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Biomedical subjects

D J Harnick

Publications and source records attributed to D J Harnick.

15 recordsLinked to original sources

Platelet glycoprotein IIb/IIIa inhibitors for acute coronary syndromes: initiate treatment early or wait for the catheterization laboratory?

Treatment of patients with acute coronary syndromes (ACS) incorporates several approaches to reverse or mitigate the thrombus, which invariably is at the center of the pathophysiologic process of ACS. Pharmacologic and mechanical strategies are designed to prevent death, reduce myocardial necrosis, and stabilize the plaque to prevent later sequelae. Conventional antithrombotic therapy includes antiplatelet and anticoagulant drugs. Medications that inhibit the platelet glycoprotein IIb/IIIa receptor have been shown to be especially efficacious in the treatment of ACS. Recent clinical trials have validated a strategy of aggressive revascularization, particularly catheter-based percutaneous procedures. This review summarizes new trial results and provides a working algorithm for care of the patient with ACS.

Angina, Unstable↗

Effects of practice setting on quality of lipid-lowering management in patients with coronary artery disease.

We undertook a study to determine whether there were differences in the quality of lipid management in patients with coronary artery disease (CAD) in 2 different practice settings (which represent different socioeconomic classes), and to determine the level of compliance with the National Cholesterol Education Program guidelines by academic physicians in managing patients with CAD. A retrospective cross-sectional study was performed using a systematic chart review of 270 medical records (131 from the cardiology clinic, 139 from the cardiology private practice) of patients with known CAD at an academic tertiary care center in New York City. The total proportion of patients with CAD having a lipid profile ordered in the clinic and private suite was 43%. Of these people, 22% had a low-density lipoprotein cholesterol (LDL) < or = 100 mg/dl and 54% had an LDL < or = 130 mg/dl (10% and 23% of the total population, respectively). The total proportion of patients taking lipid-lowering medications was 29%. When comparing the quality of treatment between the 2 settings, there were no statistically significant differences in the percentages of patients who had lipid profiles measured (40% clinic vs 47% private suite, p >0.10), in the percentage of patients with LDL < or = 130 mg/dl (50% clinic vs 57% private suite, p >0.10) or in the weighted percentage of patients taking lipid-lowering medications (29% clinic vs 48% private suite, p = 0.099). The performances of individual physicians, however, varied widely. The percentages of patients with lipid profiles measured by individual physicians ranged from 0% to 83%, while the percentages of patients on drug treatment by a physician ranged between 10% and 88%. These findings indicate that socioeconomic differences, represented by different practice settings, do not account for differences in the screening for, control of, or use of medications in managing hyperlipidemia. Rather, individual physicians are accountable for differences in lipid management.

Age Factors↗

The inositol 1,4,5-trisphosphate receptor is essential for T-cell receptor signaling.

Antigen-specific activation of T lymphocytes, via stimulation of the T-cell antigen receptor (TCR) complex, is marked by a rapid and sustained increase in the concentration of cytoplasmic free Ca2+ ([Ca2+]i). It has been suggested that the second messenger inositol 1,4,5-trisphosphate (IP3) produced after TCR stimulation binds to the IP3 receptor (IP3R), an intracellular Ca(2+)-release channel, and triggers the increase in [Ca2+]i that activates transcription of the gene for T-cell growth factor interleukin 2 (IL-2). However, the role of the IP3R in T-cell signaling and possibly in plasma membrane Ca2+ influx in T cells remains unproven. Stable transfection of T cells (Jurkat) with antisense type 1 IP3R cDNA prevented type 1 IP3R expression, providing a tool for dissecting the role of IP3 signaling during T-cell activation. T cells lacking type 1 IP3R failed to increase [Ca2+]i or produce IL-2 after TCR stimulation. Moreover, depletion of intracellular Ca2+ stores without TCR activation stimulated Ca2+ influx in cells lacking the type 1 IP3R. These results establish that the type 1 IP3R is required for intracellular Ca2+ release that triggers antigen-specific T-cell proliferation but not for plasma membrane Ca2+ influx.

Antigens, CD↗

The human type 1 inositol 1,4,5-trisphosphate receptor from T lymphocytes. Structure, localization, and tyrosine phosphorylation.

Inositol 1,4,5-trisphosphate receptors (IP3R) are intracellular calcium release channels involved in diverse signaling pathways. An IP3R is thought to play a role in mobilizing calcium required for activation of T lymphocytes. The IP3R is a tetrameric structure comprised of four approximately 300-kDa subunits encoded by a approximately 10-kilobase mRNA. In the present study we determined the structure of the human type 1 IP3R expressed in T lymphocytes (Jurkats). The IP3R in human T cells had a predicted molecular mass of 308 kDa and was most similar to the non-neuronal form of the rodent type 1 IP3R. Two putative tyrosine phosphorylation sites were identified, one near the amino terminus and one near the putative channel pore at the carboxyl terminus. During T cell activation the IP3R was tyrosine phosphorylated. A site-specific anti-IP3R antibody was used to localize the carboxyl terminus of the IP3R to the cytoplasm in T cells.

Amino Acid Sequence↗

A multidisciplinary approach to restoring a partially edentulous patient.

A 56-year-old woman had missing teeth, severe bone loss with mobile teeth, an anterior crossbite, collapsed arches, and maxillary midline deviation. She was stabilized periodontally, then a dental implant was placed for anchorage. After selected teeth were extracted, full orthodontic treatment was initiated, and restorative treatment was provided with the implant as an abutment.

Combined Modality Therapy↗