechanism about the expression of the hyperphosphorylated p38MAPK in the central nervous system (CNS) of experimental autoimmune encephalomyelitis (EAE) mouse and its relationship to the axonal damage, and investigate the potential regulation of SB203580 to the damaged axons in the CNS of EAE mouse.Methods SJL/J mice were used to establish the EAE model. Brain and spinal cord of EAE mice in the model group, SB203580 group and control group were used respectively at different time points. Stained with HE and Luxol Fast Blue (LFB), also the immunohistochemical detection was conducted with parallel phosphorylation of p38MAPK antibody staining and APP staining at the same time. By image analysis system, the number of positive signals, the coverage and the average density value in the cytoplasm of neuron in white matter lesions were measured.Results The model of EAE mice induced by PLP peptide manifested significant neurological symptoms, signs and features of relapse and remitting. Demyelinating change was observed in local regional white matter region. Compared with the model group, SB203580 group changed lighter, with its behavioral observations and had a significant weight gain (P<0.01). In addition to the control group, amyloid precursor protein (APP) expression was detected in other groups at various time points. Compared to the model group, APP expression was slighter than in SB203580 group. The number of positive cells and strength was significantly lower in the SB203580 group (P<0.01); expression of p38MAPK in EAE mice was observed at the earlier 7th day after immunization. Compared to the model group, expression of SB203580 group was lighter, positive number and intensity decreased markedly (P<0.01).Conclusion p38MAPK blockers SB203580 can not only inhibit activation of the p38MAPK in EAE mice, but also effectively reduce expression of APP which is symbolic target of EAE axonal injury, it is confirmed that the p38MAPK is indeed involved in the EAE axonal injury.

Objective:To investigate frequency of blood stasis syndrome(BSS) defined by traditional Chinese medicine in cerebral infarction and its correlations with carotid atherosclerotic plaque(CAP).Methods: All subjects comprised 151 patients aged 40 to 80 years(Mean ? SD age,65 ?11 years) with 67.9% for males and 32.1% for females.With the use of ACUSON7 color Doppler ultrasound,carotid atherosclerosis was evaluated by the plaque score,the left plaque score,the right plaque score,the numbers of the plaque respectively as defined by the sum of all plaque heights in bilateral carotid arteries.On the basis of neurological signs and symptoms,medical history,and brain MRI,we diagnosed stroke and its subtypes as follows: stroke(n=117),and vertebrobasilar insufficiency(VBI)(n=34) without the history of the stroke,which were based on Diagnostic Criteria for Cerebral Vascular Diseases in 2005.Diagnosis for syndromes defined by traditional Chinese medicine were made according to Diagnostic Criteria for Stroke in 1994.One-way ANOVA was used in comparison between groups,and multivariant Logistic Regression Analysis was conferred in correlations between several variables.Results: 47.0% of all cases with cerebral infarction presented the BSS,with as lower than syndrome of fire-heat(51.0%),as but significantly higher than syndrome of Qi deficiency(32.0%),liver-wind syndrome(27.0%),phlegm syndrome(23.0%) and syndrome of asthenic yin causing predominant yang(6.0%).There is a significant difference between groups for 44(79.0%) cases of 56 patients with cerebral infarction and the BSS have CAP,and only 35(57.0%) cases of 61 patients with cerebral infarction but without the BSS have CAP(P

OBJECTIVETo study the cell biological mechanism of sodium selenite improving insulin sensitivity in pubertal rats with insulin resistance.

METHODSThe content of inositol 1,4,5-trisphosphate (IP3) was examined by anion resin chromatography, and mRNA levels of phosphatidylinositol 3-kinase regulatory subunits (PI3Kp85 alpha) and Se-P were detected by RT-PCR in hepatocyte isolated from pubertal rats with insulin resistance.

RESULTSThe mRNA levels of Se-P and PI3Kp85 alpha and content of IP3 in isolated hepatocyte decreased in pubertal male rats with insulin resistance. The above indices increased and reached normal level in rats supplied with selenium. The response to insulin stimulation in isolated hepatocyte in rats with selenium supply was similar to that in the control group, and both groups had higher response than those with high-fat diet. Alone when inhibited by wortmannin, the concentration of IP3 increased slightly in rats with selenium supply, but still was lower than that in the control group.

CONCLUSIONSThese results indicate that the effect of selenium improving insulin sensitivity may be related to phosphatidylinositol PI3K signalling pathway. The effect of regulation of IP3 by selenium is not as effective as that by insulin, which may explain the difference of effect between selenium and insulin.

Animals ; Cell Separation ; Hepatocytes ; cytology ; metabolism ; Inositol 1,4,5-Trisphosphate ; analysis ; Insulin ; pharmacology ; Insulin Resistance ; Male ; Phosphatidylinositol 3-Kinases ; analysis ; Proteins ; analysis ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar ; Selenoproteins ; Signal Transduction ; Sodium Selenite ; pharmacology

BACKGROUNDIt has been shown that the presence of leptin is associated with deabefes, glucose wefabolism and insulin metablism. In this research, we evaluated the presence of the leptin C-2549-A polymorphism in the Chinese population in Chongqing and verified its association with plasma leptin levels and anthropometric, metabolic, and clinical parameters.

METHODSTwo hundred and sixty-nine patients with diabetes, 135 non-diabetic first-degree relatives of the patients, and 85 healthy controls were screened for the presence of C-2549-A polymorphism using a PCR-RFLP assay. Body mass index, fasting leptin, fasting insulin, fasting glucose and homeostatic model assessment for insulin resistance (HOMA)-IR were also determined.

RESULTSIn the type 2 diabetes group, AA genotype frequency (6.32%) and A allele frequency (34.94%) was higher than in normal controls (1.18% and 25.29%, respectively). Diabetic patients with the AA genotype had lower fasting leptin and insulin levels than those with other genotypes. Carriers with the AC genotype had decreased fasting leptin and insulin levels and longer duration of disease as compared with those with CC genotype. The HOMA-IR of patients with AA or AC genotypes was lower than those with the CC genotype. In non-diabetic relatives group, individuals with the AA genotype had a lower fasting leptin level than those with the AC genotype. The fasting insulin and HOMA-IR level of carriers of the AA or AC genotype were lower than those of the CC genotype.

CONCLUSIONThe C-2549-A polymorphism in the leptin gene is associated with fasting leptin in patients with type 2 diabetes. The distribution of the genotypes in diabetic subjects from diabetic pedigrees differs from those in normal controls. The A allele frequency in diabetic patients is higher than that in normal controls. The haplotypes defined by genotypes are different in the familial subjects.

Adult ; Aged ; Diabetes Mellitus, Type 2 ; genetics ; Female ; Genotype ; Humans ; Insulin Resistance ; Leptin ; blood ; genetics ; Male ; Middle Aged ; Pedigree ; Promoter Regions, Genetic

Adult ; Appendiceal Neoplasms ; immunology ; pathology ; Dendritic Cell Sarcoma, Follicular ; immunology ; pathology ; Humans ; Immunohistochemistry ; Male ; Proto-Oncogene Proteins c-kit ; analysis ; Receptors, Complement 3b ; analysis

OBJECTIVETo compare the therapeutic effect differences between electroacupuncture at Jiaji (EX-B 2) combined with blood-letting plus cupping and western medicine therapy.

METHODSFifty-three cases were randomly divided into an observation group (n=31) and a control group (n=22). The observation group was treated by electroacupuncture at Jiaji (EX-B 2) combined with blood-letting with a plum-blossom needle at the affected parts plus cupping, once each day. The control group was treated by oral administration of Valaciclovir Hydrochlordide, Indomethacin, Vitamin B1 and Vitamin B12.

RESULTSThe cured and markedly effective rate of 96.8% in the observation group was better than that of 81.8% in the control group (P < 0.05), and improvements of pain, pruritus, burning sensation and sleep in the observation group were superior to those of the control group (all P < 0.01).

CONCLUSIONElectroacupuncture at Jiaji (EX-B 2) combined with blood-letting and cupping is a better therapy for herpes zoster and its therapeutic effect is better than that of routine western medicine therapy.

Acupuncture Points ; Adult ; Aged ; Bloodletting ; Combined Modality Therapy ; Electroacupuncture ; Female ; Herpes Zoster ; therapy ; Humans ; Male ; Middle Aged ; Young Adult