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Biomedical subjects

J T Lee

Publications and source records attributed to J T Lee.

At least 19 recordsLinked to original sources
PubMed1992

Immunoscintigraphy in the detection of tuberculosis with radiolabelled antibody fragment against Mycobacterium bovis bacillus Calmette-Guérin: a preliminary study in a rabbit model.

Immunoscintigraphy with radiolabelled monoclonal antibodies is widely used to detect solid tumours, but only a few trials have been carried out concerning the specific in vivo localization of an inflammatory process. The purpose of this study was to investigate the detectability of tuberculous foci utilizing this method with radiolabelled bacillus Calmette-Guérin (BCG)-specific F(ab')2 in rabbits. All of the tuberculous lesions (n = 8) were clearly visualized on serial scintigraphy for up to 48 h after injection of the antibody. Immunohistochemical and Ziel-Neelson staining of the tuberculous lesions confirmed the presence of the tuberculous antigens and bacilli. It failed to demonstrate any sustained retention of the BCG-specific antibody fragment in the control group with syphilitic orchitis (n = 2). Therefore, the specific in vivo localization of tuberculosis is feasible by immunoscintigraphy.

Animals↗
PubMed1992

HLA-DQ beta 57 in Hispanic patients with insulin-dependent diabetes mellitus.

OBJECTIVE: The purpose of our study was to investigate the distribution of HLA-DQ beta-chain amino acid residue 57 (HLA-DQ beta 57) as a genetic marker of susceptibility for insulin-dependent diabetes mellitus in the Hispanic population. STUDY DESIGN: Fifteen patients of Puerto Rican descent with juvenile-onset insulin-dependent diabetes mellitus underwent human leukocyte antigen typing for HLA-DQ beta 57 by polymerase chain reaction amplification of the target genomic DQ sequence followed by hybridization of the polymerase chain reaction product to phosphorus 32-labeled allele-specific oligonucleotide probes. A control group of 44 Hispanic adults without diabetes who were undergoing human leukocyte antigen typing for tissue donation were concurrently typed for comparison. RESULTS: The Hispanic insulin-dependent diabetes mellitus group showed a significant increase in homozygosity for a non-aspartate amino acid (p = 0.023) over a control group of Hispanic subjects without diabetes. A high rate of heterozygosity for aspartate (53.3%) is found in Hispanic subjects with insulin-dependent diabetes mellitus as well. CONCLUSIONS: HLA-DQ beta 57 in the Hispanic population has a distribution distinct from HLA-DQ beta 57 in the Caucasian population. A single aspartate is not protective against insulin-dependent diabetes mellitus in Hispanic subjects.

Amino Acid Sequence↗
PubMed1992

Construction and characterization of a yeast artificial chromosome library for Xpter-Xq27.3: a systematic determination of cocloning rate and X-chromosome representation.

We describe the construction and characterization of a human X-chromosome-specific yeast artificial chromosome (YAC) library. Starting with 60 micrograms of hybrid cell line genomic DNA, we generated over 150,000 recombinants, over 90% of which range from 150 to 500 kb. From these recombinants, 3300 human-positive YACs (representing coverage of 4.5 X chromosomes) were identified by genomic human DNA hybridization. Mapping of random clones revealed that they are derived from the X chromosome in a regionally unbiased fashion, and screening with single-copy X-chromosome probes has repeatedly produced YACs from the library. By determining the frequency of YAC clones containing both hamster and human repetitive sequences, we estimated that approximately 11% of clones contain discontiguous sequences. Taken together, the low cocloning rate, the unbiased coverage, and a consistent recovery of YACs using specific X-chromosome markers indicate that YAC technology can be used for extensive cloning and mapping purposes. Because a certain amount of genomic rearrangement is present in YAC libraries, chromosome walking must be undertaken with a degree of caution.

Animals↗
PubMed1992

Intestinal neurofibromatosis in von Recklinghausen's disease: presenting as chronic anemia due to recurrent intestinal hemorrhage.

Neurofibromatosis (von Recklinghausen's disease) is a neuroectodermal disorder characterized by pigmentary changes of the skin (café-au-lait spots), cutaneous and visceral tumors (neurofibromas) and systemic abnormalities. The involvement of gastrointestinal tract in neurofibromatosis is not common. The most common symptoms, refer able to lesions in the gut, are hematemesis, melena and abdominal pain. We experienced a case of intestinal neurofibroma in von Recklinghausen's disease. The patient was a 39 year-old female who had suffered from chronic iron deficiency anemia and recurrent gastrointestinal hemorrhage due to two neurofibromas of jejunum for 3 years, which was diagnosed by superior mesenteric and ileal arteriogram and 99mTc pertechnetate-labelled RBC scan, and treated by segmental resection of jejunum with end to end anastomosis.

Adult↗
PubMed1992

Wound infection surveillance.

Wound infection surveillance is the information-gathering arm of a wound infection control program. Wound infection control concerns prevention--not therapy--of an infrequent but expensive kind of surgical morbidity. Topics discussed in this article include the effectiveness of wound infection surveillance; turf issues; phenomenology; and the gathering, reporting, manipulating, and use of wound infection data.

Data Collection↗
PubMed1992

Results of a compassionate-use program using intravenous ondansetron to prevent nausea and vomiting in patients receiving emetogenic cancer chemotherapy.

This study reports the effectiveness and side effects of intravenous ondansetron as a single-agent antiemetic therapy for patients receiving emetogenic cancer chemotherapy under a compassionate-use program for patients not enrolled in controlled clinical trials. Patients were > or = 7 years old and had uncontrolled nausea and vomiting or intolerable side effects with standard antiemetics administered with previous cancer chemotherapy. All patients received ondansetron 0.15 mg/kg every 4 hours x 3 daily doses beginning 30 minutes prior to emetogenic chemotherapy. Patients could receive ondansetron for up to 5 consecutive days of chemotherapy. One hundred ninety patients received ondansetron during chemotherapy treatments that were similar to previous cycles of chemotherapy during which the patients had received standard antiemetics (identical chemotherapy or differing only by addition/deletion of chemotherapy agents of low emetogenicity). Chemotherapy regimens included cisplatin (n = 99; 52%), doxorubicin (without cisplatin, n = 52; 27%), and other drugs (n = 39; 21%). Patient experiences with nausea and vomiting and side effects with ondansetron and with previous standard antiemetics were rated on a scale of 1 to 10 (1, did not experience; 10, as bad as could be). On the nausea and vomiting scale, 74% of patients improved on ondansetron relative to standard antiemetics. Mean nausea and vomiting scales were 3.9 for ondansetron and 7.7 for standard antiemetics (P < .001). On the side effects scale, 62% of patients improved with ondansetron. Mean side effect scores were 1.8 for ondansetron and 4.5 for standard antiemetics (P < .001). One hundred nine patients assessed the effect of nausea and vomiting on their quality of life by means of the Functional Living Index-Emesis. On a 100-point scale (100=best quality of life), quality of life scores were 65.5 for ondansetron and 39.5 for standard antiemetics (P < .01). Functional Living Index-Emesis scores were higher for 76% of patients during ondansetron treatment as compared with previous chemotherapy with standard antiemetic regimens. Twenty-eight patients (15%) were withdrawn from the study because of nausea and vomiting. Forty-four patients (23%) experienced other adverse effects (headache, 17 patients; diarrhea, eight patients; all other events occurred in two or fewer patients). Only six patients were withdrawn due to adverse effects. In conclusion, ondansetron therapy resulted in significantly improved control of nausea and vomiting, fewer side effects, and better quality of life than standard antiemetic therapy in the same patients receiving similar chemotherapy regimens.

Adolescent↗
PubMed1992

Transcript RNA having trans-acting antitermination activity on the T7 transcription terminator.

The efficiency of the phage T7 intrinsic terminator was determined in pulse-labeling in vitro transcription reactions. While the factor-independent terminator subcloned in pET3a showed consistently high (approximately 80%) efficiency, the efficiency of the same terminator in pGEM3ZT was initially approximately 60% but exponentially decreased to approximately 20%, although the 39-bp terminator, and its 73-bp upstream and 32-bp downstream sequences are identical in the two plasmids. When transcription product mixture of pGEM3ZT was added to an on-going reaction of pET3a, the terminator efficiency from pET3a was immediately reduced to approximately 40%. Furthermore, when the pGEM3ZT product mixture was subjected to the promoter-cleaving HinfI digestion and then phenol/chloroform extraction, the mixture still maintained the trans-acting antitermination activity. The results suggest that the trans-acting component(s) are RNA synthesized from pGEM3ZT.

DNA-Directed RNA Polymerases↗
PubMed1991

Nodular hepatocellular carcinoma. Treatment with subsegmental intraarterial injection of iodine 131-labeled iodized oil.

Internal radiation therapy with subsegmental arterial injection of iodine 131(131I)-labeled iodized oil (Lipiodol; Laboratorie, Guerbet, France) was evaluated in 24 patients with nodular hepatocellular carcinoma (HCC) ranging from 2.5 to 8.0 cm in size. 131I Lipiodol (555 to 2220 MBq in 3 to 8 ml) was injected depending on the tumor size. Tumor reduction was seen in 88.9% of tumors smaller than 4.0 cm in diameter, 65.5% of tumors between 4.1 to 6.0 cm, and 25.0% of tumors larger than 5.1 cm. The tumor size reduction corresponded to the gradual drop of serum alpha-fetoprotein (AFP) levels and devascularization on follow-up angiography. Adverse reactions from treatment included fever, mild abdominal pain, nausea, and elevation of transaminases. These were mild and well tolerated by patients. This method provided long-term local control without complications related to the thyroid, lung, gastrointestinal tract, and bone marrow.

Adult↗
PubMed1991

Immunoglobulin gene rearrangement in abnormal lymph node hyperplasia.

The histologic designation "abnormal lymphoid hyperplasia" is applied to lymph nodes demonstrating varying degrees of architectural effacement and/or cytologic atypia. Although some of these cases may be suggestive of non-Hodgkin's lymphoma, a definitive diagnosis is not possible despite careful morphologic and immunophenotypic studies. Because the demonstration of immunoglobulin and T-cell receptor gene rearrangements by Southern blot analysis provides a sensitive marker of lineage and clonality in lymphoid malignant conditions, the frequency with which such gene rearrangements could be identified in abnormal hyperplasia and their significance were studied. DNA samples from lymph node biopsy samples of 11 patients with abnormal lymphoid hyperplasia were analyzed for rearrangements of immunoglobulin and T-cell receptor genes by Southern blot hybridization. Six of these patients had monoclonal B-cell populations identified by immunoglobulin gene rearrangements; all were found subsequently to have non-Hodgkin's lymphoma by repeated biopsy from 8 days to 46 months later. Two patients with negative Southern blot studies also developed lymphoma, one a T-cell non-Hodgkin's lymphoma and one a cutaneous B-cell non-Hodgkin's lymphoma. Three patients without detectable gene rearrangements showed no evidence of malignant lymphoma at 36-, 45-, and 60-month follow-up evaluations. Southern blot analysis thus identified monoclonal B-cell lymphoid populations in a subset of patients with abnormal lymphoid hyperplasia; the presence of clonal immunoglobulin gene rearrangement predicted progression to overt non-Hodgkin's lymphoma.

Aged↗
PubMed1991

Regulation of rat pancreatic nuclear triiodothyronine receptor by glucocorticoid.

The nuclear T3 receptors in rat pancreas exhibit a characteristic maturation pattern during development and are subjected to autologous regulation by thyroid hormones. To see if glucocorticoids also regulate T3 receptors in the pancreas, rats at various age groups were subjected to experimental conditions that altered their glucocorticoid status and the corresponding changes in nuclear T3 receptors, and exocrine enzymes in their pancreata were evaluated. Hydrocortisone administration to normal suckling and weaning rats did not change total T3 binding capacity or the dissociation constant as measured at 30 degrees C (Kd30). A significant increase in the degree of occupancy of the T3 receptor was found at 5-10 days after treatment with hydrocortisone (42.2 + 4.1% vs. 19.2 + 2.0%). T3 binding capacity and exocrine enzyme concentrations were significantly reduced in both adrenalectomized (Adx) pups and adults, indicating a continuous dependency on glucocorticoid from preweaning to adulthood. In adrenalectomized rat pups, either T4 or glucocorticoid replacement alone restored T3 binding capacity and exocrine enzyme concentrations. T4 and glucocorticoid were given together to Adx rats, the level of stimulation of both pancreatic T3 binding capacity and exocrine enzyme concentrations was found to be equal to the sum of the stimulation by each of these hormones when given alone. Furthermore, a good correlation was found between Bmax30 (Bmax measured at 30 degrees C, representing total sites) for T3 binding and exocrine enzyme activities in different groups following various experimental treatments. These findings provide further evidence that thyroxine can act directly on the rat pancreas presumably through the T3 receptor in regulating the postnatal development of the exocrine enzymes.

Adrenalectomy↗
PubMed1991

Intravenous 3-methoxy-O-desmethyl-encainide in reentrant supraventricular tachycardia: a randomized double-blind placebo-controlled trial in patients undergoing EP study.

Encainide is an agent effective in atrioventricular and atrioventricular nodal reentrant tachycardia. The metabolites O-desmethyl encainide and 3-methoxy-O-desmethyl encainide (MODE) are responsible for the clinical effects of encainide in most patients. In this study, intravenous MODE was evaluated in eight patients with reentrant supraventricular tachycardia undergoing electrophysiological testing. After tachycardia was induced at least twice to ensure reproducibility, MODE (30 micrograms/kg/min x 15 min, then 7.5 micrograms/kg/min) or placebo was administered in a double-blind fashion. If tachycardia remained inducible, the infusion was unblinded; in nonresponding subjects who received placebo, MODE was then administered. Placebo was ineffective in 3/3 patients. MODE prevented tachycardia induction in 5/8 patients and increased the tachycardia cycle length from 302 +/- 38 to 413 +/- 67 msec in the other three. At a mean concentration of 774 +/- 229 ng/ml, MODE prolonged PR, AH, HV, QRS, and QT intervals, right ventricular and accessory pathway effective refractory periods, and slowed or blocked antegrade accessory pathway conduction. Changes in intracardiac conduction were rate independent between cycle lengths 400 to 600 msec, while changes in ventricular effective refractory periods were most pronounced at rapid pacing rates. No adverse effects, hemodynamic changes, or conduction disturbances occurred. Thus, MODE can modify or suppress induction of reentrant atrioventricular or atrioventricular nodal tachycardia. The study design used here is well suited for the evaluation of newer antiarrhythmic agents by electrophysiological testing.

Adult↗
PubMed1991

Interpretation of "cost-effective" and soundness of economic evaluations in the pharmacy literature.

The varied interpretations of the term "cost-effective" in the pharmacy literature are discussed and the soundness of pharmacoeconomic analyses is assessed. Sixty-five studies concerning cost issues, which were published by six pharmacy journals from January 1985 to December 1990, were evaluated according to 10 methodological criteria. Two investigators independently reviewed each study and completed a data collection form; differences were discussed and resolved to ensure consistency of evaluation. In 36 (55%) of 65 articles, cost-effectiveness was misinterpreted as cost saving. Only 3 of the 10 criteria were fulfilled by 50% or more of the studies evaluated. Problem areas included the following: (1) identification of relevant costs and consequences of each strategy, (2) discounting--adjusting data to reflect the differential timing of costs and consequences, (3) incremental analysis--examining extra costs of a program relative to additional effects provided, and (4) sensitivity analysis. Many pharmacoeconomic studies inappropriately used the term "cost-effective" and inadequately addressed basic methodological components of an economic evaluation.

Cost Savings↗
PubMed1990

The role of genetically determined polymorphic drug metabolism in the beta-blockade produced by propafenone.

Propranolol and the sodium-channel-blocking antiarrhythmic agent propafenone share structural features. Although propafenone's beta-blocking actions are readily demonstrable in vitro, clinically significant beta-blockade occurs inconsistently in vivo. In this study, we tested the hypothesis that genetically determined variations in the biotransformation of propafenone to its 5-hydroxy metabolite account for variations in the drug's beta-blocking action. We assessed beta-blockade by measuring the reduction in tachycardia produced by boluses of isoproterenol and treadmill exercise in 14 normal subjects during treatment with placebo and with 150, 225, and 300 mg of propafenone every eight hours for five days each. Nine subjects (with the extensive-metabolizer phenotype) metabolized most of the propafenone to 5-hydroxy propafenone, and five (with the poor-metabolizer phenotype) did not produce this metabolite. At the lower dosages, beta-blockade was present in both groups but was significantly greater in the subjects with poor metabolism, in whom deficient 5-hydroxylation was associated with higher plasma propafenone levels. At the highest dose, a similar degree of beta-blockade was observed in the two groups. Propafenone also had a higher affinity for beta 2 receptors in vitro than either of its major metabolites. We conclude that the degree of beta-blockade during propafenone therapy reflects genetically determined variations in the metabolism of the parent drug, which is necessary for beta-blockade, and that this action of propafenone is considerably enhanced in patients with deficient 5-hydroxylation of propafenone.

Adrenergic beta-Antagonists↗