Sweat gland density and response during high-intensity exercise in athletes with spinal cord injuries

Sweat production is crucial for thermoregulation. However, sweating can be problematic for individuals with spinal cord injuries (SCI), as they display a blunting of sudomotor and vasomotor responses below the level of the injury. Sweat gland density and eccrine gland metabolism in SCI are not well understood. Consequently, this study examined sweat lactate (S-LA) (reflective of sweat gland metabolism), active sweat gland density (SGD), and sweat output per gland (S/G) in 7 SCI athletes and 8 able-bodied (AB) controls matched for arm ergometry VO₂peak. A sweat collection device was positioned on the upper scapular and medial calf of each subject just prior to the beginning of the trial, with iodine sweat gland density patches positioned on the upper scapular and medial calf. Participants were tested on a ramp protocol (7 min per stage, 20 W increase per stage) in a common exercise environment (21±1°C, 45-65% relative humidity). An independent t-test revealed lower (p<0.05) SGD (upper scapular) for SCI (22.3 ±14.8 glands · cm⁻²) vs. AB. (41.0 ± 8.1 glands · cm⁻²). However, there was no significant difference for S/G between groups. S-LA was significantly greater (p<0.05) during the second exercise stage for SCI (11.5±10.9 mmol · l⁻¹) vs. AB (26.8±11.07 mmol · l⁻¹). These findings suggest that SCI athletes had less active sweat glands compared to the AB group, but the sweat response was similar (SLA, S/G) between AB and SCI athletes. The results suggest similar interglandular metabolic activity irrespective of overall sweat rate.     

Inhibition of antigen-induced T-cell proliferation by antibodies to endogenous AKR-MuLV

Lymph node cells from BALB/c mice immunized with ovalbumin or human γ-globulin were restimulated in vitro with these antigens and assayed for antigen-induced proliferation. The proliferative response was shown to be antigen specific and T cell dependent. A rabbit antiserum to envelope and core proteins of AKR murine leukemia virus was found to inhibit antigen-induced T-cell proliferation. The IgG fraction and F(ab′)₂ fragments of the antiserum were also inhibitory. The inhibition occurred after the initial step of antigen-T cell interaction and viral absorption studies showed the inhibition to be specific for anti-AKR virus antibodies. A hypothesis for the mechanism of inhibition is discussed in relation to a functional role for endogenous murine leukemia virus.     

M(III)-facilitated recovery and concentration of enzymes from mesophilic and thermophilic organisms

Six enzymes isolated from organisms of widely differing thermal growth optima were flocculated from solution at constant pH by addition of Fe(III) solution. In all cases the enzyme concentration was 1 g.l-1 or less. Flocculation profiles were generated for each enzyme over a range of Fe(III) levels. The concentrated enzymes were recovered from the Fe(III)/protein complex by solubilisation with citrate and dithionite followed by precipitation with ammonium sulphate. In all cases approximately 70-80% enzyme recovery was achieved. Enzyme thermal stability did not appear to be important and protein concentration had no effect on the efficiency of enzyme recovery over the range of 0.01-1 g.l-1. Approximately 30 mmol Fe(III)/l of enzyme solution facilitated optimal enzyme recovery for all solutions studied. For protein concentrations up to 1 g.l-1 a 100-fold enzyme concentration factor can be expected.     

Genome Sequence of the Emerging Pathogen Helicobacter canadensis

We determined the genome sequence of the type strain of Helicobacter canadensis, an emerging human pathogen with diverse animal reservoirs. Potential virulence determinants carried by the genome include systems for N-linked glycosylation and capsular export. A protein-based phylogenetic analysis places H. canadensis close to Wolinella succinogenes.Helicobacter canadensis is an emerging pathogen that has been isolated from four Canadian patients with diarrhea and an Australian patient with bacteremia (3, 10). Wild geese have been identified as a reservoir in Europe (12, 13), while in China, the organism has been isolated from the feces of wild rodents (5). H. canadensis has also been isolated from laboratory rabbits (11) and from Guinea fowl in France (8). Atypical isolates have been obtained from swine feces from The Netherlands and Denmark (6). To shed light on the virulence and colonization factors of H. canadensis and to reassess its phylogenetic status, we performed whole-genome sequencing of the type strain, H. canadensis strain MIT 98-5491/NCTC 13241.Single- and paired-end whole-genome shotgun sequencing was performed using 454 pyrosequencing technology, supplemented by Solexa sequencing. An initial assembly of the 454 single-end and paired-end data was created using a Newbler assembler (Roche), generating four scaffolds with an average size of 402 kb. The genome sequence was completed using a combination of BLASTX searches and analysis of the Solexa data, followed by confirmatory PCRs, PCR-assisted contig extension (1), and combinatorial PCR, with conventional and long-PCR protocols. Annotation was performed using GenDB (7).The genome of H. canadensis NCTC 13241 consists of a single circular chromosome 1,623,845 bp in length, with a G+C content of 34%. There are 1,535 protein-coding sequences (CDSs), 40 transfer RNAs, and three rRNA loci.Although phylogenetic analyses based on 16S rRNA gene sequences place H. canadensis in the genus Helicobacter (3), analysis of 23S rRNA sequences supports a clade containing H. canadensis and Wolinella succinogenes (2). Our own phylogenetic analysis using a concatenation of 482 conserved CDSs from the H. canadensis genome and related genomes provides strong support for a W. succinogenes/H. canadensis clade (data not shown), suggesting that the current taxonomy should be reevaluated.One hundred seventeen CDSs from H. canadensis have no detectable ortholog in eight other genome-sequenced epsilonproteobacteria. We found only one contiguous region of difference longer than 10 genes (ROD1; HCAN_0630-HCAN_0663). Most CDSs in ROD1 are of unknown function, although, curiously, the region carries three versions of asparagine synthetase and contains six homopolymeric tracts. A second region of difference (ROD2; HCAN_0479-HCAN_0496) shows homology to HHGI1, a pathogenicity island from Helicobacter hepaticus strain ATCC 51449 that contributes to virulence in H. hepaticus (4).The H. canadensis NCTC 13241 genome contains 29 potentially phase-variable genes with homopolymeric tracts, including several genes that, by homology, might be implicated in virulence, e.g., an immunoglobulin A protease (HCAN_0234) and two homologues of the vacuolating cytotoxin from Helicobacter pylori (HCAN_0457 and HCAN_714). The genome contains a capsular polysaccharide export locus similar to that in Campylobacter jejuni (9). Also, like C. jejuni, H. canadensis possesses genes encoding an N-linked glycosylation pathway, including two copies of PglB (HCAN_0729 and HCAN_0930).     

Quantifying the historic contribution of Olympia oysters to filtration in Pacific Coast (USA) estuaries and the implications for restoration objectives

The Olympia oyster, Ostrea lurida Carpenter, was formerly widespread in many US Pacific coast estuaries. Following dramatic declines in the late 1800s and early 1900s, this species is now the focus of renewed restoration efforts. Restoration is undertaken for brood stock rehabilitation as well as a range of ecosystem services such as filtration; however, these ecosystem services are as yet poorly quantified. We present the first laboratory measurements of filtration rates (FR) for O. lurida, to which we fit a model of FR as a function of dry tissue weight and water temperature. We find that O. lurida has a FR at optimum temperature similar to previously established means across oyster species at 1 g dry tissue weight (DTW), but lower than many Crassostrea species. We also find that the allometric exponent relating FR to DTW in O. lurida is lower than the previously published mean across oyster species. Based on our derived filtration rates and historical data, we estimate the historic impact of filtration by O. lurida in five Pacific coast estuaries. We find that historic O. lurida populations did not have the capacity to filter the full volume of the estuary within the estuary residence time in any of the estuaries examined. This result is primarily driven by the low water temperatures and the short estuary residence times that typify the Pacific coast. We conclude that, unlike Crassostrea virginica Gmelin on the Atlantic and Gulf coasts, the Olympia oyster was not historically a dominant force in regulating seston concentrations at large scales in Pacific coast estuaries. Given the differences in the ecological role and habitat structure of these two oyster species, we recommend that analogies between them be drawn with caution. We discuss the implications of our results for developing restoration objectives.