Search PubMed⌕ Search

Biomedical subjects

H Hong

Publications and source records attributed to H Hong.

At least 91 records · Page 5Linked to original sources
PubMed1995

The life history, ultrastructure, and experimental transmission of Hepatozoon catesbianae n. comb., an apicomplexan parasite of the bullfrog, Rana catesbeiana and the mosquito, Culex territans in Algonquin Park, Ontario.

Gametogenesis and sporogonic development of a haemogregarine parasite of bullfrogs (Rana catesbeiana) was observed in cells of the Malpighian tubules of laboratory-reared Culex territans that had fed on naturally infected bullfrogs. Mature oocysts, which varied considerably in size, were multisporocystic with ellipsoidal sporocysts that contained 4 sporozoites. Sporogonic development was completed in about 20 days. Mature meronts were observed in the liver and merozoites in erythrocytes of laboratory-reared bullfrogs that had been fed sporocysts 19 days previously. Similar attempts to infect laboratory-reared green and northern leopard frogs experimentally were unsuccessful, suggesting rather narrow specificity for this parasite in ranids. Gametogenesis and sporogonic stages of this parasite were ultrastructurally similar to those described for Hepatozoon species. The parasite appears to be transmitted directly between bullfrogs and mosquitoes in the study area where Cx. territans feeds avidly on bullfrogs, which in turn were observed to naturally ingest these mosquitoes. Based on data presented in this study and the earlier description by Stebbins in 1903, the haemogregarine parasite of bullfrogs was designated as a new combination, Hepatozoon catesbianae.

Animals↗
PubMed1994

Molecular cloning and expression of a novel hydroxymethylcytosine-specific restriction enzyme (PvuRts1I) modulated by glucosylation of DNA.

The kanamycin resistance plasmid Rts1 restricts the growth of bacteriophage T2, T4 and T6. The DNA of these phage contains hydroxymethylcytosine (HMC) in place of regular cytosine and is modified by glucosylation. When HMC is not glucosylated, as in the DNA of glucosyl transferase-deficient T4 phage, this restriction becomes less apparent, a phenomenon not observed with any other known restriction systems. On the other hand, glucosylation of HMC in T6 phage leads to a less efficient restriction, while restriction of bacteriophage T2 remains unchanged. The modulating effect of glucose cannot be seen when cells contain a large amount of this enzyme, as in the case when multiple copies of its determinant are present in the cells. T-odd phage and bacteriophage lambda are not restricted by Rts1 suggesting that the restriction is specific to DNA containing HMC. The restriction phenotype is due to a single gene coding for a polypeptide of 293 amino acids. This enzyme has been named PvuRts1I. A gene with the sequence motifs similar to modification enzymes was found upstream of the gene coding for PvuRts1I. This gene, however, neither modifies the restriction phenotype of PvuRts1I, nor codes for detectable modification enzyme. T4 mutants with increased resistance to PvuRts1I appear to have deficiency in their beta-glucosyl transferase enzyme.

5-Methylcytosine↗
PubMed1994

Morphology, ultrastructure and taxonomic status of Toddia sp. in northern water snakes (Nerodia sipedon sipedon) from Ontario, Canada.

Inclusions characteristic of an infection caused by Toddia sp. were found in the erythrocytes and erythroblasts of 15 of 26 northern water snakes (Nerodia sipedon sipedon) collected near Kingston, Ontario, Canada. Erythrocytes contained translucent inclusions, small acidophilic bodies, and square-shaped crystalloid structures. Erythrocytes infected with Toddia sp. were more rounded than uninfected erythrocytes and had pycnotic nuclei. We observed icosahedral virus particles measuring 195 to 210 nm formed from a membrane-bounded viral assembly site in the cytoplasm of the host erythrocyte. As a result of the viral identity of this parasite, we recommend that the etiologic agent of Toddia sp. infections from this and other species of North American snakes be renamed Snake Erythrocytic Virus.

Animals↗
PubMed1993

Irreversible inactivation of macrophage and brain nitric oxide synthase by L-NG-methylarginine requires NADPH-dependent hydroxylation.

L-NG-Methylarginine (NMA) is an established mechanism-based inactivator of murine macrophage nitric oxide synthase (mNOS). In this report, NMA is shown to irreversibly inhibit both mNOS (k(inact) = 0.08 min-1) and the recombinant constitutive brain NOS (bNOS). For both NOS isoforms, metabolism of NMA parallels that of the natural substrate L-arginine (ARG), in that it undergoes a regiospecific, NADPH-dependent hydroxylation to form L-NG-hydroxy-NG-methylarginine (NOHNMA). This intermediate then undergoes further NADPH-dependent oxidation to form L-citrulline (CIT). Authentic NOHNMA, synthesized from L-ornithine, irreversibly inhibited both mNOS (k(inact) = 0.10 min-1) and bNOS in an NADPH-dependent reaction. The conversion of either NMA or NOHNMA to CIT correlated with irreversible enzyme inactivation. Thus, the data suggest that enzyme inhibition occurs as a consequence of oxidative metabolism of the intermediate, NOHNMA. A unified mechanism is proposed that accounts for NO biosynthesis from ARG, for the inactivation of NOS by NMA and for the intermediacy of hydroxylated ARG or NMA derivatives in these processes.

Amino Acid Oxidoreductases↗
PubMed1993

Oral immunization of rats with proteinoid microspheres encapsulating influenza virus antigens.

Influenza virus antigen microspheres were prepared by a pH-dependent process using a protein-like polymer (proteinoid) made by thermal condensation of amino acids. The efficacy of these preparations to induce specific IgG responses when used as oral vaccines in rats was evaluated. A single enteric dose of M1 entrapped in proteinoid microspheres was able to induce a significant IgG response to M1 as early as 2 weeks postdosing, while rats dosed orally with the same M1 total dose (no microspheres) showed no detectable antibody response. An unencapsulated hemagglutinin and neuraminidase (HA-NA) preparation induced a moderate anti HA-NA IgG response. A single enteric dose of HA-NA spheres induced a response in 33% of the rats; this response was up to eight times higher than that observed in the rats dosed with unencapsulated antigen.

Administration, Oral↗
PubMed1992

Ultrastructure of the development of a species of Encephalitozoon cultured from the eye of an AIDS patient.

Human fibroblast cell cultures inoculated with microsporidia-infected corneal scrapings from an AIDS patient were fixed in situ and examined by scanning and transmission electron microscopy. The parasite grew prolifically and all developmental stages were observed. Meronts underwent binary fission and the daughter cells transformed into elongate, chain-like sporonts that eventually separated into sporoblasts. The formation of components of the mature spores is described. The parasite, a species of Encephalitozoon, underwent development both in the cytoplasm and within a parasitophorous vacuole, distinguishing it from the morphologically similar species E. cuniculi and E. hellem, both of which have been described from lesions in the human eye and have been reported to develop exclusively within a parasitophorous vacuole.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Effect of L-NG-nitro-arginine, inhibitor of nitric oxide synthesis, on autoregulation of renal blood flow in dogs.

The present experiments were designed to evaluate the importance of nitric oxide in the regulation of renal hemodynamics and the autoregulation of renal blood flow (RBF) in anesthetized dogs. RBF was measured by an electromagnetic flowmeter, and renal arterial pressure (RAP) was varied by an adjustable aortic clamp. The RAP-RBF relations were examined during the intrarenal infusion of saline or agents. The intrarenal infusion of L-NG-nitro-arginine (L-NNA, 40 micrograms/kg.min) at normal RAP decreased RBF and urine flow (UF), while the infusion of L-arginine.HCI (1 mg/kg.min) increased RBF and UF. Both agents did not affect the glomerular filtration rate and mean arterial pressure. The autoregulation of RBF was impaired during the L-NNA infusion. The L-arginine infusion did not affect autoregulatory efficiency. When L-NNA (40 micrograms/kg.min) and L-arginine were infused simultaneously into the renal artery, the autoregulation of RBF was maintained. However, a higher dose of L-NNA (200 micrograms/kg.min) impaired the autoregulation of RBF. These results suggest that the basal production and/or the release of nitric oxide contributes to the regulation of renal hemodynamics and urine formation. During the reduction of RAP, nitric oxide may play an important role in the autoregulation of RBF.

Animals↗
PubMed1992

Allozyme comparison of three Trypanosoma species (Kinetoplastida: Trypanosomatidae) of toads and frogs by starch-gel electrophoresis.

Six metabolic enzymes, glucose-6-phosphate dehydrogenase, glucosephosphate isomerase, isocitrate dehydrogenase, malate dehydrogenase, phosphoglucomutase, and purine nucleoside phosphorylase, from clonal isolates of 3 presumptive species of Trypanosoma (T. fallisi, T. ranarum, and T. rotatorium) from 3 anuran hosts (Bufo americanus, Rana clamitans, and Rana catesbeiana) were compared using starch-gel electrophoresis. Although bands were shared among the different zymodemes of isolates of the same host genus, low genetic polymorphism of the enzyme loci was observed with few apparent shared bands between samples isolated from frogs and toads. A distance value calculated between toad and frog trypanosome isolates suggests the likelihood of long-time separation of species. Cluster analysis based on overall similarity distinguished the trypanosomes of toads and frogs as separate taxa, suggesting that host specificity and observed morphological differences are consistent with heritable allozyme differences.

Alleles↗
PubMed1991

Differentiation between the effects of IGF-1 and GH on PMSG-induced progesterone production by rat granulosa cells.

The effects of insulin-like growth factor-1 (IGF-1) and growth hormone (GH) on pregnant mare serum gonadotropin (PMSG)-induced progesterone production by cultured granulosa cells have been studied. Rat granulosa cells were cultured in different concentrations of PMSG (0-100 mU/ml) plus or minus IGF-1 (4 nM) or GH (hGH, 2.5 or 10 nM) in the presence or absence of cortisol (2.4 micrograms/ml) and/or insulin (68 nM) in low (5 micrograms/ml) or high (50 micrograms/ml) concentrations of transferrin (TRF). IGF-1 augmented PMSG-induced progesterone production in both low and high TRF. The maximal increments were 6.6 and 4.5 times at 20 mU/ml PMSG respectively in low and high TRF. The enhancement by IGF-1 of PMSG-induced progesterone production was greater at low TRF concentrations. When cortisol was added in both low and high TRF, the enhancement by IGF-1 of PMSG-induced progesterone production was reversed and IGF-1 inhibited PMSG-induced progesterone production by 25.9% (low TRF) and 62.3% (high TRF) respectively. When a high dose of insulin was added instead of IGF-1, there was no obvious inhibition of the insulin stimulation by cortisol. In contrast, the IGF-1 inhibition in the presence of cortisol still existed in the presence of a high dose of insulin. These data indicate that insulin must have a direct effect of its own rather than simply acting as a surrogate IGF-1. GH inhibited PMSG-induced progesterone production by 37.2% and 61% respectively at 2.5 and 10 nM GH at low TRF concentration and 100 mU/ml PMSG.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Fluorescence spectroscopic analysis of calpain II interactions with calcium and calmodulin antagonists.

1. The intrinsic fluorescence of epoxysuccinyl-inhibited calpain II undergoes a Ca2(+)-dependent decrease which contrasts with the increase observed for calmodulin. 2. Calpain II was inhibited by the calmodulin antagonist toluidinylnaphthalenesulfonate (TNS), and a Ca2(+)-dependent increase in TNS fluorescence intensity was observed for epoxysuccinyl-inhibited calpain II. 3. The calmodulin antagonists calmidazolium CDZ and felodipine both caused decreases in the intrinsic fluorescence of epoxysuccinyl-inhibited calpain II. 4. Increasing concentrations of Ca2+ caused an increase in the fluorescence intensity of the inhibited enzyme in the presence of (CDZ), and a decrease in the presence of felodipine. 5. It is concluded from these studies that Ca2+ and calmodulin antagonists induce conformational changes in calpain II, and that changes occur in regions other than the Ca2(+)-binding domains.

Binding Sites↗
PubMed1990

Effects of calcium and calmodulin antagonists on calpain II subunit conformations.

Only the 80-kD catalytic subunit of smooth muscle calpain II shows a change in intrinsic fluorescence on binding calcium, but both the 80-kD and 30-kD subunits show fluorescence changes in bound toluidinyl-naphthalenesulphonate as a result of calcium binding. Both subunits also show changes in intrinsic fluorescence in the presence of calmidazolium and felodipine. These studies indicate that both subunits have binding sites for calcium and the calmodulin antagonists, which are probably located in the calmodulin-like domain of each subunit.

Animals↗
PubMed1988

Characterization of the accessory layer of the cuticle of muscle larvae of Trichinella spiralis.

The accessory layer of the cuticle of infective larvae of Trichinella spiralis has been studied with electron microscopy using cytochemical techniques and chemical extractions. The accessory layer lacks negative charges and carbohydrates demonstrable in vivo. Staining with ruthenium red and tannic acid is interpreted as being consistent with their reactions with phospholipids. Freeze fractures demonstrate an external layer of granules that can be partially released by means of detergents (CTAB and SDS). The granules are considered to be proteins. Their removal makes the worms acid sensitive and prevents them from infecting mice. Extraction of whole worms with ethanol, acetone and methanol (via reaction with 2,2-DMP), or chloroform and methanol destroys an internal layer of filaments. Thin-layer chromatography of chloroform/methanol extracts showed principally ethanolamine phospholipids from the surface of the worms. A model is presented for the molecular organization of the accessory layer. Ethanolamine phospholipids are suggested to occur as tubular micelles. Proteins may attach to these by lipophilic moieties and perhaps by a cryptic sugar group (demonstrated by others) that may penetrate into the hydrophilic core of the lipid micelles.

Animals↗