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.     

Effect of silymarin and its polyphenolic fraction on cholesterol absorption in rats.

This study evaluated the influence of silymarin (SM) and polyphenolic fraction (PF) of silymarin on cholesterol absorption in rats fed on high cholesterol diet (HCD). HCD induced a remarkable increase in hepatic, plasma, VLDL and LDL cholesterol, a decrease in HDL cholesterol and an elevation in triacylglycerol (TAG) levels in plasma, VLDL and in the liver. SM and PF were administered as dietary supplements (1.0%) in HCD for 18 days. Intestinal cholesterol absorption was measured by dual-isotope plasma ratio method, which calculates percent of cholesterol absorption from the ratio of two labelled cholesterol doses, one given intragastrically (14C) and one intravenously (3H). Silymarin and PF significantly reduced cholesterol absorption in rats fed on HCD and caused significant decreases in plasma and VLDL cholesterol and content of cholesterol and TAG in the liver. The level of HDL cholesterol was significantly increased after silymarin, but not after administration of PF. The levels of TAG in plasma and VLDL were not affected by either silymarin or PF. These results suggest that the inhibition of cholesterol absorption caused by silymarin and its polyphenolic fraction could be a mechanism contributing to the positive changes in plasma cholesterol lipoprotein profile and in lipid content in liver.     

Effect of prostaglandin E1 infusion on leukocyte traffic and fibrosis in acute lung injury induced by bleomycin in hamsters.

OBJECTIVE: To determine whether the iv infusion of prostaglandin E1 (PGE1) could modify the early influx of neutrophils into bleomycin-injured lungs and if that would affect subsequent development of inflammation and fibrosis. BACKGROUND AND METHODS: In vivo controlled animal study performed in a university hospital pulmonary research laboratory. Male Syrian golden hamsters (100- to 110-g body weight) were divided into four treatment groups: a) No treatment; b) intratracheal bleomycin plus PGE1 infusion; c) bleomycin plus saline infusion; d) PGE1 infusion only. PGE1 (180 ng/hr.100 g) or saline were infused iv 3 to 25 hr after intratracheal instillation of bleomycin sulfate (0.5 U/0.5 mL.100 g). Total and differential counts of cells recovered by lavage, lavage fluid protein, and lung total protein and hydroxyproline levels were measured from 6 hr to 30 days later. RESULTS: PGE1 infusion reduced the influx of neutrophils 6 hr after bleomycin injury by 53% compared with saline infusion (p less than .0001), but increased inflammatory cell traffic after 24 hr for 15 days. At 4 days, protein recovered in lung lavage fluid was also decreased in PGE1-treated, bleomycin-injured animals, reflecting reduced injury to lung permeability barriers. Accumulation of lung collagen in the PGE1-treated, bleomycin-instilled hamsters tended to be lower than in the bleomycin-injured, saline-infused group at 15 and 30 days, although these differences did not achieve statistical significance. Despite this fact, greater than 33% of the animals in the PGE1-treated group died, possibly indicating an increased risk of sepsis in these animals. CONCLUSIONS: PGE1 infusion can decrease early neutrophil traffic and reduce injury to the lung permeability barriers. However, this treatment augments late inflammatory events and does not significantly alter the development of fibrosis.