Objective To display whether Interleukin-8 was involved in acute lung injury(ALI) and in acute respiratory distress syndrome(ARDS).Methods Serum IL-8 levels in 12 patients with ALI and 13 patients with ARDS were assayed by RIA,and compared with 59 normal controls.Results The level of serum IL-8 was significantly higher in the patients with ALI and ARDS than that in the normal controls(P

AIM: To discuss the effects of phytoestrogenic-genistein on cathepsin K (CK) expression stimulated by interleukin-1α (IL-1α) in osteoclast-like cells (OCLs) . METHODS: The OCLs were isolated from tissue of human giant cell tumor of bone (GCT) . The cells treated with reagents were divided into 7 groups including control (treated with phenol red-free-DMEM), vehicle (treated with 1.2 nmol· L-1 IL- 1α), 10-10-10-6genistein, genistein+ ICI 182.780, and 17[β-estrodiol (17β-E2) group. The cells were treated with 1.2 nmol· L-1IL-1α after pre-treated with genistein or 17β-E2 for 48 h (excluded the control group) . Expression of CK wasdetermined by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot in OCLs stimulated by IL-1α in the presence of genistein or 17[β-E2. RESULTS: The obvious increase of expression of CK by IL1α in vehicle group was noted in comparing with control group (P ＜ 0.01 ) . Genistein down-regulated CK gene expression stimulated by IL-1α at the transcription level in a dose-dependent manner (r = 0.68, P ＜ 0.01 ) .Genistein down-regulated CK protein expression stimulated by IL-1α also in a dose-dependent manner (r = 0.61,P ＜ 0.01 ). The effects of genistein were abrogated partly after treatment with the estrogen receptor antagonist ICI 182.780. CONCLUSION: Genistein inhibits CK expression stimulated by IL-1α partly through estrogen receptor in OCLs.

To investigate the effect of atorvastatin on lipid metabolism in type 2 elder diabetes patients with hyperlipidemia, 26 patients with type 2 elder diabetes complicated with hyperlipidemia were treated with atorvastatin (10 mg/d) for 8 weeks. The serum triglyceride (TG), high density protein cholesterol (HDL-C) and low density protein cholesterol (LDL-C) were measured before and after the treatment. Meanwhile, the non-denaturing polyacrylamide gradient gel electrophoresis was used for detection of small-sized LDL(SLDL). Our results showed that TG dropped from 4.88 +/- 0.72 mmol/L to 2.65 +/- 0.32 mmol/L; HDL-C was increased from 0.85 +/- 0.31 mmol/L to 1.28 +/- 0.29 mmol/L; LDL-C was declined from 3.71 +/- 2.98 mmol/L to 2.10 +/- 1.22 mmol/L, sLDL-A was increased from (42.49 +/- 8.1)% to (53.27 +/- 7.5)%; LDL-B was decreased from (57.91 +/- 8.1)% to (46.73 +/- 7.5% ) (P<0.05). The level of blood glucose was not changed at the end of 8th week. It is concluded that atorvastatin has satisfactory lipid-regulating effects on type 2 elder diabetes patients with hyperlipidemia.
Anticholesteremic Agents/*therapeutic use ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Diabetes Mellitus, Type 2/*complications ; Diabetes Mellitus, Type 2/drug therapy ; Heptanoic Acids/*therapeutic use ; Hyperlipidemias/complications ; Hyperlipidemias/*drug therapy ; Pyrroles/*therapeutic use ; Triglycerides/blood

To investigate the effect of atorvastatin on lipid metabolism in type 2 elder diabetes patients with hyperlipidemia, 26 patients with type 2 elder diabetes complicated with hyperlipidemia were treated with atorvastatin (10 mg/d) for 8 weeks. The serum triglyceride (TG), high density protein cholesterol (HDL-C) and low density protein cholesterol (LDL-C) were measured before and after the treatment. Meanwhile, the non-denaturing polyacrylamide gradient gel electrophoresis was used for detection of small-sized LDL(SLDL). Our results showed that TG dropped from 4.88 +/- 0.72 mmol/L to 2.65 +/- 0.32 mmol/L; HDL-C was increased from 0.85 +/- 0.31 mmol/L to 1.28 +/- 0.29 mmol/L; LDL-C was declined from 3.71 +/- 2.98 mmol/L to 2.10 +/- 1.22 mmol/L, sLDL-A was increased from (42.49 +/- 8.1)% to (53.27 +/- 7.5)%; LDL-B was decreased from (57.91 +/- 8.1)% to (46.73 +/- 7.5% ) (P<0.05). The level of blood glucose was not changed at the end of 8th week. It is concluded that atorvastatin has satisfactory lipid-regulating effects on type 2 elder diabetes patients with hyperlipidemia.
Aged ; Anticholesteremic Agents ; therapeutic use ; Atorvastatin Calcium ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Diabetes Mellitus, Type 2 ; complications ; drug therapy ; Female ; Heptanoic Acids ; therapeutic use ; Humans ; Hyperlipidemias ; complications ; drug therapy ; Male ; Middle Aged ; Pyrroles ; therapeutic use ; Triglycerides ; blood

Summary: In order to confirm whether the mRNA levels of adiponectin in adipose tissue and mRNA levels of AdipoR1 in the skeletal muscles were correlated with the serum parameters of glucose and lipid metabolism and to clarify the regulation of adiponectin receptor gene expression in diabetic states, serum adiponectin, mRNA levels of adiponectin in adipose tissue and mRNA levels of AdipoR1 in the skeletal muscles were examined in type 2 diabetic rats. The model of type 2 diabetes was prepared by feeding high fat diet and injecting low dosage of streptozotocin (STZ). The diabetic rats were screened out by oral glucose tolerance test. One group of type 2 diabetic rats received rosiglitazone. The serum adiponectin concentration was detected by using ELISA and mRNA levels were examined by RT-PCR. The serum adiponectin levels and mRNA levels of adiponectin in adipose tissue of type 2 diabetic rats were significantly decreased as compared with the normal control rats (P<0.05, P<0.01 respectively). No siglificant changes were observed in the expression of adiponectin receptor 1 in the skeletal muscle of type 2 diabetic rats. The mRNA levels of adiponectin in adipose tissue were reversely correlated with serum insulin (r=-0.66, P<0.05), triglyceride (r=-0.58, P<0.05), cholesterol (r=-0.49, P<0.05), interleukin-6 (r=-0.49, P<0.05) and tumor necrosis factor (r=-0.43, P<0.05). The expression of adiponectin receptors was not altered in the skeletal muscle of Type 2 diabetic rats. The decreased serum adiponectin was caused by the decreased expression of adiponectin mRNA in adipose tissue rather than the adiponectin receptors in the skeletal muscle, which could be improved by rosiglitazone.