Antibodies, Monoclonal ; therapeutic use ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents, Hormonal ; therapeutic use ; Breast Neoplasms ; metabolism ; pathology ; therapy ; Female ; Humans ; Lymphatic Metastasis ; Receptor, ErbB-2 ; metabolism ; Receptors, Estrogen ; metabolism ; Receptors, Progesterone ; metabolism ; Signal Transduction ; Tamoxifen ; therapeutic use ; Trastuzumab

Adolescent ; Child ; Child, Preschool ; Female ; Herpesvirus 4, Human ; Humans ; Infant ; Infectious Mononucleosis ; diagnosis ; pathology ; virology ; Liver ; pathology ; Male

Objective To explore the clinical and laboratory characteristics of langerhans cell histiocytosis (LCH) in children, so as to improve diagnosis level and decrease misdiagnosis rate.Methods Twenty-five cases of LCH from Jan.1996 to Feb.2006 were analyzed by retrospective study. The clinical data were collected and abstracted for information regarding clinical symptom, physical sign, laboratory examination, imaging,pathology,diagnosis and treatment.Results Some laboratory findings in hemogram, bone marrow examination and chest X-ray were non-specific.The X-ray characteristic of skeleton was osteolysis. Computerized tomography and magnetic resonance imaging were important in defining the extent of lesion in fundus cranii and sella.Seven cases were examined for anti-Epstein-Barr virus(EBV) IgM, 3 cases were positive;5 and 3 cases out of 10 cases showed humoral and cellular immunity abnormality,respectively. The misdiagnosis rate was 52%,1 case had been misdiagnosed for 7 years. Chemotherapy was effective in the future.Conclusions The clinical manifestations of LCH varies widely, leading to high rate of misdiagnosis.The etiology of LCH is unclear,and some of our patients show the evidence of EBV infection or immunity abnormality. Definitive diagnosis of LCH is based on pathology. Ultrastructure and immunophenotype should be done to improve diagnosis level.

Objective To investigate the relationship between metabolic syndrome(MS) and severity of coronary atherosclerosis. Methods Sixty-four hospitalized patients diagnosed as coronary heart disease were divided into MS group(n=26)and non-MS group(n=38).All the patients underwent 16-row multi-slice CT coronary angiography,and cardiovascular risk factors were evaluated. Results The prevalence of MS increased with the number of stenosed coronary arteries(P

Adult ; Burkitt Lymphoma ; genetics ; Chromosome Duplication ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 14 ; Chromosomes, Human, Pair 8 ; Female ; Humans ; Leukemia, B-Cell ; genetics ; Male ; Middle Aged ; Retrospective Studies ; Translocation, Genetic

[Summary] It has been believed that both environmental and genetic effects play roles in the pathogenesis of type 2 diabetes. Genetic factors may influence the effect of environmental factors on risk of developing type 2 diabetes. This review focused on the latest evidence of the interaction effect of genes and the environmental factors on type 2 diabetes.

Acute Coronary Syndrome ; Humans

Objective To Analyze the examination meaning of b-type brain natriuretic peptide precursor (NT-proBNP),homocysteine and coagulation-fibrinolysis indexes for patients with acute cerebral infarction.Methods Selected 40 patients with acute cerebral infarction (experimental group) to hospital from March 2014 to May 2015 and 40 healthy check-up cases (control group).Then,compared the indicators in blood between the two groups of patients,namely homocysteine (Hcy),NT-proBNP,activated clotting time live enzymes enzyme (APTT),original activator inhibitory factor (PAI-1) and tissuetype fibrinolytic enzyme original activator (tPA).Meanwhile,also compared these indicators for the experimental group before and after treatment.Results Before treatment,the levels of Hcy,t-PA,NT-proBNP,PAI-1 and ATPP for experiment group were 17.7±3.6 μmol/L,29.4±7.9 μmol/L,3 212.8±2 511.4 ng/L,130.1±17.8 μmol/L and 37.8±4.5 s,respectively.The levels of Hey,t-PA,NT-proBNP,PAI-1 and ATPP for control group were 7.2± 2.1 μmol/L,15.1 ± 3.7 μmol/ L,198.7 ± 1 14.8 ng/L,67.8 ± 7.9 μmol/L and 37.8 ± 4.5 s,respectively.After treatment,the levels of Hcy,t-PA,NT-proBNP,PAI-1 and ATPP for experiment group were 12.2±1.5 μmol/L,18.2±2.3 μmol/L,348.7±194.8 ng/L,78.6±9.8 μmol/L and 32.2±4.5 s,respectively.Before treatment,the indicator of APTT for experiment patients was significantly shorter than it after treatment and that of the control group.The other four indicators were significantly higher than them after treatment and those of the control group.The differences were statistically significant (P ＜0.05).Conclusion Hcy,NT-proBNP,APTT,PAI-1,and t-PA had closely relation with the occurrence of acute cerebral infarction development,and they can be helpful to evaluate disease progression and predict prognosis for patients with acute cerebral infarction.

OBJECTIVETo explore the effect of Shenxiong Huayu Capsule (SHC) on the cerebral ischemia-reperfusion (IR) injury and the expression of growth associated protein 43 (GAP43) after total cerebral IR in the hippocampal CA1 region of rats.

METHODSTotally 100 male adult SD rats were randomly divided into five groups, i.e., the control group, the model group, the group A (by taking SHC once daily), the group B (by taking SHC twice daily), and the group C (by taking SHC thrice daily), 20 in each group. The total IR model was prepared by improved Pulsinelli's 4-vessel occlusion method. Morphological changes of the hippocampal CA1 region were observed by HE staining at day 1, 3, 7, and 14. The expression of GAP43 in the hippocampal CA1 region was detected using immunohistochemical assay at day 1, 3, 7, and 14. Meanwhile, the behavioral score was determined. The expression of GAP43 in the hippocampal CA1 region was detected using Western blot at day 14.

RESULTSCompared with the control group, the expression of GAP43 increased in the model group, the behavioral score was elevated, degenerated neurons increased, and survival neurons decreased in the model group (all P < 0.05). Compared with the model group, the expression of GAP-43 increased (with the most significant difference seen in the group C, P < 0.01), the behavioral score significantly decreased, degenerated neurons decreased, and survival neurons increased in each HSC group (all P < 0.05). Survival neurons obviously increased at day 14, of which, most number of survival neurons and highest contents of GAP43 protein could be seen in the group C, showing statistical difference when compared with those of the group A and the group B (P < 0.01).

CONCLUSIONSHC had protective effect on total cerebral IR in the hippocampal CA1, which might be associated with increased expression of GAP43.

Animals ; Brain Ischemia ; metabolism ; CA1 Region, Hippocampal ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; GAP-43 Protein ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism

Objeceive To compare the expression of Ku70 and Bax in hippocampus CA1 between normal rats and diabetic rats following cerebral ischemia/reperfusion, so as to explore the roles of Ku70 and Bax in aggravating cerebral ischemial reperfusion mjury nn diabetes. Meehods Totally 72 male SD rats were divided into 3 groups randomly: sham operated (SO) group, normoglycemia global cerebral ischemia/reperfusion (NCI) group, and diabetic global cerebral ischemia/reperfusion (DCI) group. The rats in DCI group were treated by streptozodn (STZ) and improved Puliinelii's foue-vessel occlusion method to estabiish diabetic global cerebral ischemia/reperfusion modll. Andanimals in NCI group were not gvven STZ, and other treatments were iimllar to those in the DCI group. Animals in the SO group only had blood vessels exposed. Changes of neuron pathology in hippocampus CA1 were observed by H-E stammg under iight microscopy at 1, 6, 24, and 48 h after lschemial reperfusion; expresioon of Ku70 was detected by immunohistochemistry and Western blotting analyils, and expresioon of Bax was detected by immunohistochemistry. Resules The neuron structure in hippocampus CA1 of rats was damaged nnNCI group, and the density of survival neuronswas significanely lower than that nn the SO group at all studied time ponnts(P<0. 05); the neuron structure damage nn DCI group was more severe, and the demity of sunival neurons was signiticanely lower than that of the NCI group at all studied time points(P<0. 05). The expresioon of Ku70 at 1 and 6 h nn NCI group was signiticanely higher than that in the SO group (P<0. 05), and that at 24 and 48 h was signiticanely lower than that nn the SO group(P<0. 05); Ku70 expression nn DCI group was significanely lower than that nn the NCI group at all studied time ponnts(P<0. 05). Bax expresioon in NCI group was signiticanely higher than that in the SO group at all studied time points(P<0. 05), and that in DCI group was signiticanely higher than that in the NCI group at all studied time ponnts (P<0. 05). Conclusion Diabetes can aggravate global cerebral ischemia/reperfusion injury, which may be related to Ku70 Expression decrease and Bax Expression Increase.