Biomedical subjects
Publications and source records attributed to T L Snyder.
The use of computers in dentistry has expanded considerably in the last 15 years. Computer software can facilitate practice activities ranging from patient data management and financial management to treatment planning and electronic scheduling. This article addresses strategies for using technology to simplify and improve practice management.
Vascular cell adhesion molecule-1 (VCAM-1) is expressed not only by cytokine-activated endothelium in the kidney, but also by nonvascular cells such as renal tubular epithelial cells (TEC) and mesangial cells (MC). VCAM-1 is upregulated in these cells by the cytokines TNF-alpha, IL-1, and IFN-gamma. We have examined herein the regulation of VCAM-1 expression in TEC and the role played by protein kinase C (PKC). Activation of PKC with phorbol myristate acetate (PMA) or mezerein upregulates VCAM-1 expression by TEC dose-dependently. Maximal stimulation occurs after 6 hr, and declines thereafter. Activation of the protein kinase A pathway with forskolin does not upregulate VCAM-1. The TNF-alpha- and PMA-stimulated VCAM-1 expression is inhibited by the PKC and PKA inhibitor staurosporine (STS). The TNF-alpha-stimulated VCAM-1 expression is also inhibited by the PKC-specific inhibitor calphostin C. Protein synthesis inhibition with cycloheximide (CHX) and blocking of transcription with actinomycin D (ACT D) also inhibits the TNF-alpha and PMA-stimulated upregulation of VCAM-1. The TNF-alpha induced increase in VCAM-1 mRNA levels is blocked with STS and ACT D, but is superinduced with CHX. Thus, the TNF-alpha stimulated renal tubular VCAM-1 expression may involve activation of PKC and is transcriptionally regulated.
The high incidence of corneal ulceration in the alkali-injured rabbit eye can be reduced by topical citrate drops. Citrate interferes with polymorphonuclear leukocyte (PMN) accumulation in the corneal stroma after alkali injury. It inhibits the adherence, locomotion, respiratory burst, phagocytosis, and degranulation of human PMNs in vitro. The objective of this research was to determine if PMN adherence to the vascular endothelium could be inhibited by superfused citrate in vivo. PMN adherence to the endothelium of postcapillary venules in the hamster cheek pouch was greatly enhanced and maintained by addition of leukotriene B4 (LTB4) to the superfusate. Superfusion of the pouch with 24 mM citrate for 5 min, before addition of LTB4, inhibited PMN adherence to the endothelium. The free calcium level in the superfusate was reduced from approximately 650 to 33 microM in the presence of 24 mM citrate. When LTB4-augmented PMN adherence was allowed to occur, followed by citrate treatment (24 mM), it was reversed. Simultaneous addition of CaCl2 and MgCl2 to the superfusate raised the free Ca2+ level to 786 microM and reversed the citrate-induced inhibition of LTB4-augmented adherence. From this and other research, we conclude that citrate probably inhibits adherence of PMNs to pericorneal and conjunctival vessels in the eye, preventing their accumulation in the corneal stroma.
The therapeutic effect of citrate on alkali-burned eyes is thought to be the result of inhibition of PMN activities while ascorbate apparently stimulates the production of new collagen by scorbutic fibroblasts. Attachment of PMNs to the vascular endothelium is the initial PMN response to mediators and must occur before diapedesis and chemotaxis can produce a tissue infiltrate. The present study was undertaken to test the effects of citrate or ascorbate on the in vitro adherence of resting and leukotriene B4 (LTB4)-treated PMNs. Citrate preincubation of resting or LTB4-treated PMNs inhibited adherence in a dose-dependent manner. Inhibition of LTB4 augmented adherence by 12 mM citrate was effectively reversed by the addition of Ca2+ and Mg2+ (6 mM each). Ascorbate had no significant effect on the adherence of resting or LTB4 treated PMNs. In addition we wished to test the effectiveness of the breakdown product(s) from alkali burned collagen (Type 1) as an augmentor of adherence because of its effectiveness as a locomotory and respiratory burst stimulant. These break-down product(s) had no effect on the adherence of resting or LTB4-treated PMNs unless bovine serum albumin (BSA) was omitted from the incubation mixture. In the absence of BSA, these breakdown products inhibited both types of adherence in a dose-dependent manner with dilutions from 1:10 to 1:1000. This inhibition is probably not clinically meaningful since PMN adherence takes place in the vasculature where BSA would always be present. As a consequence of citrate inhibition of adherence in vivo, PMNs would be denied access to the injury site, trapping them in a resting state within the circulatory system.
Topical citrate has been shown to significantly reduce the severity and incidence of corneal ulceration in alkali-burned rabbit eyes. Subcutaneous injection of citrate significantly reduced the severity of ulceration. This study was performed to determine the plasma citrate and ionized calcium levels after systemic administration of citrate. Repeated ingestion of citric acid capsules showed a small increase in the plasma citrate level, but no significant change in the level of ionized serum calcium 30 min after the last ingestion. A single dose of Polycitra-LC (6.672 g of citrate) more than doubled the baseline citrate concentration but only induced a 5% decrease in the level of ionized serum calcium 30 min after ingestion. Neither regimen of orally administered citrate produced any significant effect on the respiratory burst or adherence of in vitro polymorphonuclear leukocytes (PMNs) resuspended in their respective plasma. In comparison studies, higher levels of plasma citrate and lower levels of ionized serum calcium were achieved through plateletpheresis. The respiratory burst and adherence of PMNs were not statistically different from baseline PMNs. However, there was an inverse correlation between the micromolar increase in citrate or the micromolar decrease in calcium and the respiratory burst. These results suggest that the use of oral citrate alone may not be practical, but does not preclude the use of oral citrate as a supplement to topical citrate.
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Water-shock treatment of group A Streptococcus pyogenes released a mixture of nucleotide-like substances and small amounts of protein. The amount of protein was much less than found with osmotic shock of Gram-negative bacteria. In group A S. pyogenes the osmolytes released exhibited as much as a 6-fold change in respect to different growth phases. Osmolyte release was dependent on the stabilization agent used and independent of cellular metabolic activity. The released osmolytes were found to be required for optimal intracellular iodophilic polysaccharide (IPS) storage. Stabilization of washing solutions, and IPS storage medium with metabolically inert non-ionic organic compounds prevented osmolyte loss and enhanced IPS storage. Polyvinyl pyrrolidone and polyethyleneglycol (MW greater than 1000) exhibited the same protective effects as found with calf serum. Smaller non-ionic organic compounds provided similar protective action but the bacteria were more susceptible to osmotic stress.
Calf serum, pooled human plasma, polyvinylpyrollidones (PVP) and polyethylene glycols (PEG) were required as medium components by many cultures of group A.S. pyogenes for intracellular polysaccharide accumulation. These supplements produced a stabilizing effect, probably at the cell surface, and were not associated with nutrition during intracellular iodophilic polysaccharide (IPS) storage. Medium stabilization and the presence of maltose or maltose yielding polysaccharides was found to be a property unique to the group A streptococci. Cariogenic streptococci and Streptococcus agalactive did not require medium stabilization for IPS storage although addition of PVP or PEG was stimulatory. Different degrees of IPS storage in group A.S. pyogenes was found to be strain related and probably dependent on the size and degree of branching of the storage polymer.
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The purpose of this study was to identify correlates of dental anxiety in university students. Dental anxiety was measured by means of the Corah Dental Anxiety Scale. Information about the students' dental attitudes, perceptions, and past dental experiences was collected by a written questionnaire administered to an approximately 13 percent random sample of all full-time students. The response rate was 27.3 percent (n = 846). The mean dental anxiety score for the entire study group was 8.77; mean scores for men (8.44) and women (9.10) were significantly different. Of the 18 independent variables studied, seven were found to be significantly associated with dental anxiety scores: sex, frequency of childhood visits to the dentist, childhood experience with dentists, frequency of mothers' visits to a dentist, perceived number of types of services required, symptoms as reason for last dental visit, and number of preventive actions taken prior day. As a group, the independent variables explained 22.8 percent of the observed variation in dental anxiety scores. When the amount of variation which was explained by each of the independent variables was considered separately four variables were found to be significant: childhood experience with dentists, gender, attitudes toward dentists, and number of preventive actions taken the prior day. Further studies are required to identify additional antecedents of dental anxiety in university students. These studies should focus on the ability of the antecedents to explain observed variation in anxiety levels.
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