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Biomedical subjects

H Myung

Publications and source records attributed to H Myung.

10 recordsLinked to original sources
PubMed1997

A novel mechanism of virus-virus interactions: bacteriophage P2 Tin protein inhibits phage T4 DNA synthesis by poisoning the T4 single-stranded DNA binding protein, gp32.

P2 prophages have been known to inhibit DNA replication and growth of T-even phages. We show here that this inhibition is due to poisoning of the T-even single-stranded DNA binding protein gp32 by the product of the nonessential P2 tin gene. Synthesis of Tin protein from a gene cloned in a multicopy plasmid is necessary and sufficient to completely prevent de novo DNA replication and growth of wild-type T2 or T4 phage. We isolated more than 20 independent mutants that render T-even phages resistant to poisoning by the P2 Tin protein. In all of these mutants, which we call asp, Asp codon 163 of gene 32 is changed to a Gly or Asn codon. The mutant alleles are recessive; i.e., when wild-type and asp mutants coinfect the same host cells, most DNA replication is poisoned by P2 Tin protein. To explain our results, we propose that the P2 Tin protein interacts with T-even gp32 at position 163 and distorts the helical filament of gene 32 protein on single-stranded DNA. Thereby Tin protein inhibits either assembly or function, or both, of the T4 replisome. The inhibition of late gene expression by P2 Tin protein may be an indirect consequence of inhibition of DNA replication.

Bacteriophage P2↗
PubMed1996

Hybrid evolutionary programming for heavily constrained problems.

A hybrid of evolutionary programming (EP) and a deterministic optimization procedure is applied to a series of non-linear and quadratic optimization problems. The hybrid scheme is compared with other existing schemes such as EP alone, two-phase (TP) optimization, and EP with a non-stationary penalty function (NS-EP). The results indicate that the hybrid method can outperform the other methods when addressing heavily constrained optimization problems in terms of computational efficiency and solution accuracy.

Biological Evolution↗
PubMed1995

The old exonuclease of bacteriophage P2.

The Old protein of bacteriophage P2 is responsible for interference with the growth of phage lambda and for killing of recBC mutant Escherichia coli. We have purified Old fused to the maltose-binding protein to 95% purity and characterized its enzymatic properties. The Old protein fused to maltose-binding protein has exonuclease activity on double-stranded DNA as well as nuclease activity on single-stranded DNA and RNA. The direction of digestion of double-stranded DNA is from 5' to 3', and digestion initiates at either the 5'-phosphoryl or 5'-hydroxyl terminus. The nuclease is active on nicked circular DNA, degrades DNA in a processive manner, and releases 5'-phosphoryl mononucleotides.

Adenosine Triphosphatases↗
PubMed1994

The major capsid protein of the lipid-containing bacteriophage PR4 is the precursor of two other capsid proteins.

We report that capsid proteins P16 and P18 of bacteriophage PR4 are synthesized by post-translational processing of a portion of the major capsid protein, P2. A polyclonal antibody raised against purified P2 reacted with P16 and P18 as well as with P2. A monoclonal antibody reacted with both P2 and P18. The amino acid sequences of the N-termini of P2 and P18 exactly matched, indicating that P18 is derived from the N-terminal segment of P2. These data were confirmed by the analysis of the proteins encoded by various nonsense and missense P2 mutants. The 3129-bp MnlI-C fragment of the PR4 genome was shown to encode P2. The nucleotide sequence of this fragment was obtained and a single continuous ORF was found to encode P2, thus excluding introns and transcript processing in the production of P16 and P18. The DNA segment contained eight ORFs sized > 200 bp and the genes encoding proteins P6 and P6A as well as P2 were mapped by marker rescue analysis. We also report the isolation and characterization of a new class of P2 missense mutants.

Capsid↗
PubMed1994

Lipid selection in the assembly of the phospholipid bilayer membrane of the lipid-containing bacteriophage PR4.

Phage PR4 contains a lipid bilayer within the phage protein capsid. The phospholipids of the bilayer are derived from those of the host. We report that phage morphogenesis selects against the unusually bulky phospholipids synthesized by Escherichia coli grown in the presence of various sugar alcohols. These data indicate that assembly of the PR4 lipid bilayer is a selective process rather than the bulk appropriation of host membrane lipids. We also demonstrates that phage PR4 morphogenesis is compatible with the incorporation of several abnormal lipids, monoacylglycerol, diacylglycerol, and phosphatidylinositol into the phage particle.

Coliphages↗
PubMed1992

The effect of hyperglycemia on lipid peroxidation in the global cerebral ischemia of the rat.

To investigate the influence of hyperglycemia on ischemic brain damage, we measured brain ATP, lactate and malondialdehyde (MDA) levels in global cerebral ischemic models of Wistar rats. We induced global cerebral ischemia by the 4-vessel occlusion method. After 30 or 60 min of occlusion, and after 30 min of reperfusion, we measured brain ATP, lactate and MDA levels. During the ischemic period, brain ATP levels decreased to 30-70% of sham groups both in normoglycemic and hyperglycemic groups. But during the reperfusion period, the recovery rate of ATP levels was significantly lower in the hyperglycemic than in the normoglycemic groups (p less than 0.05). After 60 min of global ischemia, brain lactate increased much more in the hyperglycemic than in the normoglycemic group, and, during reperfusion, was washed out slowly in the hyperglycemic group. The MDA level, a parameter of lipid peroxidation, increased more in the hyperglycemic group than in the normoglycemic group during reperfusion periods (p less than 0.05). We conclude that hyperglycemia increases lactate accumulation, delays the recovery of energy metabolism, and enhances the lipid peroxidation in the transient global ischemia of rat brain. These findings may suggest the harmfulness of hyperglycemia in clinical cerebral ischemia.

3,4-Methylenedioxyamphetamine↗
PubMed1991

Magnetic resonance imaging in brainstem ischemic stroke.

To evaluate the efficacy of magnetic resonance imaging in brainstem stroke, we studied 21 cases of clinically definite brainstem ischemic stroke with brain magnetic resonance imaging (MRI) and conventional computed tomography (CT). MRI demonstrated brainstem lesions in 79% of the cases (16.5 out of 21), while CT revealed 33% (7 out of 21) when cases with suspicious lesions counted as 0.5. Although MRI was done a few days later than CT in most cases, MRI was superior to CT in detecting the number and the size of ischemic lesions, with clear delineation of anatomy and visualization of the status of the blood flow in the vertebral-basilar artery. Disappearance of the flow signal void in the basilar artery can be an important clue in diagnosing occlusion or thrombus of the basilar artery. By delineating the extent and the location of the infarction, MRI findings allowed an interpretation of whether the ischemic vessel is a small basilar branch or a large vessel vertebral or basilar artery.

Adult↗
PubMed1989

Hypesthetic ataxic hemiparesis in a thalamic lacune.

Right hemiparesis with an ipsilateral hypesthesia and ataxia developed in a 57-year-old man. Magnetic resonance imaging showed a left thalamic lacune bordering the medial portion of the posterior limb of the internal capsule. This finding implicated some pathogenetic mechanism of ataxic hemiparesis.

Ataxia↗
PubMed1987

Cerebral sparganosis: CT characteristics.

Cerebral sparganosis is an extremely rare parasitic zoonosis caused by a migrating plerocercoid tapeworm larva, genus Spirometra. Nineteen computed tomography (CT) scans of 12 patients with cerebral sparganosis were retrospectively analyzed and correlated with clinical and pathologic data. On CT scans, the following characteristics were noted: (a) unilateral involvement; (b) extensive or multifocal areas of low density along white matter bundles, with ipsilateral ventricular dilatation and localized cortical atrophy; (c) nodular or irregular enhancement with spotty calcification; and (d) change in location of enhancing nodules on sequential scans. These pathognomonic features reflect a chronic inflammatory process with both active granulomatous lesions and widespread degeneration of brain tissue, especially in the white matter. Degeneration is probably caused by migration of the long-surviving larva along the fiber tracts of white matter.

Adult↗