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Biomedical subjects

J Yuen

Publications and source records attributed to J Yuen.

68 records · Page 4Linked to original sources
PubMed1993

Risk of extrahepatic bileduct cancer after cholecystectomy.

The aetiology of cancer of the extrahepatic bile duct is unknown. Gallstones have been proposed to be a risk factor on the basis of ecological and epidemiological evidence. As gallstones are formed in the gallbladder, the occurrence of extrahepatic bileduct cancer in patients after cholecystectomy is of interest. All patients (62,734) who had had a cholecystectomy during 1965-1983 within the Uppsala Health Care Region, Sweden, were followed up to the end of 1987. Excluding the first year of follow-up, 23 cancers of the extrahepatic bileduct occurred vs 26.3 expected for a standardised incidence ratio (SIR) of 0.88 (95% confidence interval [CI] 0.56-1.31). 10 years or more after operation there was a greater reduction of risk (SIR = 0.27; 95% CI 0.06-0.80). Similar patterns were observed for men and women, and among patients who had undergone cholecystectomy only compared with those who had had their common bileducts explored. To assess surveillance bias the incidence of primary liver cancer was also analysed: SIR = 1.15; 95% CI 0.91-1.44 overall, and 10 years or more after cholecystectomy SIR = 0.98; 95% CI 0.66-1.40. This study shows a reduced risk of extrahepatic bileduct cancer 10 or more years after cholecystectomy, indicating that gallstones may be a cause of this cancer.

Bias↗
PubMed1993

Detection of the (--SEA) double alpha-globin gene deletion by a simple immunologic assay for embryonic zeta-globin chains.

Homozygous alpha-thalassemia [alpha-thal-1], with loss of all four alpha-globin genes, causes lethal hydrops fetalis. The most common mutation producing this syndrome is the Southeast Asian (--SEA) double alpha-globin gene deletion. Erythrocytes from adults heterozygous for the (--SEA) deletion have minute amounts of embryonic zeta-globin chains detectable by anti-zeta-globin monoclonal antibodies. Among 225 peripheral blood samples tested by a simple anti-zeta-immunobinding tetrazolium dye test, 81 were positive and 144 were negative. The majority of subjects were of Filipino, Chinese, or Laotian ancestry. All 81 positive samples were confirmed by Bam HI digests and a zeta-cDNA probe to have the (--SEA) mutation. The (--SEA) double alpha-deletion was the only abnormality in 58. In the others, it was combined with alpha-globin or beta-globin mutations, or coincidental iron deficiency. Four other samples from (--SEA) heterozygotes were negative by this immunologic assay. Anti-zeta negative samples included 78 deletions of the total alpha-globin region, (--Tot), 23 single alpha-globin deletions, and a variety of beta-globin mutations; 16 normocytic samples with normal alpha-genes were also negative. Ten anti-zeta positive and 25 anti-zeta negative samples had benign triplicated zeta-globin genes. In this population, the sensitivity of this test was 95%; and specificity for the (--SEA) mutation was 100%. Anti-zeta immunobinding testing provides rapid, simple, and reliable screening for the (--SEA) double alpha-globin deletion, although it does not detect the (--Tot) total alpha-deletions.

Antibodies, Monoclonal↗
PubMed1993

Hormone replacement therapy and breast cancer mortality in Swedish women: results after adjustment for 'healthy drug-user' effect.

No change of breast cancer mortality has been reported previously after long-term hormone replacement therapy. A conceivable explanation for the apparent discrepancy between incidence and mortality may be selection bias due to lower prevalence of breast cancer in women who receive replacement hormones, compared with nonexposed women. We used a new approach to correct for bias due to this 'healthy drug-user effect,' by adjusting the external, population-based, mortality rates for such cases prevalent during the recruitment period of our cohort. In this cohort of some 23,000 Swedish women, who were prescribed various hormone replacement regimens, breast cancer mortality was analyzed after follow-up to 12 years. External analyses revealed overall standardized mortality ratios for breast cancer rising from 0.71 to 0.81, but not significantly different from unity, after adjustment procedures. In multivariate regression models, excluding prevalent cases in the cohort, women prescribed estradiol, conjugated estrogens, or an estrogen-progestin combination were not at a higher risk relative to those given other and weak estrogens, relative risks being 0.81 and 0.68, respectively. On the basis of the present analytical approach, we conclude that breast cancer mortality does not appear to be changed overall or in subgroups, despite increased incidence.

Aged↗
PubMed1993

Frequency of glucose-6-phosphate dehydrogenase (G6PD) mutations in Chinese, Filipinos, and Laotians from Hawaii.

In a Hawaii Hereditary Anemia Screening Project, 4,984 participants were tested for glucose-6-phosphate dehydrogenase (G6PD) deficiency by a filter paper blood spot fluorescence test. Abnormal samples and suspected heterozygotes were checked by quantitative G6PD assay (normal 4.5 to 14 units/g Hb). G6PD was deficient (< 1.5 units/g Hb) in 188 of 2,155 males; 7 other males had low activity (1.5 to 2.8 units/g Hb). The gene frequency, estimated from males after excluding referred and related cases, was 0.037 for Chinese, 0.134 for Filipinos, and 0.203 for Laotians. Among 2,829 females tested, family data showed 111 females were obliged to be at least heterozygous, regardless of G6PD activity, and 43 others had low G6PD activity. Most heterozygotes probably remained undetected by G6PD screening. In 28 females, activity was under 10%; in another 9 females, activity was < 1.5 units/g Hb. Since only 25 homozygotes would be predicted, this apparent excess of females with deficient activity could be due to unequal X-inactivation in some heterozygotes. DNA analysis by polymerase chain reaction amplification and special analytic procedures revealed 10 different missense mutations in 75 males. The nucleotide 835 A-->T and 1360 C-->T transitions were first detected in this Hawaiian Project; we found that the nucleotide 1360 mutation was the most common cause of G6PD deficiency in Filipinos. This is the first report of G6PD screening and analysis of molecular G6PD mutations in Filipino and Laotian populations.

Adult↗
PubMed1993

Cholecystectomy and colorectal cancer.

BACKGROUND: An increased risk of large bowel cancer, especially of the right colon, following cholecystectomy has been reported in some studies but contradicted in others. The aim of this study was to settle this question by creating a cohort of cholecystectomy patients that was large enough and with a sufficient follow-up time to detect even weak associations. METHODS: A population-based cohort consisting of 62,615 patients who underwent cholecystectomy was followed up for the occurrence of colorectal cancer up to 23 years. RESULTS: There were 633 colorectal cancers versus 637.9 expected (standardized incidence ratio [SIR] = 0.99; 95% confidence interval [CI] = 0.92-1.07). Analyses of an extensive number of subgroups including sex, age at operation, duration of follow-up, underlying diagnosis, type of operation, and different cancer sites did not show any association. However, for cancer of the right colon among women, the risk was increased (SIR = 1.24; 95% CI = 1.03-1.48) most prominent 15 years or more after operation (SIR = 1.54; 95% CI = 1.03-2.22). CONCLUSIONS: Overall, there is no excess risk of colorectal cancer following cholecystectomy, but consistent with some earlier reports, we observed an increased risk among women for right-sided colon cancer 15 years or more after operation.

Adult↗
PubMed1993

Genetic linkage of mild pseudoachondroplasia (PSACH) to markers in the pericentromeric region of chromosome 19.

Pseudoachondroplasia (PSACH) is a dominantly inherited form of short-limb dwarfism characterized by dysplastic changes in the spine, epiphyses, and metaphyses and early onset osteoarthropathy. Chondrocytes from affected individuals accumulate an unusual appearing material in the rough endoplasmic reticulum, which has led to the hypothesis that a structural abnormality in a cartilage-specific protein produces the phenotype. We recently identified a large family with a mild form of pseudoachondroplasia. By genetic linkage to a dinucleotide repeat polymorphic marker (D19S199), we have localized the disease gene to chromosome 19 (maximum lod score of 7.09 at a recombination fraction of 0.03). Analysis of additional markers and recombinants between the linked markers and the phenotype suggests that the disease gene resides within a 6.3-cM interval in the immediate pericentromeric region of the chromosome.

Achondroplasia↗
PubMed1993

Impaired acetylcholine-mediated vasodilation in patients with congestive heart failure. Role of endothelium-derived vasodilating and vasoconstricting factors.

BACKGROUND: The vasodilatory response to intra-arterial administration of acetylcholine is reduced in patients with congestive heart failure compared with that of normal subjects. The reduced response to acetylcholine may be related to decreased endothelial release of nitric oxide, interaction with peripheral alpha-adrenergic transmission, or production of cyclooxygenase-dependent vasoconstricting substances. The extent to which each of these mechanisms contributes to the reduced vasodilatory response to acetylcholine in patients with congestive heart failure is not known. METHODS AND RESULTS: Thirty-one patients with congestive heart failure (New York Heart Association functional class II-III) and five age-matched normal subjects were studied. Regional vascular responses in the forearm to infusions of acetylcholine, an endothelium-dependent vasodilator (10(-7) to 10(-5) mol/L) and nitroglycerin, an endothelium-independent vasodilator (10(-6) mol/L) in the brachial artery were determined with venous occlusion plethysmography before and after regional alpha-adrenergic blockade with intra-arterial phentolamine (25 micrograms/min) and systemic cyclooxygenase with oral indomethacin (50 mg). Administration of phentolamine significantly increased resting baseline forearm blood flow in 11 patients with congestive heart failure (2.9 +/- 0.4 to 5.4 +/- 0.8 mL.min-1.100 mL-1) and normal subjects (4.6 +/- 0.3 to 11.3 +/- 2.1 mL.min-1.100 mL-1). Before administration of phentolamine, intra-arterial infusions of acetylcholine 10(-7), 10(-6), and 10(-5) mol/L increased forearm blood flow to 4.0 +/- 1.0, 6.0 +/- 1.7, and 16.1 +/- 4.0 mL.min-1.100 mL-1, respectively, in patients with congestive heart failure and to 14.7 +/- 6.2, 20.2 +/- 4.7, and 38.7 +/- 7.9 mL.min-1.100 mL-1, respectively, in normal subjects. After administration of phentolamine, the vasodilatory responses to intra-arterial infusions of acetylcholine and nitroglycerin did not change in either patients or normal subjects. Administration of indomethacin did not alter resting forearm blood flow in 15 patients with congestive heart failure (2.7 +/- 0.4 to 2.7 +/- 0.4 mL.min-1.100 mL-1) or normal subjects (4.6 +/- 0.3 to 5.4 +/- 0.8 mL.min-1.100 mL-1). Administration of indomethacin significantly increased the vasodilatory response to infusion of acetylcholine by an average of 39% in patients with congestive heart failure but did not change the vasodilatory response to acetylcholine in normal subjects. In patients with congestive heart failure, baseline forearm blood flow and the vasodilatory responses to intra-arterial infusions of acetylcholine and nitroglycerin were significantly less than those of normal subjects both before and after administration of phentolamine and indomethacin. CONCLUSIONS: The reduced vasodilatory response to intra-arterial infusion of acetylcholine in patients with congestive heart failure probably results from several coexistent abnormalities in peripheral vascular function, including abnormal production of cyclooxygenase-dependent vasoconstricting factor, impaired endothelial release of nitric oxide, and decreased vascular smooth muscle responsiveness to cyclic GMP-mediated vasodilation.

Acetylcholine↗
PubMed1991

Clinic observations in the assessment of pervasiveness of childhood hyperactivity.

Sixty-one boys, 6-12 years old, met both the diagnostic criteria of ADHD of DSM-III-R and hyperkinetic syndrome of ICD-9. They could be subdivided into two groups: 43 showed hyperactive symptoms in the clinic situation and 18 did not. The former group were younger and showed significantly poorer performance in measures of general intelligence, attention, cognitive styles, motor clumsiness and minor neurological deficits. Controlling for age and intelligence attenuated the differences, but significant differences remained in activity level, attention, and minor neurological deficits. This result suggests that direct observation is important in the assessment of pervasiveness of childhood hyperactivity.

Attention↗
PubMed1988

The different types of alpha-thalassemia: practical and genetic aspects.

From May 1985 to October 1987, 1,564 Southeast Asians living in Hawaii were screened for hereditary anemias. Microcytosis was determined by electronic red cell indices and morphology; iron deficiency was ruled out by normal red cell distribution width and normal protoporphyrin levels; Hb E was determined by electrophoresis; beta-thalassemia (thal) heterozygotes were identified by raised Hb A2 on column chromatography. alpha-Thalassemia heterozygotes were diagnosed by exclusion. Family studies helped identify or confirm diagnoses, especially for the alpha-thal-2 heterozygotes (-alpha/alpha alpha) and homozygotes (-alpha/-alpha). Provisional diagnoses are being checked by DNA analyses. Iron deficiency prevented detection of possibly coexisting alpha-thalassemias in 97 individuals. Technical problems included the obscuring of standard criteria for recognizing the alpha-thal variants by the presence of Hb E or beta-thal. In such cases, alpha-thal could only be detected by family studies or DNA analyses. Problems with hemoglobin (Hb) electrophoresis included Hb H migrating beyond the edge of the strip if incubation was not closely monitored, and difficulty in detecting the small amounts of unstable Hb Constant Spring. DNA analyses also had limitations, since the nondeletion alpha-thalassemias would not be detected by routine Southern blotting. DNA analyses suggested that about 50% of presumed alpha-thalassemias were alpha-thal-2 (-alpha/alpha alpha) variants, and a corresponding number of alpha-thal-2 variants were among the apparent normals. Gene frequencies in the unselected Lao subjects were approximately 0.2 for Hb E, at least 0.1 for (-alpha), usually a rightward (alpha -3.7) type, 0.04 for (-), and 0.01 for a beta-thal. Multistep screening for the alpha- and beta-thalassemias was an effective and efficient strategy.

Asia, Southeastern↗
PubMed1988

Thalassemia heterozygotes in Hawaii: ethnic attitudes toward screening and prenatal diagnosis.

The attitudes toward screening and prenatal diagnosis for the hemoglobinopathies Hb E and alpha-thalassemia, prevalent in Southeast Asia, it were studied in Southeast Asians living in Hawaii. Since May 1985, one Laotian and two Filipino Outreach Workers were trained to make home visits to educate and recruit prospective subjects for a federally-funded thalassemia screening project. Volunteers over age 18 were interviewed to assess their comprehension about thalassemia and their attitudes toward screening, family planning, and prenatal diagnosis using structured questionnaires to measure subjective responses. Prenatal diagnosis was explained to all subjects using simple brochures in Laotian and in three Filipino dialects. Culturally oriented genetic counceling was offered to all heterozygotes, emphasizing that their status was common and benign. By July 1987, 597 adult participants had been interviewed; 262 were male, 335 female (65 pregnant); 250 were Laotian, 221 Filipino, 90 Chinese, and 36 of other races. Among female interviewees, 268 said they would want prenatal diagnosis and 196 said they would abort an affected fetus. Most interviewees, especially those who were pregnant, were in favor of: 1) public education about screening, 2) having relatives tested, and 3) prenatal diagnosis when indicated. These attitudes seemed to be influenced by Western culture and religious constraints. Comprehension of genetic concepts correlated closely with education. Ten pregnancies occurred in 16 couples where both partners were heterozygous for a thalassemia (thal) (at least two non-referred couples had homozygous alpha-thal-1 fetuses during this time). Five had amniocentesis for risk of alpha-thal homozygosity, two for risk of beta-thal homozygosity, two miscarried, and one was referred too late for fetal testing. After amniocentesis, one couple declined termination for a fetus with Hb E/beta-thal, and was sceptical of the results when their infant seemed normal at birth; one couple kept a homozygous beta-thal fetus, possibly modified by alpha-gene deletions.

Abortion, Eugenic↗
PubMed1987

Positive inotropic effects of acetylcholine and BAY K 8644 in embryonic chick ventricle.

BAY K 8644 augmented Ca2+-dependent action potentials and evoked a positive inotropic effect in embryonic chick ventricle. These effects are consistent with the properties of this Ca channel "agonist" whose actions are independent of adenosine 3',5'-cyclic monophosphate (cAMP)-dependent phosphorylation. At low to intermediate concentrations (10(-8) to 10(-6) M), the cholinergic agonists acetylcholine, carbachol, and oxotremorine inhibit Ca2+-dependent action potentials and contractions in embryonic ventricle only in the presence of drugs that cause cAMP accumulation. The prediction that low to intermediate concentrations of these cholinergic agonists should not inhibit the effects of BAY K 8644 on Ca2+-dependent action potentials and contractions was borne out experimentally. This result is consistent with the cAMP hypothesis for muscarinic inhibition. It is noteworthy that all cholinergic agonists tested evoked a positive inotropic effect at high concentrations (greater than 10(-6) M) in the presence or absence of BAY K 8644. The positive inotropic effect was initiated by muscarinic receptors for it was blocked by atropine and was independent of endogenous catecholamines, since it occurred in the presence of propranolol. It is speculated that the positive inotropic effect of muscarinic agonists in embryonic heart muscle is related to stimulation of phosphoinositide metabolism.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

Asian Americans.

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Asian↗