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Biomedical subjects

K Shibata

Publications and source records attributed to K Shibata.

At least 397 records · Page 22Linked to original sources
PubMed1994

[Mechanism and prevention of postoperative hemolysis in the corrective surgery of subarterial ventricular septal defects].

Intravascular hemolysis following the repair of subarterial ventricular septal defects (VSD) was studied in 34 patients. The VSD was closed through a main pulmonary arteriotomy with a Dacron double-velour patch (Meadox, Oakland, NJ) in 17 cases (Group B) and with a Dacron single-velour patch covered by autologous pericardium facing toward the right ventricular outflow tract (RVOT) in 17 cases (Group A). No significant intergroup difference in age, weight, Qp/Qs, Pp/Ps, and Rp/Rs was found. There were no significant differences in the preoperative values of serum LDH, total bilirubin, and flow velocity at the RVOT (Group A: 1.7 +/- 0.4 m/sec vs Group B 1.8 +/- 1.0 m/sec). The severity of hemolysis was evaluated by serum LDH levels, total bilirubin levels, and hemoglobinuria on the morning of the first operative day. Postoperative LDH levels were significantly lower in the Group A (812 +/- 205 IU/L) than in the Group B (1098 +/- 427 IU/L) (p < 0.05). Hemoglobinuria developed in 2 patients in Group B (12%) and none in Group A. These data suggest that the pericardium apparently protects against postoperative hemolysis. The intensity of the turbulence at the RVOT was graded as follows using color-doppler echocardiography (0: none; Grade 1: turbulence was detected near the patch only; Grade 2: turbulence was detected halfway to the RVOT; Grade 3: turbulence extended to the anterior wall of the RVOT). The relationship between the presence of hemolysis and the degree of turbulence was examined. Turbulence at the RVOT appeared in 73% of those in Group A and in 82% of those in Group B.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

[Acute arterial occlusion of the lower extremities].

The clinical course of 40 patients with acute arterial occlusions of a lower extremity was reviewed with special reference to the etiology. Patients were classified into three groups: arterial embolism (10 patients), acute atherosclerotic thrombosis (AAT) (13 patients), and miscellaneous (17 patients). Circulation was restored in 83% of cases; embolism, 100%; AAT, 55%; and miscellaneous 88%. Five patients (13%) died, including 2 of MNMS (Myo-nephropathic-metabolic syndrome). MNMS developed in 1 patient in the embolism, 2 patients in the AAT, and 5 patients in the miscellaneous group. The five patients with MNMS in the embolism and miscellaneous groups were treated between 6 to 12 hours following the onset of symptoms, while both patients in the AAT group were not treated until 24 to 72 hours following occlusion. Revascularization was successful in the AAT group even when the ischemia lasted for 6 to 8 hours. However, patients in the embolism and miscellaneous Groups, who lacked effective collateral circulation, were at greater risk for developing MNMS when ischemia last for more than 6 hours.

Acute Disease↗
PubMed1994

[Maintenance hemodialysis in IgD- lambda -type multiple myeloma associated with severe renal failure].

A 52-year-old man was admitted to our hospital because of oliguric renal failure. The patient was well until four weeks earlier, when he developed nausea and anorexia. The urea nitrogen was 179 mg/dl, creatinine 29.2 mg/dl, uric acid 19.0 mg/dl and potassium 8.6 mEq/1. Hemodialysis was started immediately after admission. Bone marrow aspiration showed atypical plasma cell infiltration consistent with multiple myeloma. The immunoelectrophoresis revealed urinary lambda -type Bence Jones protein and serum IgD- lambda -type M protein. The findings of renal biopsy study were consistent with myeloma kidney. On the fourth hospital day, administration of prednisolone 40 mg and melphalan 2 mg was started. The patient also underwent double filtration plasma-pheresis (DFPP). Serum IgD level was decreased from 950 to 113 mg/dl. After a course of chemotherapy, however, he developed severe leukopenia and was complicated with methicillin-resistant Staphylococcus aureus (MRSA) pneumonia. This complication was successfully treated with imipenem/cilastation and vancomycin combined with granulocyte colony stimulating factor (G-CSF). The patient was discharged and returned to work on maintenance hemodialysis. Fifteen months after the presentation, he manifested progressive peripheral nerve disturbances. Three months later, the patient died--not from renal failure, but from ventricular arrhythmia. The application of maintenance dialysis therapy to myelomatosis has until now been questioned. The present case, however, suggests that aggressive treatment consisting of chronic dialysis therapy as well as chemotherapy and plasma exchange should be administered even in patients with established renal failure.

Humans↗
PubMed1994

[Chemical structural analysis of steroids by NMR spectroscopy].

NMR is so convenient way to get stereochemical information of an organic compound that organic chemists have readily taken advantage of its spectra to investigate its stereochemistry by means of chemical shifts, coupling constants, nuclear Overhauser effect, etc. Especially in the steroid field, there have been reported many studies for determination of chemical structure and analysis of conformation. It is exemplified how NMR is in steroid chemistry.

Aldosterone↗
PubMed1994

[A case of intracranial arteriovenous malformation presenting with intracranial hypertension].

A case of unruptured arteriovenous malformations (AVMs) presenting benign intracranial hypertension is reported. A 14-year-old male suffered from headache and papilledema. Intracranial pressure was 260 mmH2O. Unenhanced CT demonstrated no evidence of hemorrhage or hydrocephalus. Angiogram demonstrated a large AVM in the left temporal lobe supplied by the left posterior cerebral artery and left middle cerebral artery. It drained into the transverse sinus. Surgical excision of the AVM eliminated the headache and papilledema. AVM causes hemorrhage in 50% of cases, seizure in 30%, and other focal neurological deficits in 20%. Benign intracranial hypertension is an uncommon effect of unruptured AVMs. Only 13 cases have been reported in the literature. Benign intracranial hypertension associated with unruptured AVMs occurs in young patients with high flow AVMs that drain into the major sinus. The mechanism of intracranial hypertension associated with unruptured AVM is unknown. However, there are several possible mechanisms of intracranial hypertension associated with unruptured AVMs. The arterial blood shunting into a major sinus impedes venous return from the surrounding brain. That causes the increase of cerebral blood volume and the elevation of sinus pressure. This mechanism would reduce CSF absorption and would increase intracranial pressure. Pharmacological therapy is ineffective in controlling intracranial hypertension. Surgical excision of AVM effectively reduced intracranial hypertension. Thus, surgical excision of AVMs, if it can be done with low risk, is the treatment of choice to decrease intracranial hypertension in patients with unruptured cerebral AVMs.

Adolescent↗
PubMed1994

[A case of cortical blindness confirmed by single photon emission computerized tomography and visual evoked potential].

We reported a rare case of cortical blindness in cerebral ischemia following post-anoxic state confirmed by single photon emission computerized tomography (SPECT) and visual evoked potential. A 45-year-old woman who had been suffering from bronchial asthma was admitted to our hospital because of sudden progressive dyspnea and depressed consciousness. When she arrived at the hospital by ambulance, she was in hypoxic state and fell into cardiac arrest. Her respiratory condition gradually improved with respirator assistance, and she recovered consciousness, but complained of bilateral visual loss. She had no history of any neurological or psychiatric illness, nor of drug abuse. On neurological examination, she was alert and oriented. Light reflex, optic fundi, extraocular movement and other neurological findings were all normal, with the exception of bilateral blindness. EEG showed generalized slow background activity, but cranial CT scan and MRI showed no abnormalities. 99mTc-HMPAO SPECT indicated hypoperfusion in prominent bilateral occipital and parietal lobes. Simultaneous recordings of pattern reversal visual evoked potential (VEP) and electroretinograms (ERG) using transient checkerboard pattern reversal in 15 min and 30 min checks were recorded. The results showed normal b waves but absent P100 in the bilateral eyes. From the patient's neurological symptoms and the results of SPECT and VEP, she was diagnosed as cortical blindness in post-anoxic state. On the 30th hospital day, her visual acuity and visual fields improved, but she was suspected of having visual agnosia. Eighty-five days after the onset of the neurological abnormalities, no traces of visual disturbances were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Blindness↗
PubMed1993

A radioimmunoassay for pancreatic elastase 1: use of alpha 1-antitrypsin-elastase 1 conjugate as both standard and tracer to eliminate the influence of anti-elastase 1 autoantibodies.

We have recently reported the occurrence of anti-elastase 1 autoantibodies in human sera (Asada et al., Biochim Biophys Acta, 1991;1080:34-39). The usual radioimmunoassay of elastase 1 in autoantibody-positive sera gave abnormally high levels of elastase 1 and low recoveries of elastase 1 added to the sera. Now we have established a new radioimmunoassay system for determining pancreatic elastase 1 in serum, in which alpha 1-antitrypsin elastase 1 conjugate, the major conjugation form of elastase 1 in serum, is used as standard and alpha 1-antitrypsin-[125I]elastase 1 as tracer, because we found that the conjugate could bind to the elastase 1 specific antiserum but not to the autoantibodies. Thus the new assay system completely eliminate the unfavorable effects of the autoantibodies. The elastase 1 levels determined by the new assay method exhibited a good correlation with those obtained by a commercial assay kit in the autoantibody-negative sera, while no correlation was observed in the autoantibody-positive sera.

Acute Disease↗
PubMed1993

Cell cycle-dependent suppressive effect of histone H1 on mitosis-specific H3 phosphorylation.

To analyze the mechanism by which histone H3 phosphorylation occurs specifically during mitosis, the effect of H1 on mitosis-specific H3 phosphorylation (Ser-10) was investigated in nucleosomes. H1 interaction with H1-depleted nucleosomes suppressed H3 phosphorylation including Ser-10 by approximately 50%. However, H1 interaction with DNA-free histone octamers failed to suppress H3 phosphorylation. The extent of suppression of H3 phosphorylation in nucleosomes with H1 prepared from synchronized HeLa cells was cell cycle-dependent. Binding with a highly phosphorylated mitotic H1 produced the least suppression of H3 phosphorylation, whereas binding with a lower H1 phosphorylation from G1 phase resulted in the greatest suppression. The results suggest that 1) mitotic H3 phosphorylation is suppressed with a lower level of H1 phosphorylation during interphase and 2) highly phosphorylated H1 during mitosis partially releases the suppression of mitotic H3 phosphorylation.

Animals↗
PubMed1993

Two-dimensional echocardiographic assessment of papillary muscle contractility in patients with prior myocardial infarction.

OBJECTIVES: This study was performed to assess the length and contractile performance of human left ventricular papillary muscles and to determine the relation between papillary muscle dysfunction and mitral regurgitation. BACKGROUND: Assessment of human papillary muscle contractility remains a clinical challenge. METHODS: Two-dimensional echocardiographic examinations were performed in 16 normal subjects and 31 patients with prior myocardial infarction. Apical echocardiograms were used to obtain long-axis views of the anterior and posterior papillary muscles. The end-systolic and end-diastolic lengths of the papillary muscles were measured and fractional shortening was calculated. RESULTS: Fractional shortening in normal subjects was 27 +/- 8% for the anterior papillary muscle and 30 +/- 8% for the posterior papillary muscle. In patients with prior myocardial infarction, a significant decrease in fractional shortening was observed in proportion to the severity of left ventricular wall motion abnormalities at the site of papillary muscle implantation. Moderate or severe mitral regurgitation was significantly more frequent in patients with combined anterior and posterior papillary muscle dysfunction than in those with isolated anterior or posterior dysfunction or with normal function of both papillary muscles (p < 0.05). CONCLUSIONS: Two-dimensional echocardiography is useful for demonstrating abnormal contractility of human left ventricular papillary muscles. Papillary muscle contractility should be analyzed in each case to elucidate the mechanism of mitral regurgitation in patients with papillary muscle dysfunction.

Adult↗
PubMed1993

Metabolism and toxicity of intravenously injected yttrium chloride in rats.

Although radioactive yttrium (Y) has been used for medical treatment, little attention has been directed toward the toxicity of Y. We report time-course and dose-related changes in tissue distribution, subcellular localization, clearance, and acute toxicity of iv-injected yttrium chloride (YCl3) in rats. Intravenously injected Y was predominantly distributed to plasma in the blood. At doses more than 0.2 mg Y/rat, most plasma Y appears to be in colloidal material which was composed of proteins and some minerals. Electron microscopic analyses revealed that the colloidal material was taken up by phagocytic cells in the liver and spleen. The liver Y was slowly cleared with a half-time of 144 days at a dose of 1 mg Y/rat. Glutamic-oxaloacetic and glutamic-pyruvate transaminase activities in blood plasma were increased with a peak at 20 hr postinjection at a dose of 1 mg Y/rat and returned to their control values at 170 hr postinjection, indicating that iv-injected YCl3 caused acute hepatic injury. Some of the plasma Ca was translocated to the colloidal material and plasma Ca concentration was increased transiently following injection of YCl3, probably because of resorption of bone. At a dose of 1 mg Y/rat, a significant and tremendous amount of Ca was deposited in the liver (over 10-fold) and spleen (over 100-fold), while Ca concentration was only slightly increased in the lung and kidney (less than 1.5-fold). These results indicate that the liver and spleen are primary target organs of iv-injected YCl3.

Animals↗
PubMed1993

Antagonism of central pressor response to angiotensin II by alpha-human atrial natriuretic polypeptide at the preoptic area and posterior hypothalamus in rats.

Effects of alpha-human atrial natriuretic polypeptides (alpha-hANP) on pressor responses to angiotensin II (AII) were assessed at the preoptic area, posterior hypothalamus and central amygdaloid nucleus (ACE) in spontaneously hypertensive (SHR) and control normotensive Wistar-Kyoto (WKY) rats. Angiotensin II, administered intracerebroventricularly, at a dose of 100 ng produced a marked pressor response in hypertensive, as well as in normotensive rats and the response was potentiated in hypertensive rats. The response was antagonized in a dose-dependent manner by administration of alpha-hANP into the preoptic area and posterior hypothalamus but not to the amygdaloid nucleus. The antagonism was more marked in hypertensive than in normotensive rats. Angiotensin II, when injected directly to the preoptic area at a small dose of 10 ng similarly evoked a marked pressor response, which was augmented in hypertensive rats. This response was also antagonized by coadministration of alpha-hANP to the preoptic area in hypertensive but not in normotensive rats. The results suggest that the antagonistic relationship between ANP and AII exists at the preoptic area and posterior hypothalamus, probably implying that the activity of the ANP and AII systems in brain play a role in centrally controlling the cardiovascular system and is altered at these areas in genetically hypertensive rats.

Amygdala↗