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Biomedical subjects

K Kelly

Publications and source records attributed to K Kelly.

At least 253 records · Page 14Linked to original sources
PubMed1985

Adherence of Escherichia coli to epithelial cells in the pathogenesis of urinary tract infection.

The role of bacterial adherence in the pathogenesis of recurrent urinary tract infection was investigated using an I125 E. coli-epithelial cell assay. In vitro bacterial adhesion to buccal, vaginal epithelial and uroepithelial cells of periurethral or rectal E. coli isolated from each subject was measured in 21 patients with recurrent urinary tract infection and 10 normal controls. Percent adherence of E. coli to buccal, vaginal, and uroepithelial cells was significantly (p less than .005) greater in patients with recurrent infection, compared with controls (32.9 +/- 4.0 vs. 14.1 +/- 7.3; 32.3 +/- 8.1 vs. 15.4 +/- 6.6; 34.7 +/- 5.6 vs. 17.1 +/- 4.2, mean +/- S.D., respectively). For both patients and controls, correlation in adherence between vaginal, uroepithelial, and buccal cells was observed. There were no differences in adherence between patients with or without periurethral colonization with E. coli, and adherence was not influenced by age. Patients receiving antimicrobial prophylaxis had a significantly (p less than .005) lower mean adherence to vaginal (26.7 +/- 3.7 vs. 35.1 +/- 4.1) and uroepithelial (30.4 +/- 2.8 vs. 34.6 +/- 3.2) cells, but not for buccal epithelial cells, compared with patients not receiving prophylaxis. These data support the hypothesis that increased receptivity of epithelial cells for bacteria plays a role in the increased frequency of vaginal colonization and subsequent infection in women who experience recurrent urinary tract infection.

Adhesiveness↗
PubMed1985

Nurse practitioner challenges to the orthodox structure of health care delivery: regulation and restraints on trade.

Until recently, physicians have been the primary health care providers in the United States. In response to the rising health care costs and public demand of the past decade, allied health care providers have challenged this orthodox structure of health care delivery. Among these allied health care providers are nurse practitioners, who have attempted to expand traditional roles of the registered nurse. This article focuses on the legal issues raised by several major obstacles to the expansion of nurse practitioner services: licensing restrictions, third party reimbursement policies, and denial of access to medical facilities and physician back-up services. The successful judicial challenges to discriminatory practices against other allied health care providers will be explored as a solution to the nurse practitioners' dilemma.

Delivery of Health Care↗
PubMed1984

The F plasmid origin of transfer: DNA sequence of wild-type and mutant origins and location of origin-specific nicks.

The DNA sequence of the F plasmid origin of conjugal DNA transfer, oriT , has been determined. The origin lies in an intercistronic region which contains several inverted repeat sequences and a long AT-rich tract. Introduction of a nick into one of the DNA strands in the oriT region precedes the initiation of conjugal DNA replication, and the position of the strand-specific nicks acquired by a lambda oriT genome upon propagation in Flac-carrying cells has been determined. The nicks were not uniquely positioned, rather there was a cluster of three major and up to 20 minor sites: the biological significance of this observation is not yet fully clear. Nine independent point mutations which inactivate oriT function have been sequenced and found to alter one or other of two nucleotide positions which lie 14 and 19 bp to one side of the rightmost (as drawn) major nick site. These key nucleotides may lie in a recognition sequence for the oriT endonuclease, since mutations at these sites prevent nicking at oriT .

Base Sequence↗
PubMed1984

A novel alteration in the structure of an activated c-myc gene in a variant t(2;8) Burkitt lymphoma.

We have characterized a variant Burkitt lymphoma in which translocation joins the immunoglobulin kappa locus on chromosome 2 to the c-myc gene on chromosome 8. This Burkitt lymphoma is especially interesting because, in contrast to the more common lymphomas that carry 8;14 translocations, it carries a translocation that involves a light chain locus and occurs 3' to and at least 20 kb downstream of the c-myc gene. Furthermore, the c-myc gene from the translocated chromosome is abnormally expressed in that there is a characteristic shift in c-myc promoter utilization and an increase in c-myc transcript. These disturbances could be explained by novel structural alterations that occur in the c-myc gene and include a duplication of a 2.5 kb segment of DNA containing the two c-myc promoters and their untranslated leader exons. Interestingly, these alterations arise at a considerable distance from the translocation breakpoint.

Base Sequence↗
PubMed1984

The Collaborative Lipid Research Clinics Program Family Study. II. Response rates, representativeness of the sample, and stability of lipid and lipoprotein levels.

The Collaborative Family Study (1975-1978), the third phase of the Lipid Research Clinics Program Population Studies, covers 2405 probands and 15,693 of their relatives from nine North American communities. This sample was examined for participation differences across race, sex, locality, educational level, and reason for selection. The participation rates were somewhat lower for blacks, younger age groups, and subjects with lower educational levels. The probands' reason for selection into the study had little impact on the participation of probands or relatives. Moreover, based on information gathered at earlier examinations on eligible Family Study probands, the cornary risk factor profile appeared to be similar among participants and nonparticipants . The available longitudinal lipid data on probands indicated general consistency in lipid levels within subjects over short periods of time, in cholesterol even more so than in triglycerides. Among age strata, the younger subjects showed the least intrapersonal stability, especially for triglycerides.

Adolescent↗
PubMed1984

Advance prediction of transthoracic impedance in human defibrillation and cardioversion: importance of impedance in determining the success of low-energy shocks.

The purposes of this study were to evaluate a method that predicts transthoracic impedance in advance of defibrillating shocks in humans and to assess the importance of transthoracic impedance in low-energy defibrillation. Via defibrillator electrodes we applied 31 kHz current to the chest during the defibrillator charge cycle, before the defibrillating shock was actually delivered. The current flow was limited by transthoracic impedance; a microprocessor monitored the predischarge current flow and determined the predischarge impedance by calibration against known resistance values. Actual impedance to the defibrillating shock was also determined and compared with the predicted impedance. With this approach we predicted impedance in 19 patients who received 66 shocks for ventricular and atrial arrhythmias. Predicted impedance (y) correlated very well with actual impedance (x):y = .90x + 11.3; r = .97. To determine the importance of impedance in defibrillation and cardioversion, we prospectively gathered data from 96 patients who received shocks of various energies for ventricular or atrial arrhythmias. In patients with high transthoracic impedance (greater than 97 omega), low-energy shocks (less than or equal to 100 J) for ventricular defibrillation had only a 20% success rate as opposed to a 70% success rate for low-energy shocks in patients with low or average impedance (p less than .05). We conclude that transthoracic impedance can be accurately predicted in advance of defibrillation and cardioversion. This method permits the preshock identification of patients with high impedance in whom attempts to defibrillate with low-energy shocks are inappropriate.

Arrhythmias, Cardiac↗
PubMed1984

Effects of V lambda gene diversity on generation of antigen-specific lymphocytes.

Previous studies have shown that dextran B1355 (DEX)- and (4-hydroxy-3-nitrophenyl) acetyl (NP)-coupled antigens triggered, respectively, BALB/c and C57BL/6 (B6) lymphocytes in which the V lambda 1 gene and a specific VH gene (VHDEX and VHNPb) have functionally rearranged. In this paper, we studied whether the closely-related V lambda 2 gene can be utilized in association with these VH genes to generate antigen-specific lymphocytes. We found that the VHDEX gene was restrictedly utilized by the V1 lambda 1 gene to generate anti-DEX lymphocytes, and in contrast, both the V lambda 1 and V lambda 2 genes were utilized together with a VHNPb germline gene to form anti-NP lymphocytes. Southern blot and DNA sequencing of an anti-NP hybridoma confirmed that the germline form of the (186-2) VHNPb gene can be used in association with either the V lambda 1 or V lambda 2 genes.

Animals↗
PubMed1984

Cincinnati Lipid Research Clinic.

A major limitation of the Collaborative Lipid Research Clinic's Family Study and hence, the Princeton School District's Family Study, was the insufficient data gathering relative to environmental influences, particularly nutrient intake, alcohol intake, smoking, habitual physical activity, recent weight gain and loss, etc. (Laskarzewski 1983c). In addition, inadequacies of quantitation of family history further represented major problem areas (Laskarzewski 1982c). Nevertheless, the Princeton School District Family Study had major utility in documenting within-family aggregation of CHD risk factors in children and their young adult parents in an economically variegated, biracial cohort.

Adolescent↗
PubMed1983

Familial hyper- and hypouricemias in random and hyperlipidemic recall cohorts: the Princeton School District Family Study.

Using the Princeton School Family Study, our specific aim was to estimate the prevalence of familial hyper- and hypouricemia, to estimate the proportion of probands' first-degree relatives who were similarly affected, and to evaluate the contribution of diseases, drugs, and alcohol intake (if any) to uric acid levels. We studied 379 probands and a total of 1928 subjects, 125 and 52 black probands from a randomly recalled group, 147 white and 55 black probands from a hyperlipidemic recall (top decile cholesterol and/or triglyceride) group. Familial hyper- and hypouricemias were arbitrarily identified in those kindreds having at least two first-degree relatives in the same decile as the proband, top or bottom respectively, for serum uric acid. No probands had symptomatic gout. Diseases, drugs, and alcohol intake were not consistently associated with aggregations of high and/or low uric acid levels in families, and had little relationship to uric acid levels in individuals. Of the 177 randomly recalled probands, and of the 55 black probands in hyperlipidemic recall familial hyperuricemia, with concurrent primary hyperlipoproteinemia and hypertension. Familial hypouricemia was present in 1 of 125 white and in 1 of 52 randomly recalled black kindreds, and in 3 of 147 white and 3 of 55 hyperlipidemic recall black kindreds. While familial clustering of hyperuricemia was limited, clustering of hypouricemia was much more marked. Seventy-four and 84% respectively of first-degree relatives of hypouricemic white and black probands had uric acid less than the 50th percentile. In randomly recalled probands and their first-degree relatives there were significant inverse partial correlations between uric acid and high density lipoprotein cholesterol. Inverse associations of uric acid with high density lipoprotein cholesterol and the concurrence of hyperlipoproteinemia and hypertension in hyperuricemic families points to the importance of lipoprotein and blood pressure screening in families with asymptomatic hyperuricemia. The potential ramifications of within-family clustering of hypouricemia need to be further assessed in populations, particularly in regards to uric acid nephrolithiasis.

Adolescent↗
PubMed1983

Cell-specific regulation of the c-myc gene by lymphocyte mitogens and platelet-derived growth factor.

We show that c-myc is an inducible gene that is regulated by specific growth signals in a cell-cycle-dependent manner. Specifically, agents that initiate the first phase of a proliferative response in lymphocytes (lipopolysaccharide or Concanavalin A) and fibroblasts (platelet-derived growth factor) induce c-myc mRNA. Within one to three hr after the addition of these mitogens to the appropriate cells, c-myc mRNA concentration is increased between 10- and 40-fold. This induction of c-myc mRNA occurs in the presence of cycloheximide and, therefore, does not require the synthesis of new protein species. Consequently, the induction of c-myc mRNA is not secondary to growth. In addition, c-myc mRNA is "superinduced" by the combination of cycloheximide and mitogen, a finding consistent with a model that a labile protein may regulate c-myc levels in these cells. Further, this work suggests a regulatory linkage between the function of two oncogenes--c-myc and c-sis--the latter being the putative structural gene for PDGF.

Animals↗
PubMed1983

Familial obesity and leanness.

Using the Princeton School District Family Study cohort, our specific aim was to estimate the prevalence of suspected familial ponderosity and leanness, to provide empirical risk estimates for the proportion of probands' first-degree relatives who were similarly affected, and to estimate the contributions of diseases, drugs and caloric intake to relative obesity and leanness. We studied 379 probands, 125 whites and 52 blacks from a random recall group, 147 whites and 55 blacks from a hyperlipidemic recall group. Suspected familial obesity and leanness were arbitrarily identified in those kindreds with at least two first-degree relatives in the same Quetelet index decile as the proband, top or bottom respectively. Suspected familial obesity was observed in 2.4 percent and 6 percent respectively of random and hyperlipidemic recall group whites. Suspected familial leanness was identified in 2.4 percent and 1.4 percent of random and hyperlipidemic recall whites and in 3.8 percent of randomly recalled blacks. Approximately twice as many as expected white first-degree relatives of top Quetelet index decile probands themselves had top decile Quetelet indices; approximately three times as many as expected first-degree relatives of bottom decile Quetelet index probands themselves had bottom decile Quetelet indices. Nineteen percent and 31 percent of top decile Quetelet index white probands from random and hyperlipidemic recall groups came from families where at least two other first-degree relatives were similarly obese; 18 percent and 20 percent of white random and hyperlipidemic recall group probands with bottom decile Quetelet indices had suspected familial leanness. Nearly all subjects with familial obesity or leanness had no overt metabolic or pharmacological explanations for their body habitus. Within-family clustering of hypertension was common in kindreds with suspected familial obesity and was absent in kindreds with suspected familial leanness. Marked within-family clustering of both obesity and leanness is useful diagnostically; therapeutic intervention to reduce obesity, to be most effective, should be family-wide in the many kindreds which share familial obesity.

Adolescent↗
PubMed1982

The Clinical Lipid Research Clinic Family Study: familial determinants of plasma uric acid.

Commingling analysis of plasma uric acid levels in a random sample of 160 nuclear families supports the hypothesis that there is a mixture of three distributions. Assuming one, two, and three components in the underlying distribution, we obtained the corresponding p-values (for power transformation) as 0.059, 1.040, and 1.643, respectively. Path analysis with p = 0.059, 1.040, and 1.643 respectively. Path analysis with p = 0.059 gives genetic (h2) and cultural (c2) heritabilities as 0.256 and 0.199, without much support for intergenerational differences, assortative mating, or maternal effects. Complex segregation analysis with p = 0.059 supports multifactorial inheritance, consistent with the findings of Gulbrandsen et al. (1979) and Morton (1979) in other populations. This study also fails to support a major locus hypothesis, contrary to earlier reports.

Adolescent↗