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Biomedical subjects

H Kohno

Publications and source records attributed to H Kohno.

At least 253 records · Page 14Linked to original sources

Transcranial Doppler sonography in carotid-cavernous fistulas: analysis of five cases.

Transcranial doppler sonography was performed transorbitally in five patients clinically diagnosed as unilateral carotid-cavernous fistula. Dural arteriovenous malformation related-shunts were detected in all the patients. In the normal eyes, the only doppler signals observed at an insonation depth of 45 to 55 mm were those of the ophthalmic artery. In the affected eyes, abnormal doppler signals with relatively higher flow velocity and lower resistance were observed. In three of the cases, these abnormal signals showed a flow directed anteriorly or away from the cavernous sinus, consistent with changes in the ophthalmic veins caused by the presence of the shunts. In two cases, however, the observed flows were directed posteriorly, the normal direction of these veins. The possible explanations for this discrepancy are discussed in relation with angiographic findings. The use of transcranial doppler might provide a better understanding about hemodynamic changes in carotid cavernous fistulas.

Aged↗

DNA ploidy pattern in synchronous and metachronous hepatocellular carcinomas.

DNA ploidy of hepatocellular carcinoma (HCC) was studied in 28 patients using a flow cytometric method. Fourteen patients had two HCCs synchronously, and the remaining 14 had tumor recurrence in the remnant liver 3-41 months after curative resection of primary HCCs. DNA ploidy pattern and histopathologic parameters were compared between the synchronous and metachronous HCCs. Among those with synchronous HCCs, both tumors were diploid in 7 cases and aneuploid in 2 instances. Five patients had HCCs of different DNA ploidy pattern. On the other hand, 5 of 14 patients with metachronous HCCs had a consistent DNA ploidy between primary and recurrent tumors. In 4 cases, the first tumor was diploid whereas the recurrent HCC was aneuploid or tetraploid. In the remaining 5 cases, the primary HCC was aneuploid, but the recurrent tumor was diploid. Assuming that the difference in DNA ploidy pattern indicates a different clonal origin, the current results indicate that at least 36% of synchronous HCCs and 64% of recurrent HCCs develop in a multicentric fashion.

Adult↗

Cretinism with combined hormone deficiency caused by a mutation in the PIT1 gene.

Cretinism is marked by irreversible mental and growth retardation. We describe here an entirely new case of cretinism showing combined pituitary hormone deficiencies of thyrotropin, growth hormone and prolactin that appears to be caused by homozygosity for a nonsense mutation in the gene for the pituitary specific transcription activator, Pit-1/GHF-1 (designated PIT1 in humans for pituitary specific factor 1). This is the first report in humans of a defect in a transcription activator causing deficiency of multiple target genes.

Amino Acid Sequence↗

Simultaneous establishment of myeloid and B-lymphoid cell lines with identical chromosome abnormalities from Philadelphia chromosome-positive chronic myelogenous leukaemia.

Two continuously growing cell lines, designated YOS-M and YOS-B, were established simultaneously from a patient with Philadelphia (Ph1) chromosome-positive chronic myelogenous leukaemia (CML) in myeloid blast crisis. Both YOS-M and YOS-B had the Ph1 chromosome and identical additional chromosome abnormalities, which were not detected in the chronic phase. Cytochemical analysis showed that YOS-M was significantly positive for peroxidase, whereas YOS-B was entirely negative. YOS-M expressed myeloid-associated antigens (CD14, CD33) as well as CD4, CD25 and CD34. The surface phenotype of YOS-M was identical to that of the leukaemic blasts found in the patient. On the other hand, YOS-B expressed mature B-cell markers, CD19, CD20, CD21 and surface immunoglobulin, but not myeloid-associated antigens. These two cell lines showed an identical rearrangement pattern of the break point cluster region on chromosome 22, but rearrangement of the immunoglobulin heavy chain gene was detected only in YOS-B. These findings provide definite evidence that CML cells still have the capability to differentiate and mature along different haematopoietic cell lineages even after blast crisis.

Aged↗

Hepatocellular carcinoma and sex hormones.

The liver is morphologically and functionally modulated by sex hormones. Long-term use of oral contraceptives and androgenic steroids can induce benign and malignant hepatocellular tumors. Hepatocellular carcinoma (HCC) is more prevalent in men than in women. The role of sex hormones and their receptors in the development of HCC was reviewed. Some HCCs may be androgen dependent but others may be estrogen or even both dependent. Further studies are mandatory in order to utilize such characteristics of HCC for an effective prophylaxis and therapy of this tumor.

Animals↗

Superoxide production by liver macrophages in a septic rat model--relation to arterial ketone body ratio.

The relationship between superoxide production by liver macrophages and arterial ketone body ratio (AKBR), which reflects the oxidation-reduction state in the mitochondrial compartment of hepatocytes, was studied in rats with lethal and sublethal septicemia induced by intravenous injection of live Escherichia coli 014. In the sublethal model, AKBR decreased transiently (p < 0.01) and superoxide production by isolated liver macrophages increased significantly after opsonized zymosan (OZ) stimulation (p < 0.05). On the other hand, in the lethal model, AKBR decreased markedly (p < 0.01) to below 0.4 without recovery, and superoxide production was not activated by OZ stimulation. Thus, when AKBR decreases to an irreversible level, below about 0.4, superoxide production by liver macrophages is impaired, while as long as AKBR remains reversible, more than about 0.4, it is enhanced. It is suggested that superoxide production by the Kupffer cells is related to the intrahepatic oxidation-reduction state in the septic model.

Alanine Transaminase↗

Adult T cell leukemia associated with eosinophilia: analysis of eosinophil-stimulating factors produced by leukemic cells.

The mechanism of eosinophilia in a patient with adult T cell leukemia (ATL) was investigated. A 61-year-old woman with ATL presented marked eosinophilia. No parasite infections or allergic diseases were found in this patient. The number of eosinophils fluctuated in parallel with that of ATL cells during her clinical course. The patient's serum and the culture supernatant of ATL cells showed eosinophil colony-stimulating activity. Northern blot analysis of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), and interleukin-5 (IL-5), which are known eosinophil CSFs, showed that only GM-CSF but not IL-3 or IL-5 was expressed in freshly separated and cultured ATL cells. Since neutrophil and monocyte numbers did not increase, it is suggested that GM-CSF and unknown cytokines other than IL-3 and IL-5 produced by ATL cells synergistically stimulated eosinophil precursors in the present case.

Blotting, Northern↗

Intravascular pancuronium bromide infusion for prenatal diagnosis of twin-twin transfusion syndrome.

The diagnosis of twin-twin transfusion syndrome remains a problem. Intravascular infusion of pancuronium bromide, a nondepolarizing neuromuscular blocking agent, for the smaller of a set of twins demonstrated paralysis of both twins in one case. However, in a second case, paralysis was shown only in the smaller twin who demonstrated no transplacental vascular communications postnatally. We suggest that infusion of pancuronium bromide, 'pancuronium test', is a simple and safe method for confirming transplacental communications and aids in the diagnosis of twin-twin transfusion syndrome.

Adult↗

Human parathyroid hormone-related peptide-(107-111) does not inhibit bone resorption in neonatal mouse calvariae.

Recent analysis of the structure-function relationship of human PTH-related peptide (hPTHrP) has led to the discovery that its direct inhibitory activity on osteoclastic bone resorption resides fully in the 107-111 sequence of the peptide, as assessed by a bone resorption assay using isolated rat osteoclasts. Here we report that hPTHrP-(107-111) is inactive in neonatal mouse calvariae in culture. hPTHrP-(107-111), at doses of 10(-12)-10(-6) M and incubation periods up to 96 h, did not affect either basal or agonist-stimulated 45Ca release from prelabeled neonatal mouse calvariae, while salmon calcitonin was a potent and powerful inhibitor of both basal and stimulated 45Ca release from bone. Moreover, salmon calcitonin, but not hPTHrP-(107-111), inhibited the increase in osteoclast number in hPTHrP-(1-34)-treated bones. Furthermore, hPTHrP-(107-139) also failed to inhibit 45Ca release and the hPTHrP-(1-34)-induced increase in osteoclast number in this organ culture model when tested under conditions identical to those for hPTHrP-(107-111). The addition of indomethacin to hPTHrP-(107-111)- or hPTHrP-(107-139)-treated bones was without effect, excluding the possibility that the direct inhibitory activity of these peptides on osteoclasts is ablated by a prostaglandin-mediated mechanism. Although the mechanism underlying the apparent inability of the carboxyl-terminal PTHrP fragments to inhibit osteoclastic bone resorption in neonatal mouse calvariae is unknown, it may involve the complex microenvironment of osteoclasts in intact bone, which contains a large variety of cell types other than osteoclasts.

Animals↗

Low urinary growth hormone values in patients with Turner's syndrome.

Short stature is one of the major symptoms in Turner's syndrome (TS). The cause of short stature is not clearly known at present. In this study we initially assessed GH secretory status in TS by determinations of urinary human (h) GH excretion for 2 consecutive days. Secondly, the therapeutic dose of hGH used for treatment of short stature in TS was evaluated by measurements of urinary hGH after recombinant hGH (r-hGH) injections. Twenty-four-hour urinary hGH excretion for the 2 days combined was significantly lower in patients with TS than in normal children [2.3 +/- 1.8 ng/day (n = 7) vs. 13.4 +/- 3.2 (n = 16); P less than 0.001], although four of seven patients with TS had normal GH responses to the provocative tests. The mean level of urinary hGH in TS after 2 days was comparable to that in complete GH deficiency (1.9 +/- 0.9 ng/day; n = 14) that we previously reported. Treatment with daily sc injections of 1.0 IU (0.37 mg)/kg.week r-hGH, given in seven divided doses, normalized urinary hGH excretion and induced remarkable catch-up growth in all patients with TS. These results indicate that the 24-h endogenous GH secretion in seven patients with TS is impaired. The measurement of 24-h urinary hGH excretion may prove to be useful as a marker to assess the abnormal GH secretion and the adequacy of treatment with hGH in patients with TS. The therapeutic dose of hGH in TS is approximately 0.37 mg/kg.week, given in seven divided doses. To convert international units of r-hGH to milligrams, divide by 2.7.

Adolescent↗

Accelerated aging of the brain in Werner's syndrome.

We report the electrophysiologic examination of a 55-year-old woman with Werner's syndrome. Needle EMG and peripheral conduction studies were normal. In contrast, EEG was moderately abnormal, the N20 and P25 potentials of SEPs were delayed and enlarged, and the event-related potential, P300, was delayed. These characteristic findings indicated accelerated aging of the brain, as in the other organs, in Werner's syndrome.

Brain↗

Concomitant increase in putrescine incorporation with transferrin uptake into rat reticulocytes.

Concomitant increase in putrescine incorporation with transferrin uptake into rat reticulocytes was found. [14C]Putrescine incorporation occurred in the presence of transferrin at 37 degrees C. The subcellular distribution of incorporated [14C]putrescine showed that the incorporation in the plasma membrane time dependently increased. Both 125I-labeled transferrin uptake and [14C]putrescine incorporation decreased when ethylene glycol bis(2-aminoethyl ether)-N,N,N',N'-tetraacetic acid was added, while it increased with the addition of A23187.

Animals↗

A case of biliary cystadenocarcinoma arising in the liver with a congenital retention of indocyanine green.

A case of biliary cystadenocarcinoma that occurred in a 45-year-old woman is reported. Ultrasonography and computed tomography clearly revealed papillary projections in the cyst of the liver. Percutaneous transhepatic cystography showed connection between the cyst and the common bile duct. The tumor was surgically resected and proved to be a mucinous papillary adenocarcinoma arising from a biliary cystadenoma. The patient is doing well 4 years after surgery. Interestingly, this is the first reported case of a biliary cystadenocarcinoma in the liver with markedly diminished excretion of indocyanine green.

Adenocarcinoma, Mucinous↗

Moyamoya disease associated with pituitary adenoma--report of two cases.

Moyamoya disease associated with prolactin (PRL)-producing pituitary adenomas occurred in two females with elevated blood PRL levels (285 and 120 ng/ml). Computed tomography revealed cystic tumors extending from the sella turcica to the suprasellar cistern. Carotid angiography demonstrated stenoses or obstructions of the bilateral internal carotid arteries at their end point and development of bilateral basal moyamoya vessels. Histological diagnosis in one case was PRL-producing chromophobe adenoma. No stigmata of neurofibromatosis or any history of irradiation was found. Compression of carotid arteries by the tumor was unlikely. These cases should therefore be classified as moyamoya disease accompanied by brain tumor, a very rare occurrence. The hypothalamic disturbance caused by moyamoya disease may have induced the hyperprolactinemia, resulting in secondary prolactinoma.

Adenoma, Chromophobe↗

Androgen receptor in cirrhotic liver, adenomatous hyperplastic nodule and hepatocellular carcinoma in the human.

Androgen receptors (AR) were assayed for cirrhotic liver, adenomatous hyperplastic nodule (AHN), and hepatocellular carcinoma (HCC) which were removed by partial hepatic resection from five patients. There were three men and two women. Age ranged from 59 to 68 years. Underlying cirrhosis was macronodular in three and micronodular in two. AHN was present within HCC in two patients, but these two lesions were found in different lobes of the same liver in another two patients. Only AHN was seen in the last patient. ARs in the cytosol of cirrhotic liver ranged from nil to 12.8 fmol/mg of protein with the dissociation constant (Kd) of 3.2-20.3 x 10(-10) M. AHNs possessed ARs ranging from 4.0 to 27.6 fmol/mg of protein (Kd values, 7.4-21.0 x 10(-10) M. All HCC nodules had ARs ranging from 11.8 to 72.8 fml/mg of protein with Kd values of 5.3-27.1 x 10(-10) M. Thus, cytosolic AR concentrations were highest in HCC, lowest in cirrhotic liver, and intermediate in AHN. The present study seems to indicate that AHN may be a precancerous lesion and that androgen and its receptor play an important role in human hepatocarcinogenesis.

Aged↗

[Inversion of chromosome 16 observed in acute myeloblastic leukemia (M2) with biphenotypic surface markers lacking monocytosis and eosinophilia].

Inversion of chromosome 16 was found in a 73-year-old female with acute myeloblastic leukemia (FAB:M2). Complete remission was achieved by combined chemotherapy (DNR, Ara-C, 6-MP, Prednisolone), but she relapsed 6 months later without CNS involvement and died of respiratory failure presumably due to cerebrovascular accident during remission reinduction chemotherapy. Biphenotypic surface markers (CD2+ and CD13+) were observed on relapse. Eosinophilia was not observed throughout. Our patient and the other reported case suggest that biphenotypism and the lack of eosinophilia and monocytosis in inv (16) leukemia may be correlated with a poor prognosis.

Aged↗

The relationship of putrescine incorporation to transferrin uptake by reticulocytes.

We previously reported that putrescine incorporation occurred during transferrin uptake by rat reticulocytes (1). Both the putrescine incorporation and transferrin uptake were enhanced by the presence of Ca2+ and A23187. Furthermore, putrescine dose-dependently increased the transferrin uptake. Additionally, transglutaminase inhibitors partially blocked not only the putrescine incorporation but also the transferrin uptake.

Animals↗