Biomedical subjects

Y Sakai

Publications and source records attributed to Y Sakai.

At least 559 records · Page 31Linked to original sources

PubMed1993

Venoarterial carbon dioxide tension gradient in acute heart failure.

The venoarterial carbon dioxide tension gradient (P[v-a]CO2) was studied in patients with acute myocardial infarction. Seven patients with congestive heart failure (CHF group) and 10 patients without heart failure (control) were enrolled in this study. In all patients, hemodynamics were continuously monitored. Simultaneously, arterial and mixed venous blood were sampled, and blood gases and lactate concentration were analyzed. At the initial measurement before therapy, arterial and mixed venous pH and bicarbonate values were within the normal range, and there was no significant difference between the CHF group and controls. There was also no difference in arterial oxygen tension under the differential conditions of oxygen inhalation. However, cardiac index and mixed venous oxygen saturation (SvO2) were significantly lower, while the oxygen extraction ratio (OER) and arterial lactate were significantly higher in the CHF group than in the controls. On the other hand, P[v-a]CO2 was significantly higher in the CHF group (7.8 +/- 2.6 vs. 3.5 +/- 2.2 mm Hg, p < 0.01). This finding was due to the elevated mixed venous carbon dioxide tension in the CHF group, since arterial carbon dioxide tension was the same in both groups. Analysis of a total of 42 measurements obtained during the therapeutic course in the CHF group revealed a correlation of P[v-a]CO2 with cardiac index (r = -0.3, p < 0.05), OER (r = 0.57, p < 0.001), SvO2 (r = -0.56, p < 0.001) and lactate (r = 0.62, p < 0.001). The increase in P[v-a]CO2 observed in acute heart failure suggests the evidence of intracellular acidosis despite the absence of acidemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed1993

The effect of somatostatin analogue octreotide on amylase secretion from mouse pancreatic acini.

To clarify whether somatostatin has an inhibitory effect on pancreatic acinar cells, we studied the effect of a long-acting analogue of somatostatin, octreotide, on amylase secretion from isolated mouse pancreatic acini. Octreotide (100 nM) had no inhibitory effects on amylase secretion stimulated by secretin or vasoactive intestinal polypeptide (VIP), while reducing the increase of cyclic adenosine 3',5'-monophosphate (cAMP). On the other hand, octreotide inhibited synergistic amylase secretion induced by secretin or VIP in combination with cholecystokinin (CCK). Octreotide also reduced synergistic amylase secretion by secretin or VIP in combination with calcium ionophore A23187. CCK and A23187 did not alter the increase of cAMP induced by secretin and the inhibitory effect of octreotide on cAMP production. Octreotide did not significantly inhibit amylase secretion stimulated by dibutyryl cAMP (dbcAMP) alone, but reduced synergistic amylase secretion by dbcAMP+A23187. Results obtained above reveal that octreotide has a direct inhibitory effect on amylase secretion from mouse pancreatic acini and probably affects stimulus secretion coupling at a point distal to the production of cAMP, besides inhibiting adenylate cyclase.

Amylases↗

PubMed1993

Autoimmune haemolytic anaemia, Sjögren's syndrome and idiopathic thrombocytopenic purpura in a patient with sarcoidosis.

A unique occurrence of sarcoidosis autoimmune haemolytic anaemia (AIHA), Sjögren's syndrome and idiopathic thrombocytopenic purpura (ITP) in the same patient is reported. Although the occurrence of autoimmune disease with sarcoidosis is well known, a case in which several of these diseases coexist with sarcoidosis is rare. We present a man with longstanding sarcoidosis who developed AIHA. Sjögren's syndrome and ITP. This case report seems to be the first case in which three autoimmune diseases were accompanied by sarcoidosis in 1 patient.

Adult↗

PubMed1993

Features of coronary artery lesions related to left ventricular aneurysm formation in anterior myocardial infarction.

To determine the factors of left ventricular aneurysm formation in acute myocardial infarction, the authors studied the distribution of coronary artery lesions and the left ventricular wall motion of 43 patients with anterior myocardial infarction. Of 15 patients with aneurysm, 9 (60%) showed a single-vessel disease with severe stenosis of the proximal left anterior descending artery. Of 9 patients with triple-vessel disease, 8 (89%) had no aneurysm. In patients with the aneurysm, the Gensini score of the culprit lesion was significantly higher (p < 0.05) and the score except for the culprit lesion was less (chi 2 = 5.7, p < 0.05). In 23 patients with single-vessel disease, the collateral score was significantly less (p < 0.05) in patients with the aneurysm. The systolic wall motion on the ventriculogram appeared more impaired in the anterior infarct area but well maintained in the posterior noninfarct area in patients with the aneurysm. In conclusion, the important factors of left ventricular aneurysm formation were as follows: (1) A culprit lesion of the myocardial infarction was severe, but other coronary artery lesions were mild. (2) Collateral vessels were poor. (3) The left ventricular wall motion of the infarct area was impaired, but that of the noninfarct area was relatively good.

Cardiac Catheterization↗

PubMed1993

High expression of cytochrome b5 in adrenocortical adenomas from patients with Cushing's syndrome associated with high secretion of adrenal androgens.

The mechanism of dissociated secretion between adrenal androgens and cortisol observed in several clinical situations remains unclear. We investigated whether the electron transfer systems NADPH-cytochrome P450 reductase and cytochrome b5, both of which had been shown to increase 17,20-lyase activity in vitro, were involved in the reaction selectivity between 17 alpha-hydroxylase and 17,20-lyase in adrenocortical adenomas obtained from eight patients with Cushing's syndrome producing different concentrations of adrenal androgen. In vitro enzyme assay using microsomal fraction of adenoma indicated that all adenomas from seven patients showed almost the same degree of 17 alpha-hydroxylase and 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) activities. However, the 17,20-lyase activities of two adenomas producing high concentrations of adrenal androgens were 3-fold greater than those of other five adenomas producing low concentrations of adrenal androgens. The mRNA concentrations of cytochrome P45017 alpha and 3 beta HSD were approximately the same in all adenomas, whereas those of cytochrome b5 in two adenomas possessing high 17,20-lyase activities were greater than those in other adenomas. The increased levels of cytochrome b5 in the two adenomas were further confirmed at the protein level using Western blot analysis of the microsomal fraction. No significant expression of NADPH-cytochrome P450 reductase was detected in any of the adenomas by Northern blot analysis. These results suggest that the difference in the concentration of cytochrome b5 in adrenal adenomas from patients with Cushing's syndrome may partially account for the difference in the amount of adrenal androgens produced by the tumors.

3-Hydroxysteroid Dehydrogenases↗

PubMed1993

A single amino acid substitution (gly743 --> val) in the steroid-binding domain of the human androgen receptor leads to Reifenstein syndrome.

The androgen receptor (AR) from a patient with Reifenstein syndrome (incomplete androgen insensitivity syndrome) was characterized. The patient's pubic skin fibroblasts had normal androgen binding. However, when incubated at 41 C, fibroblasts from the patient had a marked decrease in androgen binding as compared with normal fibroblasts. Analysis of coding sequences of the androgen receptor gene revealed a single nucleotide substitution in exon E, resulting in an amino acid change from glycine (GGG) to valine (GTG) at amino acid 743 within the steroid binding domain of AR. Reconstruction of this mutation by site-directed mutagenesis into a human AR complementary DNA followed by expression in COS1 cells led to production of a mutant AR with no significant difference in androgen binding when cells were incubated with androgen at room temperature. However, in contrast to wild type AR expressed in COS1 cells, the mutant AR had markedly lower androgen-binding affinity at 41 C. The mutant receptor could still stimulate a reporter gene at 37 C but this transcriptional stimulation was also decreased when compared with wild type AR receptor in a chloramphenicol acetyltransferase assay. These results suggest that partial androgen resistance in this patient with Reifenstein syndrome is due to a single point mutation in the steroid binding domain of the androgen receptor.

Adult↗

PubMed1993

Pronounced ST-segment depression during paroxysmal supraventricular tachycardia.

To determine the clinical significance of ST-segment depression observed in paroxysmal supraventricular tachycardia (PSVT), we evaluated the 12-lead electrocardiogram (ECG) during spontaneous PSVT in 54 patients (27 men and 27 women: mean age +/- SD; 47 +/- 18 years), who came to our clinic for the treatment of PSVT. Coronary angiography was performed in 16 patients (16 to 74 years; mean = 50 +/- 18) and treadmill exercise testing was performed in 21 patients. A cardiac electrophysiological study was carried out in 24 patients. During PSVT, ST-segment score was calculated as the sum of the ST-segment depression in 12 leads. The correlations between the ST-segment score, PSVT rate and age of the patient were analyzed as follows: The most significant positive correlation was observed between the ST-segment score and the PSVT rate (r = 0.615, p < 0.000001). The next most significant correlation was found between the PSVT rate and the age of the patient (r = -0.500, p = 0.00011). A negative correlation was also observed between the ST-segment score and the age of the patient (r = -0.429, p = 0.0012). In 13 of 16 patients, coronary angiography did not reveal any significant (> or = 75% in area) stenosis. Exercise testing induced significant ST-segment depression in 3 patients, of whom two had significant coronary artery lesions. PSVT was due to atrioventricular reentry via an overt (n = 3) or concealed accessory pathway (n = 15), atrioventricular nodal reentry (n = 5) and sinus node reentry (n = 1). In conclusion, patients with a faster PSVT rate revealed more pronounced ST-segment depression than did those with a slower PSVT rate, possibly reflecting the modified repolarization process instead of coronary artery involvement.

Adult↗

PubMed1993

[Motor impersistence].

Motor impersistence is the term introduced by Fisher to describe the inability to sustain certain simple voluntary acts such as keeping eyes closed, protruding the tongue etc. He considered it a specific, nondominant hemisphere symptom, but some investigators denied its relationship to the right hemisphere damage. We considered that this difference might depend on the following two features of MI; the one is inability to maintain one of these simple acts so long as normal persons do, the other is inability to perform more than two of these acts simultaneously. When we attached importance to the latter feature and defined MI as inability to protrude the tongue with eyes closed, this phenomenon was clearly related to the right hemisphere damage. The responsible lesion was suggested to be located in area 6 or 8 in the territory of the right middle cerebral artery. The mechanism of MI was also reported.

Cerebrovascular Disorders↗

PubMed1993

Expression of proto-oncogenes and tumor suppressor genes in in vitro cell lines derived from a thymus, thymoma, and malignant thymoma of rats.

To analyze the processes of the development of thymoma and malignant thymoma from normal thymic epithelial cells, we have examined the expression of 15 proto-oncogenes and tumor suppressor genes in seven in vitro epithelial cell lines established from a normal thymus (TuD1-1, TuD1-3, and TuD1-5), thymoma (TaD1-3 and TaD1-8), and malignant thymoma (MTHC-1 and MTHC-3) of rats. Northern blot analysis indicated that most of these genes examined were transcribed at similar levels. However, higher levels of transcription of epidermal growth factor receptor (EGFR) were observed in TuD1-1, TuD1-3, TuD1-5, TaD1-3, and TaD1-8 cells than in MTHC-1 and MTHC-3 cells. Conversely, four of the former five cell lines showed no TGF-beta transcription while the latter two cell lines had high levels of its expression. In addition, c-fos proto-oncogene was highly expressed in TuD1-5 cells, which showed the fastest growth rate among the seven cell lines. These results denote that some molecular changes in the regulation of gene expression occurred in the processes of malignant transformation of thymic epithelial cells.

Animals↗

PubMed1993

[Adrenocorticotropin receptor in familial glucocorticoid deficiency].

Recent studies have revealed the presence of four subtypes for the melanocortin receptor (MC-R). Among these MC-Rs, MC2-R is considered to be an adrenocorticotropin (ACTH) receptor because its expression is almost localized in the adrenal cortex. Five Japanese patients with ACTH unresponsiveness were examined as to whether they have mutations in the putative ACTH receptor. Among these patients, there are two groups of siblings, each of which consists of two individuals. The coding region of the ACTH receptor gene was amplified by polymerase chain reaction and directly sequenced on both strands, however, no point mutation was found in any of the five patients, suggesting that familial glucocorticoid deficiency, caused by the mutated ACTH receptor, may be rare.

Adrenal Cortex↗

PubMed1993

[Experimental studies on superinfection of acute simple urinary tract infection].

Experimental acute simple urinary tract infections were induced in female rats to determine whether low-virulent bacteria can reside in the simple urinary tract, whether minor flora can co-exist with major flora, and whether the bacterial population changes when antibiotics, to which major flora is sensitive and minor flora is resistant, is administered. "Enterococcus faecalis (E. faecalis) and Pseudomonas aeruginosa (P. aeruginosa) were instilled into the bladder transurethrally. Most rats had more than 1 x 10(4) CFU/ml of E. faecalis and P. aeruginosa two and four days after inoculation. Rats were divided into three groups. Mitomycin C injection group, acetic acid bladder instillation group, hydrocortisone injection group. E. faecalis (1 x 10(7) CFS/ml) and P. aeruginosa (1 x 10(4) CFS/ml) were instilled into the bladder. Bacterial count of E. faecalis was over 1,000 times that of P. aeruginosa in 14 rats two days after inoculation and in two rats six days after inoculation. Ampicillin (ABPC) was administered once a day for four days from two to five days after inoculation under the same condition. Bacterial count of E. faecalis was over 1,000 times that of P. aeruginosa in 26 rats two days after inoculation. The bacterial population changed in seven of the 26 rats after administration of ABPC, and in three of the 12 untreated rats.

Acute Disease↗

PubMed1993

[Study of patients with spinocerebellar degeneration using positron emission tomography].

We studied cerebral blood flow, oxygen metabolism and their relation to clinical symptoms in 45 patients with spinocerebellar degeneration (SCD) and 12 normal control subjects using positron emission tomography (PET). Regions of interest were acquired for the cerebellar hemispheres, cerebellar vermis, brainstem, thalami, and cerebral cortices. PET studies in these patients revealed that regional cerebral blood flow (CBF), regional cerebral oxygen metabolic rate (CMRO2), CBF/mean CBF of each cerebral cortex (CBF/mCBF) and CMRO2/mean CMRO2 of each cerebral cortex (CMRO2/mCMRO2) in the cerebellar hemispheres, cerebellar vermis, and brainstem showed a significant decrease in comparison with the normal control subjects, while in the cerebral cortices and thalami, SCD patients showed normal values. CBF/mCBF and CMRO2/mCMRO2 were significantly decreased in patients with olivopontocerebellar atrophy (OPCA) and Menzel type of hereditary ataxia (Menzel type) in the cerebellar hemispheres, cerebellar vermis, and brainstem, whereas patients with late cortical cerebellar atrophy (LCCA) and Holmes type of hereditary ataxia (Holmes type) revealed a significant decrease of CBF/mCBF and CMRO2/mCMRO2 in the cerebellar hemispheres and cerebellar vermis, but not in the brainstem. Patients with OPCA showed a significant decrease of CBF in the cerebellar hemispheres, cerebellar vermis, brainstem and that of CMRO2 in the cerebellar hemispheres and cerebellar vermis. Patients with LCCA showed a significant decrease of CBF in the right cerebellar hemisphere and cerebellar vermis. However, a significant reduction of CBF and CMRO2 was not observed in patients with Menzel type or Holmes type in these regions. In patients with LCCA and Holmes type, the severity of upper limb ataxia and dysdiadochokinesis were significantly correlated with CBF/mCBF and CMRO2/mCMRO2 in the cerebellar hemispheres and brainstem.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

[An emergent surgical case of the traumatic mitral regurgitation due to complete rupture of the papillary muscles].

We present a case of an emergency operation on acute MR and cardiac rupture due to a blunt thoracic trauma. This 27-year-old male suffered a severe blow to the chest when his motorcycle crashed to a tree. He was brought to this hospital by ambulance. On admission, the patient was in shock due to hypotension. Echocardiogram revealed cardiac tamponade and MR of grade 3/4. Pericardial drainage was performed immediately and his condition improved. Systolic pressure of the pulmonary artery was high at 70 mmHg which measured by Swan Ganz catheter. Isolated cardiac injury was diagnosed based on the results of various tests. A sign of acute pulmonary edema progressively deteriolated, therefore, emergent operation was performed on the same day. As cardiac fissure lesions were confirmed under cardiopulmonary bypass, we repaired the inferior side of the left ventricle and then closely examined the mitral valve. Both anterior and posterior papillary muscles were completely torn, so we immediately commenced with procedures to, replace a prosthetic valve. No complication were encountered, and the postoperative course was good. Complete ruptures of the papillary muscles due to trauma is rarely reported. We believe this case is exceptionally uncommon and worthy of reporting.

Accidents, Traffic↗

PubMed1993

Improvement of ischemia/reperfusion-induced contractile dysfunction of perfused hearts by class Ic antiarrhythmic agents.

The present study was undertaken to determine whether class Ic antiarrhythmic agents, flecainide and pilsicainide, improve ischemia/reperfusion-induced cardiac contractile dysfunction. Isolated rat hearts were subjected to a 35-min global ischemia, followed by a 60-min reperfusion, and the functional and metabolic consequences were examined. Ischemia/reperfusion resulted in no recovery of contractile function and a sustained rise in left ventricular and diastolic pressure of the perfused heart during reperfusion. The ischemia/reperfusion also induced increases in tissue sodium and calcium levels, decreases in potassium and magnesium ion contents and the release of creatine kinase and purine nucleosides and bases (ATP metabolites) from the heart, suggesting a pronounced change in cardiac transmembrane flux of ions, substrates and macromolecules. Treatment of the perfused heart with either 5 to 50 microM flecainide or 10 to 100 microM pilsicainide during preischemia resulted in diminishing the postischemic contractile dysfunction; suppressing the changes in tissue sodium, potassium, calcium and magnesium contents; and attenuating the release of creatine kinase and ATP metabolites in a concentration-dependent manner. Tissue sodium accumulation and potassium loss were also observed at the end of ischemia, which was attenuated by pretreatment with these agents. These results provided evidence that class Ic antiarrhythmic agents are capable of diminishing ischemia/reperfusion-induced contractile dysfunction and tissue ionic disturbance.

Adenosine Triphosphate↗

PubMed1993

Change in responsiveness of airway and beta-adrenoceptor in guinea pigs.

Allergen inhalation challenge resulted in significant (p < 0.05) increase in airway responsiveness to methacholine soon after immediate airway response (IAR) in guinea pigs actively sensitized with inhaled ovalbumin (OA) in vivo. We have investigated the involvement of thromboxane (Tx) A2 and platelet activating factor (PAF) in this airway hyperresponsiveness (AH). Pretreatment with CS-518, a selective thromboxane synthetase inhibitor, significantly inhibited both IAR (p < 0.07) and AH (p < 0.01), while pretreatment with WEB 2086, a PAF receptor antagonist, significantly inhibited only IAR (p < 0.05), but not AH after IAR. Propranolol, when inhaled before OA exposure, had no effect on bronchomotor tone, but if inhaled after IAR, it caused immediate death of guinea pigs. This result suggests that hyperresponsiveness of beta-adrenoceptor to propranolol may be induced by IAR. Examination of bronchoalveolar lavage (BAL) fluid revealed that no changes in cellular content were observed 60 min after OA exposure. In vitro, responsiveness of tracheal smooth muscle to carbachol was not changed by sensitization. Furthermore, anaphylactic reaction in vitro had no effect on the responsiveness. We conclude that airway responsiveness increases soon after IAR when infiltration of inflammatory cells is not yet found in vivo. It is also suggested that TxA2 but not PAF is involved in AH. Hyperresponsiveness to propranolol after IAR in OA sensitized guinea pigs illustrates the possibility of changes in function of beta-adrenoceptor after IAR.

Animals↗

PubMed1993

[The effect of Ryanodine for the myocardial protection in the working heart model of rabbit].

The purpose of this paper is to evaluate the effects of Ryanodine for myocardial protection. Twenty-four rabbits were studied using the working heart model divided four groups. The first is control group with no Ryanodine, the second is 10(-9) M, the third is 10(-8) M and the last one is 10(-7) M Ryanodine with GIK cardioplegic solution respectively. The hemodynamics was studied and the elemental concentrations (Ca, Mg, K, Na, Cl) of myocardial cell was measured using X-ray microanalysis. The results showed that intracellular Ca accumulation was dose-dependently suppressed with Ryanodine during reperfusion and also Ryanodine was significantly effective to maintain the hemodynamics during same one.

Animals↗

PubMed1993

[Coexistence of essential thrombocythemia and gastric cancer].

A 74-year-old man was admitted because of swelling, pain and ecchymosis in the night lower extremity. A blood analysis revealed that Hb was 11.8g/dl, WBC 37,600/microliters, and platelet count 137.1 x 10(4)/microliters. The NAP value was high. Bone marrow examination disclosed marked megakaryocytic hyperplasia. Chromosomal analysis revealed 47, XY, +9. Hemostatic data were within normal ranges, but the 2nd aggregation of platelet by ADP was diminished. The serum beta-TG was 159, PF-4 56ng/ml, B12 1,100, UB12 BC 1,800pg/ml. Gastric fiberoscopy revealed gastric cancer and CT scan disclosed marked splenomegaly. Essential thrombocythemia (ET) coexisting with gastric cancer was diagnosed based on these examinations. He was treated with anti-platelet agents, busulfan and tegafur uracil, however thromboembolic symptoms suggesting central nervous system and peripheral vascular ischemia and gastrointestinal bleeding occurred. Among diagnostic criteria for ET established by the polycythemia vera study group, there is a category "No known cause for reactive thrombocytosis." The case reported here had gastric cancer which may have contributed to the elevated platelet count, however this case could be diagnosed as ET coexisting with gastric cancer because of the above various clinical signs and laboratory results. Although then are few reports of the coexistence of other malignancies in ET, there may be many more similar cases because of the age preponderance in ET. In order to diagnose ET more precisely, more strict diagnostic criteria are needed.

Aged↗

PubMed1992

Inactivation of glibenclamide-sensitive K+ channels in Xenopus oocytes by various calmodulin antagonists.

In follicle-enclosed Xenopus oocytes, extracellular application of cromakalim (a K+ channel opener) or intracellular injection of cAMP induces the smooth outward K+ current which is inactivated by glibenclamide. We found that cromakalim- or cAMP-induced K+ currents in the oocytes were rapidly, reversibly and dose-dependently blocked by various drugs having a calmodulin antagonizing activity in common, namely, by a selective calmodulin antagonist (W-7), antipsychotics (trifluoperazine, chlorpromazine, haloperidol), an antidepressant (amitriptyline), a beta-adrenoceptor blocker (propranolol), a local anesthetic (lidocaine) and a calcium antagonist (prenylamine). W-7, trifluoperazine, chlorpromazine and prenylamine were relatively potent blockers. For example, IC50 values to block cromakalim (100 microM)-induced K+ currents were 12 microM for trifluoperazine and 16 microM for W-7, which were close to their IC50 values to inhibit Ca2+/calmodulin-dependent phosphodiesterase (an index of the potency of calmodulin antagonists). IC50 values to inhibit cAMP (20 pmol/oocyte)-induced K+ currents were 126 microM for prenylamine and 129 microM for chlorpromazine. The IC50 values of all drugs tested to block cromakalim or cAMP responses were significantly correlated with their calmodulin-antagonizing potencies. Isoproterenol-induced K+ currents in the oocytes were also dose-dependently inhibited by glibenclamide, W-7 and trifluoperazine. These results suggest the possibility that the activity of glibenclamide-sensitive K+ channels in follicle-enclosed oocytes are regulated by calmodulin or a calmodulin-dependent process.

Animals↗