[Computed tomography of amenorrhea-galactorrhea syndrome].
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Biomedical subjects
Publications and source records attributed to S Nishimura.
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Electrocardiographic features of apical hypertrophic cardiomyopathy are high QRS voltage and giant negative T waves greater than 10 mm in left precordial leads. We analyzed thirty patients with apical hypertrophic cardiomyopathy to clarify the correlation between left ventricular (LV) wall thickness and the depth of negative T waves. LV anterior wall thickness was measured by the left ventriculogram (LVG) in the RAO projection. LV posterior wall and septal thickness were measured by echocardiograms recorded from the left sternal border. THA and THM were defined as apical thickness and mid ventricular wall thickness, respectively. The results were as follows: LVG disclosed that the depth of negative T waves in apical hypertrophic cardiomyopathy was significantly related to the absolute thickness of apical segment itself rather than the difference in the distribution of thickness from the basal to apical segment of the left ventricle. This results support the clinical observation that giant negative T waves in some cases are associated with diffuse hypertrophy of the LV without a spade like configuration in LVG. Results of the echocardiographic analysis, however, revealed that the depth of negative T waves had no relation to the distribution of left ventricular hypertrophy. This is partly because of unsatisfied and difficult recordings and measurements of the true LV apical segment by echocardiography. The presence of both high QRS voltage and giant negative T waves is indispensable for the diagnosis of apical hypertrophy.
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Chemotherapy was applied for experimental subarachnoid dissemination model of brain tumor which was established in male Wister-SPF (SLC) rats inoculated intracisternally with 2 X 10(5) C6 rat glioma cells. Nontreated animals died about 24 days after inoculation. Autopsy findings of the animals showed localized or multifocal invasion of the tumor on leptomeninges in cisterna magna, and partially infiltration into the parenchyma of the cerebellum and medulla oblongata. Three days after inoculation, the tumor deposition and proliferation already occurred. Several tumor cell layers were found in the subarachnoid space over the cerebellomedullary surface. Tumor bearing animals were at first treated by single agent. These are ACNU administered intraperitoneally, methotrexate administered intracisternally, and OK-432 administered intraperitoneally. In the next stage, combination of these drugs was applied. ACNU, 3 mg/kg i. p., on Day 3, was effective in elongation of median survival time by 23.6%, statistically significant (P less than 0.02). Methotrexate, 0.25 mg/kg i.th., on Day 3, was also effective in elongation of median survival time by 8.4%, statistically significant (P less than 0.05). OK-432, 0.1 KE/kg i. p., daily, 14 times, from Day 3 to Day 16, was ineffective in elongation of median survival time. Combination of ACNU, methotrexate and OK-432, in the same schedule as described above, produced the longest median survival time of 42.4%, statistically significant (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
A 63-year-old woman with localized lipomatosis in the pancreatic head is reported. She was diagnosed to have a lipoma by clinical data including CT scanning. Histopathological examination of the extirpated mass revealed that the lesion was mostly composed of mature fatty tissue without any lobulation or encapsulation by connective tissue, there was a small amount of scattered pancreatic parenchyma at the peripheral and deeper parts of the mass. No Langerhans' islets were detected. Based on these findings, the lesion was diagnosed as localized lipomatosis in the pancreatic head.
We determined the primary structures of various tumor-specific tRNAs as well as of their normal counterparts by postlabeling RNA-sequencing procedures. The results clearly indicated that tumor-specific tRNAs are mostly formed by undermodification of hypermodified nucleosides located in the anticodon loop: no new tRNA transcripts have so far been found in tumor cells. Among the modified nucleosides affected by tumorigenesis, queuosine and Y base are the most interesting. In various tumor tRNAPhe species, hydroxy Y base located next to the anticodon is undermodified to form hypomodified hydroxy Y base lacking methyl and carboxymethyl groups. This Y base analog should be a good marker for analyzing the state of cancer cells. Queuosine, located in the first position of the anticodon, is partly or completely replaced by guanosine in all tumor cells tested so far. The amount of G-tRNA decreased markedly when the cells differentiated into mature erythroid cells, with concomitant increase of Q-tRNA. This indicates that the presence of G-tRNA is closely related to the state of the cells, not merely to the fast growth rate of tumor cells. The enzyme tRNA-guanine transglycosylase, which is a key enzyme in biosynthesis of queuosine in tRNA (inserting Q base into tRNA by a transglycosylase reaction), is active in both tumor cells and normal cells. Administration of chemically synthesized Q base to tumor-bearing mice resulted in complete conversion of G-tRNA to Q-tRNA in tumor cells, indicating that exogenously added Q base is effectively incorporated into G-tRNA. Various Q base analogs that can be used as substrates for tRNA-guanine transglycosylase were synthesized chemically. These compounds may be used for clinical cancer diagnosis, since they should be incorporated selectively into tRNA in tumor cells. In addition to use as cancer chemotherapeutic reagents, it should be possible to develop new Q base analogs that induce miscoding or blocking of protein synthesis after insertion into G-tRNA.
Various tumor cells contain chromatographically distinct isoacceptor tRNA species. To decide whether the tumor-specific species represent an expression of a separate tRNA gene or only an undermodified form of normal tRNAPhe, nucleotide sequences of tRNAPhe isolated from neuroblastoma and normal mouse liver were determined by postlabeling techniques. The results showed identical sequences except for the changes of post-transcriptional modifications in the anticodon loop. Normal mouse liver tRNAPhe contained Cm32, Gm34, and the hypermodified YOH next to the 3' end of the anticodon. On the contrary, tRNAPhe from neuroblastoma contained C32, G34, and, instead of YOH base m1G. A small proportion of tRNAPhe species contained an undermodified YOH base. For the examination of the conditions leading to the undermodified tRNAPhe, Vero cells derived from the kidney of African green monkey in culture were used. In these cells, deprivation of methionine or lysine resulted in changes in tRNAPhe modification similar to those in tumor cells. Ehrlich ascites tumor cells were examined to determine whether the presence of altered tRNAPhe species in various tumors is also the result of starvation of some nutritional factors. Results obtained with these cells showed that tRNAPhe species lacking the Y base disappeared in tumor-bearing mice after intraperitoneal injection with a mixture of amino acids and vitamins. Thus it is concluded that tumor-specific tRNAPhe species are the products of aberrant post-transcriptional modification, not the transcripts of different, normally repressed genes.
Evidence from a variety of experimental models has suggested the existence of mu 1, mu 2 and delta binding sites for morphine and the enkephalins in the central nervous system. Additional biochemical experiments now support this concept of a common high affinity site for opiates and opioid peptides. Mu sites have now been implicated in a number of pharmacological actions, including supraspinal analgesia, prolactin release, and catalepsy, but not in others (spinal analgesia, respiratory depression, and the guinea pig ileum). The hypothesis of mu 1 sites was supported by the unique opioid meptazinol, which selectively bound to mu 1 sites. As expected from its mu 1 binding selectivity, its analgesic actions in the mouse, localized supraspinally, were antagonized by the selective mu 1 antagonist naloxonazine and it had no respiratory depressant actions. Other binding studies suggested the presence of discrete SKF10,047-selective (KD approximately 5 nM) binding sites in rat brain which differed from both kappa sites and the previously reported PCP-binding sigma sites. Additional binding and autoradiographical studies have also implied the presence of beta-endorphin, or epsilon, sites in the CNS.
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A procedure based on multiple quantum two-dimensional nuclear magnetic resonance spectroscopy is described for generation of 1H--15N chemical shift correlation maps. The method is used to obtain 15N chemical shifts for the exchangeable imino protons in 1H--15N units of site-specifically labeled Escherichia coli tRNAMetf in water. The high sensitivity and excellent chemical shift dispersion of the multiple quantum two-dimensional technique make it ideally suited for studying protonated nitrogens by NMR.
HNCM tends to have more diffuse or generalized hypertrophy than HOCM, although these two types are not fundamentally different in aetiology (genetic). Extreme ASH is primarily related to a hereditary factor while HNCM, including apical hypertrophy, seems to be based on an abnormal disposition to produce myocardial hypertrophy in response to endogenous or exogenous stimulation such as catecholamines, chronic anoxia, hypertension or even aging. Hypertension by itself, however, can not be a cause of apical hypertrophy. The configuration of left ventricular hypertrophy in HCM can be divided roughly into several patterns: ASH, apical, postero-inferior, generalized or diffuse types, etc. ASH is not an essential morphology for HNCM. Apical hypertrophy is the only specific hypertrophic pattern which shows characteristic ECG abnormalities (giant negative T waves and high QRS voltage in left precordial leads). Inverted T waves combined with high QRS voltage tends to be a reflection of a localized hypertrophic portion in the left ventricular free wall. Abnormal Q waves associated with left axis deviation usually suggest marked septal hypertrophy. They seem to be related to conduction disturbances in myopathic septum.
The nucleotide sequence of a cloned section of the Escherichia coli chromosome containing the promoter regions of the malB divergent operons was determined. The region of the proximal gene, malE of the malEFG operon, was identified on the basis of the known amino acid sequence of the precursor molecule of maltose-binding protein. The region of malK, the proximal gene of the malKlamB operon, was deduced from the observation that a cloned segment contains an amino-terminal portion of the malK gene. The non-coding region between malE and malK is 299 base pairs long and contains two long GC clusters. Another feature of this region that may be related to the regulation of gene expression is the presence of two palindromic structures between the GC clusters. The DNA regions binding to cyclic AMP binding protein were determined by a method using polyacrylamide gel electrophoresis. The sites are thought to be located close to GC clusters.
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In the cat adrenal perfused with a medium containing ouabain, raising the external concentration of K to 10 mM abruptly increased the rate of catecholamine secretion. Increased response to 10 mM K were also observed in the adrenals treated with monoiodoacetate or cyanide, which was suggested to reduce the Na pumping activity indirectly. Since both the onset time and the magnitude of K-induced secretion are dependent on the concentration of external Na, it was suggested that a small increase of K concentration accelerates Ca influx in exchange for internal Na.
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Twenty liver cancer patients, including 9 hepatocellular carcinoma and 11 with metastatic liver cancer, were treated by intra-arteral one-shot chemotherapy. Alterations in blood coagulation and fibrinolysis were observed serially after one-shot chemotherapy by testing the levels of PT, APTT, FDP, fibrinogen, AT III, alpha 2-macroglobulin, and plasminogen. APTT was prolonged, FDP increased, Fbg increased after a transicent decrease, and AT III, alpha 2-M, and plasminogen decreased. The peaks of these alterations occurred within 7 days after the one-shot treatment; recovery was observed after about weeks. The more advanced the cancer, the greater were the alterations.
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