Seasonal changes in glycerol content and cold hardiness in two ecotypes of the rice stem borer, Chilo suppressalis, exposed to the environment in the Shonai district, Japan

The rice stem borer, Chilo suppressalis, is divided into at least two ecotypes in Japan, the Shonai ecotype (SN) which is distributed in the northern part of Japan, and the Saigoku ecotype (SG) which is distributed in the southwestern region. Cold hardiness is positively correlated with the level of glycerol in both ecotypes. To investigate whether ecological distribution affects glycerol accumulation and cold hardiness development in these two ecotypes, overwintering larvae of the SN and SG ecotypes were concurrently exposed to the Shonai district. Obvious differences in the progress of glycerol accumulation and cold hardiness development in SN and SG larvae were found in early winter in the Shonai district. The levels of glycerol content and cold hardiness were low in October and high in January in both ecotypes, but those levels were different within this period (November and December) between ecotypes; the levels in SN larvae quickly reached their maximum, whereas, in SG larvae levels increased slowly. Under controlled conditions, the effect of the period of acclimation at 10 degrees C and subsequent low-temperature (5 degrees C) exposure on glycerol accumulation was investigated. These results indicated that glycerol accumulation in SN was stimulated by the progression of diapause termination, whereas a higher cumulative effect on glycerol production in SG was found when diapause was in a deep state.     

Different susceptibility of various immune reactions to suppressive effect in the tumor-bearing state

Summary Suppression of various types of immune reactions including antibody (Ab) production, cell-mediated cytolysis (CMC), and delayed footpad reaction (DFR) was compared in EL-4 lymphoma-bearing syngeneic mice. In the primary response, the suppression of Ab production and CMC was detected 4 days after tumor inoculation, reached a peak on day 8, and then disappeared. The suppression of DFR was detected on day 1 and persisted to day 12. The suppressive effects of tumor-bearing mice could be transferred with sera to normal recipients, and the degree of the suppressive effect in tumor-bearing hosts correlated with the suppressive effect of sera but not with tumor size. In the secondary response, the suppressive effect of the tumor-bearing state was detected only on DFR. Spleen cells of these hosts were able to transfer positive DFR adoptively to normal recipients, indicating the presence of sensitized lymphocytes in the absence of expression. DFR of normal mice in the primary response was suppressed by transfer of sera of tumor-bearing mice befor elicitation, at which time sensitized lymphocytes should already have been raised. The very high susceptibility of DFR to the suppressive effects of the tumor-bearing state may be ascribed to the distinct susceptibility of mononuclear cells, probably of the macrophage series, which are required as secondary cells for expression of DFR. Further studies with Sephadex G-200 fractionation of the sera from the tumor-bearing mice showed that the immunosuppressive activity appeared in the initial fraction containing relatively high-molecular-weight materials.     

Possible involvement of PI3K-dependent pathways in the increased VEGF120 release from osteoblastic cells preloaded with palmitate in vitro

It have been reported that abnormal bone metabolism often occurs in patients with type 2 diabetes, but the underlying mechanisms remain to be elucidated. In recent years dyslipidemia (hyperlipidemia) has been presumed to have an influence on bone metabolism. In addition, the involvements of VEGF and MCP-1 derived from osteoblasts in bone abnormal metabolism were also observed. Thus, we investigated the pathogenic mechanism of this abnormal bone metabolism, which is included in the regulation of VEGF and MCP-1 secretions from osteoblasts, by using UMR-106 osteosarcoma cells as an osteoblast cell model and treating them with palmitate in order to mimic a state of hyperlipidemia.     

Whole-Genome Sequence of the Hypervirulent Clinical Strain Mycobacterium intracellulare M.i.198

We report herein the draft genome sequence of Mycobacterium intracellulare clinical strain M.i.198, which consistently exhibits hypervirulence in human patients, human macrophages in vitro, and immunocompetent mice.     

A human IAP-family gene, apollon, expressed in human brain cancer cells.

IAP is a family of protein that has baculovirus IAP repeat (BIR) domains and inhibits apoptosis. We found a human IAP family gene, which we named Apollon, encoding a huge protein (530 kDa) that contains a single BIR domain and a ubiquitin-conjugating enzyme domain, that is a human homolog of BRUCE. Apollon protein was expressed in four of six brain cancers (gliomas), and one of five ovarian cancers in 38 human cancer cell lines that we examined. Among the brain cancer cell lines, SNB-78 expressed a high level of Apollon, and this cell line shows resistance against various anticancer drugs. Treating SNB-78 cells with antisense oligonucleotide against Apollon reduced the expression of Apollon protein, and significantly sensitized the cells to apoptosis induced by cisplatin and camptothecin. These results suggest that Apollon protects SNB-78 cells from undergoing apoptosis and, at least in part, plays a role in tumorigenesis and drug resistance of this cell line.     

Genetically recessive mutant of human monocytic leukemia U937 resistant to tumor necrosis factor-α-induced apoptosis

Tumor necrosis factor-α (TNF-α) is a cytokine that induces apoptosis in various cell systems by binding to the TNF receptor (TNFR). To study TNF-α-induced apoptosis, we isolated and characterized a novel TNF-α-resistant variant, U937/TNF clone UA, from human monocytic leukemia U937 cells. The UA cells resist apoptosis induced by TNF-α and anti-Fas antibody but not by anticancer drugs, such as VP-16 and Ara-C. Somatic cell hybridization between U937 and UA showed that apoptosis resistance to TNF-α in UA was genetically recessive. The hybridization analysis also showed that UA and another recessive mutant clone, UC, belong to different complementation groups in TNF-α-induced apoptosis signaling. In UA cells, TNF-α-induced disruption of mitochondrial membrane potential and CPP32 activation were abrogated. Expression of TNFR, Fas, and Bcl-2 family proteins was not changed in UA cells. These results suggest that the apoptosis resistant UA cells could have a functional defect in apoptosis signaling from the TNFR to mitochondria and interleukin-1β converting enzyme (ICE) family protease activation. UA cells could be used to study signaling linkage between cell death-inducing receptor and mitochondria. J. Cell. Physiol. 174:179–185, 1998. © 1998 Wiley-Liss, Inc.     

Down-Regulation of KCC2 Expression and Phosphorylation in Motoneurons,and Increases the Number of in Primary Afferent Projections to Motoneurons in Mice with Post-Stroke Spasticity

Spasticity obstructs motor function recovery post-stroke, and has been reported to occur in spinal cord injury and electrophysiological studies. The purpose of the present study was to assess spinal cord circuit spasticity in post-stroke mice. At 3, 7, 21, and 42 d after photothrombotic ischemic cortical injury in C57BL/6J mice, we observed decreased rate-dependent depression (RDD) of the Hoffmann reflex (H reflex) in the affected forelimb of mice compared with the limbs of sham mice and the non-affected forelimb. This finding suggests a hyper-excitable stretch reflex in the affected forelimb. We then performed immunohistochemical and western blot analyses to examine the expression of the potassium-chloride cotransporter 2 (KCC2) and phosphorylation of the KCC2 serine residue, 940 (S940), since this is the main chloride extruder that affects neuronal excitability. We also performed immunohistochemical analyses on the number of vesicular glutamate transporter 1 (vGluT1)-positive boutons to count the number of Ia afferent fibers that connect to motoneurons. Western bolts revealed that, compared with sham mice, experimental mice had significantly reduced KCC2 expression at 7 d post-stroke, and dephosphorylated S940 at 3 and 7 d post-stroke in motoneuron plasma membranes. We also observed a lower density of KCC2-positive areas in the plasma membrane of motoneurons at 3 and 7 d post-stroke. However, western blot and immunohistochemical analyses revealed that there were no differences between groups 21 and 42 d post-stroke, respectively. In addition, at 7 and 42 d post-stroke, experimental mice exhibited a significant increase in vGluT1 boutons compared with sham mice. Our findings suggest that both the down-regulation of KCC2 and increases in Ia afferent fibers are involved in post-stroke spasticity.