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Biomedical subjects

K Takeda

Publications and source records attributed to K Takeda.

At least 739 records · Page 41Linked to original sources
PubMed1994

[Influential clinical and pathological factors on prognosis of renal cell carcinoma].

The clinical, pathological and survival data were analyzed for 42 patients with nephrectomy for renal cell carcinoma, who visited our department between 1987 and 1992. The factors influencing prognosis were evaluated. There were 33 males and 9 females with an average age of 59.1 years old. Forty-five percent (19 patients) of the cases were detected incidentally. These incidental cases showed a higher survival rate than the cases with symptoms although the difference was not statistically significant. Positive acute phase reactant, clinical stage, grade and type of infiltration were to be considerably predictive factors indicating poor prognosis. Embolization of renal artery for neo -adjuvant therapy could not improve the survival rate. Interferon-alpha for adjuvant therapy did not prolong the survival team clearly.

Acute-Phase Proteins↗
PubMed1994

[The role of intestinal flora in the pathogenesis of infection and aggravation of experimental acute pancreatitis in rats].

This study was undertaken to determine the role of bacterial translocation in the pathogenesis of infection and aggravation of the course of experimental acute pancreatitis in rats. Acute pancreatitis was induced by the injection of 3% sodium taurocholate. The rats were divided into following 3 groups: acute pancreatitis only (AP), total colectomy + pancreatitis (TCAP), acute pancreatitis with ED preparation (EDAP). The positive rate of bacteriological culture of pancreatic tissue was 40.7% at 24 hours in AP group and 50.0% in EDAP group, but in TCAP group, pancreatic tissue was sterile at 6.12 hours and at 24 hours positive rate was only 6%. There was a significant reduction of bacterial contamination in TCAP group compared with AP and EDAP groups. In the bacteriological culture of the liver, spleen and MLN, bacterial contamination was reduced in TCAP group. Blood endotoxin level elevated gradually compared to the level before induction of acute pancreatitis. At 24 hours, there was a significant difference between TCAP group and EDAP group. In TCAP group, survival rate was improved at 24 hours compared to AP group and EDAP group. Infectious complication during the experimental acute pancreatitis in rats can be explained by the bacterial translocation of intestinal flora, especially colonal bacteria, which may result in aggravation of pancreatitis.

Acute Disease↗
PubMed1994

[Clinical studies on cefozopran in pediatrics].

We conducted clinical studies on cefozopran (CZOP), a newly developed parenteral cephalosporin, for its clinical application in the field of pediatrics. 1. A clinical study was performed on 16 children with infections, including 9 with pneumonia, 1 each with acute bronchitis, enterocolitis, purulent lymphadenitis, 4 with skin and soft tissue infections. CZOP was administered by 30 minutes intravenous drip infusion. Doses varying from 20 to 35 mg/kg body weight were given t.i.d. Lengths of treatment ranged from 4 to 14 days. 2. Clinical efficacies were excellent in 10 and good in 6 cases, with an efficacy rate of 100%. The overall bacterial eradication rate for the pathogenic bacteria was also 100%. 3. Side effect was noted in 1 case with skin rash. Abnormal laboratory test data were found in 5 cases including slight elevations of GPT in 4 cases and GOT in 2 cases.

Adolescent↗
PubMed1994

Effect of an angiotensin II receptor antagonist, TCV-116, on cardiac hypertrophy and coronary circulation in spontaneously hypertensive rats.

To determine whether an angiotensin II receptor antagonist (AT antagonist) could improve the impaired coronary circulation as well as induce regression of cardiac hypertrophy in the hypertensive heart, and to elucidate whether the nitric oxide system in the coronary artery was involved in this mechanism, the AT1 antagonist, TCV-116 (10 mg/kg), was administered orally to spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY), and coronary flow was measured in the isolated hearts. High systolic blood pressure in SHR was significantly reduced by a 2-week treatment with TCV. Left ventricular (LV) hypertrophy in SHR regressed after TCV treatment, while LV weight in WKY was not reduced. Total minimum coronary vascular resistance (MCVR) obtained with adenosine (10(-5) M) infusions in a Langendorff apparatus was significantly greater in SHR than in WKY. Increased MCVR in SHR was reduced after TCV treatment. Coronary perfusion with NG-monomethyl-L-arginine monoacetate (L-NMMA) increased coronary vascular resistance (CVR) in WKY, while it failed to increase CVR in SHR. TCV treatment restored the responses to L-NMMA in SHR. These findings suggest that the AT1 antagonist, TCV-116, lowered the high blood pressure in SHR, concomitantly improving the impaired coronary circulation, and that it induced regression of the cardiac hypertrophy. The suppressed nitric oxide (NO) system in the coronary vessels in SHR appeared to be activated by TCV treatment.

Angiotensin Receptor Antagonists↗
PubMed1994

[A case of dissecting aneurysm associated with mixed connective tissue disease].

A 41 year-old-female with mixed connective tissue disease (MCTD) associated with dissecting aneurysm (DA) of the right posterior cerebral artery is reported. This case satisfied the diagnostic criteria for MCTD, and cerebral angiography revealed the double-lumen sign and pooling of the contrast medium. Thus it was possible to make a definite diagnosis of both MCTD and DA. Fragility of the arterial wall due to the primary disease, MCTD, appeared to have played a role in the occurrence of dissection and the subarachnoid hemorrhage.

Adult↗
PubMed1994

Lymphotoxin and TNF differ greatly in capacity to induce differentiation of human myeloblastic leukemia ML-1 cells.

We found that recombinant and natural lymphotoxin differ from TNF in that they only marginally induce differentiation of human myeloblastic leukemia ML-1 cells. Even at 1,000-fold concentrations, lymphotoxin was significantly less potent than TNF. Lymphotoxin competitively, but not completely, inhibited TNF-induced differentiation. Based on studies of the two types of TNF receptors (55 kDa and 75 kDa) using monoclonal antibodies, the binding activity of lymphotoxin to the receptors was less than 1/3 that of TNF, but lymphotoxin could bind to both TNF receptors. Both receptors were involved in induction of differentiation by TNF. However, lymphotoxin, differed from TNF; it seemed to be weak in sending signals for differentiation through the 75 kDa receptor.

Cell Differentiation↗
PubMed1994

[A case of congenital protein C deficiency with pulmonary thromboembolism].

A 47-year-old woman, with a history of recurrent venous thrombosis in her lower limbs (1988 and June, 1992), was admitted because of pulmonary thromboembolism in the right middle lung lobe. She was given anti-coagulant therapy with warfarin. The consolidation in the right middle lobe disappeared within two months. Hematological examinations concerning the coagulation and fibrinolytic system showed a significant decrease in both the serum concentration and the activity of protein C, a vitamin K-dependent hepatic protein which acts as an anticoagulant by shutting off fibrin formation and stimulating fibrinolysis. Since a sister of the patient also has a history of venous thrombosis, several members of her family were tested for protein C deficiency. The familial study revealed that her sister and mother had both a decreased concentration and depressed activity of protein C, indicating that this is a case of congenital protein C deficiency. Warfarin therapy has been continued to reduce the prothrombin time to 70% of the normal control level, resulting in no further episodes of thrombosis.

Female↗
PubMed1994

[Clinical analysis of cases with acute exacerbation of chronic renal failure].

We analyzed the total number of 42 events of acute exacerbation of chronic renal failure (CRF) in 35 patients who were admitted to the Matsuyama Red Cross Hospital Kidney Center between 1985 and 1990. These patients consisted of 16 males and 19 females with a mean age of 59.8 +/- 12.7 years. The most frequent original renal diseases were diabetic nephropathy (DM) and arteriosclerotic nephrosclerosis (NS). The most frequent acute exacerbation factors were dehydration and infection. Four cases died and one case transferred to chronic hemodialysis, but the other 37 events (88%) in 31 cases recovered to normal renal functioning. Tentative dialysis therapy was performed for 12 events, in which the cases with DM as the original disease and infection as the exacerbation factor were responsive to this therapy. In the analysis of long-term prognosis, 7 out of 26 cases died of non-renal diseases, 15 transferred to chronic dialysis therapy and only 4 remained in a CRF state. The intervals between the date of discharge and that of the start of dialysis therapy was shorter in the cases with DM (mean of 5 months) or chronic glomerulonephritis (mean of 7.6 months) than in cases with chronic interstitial nephritis, polycystic kidney disease and NS (mean of 17.7 months). We concluded that even though many of the cases eventually transferred to chronic dialysis therapy, appropriate therapy during the acute exacerbation period could allow recovery to a natural progressive or nonprogressive course in each case.

Acute Kidney Injury↗
PubMed1994

Diffusional anisotropy of the human brain assessed with diffusion-weighted MR: relation with normal brain development and aging.

PURPOSE: To analyze diffusional anisotropy in frontal and occipital white matter of human brain quantitatively as a function of age by using diffusion-weighted MR imaging. METHODS: Ten neonates (< 1 month), 13 infants (1-10 months), 9 children (1-11 years), and 16 adults (20-79 years) were examined. After taking axial spin-echo images of the brain, diffusion-sensitive gradients were added parallel or perpendicular to the orientation of nerve fibers. The apparent diffusion coefficient parallel to the nerve fibers (0) and that perpendicular to the fibers (90) were computed. The anisotropic ratio (90/0) was calculated as a function of age. RESULTS: Anisotropic ratios of frontal white matter were significantly larger in neonates as compared with infants, children, or adults. The ratios showed rapid decrease until 6 months and thereafter were identical in all subjects. In the occipital lobe, the ratios were also greater in neonates, but the differences from other age groups were not so prominent as in the frontal lobe. Comparing anisotropic ratios between frontal and occipital lobes, a significant difference was observed only in neonates. CONCLUSIONS: Diffusion-weighted images demonstrated that the myelination process starts earlier in the occipital lobe than in the frontal lobe. The changes of diffusional anisotropy in white matter are completed within 6 months after birth. Diffusion-weighted imaging provides earlier detection of brain myelination compared with the conventional T1- and T2-weighted images.

Adolescent↗
PubMed1994

[Resistance to thyroid hormone].

Resistance to thyroid hormone (RTH), Refetoff's syndrome, is a syndrome of reduced responsiveness of target tissue to thyroid hormone (TH). Inheritance is usually autosomal dominant except in one family, being recessive. Since a point mutation was first discovered in the thyroid hormone receptor (TR) beta gene of a subject with RTH, approximately 93 unrelated families with RTH have been found to have mutations on TR beta gene. Clinically they presented either generalized (GRTH) or dominantly pituitary (PRTH) resistance to TH. In one family, affected consanguineous individuals lacked the entire protein coding region of both hTR beta alleles. In this family with recessively inherited RTH, the obligate heterozygous parents exhibited no clinical and laboratory abnormalities. Thus, manifestation of RTH in heterozygous individuals required the expression of a mutant receptor that interferes with the function of normal allele ("dominant negative effect"). The formation of mutant TR/TRAP (RXR etc.) heterodimer or mutant TR homodimer having the capability to bind the DNA for this dominant negative suppression of mutant TR beta, and the variation of TRE types, receptor isoforms and auxiliary proteins depending on the target tissue may play an important role in the manifestation of TH resistance. This may explain in part the intra- and inter-individual differences in organ resistance in patients with RTH. Studying the errors of nature would contribute to understand the molecular mechanism of TH action.

Genes, Dominant↗
PubMed1993

Suppression of stress protein GRP78 induction in tumor B/C10ME eliminates resistance to cell mediated cytotoxicity.

Tumor cells undergo self-destruction when incubated with cytotoxic T-cells (CTL) consistent with the observation that suppression of target protein synthesis causes resistance to apoptosis. Resistance to CTL is also induced by stress, suggesting that pathways exist suppressing apoptosis. Here we examine whether stress induced lysis resistance to CTL and tumor necrosis factor alpha involves stress proteins GRP78 and GRP94. We show that inhibition of GRP78 synthesis by transfection of cells with grp78 antisense vector pRSV-78WO leads to inability to induce resistance to CTL or tumor necrosis factor alpha. Resistance induced in untransfected cells is reversible upon stress removal and correlates with GRP78 rephosphorylation, consistent with the notion that phosphorylated GRP78 is nonfunctional. The possibility that GRP78 plays a role in defense against CTL mediated apoptosis is supported by the finding that CTL but not CD4+ cells express a high level of unphosphorylated GRP78.

Animals↗
PubMed1993

Expression of intercellular adhesion molecule-1 on cardiac myocytes for myocarditis before and during immunosuppressive therapy.

Right ventricular endomyocardial biopsies were performed in 15 patients with unexplained cardiac dysfunction, and the expression of intercellular adhesion molecule-1 (ICAM-1) on the myocardium was examined using the streptavidin-biotin complex method. Three of 15 patients (20%) had histologic evidence of myocarditis, and 2 of 15 patients (13%) had borderline myocarditis. The patients with biopsy-proven myocarditis received immunosuppressive therapy (prednisolone 60 mg/day). Two of the 3 patients demonstrated a substantial increase (> 10%) in percent fractional shortening and left ventricular ejection fraction during therapy. Subsequent biopsies revealed ongoing myocarditis in 1 patient, and resolved myocarditis in the other. The remaining patient had persistent cardiac dysfunction, but the subsequent biopsy revealed resolving myocarditis. ICAM-1 immunoreactivity was observed on cardiac myocytes, vascular endothelial cells, and interstitial cells of the patients with myocarditis. However, in patients without myocarditis, ICAM-1 immunoreactivity was observed only on vascular endothelial cells and interstitial cells. ICAM-1 immunoreactivity was still observed on cardiac myocytes in the patients with ongoing or resolving myocarditis during immunosuppressive therapy, but was not detected in the patient with resolved myocarditis. This study demonstrates that ICAM-1 is expressed on cardiac myocytes of patients with myocarditis and persistent cardiac dysfunction despite immunosuppressive therapy. The persistent expression of ICAM-1 may cause chronic inflammation of the myocardium.

Adult↗
PubMed1993

[MR tractography--visualization of structure of nerve fiber system from diffusion weighted images with maximum intensity projection method].

We developed a new noninvasive technique to visualize the anatomical structure of the nerve fiber system in vivo, and named this technique magnetic resonance (MR) tractography and the acquired image an MR tractogram. MR tractography has two steps. One is to obtain diffusion-weighted images sensitized along axes appropriate for depicting the intended nerve fibers with anisotropic water diffusion MR imaging. The other is to extract the anatomical structure of the nerve fiber system from a series of diffusion-weighted images by the maximum intensity projection method. To examine the clinical usefulness of the proposed technique, many contiguous, thin (3 mm) coronal two-dimensional sections of the brain were acquired sequentially in normal volunteers and selected patients with paralyses, on a 1.5 Tesla MR system (Signa, GE) with an ECG-gated Stejskal-Tanner pulse sequence. The structure of the nerve fiber system of normal volunteers was almost the same as the anatomy. The tractograms of patients with paralyses clearly showed the degeneration of nerve fibers and were correlated with clinical symptoms. MR tractography showed great promise for the study of neuroanatomy and neuroradiology.

Aged↗
PubMed1993

The development of autoimmunity in C57BL/6 lpr mice correlates with the disappearance of natural killer type 1-positive cells: evidence for their suppressive action on bone marrow stem cell proliferation, B cell immunoglobulin secretion, and autoimmune symptoms.

F1 hybrid mice are able to acutely reject parental marrow grafts, a phenomenon that is due to natural killer type 1-positive (NK1+) cells. Circumstantial evidence had suggested that the antigenic determinants recognized by these cells are self-antigens, leading to the hypothesis that the physiological role of NK1+ cells is a downregulatory or suppressive function on bone marrow stem cell proliferation and lymphocyte function. In analyzing this hypothesis it is shown here that in young mice there is a temporal correlation between appearance of NK1+ cells in the spleen and the ability to reject allogeneic marrow or to suppress endogenous stem cell proliferation. The reverse situation exists in mice expressing the homozygous lpr gene. Whereas in young mice cells with NK1+ phenotype are demonstrable, these cells disappear with age, i.e., at the time autoimmunity develops. Concomitant with the disappearance of NK1+ cells, the ability to reject marrow grafts and to control endogenous stem cell proliferation also vanishes. The suggestion that the development of autoimmunity is causally related to the disappearance of NK1+ cells is supported by experiments in which NK1+ cells were either eliminated by antibody injection or increased by adoptively transferring cell populations enriched for NK1+ cells into lpr mice. It is shown that removal of cells enhances autoimmunity, whereas injection of NK1+ cells delays the onset of autoimmunity. In vitro assays are presented that demonstrate that suppression of autoantibody-secreting B cells is due to two NK1+ cell populations, one that expresses CD3 and causes specific suppression and one that lacks CD3 and causes nonspecific suppression.

Aging↗