Biomedical subjects
Publications and source records attributed to H Miyawaki.
An unusual alkaloid, the 2-aza-anthraquinone derivative, 5-deoxy-7-methyl bostrycoidin, was identified in the cultures of the spore-derived mycobionts of the lichen Haematomma sp., but not in the natural lichen thallus.
Acute and chronic alterations of right ventricular (RV) wall properties can change left ventricular (LV) performance. We investigated whether and how stiffening of the RV free wall alters LV diastolic distensibility. We used cross-circulated isolated hearts, in which the LV and RV were independently controllable. Stiffness of the RV free wall was altered by intramuscular injections of glutaraldehyde into the RV free wall after right coronary artery ligation. We measured circumferential and longitudinal regional lengths in the septum and LV free wall. During data acquisition, RV volume was held constant. After the RV free wall was stiffened by glutaraldehyde, the LV diastolic pressure-volume relation shifted upward and became steeper. Importantly, stiffening of the RV free wall increased the diastolic regional area in the septum and LV free wall under constant LV volume. The augmented regional dimensions may result in enhanced regional tension under constant LV volume and may be related to the observed increase in LV diastolic intracavitary pressure. The impaired LV diastolic distensibility by stiffening of the RV free wall may be at least partly explained by myocardial stretch, probably due to LV deformation.
We compared midline approach with paramedian approach for combined spinal-epidural anesthesia (CSEA) by needle through needle technique. Seventy patients undergoing elective gynecological surgery received CSEA with a 27 G Whitacre spinal needle, which protrudes 12 mm beyond the tip of the Tuohy needle. The successful subarachnoid puncture with first attempt was noted in 33 patients (94%) of midline group (M group), in 31 patients (89%) of paramedian group (P group). At the subarachnoid puncture, skin to epidural space distance (43.2 mm vs 53.4 mm) and protrusion length of spinal needle (5.5 mm vs 8 mm) were significantly longer in the P group than in the M group. Abdominal radiography revealed the flexion of epidural catheter in 19 patients (54%) of M group and in 2 patients (6%) of P group. The choice of midline or paramedian approach for CSEA did not affect the success rate of the subarachnoid puncture, but paramedian approach required longer protrusion length of the spinal needle than midline approach. To raise the success rate of subarachnoid puncture by paramedian approach, a long protruded spinal needle is recommended.
There are several unsolved clinical findings in patients with idiopathic pulmonary fibrosis (IPF); (i) predominance of fibrosis in the lower lung fields, (ii) digital clubbing, and (iii) patchy distribution of pulmonary fibrosis. To explain these unsolved problems, we hypothesized that regenerated or premature bronchoepithelial cells may circulate in the blood in patients with IPF. To prove this, we performed the reverse transcriptase-polymerase chain reaction (RT-PCR) for cytokeratin 19 (CK19) and pulmonary surfactant protein A (SPA) in peripheral blood in patients with IPF and pulmonary fibrosis associated with collagen vascular disorders. In addition, 20 patients with chronic pulmonary emphysema as a disease control and 19 normal volunteers were also evaluated for the existence of circulating bronchoepithelial cells. RT-PCR analysis showed that CK19 was expressed in 12 of 38 blood samples (31.6%) of IPF and pulmonary fibrosis associated with collagen vascular disorders, seven of 20 (35.0%) blood samples of chronic pulmonary emphysema, and four of 19 (21.1%) blood samples of normal volunteers. mRNA for SPA was positive in eight of 38 (21.1%) blood samples of IPF. In contrast, SPA expressing cells were not detected in any blood samples obtained from patients with chronic pulmonary emphysema or normal volunteers. This evidence suggests that there were some circulating bronchoepithelial cells expressing mRNA for SPA in peripheral blood of patients with IPF and pulmonary fibrosis associated with collagen vascular disorders.
Bradycardia during propofol anesthesia is well known, but bradycardia after propofol anesthesia has not been studied well. We compared perioperative heart rates in patients who had undergone gynecological surgery under lumbar epidural anesthesia supplemented with light general anesthesia using isoflurane and nitrous oxide in oxygen (Group Iso, n = 25) with those who had received lumbar epidural anesthesia supplemented with propofol (Group Prop, n = 25). The heart rates for the Group Prop were significantly lower (P < 0.05) than those for the Group Iso after the induction of anesthesia up to 2 hours after surgery. Two patients in the Group Prop developed bradycardia below 50 bpm 1 and 2 hours after surgery. In one of them intravenous atropine was necessary to treat bradycardia. We conclude that more attention should be paid to postoperative as well as intraoperative bradycardia in patients who receive propofol.
There is increasing evidence that reactive oxygen species (ROS) contribute to post-ischemic reperfusion injury, but determination of the specific ROS involved has proven elusive. In the present study electron paramagnetic resonance (EPR) spectroscopy was used in vitro to measure the relative quenching of singlet oxygen (1O2) by histidine and carnosine (beta-alanyl-L-histidine) utilizing the hindered secondary amine 2,2,6,6-tetramethyl-4-piperidone HCl (4-oxo-TEMP). The relative effect of histidine and carnosine on functional recovery of isolated perfused rat hearts was also studied. Functional recovery was measured by left ventricular developed pressure (LVDP), first derivative of left ventricular pressure (dP/dt), heart rate (HR) and coronary flow (CF). EPR measurements and Stern-Volmer plots showed that 400 microM carnosine quenched 1O2 twice as effectively as equimolar histidine in vitro. Moreover, 10 mM histidine improved functional recovery of isolated rat hearts significantly more than 1 mM histidine. Furthermore, 1 mM carnosine improved functional recovery significantly more than equimolar histidine and as effectively as 10 mM histidine. Experiments with 1 mM mannitol, a known hydroxyl radical scavenger, did not show an improvement in functional recovery relative to control hearts, thereby decreasing the likelihood that hydroxyl radicals are the major damaging species. On the other hand, the correlation between improved functional recovery of isolated rat hearts with histidine and carnosine and their relative 1O2 quenching effectiveness in vitro provides indirect evidence for 1O2 as ROS participating in reperfusion injury.
The present study was designed to evaluate the pathological and immunohistochemical findings of Mycobacterium avium intracellulare complex (MAC) lung infection. A retrospective study was performed in five cases with positive cultures for MAC in whom lung resections were performed between January 1989 and December 1996. A determination of whether or not MAC caused pulmonary disease was made using the 1997 criteria defined by the American Thoracic Society. In addition, MAC was cultured from all of the five lung specimens. Pathological and immunohistochemical findings as well as chest computed tomography (CT) findings were evaluated in these five patients. Pathological findings of bronchiectasis, bronchiolitis, centrilobular lesion, consolidation, cavity wall and nodules were demonstrated, respectively, in relation to chest CT findings. Extensive granuloma formation throughout the airways was clearly demonstrated. Immunohistochemical staining demonstrated: 1) epithelioid cells and giant cells; 2) myofibroblasts extensively infiltrating the cavity wall; and 3) B-cells detected in aggregates in the vicinity of the epithelioid granulomas. This study identified pathological and immunohistochemical characteristics of Mycobacterium avium complex infection relative to chest computed tomography findings and allowed the conclusion that bronchiectasis and bronchiolitis were definitely caused by Mycobacterium avium complex infection.
OBJECTIVE: We tested the hypotheses that low concentration of H2O2 attenuates the Ca2+ paradox (Ca2+ PD) injury, and that activation of protein kinase C (PKC) and/or ATP-sensitive potassium channel (KATP) are involved in the protective effects of H2O2. METHODS: Langendorff-perfused rat hearts were subjected to the Ca2+ PD (10 min of Ca2+ depletion followed by 10 min of Ca2+ repletion). Functional and biochemical effects of H2O2 and other interventions on the cell injury induced by the Ca2+ PD were assessed. RESULTS: In the Ca2+ PD hearts pretreated with 20 mumol/l H2O2, left ventricular end-diastolic pressure and coronary flow were significantly preserved. Furthermore, peak lactate dehydrogenase release was significantly decreased and ATP contents were more preserved, compared with non-treated Ca2+ PD hearts. H2O2-treated hearts also showed remarkable preservation of cell structure. Addition of a specific PKC inhibitor, chelerythrine during H2O2 treatment completely abolished the beneficial effects of H2O2 on the Ca2+ PD. Similarly, an activator of PKC. Phorbol 12-myristate 13 acetate mimicked the protection by H2O2. Furthermore, pretreatment with a KATP opener, cromakalim also provided protection similar to H2O2 against the Ca2+ PD injury. However, a specific KATP inhibitor, glibenclamide was not able to completely block the effects of H2O2. CONCLUSIONS: These findings suggest that pretreatment with low concentration of H2O2 provides significant protection against the lethal injury of Ca2+ PD in rat hearts. PKC-mediated signaling pathways appear to play a crucial role in the protection against the Ca2+ PD injury.
Explore the source record for details and available documents.
This report is concerned with twins with cystic fibrosis (CF). They are of mixed parentage: Japanese mother and German father. One case is presented with meconium ileus as a neonate. The other patient did relatively well until the age of 6 years when she was first hospitalized and diagnosed with pulmonary aspergillosis. They have been receiving standard therapies for CF including digestive enzymes, vitamins and periodic antibiotic therapy in the US. At 19 years of age, they were tested for common mutations and one AF508 cystic fibrosis transmembrane conductance regulator (CFTR) allele was found. Further testing of their CFTR gene as well as those of their Japanese mother and grandmother revealed missense mutations in exon 7 (R347H) and exon 16 (D979A). Although the D979A mutant is very rare, this mutation combination seemed to be responsible for severe CF phenotypes.
A 53-year-old Japanese female, who had been suffering from idiopathic pulmonary fibrosis (IPF) for 3 years, was admitted with dyspnoea. The important laboratory finding on admission was a serum CA19-9 level of 649 U/mL. Despite steroid treatment for IPF, her respiratory condition gradually deteriorated with the increase of serum CA19-9 level up to 3020 U/mL and she died of respiratory failure. Immunohistochemistry showed the positive stain of CA19-9 in bronchoepithelial cells. We also reviewed the Index Medics and picked up the cases who had elevation of CA19-9 more than 1000 U/mL, and six patients were listed. Five of these six patients died within 6 months, therefore the marked elevation of CA19-9 seemed to be a bad prognostic factor in patients with pulmonary fibrosis.
We have purified to apparent homogeneity and characterized a molecular chaperonin GroEL homologue (hpGroEL) from a moderately halophilic eubacterium, Pseudomonas sp. #43. Although this halophilic bacterium requires 1-2 M NaCl for growth, hpGroEL did not require a high concentration of salt for its stability, ATPase activity and refold-promoting activity for denatured protein. The ATPase activity was even more halo-sensitive than that of GroEL from Escherichia coli. The hpGroEL protein promotes Mg(2+)-ATP-dependent refolding of urea-denatured alpha-glucosidase in the presence of E. coli-GroES, indicating that chaperonins 60 and 10 isolated from halophilic and nonhalophilic eubacteria, respectively, can cooperate with each other.
This study was undertaken to compare axial images of 99mTc-Technegas SPECT (Technegas) with those of 133Xe gas dynamic SPECT in patients with pulmonary emphysema. There were 20 patients, 19 males and 1 female. All patients except one ex-smoker were heavy smokers with a mean age of 68.1 years. For Technegas scintigraphy, the patients inhaled 505 MBq 99mTc-Technegas in several tidal volume breaths in the supine position without breath holding. For 133Xe gas scintigraphy, the patients inhaled 370 MBq 133Xe gas. 133Xe gas dynamic SPECT was performed in the equilibrium phase for the last minute of the 3 minute inhalation in a closed circuit, and in the washout phase for 6 minutes of inhalation in a semi-closed circuit, by means of a gamma camera with dual detectors (Picker model Prism 2000). Abnormal findings included heterogeneity, defects and hot spots on Technegas images and on retention images taken 3 minutes after 133Xe gas washout. In 2 of 20 patients, the degree of abnormal findings on Technegas images depended on the area of 133Xe gas retention in the washout phase. In 3 patients, the degree of abnormal findings on both Technegas SPECT and 133Xe gas dynamic SPECT images were equivalent. In the remaining 15 patients, more detailed findings and a greater area were shown by Technegas SPECT than 133Xe gas dynamic SPECT. We conclude that in patients with pulmonary emphysema Technegas SPECT can demonstrate ventilation impairment more easily than 133Xe gas dynamic SPECT.
An outbreak of coagulase VII-producing, arbekacin (ABK)-resistant, methicillin-resistant Staphylococcus aureus (MRSA) occurred between September 1994 and December 1995, involving five different wards. Twenty-one patients developed skin, wound, drainage, or respiratory tract colonization with coagulase VII-producing, (ABK)-resistant MRSA. Phenotypic characteristics (production of enterotoxin and TSST-1, antimicrobial susceptibility) and molecular-typing procedure (plasmid DNA profile, pulsed-field gel electrophoresis [PFGE] and arbitrarily primed polymerase chain reaction [AP-PCR] of chromosomal DNA) in isolated strains were compared. Plasmid analysis identified four different profiles and 19 of 22 strains recovered had identical patterns. PFGE of chromosomal DNA identified three different subtypes and 18 (81.8%) isolates shared the same subtype. AP-PCR also demonstrated that most strains had the same phenotypic characteristics. Although traditional epidemiological methods; for example, coagulase typing, plays a central role in hospital infection control, combination of plasmid DNA profile, AP-PCR, and PFGE may prove to be a particularly informative means of tracking the nosocomial spread of MRSA.
We tested the hypothesis that a transient increase in intracellular calcium concentration ([Ca2+]i) before prolonged ischemia triggers the activation of protein kinase C (PKC), resulting in significant protection against ischemic injury. Ca2+ preconditioning (3 cycles of 1-min Ca2+ depletion and 5-min Ca2+ repletion) and pharmacological intervention with isoproterenol (Iso) were employed to increase the Ca2+ influx. Langendorff-perfused rat hearts were subjected to 40 min of global ischemia followed by 30 min of reperfusion (I/R). A significant functional recovery and minimal biochemical changes were observed in Ca2+-preconditioned hearts after I/R. Pretreatment with 0.1 micromol/l Iso caused a sudden increase in left ventricular contractility, a significant decrease in lactate dehydrogenase release, preservation of ATP content, and left ventricular function compared with nontreated I/R hearts. Administration of verapamil during Iso treatment blunted the salutary effects of Iso on I/R and pretreatment with BAY K 8644, an L-type Ca2+-channel opener, mimicked Iso-induced protection. Addition of propranolol or specific PKC inhibitors (chelerythrine or bisindolylmaleimide) during Iso infusion completely abolished the beneficial effects of Iso. These results demonstrate that 1) treatment with a low dose of Iso provides significant protection against ischemic injury, 2) transient elevation of [Ca2+]i is a strong activator of PKC, and 3) PKC plays a crucial role in the subcellular mechanisms of protection by activating second messenger signals during Iso-induced preconditioning.
We tested the hypothesis that elevation of [Ca2+]i during ischemic preconditioning (IPC) stimulates protein kinase C (PKC), which confers the protection against the ischemic injury. Langendorff-perfused rat hearts were subjected to 40-minute global ischemia followed by 30-minute reperfusion (I/R). In preconditioned groups, hearts were subjected to either IPC, consisting of 5-minute global ischemia and 10-minute reperfusion, or high-Ca2+ preconditioning (HCPC), ie, the 5-minute perfusion of higher Ca2+ perfusate (2.3 mmol/L Ca2+) followed by 10-minute perfusion of normal perfusate (1.8 mmol/L Ca2+), and then were subjected to I/R. A significant functional recovery and decreased lactate dehydrogenase release were observed in HCPC and IPC hearts compared with ischemic control hearts. ATP contents of preconditioned hearts were significantly higher than those of the ischemic control hearts. The cell structure in preconditioned hearts was preserved better than that in the ischemic control hearts. Furthermore, the activation and translocation of PKC from cytoplasm to sarcolemma were observed in the preconditioned hearts. Verapamil administered during IPC significantly attenuated the salutary effects of IPC. Administration of chelerythrine, a specific PKC inhibitor, completely abolished the HCPC- and IPC-induced cardioprotection. The translocation of PKC by IPC was blocked by verapamil or chelerythrine. Immunohistochemical study using rabbit polyclonal antibody against PKC isoforms indicated that stress induced by IPC or HCPC evoked the translocation of PKC alpha and PKC delta to the cell membrane. Translocation of PKC isoforms was attenuated by the treatment with verapamil or chelerythrine. These results demonstrate that (1) a transient increase in [Ca2+]i during IPC is an important trigger for the activation of PKC, which is responsible for cardioprotection; (2) the elevation of [Ca2+]i during IPC, at least partly, resulted from Ca2+ entry via voltage-dependent Ca2+ channel; and (3) activation and translocation of PKC alpha and PKC delta occur during IPC and HCPC and may be important in preconditioning.
The cause of digital clubbing is unknown. Hepatocyte growth factor (HGF) is a pleotrophic factor which has various biological effects. We measured serum HGF in 12 patients with digital clubbing; the underlying diseases of these patients were: lung cancer, 2; cystic fibrosis, 2; idiopathic pulmonary fibrosis, 3; lung cancer with idiopathic pulmonary fibrosis, 1; chronic hepatitis, 1; interstitial pneumonia with collagen disease, 2; and bronchiectasis, 1; nine hundred and fifty-seven normal volunteers and 17 lung cancer patients without clubbing served as the control. As a result, the serum HGF concentration in patients with digital clubbing (0.47 +/- 0.29 ng/ml) was significantly higher when compared to that of lung cancer patients without digital clubbing (0.15 +/- 0.04, p < 0.01). Therefore, we suggest that HGF may play a role in the formation of digital clubbing.
We investigated consecutive patients undergoing primary total hip replacement surgery who were randomly assigned into two groups; those who received a blinded solution of aprotinin 2 million KIU (kallikrein inactivation units) (n = 11) and those who received an equivalent volume of normal saline placebo (n = 10) throughout the surgical procedure. Anesthesia and surgical techniques were standardized. All patients received spinal anesthesia combined with general anesthesia. There was no significant difference in blood loss during operation between the two groups. However, postoperative blood loss in the aprotinin group (284 +/- 155g, mean +/- SD) was significantly less compared with that in the control group (723 +/- 334g). Total blood loss in the aprotinin group (820 +/- 255g) was also significantly less than in control group (1265 +/- 389g). We conclude that the use of aprotinin 2 million KIU during total hip replacement results in significantly less perioperative blood loss, especially during the postoperative period.