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Biomedical subjects

M Choi

Publications and source records attributed to M Choi.

At least 55 records · Page 3Linked to original sources
PubMed1998

A case control study of proximal calciphylaxis.

The purpose of this investigation was to describe the clinical presentation of nine patients with calciphylaxis involving the proximal lower extremities or trunk and to compare the clinical characteristics of these patients with those of 347 hemodialysis patients from the same geographic area. Patients were identified primarily through a computer search of pathology records, identifying patients with the term "calciphylaxis" in the biopsy report. All patients had pathologic specimens consistent with calciphylaxis. All the calciphylaxis patients were white and were markedly obese. While two patients had markedly elevated parathyroid hormone levels, most patients did not show severe derangements of calcium phosphate metabolism compared with other dialysis patients. A logistic regression model identified body mass index and low serum albumin 3 months before diagnosis as being highly associated with a diagnosis of calciphylaxis. Diabetes mellitus and parameters of calcium-phosphate metabolism were not significantly associated with proximal calciphylaxis. These findings suggest that white race, morbid obesity, and poor nutritional status are associated with proximal calciphylaxis in dialysis patients.

Aged↗
PubMed1997

A novel antioxidant gene from Mycobacterium tuberculosis.

Among the major antimicrobial products of macrophages are reactive intermediates of the oxidation of nitrogen (RNI) and the reduction of oxygen (ROI). Selection of recombinants in acidified nitrite led to the cloning of a novel gene, noxR1, from a pathogenic clinical isolate of Mycobacterium tuberculosis. Expression of noxR1 conferred upon Escherichia coli and Mycobacterium smegmatis enhanced ability to resist RNI and ROI, whether the bacteria were exposed to exogenous compounds in medium or to endogenous products in macrophages. These studies provide the first identification of an RNI resistance mechanism in mycobacteria, point to a new mechanism for resistance to ROI, and raise the possibility that inhibition of the noxR1 pathway might enhance the ability of macrophages to control tuberculosis.

Amino Acid Sequence↗
PubMed1997

Peptide-induced positive selection of TCR transgenic thymocytes in a coreceptor-independent manner.

T cell receptor (TCR) transgenic thymocytes specific for the LCMV gp peptide are normally positively selected to the CD8 lineage. Transgenic thymocyte development was substantially reduced in the absence of these CD8 coreceptors. However, efficient positive selection was restored when TCR transgenic CD8-/- fetal thymic lobes were cultured with a peptide variant of the wild-type ligand. These mature thymocytes were functional, as shown by their ability to respond against strong peptide agonists. Additional experiments demonstrated that transgenic positive selection was peptide-specific. These results prove that CD8 does not possess essential signaling properties that are necessary for T cell development. In addition, the unilateral commitment of transgenic thymocytes to mature CD4-TCR(hi) T cells expressing intracellular perforin suggests that there must be some instructive component to CD4 down-regulation and lineage commitment during thymocyte selection.

Animals↗
PubMed1995

A nuclear export signal in hnRNP A1: a signal-mediated, temperature-dependent nuclear protein export pathway.

Pre-mRNAs are associated with hnRNPs, and these proteins play important roles in the biogenesis of mRNAs. The hnRNP A1 is one of the most abundant hnRNPs, and although localized primarily in the nucleoplasm, shuttles continuously between the nucleus and the cytoplasm. A 38 amino acid domain within A1, termed M9, which bears no resemblance to classical nuclear localization signal (NLS) sequences, localizes A1 to the nucleus. Here we show that M9 is also a nuclear export signal; placing M9 on a protein that is otherwise restricted to the nucleus, the nucleoplasmin core domain (NPc), efficiently exports it to the cytoplasm in a temperature-dependent manner. In contrast, classical NLSs cannot promote the export of NPc. These findings demonstrate that there is a signal-dependent, temperature-sensitive nuclear export pathway and strengthen the suggestion that A1 and other shuttling hnRNPs function as carriers for RNA during export to the cytoplasm.

Amino Acid Sequence↗
PubMed1995

Identification, cloning, and characterization of the bacteriophage N4 gene encoding the single-stranded DNA-binding protein. A protein required for phage replication, recombination, and late transcription.

The coliphage N4-coded single-stranded DNA-binding protein (N4SSB) is essential for phage replication and for expression of the phage late genes, which are transcribed by the Escherichia coli sigma 70 RNA polymerase. As a first step in investigating the role of N4SSB in replication and transcriptional activation, we have identified and sequenced the N4SSB gene. The gene encodes a 265-amino acid protein with no apparent sequence homology to other single-stranded DNA-binding proteins. We present data indicating that N4SSB is also essential for phage recombination. Mutational analysis of the carboxyl terminus of the protein indicates that this region is required for protein-protein interactions with the N4 replication, N4 recombination, and E. coli transcriptional machineries, while the rest of the protein contains the determinants for single-stranded DNA binding.

Amino Acid Sequence↗
PubMed1995

The bacteriophage N4-coded single-stranded DNA-binding protein (N4SSB) is the transcriptional activator of Escherichia coli RNA polymerase at N4 late promoters.

Transcription of the 72kb linear double-stranded DNA genome of coliphage N4 is carried out by the sequential activity of three different RNA polymerases. Early and middle viral transcripts are synthesized by two phage-coded RNA polymerases while late transcription is carried out by the Escherichia coli sigma 70-RNA polymerase. We have determined the sequences and sites of initiation of several N4 late transcripts; N4 late promoters share weak homology with the E. coli sigma 70 promoter consensus sequence. Indeed, N4 late promoters are weak templates for the host enzyme. We present evidence that the phage-coded, single-stranded DNA-binding protein (N4SSB), a protein that is required for phage DNA replication and recombination and does not bind with sequence specificity to DNA, is the activator of E. coli RNA polymerase at late N4 promoters. Models for the mechanism of action of N4SSB as a transcriptional activator are discussed.

Base Sequence↗
PubMed1995

A dose-response study of the effects of intravenous midazolam on cold pressor-induced pain.

The effects of intravenous midazolam (0.75, 1.5, and 3 mg/70 kg) were examined and compared to that of fentanyl (0.1 mg/70 kg; positive control) and saline on pain induced by a cold pressor test. Both sensory and affective components of the pain response were assessed, as there is some evidence that benzodiazepines reduce the affective component. Healthy volunteers (three females, nine males) were enrolled in a prospective, double-blind, randomized, cross-over trial in which mood and psychomotor performance were also examined. Five minutes and 135 min postinjection, subjects immersed their forearm in ice-cold water for 3 min while assessments of pain were recorded. During the first immersion, subjects reported significantly lower pain intensity and bothersomeness ratings after having been injected with fentanyl, relative to the saline and midazolam conditions, which did not differ significantly from each other. Fentanyl and midazolam had prototypical mood altering and psychomotor impairing effects. We conclude that midazolam in our laboratory setting at the doses and route of administration studied had no effects on either the sensory or affective components of the pain experience.

Adult↗
PubMed1995

Objective and subjective impairment from often-used sedative/analgesic combinations in ambulatory surgery, using alcohol as a benchmark.

Impairment caused by different sedative/analgesic combinations commonly used in ambulatory settings was compared to that of alcohol at blood alcohol concentrations (BACs) higher than or equal to 0.10%. Impairment was measured via subjective (mood) and objective (psychomotor performance) assays. Twelve healthy human volunteers (10 males and 2 females; age range 21-34 yr) participated in this prospective, double-blind, randomized, cross-over study. Each subject was exposed to five drug conditions across 5 wk. Each of the following drug conditions were adjusted for body weight (per 70 kg):fentanyl 50 micrograms and propofol 35 mg (FP), fentanyl 50 micrograms and midazolam 2 mg (FM), fentanyl 50 micrograms, midazolam 2 mg, and propofol 35 mg (FMP), alcohol 56 g (orally administered), and placebo (PLC). With the exception of alcohol, the other drugs were administered via the intravenous route. Tests for psychomotor performance, subjective effects, and short-term memory were done at baseline, and at different intervals until 240 min postinjection. Psychomotor impairment caused by alcohol at 15 min postingestion (at a BAC of 0.11% +/- 0.03% [mean +/- SE]) was used as a benchmark with which impairment caused by other sedative/analgesic combinations was compared. All the study drug combinations produced impairment (i.e., impairment greater than that seen with PLC), similar to that observed with alcohol at a BAC of 0.11%. We have demonstrated that some sedative/analgesic drug combinations used in anesthesia for ambulatory procedures produce impairment similar to or greater than that observed with a large dose of alcohol.

Adult↗
PubMed1995

Preventing the infiltration of leukocytes by monoclonal antibody blocks the development of progressive ischemia in rat burns.

Tissue loss as a consequence of thermal trauma occurs in two stages. There is immediate necrosis in tissues directly killed by the thermal energy, followed by a delayed secondary necrosis in neighboring tissues. The infiltration of neutrophils into traumatized tissues is a hallmark of the inflammatory response. Neutrophils have the machinery to kill invading microorganisms, but these same weapons have the capacity to destroy the host's viable tissues as well. Leukocyte infiltration requires their adherence to the vascular endothelial cell surface. Masking these adhesion sites on neutrophils will block the adhesion of neutrophils to the endothelium. A monoclonal antibody (mAb) was developed to guinea pig leukocyte adhesion sites CD11b/ CD18, and this mAb cross-reacts with rat leukocytes, blocking their adherence. Rats received a "comb burn" composed of four rectangular full-thickness burns placed in a row and separated by three areas left unburned. The four individual burns convert into a single large wound because the blood flow to the interspaces was terminated, blood vessels were occluded, and leukocytes were present in the extravascular space. The systemic administration of the mAb (50 to 150 microliters) immediately following a comb burn promoted the survival of the interspace, demonstrated by the prevention of loss of blood flow by laser Doppler monitoring, maintained patent vessels by latex vascular casts, blocked extravascular migration of neutrophils histologically at 2 hours, and limited the tissue loss to the original four burns.

Animals↗
PubMed1994

Essential role for KH domains in RNA binding: impaired RNA binding by a mutation in the KH domain of FMR1 that causes fragile X syndrome.

The KH domain is an evolutionarily conserved sequence motif present in many RNA-binding proteins, including the pre-mRNA-binding (hnRNP) K protein and the fragile X mental retardation gene product (FMR1). We assessed the role of KH domains in RNA binding by mutagenesis of KH domains in hnRNP K and FMR1. Conserved residues of all three hnRNP K KH domains are required for its wild-type RNA binding. Interestingly, while fragile X syndrome is usually caused by lack of FMR1 expression, a previously reported mutation in a highly conserved residue of one of its two KH domains (Ile-304-->Asn) also results in mental retardation. We found that the binding of this mutant protein to RNA is severely impaired. These results demonstrate an essential role for KH domains in RNA binding. Furthermore, they strengthen the connection between fragile X syndrome and loss of the RNA binding activity of FMR1.

Amino Acid Sequence↗
PubMed1994

Silicone breakdown and capsular synovial metaplasia in textured-wall saline breast prostheses.

Saline-filled prostheses are currently the only type of prostheses available for cosmetic use in the United States because of concerns raised about the possibility of systemic toxicity of silicone-filled artificial mammary implants. Although the approved implants are saline-filled, their potential to release silicone particles from the shells has not been systematically evaluated. We performed microscopic examination of the pericapsular tissue of 54 patients with textured-surface implants and compared these with 51 patients with smooth-walled implants over a 2-year period. The capsules that had formed around virtually all textured-surface implants had silicone fragments present either in extracellular spaces, in vacuolated histiocytes, or in the form of foreign-body granulomas in surrounding fibroadipose tissue but not in capsules associated with smooth-walled implants. In 87 percent of samples of pericapsular tissue from textured saline implants, the contact surface displayed exuberant reactive synovial metaplasia, a histologic pattern not previously described with these devices. Our findings suggest that smooth-walled prostheses are associated with less silicone fragmentation than textured devices in the peri-implant tissue capsules that tend to form around artificial surfaces used for this purpose.

Breast↗
PubMed1994

Influence of dietary fat on the pharmacodynamics of quinidine, procainamide and tocainide in isolated perfused rabbit hearts.

We have reported previously that propafenone decreased ventricular excitability and prolonged ventricular conduction time in hearts from rabbits treated with a lard diet compared to those from rabbits treated with a safflower oil diet. We hypothesized that these effects might be modulated by the lipid solubility of the drug. Accordingly, we studied the effects of dietary fat on the pharmacodynamics of the hydrophilic drugs, procainamide and tocainide, and the lipophilic drug, quinidine. Weanling rabbits were fed diets of 10% w/w lard or safflower oil for 40 days. Differences in electrophysiological variables were compared at base line and during drug perfusion. The linoleic acid content of isolated sarcolemma was significantly higher in the safflower oil group (31.1 +/- 5.6%) than in the lard group (18.8 +/- 3.9%, P < .001). During quinidine (3 microM) perfusion, the threshold current was significantly greater in the lard group (0.44 +/- 0.18 mA) compared to the safflower oil group (0.24 +/- 0.11 mA, P < .05). During procainamide and tocainide perfusion, the threshold current was similar in the lard and safflower oil groups. During quinidine perfusion, greater prolongation of the endocardial monophasic action potential duration was observed in the safflower oil group (217 +/- 15 msec) compared to the lard group (196 +/- 24 msec, P < .05). Procainamide and tocainide effects on monophasic action potential duration were similar in the lard and safflower oil groups. Thus, dietary fat modulates the effects of the lipophilic drug quinidine on ventricular excitability and repolarization.

Action Potentials↗
PubMed1993

U75412E, a lazaroid, prevents progressive burn ischemia in a rat burn model.

Thermal energy causes an immediate, irreversible injury at the burn site, followed by a delayed, reversible tissue loss in the area surrounding the burn site due to progressive ischemia. We investigated the role of lipid peroxidation in the pathogenesis of progressive ischemia in a rat burn model. The burn model consisted of a row of four 10 x 20 mm burns separated by three unburned 5 x 20 mm skin bridges (interspaces). The interspaces became ischemic and necrotic by 24 hours, producing a single wound with the merger of the burn sites. U75412E, a lipid peroxidation inhibitor, preserved vascular patency, restored blood flow, prevented a rise in tissue conjugated dienes, and maintained tissue viability in the interspaces. Four separate burn wounds healed between three viable strips of hair-bearing interspaces. The treatment was effective, when given systemically during the period between 2 hours before and 1 hour after the burn. U75412E prevented progressive burn ischemia and the expansion of tissue loss.

Animals↗