Search PubMed⌕ Search

Biomedical subjects

F Y Hsieh

Publications and source records attributed to F Y Hsieh.

26 records · Page 2Linked to original sources
PubMed1991

Atypical presentations of tuberculous meningitis--a case report.

A case of tuberculous meningitis, proved by cerebrospinal fluid (CSF) cultures, is reported due to atypical findings in CSF. This 19-year-old man developed subacute headache and fever for 2 weeks, followed by focal seizure and left hemiparesis. Initial CSF study showed hemorrhagic lymphocytic pleocytosis with mildly elevated protein and normal sugar content, mimicking viral or postinfectious meningoencephalitis. Follow-up CSF studies showed polymorphonuclear pleocytosis. A concomitant bacterial meningoencephalitis was suspected, though repeated CSF cultures did not isolate any bacteria. The activity of adenosine deaminase in CSF was 12 U/L, highly suggestive of tuberculous meningitis. Magnetic resonance imaging (MRI) showed only a focal meningoencephalitis in the right lateral frontal cortex. Due to progressive deterioration of the clinical status, umbrella therapy, including antimycobacterial drugs and strong antibiotics were given. At a later time, growth of tubercle bacilli was reported in the CSF cultures. Follow-up study of MRI 4 months later, showed thick abnormal enhancement in the basal cisterns and obstructive hydrocephalus, typical findings of chronic basal meningitis.

Adenosine Deaminase↗
PubMed1990

Antibodies to Epstein-Barr virus in iridocorneal endothelial syndrome.

Antibody titers to Epstein-Barr virus were determined in 13 patients with iridocorneal endothelial syndrome and in 13 healthy race-, age-, and sex-matched controls. Both the geometric mean titer of IgG antibodies to the Epstein-Barr virus capsid antigen and the proportion with high titers of IgG antibodies to the Epstein-Barr virus capsid antigen (greater than or equal to 1:640) were significantly higher in 12 seropositive patients with iridocorneal endothelial syndrome than in 12 seropositive controls (1/761:1/202, P = .001; 83.3%:8.3%, P less than .001). Ten of 12 seropositive patients with iridocorneal endothelial syndrome and five of 12 seropositive controls had antibodies to Epstein-Barr virus-induced early antigens (greater than or equal to 1:10) (Fisher's Exact Test, P less than .05), while four seropositive patients with iridocorneal endothelial syndrome and one seropositive control had low to undetectable levels of antibodies to Epstein-Barr virus-associated nuclear antigen (less than or equal to 1:5) (P greater than .1). Antibody levels to cytomegalovirus or measles virus were not different between patients with iridocorneal endothelial syndrome and controls. Additional studies showed no evidence of humoral immune disorder or collagen vascular disease in the patients with iridocorneal endothelial syndrome. The serologic profiles suggest that the patients with iridocorneal endothelial syndrome examined had a cellular immune abnormality sufficient to permit reactivation of latent Epstein-Barr virus infection and imply, but do not establish, a role for Epstein-Barr virus infection in the pathogenesis of some cases of the iridocorneal endothelial syndrome.

Adult↗
PubMed1990

Distribution of cerebral infarcts on computed tomography.

Locations of cerebral infarcts on computed tomography were analyzed on all patients admitted for ischemic stroke or status lacunaris in 1984. Patients who had only one symptomatic infarct, without histories of strokes or transient ischemic attacks, were allocated to group A, the rest made up group B. Group A showed that 47.6% of symptomatic infarcts were lacunes with similar percentages in the following areas: lenticular nucleus (12.7%), internal capsule (12.7%), and subcortical white matter (11.1%). In group A, the cortex (49.2%) was the most common site of infarction, while in group B, it was the subcortical white matter (31.7%). However, if the structures supplied by the basal perforating arteries (basal ganglia, thalami, and internal capsules) were considered as a whole, this area (41.8%) was the most common site for infarcts in group B. Thus, asymptomatic infarcts and those of status lacunaris contributed greatly to the overall distribution of cerebral infarcts.

Adult↗
PubMed1989

Racial differences in optic nerve head parameters.

Results of previous studies have strongly indicated that the prevalence of elevated intraocular pressure is greater in blacks than in whites and that blacks are more susceptible than whites to glaucomatous damage at any given level of pressure. It has also been suggested that a larger disc area might predispose an eye to glaucomatous damage. We investigated the possibility that clinically quantifiable differences might exist in optic disc parameters between normotensive white and black patients. Disc area, cup-to-disc ratio, and cup volume measured with a video-ophthalmograph (Rodenstock Optic Disc Analyzer) were significantly larger in blacks than in whites, while there was no difference in the disc rim area between the two groups. We derived a mathematical model of the optic disc that relates posterior displacement of the lamina cribrosa to the disc area, distensibility of the disc, and intraocular pressure.

Adolescent↗
PubMed1989

Sample size tables for logistic regression.

Sample size tables are presented for epidemiologic studies which extend the use of Whittemore's formula. The tables are easy to use for both simple and multiple logistic regressions. Monte Carlo simulations are performed which show three important results. Firstly, the sample size tables are suitable for studies with either high or low event proportions. Secondly, although the tables can be inaccurate for risk factors having double exponential distributions, they are reasonably adequate for normal distributions and exponential distributions. Finally, the power of a study varies both with the number of events and the number of individuals at risk.

Adult↗
PubMed1988

Sample size formulae for intervention studies with the cluster as unit of randomization.

This paper presents sample size formulae for both continuous and dichotomous endpoints obtained from intervention studies that use the cluster as the unit of randomization. The formulae provide the required number of clusters or the required number of individuals per cluster when the other number is given. The proposed formulae derive from Student's t-test with use of cluster summary measures and a variance that consists of within and between cluster components. Power contours are provided to help in the design of intervention studies that use cluster randomization. Sample size formulae for designs with and without stratification of clusters appear separately.

Cardiovascular Diseases↗
PubMedDate not supplied

A simple method of sample size calculation for unequal-sample-size designs that use the logrank or t-test.

This paper presents a simple method of calculating sample sizes for unequal-sample-size designs with use of published tables applicable to equal-sample-size design. The method applies to both the logrank test and the t-test. For the power of logrank test, this paper compares the proposed method with existing methods and with the Monte Carlo simulation.

Clinical Trials as Topic↗