Biomedical subjects

Y Honma

Publications and source records attributed to Y Honma.

At least 55 records · Page 3Linked to original sources

PubMed2000

Predictive variables of hypothermia in the early phase of general anesthesia.

UNLABELLED: Core temperature decreases precipitously for 1 h and then decreases slowly for 2-3 h after the induction of general anesthesia. We investigated the predictive variables of hypothermia by measuring peripheral skin temperature and total body fat (TBF). We studied 60 adult patients who required general anesthesia with isoflurane. The following variables were measured preoperatively: right palmar skin temperature by using an infrared thermometer and skin thickness at arm and scapula by using a standard caliper. TBF was calculated by using the regression equation of Durnin and Womersley. Rectal temperature, taken to represent core temperature, was measured during the operation. The gradient of hypothermia induced by general anesthesia was divided into two parts: 1) a precipitous decrease for the first hour and 2) a slow decrease for the following 2-3 h. Preoperative palmar skin temperature had a significant linear relationship with the precipitous decrease in temperature over the first hour (r = 0.69, P < 0.0001), and TBF had a significant linear relationship with the subsequent slow decrease in temperature (r = 0. 63, P < 0.0001). By simple measurements, we can predict the extent of hypothermia in the early phase of general anesthesia and prevent its onset by using body-warming techniques. IMPLICATIONS: After the induction of general anesthesia, palmar skin temperature had a linear relationship with the precipitous decrease in rectal temperature over the first hour, and total body fat had a linear relationship with the subsequent decrease in temperature. Thus, by simple measurements, we can predict the extent of hypothermia in the early phase of general anesthesia.

Aged↗

PubMed2000

Oxalate-degrading Enterococcus faecalis.

An oxalate-degrading Enterococcus faecalis was isolated from human stools under anaerobic conditions. The bacteria required a poor nutritional environment and repeated subculturing to maintain their oxalate-degrading ability. The E. faecalis produced 3 proteins (65, 48, and 40 kDa) that were not produced by non-oxalate-degrading E. faecalis as examined by SDS-PAGE. Antibodies against oxalyl-coenzyme A decarboxylase (65 kDa) and formyl-coenzyme A transferase (48 kDa) obtained from Oxalobacter formigenes (an oxalate-degrading anaerobic bacterium in the human intestine) reacted with 2 of the proteins (65 and 48 kDa) from the E. faecalis as examined by Western blottings. This is the first report on the isolation of oxalate-degrading facultative anaerobic bacteria from humans.

Adult↗

PubMed2000

Cloning, sequencing and expression of the gene encoding the extracellular metalloprotease of Aeromonas caviae.

A gene (apk) encoding the extracellular protease of Aeromonas caviae Ae6 has been cloned and sequenced. For cloning the gene, the DNA genomic library was screened using skim milk LB agar. One clone harboring plasmid pKK3 was selected for sequencing. Nucleotide sequencing of the 3.5 kb region of pKK3 revealed a single open reading frame (ORF) of 1,785 bp encoding 595 amino acids. The deduced polypeptide contained a putative 16-amino acid signal peptide followed by a large propeptide. The N-terminal amino acid sequence of purified recombinant protein (APK) was consistent with the DNA sequence. This result suggested a mature protein of 412 amino acids with a molecular mass of 44 kDa. However, the molecular mass of purified recombinant APK revealed 34 kDa by SDS-PAGE, suggesting that further processing at the C-terminal region took place. The 2 motifs of zinc binding sites deduced are highly conserved in the APK as well as in other zinc metalloproteases including Vibrio proteolyticus neutral protease, Emp V from Vibrio vulnificus, HA/P from Vibrio cholerae, and Pseudomonas aeruginosa elastase. Proteolytic activity was inhibited by EDTA, Zincov, 1,10-phenanthroline and tetraethylenepentamine while unaffected by the other inhibitors tested. The protease showed maximum activity at pH 7.0 and was inactivated by heating at 80 C for 15 min. These results together suggest that APK belongs to the thermolysin family of metalloendopeptidases.

Aeromonas↗

PubMed2000

Effect of erythromycin on Shigella infection of Caco-2 cells.

Erythromycin (EM), one of the macrolides, shows a dose-dependent effect on Shigella flexneri invasion of Caco-2 cells even at concentrations less than the minimum inhibitory concentration (subMIC). LS13, a strain of S. flexneri 1b, invaded Caco-2 cells in vitro. When the strain was treated with subMIC of EM, the invasion efficiency decreased. The carrier rate of the invasion plasmid containing virulence genes was reduced by EM treatment, as determined by the colony pigmentation test on Congo red agar plates. Presence of the invasion plasmid was found to increase susceptibility of the organisms to EM. The growth of virulent organisms carrying the invasion plasmid was inhibited at 25 microg ml(-1) of EM, whereas the growth of organisms without the plasmid was inhibited at 100 microg ml(-1) of EM. This was supported by the finding that the MIC of EM for a virulent isolate of S. flexneri 2a YSH6000 (6.25 microg ml(-1)) and for the mutant strain del-17 (50 microg ml(-1)), carrying the type III apparatus, impaired plasmid. These findings suggested that EM passed through the type III apparatus and suppressed the growth of invasive organisms selectively. This mechanism may account for the clinical effect of EM on shigellosis.

Anti-Bacterial Agents↗

PubMed2000

Anticancer derivative of butyric acid (Pivalyloxymethyl butyrate) specifically potentiates the cytotoxicity of doxorubicin and daunorubicin through the suppression of microsomal glycosidic activity.

Pivalyloxymethyl butyrate (AN9) is an anticancer derivative of butyric acid. In this study, doxorubicin (DXR) and AN9 synergistically inhibited the growth of lymphoma and lung carcinoma cells, whereas there was no synergy between AN9 and antimetabolites. AN9 did not affect the intracellular uptake of DXR. Among anthracyclines and their derivatives, the synergistic effect was prominent in compounds with a daunosamine moiety, suggesting that AN9 may affect the catabolism of these compounds. The degradation of DXR in the extract from AN9-treated cells was much less than that in extract from untreated cells. AN9 did not directly inhibit the enzyme activity but rather suppressed expression of the enzyme. With respect to the expression of drug resistance-related genes, there was no significant difference between untreated and AN9-treated cells. However, AN9 significantly down-regulated the levels NADPH-cytochrome P450 reductase and DT-diaphorase mRNA in the presence of DXR but not the level of xanthine oxidase mRNA. The enhancement of the sensitivity to anthracyclines was closely associated with the suppression of the mRNA expression.

Antibiotics, Antineoplastic↗

PubMed2000

Vidarabine and 2-deoxycoformycin as antileukemic agents against monocytic leukemia.

Although 2'-deoxycoformycin (dCF) has been reported in clinical trials to be less effective against myeloid than lymphoid malignancies, it may be useful for treating monocytic leukemia with the aid of 2'-deoxyadenosine (dAd) analogs. In the presence of 10 microM dAd, the concentration of dCF required to inhibit the viability of monocytoid leukemia cells was much lower than that required on normal or non-monocytoid malignant cells in primary culture. Among the dAd analogs, 9-beta-D-arabinofuranosyladenine (AraA) was also effective in combination with dCF. Although dCF alone slightly but significantly prolonged the survival of mice inoculated with U937 monocytic leukemia cells, combined treatment with dCF and AraA markedly prolonged the survival. These results suggest that the combination of dCF and AraA may be useful for the clinical treatment of acute monocytic leukemia.

Animals↗

PubMed2000

Influence of chorioamnionitis on survival and morbidity in singletons live-born at < 32 weeks of gestation.

BACKGROUND: Chorioamnionitis (CAM) may accelerate lung maturation in fetuses. It is possible that CAM prevents infant death after live birth. METHODS: A retrospective study of live-born singletons at < 32 weeks of gestation between 1993 and 1997. Perinatal risk factors for adverse outcomes were analyzed using a logistic regression model, with special reference to the presence of histologically confirmed CAM. Adverse outcomes included infant death before 1 year of age, and survival with cerebral palsy and/or mental retardation. RESULTS: A total of 81 infants, weighing 1181 +/- 426 g, were born at 28.1 +/- 2.3 weeks of gestation. Of those, 15 (19%) died before 1 year of age, while 16 (20%) infants developed major handicaps by 1.5 years of age (six with cerebral palsy, eight with mental retardation, and two with both cerebral palsy and mental retardation). CAM, present in 44 women, was significantly associated with a reduced risk of death after live birth, with an odds ratio of 0.11 (p = 0.01). Only the presence of such intracranial lesions as periventricular leukomalacia and intraventricular hemorrhage were significantly associated with an increased risk of major handicaps (odds ratio of 11.0, p = 0.04). Adverse outcomes occurred in a similar proportion of infants in groups without CAM (14/37) and with CAM (17/44). However, among infants with adverse outcomes, the number of deaths was significantly higher in the group without CAM (10/14) vs. with CAM (5/12) (p < 0.05). CONCLUSIONS: The presence of CAM may somehow prevent infant death after live birth. Larger studies are required to confirm this phenomenon.

Adult↗

PubMed1999

Prognostic implications of the differentiation inhibitory factor nm23-H1 protein in the plasma of aggressive non-Hodgkin's lymphoma.

The outcome of patients with non-Hodgkin's lymphoma has been improved by current approaches to treatment. Nevertheless, many patients either do not have a complete remission or ultimately relapse. To identify such patients, it is important to be able to predict the outcome. We previously found that the differentiation inhibitory factor/nm23 was correlated with the prognosis of acute myeloid leukemia. To examine the prognostic effect of nm23 on non-Hodgkin's lymphoma, we established an enzyme-linked immunosorbent assay procedure to determine nm23-H1 protein levels in plasma and assessed the association of this protein level with the response to chemotherapy, overall survival, and progression-free survival in patients with aggressive non-Hodgkin's lymphoma. The plasma concentration of nm23-H1 was significantly higher in patients with malignant lymphoma than in normal controls, especially in aggressive non-Hodgkin's lymphoma. The complete remission rate in patients with higher nm23-H1 levels was significantly worse than that in patients with lower nm23-H1 levels. Overall survival and progression-free survival were also lower in patients with higher nm23-H1 levels than in those with lower levels. The 3-year survival rates in patients with low and high nm23-H1 levels were 79.5% and 6. 7% (P =.0001). A multivariate analysis of prognostic factors showed that the plasma nm23-H1 level was independently associated with the survival and progression-free survival. An elevated plasma nm23-H1 concentration predicts a poor outcome of advanced non-Hodgkin's lymphoma. Therefore, nm23-H1 in plasma may be useful for identifying a distinct group of patients at very high risk.

Adult↗

PubMed1999

Expression of type I pili is abolished in verotoxin-producing Escherichia coli O157.

Verotoxin-producing Escherichia coli (VTEC) were examined for production of type I pili. None of 34 strains of VTEC serogroup O157 examined expressed any pili, whereas 26 strains of 27 VTEC serogroup O26 and seven strains of nine non-VTEC O157 produced type I pili. These VTEC strains were collected from sporadic human cases and cattle in Okinawa in 1997. The genes encoding the major structural component (FimA) and the adhesin (FimH) of type I pili were detected in all 70 strains examined. The inability to express type I pili could be a unique character of VTEC O157 and this trait could be a new candidate to identify the organisms.

Adhesins, Bacterial↗

PubMed1999

Effects of adrenergic stimulus on the activities of Ca2+ and K+ channels of dorsal root ganglion neurons in a neuropathic pain model.

We hypothesized that abnormal activity and adrenergic sensitivity in injured dorsal root ganglion (DRG) neurons are due to an intrinsic alteration of the cell body membrane. We investigated the effects of adrenergic stimulus on the activities of Ca2+ and K+ channels of DRG neurons in a rat chronic constriction injury (CCI) model. At first, we demonstrated thermal hyperalgesia and sprouting sympathetic nerve fibers in the ipsilateral L4-L5 DRGs. Using whole-cell patch clamp techniques, we found that alpha2-adrenergic stimulus by 10 microM norepinephrine (NE) inhibited inward currents (IBa, Ba2+ as a charge carrier) through voltage-dependent Ca2+ channels (VDCCs) of DRGs in the CCI model by 42%, whereas it enhanced the IBa by 18% in control animals. The inhibitory effect of NE disappeared by pretreatment with the N-type VDCC antagonist omega-conotoxin GVIA (1 microM). NE shifted the inactivation curve to a more negative potential, showing that it has inhibitory effects on IBa both in activated and in inactivated states. alpha2-Adrenergic stimulus also inhibited outward K+ currents by 24% in the CCI model, while it had no effect on the currents in control animals. The inhibitory effect of NE was blocked by pretreatment with the Ca2+-activated K+ (KCa) channel antagonist charybdotoxin (40 nM). The NE-induced inhibitory effects both on N-type VDCC and on KCa channels in injured DRG neurons of the CCI model could lead to cell membrane depolarization, resulting in a spontaneous discharge of action potential and an increase in sensitivity to adrenergic stimulus.

Animals↗

PubMed1999

Identification of a novel gene, OASIS, which encodes for a putative CREB/ATF family transcription factor in the long-term cultured astrocytes and gliotic tissue.

Gliosis is a characteristic response of astrocytes to inflammation and trauma of the central nervous system (CNS). To study the mechanisms underlying gliosis, we performed differential display screening for genes specifically induced in long-term cultured astrocytes used as an in vitro gliosis model. We identified and characterized a gene (named OASIS, for old astrocyte specifically-induced substance) expressed in long-term cultured mouse astrocytes, or 'old astrocytes (OA)'. The OASIS gene encoded a putative transcription factor belonging to the cyclic AMP responsive element binding protein/activating transcription factor (CREB/ATF) gene family, with homology to box B-binding factor-2 (BBF-2), a Drosophila transcription factor. Its expression was developmentally regulated; OASIS mRNA was primarily expressed in the salivary gland and cartilage in the mouse embryo and it was transiently upregulated in the brain during postnatal two weeks. The expression became weaker in the adult brain. We also demonstrated that an expression of the OASIS mRNA was induced in response to the cryo-injury of the mouse cerebral cortex. The distribution pattern of the OASIS-positive cells in the injured cortex was very similar to that of the glial fibrillary acidic protein (GFAP)-positive cells. These results suggest that OASIS protein may play a role in gliotic events.

Activating Transcription Factors↗

PubMed1999

Eos: a novel member of the Ikaros gene family expressed predominantly in the developing nervous system.

We identified a novel member of the Ikaros gene family, which has critical roles in the development of lymphoid lineages. This gene, which we named Eos, was expressed predominantly in the developing central and peripheral nervous system. Eos protein could interact with itself and Ikaros protein through its C-terminal portion in the yeast two hybrid assay. These findings suggested that Eos may have important roles in neural development similarly to the Ikaros family in the development of hemolymphoid tissue.

Amino Acid Sequence↗

PubMed1999

Greater synergism of retinoic acid receptor (RAR) agonists with vitamin D3 than that of retinoid X receptor (RXR) agonists with regard to growth inhibition and differentiation induction in monoblastic leukemia cells.

Retinoids and 1alpha,25-dihydroxyvitamin D3 (VD3) cooperatively induce the differentiation of myeloid leukemia cells. We investigated the role of retinoid receptors (RARs and RXRs) in the combined effects of retinoids and VD3 on growth inhibition and differentiation induction in human monoblastic leukemia U937 cells by using RAR- or RXR-selective retinoids. An isobologram analysis showed that both combinations were synergistic with regard to inhibiting the proliferation, and RAR agonists exhibited greater synergism with VD3 than did RXR agonists. RXR agonists alone induced nitroblue tetrazolium (NBT) reduction and expression of CD11b in U937 cells, whereas RAR agonists alone did not. On the other hand, RAR agonists and RXR agonists enhanced the differentiation induced by VD3, but RXR agonists required higher concentrations. An RAR antagonist inhibited the differentiation induced by RAR agonists plus VD3, but not that induced by RXR agonists plus VD3. Thus, RARs and RXRs act differently in their synergism with VD3. RAR agonists are more potent than RXR agonists with regard to synergism with VD3, and their combination may be useful in differentiation therapy against myeloid leukemia.

Alitretinoin↗

PubMed1999

Loss of protection by hypoxic preconditioning in aging Fischer 344 rat hearts related to myocardial glycogen content and Na+ imbalance.

OBJECTIVES: The objective of this study was to determine whether hypoxic preconditioning (HP) could lessen the myocardial increase in [Na+]i, thus protecting the aging myocardium against ischemia. BACKGROUND: A decrease in ischemic tolerance with aging is associated with an accelerated increase in [Na+]i during ischemia. Ischemic preconditioning fails to protect the middle-aged and senescent myocardium against ischemia. METHODS: Isolated hearts of young adult (12-week-old), middle-aged (50-week-old) and senescent (100-week-old) Fischer 344 rats were subjected to 25 min of ischemia with or without HP followed by 30 min of reperfusion. Left ventricular (LV) function, myocardial energy metabolites and [Na+]i were measured. RESULTS: In the older groups, the recovery of LV function and high-energy phosphates (HEPs) was lower with an increased release of creatine kinase (CK) during reperfusion than in the young group. The increased [Na+]i at the end of ischemia was greater in the former groups than in the young group. HP decreased myocardial glycogen and lessened the increased [Na+]i in the young group, resulting in an improved recovery of LV function and HEPs, as well as decreased CK release. However, the levels of glycogen before HP in the older groups were higher than in the young group and its levels after HP were similar to that before HP in the young group. HP did not affect the [Na+]i, exacerbated CK release and inhibited the recovery of LV function and HEPs in the older groups. CONCLUSIONS: HP failed to lessen the increased [Na+]i or to protect the aging hearts, probably due to the preexistence of increased glycogen level.

Aging↗

PubMed1999

Localization of huntingtin-interacting protein-2 (Hip-2) mRNA in the developing mouse brain.

Huntingtin-interacting protein-2 (Hip-2) was identified as a human protein specifically associated with huntingtin in vitro, a gene product affected in patients with Huntington disease (HD). It is a ubiquitin-conjugating enzyme identical to the previously characterized bovine E2-25k. We identified the mouse Hip-2 homologue (mHip-2) and examined its distribution patterns in the developing mouse brain in order to gain an insight into the functional significance of the Hip-2 protein in the normal brain as well as in the pathogenesis of HD. As reported with huntingtin, the mHip-2 mRNA expression developed in parallel with neuronal maturation and became distributed widely in the postnatal mouse brain. This spatiotemporal pattern of mHip-2 mRNA expression resembled that of huntingtin. We further demonstrated that mHip-2 mRNA was colocalized with huntingtin-like immunoreactivity in a single neuron. These findings suggested that the Hip-2 interacted with huntingtin in vivo and played an important role in HD pathogenesis.

Amino Acid Sequence↗

PubMed1999

Changes in respiratory pattern and arterial blood gases during sedation with propofol or midazolam in spinal anesthesia.

STUDY OBJECTIVE: To investigate changes in respiratory pattern and arterial blood gases during sedation with propofol or midazolam in spinal anesthesia. DESIGN: Randomized, placebo-controlled study. SETTING: Operating room of a university-affiliated hospital. PATIENTS: 40 ASA physical status I and II patients who required spinal anesthesia. INTERVENTIONS: Spinal anesthesia with tetracaine and subsequent sedation with propofol (n = 15), midazolam (n = 15), or placebo (n = 10) was performed. MEASUREMENTS: Respiratory pattern [rib cage contribution to the tidal volume (%RC) and phase shift between rib cage and abdominal movements (PSrc-ab)] with a respiratory inductive plethysmograph (Respigraph) and arterial blood gas analysis (pH, pO2, and pCO2) were recorded. MAIN RESULTS: Spinal anesthesia per se increased %RC by 35% without changing PSrc-ab values (1.00). Sedation with propofol and midazolam decreased %RC by 60% and by 40%, respectively. PSrc-ab increased in both groups following sedation, and the increase in this parameter was higher in the propofol group (1.12) than in the midazolam group (1.04). In the placebo group, %RC decreased by 20% without any change in PSrc-ab. The decrease in pO2 was more significant in the propofol group (65.1 mmHg) than in the midazolam (74.2 mmHg) and placebo (83.1 mmHg) groups. CONCLUSION: Significant decreases in %RC and pO2 during propofol sedation seem to depend on paradoxical respiration due, in part, to upper airway obstruction; therefore, attention should be directed to the respiratory pattern during sedation, especially with propofol.

Adult↗

PubMed1999

Vesnarinone and glucocorticoids cooperatively induce G1 arrest and have an anti-tumour effect on human non-small cell lung carcinoma cells grown in nude mice.

Vesnarinone, an oral cardiotonic, inhibited the growth of several human non-small cell lung carcinoma cell lines, and its anti-proliferative effects in vitro and in vivo were greatly enhanced by combination with glucocorticoids, but not other steroids. Simultaneous treatment with vesnarinone and dexamethasone is the most effective to evoke the synergistic effect in the growth inhibition of lung carcinoma EBC-1 cells. Dexamethasone and other glucocorticoids induced morphological changes in EBC-1 cells and these agents together with vesnarinone induced alkaline phosphatase activity, which is a typical marker of type II pneumocyte maturation. This treatment arrested the growth of the cells at the G1 phase, indicating that this treatment is cytostatic rather than cytotoxic. These results suggest that vesnarinone plus glucocorticoid might be useful in lung cancer therapy.

Alkaline Phosphatase↗

PubMed1999

Expression of sonic hedgehog signal transducers, patched and smoothened, in human basal cell carcinoma.

In basal cell nevus syndrome (BCNS) patients, mutations of a gene, patched (ptc), which encodes a putative signal transducer of sonic hedgehog protein (SHH), were found and are thought to be one of the major causes of BCNS. The SHH signaling pathway is an important developmental pathway, and ptc protein (PTC) is a suppressive component serving as a receptor for the secreted SHH. Another transmembrane protein, smoothened (SMO), forms a complex with PTC and regulates this signaling pathway. Recent transgenic studies have strengthened the importance of the SHH signaling system in the etiology of basal cell carcinoma (BCC). In this study, we examined the expression patterns of mRNA for ptc and smo in two different BCC subtypes and normal skin. We found that the expressions of ptc and smo mRNA were enhanced in the tumor nests of the nodular BCC, especially at the advancing portions, but were under the detectable level in the superficial BCC cases examined, indicating that ptc and smo mRNA expressions might be associated with BCC tumor progression and divide the BCC histologic types into two subtypes, superficial and nodular types. In addition, no obvious signals for ptc and smo mRNA were detected in the normal human epidermis, appendages, or seborrheic keratosis, indicating that the abnormal proliferation of follicular epithelial cells caused by ptc, smo and/or other genetic changes, which also cause ptc and smo overexpressions, might result in BCC tumor formation.

Aged↗