Improvement of the thermoregulation efficiency of man above 1500 m altitude

Zusammenfassung Nachweis, dass vor allem atmosphärische Abkühlungsfaktoren Asthmaanfälle auslösen können und dass der menschliche Organismus über einer kritischen Höhe von 1500 m gegen solche Temperaturreize weniger empfindlich ist. Permanente Besserung nach wiederholter Höhenbehandlung.     

The plasma volume of the Wistar rat in relation to the body weight

Summary The plasma volume of 43 male Wistar rats, weighing between 140 and 350 g, was determined. A close linear relationship between plasma volume and body weight was found: plasma volume (ml)=0.0291×body weight (g)+2.54.Acknowledgment. The excellent assistance of Mr J.S. Bouwer in animal experiments is gratefully acknowledged.     

岷江上游花椒地/林地边界土壤水分分布及影响域

在岷江上游干旱河谷区选取典型的花椒地,林地边界,利用TDR仪测定干旱条件下和雨后0-15cm表土层水分体积分数,刻画沿样带梯度土壤水分分布以及不同时段土壤水分变化,同时用移动窗口法判定土壤水分的边界影响域。结果表明,在干旱河谷区土壤水分体积分数较低并沿样带存在明显的变化,从林地到边界到花椒地土壤水分体积分数基本呈“V”字型变化;而在林地和花椒地内部,水分体积分数呈“W”型波动。干旱时土壤水分体积分数日间变化不大,而雨后水分体积分数逐日递减。土壤水分的影响域在雨后可达14m,干旱时为8m。     

Inapparent infections and cholera dynamics

In many infectious diseases, an unknown fraction of infections produce symptoms mild enough to go unrecorded, a fact that can seriously compromise the interpretation of epidemiological records. This is true for cholera, a pandemic bacterial disease, where estimates of the ratio of asymptomatic to symptomatic infections have ranged from 3 to 100 (refs 1-5). In the absence of direct evidence, understanding of fundamental aspects of cholera transmission, immunology and control has been based on assumptions about this ratio and about the immunological consequences of inapparent infections. Here we show that a model incorporating high asymptomatic ratio and rapidly waning immunity, with infection both from human and environmental sources, explains 50 yr of mortality data from 26 districts of Bengal, the pathogen's endemic home. We find that the asymptomatic ratio in cholera is far higher than had been previously supposed and that the immunity derived from mild infections wanes much more rapidly than earlier analyses have indicated. We find, too, that the environmental reservoir (free-living pathogen) is directly responsible for relatively few infections but that it may be critical to the disease's endemicity. Our results demonstrate that inapparent infections can hold the key to interpreting the patterns of disease outbreaks. New statistical methods, which allow rigorous maximum likelihood inference based on dynamical models incorporating multiple sources and outcomes of infection, seasonality, process noise, hidden variables and measurement error, make it possible to test more precise hypotheses and obtain unexpected results. Our experience suggests that the confrontation of time-series data with mechanistic models is likely to revise our understanding of the ecology of many infectious diseases.     

Evolution of a bacteria/plasmid association

Associations between bacteria and their accessory elements (viruses, plasmids and transposons) range from antagonistic to mutualistic. A number of previous studies have demonstrated that plasmid carriage reduces bacterial fitness in the absence of selection for specific functions such as antibiotic resistance. Many studies have demonstrated increased fitness of evolving microbial populations in laboratory environments, but we are aware of only one study in which fitness gains were partitioned between a plasmid and its host. Here, we examine the evolution of an association between a plasmid and its bacterial host. Carriage of the non-conjugative plasmid pACYC184 initially reduced the fitness of Escherichia coli B in the absence of antibiotic. We then cultured plasmid-bearing bacteria for 500 generations in the presence of antibiotic. The fitness of each combination of host and plasmid, with and without the culture history, was determined by competing it against a baseline strain. The results indicate adaptation by the host genome, but no plasmid adaptation. We also competed the evolved host, transformed with the baseline plasmid, against its isogenic plasmid-free counterpart. The plasmid now increased the fitness of its host.