[Prognosis in 550 cases with renal cell carcinoma].
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Biomedical subjects
Publications and source records attributed to S Yoshimura.
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Forty-one patients with advanced gastric cancer underwent gastrectomy, and the correlation between tissue uptake of the adjuvant drug and the prognosis were studied. The patients were preoperatively administered Tegafur and samples of tissue were obtained intraoperatively. 5-FU levels in the tumor and lymphnodes were measured by gas chromato-mass fragmentography (GCMF). The patients measured for 5-FU tissue uptake were given more than 60 g of tegafur as postoperative adjuvant chemotherapy, and divided into two groups; one in which the 5-FU uptake by tumor tissue and lymphnode was over 0.05 microgram/g and the other lower than 0.05 microgram/g. In both groups there were no significant differences in background factors. Each survival rate was calculated by the Kaplan-Meier method, and the generalized Wilcoxon method was used for statistical analysis. There was no statistically significant correlation between 5-FU uptake by the tumor and the prognosis, but the 5-year survival rate in the group with over 0.05 microgram/g uptake by lymphnodes was statistically significant (p = 0.018).
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[3H]Prostaglandin D2 binding to rabbit platelets was increased by about 150% in the presence of beta-adrenoceptor agonist, isoproterenol. The isoproterenol-induced potentiation of the [3H]prostaglandin D2 binding gave a bell-shaped dose-response relationship (maximum response at 3 X 10(-8) M) in a stereospecific manner. Similar and moderate potentiation was obtained with terbutaline. On the other hand, beta-adrenoceptor antagonists such as alprenolol, propranolol and butoxamine (beta 2-specific) had no potentiating effect on [3H]prostaglandin D2 binding; rather, they abolished the isoproterenol-induced increase of [3H]prostaglandin D2 binding. The beta 1-specific antagonist, metoprolol, did not have any effect. Rabbit platelets were found to possess one [3H]prostaglandin D2 binding site (Kd = 6 X 10(-7) M, Bmax = 787 fmol/mg protein). In the presence of isoproterenol at 3 X 10(-8) M, Bmax was increased with unaltering Kd value. Isoproterenol did not increase [3H]prostaglandin E1, [3H]prostaglandin E2 and [3H]prostaglandin F2 alpha bindings to platelets. The potential effect of isoproterenol was mimicked by forskolin, theophylline, dibutyryl cyclic AMP, prostaglandin E1 and prostaglandin I2, but it was abolished by 2', 5'-dideoxyadenosine, an inhibitor of adenylate cyclase, indicating that elevated level of cyclic AMP may be available for the induction of the increase of [3H]prostaglandin D2 binding. Prostaglandin D2-induced cyclic AMP synthesis and antiaggregation activity were also augmented in the presence of isoproterenol. These results suggest a beta 2-adrenoceptor-mediated cyclic AMP-dependent mechanism for the regulation of prostaglandin D2 receptor binding in rabbit platelets.
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To examine the effects of transient hyperprolactinemia on in vitro fertilization and embryo transfer, 61 cycles in 50 euprolactinemic ovulatory women with irreparable tubal diseases were stimulated with clomiphene (CC) alone or CC and human menopausal gonadotropin followed by human chorionic gonadotropin (hCG). Serum prolactin (PRL) increased after hCG administration with peak values of 45.4 +/- 4.2 ng/ml on the day of laparoscopic oocyte aspiration. The highest serum estradiol (E2) concentration was found on the day before PRL peak and serum progesterone (P) began to increase after hCG injection concomitant with the PRL rise. The group having 50 ng/ml or more of PRL (34 cycles) had significantly higher levels of E2 during preovulatory and early luteal phase compared to those of the group having less than 50 ng/ml of PRL (27 cycles) but there was no significant difference between the P levels in the two groups. In the higher PRL group 72 (62.1%) of 116 collected oocytes were fertilized and 6 (20.0%) conceived. In the lower PRL group 45 oocytes (58.4%) of 77 were fertilized and 3 (12.5%) became pregnant. These data suggest that elevated serum PRL concentrations may have no effect on fertilization of oocytes in vitro or embryonic development.
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One of the limitations of immunoperoxidase methods applied in surgical pathology is the loss of immunoreactivity during fixation and processing. In this study, the effects of decalcification on the immunoreactivity of various antigens in formalin fixed tissues were examined. The pieces of fixed tissue were placed in four different decalcifying solutions (EDTA, formic acid, nitric acid, and Plank-Rychlo solution) for various time periods and then processed routinely and embedded in paraffin. The paraffin sections of the tissues were stained with immunoperoxidase methods for immunoglobulins, hormones, or tissue/tumor-specific markers. Sections of nondecalcified tissues were used as a control. The immunohistochemical staining intensity and the number of positive cells were not reduced significantly in decalcified tissues within the usual time period of routine decalcification procedures. Many antigens survived even prolonged decalcification. The results of this study indicate that routinely decalcified tissues can be used for immunoperoxidase staining without significant loss of immunoreactivity.
In the normal rat kidney, immunohistochemical localization of glutathione peroxidase (GSH-Po) was mainly in the proximal tubules (PTs), where the proximal portions (S1 + S2) were more intensely stained than the distal portion (S3). Immunocytochemically, GSH-Po was localized in cytosol including the core of microvilli and lysosomes of the epithelial cells in the PTs. Since albumin and IgG were not found in cytosol, it is suggested that cytosolic GSH-Po may be generated in situ, but is not derived from the serum.
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The electrophysiological effects of antiarrhythmic drugs were tested in 36 patients with recurrent paroxysmal supraventricular tachycardia (PSVT), 25 of whom had accessory pathway reentrant tachycardia (APRT) and 11 A-V nodal reentrant tachycardia (AVNRT; 10 of the slow-fast type one of the fast-slow type). The test drugs were procainamide (used in 19 patients), verapamil (in 27), disopyramide (in 31), and propranolol (in 15). The drugs were tested for their ability to terminate episodes of PSVT as well as to inhibit their induction. Procainamide had an inhibitory effect on APRT in nine of 12 patients (75%) and terminated episodes of APRT in seven of 11 patients (63.6%); in all of them V-A block was responsible for the termination. In four of six patients (66.7%) with slow-fast AVNRT and in one patient with fast-slow AVNRT, inhibition of the induction of tachycardia attacks was noted after procainamide. Termination of AVNRT was seen in the same number of patients. Verapamil inhibited the induction of APRT in 12 of 18 patients (66.7%) and terminated episodes of APRT in 10 of 16 patients (62.5%), all by A-V block. In six of eight patients (75%) with slow-fast AVNRT, inhibition of the induction as well as termination of tachycardia were noted after verapamil. Disopyramide had an inhibitory effect on APRT in seven of 23 patients (30.4%) and terminated APRT in five of 21 patients (23.8%) by V-A block, while AVNRT (all slow-fast type) was terminated in only one of eight patients (12.5%) by disopyramide. Disopyramide was less effective than previously reported. This could be attributed to a relatively low dosage and slow infusion speed. Propranolol inhibited the induction of APRT and terminated episodes of APRT in only one of 10 patients (10%). In two of four patients (50%) with slow-fast AVNRT, an inhibitory effect by propranolol was noted, but termination was seen in only one patients.
A case of prepubertal periodontitis was observed and examined immunohistologically with peroxidase-antiperoxidase staining. The patient was an 11-year and 7-month-old Japanese girl, well-developed and well-nourished. Her parents were first cousins. Her chief complaint was the loosening and loss of the permanent teeth. There was a similar history of primary dentition. Her remaining permanent teeth were loosened with severe alveolar bone loss, but calculus deposit was minimal. Significantly, there was no palmar-plantar hyperkeratosis. General examination showed normal data except for the increase of the immunoglobulin concentrations. In neutrophil function tests chemotaxis was depressed, although phagocytosis, random migration and superoxide production were within normal limits. Histologically, neutrophils were seen in the gingival tissue and other findings were also similar to those of adult periodontitis. In immunohistological examination, IgG-bearing cells which mostly consisted of plasma cells predominated in the lesion. Considering the past history, the immunodeficiency and the absence of palmar-plantar hyperkeratosis, the case was diagnosed as prepubertal periodontitis.
To evaluate cardiac function, ventricular power during ejection (power) and the rate of change of power (dPower/dt) were assessed noninvasively. Power was determined from the product of aortic flow (Fa(t] and brachial arterial pressure (Pa(t]. Fa(t) was measured at the suprasternal notch using an ultrasonic pulsed Doppler flowmeter with a 2 MHz carrier frequency and 10 KHz repetition frequency. The maximum detectable blood velocity was 380 cm/sec. Pa(t) was measured using a newly-developed method based on indirect unloading techniques and an air pressure system. There were 21 normal subjects and seven patients with coronary artery disease in this study. The following results were obtained. There was no significant difference between power patterns calculated by Pa(t) and Pao(t) (aortic pressure measured by catheter). The average peak dPower/dt was 160.2 J/sec2 in normal subjects, 145.2 L/sec2 in patients with ejection fractions greater than 50%, and 93.5 J/sec2 in patients with ejection fraction less than 50%. Peak dPower/dt was significantly decreased in patients with the lower ejection fraction (p less than 0.005). The results indicated that this index is clinically useful in evaluating cardiac contractility.