1 alpha, 25-Dihydroxyvitamin D3 directly induces fusion of alveolar macrophages by a mechanism involving RNA and protein synthesis, but not DNA synthesis

The results of our present study indicate that 1 alpha, 25-dihydroxyvitamin D3[1 alpha, 25(OH)2D3] directly induces fusion of mouse alveolar macrophages without any participation of T-lymphocytes by a mechanism involving RNA and protein synthesis but not DNA synthesis. We have reported that 1 alpha, 25(OH)2D3 induces fusion of alveolar macrophages by a direct mechanism and by a spleen cell-mediated indirect mechanism [(1983) Proc. Natl. Acad. Sci. USA 80, 5583-5587]. Alveolar macrophages pretreated with or without anti-Thy 1.2 antibody and complement fused similarly when they were incubated with 1 alpha, 25(OH)2D3. The vitamin suppressed DNA synthesis, but it significantly enhanced RNA and protein synthesis. The 1 alpha, 25(OH)2D3-induced fusion was blocked by adding actinomycin D or cycloheximide, but not by hydroxyurea.     

Spatial distribution of dispersing animals

Summary A mathematical model for the dispersal of an animal population is presented for a system in which animals are initially released in the central region of a uniform field and migrate randomly, exerting mutually repulsive influences (population pressure) until they eventually become sedentary. The effect of the population pressure, which acts to enhance the dispersal of animals as their density becomes high, is modeled in terms of a nonlinear-diffusion equation. From this model, the density distribution of animals is obtained as a function of time and the initial number of released animals. The analysis of this function shows that the population ultimately reaches a nonzero stationary distribution which is confined to a finite region if both the sedentary effect and the population pressure are present. Our results are in good agreement with the experimental data on ant lions reported by Morisita, and we can also interpret some general features known for the spatial distribution of dispersing insects.     

Circadian Rhythm of Cardiac Output, Peripheral Vascular Resistance, and Related Variables by a Beat-to-Beat Monitoring

This study aimed to explore the 24-h patterns of stroke volume, cardiac output, and peripheral vascular resistance along with other correlated variables, such as left ventricular ejection time, ejection velocity index, thoracic fluid index, heart rate, and blood pressure. The study was performed on 12 clinically healthy subjects by means of a noninvasive beat-to-beat monitoring using the thoracic electric bioimpedance technique associated with the automated sphygmomano-metric recording. Time data series were analyzed by means of chronobiological procedures. The results documented the occurrence of a circadian rhythm for all the variables investigated, giving relevance to the beat-to-beat bioperiodicity of cardiac output and peripheral vascular resistance. Temporal quantification of the investigated variables may be useful for a better insight of the chronophysiology of the cardiovascular apparatus.     

城镇化进程中居民生活消费的生态环境压力评估—— 以江苏省江阴市为例

消费问题是区域生态环境压力增大和生态环境问题产生的根本原因。提出人口环境消费的概念和理论模型,并在生态足迹理论和方法的支撑下分别计算江苏省江阴市1997～2004年城镇居民和农村居民生活消费的环境压力;采用SPSS14.0软件,分析城镇和农村居民这两类人群人均环境消费的变化规律及其影响因素,并通过建立多元线性回归预测模型,估算在城镇化快速发展的情况下江阴市人口环境消费期望值。研究表明：江阴市城镇居民人均环境消费从1997年的1.395hm^2上升到2004年的1.960hm^2,年均递增0.081hm^2;农村居民则从1997年的1.345hm^2上升到2004年的1.465hm^2,年均递增0.017hm^2。城乡居民人均环境消费与人均可支配收入、人均受教育年限、恩格尔系数、人均地区生产总值等社会经济指标呈显著线性相关。预计到2010年城乡居民人均环境消费将分别达到2.258hm^2和1.919hm^2,到2020年将分别达到2.807hm^2和2.303hm2;2010年和2020年区域生态赤字将比2004年分别增长55%和107%,给区域生态环境造成巨大压力。为有效缓解区域环境压力,论文提出合理控制区域人口规模和城镇化发展速度,大力发展生态产业,培养可持续消费观念,引导绿色、健康和环境友好型的消费模式等对策措施。     

Relationship of visceral adiposity to cardiovascular disease risk factors in black and white teens

Objective: We tested the hypothesis that visceral adiposity, compared with general adiposity, would explain more of the variance in cardiovascular disease (CVD) risk factors. Research Method and Procedures: Subjects were 464 adolescents (238 black and 205 girls). Adiposity measures included visceral adipose tissue (VAT; magnetic resonance imaging), percent body fat (%BF; DXA), BMI, and waist girth (anthropometry). CVD risk factors were fasting insulin, fibrinogen, total to high‐density lipoprotein‐cholesterol ratio, triglycerides (TGs), systolic blood pressure, and left ventricular mass indexed to height^2.7. Results: After adjustment for age, race, and sex, all adiposity indices explained significant proportions of the variance in all of the CVD risk factors; %BF tended to explain more variance than VAT. Regression models that included both %BF and VAT found that both indices explained independent proportions of the variance only for total to high‐density lipoprotein‐cholesterol ratio. For TGs, the model that included both %BF and VAT found that only VAT was significant. For systolic blood pressure and left ventricular mass indexed to height^2.7, anthropometric measures explained more of the variance than VAT and %BF. Discussion: The hypothesis that visceral adiposity would explain more variance in CVD risk than general adiposity was not supported in this relatively large sample of black and white adolescents. Only for TGs did it seem that VAT was more influential than %BF. Perhaps the deleterious effect of visceral adiposity becomes greater later in life as it increases in proportion to general adiposity.     

On the role of NMDA receptors in blood pressure regulation in spontaneously hypertensive rats (SHR)

Summary In the present study the binding of [³H]MK-801 to glutamatergic receptors of the NMDA type was compared in spontaneously hypertensive (SHR) and normotensive (WKY) rats in various brain structures (including nucleus tractus solitarii) by quantitative receptor autoradiography. Additionally, blood pressure changes after treatment with the NMDA antagonist MK-801 were studied in both strains. There were no differences between SHR and WKY rats either in the level of [³H]MK-801 binding or in the hypertensive reaction to MK-801.     

Mechanical Testing of Mouse Carotid Arteries: from Newborn to Adult

The large conducting arteries in vertebrates are composed of a specialized extracellular matrix designed to provide pulse dampening and reduce the work performed by the heart. The mix of matrix proteins determines the passive mechanical properties of the arterial wall¹. When the matrix proteins are altered in development, aging, disease or injury, the arterial wall remodels, changing the mechanical properties and leading to subsequent cardiac adaptation². In normal development, the remodeling leads to a functional cardiac and cardiovascular system optimized for the needs of the adult organism. In disease, the remodeling often leads to a negative feedback cycle that can cause cardiac failure and death. By quantifying passive arterial mechanical properties in development and disease, we can begin to understand the normal remodeling process to recreate it in tissue engineering and the pathological remodeling process to test disease treatments.Mice are useful models for studying passive arterial mechanics in development and disease. They have a relatively short lifespan (mature adults by 3 months and aged adults by 2 years), so developmental³ and aging studies⁴ can be carried out over a limited time course. The advances in mouse genetics provide numerous genotypes and phenotypes to study changes in arterial mechanics with disease progression⁵ and disease treatment⁶. Mice can also be manipulated experimentally to study the effects of changes in hemodynamic parameters on the arterial remodeling process⁷. One drawback of the mouse model, especially for examining young ages, is the size of the arteries. We describe a method for passive mechanical testing of carotid arteries from mice aged 3 days to adult (approximately 90 days). We adapt a commercial myograph system to mount the arteries and perform multiple pressure or axial stretch protocols on each specimen. We discuss suitable protocols for each age, the necessary measurements and provide example data. We also include data analysis strategies for rigorous mechanical characterization of the arteries.     

Possible involvement of neuronal nitric oxide synthase enzyme in early-phase isoflurane-induced hypotension in rats

This study was conducted to demonstrate the involvement of nitric oxide synthase (NOS) in the early-phase isoflurane-induced hypotension and to ascertain whether this NOS is neuronal NOS (nNOS) or endothelial NOS (eNOS). Mean arterial pressures (MAPs) were directly measured from the femoral arteries of urethane-anesthetized rats. Isoflurane-induced changes in MAP were monitored in rats following pretreatment with vehicle or one of the following NOS inhibitors: L-N^G-monomethyl-L-arginine (L-NMMA), which is non-selective; L-N^G-nitro arginine (L-NOARG), which is more selective for nNOS and eNOS; and 7-nitroindazole (7-NI), which is selective for nNOS. Exposure to 2% isoflurane in oxygen produced a triphasic reduction in MAP, including an early phase in which mean arterial pressure (MAP) fell by 25-30% during the initial 2½ min. This early hypotensive response, but not subsequent phases, was abolished by i.v. pretreatment with either L-NMMA or L-NOARG. The early-phase hypotension was also significantly attenuated by i.p. pretreatment with 7-NI; however, the blockade was not as complete as with L-NMMA or L-NOARG. Cerebella and aorta were removed from vehicle- and 7-NI pretreated rats and assayed for NOS activity by determining the conversion of [¹⁴C]L-arginine to [¹⁴C]L-citrulline. The 7-NI pretreatment significantly reduced NOS activity in the cerebellum but not the aorta. These findings indicate that the early-phase isoflurane-induced hypotension may involve nNOS as well as eNOS. The nNOS may participate in regulation of isoflurane-induced neuronal release of endogenous opioid peptide, which produces a vasodilation that is dependent on NO derived from an action of eNOS.