Camp Okizu: Preliminary Investigation of a Psychological Intervention for Siblings of Pediatric Cancer Patients

This research was conducted at a summer camp for siblings of children with cancer. The camp is designed to address emotional problems, provide peer interaction and validation, and bolster siblings' self-esteem. Standardized measures assessing posttraumatic stress, anxiety, quality of life, and self-esteem were administered to 77 siblings (ages 6-17) prior to attending camp and again 3 months after camp. From pre- to post-camp, the siblings reported statistically significant decreases in symptoms of posttraumatic stress and anxiety, and statistically significant improvements in quality of life and self-esteem. These preliminary findings are encouraging and suggest the value of camp as a psychological intervention and provide a model for other pediatric cancer facilities designing intervention programs for siblings.     

血管细胞粘附分子调控造血的研究进展

本文简述了血管细胞粘附分子 (Vascularcelladhesionmolecule 1,VCAM 1)的结构和生物学功能 ,总结了VCAM 1在恶性血液病骨髓基质中的表达和意义 ,探讨了VCAM 1在造血干细胞动员和归巢中的作用 ,指出VCAM 1作用机制的深入研究将对恶性血液病的治疗提供更为有效的方法。     

Effects of heparin and endothelial cell growth supplement on haemostatic functions of vascular endothelium.

Heparin in combination with endothelial cell growth factor (ECGF) affects physiological responses and growth of human umbilical vein endothelial cells (HUVEC). We have examined the effect of heparin, crude ECGF (endothelial cell growth supplement [ECGS]), or both on the basal and thrombin challenged output of metabolites by HUVEC. The supernatant and/or cell lysate was assayed for released prostacyclin, von Willebrand factor, tissue plasminogen activator, plasminogen activator inhibitor and thrombospondin. Heparin modified release of all these metabolites when in combination with ECGS, and in general these responses were the opposite of those generated by inflammatory mediators such as interleukin-1. It has been postulated that heparin acts by potentiating the effect of ECGF, but heparin inhibited thrombospondin release and enhanced that of von Willebrand factor in the absence of ECGS, while ECGS alone inhibited release of plasminogen activator inhibitor. Thus, under our experimental conditions it would appear that heparin and crude ECGF can affect HUVEC independently of one another.     

Glycoproteins present in human follicular fluid that inhibit the zona- binding capacity of spermatozoa

Previous studies have suggested that human follicular fluid contains factors that reduce the zona-binding capacity of spermatozoa. The present study provides further evidence of the existence of such factors. Using the hemizona binding assay (HZA), we have shown that the inhibitory effect of human follicular fluid on the zona-binding capacity of spermatozoa is concentration-dependent, an inhibitory effect being detected when the concentration of human follicular fluid was > or = 10%. A 1% concentration of human follicular fluid did not possess this inhibitory activity. Heating human follicular fluid at 56 degrees C for 30 min did not affect its inhibitory properties; treatment with proteinase-K abolished such inhibition. Human follicular fluid was fractionated sequentially by concanavalin-A affinity chromatography, Mono Q ion-exchange chromatography and Superose-12 gel filtration. The zona binding inhibitory activity resided in the fraction which bound to the lectin and Mono Q column and contained molecules with native molecular weights of 32 and 192 kDa. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis analysis suggested that the 192 kDa glycoprotein was a tetramer, while the 32 kDa glycoprotein remained as a single molecular species under denaturing conditions. We conclude that two glycoproteins were responsible for the zona binding inhibitory activity of human follicular fluid. The physiological role of these factors remains unclear.      

Response from lieberman and colleagues

Respond on comments on Lieberman's article: Cyclosiloxanes Produce Fatal Liver and Lung Damage in Mice. Environ Health Perspect 107:161-165     

Will There Ever Be a Drug with No or Negligible Side Effects? Evidence from Neuroscience

Arguments in the neuroenhancement debate are sometimes based upon idealistic scenarios involving the assumption of using a drug that has no or negligible side effects. At least it is often implicitly assumed – as technology and scientific knowledge advances - that there soon will be a drug with no or negligible side effects. We will review evidence from neuroscience, complex network research and evolution theory and demonstrate that - at least in terms of psychopharmacological intervention – on the basis of our understanding of brain function it seems inconceivable that there ever will be a drug that has the desired effect without undesirable side effects. We will illustrate this by reference to enhancing edge detection in V2 in monkeys and demonstrate that even for this localised single neuron coded function there would be numerous side effects. Taking the more realistic case of pharmacological enhancement that is inevitably associated with side effects will change consequentialist arguments for neuroenhancement and have implications for the conception of autonomy, specifically in the case of performance enhancement. We conclude that a neuroethics debate that aims to inform policy decisions should take these findings into account. We hope that our article will precipitate more interdisciplinary research in neuroscience and philosophy.