PubMed Health⌕ Search

Biomedical subjects

L N Russek

Publications and source records attributed to L N Russek.

4 recordsLinked to original sources
PubMed2000

Examination and treatment of a patient with hypermobility syndrome.

BACKGROUND AND PURPOSE: The purpose of this case report is to present the patient examination, evaluation/diagnosis/prognosis, intervention, and outcome of a patient with hypermobility syndrome (HMS). Hypermobility syndrome has been widely recognized in the rheumatology literature, but it has seldom been discussed in the orthopedic literature and has only recently been described in the physical therapy literature. The signs and symptoms of HMS are common among patients seen in orthopedic physical therapy clinics; however, the underlying HMS may be overlooked while treating individual joints or tissues causing pain. CSE DESCRIPTION: The patient was a 28-year-old woman with complaints of chronic, multiple-joint pain. After years without a diagnosis, a rheumatologist had recently diagnosed underlying HMS. OUTCOMES: Following intervention that emphasized patient education and activity modification, the patient's complaints decreased. DISCUSSION: Recognition of HMS underlying common orthopedic problems may facilitate appropriate patient education and management.

Adult↗
PubMed1996

Mechanisms for Ca signaling in vascular smooth muscle: resolved from 45Ca uptake and efflux experiments.

Established cell lines are now widely used in experiments concerning vascular smooth muscle (VSM) function; however, considerable evidence suggests that cultured VSM cells are functionally different from VSM cells in intact blood vessels. In order to test the hypothesis that calcium signaling mechanisms are comparable in these two preparations, we developed a new method for high resolution 45Ca efflux studies in A7r5 cells. Briefly, this method involves plating cells in the lumen of a tubular glass efflux chamber and, after loading the cells with 45Ca, perfusing the chamber with a physiological saline solution and collecting the effluent. Using this method we found that the plasma membrane in cultured cells is not rate limiting for calcium efflux, since the efflux curves from both permeabilized and intact cells are kinetically the same. We also found the plasma membrane is not rate limiting in whole aortic segments by using a depolarizing solution followed by dihydropyridine solution. Thus, we demonstrated that the data obtained from cells or tissues with intact membranes reveal information about the intracellular stores (sarcoplasmic reticulum and mitochondria). Combining efflux data with a detailed kinetic model of cellular Ca transport allows least-squares estimation of the rate constants for release and uptake of Ca2+ by intracellular stores with a high degree of confidence (CV < 25%) as well as the Ca2+ contents and transmembrane fluxes associated with these stores. Quantitative comparison of results obtained from A7r5 cells with those we previously obtained for rabbit aortic segments reveals marked similarities and suggests that A7r5 cells serve as excellent model experiments for VSM cell Ca2+ homeostasis.

Animals↗
PubMed1988

Evidence for increased aortic plasma membrane calcium transport caused by experimental atherosclerosis in rabbits.

Several lines of evidence, including the reported ability of calcium channel blockers to prevent atherogenesis in cholesterol-fed rabbits, suggest that calcium mediates one or more of the pathologic changes in atherosclerosis. Moreover, it has long been known that calcium accumulates in atherosclerotic blood vessels. To test the hypothesis that a substantial fraction of this accumulated calcium is intracellular and to identify possible causes of this accumulation, calcium fluxes and contents were determined in aortic segments from cholesterol-fed rabbits and age-matched controls. A new method, based on 45Ca efflux experiments and computer-assisted kinetic analysis, was used to measure intracellular and extracellular calcium contents (nmol calcium/g wet wt tissue) and fluxes. Total intracellular calcium increased from 269 +/- 11.6 to 1,300 +/- 352 nmol/g in cholesterol-fed animals compared with controls (p less than 0.01). This change was sufficient to account for the observed increase in total tissue calcium from 4,190 +/- 211 to 5,240 +/- 477 nmol/g (p less than 0.05). Thus, the fraction of tissue calcium that is intracellular increased significantly from 0.065 +/- 0.006 to 0.223 +/- 0.048 (p less than 0.01) in experimental atherosclerosis. In addition, the data were quantitatively consistent with the hypothesis that these changes are brought about by a 4.8-fold increase in the plasma membrane calcium permeability of aortic smooth muscle cells. These results provide evidence that increased intracellular calcium is a possible mediator of cholesterol-induced atherogenesis.

Animals↗