The aim of this study was to investigate the circulating levels of IL-11 in the patients with chronic idiopathic thrombocytopenic purpura (CITP), and its significance, and to evaluate the curative effect of rhIL-11 on CITP. The level of IL-11 in patients with CITP was determined by ELISA before and after treatment, respectively. 1.5 mg of rhIL-11 were injected subcutaneously, once a day, continuously for 14 days as one course, treatment time 1 - 2 courses as total. The results showed that the higher blood IL-11 level was found in CITP patients than that in controls (P < 0.01) and during the course of treatment the number of platelets in peripheral blood of patients with CITP parallelled to the level of IL-11. The platelet counts were obviously increased in all CITP patients after rhIL-11 treatment. It is concluded that the serum level of IL-11 in patients is correlated to the number of platelets in patients. rhIL-11 can be used as an effective treatment for CITP.
Adolescent ; Adult ; Aged ; Chronic Disease ; Female ; Humans ; Interleukin-11 ; blood ; therapeutic use ; Male ; Middle Aged ; Platelet Count ; Purpura, Thrombocytopenic, Idiopathic ; drug therapy ; Recombinant Proteins ; therapeutic use ; Treatment Outcome

OBJECTIVETo assess the role of direct thrombin inhibitor argatroban in the renal replacement therapy.

METHODSElectronic databases including Cochrane library, PubMed, EMBASE, Highwire, MEDLINE, CBM, CNKI, and CSJD were searched using keywords including "Argatroban", "hemodialysis", "renal function", "renal failure", and "renal replacement therapy". A meta-analysis of all randomized controlled trials(RCTs)comparing argatroban with controls in renal replacement therapy was performed. Both the study selection and the meta-analysis were conducted according to the Cochrane Handbook for systematic reviews. Data were extracted from these trials and analyzed by RevMan 5.0 software.

RESULTSCompared with the control group, argatroban in renal replacement therapy showed no significant difference in mortality(RR=0.97, 95%CI: 0.48-1.97, P=0.93)and bleeding rate(RR=0.71, 95%CI: 0.37-1.34, P=0.29). Argatroban significantly decreased the incidence of new thrombosis in renal replacement therapy for patients with heparin-induced Thrombocytopenia(RR=0.40, 95%CI: 0.21-0.75, P=0.004). Also, argatroban significantly decreased the clotting events in extracorporeal circuit during the renal replacement therapy(RR=0.06, 95%CI: 0.01-0.23, P<0.0001). CONCLUSION Argatroban applied in renal replacement therapy can decrease the incidences of new thrombosis and clotting events in extracorporeal circuit and meanwhile will not increase the mortality and bleeding.

Antithrombins ; therapeutic use ; Hemorrhage ; epidemiology ; Humans ; Incidence ; Pipecolic Acids ; therapeutic use ; Renal Dialysis ; Renal Insufficiency ; Renal Replacement Therapy ; methods ; Thrombosis ; drug therapy

OBJECTIVE: To evaluate whether ultrafine particulates (UFPs) have direct deleterious effects on cardiac function through activating MAPK signaling. METHODS: Langendorff-perfused Sprague-Dawley rat hearts were randomly divided into 2 groups (n=10/each group). In control group, the rat hearts were perfused with Tyrode's buffer for 40 min; in UFPs-treated group, the hearts were perfused with UFPs at a concentration of 12.5 mg/L. Cardiac function was determined by measuring left ventricular developed pressure (LVDP), left ventricular peak rate of contraction and relaxation (±dp/dt_max) and coronary flow (CF). The levels of malondialdehyde (MDA), superoxide dismutase (SOD), total anti-oxidant capacity (TAOC) were detected in order to evaluate cardiac oxidative stress via the thiobarbituric acid assay, water soluble tetrazolium salt assay and colorimetry, respectively. The expressions of p-p38 MAPK, p-ERKs and p-JNKs in the myocardium were observed using immunohistochemical staining and Western blots. RESULTS: No significant changes in cardiac function were detected before and after the perfusion in control group while UFPs perfused hearts showed a decline in cardiac function in a time-dependent manner (all P < 0.05). In UFPs-treated group, LVDP, +dp/dt_max, -dp/dt_max and CF were statistically reduced from (82.6±2.1) mmHg, (1 624±113) mmHg/s, (1 565±116) mmHg/s, (12.0±0.2) mL/min to (56.8±4.4) mmHg, (1 066±177) mmHg/s, (1 082±134) mmHg/s, (8.7±0.3) mL/min (all P < 0.05), respectively. Furthermore, The comparison between the two groups observed that UFPs perfusion caused a significant decrease in cardiac function at 30 and 40 min compared with the control group (all P < 0.05). At the end of the perfusion, the level of MDA was increased from (0.98±0.14) nmol/L to (1.95±0.18) nmol/L, while SOD and TAOC were reduced from (12.50±1.87) U/mL and (6.83±1.16) U/mL to (6.50 ±1.04) U/mL and (3.67±0.82) U/mL (all P < 0.001) in UFPs group, respectively. In coincidence with these changes, immunohistochemistry and Western blots results showed that the levels of p-p38 MAPK, p-ERKs and p-JNKs in the myocardium significantly increased in UFPs group as compared with control group (all P < 0.05). CONCLUSION The results of this study demonstrated that the short-term exposure of UFPs to the isolated rat hearts has direct and acute toxic effects on cardiac function, probably related to attenuation of anti-oxidative capacity and activation of MAPK signaling pathways.
Animals ; Heart ; Malondialdehyde/metabolism* ; Myocardium ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley