Aim To investigate the effects of paclitaxel(PTX) on the expression of CD69, CD25 and proliferation of T cells by polyclonal stimulas in vitro, and explore the molecular mechanism of paclitaxel. Methods Fluorescence conjugated monoclonal antibodies and flow cytometry were used to detect the express of CD69 and CD25 by activated T cells in vitro in response to Concanavalin(Con A) and Phorbol 12,13-dibutyrate(PDB) or T cell proliferation index stained by CFDA-SE in response to PDB+Ion or Con A. Results Paclitaxel had no effect on the expression of CD69, but inhibited the expression of CD25 in activated T cells in response to Con A or PDB in a concentration-dependent manner. Paclitaxel caused a dose-dependent suppression of T cell proliferation to Con A as well as to PDB+Ion. Whether added at the beginning or after 24 h of stimulation by Con A or PDB+Ion, paclitaxel had identical effects. Conclusion The mid and later activation and proliferation of murine T cells stimulated by Con A or PDB+Ion were significantly inhibited by paclitaxel, suggesting that paclitaxel acts on the downstream signaling pathways of PKC?,and not act on the intitial activated associated proteins such as PTK and PKC?.

With the development of basic disciplines such as molecular biology,immunology,cell biology and so on. the pathogen biology research do not stop at the organ and cellular level,but go deep into the protein and gene level. It is a great boost to the deep studies of pathogen biology in diagnosis,treatment,pathogenesis,prevention and epidemiology.

Animals ; Macrophages, Alveolar ; drug effects ; enzymology ; Male ; Muramidase ; biosynthesis ; Quartz ; toxicity ; Rats ; Rats, Sprague-Dawley

Objective To evaluate the incidence and severity of pulmonary embolism (PE) in patients with different leg deep vein thrombosis (DVT) by computed tomography pulmonary angiography (CTPA).Methods A total of 145 cases who had been confirmed DVT and undergone CTPA were retrospectively analyzed.The DVTs were divided into left side DVT,right side DVT,and bilateral lower DVT groups.The incidence of PE was compared among different groups.CT obstruction index (CTI) was used to estimate the severity of pulmonary artery obstruction.DVT/PEs with CTI were compared among different groups.Results The incidence of PE of the bilateral lower DVT group was 71.4％,which was higher than that in left side DVT group (39.2％).However,no significant difference was found between bilateral lower DVT group and right side DVT group (52.9％) (P ＞ 0.05).The CTI of the bilateral lower DVT (30.20±14.20)％ was higher than that of the left side DVT (19.26 ± 14.02)％ and the right side DVT (18.56 ±11.79) ％ (P ＜ 0.05).Conclusions The bilateral lower DVT was more likely complicated with PE than the left side DVT,the severity of pulmonary artery obstruction of the bilateral lower DVT with PE patient was higher than that of single side DVT with PE patient.

Objective To explore the effect of lysophosphatidic acid(LPA)on blood-brain barrier(BBB) permeability and its possible mechanism.Methods LPA or LPA+suramin(L+S)were stereotaxically injected into the right eaudate nucleus in SD rats in vivo.Evans blue(EB)was used to quantitatively measure the permeability of BBB at different time points.The expression of matrix metalloproteinase-9 was detected by immunohistochemistry technique.The pathological ultrastruetural changes of BBB were assessed by transmission electron microscopy.Results The BBB permeability began to increase after LPA administered into ipsilateral eaudate nucleus,and reached the peak at 24h.Then the permeability of BBB gradually lowered after 48h.In comparison with the same time points of control group,there were quite significant differences(P＜0.01).After L+S was injected,the change of BBB permeability had differences in comparison with those of LPA group in the same time points,(P＜0.05).MMP-9 positive cells were mainly vascular endothelial cells.The numbers of MMP-9 positive blood vessels grew at 6h in LPA group,and the expression of it reached maximum at 24h,then the number of it decreased at 48h,showing significant statistical differences in comparison with the L+S group(P＜0.01),It was observed microscopically that ultrastrueture of BBB of the LPA group was changed sharply,such as basement membrane roughed and fragmented,astroeyte end-feet swolled markedly and perivaseular space enlarged obviously.But there were no remarkable changes in BBB in L+S group.Conclusion LPA can induce increase of BBB permeability and its possible mechanism is the strong expression of MMP-9 protein produeted by endothelial cells through the mediation of LPA receptor,leading to degradation of basement membrane.

A 29-year-old woman was admitted to the Department of Rheumatology,Peking Union Medical College Hospital due to intermittent rashes,fever and headache.Palpable purpura were symmetrically distributed on the extremities and trunk.Other manifestations included headache with nausea and vomiting.Elevated white blood cell (WBC) count,platelet (PLT) count,erythrocyte sedimentation rate (ESR) and C-reactive protein were the main laboratory findings.Antinuclear antibodies and antineutrophil cytoplasmic antibodies were negative.Examination of the cerebrospinal fluid (CSF) revealed high intracranial pressure,while routine cytology and biochemical tests of CSF were normal.Head MRI scan and PET-CT did not detect remarkable findings.A diagnosis of systemic vasculitis was confirmed by the biopsy of skin lesion which showed inflammatory infiltration of the muscular vessel wall.Combination therapy of corticosteroids and cyclophosphamide lead to a rapid improvement in clinical symptoms and laboratory parameters.The patient was in stable remission till 6 month follow-up.

The clinical characteristics of painless aortic dissection were investigated in order to improve the awareness of diagnosis and treatment of atypical aortic dissection. The 482 cases of aortic dissection were divided into painless group and pain group, and the data of the two groups were retrospectively analyzed. The major clinical symptom was pain in 447 cases (92.74%), while 35 patients (7.26%) had no typical pain. The gender, age, hypertension, hyperlipidemia, diabetes, smoking and drinking history had no statistically significant differences between the two groups (P>0.05). The proportion of Stanford type A in painless group was significantly higher than that in pain group (48.57% vs. 21.03%, P=0.006). The incidence of unconsciousness in the painless group was significantly higher than that in the pain group (14.29% vs. 3.58%, P=0.011). The incidence of hypotension in painless group was significantly higher than that in pain group for 4.26 folds (P=0.01). Computed tomography angiography (CTA) examination revealed that the incidence of aortic arch involved in the painless group was significantly higher than that in the pain group (19.23% vs. 5.52%, P=0.019). It was concluded that the incidence of painless aortic dissection was higher in Stanford A type patients, commonly seen in the patients complicated with hypotension and unconsciousness. CTA examination revealed higher incidence of aortic arch involvement.

Objective To determine the activities of 131I for treating differentiated thyroid carcinoma with diffuse pulmonary metastases ( DTC-DPM ) from the perspective of internal radiation dosimetry.Methods According to Medical Internal Radiation Dosimetry (MIRD) schema, the activity constraint,from which the whole bdy retention at 48 h should not exceed 2.96 GBq (2.96 GBq rule), was converted to dose-rate constraint(DRC) to lungs at 48 h ( DRCLU ·48 h ) in 131I therapy for DTC-DPM. Based on the assumption of DRCLU·48 h at 48 h in lung, the fractions of whole body activities ( F48 ), the effective half times of 131I in lungs ( TLL ) and the remainder of body ( TRB ) were 0.6-0.9, 20- 120 h, and 10- 20 h, respectively. The maximum safe activities of 131I for different human phantoms from the Organ Level Internal Dose Assessment (OLINDA) software were calculated. Results According to MIRD schema and 2.96 GBq rule, DRCLU ·48 h should not exceed 46.4 mGy/h in 131I therapy for DTC-DPM. Depending on varying F48 h,TLL and TRB, the maximum safe activities of 131I were 6.77-81.36, 5.29-56.20, 5.08-55.19 and 3.87-40. 52 GBq for the male adult, female adult, 15-year-old, and 10-year-old patients with DTC-DPM, respec tively. Conclusion Dosimetry-guided 131I therapy for DTC-DPM considers adequately the differences of 131I kinetics in individual patients and can adjust administered activities of 131I on the precondition of avoiding radiological pneumonitis and pulmonary fibrosis.

OBJECTIVE To discuss the characteristics and risk factors of nosocomial infection inpatients with chronic kidney disease.METHODS The data from chronic kidney disease(CKD) patients retrospectively analyzed.RESULTS The nosocomial infection rate of CKD patients was 14.73%,urinary tract was the most comun site,The main-pathogens were Gram-negative bacteria,and then Gram-positive bacteria and fungii.The patients with diabetic nephropathy,lupus nephritis,aging,lower glomerular filtration rate,hypoproteinemia,anemia,and long time duration were easy to get nosocomial infection.CONCLUSIONS Nosocomial infection in CKD patients is related to underlying diseases,age,kidney function,serum albumin level,hemoglobin level,duration time in the hospital.

Objective:To investigate the role of sterol regulatory element binding protein-1 (SREBP1) in atorvastatin-induced reduction of nucleotide-binding oligomerization domain-like receptor protein 1 ( NLRP1 ) inflammasome expression. Methods:THP-1 cells were treated with phorbol 12-myristate 13-acetate (160 nmol/L) for 12 h to be differentiated into macrophages. The medium was then replaced with serum-free medium containing lipopolysaccharide and ( or ) atorvastatin. The mRNA expression of NLRP1 and SREBP1 were detected by Real-time PCR. The protein expression of NLRP1 and SREBP1 were determined by Western blot. Furthermore, we observed the effect of SREBP1 siRNA on atorvastatin-induced reduction of NLRP1 expression. Results:Atorvastatin inhibited the mRNA and protein expression of NLRP1 and SREBP1 in the THP-1 macrophages. SREBP1 siRNA showed no significant difference on lowering NLRP1 expression when compared with atorvastatin. Treating cells with SREBP1 siRNA and atorvastatin at the same time resulted in more obvious reduction of NLRP1 expression than single use of SREBP1 siRNA or atorvastatin. Conclusion:Atorvastatin might exert anti-inflammatory effect by repressing NLRP1 expression through the SREBP1 path-way.