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T Harada

Publications and source records attributed to T Harada.

At least 253 records · Page 14Linked to original sources

Enhanced Formation of Roots and Subsequent Promotion of Growth of Shoots on Cryopreserved Nodal Segments of Asparagus officinalis L.

This study was designed to investigate the effects of cryopreservation on the survival, organogenesis, and growth of plants regenerated from nodal segments of asparagus (Asparagus officinalis L.) that had been cut from cultures in vitro. The addition of dimethylsulfoxide (Me2SO) to the freezing solution at 8-16% (v/v) with or without a sugar (glucose, sorbitol, or sucrose) was effective for successful cryopreservation by a slow prefreezing method. Frequencies of root formation (average, 59.3%) from cryopreserved and surviving nodal segments were significantly higher (P < 0.005) than those (average, 13.9%) from nodal segments that had only been treated with freezing solution supplemented with 12% (v/v) Me2SO and various sugars without freeze-thawing. The increased frequency of root formation from cryopreserved nodal segments appears to have been induced by the freeze-thaw step of the cryopreservation procedure. Numbers and lengths of shoots derived from cryopreserved nodal segments were initially lower but were subsequently higher, after 60-90 days of culture, than those of shoots derived from nodal segments without freeze-thawing. The promotion of growth of shoots from cryopreserved nodal segments seemed to have been due to the increased percentage of root formation. Histological observations revealed that only dome-shaped meristematic tissue and a few cells of cladophyll primordia survived in cryopreserved nodal segments that had been cultured for 5 days after thawing. Many mitochondria and well developed rER were observed in these cells. Disorganization and/or physiological changes might have occurred in the surviving tissues and/or cells of the cryopreserved nodal segments that were responsible for the subsequent increased formation of roots. Copyright 1998 Academic Press.

Journal Article↗

QTc interval, and autonomic and somatic nerve function in diabetic neuropathy.

QTc intervals were measured using an electrocardiogram and other autonomic function tests, in 66 neuropathy patients with non-insulin-dependent diabetes mellitus (59.0 +/- 12.5 years; mean +/- SD). The change in R-R interval did not influence the QTc interval, as calculated by the equation: QTc = QT + (1000 - R-R)/7 (ms), compared with the conventional Bazett's equation which appeared to overcompensate in the case of a small R-R interval. The QTc interval in the diabetic patients was significantly longer than that in age-matched controls. The QTc interval showed an inverse correlation with the coefficient of variation of the R-R interval and skin blood flow at rest. However, no correlation was found between QTc interval and blood pressure change, change in heart rate on standing, or results of the sympathetic skin response. The QTc interval did not correlate significantly with motor or sensory nerve conduction parameters. We conclude that the QTc interval can be a simple and useful autonomic indicator for diabetic neuropathy relatively independent of other abnormalities of autonomic and somatic nervous system function.

Aged↗

A study of sternocleidomastoid muscular atrophy after modified neck dissection.

To elucidate the conditions of atrophy in the sternocleidomastoid muscle (SCM) after modified neck dissection (MND), we tried to scrutinize the atrophic regions in the SCM and determine the cause of atrophy, by electromyography in 40 patients with SCM atrophy following MND. We also examined the detailed anatomy of the SCM in 40 cadavers. Atrophy was observed in the caudal portion in the SCM in 90% of the patients. Electromyographic examination revealed neurogenic atrophy in 24 patients, ischemic atrophy in 11, and a mixing of both types in 5. The SCM was found to be innervated by the spinal accessory nerve (SAN) and the SCM branch of the cervical nerve. The main artery feeding the cranial half of the SCM was a branch of the occipital artery (Oc) or the external carotid artery (Ex), and the auxiliary artery was a branch of the posterior auricular artery (Ap). The main artery feeding the caudal half of the SCM was a branch of the superior thyroidal artery (St), and the auxiliary artery was a branch of the subclavian artery (Sc). Postoperative SCM atrophy is attributed to damage of the feeding artery in the SCM caudal portion and local damage in the nerve fibers running through the SCM. To prevent this type of atrophy, it is important to carefully handle this muscle itself and protect the nerve fibers running through it, as well as to conserve the SCM branches of the St and Sc.

Aged↗

[A resected case of malignant peripheral nerve sheath tumor (MPNST) necessary to distinguish from Askin tumor].

We have treated a patient with malignant peripheral nerve sheath tumor (MPNST) for 7 years by interdisciplinary therapy. The diagnosis and treatment are reported with the clinical course so far. A 20-year-old man underwent surgical resection of a tumor on the left side of the chest in 1990, and a diagnosis of Askin tumor was made. In 1993, the disease recurred in the left axilla and was surgically resected. The surgical specimen was investigated histologically, and a diagnosis of MPNST was made instead of Askin tumor. Recently, a tumor began to grow in the left pleural cavity and was surgical resected. The tumor tissue contained both cells with oval and long spindle nuclei, which were intermingled with each other. Immunohistochemically, the tumor cells were positive for vimentin and some of them were positive for S100 protein. Because electron microscopy showed cytoplasmic processes on the tumor cell and basal lamina-like structures, a diagnosis of recurrent MPNST was made. Because this lesion resembled Askin tumor in its clinical manifestations and histological characteristics, differential diagnosis from Askin tumor was necessary. When a malignant soft tissue tumor arising from the mediastinum or chest walls is detected, immunohistochemical and electron microscopic studies should be performed. The diagnosis should be based on the overall findings including the location and clinical data.

Adult↗

Effect of exercise-induced acidosis on aldosterone secretion in men.

The present study was carried out to elucidate whether an exercise-induced increase in plasma hydrogen ion concentration influences aldosterone secretion. Six healthy men (aged 22-25 years) performed two intermittent exercise tests with and without drug administration. The intensities of these exercise tests were 40% maximal oxygen uptake (VO2max) and 90% VO2max, respectively. Administration of 2-mg Dexamethasone and 50-mg Captopril caused an almost complete suppression of adrenocorticotropic hormone (ACTH) and an enhancement of the elevation in renin concentration during exercise, indicating successful inhibition of ACTH release and angiotensin II production during exercise. While the magnitude of the increase in aldosterone in the drug experiment was depressed compared with the control experiment, a significant increase in aldosterone concentration was observed at the end of the 90% VO2max exercise. Whilst the change in aldosterone concentration did not correlate with the change in plasma potassium concentration, there was a significant correlation between aldosterone and plasma hydrogen ion concentrations in the drug experiment. Since the correlation coefficient was low (r = 0.455), the biological meaning of this correlation should be further investigated. These results would suggest that an elevation of plasma hydrogen ion concentration induced by exercise per se appears to be related, at least in part, with increased aldosterone secretion, independent of the pituitary-adrenal axis, and the renin-angiotensin system.

Acidosis↗

Expression of membrane-type matrix metalloproteinase-1 in human pancreatic adenocarcinomas.

The expression of a new type of matrix metalloproteinase, membrane-type matrix metalloproteinase-1 (MT-MMP-1), was examined in 24 cases of primary pancreatic adenocarcinomas and 9 cases of secondary liver tumors derived from pancreatic adenocarcinomas, using a non-radioactive in situ hybridization and immunohistochemical methods. Out of 24 cases of primary pancreatic adenocarcinomas, 18 showed positive expression of MT-MMP-1 transcripts in cancer cells and 20 of 24 showed positive expression in the tumor stromal cells. The immunoreactivity of the gene products for MT-MMP-1 was demonstrated to be almost the same, as shown by in situ hybridization in these 24 cases. In particular, both the staining intensity for MT-MMP-1 transcripts and the immunoreactivity of the gene products in the tumor stromal cells of mucinous cystadenocarcinomas were significantly weaker than those of common-type ductal adenocarcinomas among the 24 cases. All of the 9 cases of secondary liver tumors derived from pancreatic adenocarcinomas showed positive expression for MT-MMP- transcripts but less immunoreactivity for the gene products. These results suggest that MT-MMP-1 is transcribed and translated in both cancer cells and the tumor stromal cells in human pancreatic adenocarcinomas. Furthermore, considering that common-type ductal adenocarcinoma of the pancreas usually shows a strong desmoplastic reaction, while mucinous cystadenocarcinoma typically does not, MT-MMP-1 expressed in the tumor stromal cells of common-type adenocarcinomas may be involved in processes leading to the desmoplastic reaction.

Adenocarcinoma↗

Inhibition of tumor growth and microvascular angiogenesis by the potent angiogenesis inhibitor, TNP-470, in rats.

The antiangiogenic effects of TNP-470 on the neovascularization of tumors were studied by examining ultrastructural alterations in the vasculature and interstitial fluid pressure (IFP) of tumors. Wistar rats were first inoculated subcutaneously (s.c.) with the Walker 256 carcinosarcoma cell line, then either vehicle medium or TNP-470, 30 mg/kg, was injected s.c. on day 1. A tumor growth assay, the necrotic area, and the IFP in the tumor were all measured on day 12. The antiangiogenic effects of TNP-470 were studied by scanning electron microscopic images of tumor vascular casts. TNP-470 was observed to inhibit tumor growth and increase the necrotic area significantly. In the TNP-470-treated group, the IFP in the superficial layer, defined as 2-3 mm from the tumor capsule, and in the deep layer, defined as 8-10 mm from the tumor capsule, were significantly higher than the corresponding values in the control. Moreover, vascular casts showed a significant reduction in the budding of sprouts in the superficial layer, and a decrease in the maximum diameter of the tumor vessels in the deep layer. It is possible that the higher IFP in the TNP-470-treated tumors might have prevented tumor vessel dilation. The findings of this study demonstrated that TNP-470 inhibited the budding of tumor vessel sprouts, and increased the IFP. These processes seem to act synergistically to suppress tumor angiogenesis.

Animals↗

Surgical drainage for idiopathic suppurative pylephlebitis.

Idiopathic suppurative pylephlebitis is quite rare and only a few cases have been reported. Conservative systemic administration of antibiotics and urokinase is reported to be effective. In this report, surgical drainage was performed on an 18-year-old man who complained of fever and abdominal pain. He had no past history of abdominal inflammatory disease or abdominal surgery. Ultrasonography and computed tomography showed wide spread thrombosis of the portal vein. Laparotomy was performed and the occluded superior mesenteric vein was incised. Massive pus was removed. Thereafter, a drain was placed at the opened mesenteric vein. Drainage resulted in a dramatic decrease in fever. Postoperative radiographic studies of the colon, the small intestine, and other organs did not show any abnormalities. Emergency surgical drainage was performed successfully, instead of systemic administration of antibiotics and urokinase. Surgical drainage may be useful for wide spread pylephlebitis and pylethrombosis.

Abdomen, Acute↗

Membrane-type matrix metalloproteinase-1(MT1-MTP) gene is overexpressed in highly invasive hepatocellular carcinomas.

BACKGROUND/AIMS: The matrix metalloproteinase (MMP) family play important roles in the invasion of cancer cells by degrading the extracellular matrices. The current study was designed to determine the expression pattern of membrane-type matrix metalloproteinase-1 (MT1-MMP) in hepatocellular carcinomas and its participation in invasion potential. METHODS: MT1-MMP mRNA expression was examined in 25 human hepatocellular carcinoma specimens using Northern blot, and the correlation to clinicopathological features was evaluated. In situ hybridization and immunohistochemistry were performed to study the localization and the cells responsible for the production. RESULTS: Northern blot analysis revealed high levels of MT1-MMP mRNA expression in tumorous portions in all cases, whereas in non-tumorous portions moderate or faint expression was evident in 22/25 cases. In 21/25 cases, the expression levels in tumorous portion were higher than those in non-tumorous portion. In particular, hepatocellular carcinoma with capsule infiltration demonstrated significantly higher expression than those without (p<0.05). In situ hybridization and immunohistochemical study revealed MT1-MMP transcripts and proteins in cancer cells and stromal cells, respectively. MT1-MMP positive cells were preferentially observed in the invading border of tumor nests. The MMP-2 transcript showed a similar pattern to that of MT1-MMP by in situ hybridization. CONCLUSION: The present study showed that the MT1-MMP gene is strongly expressed in hepatocellular carcinoma cells and is involved in the invasion potential of hepatocellular carcinoma, and also that MT1-MMP may be one of the key molecules responsible for the invasion potential of hepatocellular carcinoma. Furthermore, the evidence suggests that MT1-MMP and MMP-2 cooperate in the process of cancer invasion.

Adult↗

Pathogenetic significance of increased levels of interleukin-8 in the peritoneal fluid of patients with endometriosis.

OBJECTIVE: To investigate the role of interleukin-8 (IL-8) in peritoneal fluid of patients with endometriosis in the pathogenesis of endometriosis. DESIGN: Peritoneal fluid was collected by laparoscopy. Endometrial and endometriotic stromal cells were obtained from normal endometrium and from chocolate cyst linings of the ovary. SETTING: Department of Obstetrics and Gynecology of Tottori University Hospital, Yonago, Japan. PATIENT(S): Forty women who underwent either laparoscopy or laparoscopic surgery. MAIN OUTCOME MEASURE(S): The peritoneal fluid concentration of IL-8 was analyzed by enzyme-linked immunosorbent assay, and the correlation between the IL-8 concentration and the extent of active endometriosis was investigated. The effect of IL-8 on cell proliferation was examined by tetrazolium bromide and thymidine incorporation. The expression of IL-8 receptor was examined in stromal cells by reverse transcription polymerase chain reaction. RESULT(S): The level of IL-8 in peritoneal fluid was significantly higher in patients with endometriosis than in patients without endometriosis. A significant correlation was noted with the extent of active endometriosis. Interleukin-8 significantly increased the number of cells and DNA synthesis in the endometrial and endometriotic stromal cells in a dose-dependent manner. Transcripts of IL-8 receptor type A were detected in stromal cells. CONCLUSION(S): The present study suggests that IL-8 found in the peritoneal fluid of patients with endometriosis contributes to the pathogenesis of endometriosis.

Antigens, CD↗

Coronary sinus pacing initiates counterclockwise atrial flutter while pacing from the low lateral right atrium initiates clockwise atrial flutter. Analysis of episodes of direct initiation of atrial flutter.

INTRODUCTION: Rapid atrial pacing in sinus rhythm may directly induce atrial flutter without provoking intervening atrial fibrillation, or initiate atrial flutter indirectly, by a conversion from an episode of transient atrial fibrillation provoked by rapid atrial pacing. The present study was performed to examine whether or not the direct induction of clockwise or counterclockwise atrial flutter was pacing-site (right or left atrium) dependent. METHODS AND RESULTS: We analyzed the mode of direct induction of atrial flutter by rapid atrial pacing. In 46 patients with a history of atrial flutter, rapid atrial pacing with 3 to 20 stimuli (cycle length = 500 - 170 ms) was performed in sinus rhythm to induce atrial flutter from 3 atrial sites, including the high right atrium, the low lateral right atrium, and the proximal coronary sinus, while recording multiple intracardiac electrograms of the atria. Direct induction of atrial flutter by rapid atrial pacing was a rare phenomenon and was documented only 22 times in 15 patients: 3, 11, and 8 times during stimulation, respectively, from the high right atrium, low lateral right atrium, and the proximal coronary sinus. Counterclockwise atrial flutter (12 times) was more frequently induced with stimulation from the proximal coronary sinus than from the low lateral right atrium (8 vs 1, P = .0001); clockwise atrial flutter (10 times) was induced exclusively from the low lateral right atrium (P = .0001 for low lateral right atrium vs proximal coronary sinus, P = .011 for low lateral right atrium vs high right atrium). CONCLUSIONS: Direct induction of either counterclockwise or clockwise atrial flutter was definitively pacing-site dependent; low lateral right atrial pacing induced clockwise, while proximal coronary sinus pacing induced counterclockwise atrial flutter. Anatomic correlation between the flutter circuit and the atrial pacing site may play an important role in the inducibility of counterclockwise or clockwise atrial flutter.

Adult↗

Extrinsic nerve strands in the aganglionic segment of Hirschsprung's disease.

BACKGROUND/PURPOSE: The distributions and pathways of the extrinsic enteric nerves in the aganglionic segment in Hirschsprung's disease (HD) have not been delineated completely. The authors have clarified the major pathways and the details of fine distribution of the extrinsic nerves in the aganglionic segment of a congenital aganglionosis rat. Further investigation was extended to apply those findings in human materials. METHODS: Five HD patients, eight fetuses, and two postmortem neonates with normally innervated colon were examined. Specimens were observed by histochemical technique using light microscopy in whole-mount preparations. RESULTS: Two sets of extrinsic nerve strands were observed in the distal aganglionic colon; one consisted of a continuous network located between the longitudinal and circular muscle coats, and the other involved branches that mainly coursed along the blood vessels in the submucosal layer originating from the nearby mesentery. These two sets of nerve strands were similar to those of aganglionosis rats. Also, thick nerve strands were found running longitudinally in the myenteric layer in the normally ganglionated colon of 18- and 21-week-old fetuses. These nerve strands were unclear in a 32-week-old fetus. CONCLUSIONS: This study showed the following: (1) the origin of the nerve strands in the myenteric layer is mainly the pelvic nerve plexus and (2) the number of ascending extrinsic nerve strands decreases from the proximal colon in cases of long-segment aganglionosis, which may be caused by the same process that occurs in the normally innervated bowel.

Colon↗

Surgical removal of protein plugs complicating choledochal cysts: primary repair after adequate opening of the pancreatic duct.

BACKGROUND/PURPOSE: Recently, pancreaticoduodenectomies have been performed for choledochal cysts complicated by protein plugs. The authors describe a new surgical procedure for removal of protein plugs or pancreatic stones that does not involve pancreatectomy. METHODS: Protein plugs were detected in 43 (34.1%) of 126 pediatric patients with choledochal cysts. The plugs disappeared spontaneously in 26 patients and were removed using nonsurgical methods in seven. The 10 patients treated surgically are considered here. RESULTS: Protein plugs were removed with the residual cyst in one patient. The plugs in the common channel were flushed into the duodenum by irrigation with saline through the narrow segment beneath choledochal cyst in another. The plugs were removed through the narrow segment using a blunt spoon in four. In the other four patients, the plugs that were too large or too hard to be removed through the narrow segment were taken away through an incision in the main pancreatic duct. This was followed by primary closure of the main pancreatic duct using the narrow segment as a flap to prevent stricture formation. All of the patients have done well. CONCLUSIONS: Protein plugs complicating choledochal cysts can be removed without pancreatectomy. Particularly, primary repair of the pancreatic duct using a flap made of the narrow segment beneath the choledochal cyst is a safe and feasible method to remove large or hard protein plugs.

Adolescent↗

Combined resection of abdominal aorta and inferior vena cava for retroperitoneal rhabdomyosarcoma invading the aortoiliac bifurcation.

The authors report on an 11-year-old boy with retroperitoneal alveolar rhabdomyosarcoma at the aortoiliac bifurcation. The tumor was resected en bloc together with the infrarenal abdominal aorta and the inferior vena cava. The aortic defect was repaired successfully with a Y-shaped Dacron graft. The authors conclude that tumor resection with aortic reconstruction can be a choice for unresectable retroperitoneal tumors in children.

Aorta, Abdominal↗

Muscle damage induced by experimental hypoglycemia.

To determine organ damage due to hypoglycemia, we studied the effects of insulin dose and hypoglycemia duration on serum enzyme activity in rabbits. Thirty rabbits were randomly divided into five groups according to hypoglycemia duration and insulin dose: A2, hypoglycemia for 30 minutes with 2 U/kg insulin; A10, hypoglycemia for 30 minutes with 10 U/kg insulin; B2, hypoglycemia for 60 minutes with 2 U/kg insulin; B10, hypoglycemia for 60 minutes with 10 U/kg insulin; and C, no hypoglycemia with 10 U/kg insulin and 50% glucose. Insulin-induced hypoglycemia was reversed by intravenous injection of glucose. Alterations in serum enzyme activity and creatine kinase (CK) isoenzyme distribution were determined before and after insulin injection. Serum CK activity increased significantly in all hypoglycemic groups compared with preinjection values, and tended to remain high for 24 hours in both groups A10 and B10. Serum activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) increased only in group B10. In addition, the level of band 4 of serum CK isoenzymes, which exists predominantly in skeletal muscle and myocardium, increased significantly in group B10. These results suggest that the increase in both serum enzyme and CK band 4 isoenzyme activities during hypoglycemia is primarily due to damage in muscle rather than liver, and that the hypoglycemia duration and insulin dosage may influence the extent of organ damage.

Alanine Transaminase↗

Detection of gains and losses in 18 meningiomas by comparative genomic hybridization.

Comparative genomic hybridization (CGH) was used to examine gains and losses in 18 meningioma tumors that had been previously analyzed for loss of heterozygosity (LOH) at 22q12. Partial or complete losses were seen by CGH in only 9 of 18 cases on chromosome 22. This compares with 11 of 18 losses of single or more loci by LOH. The discrepancy in these results in probably explained by the increased sensitivity of LOH by using microsatellite markers that are able to detect small deletions, whereas losses on the order of 10-15 megabases are required for confident identification by CGH. There was no consistent pattern of gains or losses by CGH, including those tumors that lacked LOH at 22q12. In one tumor of interest in which CGH and LOH studies failed to demonstrate loss on chromosome 22, CGH identified an area of amplification at 17q22-23.

Chromosome Deletion↗