左旋卡尼汀联合环磷腺苷葡胺治疗慢性充血性心力衰竭

目的:探究左旋卡尼汀联合环磷腺苷葡胺治疗慢性充血性心力衰竭(chronic congestive heart failure,CHF)的临床疗效。方法:选取我院心内科CHF患者58例,随机分为对照组28例与实验组30例,其中对照组28例,予地高辛、氢氯噻嗪、环磷腺苷葡胺常规治疗;实验组30例,在常规治疗的基础上加用左旋卡尼汀治疗。观察两组患者治疗前后心功能分级(NYHA)、6 min步行距离、左心室射血分数(LVEF)及左心室舒张末容积(LVEDD)等。结果:与对照组比较,实验组患者治疗后心率和NYHA心功能分级明显改善,6 min步行实验明显提高,患者LVEDD、LVEF明显改善,差异具有统计学意义(P<0.05);两组患者接受相应治疗后均未出现任何不良反应(P>0.05)。结论:左旋卡尼汀联合环磷腺苷葡胺能够明显改善慢性充血性心力衰竭,对临床具有指导意义,值得临床推广。     

Diapause in Monogonont Rotifers

This review focuses on more recent findings on the diapause in Monogonont rotifers, since the major reviews by Pourriot & Snell (1983, Hydrobiologia 104: 213–224) and Gilbert (1992, Rotifera. In Adiyodi, K. G. & R. G. Adiyodi (eds), Reproductive Biology of Invertebrates, Vol. 5 – Sexual Differentiation and Behaviour. IBH Publishing Co., Oxford: 115–136; Vol. 6A – Asexual Propagation and Reproductive Strategies. IBH Publishing Co., Oxford: 231–263.). It covers diapausing egg formation, diapausing egg survival, and diapausing egg hatching as well as possible strategies involved in these processes. Data from laboratory and field studies exist, but little information is available on diapausing egg hatching in the field. Resting or diapausing egg production can be mictic and in some cases amictic. Mictic diapausing egg production depends on the balance between cues promoting and inhibiting mictic female production. Such cues can be either environmental or endogenous. Our knowledge on factors inducing mixis is still limited to a few species, but effects of crowding on mixis induction may be more widespread. Recent results also show that male mating behavior may play an important role in the successful production of diapausing eggs. Hatching may be induced by factors related to temperature and light conditions; also desiccation may have a role. However, desiccation of temporary habitats may also be damaging to diapausing stages. Although few data are available, those existing point to distinct differences between populations and the importance of clonal variation within populations regarding the initiation as well as the termination of diapause.     

ATP modulates load-inducible IL-1beta,COX 2, and MMP-3 gene expression in human tendon cells

Tendon cells receive mechanical signals from the load bearing matrices. The response to mechanical stimulation is crucial for tendon function. However, overloading tendon cells may deteriorate extracellular matrix integrity by activating intrinsic factors such as matrix metalloproteinases (MMPs) that trigger matrix destruction. We hypothesized that mechanical loading might induce interleukin-1beta (IL-1beta) in tendon cells, which can induce MMPs, and that extracellular ATP might inhibit the load-inducible gene expression. Human tendon cells isolated from flexor digitorum profundus tendons (FDPs) of four patients were made quiescent and treated with ATP (10 or 100 microM) for 5 min, then stretched equibiaxially (1 Hz, 3.5% elongation) for 2 h followed by an 18-h-rest period. Stretching induced IL-1beta, cyclooxygenase 2 (COX 2), and MMP-3 genes but not MMP-1. ATP reduced the load-inducible gene expression but had no effect alone. A medium change caused tendon cells to secrete ATP into the medium, as did exogenous UTP. The data demonstrate that mechanical loading induces ATP release in tendon cells and stimulates expression of IL-1beta, COX 2, and MMP-3. Load-induced endogenous IL-1beta may trigger matrix remodeling or a more destructive pathway(s) involving IL-1beta, COX 2, and MMP-3. Concomitant autocrine and paracrine release of ATP may serve as a negative feedback mechanism to limit activation of such an injurious pathway. Attenuation or failure of this negative feedback mechanism may result in the progression to tendinosis.     

Extracellular potassium controls responsiveness of the noradrenergic cAMP system in the rat retina to fluphenazine

The effects of fluphenazine (FLU) on the noradrenaline (NA) induced cAMP-synthesis in intact rat retinae were studied as a function of extracellular K⁺- and Ca²⁺-ions. Thus NA-induced cAMP levels were measured after incubating intact rat retinae with 50 μM NA in the presence or absence of FLU and in the presence of 1 or 10 mM theophylline. Results were: (1) Experimental condition a: standard NA-responses were measured after incubating retinae at 0.75 mM Ca²⁺, at 10 mM theophylline, at 10 μM FLU and at 2 and 0 mM K⁺. FLU does not affect the NA-response at 2 mM K⁺ significantly; however, it inhibits the NA-response at 0 mM K⁺ in this condition. (2) Experimental condition b: NA-responses were measured after incubating retinae at 0.125 mM Ca²⁺, 10 mM theophylline, 10 μM FLU and at 2 and 0 mM K⁺. At 2 mM K⁺ FLU replaces a Ca²⁺ function probably connected with the synthesis part of the NA-cAMP system and NA-responses in this low Ca²⁺ condition are consequently enhanced by FLU; however, FLU inhibits the NA-response at 0 mM K⁺ in this condition. (3) Experimental condition c: NA-responses were measured after incubating retinae at 0.75 mM Ca²⁺, 1 mM theophylline, 10 μM FLU and at 2 and 0 mM K⁺. At 2 mM K⁺ FLU enhances the NA-response by further inhibition of the degradation part of the NA-cAMP system; FLU inhibits the NA-response at 0 mM K⁺ in this condition. (4) The inhibitions of the NA-responses by FLU at 0 mM K⁺ in all three conditions a, b and c showed an apparent K_m of 1 μM. (5) Low concentrations of K⁺ (0.4–0.8 mM) maintain the property of FLU to enhance the NA-responses at condition b (0.125 mM Ca²⁺) and at condition c (1 mM theophylline). Results suggest that the activation of NA-receptor coupled adenylate cyclases (NA-AC-ases) by NA, resulting in activation of phosphodiesterase activity by the NA-elevated cAMP-levels, is sustained by (a) membraneous factor(s) connected to the NA-receptor. This (these) factor(s) is (are) switched off in the absence of K⁺. Evidence has been presented, that Ca²⁺ and FLU do not have access to this intramembraneous factor-enzyme activating moiety of the NA-cAMP system at 0 mM K⁺. Between 0.4 and 0.8 mM K⁺ the factor-enzyme-NA-receptor complex is still intact.     

Differences in the reducing power along the rat GI tract: Lower antioxidant capacity of the colon

The ability of the gastrointestinal (GI) tract, as well as other tissues, to cope with reactive oxygen species (ROS) efflux in pathological events is determined partly by epithelial antioxidant levels. These levels are comprized of tissue antioxidant enzymes and low molecular weight antioxidants (LMWA). While glutathione levels and the activity of enzymatic antioxidants along the GI tract have been studied, the contribution of the overall LMWA to the total antioxidant capacity has not yet been determined. In this study the overall antioxidant activity in the mucosa/submucosa and muscularis/serosa of various sections along the small intestine and colon of the rat was evaluated by determining the reducing power, which reflects the total antioxidant activity derived from LMWA, using cyclic voltammetry. The activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase was also measured. The reducing power (total antioxidant activity) was higher in the mucosa/submucosa of the small intestine as compared to the mucosa/submucosa of the colon. Similarly, catalase and SOD activity in the mucosa/submucosa of the small intestine was significantly higher than in the mucosa/submucosa of the colon. Differences were also observed in the reducing power and SOD activity in the muscularis/serosa of the rat small intestine as compared to the colon. The low antioxidant capacity in the colon may facilitate reactive oxygen species (ROS)-mediated injury and lead to inflammatory diseases such as ulcerative colitis, specifically in the colon.     

Studies on the iodinated surface membrane proteins and concanavalin A agglutination of transformed Syrian hamster cells

Chemically transformed Syrian hamster cells exhibit marked agglutination in the presence of the plant lectin, concanavalin A. In this report, we describe conditions which can alter this concanavalin A agglutinability, and compare the surface proteins from transformed cells which express different degrees of agglutinability. Lactoperoxidase-catalyzed iodination of tertiary Syrian hamster cells reveals the major iodinatable protein to be approximately 220 000 daltons. The transformed Syrian hamster cells do not contain this protein in an iodinatable form. Analyses of the transformed cells grown under conditions which decrease the concanavalin A agglutinability do not demonstrate any iodination of the 220 000 mol. wt. protein. These results depict the effects of growth and dibutyryl cyclic AMP on the iodinatable cell surface proteins of transformed cells and indicate that the absence of the 1–220 000 mol. wt. protein is probably not a major determinant of concanavalin A agglutination.     

Adentylate cyclase activity in myocardium of spontaneously hypertensive rat: effect of endogenous factors and solubilization

The isoproterenol- and glucagon-stimulated adenylate cyclase activities in the myocardial membranes of hypertensive rat were consistantly lower as compared with normal controls. Addition of cytosolic fraction (100,000 x$\text{g}$ supernatant) to the particulate preparation had an additive effect for glucagon and Gpp(NH)p stimulated enzyme activity and a synergistic effect for isoproterenol stimulation. Cytosolic fraction of normal control animals did not bring the adenylate cyclase activity in SHR equivalent to the control values. The basal and F^?-stimulated enzyme activity of solubilized adenylate cyclase was reduced by about 30% in SHR as compared with WKY, which could be due to a decrease in the actual amount of adenylate cyclase in the myocardium of SHR.