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Biomedical subjects

J H Ryu

Publications and source records attributed to J H Ryu.

At least 19 recordsLinked to original sources
PubMed1995

Ontogenetic development of histamine receptor subtypes in rat brain demonstrated by quantitative autoradiography.

The postnatal ontogenetic development of the histamine receptor subtypes was studied in rat brain by quantitative receptor autoradiography with highly sensitive imaging plates. H1 receptor binding sites labeled with [3H]pyrilamine were detected on postnatal day 2 (P2) and increased very slowly until P9, and then rapidly reaching the adult levels in the hypothalamus, hippocampus, and amygdala by P16. The densities of H1 receptor binding sites in the cortex, striatum, thalamus, and substantia nigra were relatively low during development. H3 receptor binding sites labeled with [3H](R) alpha-methylhistamine were not detectable until P9. On P9, their density was higher in the substantia nigra than in other regions. Subsequently, H3 receptor binding increased, reaching the adult levels in the substantia nigra on P16 and in the other regions on P23. The histamine concentration was initially very high, but decreased to the adult level by P16. On the contrary, the activity of L-histidine decarboxylase of whole brain tissue was low on P5, and increased markedly from P16 to P23, to the adult level on P30. Administration of (S) alpha-fluoromethylhistidine (FMH), a specific inhibitor of L-histidine decarboxylase (HDC), significantly decreased both the HDC activity and histamine concentration during postnatal development. FMH treatment did not change H1 receptor binding in any brain region, but significantly increased H3 receptors in the substantia nigra and striatum on P23. Unilateral injection of 6-hydroxydopamine into the striatum on P2 resulted in up-regulation of H3 receptor binding sites in the dorsomedial (11%) and dorsolateral (18%) regions of the striatum and substantia nigra (31%) on P23, but no change in the H3 receptor density in the nucleus accumbens or frontal cortex on P11 and P23. These results demonstrate that the developmental patterns of H1 and H3 receptors are heterogeneous and independent of each other. There are marked mismatches of presynaptic and postsynaptic markers of the histaminergic neuron system as in other aminergic systems.

Aging↗
PubMed1995

Idiopathic perilymphatic fistulas. A temporal bone histopathologic study with clinical, surgical, and histopathologic correlations.

OBJECTIVE: To report a case of idiopathic perilymphatic fistulas diagnosed and successfully treated during life and confirmed histopathologically post mortem. METHODS: Perilymphatic fistulas were diagnosed clinically and repaired surgically. Light microscopic histopathologic studies were made of both temporal bones after death. RESULTS: Vestibular symptoms had improved postoperatively. Postmortem histopathologic examination of the temporal bones demonstrated patencies of the labyrinth capsule that had been predicted clinically during life, the qualities of the membranous labyrinth in both the operated-on and the unoperated-on ears, and the elements of the surgical repair. Notably, there was no evidence of endolymphatic hydrops. CONCLUSIONS: The histopathologic findings document the relationships of the fistula ante fenestram and the fissure connecting the round window niche and the posterior semicircular canal to idiopathic perilymphatic fistulas. Also, the diagnostic features reported herein allowed this patient with fluctuating hearing loss, episodic vertigo, and tinnitus to be distinguished from a patient with Meniere's syndrome. These findings have implications regarding past and future studies of vestibular and cochlear disorders.

Aged↗
PubMed1995

Cavitary pulmonary infarct in immunocompromised hosts.

Pulmonary disease in immunocompromised patients is common, but cavitary lung disease is less common and is usually associated with a fungal or mycobacterial infection. Pulmonary embolism is a noninfectious cause of a cavitary pulmonary process. Pulmonary embolism causes infarction in fewer than 15% of cases, and only about 5% of infarctions cavitate. Herein we describe two cases of cavitary infarcts in immunocompromised patients and review the clinical aspects of pulmonary infarcts and cavitation. Cavitary pulmonary infarction has been reported only rarely in immunocompromised patients. It is a dangerous but treatable pulmonary disease that must be considered in the differential diagnosis of immuno-compromised patients with lung disease.

Aged↗
PubMed1995

Stationary organization of the actin cytoskeleton in Vallisneria: the role of stable microfilaments at the end walls.

In mesophyll cells of the aquatic angiosperm Vallisneria gigantea, bundles of microfilaments (MFs) serve as tracks for the rotational streaming of the cytoplasm, which occurs along the two longer side walls and the two shorter end walls. The stationary organization of these bundles has been shown to depend on the association of the bundles with the plasma membrane at the end walls. To identify the sites of such association, the effects of cytochalasin B (CB) on the configuration of the bundles of MFs were examined. In the case of the side walls, MFs were completely disrupted after treatment with CB at 100 micrograms/ml for 24 hours. By contrast, in the case of the end walls, a number of partially disrupted MFs remained even after 48 hours of treatment. After removal of CB, a completely normal arrangement of bundles of MFs was once again evident within 24 hours after a rather complicated process of reassembly. When reassembly had been completed, the direction of cytoplasmic streaming was reversed only in a small fraction of the treated cells, suggesting that bundles of MFs are anchored and stabilized at the end walls of each cell and that the polarity of reorganized bundles and, therefore, the direction of the cytoplasmic streaming is determined in a manner that depends on the original polarity of MFs that remained in spite of the disruptive action of CB. By contrast, the direction of reinitiated cytoplasmic streaming was reversed in 50% of cells in which the bundles of MFs had been completely disrupted by exogenously applied trypsin prior treatment with CB.(ABSTRACT TRUNCATED AT 250 WORDS)

Actin Cytoskeleton↗
PubMed1995

Pulmonary tuberous sclerosis.

We describe the clinical presentation, pulmonary function tests, chest radiograph, and computed tomography findings, response to hormonal treatment, and duration of survival of nine patients with pulmonary involvement in tuberous sclerosis complex with follow-up over an average of 17 years (range, 1 to 35 years) since diagnosis. All patients were female, and the average age at onset of symptoms was 16 years (range, 3 months to 39 years); pulmonary symptoms did not develop until an average age of 33 years (range, 22 to 46 years). There was an average delay of 8 years before the correct diagnosis was made. The most common presenting clinical features were seizures, pneumothorax, bleeding into a renal angiomyolipoma, dyspnea, and typical skin changes. Pulmonary function tests commonly demonstrated obstruction to airflow and reduced single-breath diffusing capacity. Chest radiograph and computed tomography characteristically demonstrated diffuse interstitial infiltrates with cystic changes. Two asymptomatic patients with mild pulmonary involvement have remained in stable condition without hormonal therapy. The remaining seven patients had moderate to severe airflow obstruction; of these, five underwent hormonal therapy. Three patients had a clinical response to treatment. Two patients who did not receive hormonal treatment died of progressive respiratory failure. Most patients with pulmonary involvement in tuberous sclerosis have a slowly declining clinical course. Although the available data are limited, they suggest that a trial of hormonal therapy is recommended both for symptomatic patients and for those with declining pulmonary function. Tuberous sclerosis complex should be suspected in all patients with the diagnosis of lymphangioleiomyomatosis.

Adult↗
PubMed1995

Clinical characteristics of fatal pulmonary embolism in a referral hospital.

OBJECTIVE: To determine the clinical characteristics of hospitalized patients who died of pulmonary embolism, confirmed by evaluative autopsy. DESIGN: We retrospectively analyzed a series of autopsy cases of pulmonary embolism at a tertiary-care center for the period Jan. 1, 1985, through Dec. 31, 1989. MATERIAL AND METHODS: The medical and autopsy records of all hospitalized patients with autopsy-proven fatal pulmonary embolism were reviewed. Cases of tumor emboli, fat emboli, and contributory-only thromboembolic disease were excluded from the study. Specific symptoms and signs, diagnostic studies, and prophylactic measures were noted. RESULTS: Among 2,427 autopsies performed during the 5-year study period, death in 92 (3.8%) was clinically and pathologically judged to be caused by pulmonary embolism. No risk factors were noted in only 11 patients (12%). Prophylaxis against thromboembolism was used in 46%. Classic symptoms were often absent: dyspnea was present in only 59%, chest pain in only 17%, and hemoptysis in 3%. Pulmonary embolism was considered in 49% of the 92 patients and was correctly assigned as the cause of death on the death certificate or in the medical records in 32%. Testing for venous thromboembolic disease was performed in 22%. Comorbidity was present in most patients: 54% had guarded or poor prognoses independent of pulmonary embolism. CONCLUSION: The usual signs and symptoms associated with pulmonary embolism did not adequately identify most of our patients who died of pulmonary embolism. The reasons included the absence of these signs and symptoms, inability to communicate (for example, sedated or comatose patient), sudden death from acute massive pulmonary embolism, and presence of comorbid factors.

Adult↗
PubMed1994

Marked increase in histamine H3 receptors in the striatum and substantia nigra after 6-hydroxydopamine-induced denervation of dopaminergic neurons: an autoradiographic study.

The bindings of [3H](R) alpha-methylhistamine to histamine H3 receptors were investigated in rat brain following intranigral treatment with 6-hydroxydopamine (6-OHDA) by quantitative receptor autoradiography. The levels of [3H](R) alpha-methylhistamine binding sites in the denervated striatum (dorsomedial and dorsolateral) and substantia nigra were significantly higher than those in the contralateral side 21 days after nigral lesions. Saturation kinetic analysis revealed that the maximum binding capacities were up-regulated to about 1.7- and 1.2-fold those in the contralateral substantia nigra and striatum, respectively. These results strongly suggest that H3 receptors in the striatum and substantia nigra are influenced by tonic dopaminergic inputs.

Animals↗
PubMed1994

Heterogeneous distributions of histamine H3, dopamine D1 and D2 receptors in rat brain.

The changes of the histamine H3 and dopamine D1 or D2 receptor binding sites induced by quinolinic acid treatment were studied in order to discriminate the comparative distribution. This treatment resulted in similar decreases in histamine H3 and dopamine D1 receptor binding sites in the striatum and ipsilateral substantia nigra. Dopamine D2 receptor binding sites were relatively well conserved, whereas H3 receptors decreased considerably. These results suggest that histamine H3 and dopamine D1 receptor binding sites are localized on the striatonigral projection neurones which are together sensitive to quinolinic acid, and that the distributional compartment of dopamine D2 receptor binding sites is quite different from those of histamine H3 and dopamine D1 receptors.

Animals↗
PubMed1994

Binding characteristics of a histamine H3-receptor antagonist, [3H]S-methylthioperamide: comparison with [3H](R)alpha-methylhistamine binding to rat tissues.

The release and synthesis of neuronal histamine are regulated by histaminergic autoreceptors named as histamine H3 receptors. The development of radiolabeled histamine H3 antagonists is needed to characterize the binding of antagonists to these receptors. Here we describe the binding characteristics of a new histamine H3-receptor antagonist, [3H]S-methylthioperamide (SMT), to rat tissues, and compare its binding with that of [3H](R)alpha-methylhistamine ((R)alpha MH), a selective histamine H3-receptor agonist. The binding of [3H]SMT to the membranes of rat forebrain was found to be stereoselective, saturable, reversible and temperature-dependent. Saturation binding experiments indicated a single class of high affinity sites for [3H]SMT in forebrain membranes (KD = 2.1 nM, Bmax = 24.3 pmol/g of tissue at 4 degrees C). The Bmax was approximately 3 times that of [3H](R)alpha MH binding to rat forebrain membranes (KD = 2.5 nM, Bmax = 7.3 pmol/g of tissue at 25 degrees C). Autoradiographic images of [3H]SMT binding in the brain were essentially the same as those of [3H](R)alpha MH. [3H]SMT also bound appreciably to peripheral tissues (the liver, adrenal, stomach, ileum, kidney, lung and bladder), whereas the [3H](R)alpha MH bindings to these peripheral tissues were negligible. These results indicate that [3H]SMT binds to H3 receptors primarily in the central nervous system, and that it also has high affinity toward non-H3 receptors, probably hemoproteins, in peripheral tissues.

Animals↗
PubMed1992

Syphilis: a disease to exclude in diagnosing sarcoidosis.

A 37-year-old man was referred to our institution for assessment of possible sarcoidosis with involvement of the central nervous system. Before referral, he experienced a systemic illness that persisted for several months, during which time ocular and pulmonary noncaseating granulomas were identified. Sarcoidosis with involvement of the central nervous system was tentatively diagnosed. Because of several inconsistencies in the preliminary diagnosis of sarcoidosis, further assessment was pursued, and syphilis was diagnosed. Herein we emphasize the useful clinical features for distinguishing syphilis from sarcoidosis and review the clinical manifestations of pulmonary syphilis.

Adult↗
PubMed1992

Receptor autoradiography with 11C and [3H]-labelled ligands visualized by imaging plates.

The distribution of histamine H1, H3, dopamine D1 and D2 receptors in the brain was studied by receptor autoradiography using a high-sensitivity and high-resolution imaging plate system. [3H]Pyrilamine, [3H](R)alpha-methyl-histamine, [11C]SCH23390, and [11C]N-methylspiperone (or [11C]YM-09151-2) were used as ligands to identify H1, H3, D1 and D2 receptors, respectively. Two different receptors (dopamine D2 and histamine H3) could be also labelled simultaneously in a single cryostat-sliced section using [11C]N-methylspiperone and [3H](R)alpha-methylhistamine, respectively. The imaging plate system is useful for receptor autoradiography of positron emitter-labelled and tritium-labelled receptor-ligands because of its high sensitivity.

Animals↗
PubMed1992

Monocyte heterogeneity in angiotensin-converting enzyme induction mediated by autologous T lymphocytes.

The ability of monocyte subpopulations to be induced selectively by T lymphocytes to synthesize enhanced levels of angiotensin-converting enzyme (ACE) was examined using an in vitro model employing normal peripheral blood monocytes and T lymphocytes. Separation of monocytes into subpopulations on the basis of buoyant density indicated no difference in the ability of the resulting monocyte subpopulations to produce basal levels of ACE when cultured in the absence of T lymphocytes. However, the subpopulations differed significantly in their ability to synthesize enhanced levels of ACE in response to the presence of autologous T lymphocytes; low-density monocytes were induced by T lymphocytes to synthesize three-fold more ACE than were high-density monocytes. Surface antigen labelling using MoAbs demonstrated that the low-density monocyte subpopulations also had a significantly higher percentage of Leu-M2+ monocytes compared with the high-density monocyte subpopulations. When monocytes were separated on the basis of the presence of the Leu-M2 antigen using an immune rosetting technique, T lymphocytes were able to induce significantly elevated levels of ACE in the Leu-M2+ enriched monocyte subpopulation but were unable to induce ACE beyond basal levels in the Leu-M2(+)-depleted monocyte subpopulation. These results demonstrate that monocytes are heterogeneous with respect to their ability to be induced by T lymphocytes to synthesize ACE. This raises the possibility that selective accumulation of a monocyte subpopulation in the granulomatous inflammation of sarcoidosis may be one of the factors required for elevated ACE synthesis in the resulting granuloma epithelioid cells.

Adult↗
PubMed1992

Selective effect of chronic lead ingestion on tyrosine hydroxylase activity in brain regions of rats.

Alterations of tyrosine hydroxylase activity in various regions of brain from rats postnatally exposed to lead were tested. Three groups of animals were prepared; (1) Rats exposed to lead at a low dose (0.05% lead acetate, PbAc); (2) Rats exposed to lead at a high dose (0.2% PbAc); (3) Age-matched normal control rats. At 2, 4, 6, and 8 weeks of age, weight of brain and body, and concentrations of lead in whole brain of animals in each group were measured. Activities of tyrosine hydroxylase and Na(+)-K+ ATPase were also measured at the same ages in 4 brain regions of each animal. Body weight gain was decreased after 6 weeks of age in rats exposed to lead at a high dose. Concentrations of lead in whole brain were increased from 0.37 to 0.83 (ng/mg wet tissue) in these animals. Exposure of rats to lead generally increased tyrosine hydroxylase activity and decreased Na(+)-K+ ATPase activity. However, changes of tyrosine hydroxylase activity were detected without concomitant changes of Na(+)-K+ ATPase activity in pons-medulla at 2 weeks of age and telencephalon at 6 weeks of age in rats exposed to lead at a low dose, and in midbrain at 4 and 6 weeks of age in rats exposed to lead at a high dose. These data imply that catecholaminergic nervous system in the brain regions described above could be selectively affected by lead.

Animals↗
PubMed1991

Microscopic pulmonary tumor embolism causing subacute cor pulmonale: a difficult antemortem diagnosis.

Microscopic pulmonary tumor embolism is difficult to diagnose. The most common initial clinical symptom is subacute progressive dyspnea, and the initial laboratory evaluation typically shows hypoxemia in a patient with clear lung fields on a chest roentgenogram. Another distinguishing feature may be hepatic abnormalities. In general, pulmonary angiography discloses no evidence of emboli, but multiple subsegmental peripheral perfusion defects are noted on ventilation-perfusion lung scans. The diagnosis of microscopic pulmonary tumor embolism can be confirmed by open-lung or transbronchial lung biopsy or by microvascular pulmonary cytology, a less invasive procedure that could be performed at the time of pulmonary angiography. Herein we describe two patients with unsuspected microscopic pulmonary tumor embolism that eventuated in subacute cor pulmonale and death. These cases illustrate the characteristic findings of this entity and emphasize the need for early diagnosis.

Adenocarcinoma↗
PubMed1991

Oxygen-exacerbated bleomycin pulmonary toxicity.

Bleomycin is an antineoplastic agent with potential for producing pulmonary toxicity, attributed in part to its free radical-promoting ability. Clinical and research experiences have suggested that the risk of bleomycin-induced pulmonary injury is increased with the administration of oxygen. We report a case in which the intraoperative administration of oxygen in the setting of previous bleomycin therapy contributed to postoperative ventilatory failure. Our patient recovered with corticosteroid therapy. Physician awareness of a potential interaction between oxygen and bleomycin may help reduce the morbidity and mortality related to bleomycin therapy.

Acute Disease↗
PubMed1991

Effects of acetate dialysate on transforming growth factor beta 1, interleukin, and beta 2-microglobulin plasma levels.

To evaluate potential adverse effects of acetate use in hemodialysis (HD), we measured plasma interleukin (IL-1 alpha, IL-1 beta, IL-6), TNF alpha, TGF beta 1, and beta 2-microglobulin levels with ELISA assays in normal (N = 9), CRF (N = 6), CAPD (N = 7) and HD (N = 8) subjects and compared the effects of acetate (Ac) and acetate-free (Ac-free) dialysate. TGF beta 1 was the only cytokine consistently detected. Compared to normals (median 57, range 53 to 68 pg/ml, one undetected; N = 8), TGF beta 1 was higher in the CRF (75, 70 to 97 pg/ml, one undetected) and CAPD (75.5, 66 to 116 pg/ml, N = 6) groups (P less than 0.05), and was somewhat higher in the HD (68, 52 to 88 pg/ml) group (P less than 0.10). Acutely, TGF beta 1 pre-HD (70, 63 to 88 pg/ml) increased above normals post AcHD [79.5, 65 to 140 pg/ml uncorrected for ultrafiltration (UF)] and was higher after AcHD versus Ac-free HD both uncorrected (79.5, 65 to 140 pg/ml vs. 70, 52 to 86 pg/ml) and corrected for UF (68, 51 to 115 pg/ml vs. 57, 43 to 69 pg/ml; P less than 0.05). beta 2-microglobulin was not different after AcHD (81.2 +/- 8.0 mg/ml) versus Ac-free HD (72.5 +/- 6.9 mg/ml). Significantly lower serum inorganic phosphorus was also found four hours post-AcHD compared to four hours post-Ac-free HD (0.87 mmol +/- 0.10 SEM vs. 1.05 mmol +/- 0.07 SEM; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗