Arterial blood pressure response to heavy resistance exercise

The purpose of this study was to record the blood pressure response to heavy weight-lifting exercise in five experienced body builders. Blood pressure was directly recorded by means of a capacitance transducer connected to a catheter in the brachial artery. Intrathoracic pressure with the Valsalva maneuver was recorded as mouth pressure by having the subject maintain an open glottis while expiring against a column of Hg during the lifts. Exercises included single-arm curls, overhead presses, and both double- and single-leg presses performed to failure at 80, 90, 95, and 100% of maximum. Systolic and diastolic blood pressures rose rapidly to extremely high values during the concentric contraction phase for each lift and declined with the eccentric contraction. The greatest peak pressures occurred during the double-leg press where the mean value for the group was 320/250 mmHg, with pressures in one subject exceeding 480/350 mmHg. Peak pressures with the single-arm curl exercise reached a mean group value of 255/190 mmHg when repetitions were continued to failure. Mouth pressures of 30-50 Torr during a single maximum lift, or as subjects approached failure with a submaximal weight, indicate that a portion of the observed increase in blood pressure was caused by a Valsalva maneuver. It was concluded that when healthy young subjects perform weight-lifting exercises the mechanical compression of blood vessels combines with a potent pressor response and a Valsalva response to produce extreme elevations in blood pressure. Pressures are extreme even when exercise is performed with a relatively small muscle mass.     

Comparison of the functional and numerical responses of resistant versus non-resistant populations of the copepod Acartia hudsonica fed the toxic dinoflagellate Alexandrium tamarense

The functional and numerical responses of grazers are key pieces of information in predicting and modeling predator–prey interactions. It has been demonstrated that exposure to toxic algae can lead to evolved resistance in grazer populations. However, the influence of resistance on the functional and numerical response of grazers has not been studied to date. Here, we compared the functional and numerical responses of populations of the copepod Acartia hudsonica that vary in their degree of resistance to the toxic dinoflagellate Alexandrium tamarense. In common environment experiments carried out after populations had been grown under identical conditions for several generations, female copepods were offered solutions containing different concentrations of either toxic A. tamarense or the non-toxic green flagellate Tetraselmis sp. ranging from 25 to 500 μgC L⁻¹, and ingestion and egg production rates were measured. Throughout most of the range of concentrations of the toxic diet, copepod populations that had been historically exposed to toxic blooms of Alexandrium exhibited significantly higher ingestion and egg production rates than populations that had little or no exposure to these blooms. In contrast, there were no significant differences between populations in ingestion or egg production for the non-toxic diet. Hence, the between population differences in functional and numerical response to A. tamarense were indeed related to resistance. We suggest that the effect of grazer toxin resistance should be incorporated in models of predator and toxic prey interactions. The potential effects of grazer toxin resistance in the development and control of Alexandrium blooms are illustrated here with a simple simulation exercise.     

Genetic mapping of meander tail, a mouse mutation affecting cerebellar development

The meander tail mouse harbors a recessive mutation on chromosome 4 that affects the anterior lobes of the cerebellum and the caudal vertebrae. Examination of the mea/mea cerebellum reveals that the complete disorganization of all cell types seen in the anterior lobes is separated by a sharp and consistent boundary from the normal cytoarchitecture of the posterior lobes. In the absence of any biochemical information regarding the affected gene product, attempts to clone the gene must rely on the strategy of reverse genetics. As an initial step in this process we have constructed a genetic linkage map spanning 68 cM of chromosome 4 using an intersubspecific phenotypic backcross. The loci included in this analysis are Calb, Ggtb, Lv, b, Ifa, mea, D4Rp1, Glut-1, Lck, Lmyc-1, and Eno-1. This analysis positions the mea phenotypic locus in the interval between Ifa and Glut1. These results also further define regions of homology between mouse chromosome 4 and human chromosomes 8, 1, and 9. This linkage map provides the means to evaluate candidate genes, and to identify tightly linked markers useful for cloning the meander tail locus.     

Interactions between Kar2p and Its Nucleotide Exchange Factors Sil1p and Lhs1p Are Mechanistically Distinct

Kar2p, an essential Hsp70 chaperone in the endoplasmic reticulum of Saccharomyces cerevisiae, facilitates the transport and folding of nascent polypeptides within the endoplasmic reticulum lumen. The chaperone activity of Kar2p is regulated by its intrinsic ATPase activity that can be stimulated by two different nucleotide exchange factors, namely Sil1p and Lhs1p. Here, we demonstrate that the binding requirements for Lhs1p are complex, requiring both the nucleotide binding domain plus the linker domain of Kar2p. In contrast, the IIB domain of Kar2p is sufficient for binding of Sil1p, and point mutations within IIB specifically blocked Sil1p-dependent activation while remaining competent for activation by Lhs1p. Taken together, these results demonstrate that the interactions between Kar2p and its two nucleotide exchange factors can be functionally resolved and are thus mechanistically distinct.     

Prostaglandin inhibition of cyclic-AMP accumulation and rate of lipolysis in fat cells

A direct relationship between the rate of cyclic AMP accumulation for 2 minutes and the rate of free fatty acid mobilization for 20 minutes was found in rat isolated fat cells stimulated with norepinephrine or theophylline. The concentration-dependent inhibition of cAMP accumulation by prostaglandin E₂ was reflected in proportional inhibition of lipolysis. These data suggest that the anti-lipolytic mechanism of action of prostaglandin E₂ is mediated by inhibition of the early rate of cAMP accumulation rather than the total production of cAMP.