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Biomedical subjects

A Imai

Publications and source records attributed to A Imai.

At least 235 records · Page 13Linked to original sources
PubMed1984

Platelet cyclo-oxygenase deficiency in a Japanese.

A case of platelet cyclo-oxygenase deficiency in a Japanese was investigated. There was a marked decrease of aggregation with collagen and absence of aggregation with epinephrine and arachidonic acid. The platelet response to a labile aggregation stimulating substance (LASS) was normal. There was no biosynthesis of prostaglandin endoperoxides from arachidonate. The platelets, including granular volume, showed no ultrastructural abnormalities. The responses to various inducers of platelet aggregation, except for arachidonate, were different from the cases described by others. It is concluded that the defective platelet function, due to a deficiency of platelet cyclo-oxygenase, is heterogeneous.

Adult↗
PubMed1984

Indigenous microfloras and resistance to bacterial infection in mice with experimentally induced diabetes: a possible animal model for opportunistic infection.

Persistent diabetes was induced in male Slc:ddY mice by a single intraperitoneal injection of 200 mg/kg streptozotocin (STZ). In these mice, the numbers of aerobic gram-negative bacilli, staphylococci (including micrococci), and streptococci increased, while those of other bacteria were almost unchanged in both oral and caecal floras. The mice were vulnerable to oral infection of Salmonella enteritidis, intranasal infection of Klebsiella pneumoniae and Serratia marcescens, and contact infection with mice infected with S. enteritidis and K. pneumoniae. These findings suggest that STZ-treated mice might be a useful model for investigating opportunistic infection.

Alloxan↗
PubMed1984

Endogenous infection in mice with streptozotocin-induced diabetes. A feature of bacterial translocation.

Slc:ddY mice that received a single intraperitoneal injection of 200 mg/kg streptozotocin (STZ) were examined for persistency of diabetes (changes of indigenous bacterial floras, and bacterial translocation. Significant diabetes (increase in plasma glucose and decrease in insulin) was recognized 2 weeks after the injection, and persisted for 12 weeks. The numbers of aerobic gram-negative bacilli, staphylococci (including micrococci), and streptococci in caecal and oral floras were significantly increased, but the numbers of anaerobic bacteria in caecal flora were hardly changed. Bacterial translocation of indigenous bacteria to the mesenteric lymph node, lung, or kidney was detectable in some mice 2 weeks after the injection. The incidence of bacterial translocation in these STZ-treated mice then increased; infection caused by several organisms, e.g., Klebsiella pneumoniae, Staphylococcus epidermidis, streptococci, or Lactobacillus sp., occurred in lung, liver, spleen, kidneys, and mesenteric lymph node. No indigenous bacteria were cultured from these organs of control mice. This endogenous infection may have been due to the over population of several bacterial strains caused by disruption of indigenous floras along with depression of immunological function.

Animals↗
PubMed1984

"Enveloped" rotavirus particles detected in culture fluid.

In a negative contrast preparation of human rotavirus culture fluid were found membrane-bound "enveloped" virus particles which had been observed only in thin sections of the infected cells. The "enveloped" particles comprised a single-shelled particle and degenerating membrane structure.

Cells, Cultured↗
PubMed1984

Effects of cellular Ca2+ depletion on phospholipid turnover and glycogen phosphorylase a in rat hepatocytes.

The influences of changes in cellular Ca2+ level on membrane phospholipid turnover and cellular function (monitored by glycogen phosphorylase a activity) were investigated in vasopressin- and ionophore A23187-stimulated rat hepatocytes. Addition of vasopressin or A23187 to rat hepatocytes in the presence of extracellular Ca2+ enhanced the phosphorylase a activity by 3 to 4-fold within 1 min, returning to initial activity with further incubation. There was the marked generation of 1,2-diacylglycerol resulted from phospholipase C activation, which followed the transient activation of phosphorylase a. When the incorporation of [32P]phosphate into phospholipids was examined, phosphatidylinositol (PI) labeling due to vasopressin-stimulation remained rather unchanged up to 5 min but then rose gradually. On the other hand, A23187 had little effect on the incorporation into phosphatidylinositol although marked phosphatidic acid (PA) labeling was consequently produced, showing inhibitory effect on the conversion of PA to PI. Deprivation of extracellular Ca2+, which also reduced slightly the intracellular Ca2+ from 3.33 micrograms to 1.38 micrograms/10(7) cells, suppressed but not abolished stimuli-induced phosphorylase a activation without affecting the enhancement of phospholipid metabolism. Hepatocytes depleted of intracellular Ca2+ (0.50 microgram/10(7) cells) no longer showed both phosphorylase a activation and the enhancement of phospholipid metabolism. These findings seem to indicate that phosphorylase a activity is more sensitive than membrane phospholipid turnover to changes of intracellular Ca2+ concentration. The results demonstrate that marked and selective changes in membrane phospholipids depending on the type of stimulants occur upon stimulation of hepatocytes and provide the possibility that these reactions do not trigger glycogen phosphorylase a activation through Ca2+ mobilization.

Animals↗
PubMed1983

Possible involvement of 1-acyl-glycerophosphorylinositol acyltransferase in arachidonate enrichment of phosphatidylinositol in human platelets.

Microsomes isolated from human platelets synthesize phosphatidylinositol by the action of acyl-CoA: 1-acyl-sn-glycerol-3-phosphorylinositol(1-acyl-GPI) acyltransferase. The properties of 1-acyl-GPI acyltransferase were compared with those of 1-acyl-glycerophosphorylcholine (1-acyl-GPC) acyltransferase. Apparent Km values of 1-acyl-GPI and 1-acyl-GPC acyltransferases for the corresponding acyl acceptor (lysophospholipid) were 22 and 20 microM, respectively, in the presence of arachidonoyl-CoA as fatty acyl donor. However, the Km value (1.3 microM) of 1-acyl-GPI acyltransferase for arachidonoyl-CoA was much lower than that (5.0 microM) of 1-acyl-GPC acyltransferase. Under optimal conditions, the acylation rate of 1-acyl-GPI with arachidonoyl-CoA was 2-6 times higher than with oleoyl-CoA and linoleoyl-CoA, and was very low with saturated fatty acyl-CoAs. The acylation rates with various acyl-CoAs for 1-acyl-GPI were different from those for 1-acyl-GPC. These results suggest that the reacylation pathway of 1-acyl-GPI participates in the incorporation of arachidonic acid to phosphatidylinositol in platelet microsomes. Furthermore, there were no significant effects of thrombin-activation on acyl-CoA specificity for 1-acyl-GPI and 1-acyl-GPC acyltransferase in human platelets.

Acyl Coenzyme A↗
PubMed1983

Modification of positional distribution of fatty acids in phosphatidylinositol of rabbit neutrophils stimulated with formylmethionyl-leucyl-phenylalanine.

The effects of formylmethionyl-leucyl-phenylalanine (fMet-Leu-Phe) on the positional distribution of fatty acids in phosphatidylinositol (PI), phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were investigated with rabbit neutrophils. The proportion of arachidonate at the C-2 position of PI was 35.0% in resting neutrophils and declined to 30.8% after 5 min stimulation with the peptide at a concentration of 10(-7) M. In contrast, the profiles of the positional distribution of fatty acids in PC and PE were not affected upon stimulation with fMet-Leu-Phe. The phospholipid composition of rabbit neutrophils was examined at different time intervals following the addition of fMet-Leu-Phe. PI and PC, but no other phospholipids, exhibited significant changes in their quantities. The quantity of PC decreased at 5 min with a concurrent increase in that of lysophosphatidylcholine (lysoPC), suggesting a phospholipase A2 action on PC. The quantity of PI, on the other hand, decreased at 1 min with an accompanying increase in phosphatidic acid when the profile of the positional distribution of fatty acids in PI remained unchanged. No lysophosphatidylinositol (lysoPI) was detected. This indicates the enhancement of the PI cycle in the fMet-Leu-Phe-stimulated neutrophils. The augmented PI cycle in response to fMet-Leu-Phe was further supported by the finding that [3H]arachidonyl-diacylglycerol and -phosphatidic acid accumulated at the expense of [3H]arachidonylPI in rabbit neutrophils prelabelled with [3H]arachidonate. Restoration of the content of PI to the higher than the original level at 5 min after stimulation with fMet-Leu-Phe, however, leads to the suggestion that de novo synthesis of PI as well as PI resynthesis along the closed cycle of PI has occurred at 5 min and that this newly synthesized PI, via a de novo pathway with a different pattern of the positional fatty acyl composition, is the cause of the decreased proportion of arachidonate.

Animals↗
PubMed1983

Evidence that cyclic AMP may regulate Ca2+-mobilization and phospholipases in thrombin-stimulated human platelets.

The regulation of human platelet responses by cyclic AMP (cAMP) has been investigated by measuring thrombin-stimulated serotonin release, Ca2+ uptake and phospholipase activity. Thrombin-induced 1,2-diacylglycerol (DG) formation as a result of phospholipase C activation was inhibited by pretreatment with dibutyryl cAMP (dbcAMP) in a dose-dependent manner. Subsequent failure to produce phosphatidic acid (PA), which is converted from 1,2-DG by phosphorylation and would serve as intracellular Ca2+ ionophore, appeared to parallel the decrease in Ca2+ uptake activity. Phospholipase A2 activity, monitored by the production of [3H]lysophosphatidylcholine and [3H]lysophosphatidylethanolamine, was also suppressed by dbcAMP. These data indicate that the intracellular cAMP level may be closely associated with Ca2+ uptake and phospholipases activation. In addition, it is suggested that alteration of intracellular cAMP regulates phospholipase activation and consequently platelet responses, perhaps by controlling available Ca2+ content.

Blood Platelets↗
PubMed1983

Evidence for de novo synthesis of phosphatidylinositol coupled with histamine release in activated rat mast cells.

Phospholipid metabolisms in rat mast cells activated by ionophore A23187 and compound 48/80 were examined with reference to 'phosphatidylinositol (PI) cycle'. The addition of A23187 to [3H]glycerol-prelabeled mast cells induced a marked accumulation of the radioactivity in 1,2-diacylglycerol(DG) and phosphatidic acid(PA) within 10 to 30 sec. A great enhancement of [3H]glycerol incorporation into PA and PI was also detected during histamine release. On the other hand, 48/80 was far less effective than A23187 both in producing 1,2- DG and PA and in accerelating [3H]glycerol incorporation into PA and PI, despite the comparable ability of histamine release. The activity of Ca2+ uptake into mast cells, as measured by pulse-labeling with 45Ca2+, was increased when exposed to both of two agents. These data provide circumstantial evidence that phospholipid metabolisms, mainly de novo PI synthesis, may be a part of the triggering events for Ca2+ mobilization and secretory process. The PI metabolism induced by two different stimulants appears to behave in a different manner.

Animals↗
PubMed1983

The rapid polyphosphoinositide metabolism may be a triggering event for thrombin-mediated stimulation of human platelets.

The metabolism of polyphosphoinositides was examined in human platelets activated by thrombin. The addition of thrombin to [3H]glycerol-labeled platelets induced an initial loss and a subsequent increase of the radioactivity in phosphatidylinositol-4,5-bisphosphate (TPI) without any significant change in phosphatidylinositol-4-phosphate (DPI). A marked enhancement of [32P]Pi incorporation into TPI occurred in parallel with an increase in this lipid content, which was accompanied with a conccurent decrease in phosphatidylinositol (PI). The rate of this subsequent increase in TPI was smaller than that observed in [3H]arachidonic acid-labeled platelets, suggesting that formed TPI in activated platelets may contain much greater amount of arachidonate than preexisting TPI in resting platelets. These data indicate that thrombin causes a rapid change in TPI metabolism (initial degradation of preexisting TPI and subsequent production of arachidonate-rich TPI), which might be a primary candidate to modulate thrombin-induced function in human platelets.

Arachidonic Acid↗
PubMed1983

Influence of temperature and relative humidity on human rotavirus infection in Japan.

A climatologic analysis of human rotavirus infection in inpatients with acute diarrhea was conducted over a seven-year period. The infection frequency appeared to be related to temperature, but not to relative humidity. Human rotavirus infection was found to appear abruptly when the mean temperature of any 10-day period became less than 5 C (November or December), reached a peak when it was less than 0 C (January and February), and waned when it became greater than 20 C (June and July) in the city of Yamagata in northern Japan.

Adolescent↗
PubMed1983

Relationships of volatile components and bacterial flora in mouse caecum.

The relations between volatile components and bacterial flora in mouse caecum were studied in germ-free, gnotobiotic and SPF mice and in gnotobiotes given heated caecal homogenate from SPF mice. Anaerobic fusiform bacteria were present in SPF mice and ex-gnotobiotic (gnotobiotic plus SPF caecum) mice only. Low concentrations of furfural correlated with the presence of intestinal fusiform bacteria, suggesting that furfural may be decomposed by these organisms. Fusiform bacteria were also associated with the highest concentrations of acetic and butyric acids and may play an important role in regulating the composition of the mouse caecal flora.

Acetates↗