Biomedical subjects
Publications and source records attributed to T Ohno.
A 67-year-old man with angiomyolipoma on the sigmoid colon is reported. The colonic polyp was pedunculated and diagnosed histologically after endoscopic polypectomy. Angiomyolipoma is one of the benign hamartomas arising principally in the kidneys of patients with or without tuberous sclerosis. Extrarenal angiomyolipoma is rare and this may be the first report of colonic angiomyolipoma.
Patterns of EMG activities of neck muscles underlying the initiation of head-turning, induced by stimulation of the caudate nucleus, were analyzed with special reference to temporal relations between the onset of head-turning and that of changes in EMG activities. These patterns were compared with those associated with the initiation of lateral flexion of the neck which occurred without electrical stimulation of the caudate nucleus in order to examine whether the caudate-induced head-turning was initiated via the same muscular system as that used in non-caudate-induced head movements. Experiments were carried out using 5 awake, unrestrained cats which were trained to stand still with one limb on each of 4 footplates. Trains of stimulating current pulses were applied to several stimulation points in the caudate nucleus while the animal maintained a stable standing posture with its neck extended. Head movements in the horizontal plane and EMGs of 6 neck muscles (splenius, longissimus cervicis, obliquus capitis caudalis, biventer cervicis, complexus and cervical multifidus) were recorded. Patterns of EMG activities of neck muscles around the onset of the caudate-induced head-turning were characterized by an increase in activity of the splenius, the longissimus cervicis and the obliquus capitis caudalis muscles, and by a decrease in activity of the complexus, the biventer cervicis and the cervical multifidus on the side of flexion. It is suggested that an increase in activity of the splenius, the longissimus cervicis and the obliques capitis caudalis muscles was responsible for the initiation of this evoked response. In non-caudate-induced lateral flexion of the neck, patterns of activities of neck muscles were similar to those in caudate-induced head-turning. It is therefore concluded that the caudate-induced head-turning as an evoked behavioral response was initiated through a muscular system similar to that utilized for similar head movements occurring without electrical stimulation of the caudate nucleus, although the pathways involved are thought to be different.
The pharmacokinetics and pharmacodynamics (blood pressure, heart rate, serum angiotensin-converting enzyme, and plasma renin activity) of enalapril and enalaprilat were studied after oral administration of enalapril maleate (10 mg) to seven biopsy-proven cirrhotic patients and to seven healthy subjects. The mean Cmax, AUC, and urinary excretion of enalapril and enalaprilat were greater and less (p less than 0.01), respectively, and mean oral clearance of enalapril was less (p less than 0.01) in the cirrhotic group than in the healthy group. However, there was no significant difference in the mean total drug (enalapril plus enalaprilat) excretion between the two groups. Blood pressure fell (p less than 0.05) only at 3 or 4 hours postdose, with no change in heart rate in the two groups. Serum angiotensin-convering enzyme (ACE) decreased (p less than 0.001) and plasma renin activity (PRA) increased (p less than 0.05) in the two groups. The magnitude of the percentage of inhibition of ACE activity was comparable between the two groups. Serum enalaprilat concentration correlated (p less than 0.001) with the percentage of inhibition of ACE activity. The results suggest that the bioactivation of enalapril to enalaprilat is considerably impaired in patients with cirrhosis but that the pharmacodynamic effects do not appear to be blunted in those patients. The mechanism and clinical implications remained unclear.
The authors produced immunotoxin by coupling the diphtheria toxin fragment A to the monoclonal antibody against a human glioma cell line. This toxin selectively inhibited protein synthesis of glioma cells in culture.
The goal of surgical treatment of metastatic spinal tumors is to maintain neurologic functioning without pain for the duration of the life expectancy. Of 28 patients in this series, 25 who had metastasis in the vertebral body underwent direct decompression by removal of the tumor, followed by vertebral reconstruction. A combined anterior or posterior instrumentation provided rigid spinal stability immediately after surgery. Three patients with involvement of the posterior part of the vertebra were treated by laminectomy for removal of the tumor, followed by posterior instrumentation. As a result, of nine patients who are alive with improved neurologic functions, seven have been ambulatory for an average duration of 13 months. Of 19 patients who have already died, recurrence of neurologic deficits was observed in five (26%), and 14 had no neurologic deterioration until they succumbed to the malignancy. Removal of the tumor and reconstructive surgery may be expected to produce satisfactory results.
The purpose of the present study of experimental spinal metastasis, developed in rats by inoculation of tumor cells through the spinous process, was to find the factor that causes the initial damage to the cord in this disorder. In the early stage of paralysis, the degenerated posterior funiculus originated from a small hemorrhagic area in the posterior column of the involved cord. Using the scanning electron microscope, the hemorrhage was found to be from the intrinsic vein, resulting from the disturbance of venous drainage in the compressed portion. In the early stage of compression, extravasation of horseradish peroxidase was observed in the white matter, but histologic degeneration was not. A hemorrhage existed wherever degeneration of the funiculus was observed. Therefore, the trigger to induce the initial damage on the cord in spinal metastasis was not likely to be vasogenic edema, but instead the intrinsic venous hemorrhage.
Botulinum toxins are potent neurotoxins which block the release of neurotransmitters. The effects of these toxins on hematopoietic cells, however, are unknown. Monocytes secrete a variety of polypeptide growth factors, including tumor necrosis factor (TNF). In the study reported here, the effects of botulinum toxin type D on the secretion of TNF from human monocytes were examined. The results demonstrate that botulinum toxin type D inhibits the release of TNF from monocytes activated by lipopolysaccharide (LPS) but not by 12-O-tetradecanoylphorbol-13-acetate. Botulinum toxin type D had no detectable effect on intracellular TNF levels in LPS-treated monocytes, indicating that the effects of this toxin involve the secretory process. This inhibitory effect of botulinum toxin type D on TNF secretion from LPS-treated monocytes was partially reversed by treatment with 12-O-tetradecanoylphorbol-13-acetate or introduction of guanosine 5'-[gamma-thio]triphosphate into these cells. The results demonstrate that TNF secretion is regulated by at least two distinct guanine nucleotide-binding proteins, one responsible for the activation of phospholipase C and another which acts as a substrate for botulinum toxin type D. ADP-ribosylation of monocyte membranes by botulinum toxin type D demonstrated the presence of three substrates with Mrs of 45,000, 21,000, and 17,000. While the role of these substrates in exocytosis is unknown, the results suggest that the Mr 21,000 substrate is involved in a process other than TNF secretion.
Sixteen of 75 patients with dilated cardiomyopathy (DCM) died during a mean follow-up period of 39.7 months. In non-survivors, the cardiothoracic ratio and the left ventricular end-diastolic dimensions were greater, the left ventricular end-diastolic pressures were more elevated, and the cardiac index was lower than in the survivors at the time of initial diagnosis. There were no significant differences between survivors and non-survivors in the magnitude of the maximum QRS and T vectors or in the maximum T angle. In the non-survivors, the maximum QRS vector was directed more posteriorly and the width/length ratio of the loop in the horizontal plane was smaller than in survivors. The QRS loop in the horizontal plane was often distorted in non-survivors or showed a bizarre figure-of-eight configuration. It appears that in DCM a marked posterior displacement of a QRS loop that is narrow and distorted or is in a bizarre figure-of-eight configuration in the horizontal plane indicates an unfavorable prognosis.
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The effects of aging on stress ulcer formation were examined in male Fischer 344 rats at 2, 8-9, 11-12, 17-18 and 21-24 months old. The animals were restrained and immersed in a water bath (22 degrees C) for 1, 2, 4 and 8 h. The incidence and severity of gastric corpus ulceration increased linearly with age. Basal acid secretion, determined 4 h after pylorus ligation, decreased with age, but there were no age-related differences in the effect on acid secretion of histamine and vagal nerve stimulation in the lumen-perfused stomachs of anesthetized rats. On morphological examination, surface epithelial cells in aged rats (21-24 months) were found to be intact, but the gastric foveolae were shallow and the chief cell layer was thick in aged rats. Deficiencies of vascular networks were observed in aged rat stomachs. These results indicate that an insufficiency of gastric mucosal microvascular networks and the preserved gastric acid response in the vulnerable mucosa may be involved in the mechanisms underlying aggravation of stress ulcer formation in aged rats.
A case of large granular lymphocyte (LGL) leukemia with ascites and CNS involvement was reported. A 39-year-old Japanese female was admitted to our hospital in March, 1987 because of high fever. Her clinical and hematological features were characterized by generalized lymphadenopathy, marked hepatosplenomegaly, high serum LDH level (3,257 mU/ml), marked leukocytosis (71,000/microliters) with 74% LGLs and bone marrow infiltration with 57% LGLs. Despite of chemotherapy, ascites, retroperitoneal mass and CNS involvement developed and she died of sepsis after three months. LGLs from the patient's blood, marrow and ascites, stained positively for acid phosphatase. These LGLs were E rossete+ and Fc (IgG) receptor+ and were positive for CD2, OKM1, HLA-DR and Leu11, but were negative for CD1, CD3, CD4, CD8 and Leu7 as well as for terminal deoxynucleotidyl transferase activity. The natural killer activity against K562 target cells was high and was significantly augmented after stimulation by recombinant human interleukin 2. These LGLs also demonstrated normal antibody-dependent cytotoxicity activity. Cytogenetic study on bone marrow cells and ascitic cells revealed clonal chromosomal abnormalities. These clinical, hematological, immunological and cytogenetic findings suggest that this patient had a neoplastic proliferation of natural killer cells.
Five odontogenic keratocysts were examined by using a scanning electron microscope (SEM) on the three-dimensional ultrastructure of epithelial lining cells. The fractured surface of the specimens showed a single row of columnar or cuboidal cells perpendicular to the flat basal lamina, a four- to five-cell layer of spinous cells, and a superficial layer of flattened parakeratinized cells. At high magnification of superficial cell surface, microvillis, short discontinuous branched or anastomosing microridges were observed.
We report a 35-year-old male with leukemic change and gastric involvement of Burkitt's lymphoma. A monoclonal immunoglobulin (Ig), IgM-kappa, was detected in the serum by means of immunoelectrophoresis. Immunophenotypical analysis showed that the neoplastic cells were CD20+, OKIal+, CD10-, CD21-, surface Ig+ (M-kappa), and cytoplasmic Ig-. The neoplastic cells did not secret Ig by using of protein A plaque forming cell assay. Active transcription of Ig heavy chain genes was not detected by cell dot analysis of the neoplastic cells. These findings support the possibility that the presence of the monoclonal Ig in the serum does not result from secretion of Ig from the neoplastic cells. The shedding of surface Ig from the neoplastic cells might result in the occurrence of monoclonal Ig in the serum.
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Gene configurations of immunoglobulin (Ig), T-cell antigen receptor (TCR) beta chain, and T-cell rearranging gene gamma (TRG gamma) were studied in human B-precursor lymphoblastic leukemic cells. These cells were phenotypically classified into three developmental stages (stages II through IV) according to Nadler's criteria. All of them showed the Ig heavy chain (IgH) gene rearrangement, and 67% of the cells in stage IV had the rearranged TRG gamma, albeit seldom in other stages. We further analyzed IgH gene rearrangements in detail using upstream to DH (diversity region of IgH) region probe to distinguish DJ from V-DJ recombination. All dual genotyped cells in each stage except one case in stage II showed the V-DJ rearrangements. This suggests the cross-lineage involvement of the putative recombinase, particularly in the process of V-DJ rearrangements. We next examined the transcriptional status of Ig genes as an indirect reflection of the accessibility of these genes to the recombinase. Properly spliced IgH transcripts of normal size were observed in stage IV and surface Ig positive stage, but not in stage II nor III. However, IgH transcripts of aberrant sizes were seen in stage II, III, and also IV. Cross-lineage gene rearrangements were shown to occur frequently when normally spliced IgH gene begins to be transcribed or just before this. These findings may implicate that V-DJ or V-VDJ gene rearrangements forming functional IgH genes, induce frequently TCR or TRG gene rearrangements. We propose these dual genotypes are different in origin from those observed in stem cell leukemia.
The purpose of the present experimental spinal metastasis developed in rats by inoculation of Walker's cancer cells through the spinous process is to find the factor which causes the initial damage of the cord in this disorder. In the early stage of paralysis, microangiogram exhibited that the degenerated posterior funiculus originated from the small hemorrhagic area in the posterior column of the involved cord. Scanning electron microscopic findings showed that the hemorrhage was of the intrinsic vein resulting from the disturbance of venous drainage in the compressed portion. In the early stage of compression, however, vascular permeability was observed in the white matter, but histologic degeneration was not. It was concluded that the trigger to induce the initial damage on the cord in spinal metastasis was likely to be the intrinsic venous hemorrhage.
A 65-year-old female with a history of cancer of the uterine body and a strong family history of cancer, was admitted with abdominal pain and anemia. During roentgenographic examination of the small intestine, a tumor was recognized about 25 cm from the ileocecal valve, leading us to suspect a carcinoma of the ileum. A colonoscopy demonstrated a constricting, ulcerated lesion, with a round wall: and a subsequent biopsy proved that the patient had a moderately differentiated adenocarcinoma. At surgery, a tumor, measuring 52 x 50 mm, was found to have infiltrated the serosa with a metastasis to the mesenteric lymph node.
We examined activities of procoagulant and fibrinolysis in homogenate of leukemic cells. Procoagulant activity (PCA) was increased in patients with acute myelocytic leukemia (AML) and acute promyelocytic leukemia (APL), but it was significantly decreased in patients with chronic myelocytic leukemia (CML) and adult T cell leukemia. In CML, PCA was increased in the blastic phase. Plasminogen activator activity (PLGAA) was also increased in patients with AML, APL and acute lymphocytic leukemia (ALL) associated with disseminated intravascular coagulation (DIC). Elastase-like activity, trypsin-like activity and chymotrypsin-like activity (CTLA) were increased in those with myelocytic leukemia, but they were low in those with lymphocytic leukemia. PCA, PLGAA and CTLA were significantly higher in patients with DIC than in those without DIC. Measurement of procoagulant and fibrinolytic activity in leukemic cells homogenate may be useful not only for studying hemostatic abnormalities but also for classification of leukemic cells.