Biomedical subjects

K L Hayes

Publications and source records attributed to K L Hayes.

6 recordsLinked to original sources

PubMed2001

Training status and interest in certification of nondiplomate faculty teaching predoctoral dental public health.

OBJECTIVES: A survey was conducted to better understand the training needs of faculty members without dental public health (DPH) specialty board certification who teach DPH to dental students. METHODS: An 11-item questionnaire was sent to 193 non-DPH diplomate faculty members at US dental schools who were dentists and at least one of the following: a member of the American Association of Dental Schools Community and Preventive Dentistry Section, a referral from an academic American Board of Dental Public Health diplomate, a DPH faculty listed on the school's Web pages, a DPH contact from the AADS Institutional Directory, or the school's dean if no other contact. RESULTS: A 70 percent response rate was obtained. Seventy-nine percent of the respondents taught at least one national board-related DPH topic. Among these faculty members, 67 percent have or are in training for the master of public health, 26 percent have completed or are in a DPH residency, and 63 percent desire training in one or more of the DPH topics. The majority (64%) does not plan to take the specialty exam, while 28 percent plan to take the exam within five years. About half reported no personal incentives to take the exam and 39 percent perceived no institutional incentives. CONCLUSIONS: These nondiplomate teachers of predoctoral DPH desire training, but appear to have barriers and perceive few benefits to achieving DPH board certification.

Attitude of Health Personnel↗

PubMed1999

The platelet high affinity binding site for thrombin mimics hirudin, modulates thrombin-induced platelet activation, and is distinct from the glycoprotein Ib-IX-V complex.

The platelet high affinity binding site for thrombin appears to be described by a classical receptor-ligand interaction that is distinct from the platelet thrombin receptor/substrate, PAR-1. However, the identification and function of the high affinity binding site with respect to its physiological importance have continued to elude investigators. Prior studies using two mutant thrombins suggested that thrombin interaction with the platelet high affinity binding site is mediated through an extensive portion of the thrombin molecule involving residues within the substrate binding pocket and the anion binding exosite (Leong, L., Henriksen, R. A., Kermode, J. C., Rittenhouse, S. E., and Tracy, P. B. (1992) Biochemistry 31, 2567-2575) and may mimic a thrombin-hirudin interaction. To test this hypothesis, an anti-hirudin peptide antibody (anti-hirpeptide Ab) was raised against a peptide mimicking the COOH terminus of hirudin. The Ab recognized adherent platelets and those in suspension as determined by enzyme-linked immunosorbent assay and immunofluorescence microscopy, respectively. 125I-Thrombin binding to platelets was inhibited in the presence of the anti-hirpeptide Ab in a dose-dependent manner with maximal inhibition >90%. Analyses of data from binding studies of 125I-thrombin to platelets at a fixed Ab concentration indicated that the anti-hirpeptide Ab inhibited the high affinity binding interaction exclusively. In addition, thrombin-induced increases in platelet [Ca2+]i were enhanced by blocking the high affinity binding site with the Ab due to redistribution of the agonist to PAR-1. Thrombin Quick I-induced platelet calcium mobilization was unaffected by the presence of the Ab, consistent with the inability of thrombin Quick I to bind to the high affinity site. Even though glycoprotein (GP) Ib contains a hirudin-like region within the alpha subunit, the postulated high affinity binding site, direct binding of 125I-thrombin could not be demonstrated to transfected Chinese hamster ovary and L cells expressing the GP Ib-IX-V complex. Furthermore, an anti-GP Ib Ab, raised to the peptide region proposed as the thrombin high affinity site, did not enhance thrombin-induced platelet calcium mobilization. The anti-hirpeptide Ab recognized a population of platelet membrane proteins distinct from PAR-1 and GP Ib by three-color immunofluorescence using confocal microscopy. These combined studies demonstrate that the high affinity binding site for thrombin is a unique platelet protein distinct from GP Ib which modulates the effective thrombin concentration localized at the human platelet surface.

Amino Acid Sequence↗

PubMed1998

Academic dental public health diplomates: their distribution and recommendations concerning the predoctoral dental public health faculty.

OBJECTIVE: The purpose of this study was to assess the representation of academically based diplomates of the American Board of Dental Public Health (ABDPH) and to identify their perceptions on the training of dental public health predoctoral faculty. METHODS: Data were collected by a mailed, self-administered, 13-item questionnaire. The population was the 48 diplomates of the ABDPH as of March 1997 associated with academic institutions. RESULTS: Twenty of the 55 US dental schools had a diplomate of the ABDPH with a mean of 1.8 diplomates per school with a diplomate. An average of 4.5 full-time faculty members per school were associated with teaching dental public health. A master's degree in public health (MPH) was the most frequently suggested educational requirement for dental public health faculty. Continuing education courses were training needs perceived for dental public health faculty. The lack of time, money, and incentives, along with perceived rigidity of requirements for board certification, were reported as major barriers for faculty becoming dental public health board certified. CONCLUSIONS: Numerous challenges confront the development of a strong dental public health presence in US dental schools. These challenges include, among others, insufficient numbers of academic dental public health specialists and insufficient motivations to encourage promising candidates to pursue specialty status.

Attitude of Health Personnel↗

PubMed1998

Linking postdoctoral general dentistry programs with managed care programs and settings.

This report presents the results of a small workgroup convened by the American Association of Dental Schools to examine experiences related to postdoctoral general dentistry programs linked with managed care systems and clinical settings. The workgroup was a component of an Association effort to identify and promote innovative and nontraditional methods by which the number of postdoctoral general dentistry (PGD) positions can be increased to meet current demand for PGD education. The participants identified factors and conditions that they believed to be critical to the planning, development, and conduct of PGD programs with substantial linkages with managed care systems and settings. The information should be helpful to others as they consider opportunities to establish PGD programs or increase their number of PGD training positions.

Academic Medical Centers↗

PubMed1997

General dentistry grant program: 1976-1996.

The federal general dentistry grant program supports the development of new programs and first-year positions in postdoctoral general dentistry (PGD) education. One hundred and fifteen institutions have participated in the grant program since awards were first made in 1978. The grant program assisted in establishing 59 new PGD programs and 560 new positions. Eighty-eight percent of the new programs are still in operation; 69 percent of the positions are still being filled. These retained programs and positions represent 72 percent and 77 percent of the net growth in PGD programs and positions, respectively, that has occurred since 1977.

Education, Dental, Graduate↗

PubMed1994

alpha-Thrombin-induced human platelet activation results solely from formation of a specific enzyme-substrate complex.

Prior studies using the mutant thrombin, thrombin Quick I, indicate that this protease induces maximum platelet aggregation and intraplatelet [Ca2+] fluxes at agonist concentrations where dissociable, equilibrium platelet binding is undetectable and led to the conclusion that thrombin interaction with its platelet "receptor" is best described kinetically by formation of an enzyme-substrate complex. This conclusion was substantiated further in the present studies by demonstrating that both thrombin Quick I and thrombin mimicked the thrombin receptor agonist peptide in the induction of the platelet activation-dependent events required for functional Prothrombinase assembly and that a rabbit antibody raised against KATNATLDPRSFLLR, a pentadecapeptide which represents amino acids 32-46 in the platelet thrombin receptor/substrate and spans the thrombin cleavage site, inhibited both thrombin- and thrombin Quick I-induced platelet activation responses equivalently. The antipeptide antibody had a more pronounced inhibitory effect on the rate of the thrombin-induced response rather than the magnitude of the response suggesting competition for the cleavage site, consistent with the observation that pretreatment of metabolically-inhibited platelets with thrombin, which was removed by washing, eliminated specific antibody binding due to removal and/or masking of antibody epitopes. Concentrations of the antipeptide antibody that inhibited thrombin- and thrombin Quick I-induced increases in intracellular [Ca2+] flux by as much as 97% did not alter the dissociable equilibrium binding of 125-I-FPR-thrombin to platelets. These combined data indicate that the hydrolytic event initiated by thrombin or thrombin Quick I interaction with the platelet receptor/substrate for thrombin is unrelated to the dissociable equilibrium binding of thrombin to membrane sites described previously by classical receptor-ligand binding analyses.

Amino Acid Sequence↗