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Biomedical subjects

C W Ko

Publications and source records attributed to C W Ko.

At least 37 records · Page 2Linked to original sources
PubMed2000

Automatic spike detection via an artificial neural network using raw EEG data: effects of data preparation and implications in the limitations of online recognition.

OBJECTIVE: Automatic detection of epileptic EEG spikes via an artificial neural network has been reported to be feasible using raw EEG data as input. This study re-investigated its suitability by further exploring the effects of data preparation on classification performance testing. METHODS: Six hundred EEG files (300 spikes and 300 non-spikes) taken from 20 patients were included in this study. Raw EEG data were sent to the neural network using the architecture reported to give best performance (30 input-layer and 6 hidden-layer neurons). RESULTS: Significantly larger weighting of the 10th input-layer neuron was found after training with prepared raw EEG data. The classification process was thus dominated by the peak location. Subsequent analysis showed that online spike detection with an erroneously trained network yielded an area less than 0.5 under the receiver-operating-characteristic curve, and hence performed inferiorly to random assignments. Networks trained and tested using the same unprepared EEG data achieved no better than about 87% true classification rate at equal sensitivity and specificity. CONCLUSIONS: The high true classification rate reported previously is believed to be an artifact arising from erroneous data preparation and off-line validation. Spike detection using raw EEG data as input is unlikely to be feasible under current computer technology.

Brain↗
PubMed2000

Nasogastric lansoprazole is effective in suppressing gastric acid secretion in critically ill patients.

AIM: To evaluate the effect of nasogastric lansoprazole on acid suppression in critically ill patients. METHODS: Patients were eligible for the study if they had a nasogastric tube in place and had not received acid-suppressive agents for 3 days prior to enrolment into the study. Patients with active gastrointestinal bleeding or a baseline gastric pH > 4.0 were excluded. Patients served as their own controls during a 24 h lead-in period. Lansoprazole 30 mg was administered once daily with water through a nasogastric tube for 2 days. Intragastric pH was measured by continuous 24 h pH-metry for 3 days. RESULTS: Fifteen patients were enrolled into the study. The baseline median 24 h intragastric pH was 2.25 +/- 1.01, and increased to 6.70 +/- 0.82 (P= 0.001) after 2 days of lansoprazole. Mean percentage of time intragastric pH was > or = 4.0 was 25 +/- 13% at baseline, and increased to 84 +/- 14% (P=0. 001) after 2 days of lansoprazole. CONCLUSIONS: Nasogastric lansoprazole 30 mg daily is effective in suppressing gastric acid secretion in critically ill patients.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2000

Cost-effectiveness of strategies for primary prevention of nonsteroidal anti-inflammatory drug-induced peptic ulcer disease.

OBJECTIVE: Nonsteroidal anti-inflammatory drugs (NSAIDs) increase the risk of peptic ulcer disease by 5- to 7-fold in the first 3 months of treatment. This study examined the relative cost-effectiveness of different strategies for the primary prevention of NSAID-induced ulcers in patients that are starting NSAID treatment. MEASUREMENTS AND MAIN RESULTS: A decision analysis model was developed to compare the cost-effectiveness of 6 prophylactic strategies relative to no prophylaxis for patients 65 years of age starting a 3-month course of NSAIDs: (1) testing for Helicobacter pylori infection and treating those with positive tests; (2) empiric treatment of all patients for Helicobacter pylori; (3) conventional-dose histamine2 receptor antagonists; (4) high-dose histamine2 receptor antagonists; (5) misoprostol; and (6) omeprazole. Costs were estimated from 1997 Medicare reimbursement schedules and the Drug Topics Red Book. Empiric treatment of Helicobacter pylori with bismuth, metronidazole, and tetracycline was cost-saving in the baseline analysis. Selective treatment of Helicobacter pylori, misoprostol, omeprazole, and conventional-dose or high-dose histamine2 receptor antagonists cost $23,800, $46,100, $34,400, and $15,600 or $21,500 per year of life saved, respectively, relative to prophylaxis. The results were sensitive to the probability of an ulcer, the probability and mortality of ulcer complications, and the cost of, efficacy of, and compliance with prophylaxis. The cost-effectiveness estimates did not change substantially when costs associated with antibiotic resistance of Helicobacter pylori were incorporated. CONCLUSIONS: Several strategies for primary prevention of NSAID-induced ulcers in patients starting NSAIDs were estimated to have acceptable cost-effectiveness relative to prophylaxis. Empirically treating all patients for Helicobacter pylori with bismuth, metronidazole, and tetracycline was projected to be cost-saving in older patients.

Adult↗
PubMed1999

Nasopharyngeal carcinoma cell line (C666-1) consistently harbouring Epstein-Barr virus.

We have established a cell line (C666-1) from undifferentiated nasopharyngeal carcinoma (NPC). This cell line consistently carries the Epstein-Barr virus (EBV) in long-term cultures. C666-1 is a subclone of its parental cell line, C666, derived from an NPC xenograft of southern Chinese origin. It grows as an adherent culture and lacks contact inhibition. In addition, it is tumorigenic in athymic nude mice. The cells consistently express EBV-encoded RNAs and are positively stained for cytokeratin, an epithelial marker. In addition, they express EBNA1 protein, LMP1 and LMP2 transcripts and thus resemble the EBV latency II pattern. The virus genotype is EBV-1 with the latent membrane protein 1 gene showing a 30-bp deletion at the carboxyl terminus, both consistent with findings in southern Chinese NPC tumours. Cytogenetic analysis revealed a sub-diploid status with a chromosomal modal number of 45. C666-1 is unique among NPC cell lines in that it carries EBV. These cells may serve as a good investigative tool as the viral latency pattern and genotype are observed in the majority of primary NPC biopsies from Chinese patients.

Animals↗
PubMed1999

Biliary sludge.

Biliary sludge was first described with the advent of ultrasonography in the 1970s. It is defined as a mixture of particulate matter and bile that occurs when solutes in bile precipitate. Its composition varies, but cholesterol monohydrate crystals, calcium bilirubinate, and other calcium salts are the most common components. The clinical course of biliary sludge varies, and complete resolution, a waxing and waning course, and progression to gallstones are all possible outcomes. Biliary sludge may cause complications, including biliary colic, acute pancreatitis, and acute cholecystitis. Clinical conditions and events associated with the formation of biliary sludge include rapid weight loss, pregnancy, ceftriaxone therapy, octreotide therapy, and bone marrow or solid organ transplantation. Sludge may be diagnosed on ultrasonography or bile microscopy, and the optimal diagnostic method depends on the clinical setting. This paper proposes a protocol for the microscopic diagnosis of sludge. There are no proven methods for the prevention of sludge formation, even in high-risk patients, and patients should not be routinely monitored for the development of sludge. Asymptomatic patients with sludge can be managed expectantly. If patients with sludge develop symptoms or complications, cholecystectomy should be considered as the definitive therapy. Further studies of the pathogenesis, natural history, and clinical associations of biliary sludge will be essential to our understanding of gallstones and other biliary tract abnormalities.

Acute Disease↗
PubMed1999

Detection of chromosomal imbalances in growth hormone-secreting pituitary tumors by comparative genomic hybridization.

Although recent molecular investigations have identified a number of genetic alterations that are associated with the development of pituitary adenomas, the exact pathogenesis mechanism of these tumors remains largely unknown. In this study, we used a genome-wide survey to detect specific genetic changes within the genome of pituitary adenomas. A series of 10 growth hormone-secreting adenomas were analyzed for their genetic imbalances on all 22 autosomes by comparative genomic hybridization (CGH). Chromosomal imbalances were detected in 8 GH-secreting adenomas, whereas 2 tumors had no detectable genetic abnormalities. Chromosome gains were more frequent than losses. Overrepresentation of whole or parts of chromosomes were detected in 5/10 (50%) in 19, 3/10 (30%) in each of 5, 9, and 22q, 2/10 (20%) in 17p12-q21, whereas DNA loss were 3/10 (30%) in 13q and 2/10 (20%) in 18. No detectable gain or loss of genetic material was observed in chromosomes 7, 8, 10, 12, 15, and 20. The findings of overrepresentation of chromosomes 5q, 9p, 17q and DNA loss of chromosome 18 were consistent with those detected in nonfunctioning adenomas (Daniely M, Aviram A, Adams EF, et al:J Clin Endocrinol Metab 83:1801-1805, 1998) suggesting that the development of pituitary tumors, at least in somatotroph and nonfunctioning adenomas, may share common pathway. Frequent amplifications in chromosomes 19 and 22q imply that candidate genes residing in these chromosomal regions may be involved in the pathogenesis of GH-secreting adenomas.

Adenoma↗
PubMed1999

Recombinant human growth hormone and Gitelman's syndrome.

Gitelman's syndrome is a primary renal tubular disorder with hypokalemic metabolic alkalosis, hypocalciuria, and magnesium deficiency. Short stature is one of clinical manifestations in children. The pathogenesis of short stature in Gitelman's syndrome is not known. To evaluate whether growth hormone (GH) is deficient and whether recombinant human GH (rhGH) improves growth rate, rhGH therapy was tried in a child with Gitelman's syndrome. Both height and body weight were less than the third percentile. Laboratory and radiologic findings suggested GH deficiency. During the first 6 months, rhGH therapy with potassium supplement markedly elevated growth rate from 3.8 cm/yr to 12.0 cm/yr. After cessation of rhGH, height increment markedly decreased to the pretreatment level of 3.6 cm/yr during the second 6 months. Additionally, hypomagnesemia was corrected after rhGH therapy. Accordingly, GH deficiency may contribute to short stature in children with Gitelman's syndrome, and rhGH therapy would be an excellent adjunctive treatment for short children with Gitelman's syndrome whose condition is resistant to conventional therapies in terms of growth.

Bartter Syndrome↗
PubMed1999

Gallstone formation. Local factors.

Bile supersaturation is necessary for cholesterol gallstones to form. Not all people with supersaturated bile form gallstones, however, and additional factors must be present. The role of pronucleating substances has been extensively studied. Of these, proteins, especially mucin, are best understood. Mucin is secreted by the gallbladder epithelium and may act as a nidus for crystal nucleation. Other proteins that may act as pronucleators include alpha 1-acid glycoprotein, alpha 1-antichymotrypsin, phospholipase C, and a small calcium binding protein. The role of antinucleating factors is less well understood. Certain drugs, including octreotide and ceftriaxone, may also predispose to stone formation. Another local factor is gallbladder stasis, a well-known risk factor for pigment stone formation. More recent research has focused on the role of bacterial infection, which has long been believed to be a factor in pigment gallstone formation. Newer data also support a role for infection in cholesterol gallstone pathogenesis. Additionally, genetic factors that may predispose a patient to cholesterol gallstones have been identified in mice and in humans.

Animals↗
PubMed1999

Regulation of renal laminin in mice with type II diabetes.

This study examines the regulation of renal laminin in the db/db mouse, a model of type II diabetes characterized by extensive remodeling of extracellular matrix. Immunohistochemistry demonstrated an increase in the contents of laminin chains including beta1 chain in the mesangium and tubular basement membranes at 1, 2, 3, and 4 mo of diabetes. Immunofluorescence with an antibody against the recently discovered laminin alpha5 chain showed that in the normal mouse, the protein had a restricted distribution to the glomerular and tubular basement membranes with scant expression in the mesangium of older mice. In the diabetic mouse, the laminin alpha5 chain content of the glomerular and tubular basement membranes was increased, with marked expression in the mesangium. Northern analysis revealed a significant decrease in the renal cortical contents of alpha5, beta1, and gamma1 chain mRNA in the diabetic mice compared to control, at each of the time points. In situ hybridization showed decreased abundance of alpha5 transcripts in the glomeruli of diabetic mice compared to nondiabetic controls. Analysis of mRNA changes by Northern and in situ hybridization studies demonstrated that the reduction in laminin transcripts involved both glomerular and tubular elements. These observations demonstrate that laminin accumulation in the db/db mice with type II diabetes is due to nontranscriptional mechanisms. Because previous investigations in rodents with type I diabetes have shown that the increase in renal laminin content was associated with a corresponding increment in laminin chain transcript levels, it appears that the mechanisms underlying augmentation in renal matrix laminin content may be distinct in the two types of diabetes.

Animals↗
PubMed1998

Biliary lipid composition after liver transplantation: effect of allograft function and cyclosporine.

Biliary lipid composition and bile flow are altered after orthotopic liver transplantation. Cyclosporine may have additional effects on biliary lipid composition and secretion. We studied the effects of liver transplantation, allograft function, and cyclosporine on biliary lipids in humans. Changes in lipid composition and secretion were correlated with serum cyclosporine levels, clinical events, and allograft function. Bile samples were withdrawn via a T-tube at interval time points in 17 patients during the first 3 months posttransplantation. Total and individual bile acid, cholesterol, and phospholipid were determined using high-performance liquid chromatography. Biliary lipid profiles were then correlated with clinical events, serum cyclosporine levels, and other clinical laboratory values. Biliary lipid concentrations decreased in 3 patients during periods of graft dysfunction (acute cellular rejection, drug-induced hepatitis, and inferior vena caval thrombosis) and increased with resolution of the graft injury. Serum cyclosporine levels were positively correlated with total bile acid, cholesterol, and phospholipid concentrations in bile. There was no relationship between the composition of secreted bile acids and serum cyclosporine levels. Bile acid, cholesterol, and phospholipid secretion were not uncoupled in the presence of cyclosporine. We concluded that (1) a decrease in biliary lipid concentrations may be an indicator of worsened graft function in some allografts; (2) biliary lipid concentrations are correlated with increasing cyclosporine levels; and (3) bile acid composition is unchanged, and uncoupling of secretion of other biliary lipids is not observed in the presence of cyclosporine.

Adolescent↗
PubMed1998

Transient impact of hemodialysis on gastric myoelectrical activity of uremic patients.

Upper gastrointestinal discomforts are common in uremic patients. Investigators have stressed the structural, histopathological, and physiological changes in the gastrointestinal tract in the past decades. Few data are available about the electrophysiological changes in the stomach of uremic patients. It is not known whether hemodialysis alters gastric myoelectrical activity. More interestingly, what is the long-term effect? To address these questions, we measured gastric myoelectrical activity before and after hemodialysis in patients with end-stage renal disease on maintenance dialysis treatment. Twenty-one uremic patients with dyspeptic complaints were enrolled in this study. Gastric myoelectrical activity was measured noninvasively using abdominal surface electrodes (electrogastrography). The paired variables obtained before and after hemodialysis were compared statistically. We also compared the difference between two subgroups defined as new hemodialysis patients and chronic hemodialysis patients. We found that there was a significantly lower percentage of normal slow-wave frequency obtained after hemodialysis in comparison with before hemodialysis (fasting state: 49.1 +/- 4.8% vs 68.1 +/- 5.4%, P < 0.01; fed state: 53.8 +/- 6.9% vs 73.4 +/- 4.1%, P < 0.01). In comparing the subgroups, there were no differences between each EGG variable. We concluded that the hemodialysis itself compromised gastric myoelectrical activity in its immediate effect. However, there were no permanent effects regarding gastric myoelectrical activity itself.

Electrocardiography↗
PubMed1998

Gastric dysrhythmia in uremic patients on maintenance hemodialysis.

BACKGROUND: Dyspeptic symptoms are common in uremic patients receiving hemodialysis. Investigators have placed emphasis on the changes in histopathology and physiology of the gastrointestinal tract. But not much data about the gastric myoelectric activity are available. The aim of this study was to assess gastric myoelectric activity in uremic patients undergoing hemodialysis. METHODS: Fifty-eight subjects were enrolled. They were assigned to: group I, uremic patients undergoing hemodialysis with dyspeptic complaints (n = 20); group II, non-uremic patients with matched dyspeptic complaints (n = 20); and group III, healthy volunteers without dyspeptic complaints (n = 18). Gastric myoelectric activity was measured with abdominal surface electrodes in each person. Patients in group I were measured twice, before (group Ia) and after (group Ib) hemodialysis. The data were compared between the groups. RESULTS: In the prehemodialysis period there was a significantly lower percentage of normal slow-wave frequency when compared with group III (fasting, 66.54%+/-5.39% versus 84.58%+/-3.63%; P < 0.005; fed, 72.25%+/-4.16% versus 89.06%+/-2.57%; P < 0.01). In the post-hemodialysis period the difference was even more profound (fasting, 46.52%+/-4.26% versus 84.58%+/-3.63%; P < 0.001; fed, 51.49%+/-6.89% versus 89.06%+/-2.57%; P < 0.005). Yet, when compared with group II, a significant difference existed only in the post-hemodialysis period (fasting, 46.52%+/-4.26% versus 67.30%+/-3.46%; P<0.001; fed, 51.49%+/-6.89% versus 70.41%+/-4.39%; P < 0.01). Another finding is that hemodialysis decreased the gastric myoelectric activity after hemodialysis (fasting, 66.54%+/-5.39% versus 46.52%+/-4.26%; P < 0.001; fed, 72.25%+/-4.16% versus 51.49%+/-6.89%; P < 0.005). CONCLUSIONS: Uremic patients undergoing hemodialysis have impaired gastric myoelectric activity. Interestingly, hemodialysis seems to cause deterioration in gastric myoelectric activity.

Adult↗
PubMed1997

Acute pancreatitis in marrow transplant patients: prevalence at autopsy and risk factor analysis.

Pancreatitis has been described as an infrequent complication of marrow transplantation. This study investigated the prevalence of pancreatitis at autopsy in marrow transplant patients and determined risk factors for its development. We reviewed consecutive autopsy reports from 1991 to 1993. Medical records and laboratory reports were reviewed for analysis of clinical variables. Autopsy findings and clinical variables were correlated with the autopsy diagnosis of pancreatitis. Pancreatitis was found in 51 of 184 (28%) patients at autopsy. Of those with pancreatitis, 35% had abdominal pain, 10% had measurements of serum pancreatic enzymes, and 20% had abdominal imaging studies in the week prior to death. By univariable analysis, risk factors associated with development of pancreatitis included clinical grades 3 and 4 GVHD, GVHD at autopsy, liver GVHD at autopsy, major infection at autopsy, and increasing days of survival. By multivariable analysis, independent risk factors for its development included any GVHD at autopsy, increasing length of survival after transplantation, and major infection at autopsy. We conclude that pancreatitis is a common but often subclinical complication of marrow transplantation. Its development may be associated with a high prevalence of biliary sludge and prolonged treatment of GVHD with cyclosporine and prednisone.

Abdominal Pain↗
PubMed1996

Cyclic AMP regulates basement membrane heparan sulfate proteoglycan, perlecan, metabolism in rat glomerular epithelial cells.

Perlecan, the basement membrane heparan sulfate proteoglycan (HSPG), has been fully cloned from mouse and human tissues. When a cRNA probe of murine perlecan cDNA was employed in RNase protection assay to test whether rat glomerular epithelial cells (GEC) constitutively express perlecan, several bands of hybridization were seen, suggesting that sequences between rat and murine perlecan may not be identical. Using primers based on published cDNA sequences of murine and human perlecan and poly A+ RNA of rat GEC, we synthesized a 497 bp product (RPD-I) by RT-PCR. The deduced aminoacid sequence showed an 85% and 88% homology with domain I of murine and human perlecan, respectively. The three putative sites containing the consensus sequence SGD for attachment of heparan sulfate chains were fully conserved in the rat perlecan as was a site (NFT) for attachment of N-linked oligosaccharide. RPD-I detected a > 9.5 kb transcript of perlecan in RNA of GEC, similar in size to that present in rat glomeruli. Employing a riboprobe synthesized from RPD-I in RNase protection assay we examined whether dbcAMP regulated perlecan expression in the GEC. At 1, 6, 24 and 48 h of incubation, 1 mM dbcAMP caused 43%, 32%, 47% and 40% reduction in mRNA abundance of perlecan, respectively. Immunoprecipitation showed a corresponding reduction of 61%, 70% and 65% in the synthesis of 35SO4 labeled basement membrane HSPG by the GEC following 12, 24 and 48 h of incubation with dbcAMP. Following incubation for 1 and 24 h prostaglandins, PGE1 and PGE2 (1 uM), known activators of glomerular adenylate cyclase, reduced perlecan mRNA abundance to a similar extent as dbcAMP on northern analysis. Our results show that glomerular basement membrane HSPG synthesized by the GEC belongs to the perlecan family. Decrease of GEC perlecan gene expression and synthesis by cAMP and prostaglandins may be of relevance to proteinuric states characterized by activation of these mediators.

Alprostadil↗
PubMed1996

Chemical composition of gallbladder sludge in patients after marrow transplantation.

OBJECTIVES: Gallbladder sludge develops in approximately 70% of patients after bone marrow transplantation (BMT). Sludge often develops in these patients without known predisposing factors, such as fasting or narcotic use. In this study, we examined the chemical composition of sludge in BMT patients. METHODS: Gallbladder content samples from 15 patients were obtained at autopsy. Presence or absence of sludge was determined by examination of gallbladder contents. Sludge samples were examined with direct and polarizing microscopy and assayed for cholesterol, bilirubin, and calcium content and for the presence of a calcium-binding protein. RESULTS: On microscopic examination, cholesterol monohydrate crystals were almost completely absent. Calcium bilirubinate crystals were present in large amounts in all samples. Calcium-ceftriaxone crystals were found in two patients who had received ceftriaxone. A large proportion of the sludge (84.6%) was found to be "unmeasurable residue." Of this part, 5-30% was accounted for by a calcium-binding protein. CONCLUSIONS: We conclude that gallbladder sludge in patients after marrow transplantation consists primarily of "unmeasurable residue," calcium bilirubinate, and a calcium-binding protein. Cholesterol crystals are almost absent. We conclude that formation of gallbladder sludge in these patients could serve as a model for studying the pathogenesis of pigment gallstones.

Autopsy↗
PubMedDate not supplied

Hospitalizations for bacterial septicemia after renal transplantation in the united states.

BACKGROUND: It is common belief in the transplant community that rates of septicemia in transplant recipients have declined, but this has not been studied in a national population. METHODS: Therefore, 33,479 renal transplant recipients in the United States Renal Data System from July 1, 1994 to June 30, 1997 were analyzed in a retrospective registry study of the incidence, associated factors, and mortality of hospitalizations with a primary discharge diagnosis of septicemia (ICD9 Code 038.x). RESULTS: Renal transplant recipients had an adjusted incidence ratio of hospitalizations for septicemia of 41.52 (95% CI 35.45-48.96) compared to the general population. Hospitalizations for septicemia were most commonly associated with urinary tract infection as a secondary diagnosis (30.6%). In multivariate analysis, diabetes and urologic disease, female gender, delayed graft function, rejection, and pre-transplant dialysis, but not induction antibody therapy, were associated with hospitalizations for septicemia. Recipients hospitalized for septicemia had a mean patient survival of 9.03 years (95% CI 7.42-10.63) compared to 15.73 years (95% CI 14.77-16.69) for all other recipients. CONCLUSIONS: Even in the modern era, renal transplant recipients remain at high risk for hospitalizations for septicemia, which are associated with substantially decreased patient survival. Newly identified risks in this population were female recipients and pre-transplant dialysis.

Adult↗