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Biomedical subjects

J Kosaka

Publications and source records attributed to J Kosaka.

At least 37 records · Page 2Linked to original sources
PubMed1991

A case of extraadrenal pheochromocytoma with papillary thyroid carcinoma.

A 63-year-old housewife with a history of partial thyroidectomy was referred to our hospital because of a neck mass and abdominal tumor. Aspiration biopsy of the neck tumor revealed the recurrence of papillary thyroid carcinoma. Magnetic resonance imaging (MRI) of the abdomen and urinary and plasma catecholamine levels indicated that the tumor beside the abdominal aorta was an extraadrenal pheochromocytoma. Two tumors were excised and histologic studies confirmed the diagnosis. So far two cases of extraadrenal pheochromocytoma with papillary thyroid carcinoma have been reported. The present case indicates that the presence of papillary thyroid carcinoma should be considered in patients with extraadrenal pheochromocytoma.

Abdominal Neoplasms↗
PubMed1990

[Roles of the kidney in activation and release of plasma inactive renin in the rat].

Plasma inactive as well as active renin is supposed to originate from the kidney, though there is little direct evidence. As we have previously reported (Sakanaka et al., Folia Endocrinol. Jap., 63: 961-977, 1987; Miyazaki et al., J. Hypertension 4 (Suppl 6): S453-S455, 1986; Miyazaki et al., J. Hypertension 6: 33-40, 1988), the submandibular gland, but not the kidney, is thought to play an crucial role in releasing plasma inactive renin in the rat. In the present acute studies, we attempted to elucidate the roles of the kidney in the release mechanisms of plasma inactive renin. Adult male rats maintained on a regular rat chow (Na: 260 mg/100g) were uninephrectomized, and vessel clips were placed on the renal pedicles of the contralateral kidneys to make completely ischemic and non-filtered kidneys. In the first protocol, the renal pedicles were occluded for 2 h, followed by the removal of the vessel clips. During the occlusion for 2 h, plasma active renin concentration (PAC) in the peripheral blood obtained from the femoral cannulae decreased, while plasma inactive renin concentration (PIC) along with plasma total renin concentration (PTC) increased as in the case of total nephrectomy, which supports our previous studies. Then, declipping resulted in the rapid rise in PAC with the peak values at 2 min, which was followed by its gradual decrease with time during the experimental period (30 min). On the other hand, PIC decreased gradually toward control levels with no rise after declipping. In the second protocol, blood trapped in the kidney was collected through the renal venous cannulae at 0, 60, 120 and 240 min after the pedicle occlusion in the different groups of rats. The renal blood levels of PAC increased by more than three times at 240 min compared to the control values, while PIC decreased to one third of the control values. PTC increased at 120 and 240 min. Renal tissue levels of renin were also measured at 0 and 120 min in the second protocol in the kidneys of rats which were maintained on a regular rat chow. Inactive renin concentration increased, while active renin concentration decreased. These were compatible with the results obtained in plasma. In the last protocol, the second protocol was in part repeated in salt-depleted rats which were kept on a low salt diet (Na: 11.3 mg/100g) for 2 weeks.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Silent thyroiditis following rubella.

A 40-year-old housewife was referred to our hospital for evaluation of a thyrotoxic state. A month after rubella infection, she developed heat intolerance. Physical examination revealed a hard and non-tender goiter with no signs or symptoms of inflammation. Free thyroid hormones were high and TSH was undetectable. 123I-thyroidal uptake was suppressed. Antithyroglobulin and anti-microsomal antibodies were negative throughout the course. A serologic study revealed high levels of anti-rubella antibodies. After a month without any treatment, she became euthyroid. Free thyroid hormones and TSH gradually became normal and the antibodies to rubella decreased. 123I-thyroidal uptake increased. From the clinical course, the patient was diagnosed as having silent thyroiditis. We suggest that viral infection such as rubella could cause the development of silent thyroiditis.

Adult↗
PubMed1988

Reno-submandibular axis controls release of extrarenal inactive renin.

The mechanisms causing the release of plasma inactive renin (PIR) area still unclear. We have investigated the role of the kidney in the release of trypsin-activable PIR from extrarenal sources in the rat, with special reference to the submandibular gland. The activation of PIR was performed by incubation with 20 mg/ml trypsin at 4 degrees C for up to 10 min; the reaction was then terminated by addition of 20 mg/ml of soybean trypsin inhibitor. Bilateral nephrectomy resulted in a gradual, marked, sex-independent increase in PIR concentration, reaching levels 4.5 times higher than basal in 24 h (time 0: 14.8 +/- 1.0 ng/ml per h; 24 h: 66.8 +/- 3.4 ng/ml per h, mean +/- s.d., P less than 0.001). This increase was not altered by the concomitant intravenous infusion of pressor doses of either angiotensin (Ang) II (30 ng/min) or pure mouse submandibular renin (a 20-ng intravenous bolus followed by intravenous infusion at the rate of 50 ng/h) for 4 h, but was completely prevented by prior removal of the submandibular glands, in which no activity of active renin and no inactive renin was detected. These results suggest that the post-nephrectomy increase of PIR is not dependent on feedback mechanisms of the suppressed renin-angiotensin system, but is controlled by the presence of submandibular glands in the rat.

Animals↗
PubMed1987

Structural diversity of murine serum amyloid A genes. Evolutionary implications.

Mouse serum amyloid A (SAA) gene family comprises four members that are closely linked in the chromosome 7. Two of these genes encoding major mouse SAA isotypes (SAA1 and SAA2) are highly homologous not only in exons but also in introns and flanking regions; this sequence homology extends 280 base pairs upstream of major cap sites and 430 base pairs downstream of polyadenylation sites, and the 5' boundary of this homology unit is marked by the CA/GT repeat. Sequence comparison also shows that one (SAA4) of the other two genes is related to the SAA1/2 gene, whereas the other gene (SAA3) evolved independently. Based on these results and the SAA gene arrangement, we discussed mouse SAA gene evolution.

Animals↗
PubMed1987

[Roles of kidney and submandibular gland in the release of rat plasma inactive renin].

In this study we outlined the development of an enzymatic technique to activate plasma inactive renin by trypsin in rat plasma. Using this method, we reported the releasing mechanism of the trypsin-activable inactive renin which has not yet been clarified. Adult male Wistar rats (260-300 g) were kept on regular diet (Na: 260 mg/100g) unless explained and underwent operation under pentobarbital anesthesia (50 mg/kg). Blood samples were obtained from conscious rats through the cannulae, which had been inserted into the left femoral arteries 24h before the experiments. After addition of excessive renin substrate which had been obtained from the 24 h-nephrectomized rat plasma, renin was measured by the commercial RIA-kit (Dainabot). Trypsin (Worthington) treatment (20 mg/ml plasma for 10 min at 4 degrees C) was followed by addition of SBTI (Sigma) (20 mg/ml plasma). This condition maximally increased the rate of angiotensin I generation and did not alter the Km or optimum pH of the renin reaction. In this condition, trypsin reaction was completely inhibited by adding these concentrations of SBTI. The molecular weight of inactive renin (51,000) in the normal rat plasma estimated by Sephadex G-100 column (Pharmacia) was the same as that in the nephrectomized rat plasma. In conclusion, trypsin treatment of plasma (20 mg/ml plasma for 10 min at 4 degrees C) followed by SBTI (20 mg/ml plasma) was justified for trypsin activation of rat plasma. Using this method, we investigated the changes in active and inactive renin after bilateral nephrectomy in the salt-depleted rat. Active renin decreased rapidly after bilateral nephrectomy with a half life of 23.6 +/- 4.0 min. Inactive renin, on the other hand, increased gradually and reached to a plateau 24 h after bilateral nephrectomy, and was kept unchanged during the following 24 h. The infusion of mouse submandibular gland active renin or angiotensin II could not prevent the increase of plasma inactive renin in the nephrectomized rat. These suggest that there may be no feedback mechanisms between plasma inactive and active renin or angiotensin II. Furthermore, we investigated the organ-related sources of plasma inactive renin which markedly increased after total nephrectomy. Simultaneous removals of submandibular glands but not of adrenal glands completely prevented the postnephrectomy increases of plasma inactive renin. But, removals of submandibular glands or adrenal glands alone were followed by no changes in the basal levels of plasma inactive renin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

The significance of autonomic neuropathy in the elevation of inactive renin in diabetes mellitus.

Plasma renin activity (PRA) and inactive renin(IR, activated by trypsin) were measured in the plasma of 15 type II diabetics with autonomic neuropathy (group 3), 15 type II diabetics without (group 2), and 14 nondiabetic control subjects (group 1) in the recumbent position. There were no significant differences between the 3 groups with respect to age, ideal body weight, supine resting mean blood pressure, serum creatinine, daily urinary excretion of sodium, or renin substrate at the time of study. Autonomic neuropathy (AN) was assessed by measurement of the ratio of the longest to the shortest R-R interval during deep breathing (E/I-ratio) and by postural hypotension. PRA was significantly lower in group 3 than in group 1 (p less than 0.05). The IR level was significantly higher in group 3 than in groups 2 and 1 (p less than 0.005 for both comparisons). The ratio of active renin to total renin (TR) (PRA/(IR + PRA)) was significantly lower in group 3 than in groups 2 and 1 (p less than 0.001 for both comparisons). The IR level and PRA/(IR + PRA) were significantly correlated with E/I-ratio (r = -0.498, p less than 0.01 and r = 0.588, p less than 0.001, respectively) and with the severity of postural hypotension (r = 0.383, p less than 0.05 and r = 0.401, p less than 0.05, respectively), but not with the daily urinary excretion of protein or 24 h-creatinine clearance (24 h-Ccr) in the whole diabetics. From these results, we conclude that autonomic neuropathy might be a more important factor than nephropathy in the lower PRA and higher IR level in type II diabetics with AN.

Autonomic Nervous System Diseases↗
PubMed1986

The hypotensive effect of single-dose captopril in diabetics.

To determine the role of the kallikrein-kinin (KK) system in patients with diabetes mellitus in relation to nephropathy and/or hypertension, the single-dose effects of captopril (25 mg, p.o.) were examined in 9 control subjects and 32 diabetics (group 1; 11 normotensives without nephropathy, group 2;10 hypertensives without nephropathy, group 3; 11 hypertensives with nephropathy). Significant hypotensive effects of captopril were found in groups 1 and 2 as well as in the control group, but not in group 3. These hypotensive effects were completely blocked by the infusion of ethyl-p-(6-guanidinohexanoyloxy) benzoate methanesulfonate (FOY), a kallikrein inhibitor. The administration of captopril during vehicle infusion induced a significant elevation of plasma renin activity (PRA) at 60 and 120 min after captopril in each group, except for group 3. FOY cancelled these captopril-induced effects on PRA in those groups. No correlation was found between pretreatment PRA and the changes in mean blood pressure (MBP) after captopril during vehicle infusion in whole diabetics. In addition, the daily urinary excretion of kallikrein in group 3 was significantly lower than that in groups 1 and 2 as well as in the control group. These results suggest that the hypotensive action of captopril in diabetics without nephropathy may be largely due to activating the KK system, and that the KK system may be suppressed in hypertensive diabetics with nephropathy.

Blood Pressure↗
PubMed1986

Increased sodium influx into erythrocytes in diabetes mellitus and hypertension.

A variety of abnormality has been reported in the cation transport systems in erythrocytes in essential hypertension. To determine the existence of similar abnormality in diabetics with hypertension, sodium (Na+) influx into erythrocytes in the presence of ouabain (measured by using 22Na+), and the Na+ and potassium (K+) content in intact erythrocytes were examined. Subjects, all of whom were Japanese, were divided into 4 groups; 23 nondiabetic, normotensive control subjects without family history of hypertension (control group), 20 patients with essential hypertension (group 1), 21 normotensive diabetics without family history of hypertension (group 2) and 15 hypertensive diabetics (group 3). Na+-K+ pump activity (measured by using 86Rb+) was studied in some of them, too. Na+ influx in group 1 was 0.451 +/- 0.111 m mol/Kg erythrocytes/h, significantly more elevated than that in the control group (0.345 +/- 0.080, p less than 0.001). Na+ influx in group 2 (0.435 +/- 0.094) was significantly greater than that in the control group (p less than 0.005), but no significant difference was found between groups 1 and 2. Na+ influx in group 3 (0.551 +/- 0.128) was significantly higher than that in the control group (p less than 0.001), in group 1 (p less than 0.02), or in group 2 (p less than 0.005). There were no significant differences in Na+-K+ pump activity, or Na+ and K+ content among the 4 groups. These findings suggested that: Na+ influx into ouabain-treated erythrocytes was higher in patients with essential hypertension than in control subjects in Japanese, diabetes mellitus per se might increase Na+ influx, and the elevation of blood pressure in hypertensive diabetics as well as in essential hypertensives might be related to the increased Na+ influx.

Adult↗
PubMed1985

[Image diagnosis of adrenal disorders--I. CT images of control subjects and image diagnosis of primary aldosteronism].

The shape and size of the adrenals in control subjects without adrenal disorders were studied by computed tomography (CT), and a comparative assessment of diagnostic values of ultrasonography (US) by electronic linear scanner, CT, and adrenal scintigraphy was made on 9 patients with primary aldosteronism. Adrenal imaging by scintigraphy was performed on the 5th and 6th day, or further on the 7th day after the injection of 1 mCi of Adosterol. CT findings of the adrenals in control subjects: Eighty-two % of 100 control right adrenals, and 89% of 100 control left adrenals were detected by CT. Seventy-seven % of the right adrenals were in linear-shape, and the others were in V-shape. The shape of the left adrenals could be classified into triangular-shape (54%), Y-shape (28%) and V-shape (18%). The mean width and thickness of the right adrenals were 28.6 +/- 7.5 mm (M +/- SD) and 3.8 +/- 1.4 mm, respectively. Those of the left ones were 19.4 +/- 5.5 mm and 5.3 +/- 1.8 mm. Image diagnosis of primary aldosteronism: In 2 out of 3 patients examined by US, aldosteronomas were detected. In these 2 patients, one had 2 adenomas 2.8 X 1.7 X 1.2 cm and 1.0 X 1.0 X 2.0 cm in size, and the other had one adenoma 0.8 X 1.0 X 2.0 cm in size. On adrenal scintiscanning under dexamethasone pretreatment (DP), the isotope uptake of aldosteronoma was still seen with the disappearance of the contralateral adrenal in 7 out of 9 cases. In these 7 cases, the laterality of the tumor was confirmed. In one of the remaining 2 cases, the bilateral adrenal images were obtained regardless of DP. In the other case, of which aldosteronoma was the smallest (0.6 X 0.6 X 0.8 cm), the image of the affected adrenal with adenoma as well as the contralateral adrenal disappeared under DP. CT delineated all aldosteronomas in 8 cases examined including 2 cases in which adrenal scintiscanning failed to elucidate the localization of aldosteronoma. These results indicated that the combination of these 3 new image diagnostic methods was available for the detection of aldosteronomas of various sizes.

Adenoma↗
PubMed1983

Diabetic gangrene in Japan: analysis of 487 cases.

Diabetic gangrene was thought of as a rather rare complication in Japan. Since the first report in 1917, only 16 cases were reported up to 1945. However, the number of reports increased rapidly in the manner of a geometric series after 1965. Sex and age distributions of the syndrome in Japan corresponded closely with those of Western countries. A distinct tendency in the inducement of gangrene was found, i.e. thermal trauma had preceded 43.6% of the cases. This might be the result of the local habit of warming the feet using hot-water bottles or foot warmers. The number of patients with normal pulses in the affected extremities in Japan was distinctly higher compared with that reported in Western countries. But functional and morphological changes in large peripheral vessels were frequently demonstrated when more detailed examinations were conducted. The cause for the rapid increase in the incidence of diabetic gangrene has not been elucidated, but changes in lifestyle may be partly responsible. The most conspicuous change was the increase in meat and fat intake during the 1960's. The changes in total calorie, total protein or sugar intake over this period were inconspicuous. Changes in dietary habits seem to be responsible, but further research will be necessary to clarify the details.

Aged↗