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Biomedical subjects

J S Hong

Publications and source records attributed to J S Hong.

At least 109 records · Page 6Linked to original sources
PubMed1994

1H magnetic resonance imaging of freezing and thawing in freeze-tolerant frogs.

Proton magnetic resonance imaging (MRI) of the processes of freezing and thawing in the wood frog Rana sylvatica provided noninvasive and real-time analysis of the mode of ice propagation through the body of a freeze-tolerant vertebrate. MRI revealed a directional movement of ice from the exterior inward that required several hours to reach completion. Freezing in core organs such as liver, which produces and exports cryoprotectant, and heart, which circulates it, was delayed and occurred well after the organs were surrounded by extraorgan ice. Natural thawing was a very different process; thawing began uniformly throughout the body, but core organs melted more rapidly than peripheral ones, an adaptation that may be key to the early restoration of heartbeat and breathing. The images presented demonstrate the sensitivity and power of MRI and its potential to become a critical monitoring technology in the development of cryopreservation techniques for mammalian organ explants.

Acclimatization↗
PubMed1994

Freeze tolerance in turtles: visual analysis by microscopy and magnetic resonance imaging.

Two visual techniques were used to analyze the patterns of natural freezing and thawing in freeze-tolerant hatchling painted turtles Chrysemys picta marginata. Directional solidification plus light microscopy of liver, heart, and skeletal muscle slices was used to compare freezing at -4 degrees C (a survivable temperature in vivo) and -20 degrees C (not survivable). At -4 degrees C tissues showed large amounts of ice in expanded extracellular and vascular spaces, occupying 36% (liver) and 61% (muscle) of total tissue volume. Cells at -4 degrees C were shrunken, but intracellular water remained; at -20 degrees C, however, cells showed little evidence of free water. Liver micrographs showed novel spherical shells of water associated with intracellular particles (apparently glycogen granules) suggesting that a noncolligative method of cell water retention was employed. Proton magnetic resonance imaging was used for noninvasive analysis of freezing and thawing in the intact animal. Images showed that freezing propagated in a directional manner through the body with ice formed first in extraorgan spaces (e.g., abdominal cavity, brain ventricles). However, thawing occurred uniformly throughout the body core, and organs melted more rapidly than the extraorgan ice surrounding them.

Acclimatization↗
PubMed1994

A case of coincident multiple myeloma and non-Hodgkin's lymphoma.

A rare case of coexisting multiple myeloma and non-Hodgkin's lymphoma at the time of diagnosis is presented. The patient presented with petechiae, melena and weight loss. IgA lambda monoclonal gammopathy in the serum and free lambda chain in urine were documented. Bone marrow biopsy demonstrated an interstitial infiltration of neoplastic plasma cells coexisting with localized collection of neoplastic lymphoid cells composed of monotonous small lymphocytes with occasional cleaved nuclei. Immunophenotype of plasma cell was IgA lambda. The patient also had a jejunal mass, with biopsy proven malignant lymphoma, diffuse small cleaved cell type. The tumor was diffusely positive for pan-B marker. After chemotherapy, the IgA lambda monoclonal protein decreased and the patient improved. This case suggest, that the seound B-cell neoplasm may have evolved by transformation of an original neoplastic clone, or that malignant tumors may be polyclonal at onset. Definitive diagnosis and staging of each disorder is important for proper management.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

Prolonged expression of AP-1 transcription factors in the rat hippocampus after systemic kainate treatment.

Systemic administration of kainate, a glutamate receptor agonist, caused neuronal death in the CA1 and CA3 fields of the rat hippocampus. In the areas of cell loss, reactive astrocytes increased their expression of an astrocyte-specific protein, glial fibrillary acidic protein (GFAP). AP-1 DNA binding activity and the expression of a 35 kDa fos-related antigen (fra) remained elevated in the rat hippocampus for at least 2 weeks after a single systemic injection of kainate, which correlated with changes in gene expression during reactive gliosis. Immunoreactivity for fras was detected in the nuclei of neurons in the dentate gyrus, but relatively few cells in CA1 and CA3 were immunoreactive 1 week after kainate treatment. However, elevated AP-1 DNA binding activity was observed in the CA1 and CA3 regions as well as in the dentate gyrus, suggesting that proteins other than the fras were involved in the astrocytic AP-1 complex. The AP-1 DNA binding activity in hippocampus recognized an AP-1 sequence from the promoter region of the GFAP gene, suggesting that GFAP is a potential target gene. Thus, a single systemic injection of kainate causes long-term activation of AP-1 DNA binding activity in the rat hippocampus and may be important for long-term changes in gene expression in hippocampal cells.

Animals↗
PubMed1994

Regulation of preproenkephalin expression in astrocytes: is there a role for glia-derived opioid peptides in reactive gliosis?

Cultured glial cells synthesize a number of neuropeptides, growth factors, cytokines, and other factors that are not detectable in resting glia in the adult brain but that appear in response to brain injury. Enkephalin-containing peptides are produced and released by cultured astrocytes and glioma cell lines, which have provided convenient model systems to study the regulation of the preproenkephalin gene. The purpose of this review is to examine data suggesting that reactive astrocytes produce enkephalin-containing peptides, the regulatory processes that may be involved, and possible functions of glia-derived peptides in reactive gliosis.

Adult↗
PubMed1993

Biphasic generation of diacylglycerol by angiotensin and phorbol ester in bovine adrenal chromaffin cells.

Stimulation of angiotensin receptors in bovine adrenal medullary cells with Sar1-angiotensin II increased diacylglycerol levels in a biphasic fashion. An initial peak occurred at 3 min and an increase was observed again at 60 min and even at 18 hrs. Phorbol 12-myristate 13-acetate produced a similar pattern of increase in diacylglycerol levels. Both the angiotensin analog and the phorbol ester also increased the release of (3H)choline into the culture medium from prelabelled cells. The long-term diacylglycerol production could be derived from phosphatidylcholine rather than from the phosphoinositides. The latter may be the source of the angiotensin stimulated initial production of diacylglycerol and activation of PKC. Activated PKC then turns on the continuous production of DAG which maintains PKC in an active state for long periods of time in the presence of the peptide.

Adrenal Medulla↗
PubMed1993

Developmental changes in rat adrenal enkephalin precursor: peptide ratio.

Developmental changes in rat adrenal [Met5]enkephalin (ME) immunoreactivity and [Met5]enkephalinargininephenylalanine (MERF) immunoreactivity (which presumably reflects proenkephalin) were examined. The concentration of MERF appeared highest at the end of the first week postnatally and decreased fourfold to near adult values by day 21, while ME levels decreased only about twofold. This indicates a fall in the adrenal proenkephalin:ME ratio during the transition from the suckling to the weanling period in the rat. The elevated MERF levels during the suckling period may result from deficient processing of proenkephalin to free ME. An increase in the activity of the processing enzyme carboxypeptidase E was observed at day 15, which may contribute to the developmental fall in the adrenal proenkephalin to free ME ratio. Mimicking sympathetic activity by nicotine treatment (3 mg/kg i.p. twice daily from birth) produced a precocious decrease in the MERF:ME ratio at day 8, and also increased the activity of the processing enzyme. Denervation at day 10 markedly decreased adrenal ME and produced a three-fold increase in MERF:ME ratio when measured at day 30. Adrenal carboxypeptidase E activity was also decreased after denervation. In summary, these results suggest that increasing preganglionic sympathetic nerve activity during the third week postnatally stimulates proenkephalin processing and leads to the developmental decrease in MERF:ME ratio in the rat adrenal.

Adrenal Glands↗
PubMed1993

Elevated basal AP-1 DNA binding activity in developing rat brain.

Nuclear extracts from hippocampi, striata and hypothalami of postnatal day (P) 7 rats contained elevated basal levels of AP-1 DNA binding activity and c-jun protein, which decreased to the low basal levels observed in the adult by P21. In contrast to the AP-1 DNA binding complex in the adult brain, the fos-related antigens were not a major component of the P7 AP-1 DNA binding activity.

Aging↗
PubMed1993

Role of omega-conotoxin GVIA-sensitive Ca2+ entry in angiotensin II-stimulated [3H]phorbol 12,13-dibutyrate binding in bovine adrenal medullary cells.

The relative contributions of Ca2+ influx and intracellular Ca2+ mobilization were examined for angiotensin II-stimulated [3H]phorbol 12,13-dibutyrate binding, which reflects the level of activated protein kinase C in bovine chromaffin cells. Angiotensin II receptors activate phospholipase C in chromaffin cells, leading to a short-lived mobilization of intracellular Ca2+. Angiotensin II-stimulated [3H]phorbol 12,13-dibutyrate binding was largely blocked in Ca(2+)-free buffer and by pretreatment with the Ca(2+)-channel blocker omega-conotoxin GVIA. The [3H]phorbol 12,13-dibutyrate binding response to [Sar1]angiotensin II also appeared to be voltage sensitive, as no additivity was observed with the response to the depolarizing agent 4-aminopyridine (3 mM). Threshold sensitivities of the extra- and intracellular Ca(2+)-mobilizing pathways to angiotensin II were similar, and all examined effects of angiotensin II in these cells were apparently mediated by losartan-sensitive (AT1-like) receptors. The dependence of angiotensin II-stimulated [3H]phorbol 12,13-dibutyrate binding on extracellular Ca2+ entry, in contrast to stimulation by other phospholipase C-linked receptor agonists (bradykinin and methacholine), suggests that angiotensin II preferentially stimulates protein kinase C translocation to the plasma membrane, rather than to internal membranes, in bovine adrenal medullary cells.

Adrenal Medulla↗
PubMed1993

Kainate-induced changes in opioid peptide genes and AP-1 protein expression in the rat hippocampus.

In the rat hippocampus, jun, c-fos, and fos-related antigen immunoreactivity, AP-1 DNA binding, and opioid peptide gene expression were examined after kainate treatment to determine whether the induction and DNA binding of AP-1 transcription factors are correlated with the expression of the opioid peptide genes. One and one-half hours after kainate administration, fos-related antigen and jun immunoreactivity and AP-1 DNA binding were induced; maximal elevation was observed after 4.5 h. Transcription factor expression and DNA binding increased in a dose-dependent manner. Preprodynorphin and preproenkephalin mRNA induction was also dose dependent. The anticonvulsants, pentobarbital and diazepam, effectively blocked electroencephalographic seizure activity caused by kainate treatment, whereas valproic acid was approximately 50% effective. Opioid peptide gene expression, fos-related antigen and jun immunoreactivity, and AP-1 DNA binding all reflected similar reductions after anticonvulsant treatment. Therefore, expression and DNA binding activity of the AP-1 transcription factors are correlated with opioid peptide gene expression in the rat hippocampus.

Animals↗
PubMed1992

Characterization of dynorphin-containing neurons on dissociated dentate gyrus cell cultures.

In the dentate gyrus, the synthesis of the opioid peptide, dynorphin, is modulated by a variety of stimuli. In order to elucidate the cellular and molecular mechanisms regulating the synthesis of dynorphin in the hippocampus, we have established a routine primary cell culture of dentate granule neurons and identified granule-like neurons by a characteristic marker, dynorphin, in these cultures. Cultures were prepared from 7-day-old rat pups and maintained in medium with 2% fetal bovine serum. These cultures contained approximately 20% neurons and survived for over 4 weeks. After 2 weeks in culture, neurons expressing dynorphin-A and its messenger RNA were detected using immunocytochemistry and in situ hybridization, respectively. In dentate cultures, enkephalin-, cholecystokinin-, neuropeptide Y- and substance P-positive cells were observed in addition to dynorphin-positive cells with immunocytochemistry. The results suggest that dentate gyrus cell cultures provide a valid in vitro model for studying molecular mechanisms regulating prodynorphin gene expression.

Animals↗
PubMed1992

Preferential activation of [3H]phorbol-12,13-dibutyrate binding by AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) in neonatal striatal cell cultures.

Activation of excitatory amino acid receptors increased [3H]phorbol-12,13-dibutyrate ([3H]PdBu) binding in four week cultures of striatal cells from postnatal day 7 rat pups (PN7), and in PN7 cells co-cultured the fourth week with striatal cells from postnatal day 1 rat pups. Kainate (KA), trans-1-amino-cyclopentyl-1,3-dicarboxylate (ACPD), and N-methyl-D-aspartate (NMDA) increased [3H]PdBu binding equally in both types of cultures, but alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) increased binding by 3-fold in the co-cultures. Thus, [3H]PdBu binding in these two types of striatal cultures offers a simple model system for studying the regulation of AMPA/KA receptor responses.

Animals↗
PubMed1992

Constitutive expression of AP-1 transcription factors in the rat adrenal. Effects of nicotine.

The AP-1 proteins (c-fos and fos-related antigens and jun proteins) are transcription factors that are induced in most cells by various stimuli, but the expression of these proteins is low or undetectable in the basal state. Our data indicate that the rat adrenal gland contains a basally expressed elevated level of AP-1 proteins and mRNAs (40- and 35-kDa fos-related antigens, a 39-kDa c-jun protein, c-jun, junB, and junD mRNA), as well as high basal AP-1 DNA binding activity. Both the medulla and cortex contained equivalent levels of fos-related antigens and c-jun protein; however, the majority of AP-1 DNA binding was detected in the medulla. Handling of rats for several days prior to sacrifice failed to affect protein expression or binding; on the other hand, repeated injections of nicotine increased AP-1 DNA binding. A single nicotine injection 60 min prior to removing the adrenals caused a significant reduction in AP-1 DNA binding without any detectable changes in AP-1 protein expression. Pretreatment of adrenal nuclear extracts with alkaline phosphatase prior to incubation with the AP-1 oligomer decreased binding activity. Thus, unlike most tissues where AP-1 DNA binding activity is controlled by increased expression of AP-1 proteins, DNA binding in the rat adrenal gland appears to be controlled at the post-translational level, possibly through dephosphorylation.

Adrenal Glands↗
PubMed1992

A 35 kDa Fos-related antigen is co-localized with substance P and dynorphin in striatal neurons.

The rat striatum after dopamine denervation followed by repeated apomorphine treatment was examined for the co-expression of c-fos and Fos-related antigens with dynorphin, substance P and [Met5]enkephalin using Western blot and immunohistochemical techniques. Administration of apomorphine, a dopamine agonist, elevated the level of 35 kDa Fos-related antigen which co-localized with dynorphin and substance P, but not enkephalin, in striatal neurons.

Animals↗
PubMed1992

Apomorphine induction of AP-1 DNA binding in the rat striatum after dopamine depletion.

The expression of AP-1 transcription factors was assessed in the dopamine-depleted rat striatum over a 1 week period of repeated apomorphine injections. A single injection of apomorphine increased the expression of a 35 kDa Fos-related antigen and Jun proteins and their expression continued to increase until day 3 of repeated apomorphine treatment in dopamine-depleted striata. Apomorphine induces AP-1 transcription factors which may be involved in modulating gene expression in the striatum.

Animals↗
PubMed1992

Regulation of prodynorphin gene expression in the hippocampus by glucocorticoids.

The regulation of prodynorphin gene expression by glucocorticoids in the hippocampus was examined in rats that were adrenalectomized (ADX) either 7, 30, 60 and 90 days prior to sacrifice. Peptide levels in the hippocampus of ADX rats were determined by radioimmunoassay and immunocytochemistry. Prodynorphin (PDYN) mRNA was measured by Northern blot analysis and in situ hybridization. A time-dependent decrease in dynorphin A(1-8)(DYN) levels in the hippocampus (18% at 7 days; 44% at 30 days; 58% at 60 days) of ADX rats was found, which was accompanied by a comparable decrease in the abundance of PDYN mRNA. An in situ hybridization analysis revealed that both the number of positively hybridized cells and the number of silver grains per cell were decreased in the dentate gyrus after ADX. The administration of dexamethasone after surgery reversed the peptide and mRNA attenuation induced by ADX. ADX had no effect on the expression of proenkephalin mRNA or [Met5]-enkephalin immunoreactivity in the hippocampus. Examination of thionin-counterstained tissue showed that the dentate granule cell layer was intact. The decrement of DYN expression in this system is proposed to have resulted from the removal of glucocorticoid input and not dentate granule cell loss. This study provides the strong evidence for a differential susceptibility of these two opioid peptides in the hippocampus to the removal of glucocorticoids. In addition, these data provide support for a potentially selective, glucocorticoid-permissive component in PDYN gene expression.

Adrenal Glands↗
PubMed1992

Effects of [Sar1]angiotensin II on proenkephalin gene expression and secretion of [Met5]enkephalin in bovine adrenal medullary chromaffin cells.

We have studied the effect of [Sar1]angiotensin II [S1-AII; a degradation-resistant analogue of angiotensin II (AII) on the release of [Met5]enkephalin (ME) and proenkephalin A (proENK) gene expression. Short-term (15-min to 1-h) stimulation of bovine adrenal medullary chromaffin (BAMC) cells with S1-AII at concentrations from 0.1 to 100 nM had no significant effect on secretion of ME, whereas high concentrations of S1-AII (3 to 100 microM) produced a concentration-dependent increase in the concentration of ME in the incubation media. In contrast, long-term (3- to 24-h) stimulation with low concentrations (0.1 nM-1 microM) of S1-AII increased the secretion of ME in a concentration-dependent manner (EC50 = 1 nM). The intracellular level of ME was not changed by long-term treatment with S1-AII (100 nM). In addition to increased ME secretion, long-term (24-h) stimulation with S1-AII increased the expression of proENK mRNA in a concentration-dependent manner (EC50 = 4 nM). Losartan (2-n-butyl-4 chloro-5-hydroxymethyl-1-[(2'-(1 H-tetrazol-5-yl)biphenyl-4-yl)- methyl]imidazole potassium salt, a type 1 AII receptor antagonist) inhibited these effects, whereas PD123319 (50 microM, a type 2 AII receptor antagonist) was inactive. Our results suggest that AII in BAMC cells exerts a major effect on the long-term regulation of expression of proENK mRNA and secretion of ME. These effects appear to be mediated by type 1-like AII receptors.

Adrenal Medulla↗