Specimen collection, storage, and transmission to the laboratory for hematological tests.
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Blood Specimen Collection↗
Biomedical subjects
S Miwa
Publications and source records attributed to S Miwa.
Initial effects of the left ventricular repair by plication may not last long in a rat ischemic cardiomyopathy model.
BACKGROUND: Long term effects of left ventricle (LV) repair surgery (LVR) for ischemic cardiomyopathy are not well understood. METHODS AND RESULTS: Sixty-nine rats developed ischemic cardiomyopathy with large akinetic LV area 4 weeks after the left anterior descending artery was ligated. In a second surgery 4 weeks later, 33 rats underwent LVR by plication of the akinetic LV area (LVR group), and 36 underwent rethoracotomy alone (sham group). No medication was used in either group. All rats survived the second surgery. LV end-diastolic dimension as measured by echocardiography, LV fractional shortening, and the maximal end-systolic pressure-volume relationship (E(max)) as calculated from the data by catheter-tipped manometer and echocardiography improved in the LVR group after the second surgery, but LV end-diastolic dimension and E(max) gradually deteriorated as time passed. LV end-diastolic pressure improved 1 week after LVR but rose significantly 4 weeks after LVR. Brain natriuretic peptide mRNA was lower in the LVR group than in the sham group 1 week after LVR but not 4 weeks postoperatively. CONCLUSIONS: Initial improvement in LV function and neurohormonal status after LVR did not last for 4 weeks in this rat model when untreated medically. The mechanism of deterioration should be elucidated to improve long-term results of LVR.
Animals↗
A new glucose-6-phosphate dehydrogenase variant G6PD Sugao (826C-->T) exhibiting chronic hemolytic anemia with episodes of hemolytic crisis immediately after birth.
A case of glucose-6-phosphate dehydrogenase (G6PD) deficiency associated with chronic hemolysis with episodes of hemolytic crisis immediately after birth is reported. The propositus was a 1-month-old Japanese male infant. Molecular analysis of the G6PD gene revealed a novel missense mutation (826C-->4T) in exon 8 predicting a single amino acid substitution, Pro276Ser. The mother was confirmed to be heterozygous for this mutation. We designated this novel class 1 variant as G6PD Sugao. Pro276 is a phylogenetically conserved residue that may play a significant role in dimer formation.
Anemia, Hemolytic, Congenital↗
Failure of endothelin-1 to activate store-operated Ca2+ channels by lack of mobilization from intracellular Ca2+ stores in cultured bovine adrenal chromaffin cells.
We have recently shown that in addition to L-type voltage-operated Ca2+ channel (VOC), endothelin-1 (ET-1) stimulation opens two types of Ca2+-permeable nonselective cation channels [designated nonselective cation channel-1 (NSCC-1) and NSCC-2]. However, in this Ca2+ entry, the involvement of store-operated Ca2+ channel (SOCC), which is suggested to exist in chromaffin cells, was unclear. Those NSCCs as well as SOCC can be pharmacologically discriminated using Ca2+ channel blockers such as SK&F 96365 and LOE 908. To clarify whether SOCC should actually exist and play a role in Ca2+ entry in chromaffin cells stimulated with ET-1, we examined the effects of removal of extracellular Ca2+, thapsigargin (TG, an inhibitor of endoplasmic reticulum Ca2+-ATPase), LOE 908 and SK&F 96365 on cytosolic free Ca2+ concentrations ([Ca2+]i) in cultured bovine adrenal chromaffin cells. After the cells were exposed to Ca2+-free medium followed by exposure to TG to deplete Ca2+ from the intracellular Ca2+ store, restoration of extracellular Ca2+ caused a gradual increase in [Ca2+]i (to about 200% of control). The increase was unaffected by LOE 908, but completely abolished by SK&F 96365. In the Ca2+-free medium, no increase in [Ca2+]i by ET-1 was observed, but the subsequent restoration of extracellular Ca2+ induced a rapid increase in [Ca2+]i (to the same level of [Ca2+]i as that evoked by ET-1 in the normal medium (1.0 mM Ca2+)). Since SK&F 96365 is also a blocker of SOCC, these results indicate that in bovine adrenal chromaffin cells, Ca2+ entry through SOCC (Ca2+ influx through the capacitative Ca2+ entry system) occurs but is comparably weak, and that it virtually does not work on the stimulation of ET-1.
Acetamides↗
Two novel glucose-6-phosphate dehydrogenase variants found in newborn mass-screening for galactosaemia.
UNLABELLED: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked recessive disorder in which haemolytic anaemia is the major symptom. The Beutler spot test employed in mass-screening for galactosaemia in newborns requires several intrinsic erythrocyte enzymes such as G6PD for its reaction and can theoretically detect G6PD deficiency apart from galactose-1-phosphate uridyltransferase deficiency. In this study, we detected two patients with G6PD deficiency using the quantitative Beutler test which was recently developed in our laboratory. Both patients lacked erythrocyte G6PD activity but exhibited no clinical symptoms. Molecular analysis in patients 1 and 2 revealed two novel missense mutations of C853T causing R285C and A1220C causing K407T, respectively. Molecular rather than enzymatic analysis was required in familial studies to detect and diagnose the carrier state. To date these patients have avoided oxidant stress and haemolytic diatheses have not been induced. CONCLUSION: Our results indicate that the quantitative Beutler test can detect glucose-6-phosphate dehydrogenase deficiency of class 1 and 2 and is therefore useful for early intervention and prevention of haemolytic diathesis in patients with this disorder.
Galactosemias↗
Distribution of glucose-6-phosphate dehydrogenase mutations in Southeast Asia.
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a heterogeneous enzyme abnormality with high frequency in tropical areas. We performed population screening and molecular studies of G6PD variants to clarify their distribution and features in Southeast Asia. A total of 4317 participants (2019 males, 2298 females) from 16 ethnic groups in Myanmar, Lao in Laos, and Amboinese in Indonesia were screened with a single-step screening method. The prevalence of G6PD-deficient males ranged from 0% (the Akha) to 10.8% (the Shan). These G6PD-deficient individuals and 12 G6PD-deficient patients who had been diagnosed at hospitals in Indonesia and Malaysia were subjected to molecular analysis by a combination of polymerase-chain-reaction-based single-strand conformation polymorphism analysis and direct sequencing. Ten different missense mutations were identified in 63 G6PD-deficient individuals (50 hemizygotes, 11 heterozygotes, and 2 homozygotes) from 14 ethnic groups. One missense mutation (1291 G-->A) found in an Indonesian Chinese, viz., G6PD Surabaya, was previously unknown. The 487 G-->A (G6PD Mahidol) mutation was widely seen in Myanmar, 383 T-->C (G6PD Vanua Lava) was specifically found among Amboinese, 871 G-->A (G6PD Viangchan) was observed mainly in Lao, and 592 C-->T (G6PD Coimbra) was found in Malaysian aborigines (Orang Asli). The other five mutations, 95 A-->G (G6PD Gaohe), 1003 G-->A (G6PD Chatham), 1360 C-->T (G6PD Union), 1376 G-->T (G6PD Canton), and 1388 G-->A (G6PD Kaiping) were identified mostly in accordance with distributions reported previously.
Amino Acid Substitution↗
Transitional cell carcinoma of the renal pelvis in a long-term hemodialysis patient with autosomal dominant polycystic kidney.
We present a case of renal pelvic transitional cell carcinoma (TCC) accompanied by autosomal dominant polycystic kidney disease (ADPKD). An 81-year-old woman on long-term hemodialysis for ADPKD visited the Department of Urology at Kouseiren Takaoko Hospital, complaining of asymptomatic macroscopic hematuria. Retrograde pyelogram showed an irregular filling defect in the right renal pelvis, which suggested the right renal pelvic tumor. We performed right nephrectomy and transurethral removal of the right ureter. Histological diagnosis demonstrated renal pelvic TCC.
Aged↗
Value of lipiodol computed tomography and digital subtraction angiography in the era of helical biphasic computed tomography as preoperative assessment of hepatocellular carcinoma.
OBJECTIVE: To compare the diagnostic accuracies of Lipiodol computed tomography (CT) and helical biphasic CT as preoperative imaging modalities for hepatocellular carcinoma (HCC). SUMMARY BACKGROUND DATA: Lipiodol CT after digital subtraction angiography has long been used as a highly sensitive imaging modality for HCC. The recent advent of helical CT has allowed scanning the entire liver during both the arterial and portal venous phase of contrast enhancement. METHODS: The authors analyzed data from 164 patients who underwent hepatic resection for HCC to calculate the sensitivity and specificity of these modalities. Findings of intraoperative ultrasonography followed by histologic confirmation were set as the gold standard. RESULTS: Although sensitivity decreased with both modalities as tumors became small and well differentiated, helical CT showed a higher sensitivity than Lipiodol CT in detecting well-differentiated HCC nodules smaller than 2 cm. In contrast, Lipiodol CT was superior to helical CT for the detection of small but moderately to poorly differentiated nodules. The overall sensitivity of helical CT was higher than that of Lipiodol CT. These findings suggest that helical CT is superior in delineating early HCC, whereas Lipiodol CT is specific to the detection of intrahepatic metastases. In terms of specificity, helical CT was superior to Lipiodol CT. CONCLUSIONS: Helical CT and Lipiodol CT are complementary modalities. At present, helical biphasic CT does not obviate the need for invasive techniques such as angiography and Lipiodol CT as preoperative examinations for HCC.
Adult↗
[Field epidemiological investigation on an outbreak of Chlamydia pneumoniae infection--first recognized incidence in a nursing home for elderly in Japan].
Chlamydia pneumoniae (C. pneumoniae) is an emerging pathogen recognized in 1989. Although C. pneumoniae infection is known to give a great impact on public health in western countries, many aspects remain unclarified in Japan. During December 1999 and March 2000, respiratory symptoms among residents and employees in a nursing home for elderly implicated an outbreak of C. pneumoniae infection. Field epidemiological investigation confirmed that this is the first outbreak recognized in a nursing home setting in Japan, involving 31/59 (15 confirmed) residents and 9/41 (2 confirmed) employees. Fifteen residents developed severe C. pneumoniae infections including one fatal outcome with pneumonia. Epidemiological analysis did not identify risk factors which induce infection or severe illness by C. pneumoniae for the residents. However, for the employees, frequent contact with the residents was demonstrated as a significant risk factor for the infection. None of 13 employees who had no contact with the residents presented C. pneumoniae infection, while nine out of 28 employees who had frequent contact developed C. pneumoniae infections (RR infinite, P = 0.04). These results indicated that C. pneumoniae infection spread gradually by human-to-human droplet transmission without specific risk factors. This study raised current problems in diagnosing and treating the C. pneumoniae infection and the need to enhance the awareness of this disease.
Aged↗
Identification of hepatic venous territories in liver resection by using color Doppler ultrasonography: report of two cases.
OBJECTIVE: Resection of the hepatic vein because of the proximity of tumors may result in increased congestion in the noncancerous parenchyma, which in turn may lead to functional hepatic volume loss and postoperative hepatic failure, especially in a case of low hepatic reserve. However, to our knowledge, no technique for estimating the extent of dependent hepatic venous territories before hepatic resection has been established. We examined the possibility of using color Doppler ultrasonography for this purpose. METHODS: A color Doppler system and a linear array transducer equipped with multiple Doppler frequencies ranging from 7 to 13 MHz were used intraoperatively. Two patients with hepatocellular carcinomas were examined. By tracking entire branches of the targeted vessel, from the trunk to the terminal branches extending to the liver surface, it was possible for the boundaries of the dependent areas to be projected and marked on the liver surface with either ink or electrocautery. RESULTS: In both cases, this method was effective for either minimizing the congestive area or preserving the hepatic mass that was being drained via aberrant routes. CONCLUSIONS: Identification of hepatic venous territories by means of color Doppler ultrasonography may provide new information about intrahepatic blood circulation and may increase the safety and curability of hepatic resection.
Aged↗
Ca(2+) influx through nonselective cation channels plays an essential role in noradrenaline-induced arachidonic acid release in Chinese hamster ovary cells expressing alpha(1A)-, alpha(1B)-, or alpha(1D)-adrenergic receptors.
We constructed Chinese hamster ovary (CHO) cells stably expressing alpha(1A)-, alpha(1B)-, or alpha(1D)-adrenergic receptors (CHO-alpha(1A), CHO-alpha(1B), or CHO-alpha(1D), respectively) and compared the Ca(2+) channels activated by noradrenaline (NA) in these cells using whole-cell recordings and monitoring of the intracellular free Ca(2+) concentration ([Ca(2+)](i)). We also investigated the involvement of Ca(2+) channels in the NA-induced arachidonic acid release. In all three cell types, NA at concentrations > or =10 nM induced a sustained increase in [Ca(2+)](i) attributable to extracellular Ca(2+) influx in [Ca(2+)](i) monitoring and an inward current in whole-cell recording. The current-voltage relationships were linear, and their reversal potentials were close to 0 mV. The reversal potential of the currents was not affected by a change in the concentration of Cl(-) in the bath solution. Moreover, a current could be induced in a bath solution containing only Ca(2+) as the movable cation. LOE 908, a receptor-operated Ca(2+) channel blocker, inhibited the sustained increase in [Ca(2+)](i) and inward currents in a concentration-dependent manner, and complete inhibition was observed at concentrations > or = 3 microM. NA induced arachidonic acid release in all three cell types. This release was entirely dependent on extracellular Ca(2+) influx. Moreover, LOE 908 at concentrations > or = 3 microM blocked the NA-induced increase in arachidonic acid release. These results indicate that 1) NA activates LOE 908-sensitive Ca(2+)-permeable nonselective cation channels (NSCCs) in CHO-alpha(1A), CHO-alpha(1B), and CHO-alpha(1D), and 2) the Ca(2+) influx through NSCCs may play an important role in the NA-induced enhancement of arachidonic acid release in these cells.
Acetamides↗
Infection with Edwardsiella tarda causes hypertrophy of liver cells in the Japanese flounder Paralichthys olivaceus.
To study the direct cause of liver enlargement in the Japanese flounder Paralichthys olivaceus infected with Edwardsiella tarda, the fish were challenged with E. tarda and reared without feeding. The liver of fish exposed to the bacteria was markedly enlarged compared to that of the controls while no severe histopathological change appeared in the organ during the experiments. No notable difference was observed in the crude fat, glycogen, and water content of the liver between challenged and control fish. The size of liver cells and nuclei of the challenged fish was apparently larger than that of the controls. Analysis of crude DNA in the liver suggested that the number of liver cells of starved control fish significantly decreased during the experiment while that of the challenged fish was maintained at a level of the initial control. RNA/DNA ratio of the liver of challenged fish clearly increased while it decreased in the control fish during the experiment. These observations suggest that liver enlargement of flounder infected with E. tarda, at least in the early stage of infection, is not a result of any readily observable histopathological changes and that E. tarda infection causes hypertrophy of the cells, as well as preventing decrease in liver cell number.
Animals↗
An alternative method of arterial reconstruction after hepatic arterial thrombosis following living-related liver transplantation.
BACKGROUND: Hepatic artery thrombosis (HAT) remains an important cause of graft loss after liver transplantation. Emergency rearterialization methods are limited in cases of living-related liver transplantation in which the graft hepatic artery is thin and short. CASE: A 19-year-old woman who underwent living-related liver transplantation for biliary atresia developed HAT on the 4th postoperative day. During the emergency laparotomy the recipient hepatic artery was found to be too short to anastomose, so the recipient's right gastroepiploic artery was anastomosed to the graft hepatic artery. The patient is now alive and well 6 months after reoperation, and she has experienced no further episode of HAT. CONCLUSION: The right gastroepiploic artery can be used easily and safely for hepatic graft revascularization without causing ischemia of the stomach. An additional skin incision is not required, and the artery is long enough to anastomose to the graft artery directly. The method of hepatic graft rearterialization described here is an important option for patients who undergo living-related or split liver transplantation.
Adult↗
Cholesterol oxidation switches the internalization pathway of endothelin receptor type A from caveolae to clathrin-coated pits in Chinese hamster ovary cells.
We investigated the mechanism of endothelin receptor type A (ETA) internalization in Chinese hamster ovary cells using two assays; flow cytometric quantification of cell surface myc-ETA and in situ localization of Cy5-labeled ET-1. In both assays, agonist-dependent internalization of myc-ETA was inhibited by nystatin and filipin, both of which disrupt internalization via caveolae, whereas it was barely affected by chlorpromazine and hypertonic sucrose, both of which disrupt internalization via clathrin-coated pits. In addition to myc-ETA, ET-1 caused intracellular translocation of caveolin-1 and this translocation was also blocked by nystatin but not by chlorpromazine. These results strongly argue that ETA is internalized via caveolae but not clathrin-coated pits. Treatment of the cells with cholesterol oxidase reduced cellular cholesterol and caused intracellular translocation of caveolin-1 but did not affect cell surface localization of myc-ETA. In cholesterol oxidase-treated cells, however, both chlorpromazine and hypertonic sucrose effectively blocked ET-1-induced myc-ETA internalization and nystatin was less effective than in untreated cells. Accordingly, expression of a dominant negative form of beta-arrestin blocked myc-ETA internalization in cholesterol oxidase-treated cells but not in untreated cells. These results suggest that, in Chinese hamster ovary cells, 1) agonist-occupied ETA can be internalized either via caveolae or clathrin-coated pits; 2) of the two, the former is the default pathway; and 3) the oxidative state of cell surface cholesterol is one of the factors involved in the pathway selection.
Animals↗
Sonographic detection of visceral adhesion in percutaneous drainage of afferent-loop small-intestine obstruction.
To facilitate the percutaneous drainage of an afferent-loop small-intestine obstruction, we used sonography to detect visceral adhesions and select a safe puncture route. The portion of the small intestine that was fixed to the anterior abdominal wall was sonographically identified by using a high-frequency transducer to locate the area of restricted visceral sliding. The needle was then inserted into the intestine. In 3 cases, we have found that this technique improves the confidence of the physicians who perform the percutaneous drainage and may help to minimize the risks associated with the percutaneous drainage.
Afferent Loop Syndrome↗
Molecular cloning and expression profile of rat myocilin.
Myocilin is known to be associated with the pathogenesis of juvenile-onset primary open angle glaucoma. The tissue distribution of myocilin transcripts has been analyzed in both humans and mice, and a high level of expression in the retina and skeletal muscle has been reported. The functions of myocilin in these tissues are unknown. We isolated rat myocilin cDNA and examined the expression pattern of myocilin, including its expression in endocrine organs, using Northern blot analysis. The rat myocilin cDNA sequence has two in-frame initiation codons, the upstream and downstream ATGs corresponding to the initiation codon of human and murine myocilin, respectively. It is most likely that the first ATG is a translational initiation codon, since 8 of 13 amino acid residues deduced from the rat cDNA sequence between the first and the second ATGs are the same as those in human myocilin. The open reading frame encodes 502 amino acids. Rat myocilin also has both a myosin-like domain and an olfactmedin-like domain, which have been identified in human and murine myocilin. Northern analysis of rat myocilin mRNA revealed substantial expression in the thyroid gland, as well as in the retina and muscle. No transcripts were detected in other endocrine glands, including the adrenal gland, pituitary, and testis. Myocilin may play an important role in thyroid function. Further study of the expression and role of myocilin in the thyroid is required.
Amino Acid Sequence↗
Other erythrocyte enzyme deficiencies associated with non-haematological symptoms: phosphoglycerate kinase and phosphofructokinase deficiency.
Phosphoglycerate kinase (PGK) deficiency is associated with hereditary haemolytic anaemia and often with central nervous system dysfunction and/or myopathy. Twenty-three families have been discovered with this condition. Nine have manifested both symptoms, six only haemolysis, and seven central nervous system dysfunction and/or myopathy without haemolysis; one case is asymptomatic. Among them, the structural abnormalities of 14 mutants, including 11 missense mutations, 1 gene deletion, 1 gene insertion, and 1 splicing mutation, have been identified. The correlation between the phenotypic and structural differences in PGK deficiency remains to be defined. Splenectomy obviates transfusion in most patients but does not correct the haemolytic disorder. Phosphofructokinase (PFK) deficiency is associated with myopathy and/or haemolysis. More than half reported had the typical features of glycogen storage disease type VII (Tarui disease). The other cases exhibited myopathy alone, haemolytic anaemia alone, or no clinical symptom at all. Eight missense, 1 nonsense, 1 frameshift and 5 splicing mutations have been determined in the PFK-M gene. In classic PFK-M deficiency, the avoidance of undue exertion is the key to prevent muscle symptoms.
Anemia, Hemolytic, Congenital↗
Endothelin-1-induced contraction of rat thoracic aorta depends on calcium entry through three types of calcium channel.
We have recently shown that endothelin-1 (ET-1) activates two types of Ca2+-permeable nonselective cation channels (designated NSCC-1 and NSCC-2) and store-operated Ca2+ channel (SOCC). These channels can be pharmacologically discriminated using 1-[beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1-H-imidazoe l hydrochloride (SK&F 96365) (a blocker of NSCC-2 and SOCC) and (RS)-(3,4-dihydro-6,7-dimethoxyisoquinoline-1-gamma l)-2-phenyl-N,N-di-[2-(2,3,4-trimethoxyphenyl)ethyl]acetamide (LOE 908) (a blocker of NSCC-1 and NSCC-2). For our study we characterized Ca2+ channels involved in ET-1-induced contractions and increases in the intracellular free Ca2+ concentration ([Ca2+]i) using these blockers. Our results show that the response to lower concentrations of ET-1 involves only one Ca2+ channel which is sensitive to SK&F 96365 and LOE 908 (NSCC-2). In contrast, the response to higher concentrations of ET-1 involves two types of Ca2+ channel in addition to NSCC-2: one is sensitive to SK&F 96365 but resistant to LOE 908 (SOCC), and the other is resistant to SK&F 96365 but sensitive to LOE 908 (NSCC-1). Furthermore, the percentage contribution of Ca2+ entry through NSCC-1, NSCC-2 and SOCC is calculated to be 10%, 50-60% and 30-40%, respectively.
Acetamides↗