PubMed Health⌕ Search

Biomedical subjects

C Shigemasa

Publications and source records attributed to C Shigemasa.

At least 55 records · Page 3Linked to original sources
PubMed1997

Pertechnetate thyroid uptake is not always suppressed in patients with subacute thyroiditis.

The authors studied the clinical courses and immunologic aspects in 15 patients (age range, 32-69 years old; 14 women) with clinical features that were similar to subacute thyroiditis (SAT). In 2 patients (group A) whose thyrotropin-binding inhibitory immunoglobulins (TBII) and thyroid stimulating antibody (TSAb) showed strongly positive activity at the initial visit, Tc-99m pertechnetate thyroid uptake (Tc-99m uptake) was elevated (5.6% and 3.8%, respectively, normal; 0.7-3.0%). In 6 (group B) of 13 other patients, Tc-99m uptake was not completely suppressed (2 normal, 4 near normal) and imaging showed uptake in one lobe. In 7 (group C), however, there was no evidence of uptake in either lobe. Inflammatory process was localized in one lobe in all group B patients, and was in both lobes in all group C patients but one. Serum TSH levels were detectable in at least 4 patients (2 group B, 2 group C) low in all. There were no patients in both groups B and C in whom TBII and/or TSAb were detected at the initial visit. In SAT, marked suppression of Tc-99m uptake may be ascribed mainly to inflammatory follicular cell damage, but it is not always suppressed, owing to an association similar to Graves' disease and other unknown mechanism(s).

Adult↗
PubMed1997

Tonic block of the Na+ current in single atrial and ventricular guinea-pig myocytes, by a new antiarrhythmic drug, Ro 22-9194.

Ro 22-9194 reduced the Na+ current in the atrial myocytes as well as ventricular myocytes in a tonic block fashion. Ro 22-9194 had a higher affinity to the inactivated state Na+ channels (KdI = 3.3 microM in atrial myocytes, KdI = 10.3 microM in ventricular myocytes) than to those in the rested state (KdR = 91 microM in atrial myocytes, KdR = 180 microM in ventricular myocytes), which indicated that Ro 22-9194 had a higher affinity to the Na+ channels in atrial myocytes than in ventricular myocytes. Ro 22-9194 shifted the inactivation curve in the hyperpolarized direction in both atrial and ventricular myocytes. These findings suggest that Ro 22-9194 more strongly inhibited the Na+ channel of the atrial myocytes of the diseased hearts with the depolarized membranes potentials than the Na+ channels in ventricular myocytes.

Animals↗
PubMed1996

Establishment and characterization of a Chinese hamster ovary cell line, CHO-4J, stably expressing a number of Na+/I- symporters.

The cDNA of the Na+/I- symporter playing a key role in thyroid iodide transport was cloned very recently. To characterize its function, we transfected the Na+/I- symporter gene into Chinese hamster ovary (CHO) cells and established a cell line stably expressing a number of rat Na+/I- symporters, named CHO-4J. Iodide uptake was dependent on [Na+] and reached a plateau within 30 min. Kinetic studies revealed that the K(m) for iodide was 35 microM, similar to that of FRTL-5 thyroid cells. The maximal velocity (Vmax) at cell protein level was 6-10-fold higher than in FRTL-5 cells and that at single cell level was approximately 1000-fold higher. CIO4- and SCN- dose-dependently inhibited iodide uptake in a competitive manner. The Ki was 1.5 and 16 microM, respectively. Iodide efflux from CHO-4J cells was apparently slower (t1/2 = 15 min) than FRTL-5 cells (t/2 = 2 min). Electrophysiological characteristics were examined using the whole cell patch clamp technique. Rapid inward current was observed when CHO-4J cells were perfused with 50-1000 microM Nal, suggesting a transport stoichiometry of at least 2 Na+ per I-. The current-voltage relation revealed that this current was membrane potential-dependent. The reversal potential was very close to that of Na+ in agreement with dependency on the Na+ electrochemical gradient. CHO-4J cells with a slow iodide efflux, expressing a number of Na+/I-symporters whose characteristics are identical to those of FRTL-5 cells will function as a new tool for sensitive of iodide uptake.

Animals↗
PubMed1996

Amitriptyline inhibits the G protein and K+ channel in the cloned thyroid cell line.

We have reported that thyroid K+ channel is activated by extracellular application of the thyroid-stimulating hormone (TSH) using single channel recording method performed on cloned normal rat thyroid cell (FRTL-5) membrane. Treatment of dibutyryladenosine cyclic monophosphate (Bt2 cAMP) also activated the TSH-dependent K+ channel. These findings indicate that the thyroid K+ channel is activated through the TSH-adenosine cyclic monophosphate (cAMP)-protein kinase A system. We examined the effects of amitriptyline on TSH-guanosine triphosphate binding protein (G protein)-adenylate cyclase-cAMP-K+ channel system in the cloned normal rat thyroid cell line FRTL-5. Amitriptyline inhibited the cAMP production induced by TSH. Amitriptyline also inhibited the cAMP production induced by cholera toxin, indicating that amitriptyline inhibited the thyroid G protein. Amitriptyline had no effect on TSH-receptor binding and cAMP production by forskolin (adenylate cyclase stimulator). Amitriptyline inhibited the K+ channel activation by cAMP, indicating that the suppressing mechanism is not the inhibition of TSH receptor or G protein but the direct suppression of K+ channel. It was concluded that amitriptyline inhibited the thyroid G protein and K+ channel.

Amitriptyline↗
PubMed1996

A new type of familial central diabetes insipidus caused by a single base substitution in the neurophysin II coding region of the vasopressin gene.

We studied the genetic basis of familial neurohypophyseal diabetes insipidus in a Japanese family. The members had polyuria and a deficiency of plasma vasopressin (AVP). Polymerase chain reaction (PCR) amplified exons of the AVP-neurophysin-II gene were subcloned and sequenced. Exons 1 and 3 were normal, but nucleotide 1884 Guanine (G) in exon 2 was substituted with Thymine (T), which induced a substitution of glycine (Gly) for valine (Val). To examine the presence of this mutation in the affected subjects, we designed two mutated primers. One of them induced a new endonuclease restriction site in the PCR fragments from normal, and the other induced a new endonuclease restriction site from patients with the mutation. DNA fragments from two affected members of this family were amplified with this primer, and the PCR products were digested by endonuclease and resolved by electrophoresis. The results indicated that these subjects had both normal and mutant alleles, indicating that the mutation was heterozygous. We concluded that this mutation caused neurohypophyseal diabetes insipidus in this family.

Arginine Vasopressin↗
PubMed1996

Decreased heart rate variability in patients with diabetes mellitus and ischemic heart disease.

We investigated the characteristics of decreased heart rate variability (HRV) in diabetic patients with ischemic heart disease (IHD). Twenty-one healthy control subjects, 17 diabetic patients without IHD, and 33 diabetic patients with IHD were studied. The diabetic patients with IHD were subdivided into 2 groups according to the severity of their IHD: severe or mild. HRV was evaluated in all subjects using the spectral variables of the all-frequency, low-frequency, high-frequency (AF, LF, HF) components and the LF/HF ratio were determined from Holter recordings. The AF and LF components in patients with diabetes only or diabetes and severe IHD were significantly lower than in control group, but the HF component was significantly lower only in the group of patients with diabetes and severe IHD. The LF/HF ratio did not differ significantly among the 4 groups, but was the lowest in diabetic patients without IHD. Patients with diabetes and mild IHD showed a slight decrease in HRV, but this was not significant. With regard to the circadian rhythm of HRV, the AF and LF components in patients with diabetes-only or diabetes and severe IHD were significantly decreased and showed the same pattern throughout the day. However, the HF component was decreased during more time zones in patients with diabetes and severe IHD, whereas the LF/HF ratio was lower during more time zones in the diabetes-only group. All spectral variables showed a tendency to be inversely related to the duration of diabetes in all diabetic patients. In particular, the LF/HF ratio showed a significant negative correlation. The HRV of diabetic patients was characterized by a decreased LF/HF ratio. It was concluded that, although HRV in diabetic patients with severe IHD was reduced mainly as a result of diabetic neuropathy, this was also partly due to a decline in parasympathetic tone as a result of myocardial injury.

Aged↗
PubMed1996

Renal handling of urate in a patient with familial juvenile gouty nephropathy.

We encountered a case of familial juvenile gouty nephropathy (FJGN) with an autosomal dominant transmission pattern. Hyperuricemia in the propositus was caused by renal underexcretion of urate although his erythrocyte purine enzyme was normal. A renal biopsy specimen from the propositus showed interstitial fibrosis with tubular atrophy. On pyrazinamide and probenecid tests, the tubular secretion of urate selectively decreased without changes in either presecretory or postsecretory reabsorption of urate when his renal function was normal. Probenecid increased the urinary urate excretion and Cur/Ccr. The serum urate concentration was poorly controlled by allopurinol. When his renal function deteriorated, the uricosuric effects of both probenecid and benzbromarone were attenuated. However, the combined administration of probenecid with allopurinol decreased the serum urate concentration. These data suggest that the tubular secretion of urate is selectively impaired in FJGN and at the stage of renal failure, the combination of an uricosuric agent with allopurinol might be effective in treating hyperuricemia in FJGN.

Adolescent↗
PubMed1996

Cardiac angiosarcoma.

Angiosarcoma is one of the most common cardiac tumors, but early detection of this tumor is often difficult, as exemplified by our patient, a 55-year-old woman whose cardiac tumor was first detected by echocardiography. Surgical removal of the tumor was impossible due to its extensive pericardial invasion. Pathological diagnosis was not complete before autopsy because of the wide occupied necrotized area of the tumor. There is no diagnostic imaging technique available to detect such a necrotized area. An imaging technique more powerful than echocardiography and able to diagnose angiosarcoma earlier is needed.

Biopsy↗
PubMed1996

[Clinical incidence of primary cardiac tumors].

Recently, clinical diagnostic methods for heart disease, especially echocardiography, have remarkably progressed and the incidence of cardiac tumors increased. This study investigated the characteristics of tumors in 115 patients with primary cardiac tumor, diagnosed histologically in 1993-1994, in collaboration with 126 university hospitals in Japan. Histological diagnosis, location, initial clinical manifestations and prognosis of cardiac tumors are reported. Of the 115 patients, 98 (85%) had primary benign tumor. Myxoma was the most common histological group (91 cases). Primary malignant cardiac tumors occurred in 17 patients (15%) of which rhabdomyosarcoma was the most frequent (5 cases). Sixty percent of patients with myxoma were female, a similar ratio to the proportion of female patients with other primary cardiac tumors. Most patients with myxoma had the tumor in the left side of the heart [76 cases (84%) in left side, 12 (13%) in right side, 3 (3%) in both sides]. In contrast, the primary malignant cardiac tumors occurred more in the right side of the heart rather than in the left side (eight in right side, six in left side). Embolization was the characteristic initial clinical manifestation for myxoma. There were no patients with initial manifestation of embolization in the other histological groups. Reflecting the recent progress and spread of clinical diagnostic methods, 17% of all patients were discovered asymptomatically. All patients with myxoma who were asymptomatic underwent operation, and there were no surgical deaths. In contrast, only one patient with primary malignant cardiac tumor could survive longer than a year. In conclusion, the progress and the spread of cardiovascular imaging has contributed to the early diagnosis of primary cardiac tumors. These data demonstrate new clinical and pathological characteristics of primary cardiac tumors seen in recent cardiologic practice in Japan.

Adolescent↗
PubMed1996

[Renal hypouricemia].

Renal hypouricemia (serum urate < 2.0 mg/dl) is the inborn disorder due to the impaired tubular urate transport resulted in an increased urate excretion. The inheritance shows an autosomal recessive trait. The prevalence of renal hypouricemia is 0.15% in the outpatients. Based on the 4-component model, by using the pharmacological inhibitor, renal hypouricemia is classified into the 4 types as follows, 1) defective presecretory reabsorption, 2) defective postsecretory reabsorption, 3) enhanced urate secretion, and 4) both defective presecretory and postsecretory reabsorption including the three subtypes. Although renal hypouricemia has asymptomatic as usual, acute renal failure and urolithiasis (hematuria) have been reported as the complication. We further introduced the novel pathophysiology of the renal hypouricemia such as the aciduria correlating to the accelerated urate excretion and the hyperoxipurinemia in this review.

Acute Kidney Injury↗
PubMed1995

Family with nonmedullary thyroid neoplasms.

This report concerns a family in which papillary thyroid carcinoma appeared in the father and two daughters and follicular adenoma in a granddaughter. The father died of systemic metastasis of papillary thyroid carcinoma. The two daughters and granddaughter felt well postoperatively. We speculate that some gene-related factors might play an important role in familial occurrence of papillary thyroid carcinoma and follicular thyroid adenoma in the family.

Adenoma↗
PubMed1995

A patient with an autonomously functioning thyroid nodule with papillary adenocarcinoma associated with Graves' hyperthyroidism.

A 69-year-old man had concomitant findings of an autonomously functioning thyroid papillary adenocarcinoma and Graves' hyperthyroidism. The patient presented with hyperthyroidism and a right lobe thyroid nodule that was shown to be hyperfunctional on I-123 imaging. The TI-201 imaging showed uptake confined almost entirely to the right lobe nodule. Papillary adenocarcinoma in the nodule and diffuse hyperplasia surrounding the nodule along with a slightly enlarged left lobe were found at surgery.

Adenocarcinoma, Papillary↗
PubMed1995

Development of hypercalcemic crisis in a Graves' hyperthyroid patient associated with central diabetes insipidus.

A 26-year-old man with Graves' hyperthyroidism associated with central diabetes insipidus (DI), initially showed hypercalcemic crisis. Initially, very low serum levels of intact parathyroid hormone (PTH) and 1,25-dihydroxy vitamin D3 and a moderate rise of serum C-terminal PTH related protein (C-PTHrP) were observed which strongly suggested a humoral hypercalcemia of malignancy due to PTHrP. However, the serum C-PTHrP level later became normal. Mild hyperprolactinemia, no responses of growth hormone (GH) to insulin-induced hypoglycemia despite a normal growth hormone releasing hormone (GRH) test and mild thickening of the pituitary stalk on magnetic resonance imaging were observed. Thus, an autoimmune nature of his central DI is considered; it is noteworthy that the serum C-PTHrP level may be elevated by renal failure in patients with hypercalcemia due to causes other than PTHrP.

Acute Disease↗
PubMed1993

The TSH-dependent potassium channel in a cloned rat thyroid cell line.

We found a TSH-dependent K+ channel in the membrane of a rat thyroid cell line (FRTL-5 cell). This K+ channel is activated by extracellular application of the thyroid stimulating hormone (TSH). Treatment of dibutyryladenosine cyclic monophosphate (Bt2 cAMP) also activated the TSH-dependent K+ channel. Intracellular application of protein kinase A activates this K+ channel without the presence of free Ca2+. These findings indicate that the thyroid K+ channel is activated through the TSH-cAMP-protein kinase A system. This is the first report of a polypeptide hormone activated K+ channel and it should be useful for examining the effects of this K+ channel on thyroid cell functions.

Amino Acid Sequence↗
PubMed1993

Renal hypouricemia due to enhanced tubular secretion of urate associated with urolithiasis: successful treatment of urolithiasis by alkalization of urine K+, Na(+)-citrate.

We encountered a case of hypouricemia with increases both in urate clearance (Cur) and in the ratio of Cur to creatinine clearance (Cur/Ccr), the normal daily urinary excretion of urate, and urolithiasis. Pyrazinamide markedly decreased Cur and Cur/Ccr, and both probenecid and benzbromarone markedly increased Cur and Cur/Ccr, however, benzbromarone did not increase either Cur or Cur/Ccr under pretreatment with pyrazinamide in the patient. Thus, the diagnosis was made of renal hypouricemia due to enhanced tubular secretion of urate. The urinary pH of the patient tended to be acidic. Three months after the start of alkalization of the patient's urine by K+, Na(+)-citrate, both urolithiasis and the symptoms related to urolithiasis disappeared. These results suggest that renal hypouricemia due to enhanced tubular secretion of urate can result in urolithiasis and the alkalization of urine may be an effective treatment for uric acid stones.

Benzbromarone↗
PubMed1992

Evaluation of thyroid function in patients with isolated adrenocorticotropin deficiency.

Thyroid hormone and thyrotropin (TSH) levels were evaluated before and after adrenal replacement in eight patients (six men and two women, 35-62 years old) with isolated adrenocorticotropin (ACTH) deficiency. Six patients (cases 1-6) showed TSH excess before treatment. Four patients (cases 1-4), who initially had subnormal thyroid hormone levels, showed resolution of biochemical features of primary hypothyroidism after treatment, although TSH excess has persisted in two patients (cases 1 and 2). Case 1 had an extremely high titer of antimicrosomal antibody (MCHA), and cases 2 and 3 showed histologically and cytologically chronic thyroiditis, despite negative results for MCHA and antithyroglobulin antibody, respectively. Two patients (cases 5 and 6), who had had normal thyroid hormone levels and did not show the significant rise in serum T3 in TSH releasing hormone testing, showed TSH normalization without changes in serum thyroid hormone levels after treatment. The other two patients (cases 7 and 8), who initially had normal TSH and thyroid hormone levels, did not show the significant changes in serum TSH and thyroid hormone levels after treatment. The prevalence of chronic thyroiditis coexistence in isolated ACTH deficiency may be higher than predicted. Therefore, TSH excess before adrenal replacement may be attributed to not only direct enhancement of TSH release due to chronic cortisol deficiency but also to thyroid dysfunction due to chronic thyroiditis. It is possible that hypothyroidism due to chronic thyroiditis can be improved only by adrenal supplementation.

Adrenocorticotropic Hormone↗