Comparison of percutaneous endoscopic gastrostomy with Stamm gastrostomy.

In a review of 125 percutaneous endoscopic gastrostomies (PEG) and 88 Stamm gastrostomies performed at Duke University Medical Center since 1978, the average operating room time for PEG (50 +/- 20 min) was shorter than for Stamm (96 +/- 26 min) (p less than 0.0001). General anesthesia was administered in only 13% of PEG placements compared with 64% of Stamm gastrostomies. The cost of PEG was about $1000 less than for Stamm gastrostomies. The average time after surgery until use of the feeding tube was 1.8 days for PEG compared with 3.4 days for Stamm (p less than 0.0001). The overall complication rate after PEG was 8.8% (4.0% major) compared with 23.9% for Stamm gastrostomies (10.2% major) (p less than 0.005). PEG reduces operative time, necessity for general anesthesia, expense of insertion, incidence of complications, and requires less recovery time before use. PEG is the procedure of choice for gastric feeding access.     

伏尔泰《谈种痘》及蒙塔古夫人传种人痘于英国史料辨误

伏尔泰<哲学通信>中的第11封信是<谈种痘>,信中关于种痘史实细节的表述不够准确,原因在于其本人并未亲临现场,没有引征文献,多是得于传闻,甚或出于自己的想象.一些不够准确的表述,虽似无伤大雅,但容易对人痘起源和传播途径方面的研究产生误导,应当加以纠正.关于蒙塔古夫人将人痘接种术带回英国的过程,因国内罕能读到原始文献,有不少以讹传讹,更有必要于此加以澄清.     

Slow degeneration of zebrafish Rohon-Beard neurons during programmed cell death.

Rohon-Beard cells are large, mechanosensory neurons located in the dorsal spinal cord of anamniote vertebrates. In most species studied to date, these cells die during development. We followed labeled Rohon-Beard cells in living zebrafish embryos and found that they degenerate slowly, over many days. During degeneration, the soma shrinks and finally disappears, and the processes become beady in appearance and finally break apart, but they do not retract. Zebrafish Rohon-Beard cells apparently fragment their DNA, as revealed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) labeling, before undergoing degenerative morphologic changes. We also followed the development of labeled dorsal root ganglion neurons, as they are developing at the same stages that Rohon-Beard cells are degenerating. We found that, although axons of both cell types extend into similar regions, Rohon-Beard cells degenerate normally in mutants lacking dorsal root ganglia, providing evidence that interactions between the two cell types are not responsible for Rohon-Beard cell degeneration. Developmental Dynamics 229:30-41,2004.     

Influenza vaccination: a collaborative effort to improve the health of the community.

BACKGROUND: The need to improve influenza vaccination delivery in our community became painfully clear during the winter of 1997-1998 when high rates of respiratory illness led to congestion in the emergency department and a critical shortage of hospital beds. In response, the local hospital and the Department of Health launched a collaborative program to increase influenza vaccine coverage in the community. METHODS: The partnership was designed to increase the number of citizens receiving influenza vaccine and to moderate the severity of lower respiratory tract illness during the winter season. A variety of methods were used to increase public awareness, enhance vaccine delivery, and create a relatively seamless service for the community. RESULTS: During three seasons, influenza vaccination rates increased by a relative 150%. This represented immunization of 16% of the entire community and more than 75% of residents older than 65 years. Hospital employee vaccination rates also rose from 34% to 58%. When compared with other hospitals in the county, the campaign reduced the average number of annual visits to the emergency department for all respiratory diagnoses by 34% and exacerbations of chronic obstructive pulmonary disease by 46%. CONCLUSIONS: This influenza vaccination program illustrates the potential for synergy that exists between local departments of health and community hospitals in successfully increasing vaccine delivery to the community. Furthermore, it also suggests that such efforts can be successful in reducing use of the emergency department, resulting in a positive impact on the health of the community.     

Effects of weight loss in overweight/obese individuals and long-term lipid outcomes – a systematic review

This paper aims to review the evidence for long‐term effectiveness of weight loss on cholesterol, high‐density lipoprotein (HDL), low‐density lipoprotein (LDL) and triglycerides in overweight/obese people. Current evidence is mostly based on short‐term studies. A systematic review of long‐term lipid outcomes of weight loss in studies published between 1966 and 2001, was conducted. Inclusion criteria included all cohort studies and trials carried out on participants with body mass index of greater than or equal to 28 kg m^?2. Studies had at least two weight change measurements and follow‐up of more than 2 years. Thirteen long‐term studies with a follow‐up of more than 2 years were included. Cholesterol has a significant positive linear relationship with weight change (r = 0.89) where change in weight explains about 80% of the cholesterol difference variation (Adj R² = 0.80). For every 10 kg weight loss a drop of 0.23 mmol L^?1 in cholesterol may be expected for a person suffering from obesity or are grossly overweight. Weight loss has long‐term beneficial effects especially on LDL and cholesterol. Weight loss in obese patients should be encouraged and sustained.     

Flow-induced cerebral vasodilatation in vivo involves activation of phosphatidylinositol-3 kinase, NADPH-oxidase, and nitric oxide synthase.

Reactive oxygen species (ROS) such as superoxide (O2*-) and hydrogen peroxide (H2O2) are known cerebral vasodilators. A major source of vascular ROS is the flavin-containing enzyme nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase. Activation of NADPH-oxidase leads to dilatation of the basilar artery in vivo via production of H2O2, but the endogenous stimuli for this unique vasodilator mechanism are unknown. Shear stress is known to activate both NADPH-oxidase and phosphatidylinositol-3 kinase (PI3-K) in cultured cells. Hence, this study used a cranial window preparation in anesthetized rats to investigate whether increased intraluminal blood flow could induce cerebral vasodilatation via the activation of NADPH-oxidase and/or PI3-K. Bilateral occlusion of the common carotid arteries to increase basilar artery blood flow caused reproducible, reversible vasodilatation. Topical treatment of the basilar artery with the NADPH-oxidase inhibitor diphenyleneiodonium (DPI) (0.5 and 5 micromol/L) inhibited flow-induced dilatation by up to 50% without affecting dilator responses to acetylcholine. Treatment with the H2O2 scavenger, catalase similarly attenuated flow-induced dilatation, suggesting a role for NADPH-oxidase-derived H2O2 in this response. The nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) partially reduced flow-induced dilatation, and combined treatment with a ROS inhibitor (DPI or catalase) and L-NAME caused a greater reduction in flow-induced dilatation than that seen with any of these inhibitors alone. Flow-induced dilatation was also markedly inhibited by the PI3-K inhibitor, wortmannin. Increased O2*- production in the endothelium of the basilar artery during acute increases in blood flow was confirmed using dihydroethidium. Thus, flow-induced cerebral vasodilatation in vivo involves production of ROS and nitric oxide, and is dependent on PI3-K activation.