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Biomedical subjects

D Chung

Publications and source records attributed to D Chung.

At least 19 recordsLinked to original sources
PubMed2001

Design parameters for an electrochemical cell with porous electrode to treat metal-ion solution.

An electrochemical reactor was designed and operated to treat the solution containing copper ions. Design parameters for the electrochemical reactor using the porous cathode and RuO2/IrO2/Ti anode were investigated. The porous cathode was prepared by the electroless nickel deposition on polyurethane. The apparent current, the gap between cathode and anode, and hydraulic retention time (HRT) were selected as design parameters. The copper removal rate increased with an increase in apparent current. It was not affected by the gap between the cathode and the anode. A reduction in hydraulic retention time stimulated the mass transfer toward the electrode and increased the cathodic current efficiency. Dimensional analysis was conducted to obtain the design equation for scale-up of the electrochemical reactor. The dependence of Sh on Re, Sc, and characteristic lengths, DC/A/L and DW/C/L, was described in the form of a power series. The coefficients were obtained from experimental data.

Cations↗
PubMed2000

Phenotypic characteristics associated with the APC gene I1307K mutation in Ashkenazi Jewish patients with colorectal polyps.

CONTEXT: The I1307K mutation of the APC gene is found in approximately 6% of the Ashkenazi Jewish population and is associated with elevated risk of colorectal cancer. The incidence of the mutation in patients with colorectal adenomas is unknown. OBJECTIVES: To determine the carrier rate of the I1307K mutation in Ashkenazi Jewish patients with a history of colorectal polyps but without colorectal cancer and to compare phenotypic characteristics and family history of carriers vs noncarriers. DESIGN, SETTING, AND PATIENTS: A total of 231 patients who had at least 1 large bowel polyp diagnosed between January 1, 1992, and January 31, 1999, at 1 of 5 centers in Boston, Mass, were included, of whom 183 were Ashkenazi Jewish. DNA was isolated from cheek swab samples. MAIN OUTCOME MEASURES: Presence of the I1307K variant in the APC gene. RESULTS: The I1307K variant was identified in 22 (14%) of 161 Ashkenazi Jewish patients with a history of adenomatous polyps and in 1 (5%) of 20 Ashkenazi Jewish patients with hyperplastic polyps. The phenotypic features of adenomas, family history of polyps, colorectal cancer, and other cancers were indistinguishable between I1307K carriers and noncarriers. CONCLUSIONS: The frequency of the APC I1307K mutation is elevated in Ashkenazi Jewish patients with adenomatous polyps, but not hyperplastic polyps. The I1307K mutation represents a novel paradigm for cancer-predisposing genes, as it is associated with moderately increased risk of neoplasia without other associated distinguishing phenotypic features. JAMA. 2000;284:857-860

Aged↗
PubMed2000

Recurrent laryngeal nerve palsy associated with mediastinal amyloidosis.

Amyloidosis affecting peripheral nerves causing isolated nerve palsies is uncommon. Localised amyloidosis occurs less frequently than the reactive or immune related systemic forms, and mediastinal localisation is virtually unknown. We present a case of recurrent laryngeal nerve palsy associated with mediastinal AL amyloidosis in a middle aged man.

Amyloidosis↗
PubMed2000

Pancreatic pseudocyst masquerading as an incarcerated inguinal hernia.

We present a case in which a pancreatic pseudocyst dissected into the right inguinal region, thus masquerading as an incarcerated right inguinal hernia. Computed tomography (CT) confirmed the diagnosis of a pseudocyst, and the patient was treated successfully with percutaneous drainage.

Adult↗
PubMed1999

Mapping of the discontinuous H-kininogen binding site of plasma prekallikrein. Evidence for a critical role of apple domain-2.

Plasma prekallikrein, a zymogen of the contact phase system, circulates in plasma as heterodimeric complex with H-kininogen. The binding is mediated by the prekallikrein heavy chain consisting of four apple domains, A1 to A4, to which H-kininogen binds with high specificity and affinity (K(D) = 1.2 x 10(-8) M). Previous work had demonstrated that a discontinuous kininogen-binding site is formed by a proximal part located in A1, a distal part exposed by A4, and other yet unidentified portion(s) of the kallikrein heavy chain. To detect relevant binding segment(s) we recombinantly expressed single apple domains and found a rank order of binding affinity for kininogen of A2 > A4 approximately A1 > A3. Removal of single apple domains in prekallikrein deletion mutants reduced kininogen binding by 21 (A1), 64 (A2), and 24% (A4), respectively, whereas deletion of A3 was without effect. Transposition of homologous A2 domain from prekallikrein to factor XI conferred high-affinity kininogen binding from the former to the latter. The principal role of A2 for H-kininogen docking to the prekallikrein heavy chain was further substantiated by the finding that cleavage of a single peptide bond in A2 drastically diminished the H-kininogen binding affinity. Furthermore, the epitope of monoclonal antibody PKH6 which blocks kallikrein-kininogen complex formation with an IC(50) of 8 nM mapped to the center portion of domain A2. Our data indicate that domain A2 and two flanking sequence segments of A1 and A4 form a discontinuous binding platform for H-kininogen on the prekallikrein heavy chain. Domain-specific antibodies directed to these critical sites efficiently interfered with contact phase-induced bradykinin release from H-kininogen.

Binding Sites↗
PubMed1998

Peptides derived from the complementarity-determining regions of anti-Mac-1 antibodies block intercellular adhesion molecule-1 interaction with Mac-1.

Peptides or small molecules that can block the interaction of the integrin Mac-1 with its receptor, intercellular adhesion molecule-1 (ICAM-1), have not previously been developed. We studied this interaction by measuring the adherence of ICAM-1-expressing Chinese hamster ovary (CHO) cells to immobilized, purified Mac-1. Nucleotide sequence information was obtained for the complementarity determining regions (CDRs) of three antibodies (44aacb, MY904, and 118.1) shown to block Mac-1-mediated cell adherence. Peptides were synthesized based on the predicted amino acid sequences of the CDRs and tested for the ability to block cell adhesion to Mac-1. Peptides derived from CDR1 of 44aacb, CDR2 of 118.1, and CDRs 1 and 3 of MY904 heavy chains were found to possess blocking activity at 10-100 muM. This may indicate that one or two CDRs contribute disproportionately to the antibody binding affinity. The binding of ligands to Mac-1 has been shown to require a region of the alpha-chain known as the I- or A-domain. We have recombinantly produced Mac-1 I-domain, and show that it is also capable of supporting the adherence of ICAM-1-expressing CHO cells. The adherence of ICAM-1-CHO cells to the I-domain is inhibited by 44aacb and 118.1 and by the CDR peptides from 44aacb and 118.1. By using phage display of peptide libraries based on the 118.1 CDR peptide with five residues randomized, we were able to identify a novel peptide inhibitor of Mac-1 with substitutions at all five positions. These peptides provide lead structures for development of Mac-1 antagonists.

Amino Acid Sequence↗
PubMed1998

Necrotizing esophagitis presenting as a black esophagus.

A case of necrotizing esophagitis discovered during upper endoscopy is described. An 88-year-old woman was admitted to our hospital with complaints of multiple episodes of coffee ground emesis and dysphagia over 3 months. Ischemia is proposed as the etiology of necrotizing esophagitis on the basis of the patient's significant cardiac history, her age, and low-flow state.

Aged↗
PubMed1998

Lower gastrointestinal bleeding as the initial presenting symptom of renal cell carcinoma.

Renal cell carcinoma is known as one of the "great mimics encountered in clinical medicine," along with syphilis and tuberculosis. It can present clinically as a wide range of symptoms, with a classic triad described as hematuria, pain, and a palpable abdominal mass. However, this triad is present only in <20% of patients with renal cell carcinoma. Gastrointestinal bleeding has been described in renal cell carcinoma, although mainly secondary to metastasis in the upper gastrointestinal tract, with few cases due to local invasion. Lower gastrointestinal bleeding as a presenting symptom of an invasive primary renal cell carcinoma has been described in only one patient in the literature. Our patient is the first in whom a colonoscopic biopsy was used as a successful diagnostic modality.

Aged↗
PubMed1998

Two acute pediatric abdominal catastrophes from strangulated left paraduodenal hernias.

We present two cases of catastrophic intestinal obstruction from to strangulation of a left paraduodenal hernia (PDH). PDH is the most common internal hernia. Early diagnosis and treatment are essential because of the high morbidity and mortality associated with strangulation. Early involvement of the surgical team without an overly extensive evaluation in the emergency department is important if this diagnostic suspicion exists. PDH should also be considered when there is a history of chronic, intermittent abdominal pain of unclear cause. To our knowledge, these cases are the first described cases of sudden demise within a few hours of onset of symptoms of a left PDH.

Abdomen, Acute↗
PubMed1997

An alpha-helical minimal binding domain within the H3 domain of syntaxin is required for SNAP-25 binding.

The interaction between the proteins syntaxin 1A and SNAP-25 is a key step in synaptic vesicle docking and fusion. To define the SNAP-25 binding domain on syntaxin, we have prepared peptides that span the syntaxin H3 domain (residues 191-266), the region previously shown to be important for binding to SNAP-25, and then determined the affinities of these peptides for binding to SNAP-25. A minimal binding domain was identified within a region of 32 amino acids (residues 189-220). Its affinity for SNAP-25 is substantially enhanced by C-terminal extension (residues 221-266). Circular dichroism revealed the presence of substantial alpha-helicity in the H3 domain and in the 32-mer minimal binding domain, but not in H3 peptides that do not bind to SNAP-25. At temperatures that denature the alpha-helix of the minimal binding domain peptide, SNAP-25 binding is lost. Selected mutations in evolutionarily conserved residues of the amphiphilic alpha-helix within the minimal binding domain (e.g., residues 205 and 209) greatly reduce the affinity for SNAP-25 but have no major effect on secondary structure, suggesting that these residues may interact directly with SNAP-25. The H3 domain peptide and the minimal binding domain peptide inhibit norepinephrine release from PC12 cells. These results suggest that specific amino acid residues in the H3 domain, positioned by the underlying alpha-helical structure, are important for its binding to SNAP-25 and support the notion that this interaction is important for presynaptic vesicular exocytosis.

Amino Acid Sequence↗
PubMed1997

Selective inhibition of oncogenic ras-p21 in vivo by agents that block its interaction with jun-N-kinase (JNK) and jun proteins. Implications for the design of selective chemotherapeutic agents.

We have obtained evidence that oncogenic and activated normal ras-p21 proteins utilize overlapping but distinct signal transduction pathways. Recently, we found that ras-p21 binds to both jun and its kinase, jun kinase (JNK). We now present evidence that suggests that oncogenic but not normal activated p21 depends strongly on early activation of JNK/jun. This early activation most likely involves direct interaction between oncogenic p21 and JNK/jun because p21 peptides that blocked the binding of p21 to JNK and jun strongly inhibited oncogenic p21-induced oocyte maturation while they did not inhibit insulin-activated normal cellular p21-induced maturation. Very similar results were also obtained for a newly characterized specific inhibitor of JNK which blocked oncogenic but not normal activated p21-induced oocyte maturation. We also found that both jun and JNK strongly enhanced oncogenic p21-induced oocyte maturation while they inhibited insulin-activated normal p21-induced oocyte maturation. These results suggest that the peptides and JNK inhibitor may be useful agents in selectively blocking the effects of oncogenic but not normal p21 in cells.

Animals↗
PubMed1997

Inhibition of oncogenic and activated wild-type ras-p21 protein-induced oocyte maturation by peptides from the ras-binding domain of the raf-p74 protein, identified from molecular dynamics calculations.

In the preceding paper we found from molecular dynamics calculations that the structure of the ras-binding domain (RBD) of raf changes predominantly in three regions depending upon whether it binds to ras-p21 or to its inhibitor protein, rap-1A. These three regions of the RBD involve residues from the protein-protein interaction interface, e.g., between residues 60 and 72, residues 97-110, and 111-121. Since the rap-1A-RBD complex is inactive, these three regions are implicated in ras-p21-induced activation of raf. We have therefore co-microinjected peptides corresponding to these three regions, 62-76, 97-110, and 111-121, into oocytes with oncogenic p21 and microinjected them into oocytes incubated in in insulin, which activates normal p21. All three peptides, but not a control peptide, strongly inhibit both oncogenic p21- and insulin-induced oocyte maturation. These findings corroborate our conclusions from the theoretical results that these three regions constitute raf effector domains. Since the 97-110 peptide is the strongest inhibitor of oncogenic p21, while the 111-121 peptide is the strongest inhibitor of insulin-induced oocyte maturation, the possibility exists that oncogenic and activated normal p21 proteins interact differently with the RBD of raf.

Amino Acid Sequence↗
PubMed1997

Large bowel obstruction: a postoperative complication after laparoscopic bilateral inguinal hernia repair.

Each year in the United States alone over 500,000 inguinal herniorrhaphies are performed. Numerous techniques and methods have been described, all in an attempt to decrease recurrences, complications, and morbidity. One of the newer methods involves laparoscopic, transabdominal, preperitoneal placement of a mesh sheet. Several articles have described complications following this procedure--some inherent in all hernia repairs and some unique to either the laparoscopic approach or mesh placement. Our case appears to represent the first description of a large bowel obstruction secondary to an intense, inflammatory reaction to the inserted mesh. It suggests that mesh insertion, despite reperitonealizing the mesh, is not without complication.

Hernia, Inguinal↗
PubMed1997

Heterotypic protection following oral immunization with live heterologous rotaviruses in a mouse model.

A Jennerian approach using live animal viruses to immunize humans is the current lead strategy for developing rotavirus vaccines. This strategy has been modified by incorporating human rotavirus VP7 genes into vaccine strains to induce serotype-specific neutralizing antibodies to human strains. However, the role of homotypic versus heterotypic immunity in protection is unclear. To investigate the importance of serotype-specific immunity in a mouse model, mice were immunized with rhesus rotavirus (RRV: G3, P5[3]), RRV-based modified Jennerian vaccine strains DxRRV (G1, P5[3]), DS1xRRV (G2, P5[3]), or ST3xRRV (G4, P5[3]), or bovine rotavirus NCDV (G6, P6[1]) and challenged with murine rotavirus ECw (G3, P[16]). Mice immunized with modified Jennerian vaccines exhibited complete to near-complete protection from challenge. NCDV-immunized mice also showed partial protection. The protection was correlated with fecal IgA levels to VP6, not serum IgG responses. Modified Jennerian vaccines induce both heterotypic and homotypic immunity in mice.

Animals↗
PubMed1996

pRb controls proliferation, differentiation, and death of skeletal muscle cells and other lineages during embryogenesis.

Mice deficient for the RB gene (RB-/-), prior to death at embryonic day 14.5, show increased cell death in all tissues that normally express RB1: the nervous system, liver, lens, and skeletal muscle precursor cells. We have generated transgenic mice (RBlox) that express low levels of pRb, driven by an RB1 minigene. RBlox/RB-/- mutant fetuses die at birth with specific skeletal muscle defects, including increased cell death prior to myoblast fusion, shorter myotubes with fewer myofibrils, reduced muscle fibers, accumulation of elongated nuclei that actively synthesized DNA within the myotubes, and reduction in expression of the late muscle-specific genes MCK and MRF4. Thus, insufficient pRb results in failure of myogenesis in vivo, manifest in two ways. First, the massive apoptosis of myoblasts implicates a role of pRb in cell survival. Second, surviving myotubes failed to develop normally and accumulated large polyploid nuclei, implicating pRb in permanent withdrawal from the cell cycle. These results demonstrate a role for pRb during terminal differentiation of skeletal muscles in vivo and place pRb at a nodal point that controls cell proliferation, differentiation, and death.

Animals↗
PubMed1996

Organization, evolutionary conservation, expression and unusual Alu density of the human gene for pigment epithelium-derived factor, a unique neurotrophic serpin.

PEDF is a neurotrophic serpin that promotes a neuronal phenotype and augments neuronal cell survival. The isolation, sequence and structural analysis of the human PEDF gene and its promoter along with its evolutionary conservation and expression in human tissues are now described. The gene spans approximately 16 kb and is divided among 8 exons and 7 introns, the junctions of which conform to the AG/GT consensus rule. PEDF appears to fall into the ovalbumin/PAI-2 subgrouping of serpins and is structurally far different from GDN/PN-1, the only other neurotrophic serpin reported to date. The immediate 5'-flanking region is dominated by a dense cluster of Alu repeats in which are embedded several promoter consensus sequences. A CAAT box is present at -43. The putative promoter region is also far different from that reported for GDN/PN-1. Comparable hybridization signals of 23 kb EcoRI fragments containing the PEDF gene are observed by Southern blot analysis in all primate, mammal and avian species examined; conservation is particularly evident among the primates. Northern blot analysis confirms the presence of the PEDF transcript in a broad range of human fetal and adult tissues including almost all brain areas examined, underscoring differences with GDN/PN-1 which, in the adult brain, is only expressed in glia and a subset of neurons.

Animals↗
PubMed1996

Client follow-up at the Adelaide sexually transmitted disease clinic.

This study investigated the extent to which doctor-client communication is associated with follow-up rates at Clinic 275, an Adelaide sexually transmitted diseases (STD) clinic. At Clinic 275, clients are routinely screened for the major STDs at their first visit. They are then asked to return in one week's time for their results and further treatment if necessary. Over a four-week period in April-May 1994, the clinical consultations between doctors and 100 clients attending for their first visit in an episode of care were observed and recorded. Data from the observation schedules were matched with data collected from interviews, either when clients returned for their follow-up visit (n = 78) or from a telephone interview when they failed to return (n = 20). In addition, 18 clients who failed to return for follow-up (but were not part of the original observation sample) were interviewed. Sociodemographic factors did not affect follow-up rates. Of those who did not return for follow-up, social and environmental reasons were cited by about two-thirds. Reasons given by the remaining clients indicate that failure to return for follow-up was related to discrepancies in doctor-client communication in that they were confused about the need to return to obtain test results. In addition, approximately half could not name the infections for which they had been tested. Changes in clinic practice may prove a more useful method of increasing follow-up rates than seeking to identify the characteristics of noncompliant individuals.

Appointments and Schedules↗