The effect of Smac gene on the TRAIL-induced apoptosis of the prostate cancer cell line PC-3 and the molecular mechanism were investigated. The Smac gene was transfected into PC-3 cells under the induction of liposome. The intrinsic Smac gene expression was detected by Western blotting. After treatment with TRAIL as an apoptosis inducer, in vitro cell growth activity was assayed by MTT colorimetry. The apoptosis rate of PC-3 cells was determined by annexin V-FITC and propidium iodide staining flow cytometry. The expression of cellular XIAP and caspase-3 genes was examined by Western blotting. Smac-transfected cells (PC-3/Smac group) had significantly increased Smac protein level as compared with PC-3 controls (P<0.01). After induction with 100-200 ng/mL TRAIL for 12-36 h, cellular proliferation rate in PC-3/Smac group was significantly lower than in PC-3 controls (P<0.05). After induction with 100 ng/mL TRAIL for 24 h, the apoptosis rate in PC-3/Smac group was significantly enhanced as compared with that of PC-3 controls (P<0.05). Accordingly, the XIAP expression level was down-regulated significantly (P<0.05) and caspase-3 subunit P20 was up-regulated significantly (P<0.05). It is suggested that the over-expression of cellular Smac can inhibit inhibitor of apoptosis proteins (IAPs), enhance caspases activity and the apoptosis rate of PC-3 cells induced by TRAIL, which may provide a useful experimental basis for prostate cancer therapy.

An 18-year-old female presented with painful erythema and nodules on both legs for more than 2 years.Dermatological examination showed irregularly sized,mildly indurated,tender,deep subcutaneous nodules arising in diffused infiltrated dark erythematous patches in the inner and posterior region of the left leg.Histopathology showed no significant changes in the epidermis.There were perivascular lymphoid cell infiltrates in the dermis and subcutis.Multiple sites of necrosis of blood vessel walls with vascular occlusions were noted.The lumens of some blood vessels were filled with lymphocytes,among which were many atypical cells with hyperchromatic nuclei and pathologic mitotic figures.Immunohistochemistry showed that lymphocytes in the cavities of blood vessels were positive for CD3(+++),CD3ε(+++),CD2(+),CD56(+++),granzyme B(+++),perforin(+++),CD30(+),Ki67 (+++,100％ ),but negative for CD20,CD5,CD7,CD4,CD8,TdT,anaplastic lymphoma kinase,early membrane antigen (EMA) or pan cytokeratin (pCK).The endothelial cells lining the blood vessels stained positively for CD34.The intravascular lymphocytes were also positive for EBER1/2 by in situ hybridization.A diagnosis of cutaneous intravascular NK/T cell lymphoma was made.

Objective To investigate the clinical characteristics of primary gastrointestinal lymphoma (PGIL) on different origin site in order to improve its diagnosis.Methods The clinical data from 202 patients with PGIL diagnosed by histology from January 1999 to June 2007 were identified from the clinical databases of 8 hospitals in Wuhan area and retrospectively analyzed.The patients were divided into gastric,small intestinal and large intestinal lymphoma groups according to the site of origin and there clinical characteristics were compared.Results The PGIL localization was gastric in 113 (56.0%) cases, small intestine in 37(18.3%) cases and large intestine in 52 (25.7%) cases.One hundred and thirty (64.4%) were males and 72 (35.6%) were females.The male patients were predominant.The median duration of symptoms in gastric lymphoma group was longer than small intestinal lymphoma group (3.0 months vs.1.0 month,P=0.013).The most common symptoms were abdominal pain and anemia. The clinical stage was Ⅰ E and Ⅱ E in 71.3% of cases.The large intestinal lymphoma group presented more advanced-stage disease compared with gastric lymphoma group (P = 0.014).The frequent histological type was mucosa-associated lymphoid tissue lymphoma (MALT),diffuse large B-cell lymphoma and T-cell lymphoma.Gastric,small intestinal and large intestinal lymphomas presented more frequently as low-grade MALT lymphoma (56.9%),T-cell lymphoma (34.4%) and high-grade B-cell lymphoma (51.1%),respectively (all P value ＜0.05).The common macroscopic type of PGIL were nodular protruding and ulcerative type.Compared with gastric lymphoma,nodular protruding type was more common and ulcerative type was less common in large intestinal lymphoma (P = 0.000).The diagnosis confirmed by endoscopic biopsy were 58.7% (61/104),25.0% (4/16),48.2% (13/27) in gastric,small intestinal and large intestinal lymphoma groups,respectively.Conclusions The clinical characteristics are different in patients with different localization of PGIL including patient characters, initial symptoms,histological classification,clinical stage,macroscopic feature,endoscopic findings. Analysis of these clinical characteristics is helpful to improve its diagnosis.

A 20-year-old male patient presented with myalgia of upper limbs and myasthenia of extremities for more than 1 month. Physical examination showed diffuse erythema on the cheeks, upper eyelids, upper chest, neck and dorsa of the hands. The myodynamia of the proximal and distal muscles of upper and lower extremities was grade Ⅳ, Ⅴ, Ⅲ and Ⅴ respectively. Laboratory examinations revealed that the serum levels of creatine kinase, CK-MB and lactate dehydrogenase were 2103 U/L, 83 U/L and 489 U/L respectively, which were all above the normal range. Electromyogram revealed myopathic abnormality and normal nerve conduction velocity. Histopathology of gastrocnemius muscle showed hypertrophy and swelling of muscle fibers, disappearance or fuzziness of transverse striation, and intermuscular lymphoid cell infiltration. A biopsy of the skin lesion from the upper chest showed liquefaction degeneration of and colloid bodies in basal cell layer, perivascular lymphoid cell infiltration in the dermis. A diagnosis of dermatomyositis was established based on the clinical and laboratory findings. After management with intravenous prednisolone 80 mg once daily and symptomatic treatment for 4 weeks, the myodynamia of upper limbs was improved, serum levels of creatine kinase,CK-MB and lactate dehydrogenase reached the normal ranges. However, the myodynamia of lower limbs progressively deteriorated with the emergence of paresthesia. Enhanced MRI scan showed a tumor in the vertebral canal at the level of thoracic vertebra 11 to 12. A spherical encapsulated tumor measuring 3 cm in diameter was surgically removed. The tumor was diagnosed as paraganglioma in vertebral canal according to pathological and immunohistochemical findings. The patient was finally diagnosed with paraganglioma in vertebral canal superimposed on dermatomyositis.

The effect of Smac gene on the TRAIL-induced apoptosis of the prostate cancer cell line PC-3 and the molecular mechanism were investigated.The Smac gene was transfected into PC-3 cells under the induction of liposome.The intrinsic Smac gene expression was detected by Western blotting.After treatment with TRAIL as an apoptosis inducer,in vitro cell growth activity was assayed by MTT colorimetry.The apoptosis rate of PC-3 cells was determined by annexin V -FITC and propidium iodide staining flow cytometry.The expression of cellular XIAP and caspase-3 genes was examined by Western blotting.Smac-transfected cells (PC-3/Smac group) had significantly increased Smac protein level as compared with PC-3 controls (P＜0.01).After induction with 100-200 ng/mL TRAIL for 12-36 h,cellular proliferation rate in PC-3/Smac group was significantly lower than in PC-3 controls (P＜0.05).After induction with 100 ng/mL TRAIL for 24 h,the apoptosis rate in PC-3/Smac group was significantly enhanced as compared with that of PC-3 controls (P＜0.05).Accordingly,the XIAP expression level was down-regulated significantly (P＜0.05) and caspase-3 subunit P20 was up-regulated significantly (P＜0.05).It is suggested that the over-expression of cellular Smac can inhibit inhibitor of apoptosis proteins (IAPs),enhance caspases activity and the apoptosis rate of PC-3 cells induced by TRAIL,which may provide a useful experimental basis for prostate cancer therapy.

Zinc oxide nanoparticles(ZnO NPs)have been gradually introduced into people's lives due to their excellent properties.In daily contact,ZnO NPs can enter the human body in a variety of ways and accumulate in tissues and organs.Inhalation is an important means by which ZnO NPs enter the human body and deposit in lungs.Studies have shown that exposure of lungs to ZnO NPs will cause a range of negative effects.The mechanism of pulmonary toxicity induced by ZnO NPs is related to Zn2+release,oxidative stress,DNA damage,autophagy,inflammation and pulmonary surfactant dysfunction.This paper reviews the pulmonary toxicity and mechanisms of ZnO NPs,and summarizes the prevention and treatment strategies,which provides scientific basis for safer use of nanomaterials,and potential intervention strategies for the prevention and treatment of nanotoxicity.