Activity patterns in human motion-sensitive areas depend on the interpretation of global motion

Numerous imaging studies have contributed to the localization of motion-sensitive areas in the human brain. It is, however, still unclear how these areas contribute to global motion perception. Here, we investigate with functional MRI whether the motion-sensitive area hMT+/V5 is involved in perceptual segmentation and integration of motion signals. Stimuli were overlapping moving gratings that can be perceived either as two independently moving, transparent surfaces or as a single surface moving in an intermediate direction. We examined whether motion-sensitive area hMT+/V5 is involved in mediating the switches between the two percepts. The data show differential activation of hMT+/V5 with perceptual switches, suggesting that these are associated with a reconfiguration of cell assemblies in this area.     

"Stem cell" origin of the hematopoietic defect in dyskeratosis congenita

We have used the long-term bone marrow culture (LTBMC) system to analyze hematopoiesis in three patients with dyskeratosis congenita (DC), two of whom had aplastic anemia, and the third had a normal blood count (apart from mild macrocytosis) and normal BM cellularity. Hematopoiesis was severely defective in all three patients, as measured by a low incidence of colony-forming cells and a low level of hematopoiesis in LTBMC. The function of the marrow stroma was normal in its ability to support the growth of hematopoietic progenitors from normal marrows seeded onto them in all three cases, but the generation of hematopoietic progenitors from patients marrow cells inoculated onto normal stromas was reduced, thus suggesting the defect to be of stem cell origin. The parents and unaffected brother of one of the families have also been studied in LTBMC and all showed normal hematopoietic and stromal cell function. From this study we speculate that there are some similarities between DC and the defect in the W/Wv mouse.     

A comprehensive management system for heart failure improves clinical outcomes and reduces medical resource utilization]

BACKGROUND: Hospital admissions for heart failure are common and readmission rates are high. Many admissions and readmissions may be avoidable, so that alternative strategies are needed to improve long-term management. METHODS: We conducted a randomized trial of the effect of a guideline-based intervention on rates of readmission within 90 days of hospital discharge and costs of care for patients who were hospitalized due to decompensated heart failure. The intervention consisted of comprehensive education of the patient and family, a prescribed diet and intensive application of guidelines' recommendations on pharmacological therapy. The intervention started before discharge and continued thereafter with follow-up visits for up to 3 months. Two hundred and nine guideline-managed patients were compared to 209 concurrent normally-discharged patients. RESULTS: Patients in the study group were more prescribed beta-blockers, ACE-inhibitors, angiotensin receptor blockers, and spironolactone. Sixteen patients (8%) in the intervention group and 31 (15%) among controls were readmitted for DRG 127, within 3 months of discharge (Fisher's exact test, p < 0.01), while the 6-month mortality rate was similar between groups (9 and 11.5% respectively). Quality of life significantly improved from 5.6 +/- 1.0 to 6.1 +/- 1.9 (Mann-Whitney U-test, p < 0.05). The overall costs of care were lower for guideline-managed patients (110 vs 150 Euro per patient per month), due to the lower readmission rates. CONCLUSIONS: Our study showed that a guideline-based management program for patients with heart failure at discharge improves quality of life and reduces readmission for DRG 127 and total bed days, allowing relevant cost savings.     

Inactivation of purified human alpha 2-antiplasmin and purified human C1 inhibitor by synthetic fibrinolytic agents

3-Hydroxypropyl flufenamide (Flu-HPA) is one of a series of flufenamic acid derivatives that enhances blood clot lysis in vitro. Studies of possible mechanisms of action of Flu-HPA were undertaken. The profibrinolytic activity of Flu-HPA in clot lysis assays was found to be dependent on plasminogen. The influence of Flu-HPA on the ability of purified alpha 2-antiplasmin to inhibit purified plasmin was studied. Plasmin activity was determined using 125I-fibrin plates or the spectrophotometric tripeptide substrate, Val-Leu-Lys-paranitroanilide. At Flu-HPA concentrations greater than 1 mM, the inhibitory activity of alpha 2-antiplasmin was abolished in a time-dependent and concentration- dependent manner. The influence of Flu-HPA on the ability of purified Cl inhibitor to inhibit purified plasma kallikrein and beta-Factor XIIa was also studied. Cl inhibitor activity was abolished by Flu-HPA at concentrations greater than 2 mM. Notably, Flu-HPA up to 60 mM did not affect the amidolytic activities of plasmin, kallikrein, or beta-Factor XIIa. Flu-HPA did not release enzyme activity from preformed complexes of either alpha 2-antiplasmin and plasmin of Cl inhibitor and kallikrein. A water-soluble derivative of flufenamic acid, N-flufenamyl- glutamic acid, also inactivated alpha 2-antiplasm and Cl inhibitor. This inactivation was shown to be reversible. These results indicate that synthetic fibrinolytic compounds such as flufenamic acid derivatives may promote fibrinolysis by directly inactivating alpha 2- antiplasmin and Cl inhibitor.     

Relation of asymmetrical dimethylarginine levels with renal outcomes in hypertensive patients with and without type 2 diabetes mellitus

Aim

The aim of the study was to evaluate the association between high plasma ADMA levels, a biomarker of endothelial dysfunction, with the progression of albuminuria and chronic kidney disease (CKD) in hypertensive patients, with and without type 2 diabetes mellitus.

周期性压力作用下椎间盘细胞中整合素α3的表达

目的 探讨整合素在体外培养的椎间盘细胞力学传导中的作用。方法采用猪的椎间盘进行体外细胞的分离和培养，对细胞施加周期性液压负荷，通过对细胞的形态学观察、Western免疫印迹、免疫细胞化学染色和免疫荧光，分别检测整合素α3和肌动蛋白在周期性压力下椎间盘细胞中的表达。结果经加压后，纤维环细胞和髓核细胞均可见体积缩小，由多角形转变为细长形，α3和肌动蛋白在AF和NP细胞中的表达均明显减少。结论压力抑制了整合素α3的产生，整合素α3将力的信号转换到细胞内时，进一步影响到与其关系密切的肌动蛋白。     

A prospective study on TT virus infection in transfusion-dependent patients with beta-thalassemia

A novel DNA virus designated TT virus (TTV) has been reported to be involved in the development of posttransfusion non-A-C hepatitis. We evaluated the frequency and natural course of TTV infection in a cohort of transfusion-dependent thalassemic patients in a 3-year follow-up study. Ninety-three serum hepatitis C virus (HCV) antibody-negative patients (median age of 8 years; range, 0 to 25) from eight centers were studied. Of them, 34 (37%) had an abnormal alanine-aminotransferase (ALT) baseline pattern, and the other 12 (13%) showed ALT flare-ups during the follow-up. TTV DNA in patient sera collected at the time of enrollment and at the end of follow-up was determined by polymerase chain reaction (PCR). In parallel, serum samples from 100 healthy blood donors were also tested. At baseline, 87 patient sera (93.5%) tested positive for the TTV DNA. Of these TTV DNA-positive patients, 84 (96.5%) remained viremic at the end of the study period. Of the 6 TTV DNA-negative patients, 3 acquired TTV infection during follow-up. However, no definite relation was observed between the results of TTV DNA determination and ALT patterns. TTV viremia was also detectable in 22% of blood donors. In conclusion, TTV infection is frequent and persistent among Italian transfusion-dependent patients. The high rate of viremia observed in healthy donors indicates that the parenteral route is not the only mode of TTV spread.