Restricting restraint use in long-term care.
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Biomedical subjects
Publications and source records attributed to J D Kramer.
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Use of physical restraints in U.S. nursing homes has, historically, been quite high. Myths about restraints, e.g., that they prevent falls and injuries, have helped to perpetuate a practice that almost always results in long-term adverse physical and psychological effects for the resident. Recent federal law has severely restricted the use of physical restraints in nursing homes. Changing this practice of nursing home personnel requires a well thought out process and the cooperation of leaders in the facility. CNSs are uniquely qualified to move a facility toward the goal of reducing the use of restraints. Their skills as leaders, educators, change agents, consultants, and systems experts are most essential.
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The biochemical characterization of dipeptidyl aminopeptidase II activity was investigated in the supernatant of centrifuged homogenates of adult Schistosoma japonicum using a lysine-alanine oligopeptide derivative of 4-methoxy-2-naphthylamide as a substrate. It was observed that the pH optimum of the enzyme is in the acid range, with an optimum at pH 6.3. Time and enzyme concentration studies, along with temperature studies, support the premise that the reaction is enzymatic. The Km was 3.3 X 10(-3) M, at pH 5.5 and 37 C. Tris and diisopropyl phosphofluoridate, when incorporated into the assay system at final concentrations of 500 and 2 mM, respectively, significantly inhibited the reaction by 70.9 and 75%, respectively. Leupeptin (5 X 10(-4) mM) had no effect. The results indicate that the enzyme under study in the present investigation strongly resembles mammalian dipeptidyl aminopeptidase II due to its affinity for substrate, sensitivity to Tris and diisopropyl phosphofluoridate inhibition, and pH optimum. Its inhibition by diisopropyl phosphofluoridate indicates that it may belong to the serine class of proteases. Cytochemical studies revealed reaction product in the lipid-like globules in the gastrodermis, adding further credence that these globules are lysosomal.
We present a case of glycogen storage disease type II (Pompe's disease) with the classical clinical presentation and characteristic electrocardiographic changes of this disorder. An acid maltase (EC 3.2.1.20) determination in the peripheral leukocytes revealed normal activity; however, acid maltase activity was completely absent in a pre-mortem skeletal muscle biopsy. Post-mortem studies showed acid maltase activity to be absent in all tissues examined, including cultured skin fibroblasts. Massive glycogen deposition corresponded to the localization of the enzymic deficiency, except in the brain, where glycogen content was within the normal range. The acid maltase activity in mixed peripheral leukocytes was due to an isoenzyme of acid maltase in the granulocyte series. Antenatal diagnosis was accurate in a subsequent pregnancy, but discordance between enzyme activity in different cell lines in an individual with a genetic disease is a conceivable source of error in both prenatal and postnatal diagnoses.
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Cytochromes P450 (P450s) constitute a superfamily of phase I enzymes capable of oxidizing and reducing various substrates. P450 2D6 is a polymorphic enzyme, which is absent in 5-9% of the Caucasian population as a result of a recessive inheritance of gene mutations. This deficiency leads to impaired metabolism of a variety of drugs. All drugs metabolized by P450 2D6 contain a basic nitrogen atom, and a flat hydrophobic region coplanar to the oxidation site which is either 5 or 7 A away from the basic nitrogen atom. The aim of this study was to build a three-dimensional structure for the protein and more specifically for the active site of P450 2D6 in order to determine the amino acid residues possibly responsible for binding and/ or catalytic activity. Furthermore, the structural features of the active site can be implemented into the existing small molecule substrate model, thus enhancing its predictive value with respect to possible metabolism by P450 2D6. As no crystal structures are yet available for membrane-bound P450s (such as P450 2D6), the crystal structures of bacterial (soluble) P450 101 (P450cam), P450 102 (P450BM3), and P450 108 (P450terp) have been used to build a three-dimensional model for P450 2D6 with molecular modeling techniques. Several important P450 2D6 substrates were consecutively docked into the active site of the protein model. The energy optimized positions of the substrates in the protein agreed well with the original relative positions of the substrates within the substrate model. This confirms the usefulness of small molecule models in the absence of structural protein data. Furthermore, the derived protein model indicates new leads for experimental validation and extension of the substrate model.
OBJECTIVE: To examine the associations among selected patient, wound, and treatment factors and healing in pressure ulcers. DESIGN: Nonexperimental, retrospective study using data extracted from charts of patients having a Stage II, III, or IV pressure ulcer between July 1994 and November 1996. SETTING: A long-term-care facility associated with a major metropolitan medical center. RESULTS: Evidence of healing was significantly associated with patient weight (P < .05) and negatively associated with body temperature (P < .05), time on a pressure-relieving bed (P < .05), amount of exudate (P < .001), and stage of pressure ulcer (P < .001). In a regression analysis, pressure ulcer stage, patient weight, and mean body temperature explained 25% of the variability in healing; specifically, lower pressure ulcer stage, higher patient weight, and lower mean body temperature predicted improved healing. Healing was not predicted by chronologic age, pressure ulcer location, number of illnesses, use of tube feedings, use of pressure-relieving beds, mean arterial pressure, or Braden Scale score. In a regression analysis of patient factors alone, lower body temperature and higher weight together predicted 9% of the variance in healing. When wound variables were analyzed, 19% of the variability in healing was explained by the stage of the pressure ulcer. Of the treatment variables, only shorter time on a pressure-relieving bed predicted healing, explaining 6% of the variance. CONCLUSIONS: Strategies for healing pressure ulcers in nursing home patients should include programs for early recognition of pressure injury and prevention of pressure ulcer progression to higher stages; attention to weight gain and/or weight maintenance in at-risk patients; and early recognition and treatment of infections and febrile episodes.