Oligotrophic properties of heterotrophic bacteria and in situ heterotrophic activity in pelagic seawates

Abstract The distribution of heterotrophic bacteria in polluted coastal and unpolluted pelagic seawaters was studied using a ¹⁴C-MPN method with either five of seven kinds of ¹⁴C-organic compounds as substrates. The total number of heterotrophic bacteria in pelagic waters ranged from 9.2 × 10³ to 5.4. ¢ 10⁴ cell/ml and more than 85% of the heterotrophic bacteria were represented by obligate oligotrophs. In coastal waters, the number of heterotrophs was one order of magnitude higher (av. 3.5 ¢ 10⁵ cells/ml), and eutrophic and facultatively oligotrophic bacteria were predominant. Oligotrophs in pelagic waters had a high specificity for the utilization of amino acids, especially glycine, and acetate-utilizing bacteria were scarce. The in situ maximum uptake rates of glutamate and glycine were much higher than those of glycolate and acetate. Acetate uptake rates were extremely low or not detectable in pelagic waters. The specificity of uptake kinetics is assumed to depend on the existence of obligate oligotrophs as dominant bacteria in pelagic seawater.     

Selective modification of positive chemotaxis in the true slime mold Physarum polycephalum by ethylenediaminetetraacetic acid treatment.

The plasmodium of the true slime mold Physarum polycephalum was treated with EDTA or EGTA and the effect of the treatment on the chemotactic response was examined by measuring the chemotactic motive force with the double-chamber method. The results obtained were as follows: (1) The treatment of the plasmodium with 5 mM EDTA (pH 7.0, 20 min) did not give any significant effect on the protoplasmic streaming or motility. (2) The plasmodium treated with EDTA exhibited no chemotactic response to non-electrolyte attractants (D-glucose, D-galactose, D-mannose, and maltose) and negative chemotaxis to electrolyte attractants (cyclic AMP and NaH2PO4). (3) The EDTA treatment gave no effect on the chemotactic response to repellents (D-fructose, NaCl, CaCl2, MgCl2). (4) The EDTA-treated plasmodium exhibited changes in the membrane potential in response to both attractants and repellents as similar to the untreated plasmodium. (5) The treatment of the plasmodium with 5 mM EGTA (pH 7.0, 20 min) gave results similar to those obtained with the EDTA treatment. The results obtained suggested that EDTA (or EGTA) treatment did not affect the receptor sites but modified the transduction mechanism from reception into tactic movement.     

Renal Impairment with Sublethal Tubular Cell Injury in a Chronic Liver Disease Mouse Model

The pathogenesis of renal impairment in chronic liver diseases (CLDs) has been primarily studied in the advanced stages of hepatic injury. Meanwhile, the pathology of renal impairment in the early phase of CLDs is poorly understood, and animal models to elucidate its mechanisms are needed. Thus, we investigated whether an existing mouse model of CLD induced by 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) shows renal impairment in the early phase. Renal injury markers, renal histology (including immunohistochemistry for tubular injury markers and transmission electron microscopy), autophagy, and oxidative stress were studied longitudinally in DDC- and standard diet–fed BALB/c mice. Slight but significant renal dysfunction was evident in DDC-fed mice from the early phase. Meanwhile, histological examinations of the kidneys with routine light microscopy did not show definitive morphological findings, and electron microscopic analyses were required to detect limited injuries such as loss of brush border microvilli and mitochondrial deformities. Limited injuries have been recently designated as sublethal tubular cell injury. As humans with renal impairment, either with or without CLD, often show almost normal tubules, sublethal injury has been of particular interest. In this study, the injuries were associated with mitochondrial aberrations and oxidative stress, a possible mechanism for sublethal injury. Intriguingly, two defense mechanisms were associated with this injury that prevent it from progressing to apparent cell death: autophagy and single-cell extrusion with regeneration. Furthermore, the renal impairment of this model progressed to chronic kidney disease with interstitial fibrosis after long-term DDC feeding. These findings indicated that DDC induces renal impairment with sublethal tubular cell injury from the early phase, leading to chronic kidney disease. Importantly, this CLD mouse model could be useful for studying the pathophysiological mechanisms of sublethal tubular cell injury.     

Molecular conformation of achatin-I, an endogenous neuropeptide containing D-amino acid residue. X-ray crystal structure of its neutral form

The molecular conformation of achatin-I neutral form (H-Gly-D-Phe-Ala-Asp-OH), an endogenous neuropeptide, was elucidated by X-ray crystal analysis. The molecule has a type II' beta-turn structure with the D-Phe-Ala residues at the corner of the bend, which is further stabilized by two NH(Gly)...C gamma = O sigma(Asp) and NH(Asp)...C gamma = O sigma(Asp) intramolecular hydrogen bonds. This turn conformation may be an important feature of achatin-I related to its neuroexcitatory activity.     

Immunoelectron microscopic demonstration of estrogen receptors in osteogenic cells of Japanese quail

Summary The localization of estrogen receptors (ERs) in osteogenic cells was immunoelectron microscopically examined in the femurs of female and estrogen-treated male Japanese quail. An electron dense reaction product showing ER localization was observed in the nuclei of osteoblasts and immature osteocytes in the medullary bone of the female quail. However, reaction product was not seen in the osteoclasts. On the endosteal bone surface of male quail, nuclear reaction product was detected in bone lining cells. After 24 h of estrogen treatment, reaction product was observed in the nuclei of preosteoblasts on the endosteal bone surface. After 48 h, the medullary bone partly appeared along the endosteal surface. Nuclear reaction product was seen in osteoblasts on the medullary bone surface.