Animals ; Disease Models, Animal ; Ischemic Preconditioning ; methods ; Lipid A ; administration & dosage ; analogs & derivatives ; MAP Kinase Signaling System ; Male ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism

Actins ; metabolism ; Female ; Fibroma ; metabolism ; pathology ; surgery ; Foot Diseases ; metabolism ; pathology ; Humans ; Immunohistochemistry ; Inclusion Bodies ; metabolism ; pathology ; Infant ; Toes

B-Lymphocytes ; pathology ; Humans ; Lymphoma, B-Cell ; pathology ; Lymphoma, Large B-Cell, Diffuse ; pathology ; Male ; Middle Aged

Objective To retrospectively review the PET/CT imaging features of sarcoidosis and improve the diagnostic accuracy of this benign disease.Methods The PET/CT imaging characteristics and clinical data, including lesion size, distribution, standardized uptake value (SUV) and the ratio of misdiagnosis, of 11 sarcoidosis patients (5 confirmed pathologically and 6 clinically) were retrospectively analyzed.Results (1) Eleven patients had lymph node involvement:mediastinum and hilar lymphadenopathy in 11/11, supraclavicular fossa lymphadenopathy in 8/11, retroperitoneal lymphadenopathy in 8/11, pelvic cavity lymphadenopathy in 3/11.(2) Extrathoracic lesions were found in 7/11 with 4 lung involvement, 2 liver involvement, 1 parotid gland and temporalis involvement and 1 bilateral iliac and sacral bone involvement.(3) The size of the lesions ranged from 1.0 to 4.6 cm and the CT density ranged from 30 to 40 HU.The lesions in the lung are hypodense and in the liver are slightly hypo-or iso-dense.18F-fluorodeoxyglucose (FDG) uptake of all lesions was definitely increased in 6 cases; 18F-FDG uptake of some lesions was moderately or definitely increased in 2 cases, and slightly increased uptake in 3 cases.(4) The PET/CT diagnosis was consistent with the final diagnosis in 6/11.The 5 cases of misdiagnosis were malignant lymphoma (4/11) and lung cancer ( 1/11 ).Conclusions Differentiation between sarcoidosis and lymphoma in patients presenting with hilar lynphadenopathy can be difficult.Whole-body PET/CT may be helpful in the differentiation of the two diseases.

Objective To explore the role of CD 30 on CD4 + T lymphocyte and T lymphocyte subset activation in asthma pathogenesis.Methods Twenty seven asthma active attack patients,16 acute upper respiratory infection patients and 19 control children were randomly selected. Direct immunofluorescence flow cytometry was used to detect the CD 30 positive percentage on CD4 +cell; ELISA was used to detect the levels of interleukin(IL) 4 and IL 13 in culture supernatants of peripheral blood mononuclear cells(PBMC) and plasma total immunoglobulin E(IgE) level.Results Compared with control group and acute upper respiratory infection group, in asthmatic children the CD4 +CD 30 + percentage on CD4 + cell was elevated significantly; 2.The levels of IL 4 and IL 13 in supernatants of cultured lymphocyte were increased significantly, the plasma total IgE level was increased significantly;3.There was a significant positive correlation of CD4 +CD 30 + cell percentage with the levels of IL 4 and IL 13 in culture supernatants and plasma total IgE.Conclusions The cell that could produce Th2 derived cytokine may consist of CD 30 +cell;When CD 30 L combined with CD 30 on CD4 + cells ,it might result in Th2 cell proliferation ,develop and release Th2 derived cytokine; IL 4 and IL 13 could induce B cell production and secrete more IgE. It is suggested that CD 30 and imbalance of Th2 subset may play an important role in asthma pathogenesis.

Objective To determine the role of interleukin-8 (IL-8) produced by tumor induced fibroblasts in the development of cutaneous melanoma. Methods B16 melanoma cells induced L929 fibroblasts phenotype was transdifferentiated to myofibroblasts (MF) by co-culture in vitro. MF was monitored by morphology and immunophenotype for a-SMA. The level of IL-8 was detected by ELISA. The effect on B16 cell proliferation rate was estimated using MIT method in vitro. Melanoma implanting model was constructed in C57 mice. Results L929 MF phenotype could be modulated by B16 melanoma cells-derived transforming growth factor-β1 (TGF-β1) and elevated the levels of IL-8. L929 MF did not influence the B16 melanoma cells viability in vitro, but shortened the time of tumor formation and increased the incidence rates of tumors in C57 implanting model mice. Conclusion Fibroblasts can be activated by tumor cells and produce IL-8, which acts as an inflammatory cytokine promoting the development of cutaneous melanoma.

Aged ; Colorectal Neoplasms ; physiopathology ; Humans ; Intestinal Neoplasms ; complications ; Stomach Neoplasms ; complications

12E7 Antigen ; Actins ; metabolism ; Antigens, CD ; metabolism ; Cell Adhesion Molecules ; metabolism ; Female ; Granular Cell Tumor ; complications ; metabolism ; pathology ; surgery ; Humans ; Hysterectomy ; Immunohistochemistry ; Leiomyomatosis ; complications ; metabolism ; pathology ; surgery ; Middle Aged ; Ovarian Neoplasms ; complications ; metabolism ; pathology ; surgery ; Ovariectomy ; Receptors, Estrogen ; metabolism ; Uterine Neoplasms ; complications ; metabolism ; pathology ; surgery ; Vascular Neoplasms ; complications ; metabolism ; pathology ; surgery

Objective To investigate the nutritional status of elderly inpatients with benign orthopedic diseases and to assess its relationship with clinical outcomes.Methods Nutritional Risk Screening 2002 ( NRS 2002) was used to prospectively investigate undernutrition and nutritional risk in elderly patients hospitalized between April 1 and May 31, 2012 in Beijing Hospital for benign orthopedic diseases.Associations between nu-tritional status and clinical outcomes were analyzed.Results A total of 520 patients were included, with a mean age of (75 ±7.09) years.The mean body mass index (BMI) was (23.20 ±3.83) kg/m2, mean dominant-hand grip strength was (16.87 ±19.19) kg, mean mid-upper arm circumference was (25.62 ±3.81) cm, mean calf circumference was (31.92 ±4.02) cm.Compared with patients aged 65-79 years, patients≥80 years showed significantly lower hand grip strength [ (13.58 ±15.92) kg vs.(18.48 ±20.42) kg, P=0.004].All the pa-tients completed NRS 2002, which showed that 9.31%of the patients had undernutrition (BMI≤18.5 kg/m2), and 45.19%had nutritional risk (NRS 2002 score≥3).Compared with patients aged 65-79 years, patients≥80 years had significantly higher incidence of undernutrition (13.97% vs.7.21%, P=0.024) and nutritional risk (52.38%vs.41.76%, P=0.024), higher incidence of infectious complications in patients with nutritional risk (10.21%vs.5.26%, P=0.044), longer hospital stay [ (11.66 ±5.76) days vs.(10.42 ±4.37) days, P=0.016], and higher hospital expense [(20.28 ±1.811) thousand yuan vs.(16.39 ±1.362) thousand yuan, P=0.016].Conclusion Elderly patients hospitalized for benign orthopedic diseases have a high incidence of undernutrition and nutritional risk, which is associated with worse clinical outcomes.

OBJECTIVETo explore the effects of stromal interaction molecule 1 (STIM1) on the expression of apoptosis-related proteins in prostate cancer PC-3 cells.

METHODSWe transfected the lentivirus vector STIM1-pGCSIL-GFP carrying STIM shRNA into human hormone-independent prostate cancer PC-3 cells, and 3 days later observed the transfection efficiency by fluorescence microscopy. At 7 days after transfection, we determined the expression of STIM1 in the PC-3 cells by RT-PCR and Western blot and those of apoptosis-related proteins Bcl-2, Bax, survivin and activated Caspase-3 by Western blot.

RESULTSAt 3 days, inverted microscopy revealed a transfection efficiency of > 80%. At 7 days, the STIM1 expression was significantly inhibited at both mRNA and protein levels. The Bcl-2/Bax rate was remarkably decreased as compared with that of the control group (0. 31 vs 1.24 ) , and the survivin expression was markedly reduced, 0. 14 times that of the relative expression in the control. However, the Caspase-3 cleavage was significantly activated, 1.52 times that of the control (P <0.05).

CONCLUSIONSTIM1 can be regarded as an oncogene in prostate cancer PC-3 cells. Inhibition of its expression can induce PC-3 cell apoptosis by reducing the Bcl-2/Bax rate, decreasing the survivin expression, and activating the Caspase-3 pathway.

Apoptosis ; Caspase 3 ; metabolism ; Cell Line, Tumor ; Humans ; Inhibitor of Apoptosis Proteins ; metabolism ; Male ; Membrane Proteins ; genetics ; Neoplasm Proteins ; genetics ; Prostatic Neoplasms ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; RNA, Small Interfering ; genetics ; Stromal Interaction Molecule 1 ; Transfection ; bcl-2-Associated X Protein ; metabolism