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F Y Hsieh

Publications and source records attributed to F Y Hsieh.

13 recordsLinked to original sources
PubMed1992

Comparing sample size formulae for trials with unbalanced allocation using the logrank test.

This paper compares the sample size formulae given by Schoenfeld, Freedman, Hsieh and Shuster for unbalanced designs. Freedman's formula predicts the highest power for the logrank test when the sample size ratio of the two groups equals the reciprocal of the hazard ratio. The other three formulae predict highest powers when sample sizes in the two groups are equal. Results of Monte Carlo simulations performed for the power of the logrank test with various sample size ratios show that the power curve of the logrank test is almost flat between a sample size ratio of one and a sample size ratio close to the reciprocal of the hazard ratio. An equal sample-size allocation may not maximize the power of the logrank test. Monte Carlo simulations also show that, under an exponential model, when the sample size ratio is toward the reciprocal of the hazard ratio, Freedman's formula predicts more accurate powers. Schoenfeld's formula, however, seems best for predicting powers with equal sample size.

Clinical Trials as Topic↗
PubMed1992

Locations of cerebral infarctions in tuberculous meningitis.

The locations of cerebral infarctions were studied in 14 patients with tuberculous meningitis (TBM) and 173 patients with noninflammatory ischemic stroke (IS). In patients with TBM, 75% of infarctions occurred in the "TB zone" supplied by medial striate and thalamoperforating arteries; only 11% occurred in the "IS zone" supplied by lateral striate, anterior choroidal and thalamogeniculate arteries. In patients with IS, 29% of infarctions occurred in the IS zone, 29% in the subcortical white matter, and 24% in (or involving) the cerebral cortex. Only 11% occurred in the TB zone. Bilaterally symmetrical infarctions of the TB zone were common with TBM (71%) but rare with IS (5%).

Adult↗
PubMed1992

Bilateral putaminal necrosis caused by methanol poisoning: a case report.

Bilateral putaminal necrosis is characteristic of methanol poisoning. A 31-year-old male alcoholic had headache, impaired consciousness, neck stiffness, roving eyes with dilated unreactive pupils, papilloedema, abdominal pain, vomiting, and severe metabolic acidosis after a binge. Abnormalities of the cerebrospinal fluid included an initial pressure of 240 mmH2 O, RBC 286/mm3, WBC 8/mm3, and protein 179 mg/dl. Peritoneal dialysis was performed on the 2nd day after drinking. A blood test for methanol was not performed until the 5th day, and its results was negative. However, computed tomography (CT) on the 3rd day showed necrosis and hemorrhage of bilateral putamina and the cerebral cortex, and post-contrast enhancement of meninges. On the 22nd day, a CT revealed further changes: necrosis of bilateral subcortical white matter, and post-contrast gyral enhancement at the otherwise normal-looking areas of the cerebral cortex. We suggest that, in certain situations, the characteristic CT findings are helpful in the diagnosis of methanol poisoning.

Adult↗
PubMed1992

Persistent interictal aphasia after repeated partial seizures: a case report.

We reported a case of persistent interictal aphasia after repeated partial seizures. This 64-year-old man, left-handed and literate, developed repeated right facial twitching associated with head turning to the right or transient loss of awareness since October 30 1991. Persistent aphasia between seizures occurred from November 4. An electroencephalogram (EEG) on November 6 showed an epileptic focus over the left frontal area. Tc-99m HMPAO brain single photon emission computed tomography (SPECT) performed one and half and hour after an attack on November 7 showed focal hyperperfusion over the left frontal area. The aphasia recovered on November 7 after the seizures had been stopped. Follow-up EEG and Tc-99m HMPAO brain SPECT done on November 11 and November 14 respectively were normal.

Aphasia↗
PubMed1991

Optic nerve head and nerve fiber layer in Alzheimer's disease.

We compared (1) the differences in the retinal nerve fiber layer between 26 patients with Alzheimer's disease and 30 age- and race-matched normal controls with use of blue-light high-resolution photography, (2) the differences in disc pallor between 30 patients with Alzheimer's disease and 32 controls with use of a boundary-tracking program and fundus photographs, and (3) the topographic disc variables between 26 patients with Alzheimer's disease and 36 controls with use of an optic nerve head analyzer. A higher proportion of patients with Alzheimer's disease had detectable nerve fiber damage as seen by red-free photography compared with controls. Although the pallor area-to-disc area ratio was not significantly different between patients with Alzheimer's disease and controls, the patients with higher pallor area-to-disc area ratios had higher Alzheimer's Disease Assessment Scale (ADAS) scores and longer durations of disease. Patients had an increased cup-to-disc ratio and cup volume and decreased disc rim area compared with controls. These variables also correlated significantly with ADAS scores and the duration of disease. The correlation among the optic nerve head changes and the ADAS scores in patients with Alzheimer's disease suggests a potential role for optic nerve head analysis in monitoring the progression of Alzheimer's disease and in assessing the effectiveness of any treatments developed.

Aged↗
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↗