Active recovery attenuates the fall in sweat rate but not cutaneous vascular conductance after supine exercise.

The purpose of this study was to identify whether baroreceptor unloading was responsible for less efficient heat loss responses (i.e., skin blood flow and sweat rate) previously reported during inactive compared with active recovery after upright cycle exercise (Carter R III, Wilson TE, Watenpaugh DE, Smith ML, and Crandall CG. J Appl Physiol 93: 1918-1929, 2002). Eight healthy adults performed two 15-min bouts of supine cycle exercise followed by inactive or active (no-load pedaling) supine recovery. Core temperature (T(core)), mean skin temperature (T(sk)), heart rate, mean arterial blood pressure (MAP), thoracic impedance, central venous pressure (n = 4), cutaneous vascular conductance (CVC; laser-Doppler flux/MAP expressed as percentage of maximal vasodilation), and sweat rate were measured throughout exercise and during 5 min of recovery. Exercise bouts were similar in power output, heart rate, T(core), and T(sk). Baroreceptor loading and thermal status were similar during trials because MAP (90 +/- 4, 88 +/- 4 mmHg), thoracic impedance (29 +/- 1, 28 +/- 2 Omega), central venous pressure (5 +/- 1, 4 +/- 1 mmHg), T(core) (37.5 +/- 0.1, 37.5 +/- 0.1 degrees C), and T(sk) (34.1 +/- 0.3, 34.2 +/- 0.2 degrees C) were not significantly different at 3 min of recovery between active and inactive recoveries, respectively; all P > 0.05. At 3 min of recovery, chest CVC was not significantly different between active (25 +/- 6% of maximum) and inactive (28 +/- 6% of maximum; P > 0.05) recovery. In contrast, at this time point, chest sweat rate was higher during active (0.45 +/- 0.16 mg.cm(-2).min(-1)) compared with inactive (0.34 +/- 0.19 mg.cm(-2).min(-1); P < 0.05) recovery. After exercise CVC and sweat rate are differentially controlled, with CVC being primarily influenced by baroreceptor loading status while sweat rate is influenced by other factors.     

A common genetic variant in the neurexin superfamily member CNTNAP2 increases familial risk of autism

Autism is a childhood neuropsychiatric disorder that, despite exhibiting high heritability, has largely eluded efforts to identify specific genetic variants underlying its etiology. We performed a two-stage genetic study in which genome-wide linkage and family-based association mapping was followed up by association and replication studies in an independent sample. We identified a common polymorphism in contactin-associated protein-like 2 (CNTNAP2), a member of the neurexin superfamily, that is significantly associated with autism susceptibility. Importantly, the genetic variant displays a parent-of-origin and gender effect recapitulating the inheritance of autism.     

Optimal conditions for breaking medically important yeasts by an inexpensive and simple method

Conditions for breaking various medically important yeasts using glass beads, 30 ml Corex centrifuge tubes, and a Vortex mixer were determined. From 75–95% ofCandida hyphal cells and all species of yeasts exceptSporothrix schenckii were broken when 10 g of 0.45–0.50 mm glass beads, 50–300 mg of wet cells in 5 ml of buffer, and 90 s of vortexing were employed. Yeasts ofSporothrix schenckii broke more efficiently when 0.25–0.30 mm beads were used.     

Regional changes in amino acid content in developing rat brain

Abstract— The content of several amino acids was measured in five discrete regions of the central nervous system of the developing rat, using a [³H]dansylation assay procedure. Both regional differences in amino acid content and regional differences in rate of change of amino acids during maturation were found. Particularly prominent were the maturational changes and high adult contents of glutamic acid in the cerebral cortex, GABA in the hypothalamus, and aspartic acid in the medulla.     

Developmental partitioning of SYK and ZAP70 prevents autoimmunity and cancer

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Percent satellite DNA as a function of tissue and age of mice.

A selective loss of satellite DNA was found to occur to different extents as a function of tissue and age of mice using several common DNA extraction and purification procedures. This result emphasizes a serious problem that may be encountered in comparative studies of DNA structure and composition if selective loss of specific DNA sequences occurs. We have developed a DNA extraction and purification procedure that is simple and reliable and gives a high percent DNA yield, which substantially reduces the selective loss of heterochromatin DNA sequences. The method features a centrifugation step of a proteolytic digest of chromatin in 2.4 M CsCl. Percent DNA yield of 82-98% are routinely obtained with no apparent loss of satellite DNA sequences from different tissues or ages of mice. Utilizing this method, percent satellite DNA was found to remain essentially constant at 11 +/- 1% for spleen, kidney, and brain tissues obtained from mice of 10-780 days of age. However, for liver, percent satellite DNA remained at about 7-8% from 10 to 300 days of age and then increased to about 12-13% from 300 to 600 days of age. During this latter time interval (300-600 days), an increase of DNA per nucleus of about 3-fold occurred, due to the formation of tetra- and octaploid cell types. A steady loss in the total number of nuclei per gram of liver as a function of age was also found. These two opposing effects resulted in a nearly constant amount of DNA per gram and per organ for liver throughout the lifespan of the mouse.     

Mammalian Raf-1 is activated by mutations that restore Raf signaling in Drosophila.

An interaction with the Ras proto-oncogene product is a requirement for Raf-1 activation in many signaling cascades. The significance of this interaction is demonstrated by the fact that a mutation preventing the Ras-Raf interaction severely impairs the function of both mammalian (Raf-1) and Drosophila (D-Raf) Raf proteins. In D-Raf, however, dominant intragenic mutations have been identified that suppress the effect of the Ras-binding site (RBS) mutation. To address the mechanism by which these mutations restore Raf signaling, we have introduced the suppressor mutations into the analogous residues of mammalian Raf-1. Here, we show that rather than compensating for the RBS mutation by restoring the Ras-Raf-1 interaction, the suppressor mutations increase the enzymatic and biological activity of Raf-1, allowing Raf-1 to signal in the absence of Ras binding. Surprisingly, we find that while one of the suppressor mutations (P181L) increases the basal kinase activity of Raf-1, it also abolishes the ability of wild-type Raf-1 to become activated by Ras. This mutation occurs in the cysteine-rich domain (CRD) of Raf-1 and demonstrates the importance of this region for a productive Ras-Raf interaction. Finally, we present evidence that the most activating suppressor mutation (G498S) increases Raf-1 activity by introducing a novel phosphorylation site into the L12 activation loop of the Raf-1 kinase domain.