From Spencer to E-P: Eyewitnessing the Progress of Fieldwork

Strangers Abroad Series: Sir Walter Baldwin Spencer (1860–1929), Fieldwork; Franz Boas (1858–1952), The Shackles of Tradition; William Rivers (1864–1922), Everything Is Relatives; Bron-islaw Malinowski (1884–1942), Off the Verandah; Margaret Mead (1901–1978), Coming of Age; Sir Edward Evans-Pritchard (1902–1973), Strange Beliefs.     

Exercise training improves lusitropy by isoproterenol in papillary muscles from aged rats

Taffet, George E., Lloyd A. Michael, and Charlotte A. Tate.Exercise training improves lusitropy by isoproterenol in papillarymuscles from aged rats. J. Appl.Physiol. 81(4): 1488-1494, 1996.Aging isassociated with a decreased cardiac responsiveness to -adrenergicstimulation. We examined the effect of endurance exercise training ofold Fischer 344 male rats on -adrenergic stimulation of the functionof isolated left ventricular papillary muscle. Three groups wereexamined: sedentary mature (SM; 12-mo old), sedentary old (SO;23-24 mo old), and exercised old (EO; 23-24 mo old) that weretreadmill trained for 4-8 wk. The isometric contractile propertieswere studied at 0.2 Hz and 0.75 mM calcium. Without -adrenergicstimulation, there were no group differences for peak tension, maximumrate of tension development(+dP/dt), or maximum rateof tension dissipation(dP/dt). The time to peak tension was longer (P < 0.05) forboth EO and SO than for SM rats. Half relaxation time(RT_1/2) was prolonged(P < 0.05) for SO compared with SMand EO (which did not differ). The three groups did not differ in the-adrenergic stimulation by isoproterenol of peak tension,dP/dt, time to peak tension, orcontraction duration. The inotropic response(+dP/dt) of SM was greater(P < 0.05) than that in SO or EOrats (which did not differ); however, the lusitropic response(RT_1/2) was lesser(P < 0.05) in SO than in SM or EO rats (which did not differ). Thus exercise training of old rats improved the lusitropic response to isoproterenol without altering theage-associated impairment in inotropic response.

     

Mixed Infection with cagA-Positive and cagA-Negative Strains of Helicobacter pylori

Background Helicobacter pylori infection has been implicated strongly in the pathogenesis of gastritis, peptic ulcer disease, gastric adenocarcinoma, and gastric lymphoma, but the reasons for these widely different clinical outcomes are unknown. The aim of this study was to determine whether these differences could be due in part to mixed infection in the same individual, with bacteria having differences in pathogenic factors associated with ulcers.
Materials and Methods. The cagA gene of H. pylori was used to test for mixed infection because it is present in only some strains, and its presence has been associated with ulcers. Polymerase chain reaction (PCR) assays for the cagA gene were applied to H. pylori culture isolates and endoscopic gastric aspirates. Individual bacterial clones were tested for genetic similarity by random primer amplification and restriction endonuclease digestion of urease gene PCR products.
Results. The majority of H. pylori -positive patients had strongly cagA -positive culture isolates and endoscopic samples (62.5% and 69.6%, respectively). However, many of these patients had evidence of mixed infection with cagA negative and cagA positive strais in cultures isolates and endoscopic samples (25% and 17.4%, respectively). Mixed infection was found to be due to genetically unrelated strains in two patients in whom genetic analysis was performed.
Conclusion. Mixed infection with differences in substrain pathogenic factors might occur in H. pylori infection and might contribute to differences in clinical outcome.     

Primate terminal complement inhibitor homologues of human CD59

The nucleotide sequence data reported in this paper have been submitted to the GenBank nucleotide sequence database and have been assigned the accession numbers L22862 (African green monkey CD59) and L22863 (baboon CD59)     

Stem deformity inPinus radiata plantations in south-eastern Australia

Plantations of radiata pine (P. radiata D.Don) on soils previously under legume based pastures have a high incidence of stem deformity compared with forest soils. A comparison of soil properties and tree nutrition of 5 to 7 year-old radiata pine on former pastures in the first part of the study showed that stem deformity was strongly correlated with mineralisation of soil N and in particular with nitrification. Other soil properties that have changed as a result of pasture improvement, e.g. pH, available P and Mn, were only partially correlated with stem deformity. In the second part of the study, the role of N availability and other soil properties in the expression of deformity was further investigated in a separate field experiment on soils formerly under native eucalypt forest, tobacco cropping, and improved pasture. Young radiata pine plantings were treated with lime, phosphorus, and nitrogen applied as urea and sodium nitrate. Liming increased soil pH by around 1.5 units, raised exchangeable Ca²⁺ and decreased available Mn. Soil mineral N content was only marginally affected by liming. Superphosphate increased soil available P and raised levels of P in foliage. Changes in soil pH, availability of P, Mn, and B did not affect growth or stem deformity at any of the sites. In contrast, application of N fertilisers at 200 and 600 kg N ha^-1 increased mineral N content and stimulated nitrification, particularly at the forest site. The high rate of N fertiliser increased basal area at the forest site by 45%, but also raised the level of stem deformity from 12% to 56%. At the tobacco and pasture sites, this treatment did not increase growth and did not significantly raise stem deformity above the already high basic level of deformity (63%). Implications of stem deformity in young plantations of radiata pine on potential utilisation later in the rotation are discussed.     

Cloning of the mgtE Mg2+ transporter from Providencia stuartii and the distribution of mgtE in gram-negative and gram-positive bacteria.

The MM281 strain of Salmonella typhimurium possesses mutations in each of its three Mg2+ transport systems, requires 100 mM Mg2+ for growth, and was used to screen a genomic library from the gram-negative bacterium Providencia stuartii for clones that could restore the ability to grow without Mg2+ supplementation. The clones obtained also conferred sensitivity to Co2+, a phenotype similar to that seen with the S. typhimurium corA Mg2+ transport gene. The sequence of the cloned P. stuartii DNA revealed the presence of a single open reading frame, which was shown to express a protein with a gel molecular mass of 37 kDa in agreement with the deduced size of 34 kDa. Despite a phenotype similar to that of corA and the close phylogenetic relationship between P. stuartii and S. typhimurium, this new putative Mg2+ transporter lacks similarity to the CorA Mg2+ transporter and is instead homologous to MgtE, a newly discovered Mg2+ transport protein from the gram-positive bacterium Bacillus firmus OF4. The distribution of mgtE in bacteria was studied by Southern blot hybridization to PCR amplification products. In contrast to the ubiquity of the corA gene, which encodes the dominant constitutive Mg2+ influx system of bacteria, mgtE has a much more limited phylogenetic distribution.     

Transport and control of Ca by pigeon erythrocytes. II. Evidence against a simple feedback control of cell Ca and evidence for the involvement of more than one pool

Cells were subjected to a range of ⁴⁵Ca²⁺ influx loads with A23187. We measured cell ⁴⁵Ca²⁺ with time and A23187 dose, and the apparent ⁴⁵Ca²⁺ influxes (≡“J(in,app)”) at Ca²⁺ steady state. We also measured endogeneous exchangeable and total cell Ca²⁺, which were 50 and 17–220 μM respectively. The effects of A23187 and Ca²⁺ on cell ATP, swelling, net Cl⁻ permeability, and cell morphology were measured. These were modest and do not affect our conclusions.J(in,app) 3 × 10⁻⁴ [A23187]^2.9·[Ca²⁺(o)]μmoles/l·min with 92–552 μM [Ca²⁺(o)] (≡ external Ca²⁺ concentration) and 0–7 μM A23187. J(in,app) was increased an order of magnitude by vanadate and is probably much less than the true influx. The least unlikely explanation found for the high [A23187] exponent, 2.9, was that most of the Ca²⁺ crossing the membrane is expelled by the pump before it can move deeper into the cell.Calcium pumping increased rapidly in response to increased influx, but the steady state cell ⁴⁵Ca²⁺ was approximately proportional to J(in,app) rather than approximately constant between 10 and 120 μmoles/l·min with 184 μM [Ca²⁺(o)]. This is not the result expected from a simple feedback mechanism.At high A23187 doses the pump appears fully activated resulting in a linear relation between cell/medium ⁴⁵Ca²⁺ and [A23187]⁻². From the plot we calculated α≡free/total exchangeable Ca²⁺ = 0.38 ± 0.08 (n = 3) and a maximum pump rate, “Pmax” = 78 μmole/l·min. Pmax is underestimated insofar as J(in,app) is less than the true influx.     

Changes in [3H]inositol-labelled phosphoinositides of pig platelets in response to thrombin

Pig platelet phosphoinositides have been labelled with [³H]inositol and then treated with thrombin in the absence of Ca²⁺. There was a loss of labelled phosphatidylinositol 4,5-bisphosphate between 30 and 60 s after the addition of thrombin but the general picture was of increased labelling over a 4-min period. Labelling of phosphatidylinositol 4-phosphate showed no period of loss but there was an early loss of phosphatidylinositol and no increased labelling during the 4-min incubation. The small amount of lysophosphatidyl[³H]inositol in the platelets was not affected by thrombin treatment. Thrombin caused loss of [¹⁴C]arachidonate-labelled phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol.