Objective To investigate the relationship between Sfrp5 and T2DM macroangiopathy , and to evaluate the activation of calcium dobesilate. Methods T2DM patients were divided into experimental group (IMT≥0.90 mm,n = 65)and control group (IMT < 0.90 mm, n = 30)and patients in experimental group were randomly further divided into group A (n = 30,treated with calcium dobesilate) and group B (n = 35, treated with routine therapy). Another 20 healthy control were involved as normal group. Sfrp5,IL-10,TC,TG,FPG, HbA1c and IMT were observed before and after treatment. Results Sfrp5 and IL-10 in experimental group and control group were lower than those in normal group (P < 0.01)and Sfrp5 and IL-10 in experimental group were lower than those in control group (P < 0.05). Correlation analysis showed that sfrp5 and IL-10 were negatively correlated with these above-mentioned indicators and Sfrp5 was positively correlated with IL-10(P < 0.05). After 16-week treatment, the contents of FBG, lipid, HbA1c and IMT were decreased in group A and B, but Sfrp5 and IL-10 were increased in group A (P < 0.01). Sfrp5 and IL-10 didn't alter significantly in group B (P >0.05). IMT in group A were decreased when compared with group B (P < 0.05). Conclusion Sfrp5 is negatively correlated with macroangiopathy. Calcium dobesilate can elevate Sfrp5 and IL-10,thus delay the progression of macroangiopathy.

Small cell lung cancer(SCLC) is an chemosensitive and radiosensitive malignant tumor which can appear hematogenous metastasis in early stage. The treatment of SCLC is based on chemotherapy and combined with radiotherapy and operation. In spite of the high response rate, the median time from drug-resistance to death of extensive SCLC is still disappointed. As to limited SCLC, there are still 75 % ~ 80 % patients relapse after inductive chemotherapy and radiotherapy. All in all, the second-line therapy is very important in SCLC patients.

AIM To investigate the effect and mechanism of L-arginine(L-Arg) on lipopolysaccharides(LPS)-induced acute lung injury (ALI). METHODS Models of ALI were established by injection (iv) with LPS 5 mg·kg~(-1) in male SD rats. The rats were randomly divided into 3 groups: ① saline group; ② LPS group; ③ L-Arg group. The rats in each group were further divided into 2 subgroups according to L-Arg- supplemented time: 1 h+3 h group and 6 h+3 h group. L-Arg 500 mg·kg~(-1) or saline (saline and LPS groups) was administrated at 1 or 6 h after LPS injection, respectively. The treatment lasted for 3 h, and the rats were sacrificed at 4 or 9 h after LPS injection. Apoptotic rate, caspase 3, and Bcl-2 and Bax were evaluated by flow cytometry, Western blot analysis and immunohistochemistry, respectively; meanwhile, the pathological changes of lung tissue were observed by electron microscope. RESULTS Compared with saline group, apoptosis of pulmonary cells and caspase 3 expression were significantly increased, Bcl-2 was decreased, while Bax was elevated in alveolar and airway epithelial cells in LPS group. Compared with LPS 1 h+3 h group, L-Arg 1 h+3 h decreased apoptotic pulmonary cells〔(23.8±2.8)% vs (15.4±2.3)%〕; moreover, expressions of caspase 3 (0.80±0.06 vs 0.67±0.10) and Bax (0.115±0.012 vs 0.091±0.014) were significantly decreased, while expression of Bcl-2 (0.067±0.011 vs 0.075±0.009) and Bcl-2/Bax ratio (0.586±0.114 vs 0.833±0.142) in alveolar and airway epithelial cells were markedly increased, and lung damage was alleviated. L-Arg 6 h+3 h also reduced apoptotic pulmonary cells and caspase 3 expression compared with LPS group, but the lung injury relieved slightly. CONCLUSION Relatively early administration of L-Arg can protect lungs from LPS-induced injury through inhibiting cell apoptosis, as well as increasing the expression of anti-apoptotic protein Bcl-2 and decreasing the expression of proapoptotic protein Bax and caspase 3.

Aim To investigate the effect and the possible mechanism of aminoguanidine(AG)on the lipopolysaccharide(LPS)-induced acute lung injury in rats.Methods Male SD rats were randomly divided into control group,LPS group and AG group.AG was administered in AG group,saline was administered in control group and LPS group.All the groups were further divided into 2 subgroups according to the duration of ALI:3 h+3 h group and 6 h+3 h group.In AG group and LPS group,LPS was administered.Saline was administered in control group.The translocation of NF-?B and the expression of intercellular adhesion molecule-1(ICAM-1)were respectively detected with immunohistochemisty(IHC);the concentrations of TNF-? and IL-6 in lung tissue were evaluated by radioimmunoassay;the pathological changes of lung tissue were observed by light and electron microscope.Results Compared with those of the control group,NF-?B was significantly translocated from the cytoplasm into the nucleus,the expression of NF-?B and ICAM-1 protein were significantly increased.The concentrations of TNF-? and IL-6 in lung tissue were significantly increased in LPS group.Degree of ALI was gradually worsened after administration of LPS.In AG(3 h+3 h)group,the expression of NF-?B and ICAM-1 protein were significantly decreased,the concentrations of TNF-? and IL-6 in lung tissue were significantly decreased and the lung damage was improved compared with those of the LPS(3 h+3 h)group.Conclusions Administration of AG could ameliorate LPS-induced acute lung injury in rats.The possible mechanism was that AG could reduce the expression of iNOS mRNA,inhibited NF-?B activation and subsequently led to the down-regulation of NF-?B-dependent inflammatory gene expression and thus reduced the inflammatory response in lung injury.

Aim To investigate the effect of aminoguanidine (AG) on the lipopolysaccharide (LPS)-induced chronological changes of pulmonary surfactant (PS) and alveolar macrophage (AM) of rats.Methods Acute lung injury was induced by injection(iv) of lipopolysaccharide (LPS 5 mg?kg-1). AG(AG group) or saline(control and LPS group) was administrated respectively at 3 h or 6 h after LPS injection for 3 h.The expressions of SP-A mRNA and SP-A protein in the lung tissue were measured by ISH methods and Western blot;the total protein(TP),total phospholipid(TPL) in the bronchoalveolar lavage fluid (BALF) were detected.Rat AM was isolated from the BALF of adult SD rats and harvested by selective plating technique.The concentrations of Tumor necrosis factor-? (TNF-?),Interleukin-6(IL-6),Nitric oxide (NO) and the activity of lactate dehydrogenase (LDH) in the culture supernatants were detected.Results Compared with the controls,SP-A mRNA and SP-A protein in the LPS groups were significantly and progressively decreased. TPL of LPS group in the BALF was significantly decreased whereas TP concentration was significantly increased.Compared with LPS group at the same time points,treatment with AG at 3 h after LPS the expressions of SP-A mRNA and SP-A protein in lung tissue and TPL in BALF were increased markedly,whereas TP was significantly decreased.LPS treated group,LDH activity,the contents of NO,TNF-? and IL-6 in culture medium were significantly increased compared with that of normal group.The LDH activity,NO contents,TNF-? and IL-6 were decreased in AG group compared with that of LPS group.Conclusion Relatively early administration AG(selective inhibitor of iNOS),can protect lung from LPS-induced injury through increasing the expression of SP-A mRNA,SP-A protein and TPL,and inhibiting over-release of a series of cytokines and inflammatory transmitters from AM.

AIM: The quality standard for Compound Xiaojingtong Capsule(Radix Astragali, Radix Ginseng, Radix Angelicae Sinensis, Rhizoma Chuanxiong, etc.) were studied. METHODS: The TLC method for identification of Radix Ginseng, Radix Angelicae Sinensis, Rhizoma Chuanxiong in these capsules were established. Astragaloside Ⅳ was determined by single wavelength TLC-scanning(? s=530nm). RESULTS: Radix Angelicae Sinensis, Rhizoma Chuanxiong and Radix Ginseng could be detected. Astragaloside Ⅳ showed a linear relationship at the concentration range of 1.1～5.5?g (r=0.9983). The average recovery was 100.1% and RSD was 1.59% (n=6). CONCLUSION: This method is suitable for the quality control of Compound Xiaojingtong Capsule.

Objective To evaluate the effects of L-aronine(L-Arg) on LPS-induced lung mitochondrial injury in rats.Methods Twenty.four male SD rats weighing 230-270 g were randomly divided into 3 groups(n=8 each):groupⅠsham operation(S);group ⅡLPS and group Ⅲ LPS+L-Arg.LPS 5 mg/kg in normal saline(NS)1 ml/kg waft given iv in group Ⅱ and Ⅲ while in group Ⅰ NS 1 ml/kg was given iv instead of LPS. L-Arg 500 ms/kg in NS 1 ml/kg was given intrapefitoneally(IP)at 3 h after LPS administration in group Ⅲ,while in group Ⅰ I and Ⅱ NS1 ml/kg was injected IP instead of L-Arg.The animals were sacrificed at 3 h after L-Arg injection by exsanguination and the lungs were immediately removed.The mitochondrias of the lungs were isolated by differentia centrifugation.The activities of SOD,GSH-Px,ATPase,inducible,constitutive and total nitric oxide synthase(iNOS,cNOS,NOS)and MDA and NO contents,the degree of mitochondrial swelling,mitocho-ndrial activity and membrBne fluidity of mitochondria wefe measured.Ultrastructure of cells in lung was examined wlth eleciron microscope.Results The SOD,GSH-Px.ATPase and mitochondriai activities and the membrane fluidity of mitochondria were significantly decreased,while the MDA and NO contents and iNOS,NOS activities and the degree of mitochondriM swelling in the lung were significantly increased in group LPS as compared with group S.The lung cytoplasm and mitoehondria swelled,the cfistae were disrupted,dissolved or disappeared in LPS group(Ⅱ).The LPS-induced changes were ameliorated by L-Arg in group Ⅲ as compared with group Ⅱ.Conclusion L-Arg can attenuate lung mitochondrinl injury induced by LPS by enhancing antioxidative effects.

With acute lymphoblastic leukemia in skeletal muscle symptom,part of these patients may be misdiagnosed as juvenile idiopathic arthritis. How to distinguish these children has significance for the timely and proper treatment and good prognosis. This article from the history and routine laboratory examination and ima-ging examination put forward early in the disease through the analysis of joint symptoms from juvenile joint pain,blood and imaging characteristics and preliminary identification of childhood leukemia from juvenile idio-pathic arthritis in order to decrease the rate of misdiagnosis.

Objective To investigate the effects of nitric oxide(NO) and its donor(L-arginine) on focal cerebral ischemic injury in rats. Methods Forty-two healthy male SD rats weighing 250-300g were used. The animals were anesthetized with 20% urethane 1g? kg-1. Common carotid artery (CAA), external carotid artery(ECA) and internal carotid artery were(ICA) exposed through a median incision in the neck. Middle cerebral artery occlusion (MCAO) was produced by insertion of a 40 mm long nylon thread (0.3 mm in diameter) into ICA through ECA. The tip of the nylon thread was made into a ball of 0.5 mm in diameter with heat and the length of insertion was (18.5?0.5)mm on average. The animals were randomly divided into four groups: group 1: sham operation; group 2: ischemia group; group 3: low dose L-arginine(300mg?kg-1 intraperitoneal injection) and group 4: high dose L-arginine(500mg?kg-1 IP). Group 3 and 4 were further divided into 3 subgroups: subgroup A: L-arginine was given 1h after MCAO and the animals were killed 2h after medication (1h + 2h); subgroup B: L-arginine was given 3h after MCAO and the animals were killed 3h after medication(3h + 3h) and subgroup C: L-arginine was given 6h after MCAO and the animals were killed 3h after medication(6h + 3h) . The brain was removed immediately. The volume of cerebral infarct/volume of whole brain was calculated(%) . The NO, MDA content and NOS, SOD activity in the brain tissue of ischemic hemisphere were measured. Results L-arginine significantly decreased cerebral infarct volume and ameliorated focal cerebral ischemia. The effects in high dose group were better than in low dose group. L-arginine significantly increased NO content, decreased MDA content and enhanced the SOD activity in the focal ischemic cerebral tissue. Conclusions It may be concluded that L-arginine has beneficial effect on brain injury in acute ischemic stage and high dose provides better effects.

Aim To investigate the protective effect of propofol on ischemia-reperfusion(I/R)injury in isolated rat hearts and clarify the possible molecular mechanism from oxidative stress and the apoptosis initiated by mitochondria pathway. Methods The langendorff model of ischemia-reperfusion was used.Forty isolated perfused rat hearts were divided into control,I/R, propofol 15,30,60 ?mol?L-1 groups. Hearts were suffered globally ischemic for 25 min and 30 min with reperfusion. The cardiac function indexs such as the left ventricular developed pressure(LVDP), the left ventricular end diastolic pressure(LVDEP), heart rate (HR), coronary arterial flow (CF) were recorded at the time of equilibrate, before ischemia, the end of reperfusion respectively. The lactate dehydrogenase (LDH), creatine kinase (CK) activities in the flow were measured. The swelling and activity of mitochondria, the activity of Manganese Superoxide Dismutase (Mn-SOD) and content of malondialdehyde (MDA) in myocardium mitochondria were also determined. The incidence of cardiomyocyte apoptosis was evaluated by the TdT-mediated dUTP nick end labeling (TUNEL) staining and the expression of Bcl-2 and Bax were evaluated by Flow Cytometry(FCM). The expression of Caspase-3,8,9 was detected by immunohistochemistry.Results Compared with I/R group, administration of propofol at the concentration of 30 and 60 ?mol?L-1 markedly ameliorated the cardiac function in CF,LVDP and LVDEP(P