[A clinical study on 16 cases with tracheobronchial tuberculosis].
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Biomedical subjects
Publications and source records attributed to S Hashimoto.
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To determine the functional role of the striatonigral system in the circling behavior of rats and the mode of action of colchicine, we investigated the circling behavior induced by dopamine agonists after microinjection of colchicine into the unilateral striatum. Both apomorphine and methamphetamine produced ipsilateral circling behaviors in rats injected with colchicine, indicating that ipsilateral striatonigral pathways were damaged by the drug. Histological and biochemical examinations showed that intracaudate injection of colchicine damaged not only the dopaminergic neurons but also caused atrophy of the striatum with loss of neuronal perikarya. These results suggest that treatment with colchicine may be used as a model of senile atrophy or degenerative atrophy in these animals.
Monoclonal antibodies against human T cell leukemia virus type I (HTLV-I) p24 and p19 were produced and employed in the in vivo expression of HTLV-I in some HTLV-I-related subjects by Western blot analysis. The antigenic determinants of these monoclonal antibodies were different from that of natural human anti-HTLV-I antibody examined. Serum p24 was identifiable in almost all of the overt ATL patients (17 of 18, 94%), but not in the chronic ATL cases or HTLV-I carriers. On the other hand, serum p19 was detected in one of the three patients with chronic ATL examined, but not in the overt ATL patients or the HTLV-I carriers. These results indicate that the in vivo expression of HTLV-I p24 and p19 which has reacted with natural anti-HTLV-I antibody can be detected by these monoclonal antibodies. Therefore, the investigation of serum HTLV-I expression may lead to the early detection of overt ATL in an HTLV-I carrier.
Complementary DNA (cDNA) clones encoding the regulatory subunit of the type I cAMP-dependent protein kinase (R-I) were isolated by screening of rat brain cDNA libraries. A 1.5-kilobase (kb) cDNA insert containing the entire coding region was sequenced and full amino acid sequence has been deduced from the nucleotide sequence. The clone encodes for a protein of 380 amino acids that shows 97% homology to the bovine R-I subunit. Northern blot analysis demonstrated two major mRNA species (2.8 and 4.4 kb in size) in rat brain and liver.
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To evaluate the usefulness of pulsed Doppler echocardiography in assessing late diastolic mitral regurgitation (MR) and to clarify the pathophysiology of MR, 226 consecutive patients who had undergone left ventriculography were studied. By investigating blood flow patterns at the left atrial outflow tract, late diastolic disturbed flow suggesting MR was detected in 15 patients (7%), including 10 (4%) with positive left ventriculographic findings. Among these 15 patients, 14 (93%) had atrial fibrillation and had late diastolic MR in the cardiac cycle with prolonged RR interval. The limitation in number of cardiac cycles that could be analyzed and the rapid heart rate eliminating appearance of the beat with prolonged RR interval may be the reasons for the paucity of late diastolic MR by left ventriculography. Ten patients (66%) with late diastolic MR, including 1 with sinus rhythm, had aortic regurgitation, 3 had high-grade systolic MR and 2 had atrial septal defect. Simultaneous recording of pulmonary artery wedge pressure and left ventricular pressure in 3 patients showed a reversal of pressure gradient in late diastole when the RR interval was prolonged. In conclusion, pulsed Doppler echocardiography was useful for detecting late diastolic MR and in reducing overestimation of systolic MR in left ventriculography induced by erroneous addition of late diastolic MR. The difference of the incidence of this flow between left ventriculography and Doppler examination indicated that this flow depends primarily on heart rate and may come and go in a patient.
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A cDNA library in lambda-phage lambda gt11 containing DNA inserts prepared from human liver mRNA was screened with monoclonal antibodies to human protein C inhibitor. Six positive clones were isolated from 6 X 10(6) phages and plaque purified. The cDNA in the phage containing the largest insert, which hybridized to a DNA probe prepared on the basis of the amino-terminal amino acid sequence of the mature inhibitor, was sequenced. This cDNA insert contained 2106 base pairs coding for a 5'-noncoding region, a 19-amino acid signal peptide, a 387-amino acid mature protein, a stop codon, and a long 3'-noncoding region of 839 base pairs. Based on the amino acid sequence of the carboxyl-terminal peptide released by cleavage of protein C inhibitor by activated protein C as well as by thrombin, the reactive site peptide bond of protein C inhibitor is Arg354-Ser355. Five potential carbohydrate-binding sites were found in the mature protein. The high homology of the amino acid sequence of protein C inhibitor to the other known inhibitors clearly demonstrates that protein C inhibitor is a member of the superfamily of serine protease inhibitors including alpha 1-antichymotrypsin, alpha 1-antitrypsin, antithrombin III, ovalbumin, and angiotensinogen. Based on the difference matrices for these proteins, we present possible phylogenetic trees for these proteins.
Supernates of thymic epithelial cell culture (STEC) strongly inhibit aggregation induced by addition of adenosine diphosphate (ADP: 1 microM) or thrombin (0.5 unit per ml) to washed platelet suspensions and accelerated the restoration from ADP-triggered aggregation. At the same time, STEC increased the level of platelet adenosine 3',5'-cyclic monophosphate (cyclic AMP) in a dose-dependent manner. Depending on the concentration used, thymosin fraction 5 increased the level of intracellular cyclic AMP ranging between 5 and 100 micrograms per ml, as well as inhibiting ADP-induced platelet aggregation. The activities of both STEC and thymosin fraction 5 were found to act exclusively on cyclic AMP phosphodiesterase activity in platelets. In contrast the supernates from Chang, HeLa, or HCC-M cells did not affect platelet aggregation induced by ADP, but slightly increased the cyclic AMP level (Chang, HeLa). Within 2 min after the treatment with STEC, more than 50% of the maximum inhibitory activity on platelet aggregation and increases in intracellular cyclic AMP were observed. These activities disappeared following STEC treatment with pronase E. STEC activity was found predominantly in the 1,000-50,000-dalton fractions. These activities were not altered when STEC was treated by adenosine deaminase. The level of prostaglandin E (PGE) derivatives in STEC was about two times that found in the control culture medium. These data suggest that the biological activity of STEC in the platelets might be attributed to thymosinlike polypeptides and PGE1.
Subcutaneously (s.c.) administered apomorphine (0.0125-0.4 mg/kg) or physostigmine (0.025-0.4 mg/kg) to rats elicited yawning. The dose-response curves were bell-shaped. The peak effects of apomorphine and physostigmine were observed with a dose of 0.1 mg/kg of each drug. Yawning elicited by apomorphine (0.1 mg/kg) or physostigmine (0.1 mg/kg) was reduced by intraperitoneally (i.p.) administered 5-hydroxytryptophan (5-HTP, 50-200 mg/kg, given 30 min before). Yawning elicited by apomorphine but not by physostigmine was enhanced by p-chlorophenylalanine (p-CPA, 25-400 mg/kg i.p., given 24 h before). Apomorphine elicited but not physostigmine-elicited yawning was enhanced by pretreatment with 5,7-dihydroxytryptamine (5,7-DHT, 8 micrograms/rat, given 14 days before into the dorsal raphe). This treatment led to a 35% depletion of serotonin (5-HT) in the striatum. 5-HTP, p-CPA or 5,7-DHT given alone did not elicit yawning. Bilateral, intrastriatal microinjection of apomorphine (1.5-50 micrograms/site) but not physostigmine (5-50 micrograms/site) elicited yawning. The dose-response curve was also bell-shaped. These results indicate that central serotonergic pathways play an important role in modulating drug-elicited yawning in rats.
The effect of tumor cells and immunostimulants on the release of cytostatic factors (CF) from Lactobacillus casei YIT 9018 (LC)-, Corynebacterium parvum (CP)- or peptone-elicited peritoneal macrophages (PM) was investigated in vitro and in vivo. Significant release of CF into the culture medium from PM elicited with LC was induced by seven of eight mitomycin C-pretreated tumor cell lines and not by normal spleen cells, while no CF was released extracellularly from peptone-elicited PM given the same stimulus. CF were released from LC-elicited PM (LCEPM) after stimulation with LC, bacille Calmette-Guérin, streptococcal preparation OK-432, fucoidan or lipopolysaccharide, and LC but not CP induced CF production in the peritoneal cavities of LC- or CP-primed mice. The release of CF from LCEPM after stimulation with mitomycin C-pretreated 3T12-3 cells was inhibited by D-mannose and not by L-fucose. L-Rhamnose and mannose 6-phosphate, but not D-mannose or L-fucose, caused the release of CF from the PM. It was suggested that the release of CF from activated PM is caused by stimulation by some tumor cells, sugars, or bacterial immunostimulants, D-Mannose and L-rhamnose on the surface of tumor cells or bacteria, respectively, may plan an important role in the release of CF from activated macrophages.
201Tl myocardial imaging can, noninvasively, visualize the various cardiac structures; such as the left ventricle, right ventricle and, occasionally, the atrium. We have noted that certain patients exhibit a prominent appearance of the papillary muscle on a scintigram. Thus, we analyzed 201Tl myocardial scintigrams for evidence of activity which corresponded to the anterolateral (A-PM) and posteromedial (P-PM) papillary muscles. Twenty normal subjects, 81 patients with ischemic heart disease (IHD), 11 with hypertrophic cardiomyopathy (HCM) and 13 with dilated cardiomyopathy (DCM) were examined. Patients with DCM had rest imaging only, while the remaining ones performed exercise studies. The prevalence of a positive A-PM image was not high (9%-23%) and there was no significant difference among groups. The P-PM was seen in only 15% of the normal group and in 18% of the HCM group, while the prevalence was high in the IHD (34.6%) and DCM (53.8%) groups. In the IHD, the positive images of the P-PM were largely from the sub-group with single vessel left anterior descending (LAD) coronary artery disease (78.9%). However, even in the presence of a defect in the left ventricular wall supplied by the LAD coronary artery, the patients with multi-vessel coronary artery disease did not tend to disclose the P-PM on the scintigram (30.8%). Thus, we conclude that positive P-PM imaging on a planar 201Tl myocardial scintigram is frequently observed under some cardiac states and seems to be related to reduced wall motion, sound blood supply to the P-PM and the existence of a defect in the anterior left ventricular wall overlapping the P-PM.(ABSTRACT TRUNCATED AT 250 WORDS)
Cu(II)2(acetylsalicylate)4, Cu(II)(anthranilate)2, Cu(II)2[1-(p-chlorobenzoyl)-5-methoxy-2-methyl-3-indolylacetate]4, Cu(II)(3,5-diisopropylsalicylate)2, Cu(II)(salicylate)2, Cu(II)2(2-[3-(trifluoromethyl)-phenyl]aminonicotinate)4, Cu(II)(L-alaninate)2, Cu(II)(L-cystinate)2, and Cu(II)(glycinate)2 were generally found to be more effective analgesics than their parent ligands, Cu(II)(chloride)2, and Cu(II)2(acetate)4 in the Writhing Mouse and Adjuvant Arthritic Rat pain models following subcutaneous and oral administration. Comparison of the time course of analgesia for salicylic acid and Cu(II)(salicylate)2 in the adjuvant arthritis pain model revealed that this complex had more sustained activity in addition to being more potent than salicylic acid. Cu(II)2(indomethacin)4 was also found to be as effective as morphine in both pain models. These data and pertinent literature are discussed in support of the hypothesis that copper complexes activate copper-dependent opioid receptors.
Four cases of annular pancreas diagnosed by endoscopic retrograde cholangiopancreatography (ERCP) are described and 105 cases of this anomaly in adults in Japan were reviewed. Among 105 cases, abdominal pain was the most frequent symptom. Concerning associated diseases, peptic ulcer was present in 24.8% and pancreatitis in 13.3%. In case 1, duodenal ulcer and pancreatic cyst were noted. Pancreatolithiasis was found in two cases (case 1 and 2). Case 4 presented the clinical features of acute pancreatitis. Out of 105 cases, well-described 26 were divided into six types. The following results were obtained. 1) The most frequent type was that in which the annular duct arose from the duct of Wirsung. 2) The next most frequent type was that in which the main pancreatic duct encircled the duodenum. 3) The other types corresponded to those in which the annular duct arose from the duct of Santorini and the common bile duct. We emphasized that ERCP is the most important procedure to find the characteristic features and to establish the therapeutic strategy in cases of annular pancreas.
The caudate spindle in rats was observed following bilateral application of apomorphine (1.5-50 micrograms) and (+/-)-3-(3-hydroxyphenyl)-N-n-propylpiperidine (3-PPP, 0.3-3 micrograms) into the striatum. The smallest dose (1.5 micrograms) of apomorphine enhanced the spindle whereas with a larger dose (50 micrograms), suppression occurred. The preferential dopamine (DA) autoreceptor (inhibitory-receptor) agonist, (+/-)-3-PPP, enhanced the spindle, in a dose-dependent manner. The enhancing effect of apomorphine (1.5 micrograms) and (+/-)-3-PPP (3 micrograms) was prevented by neuroleptics, such as haloperidol (20 micrograms/kg, i.v.) and sulpiride (2 mg/kg, i.v.) at doses which, per se, did not affect the spindle. Small doses of neuroleptics are thought to block DA autoreceptors, suggesting that the enhancing effects of the DA agonists are mediated by autoreceptors. These results lend further support to the assumption that the development of the caudate spindle involves activation or DA receptors. Enhancement of the spindle, induced by injections of apomorphine into the striatum (small dose) and (+/-)-3-PPP, may be mediated by DA autoreceptors (inhibitory-receptors) located at presynaptic elements of the nigro-striatal DA system, while suppression may be due to stimulation of the postsynaptic DA receptors.