The impact of nursing diagnoses in a long-term care setting

Nursing diagnosis as a critical component of the nursing process provides a common taxonomy to describe problems that nurses can treat and is a convenient, logical way to reference nursing standards. Theory is translated into practice with the use of population-specific prototype care guides and a written orders system. Nurses in leadership are responsible for providing the necessary resources to promote professional growth and facilitate desired change. Recommendations to assist with the implementation of nursing diagnosis are identified in Table 1. The system is dependent on staff nurses' professional commitment to learning and willingness to actively participate in change. Involvement of staff nurses continues to be a critical factor in the improvement of nursing practice.     

The effect of social learning intervention on metabolic control of insulin-dependent diabetes mellitus in adolescents

This paper reports the results of an experimental study modeled after a study conducted by Kaplan et al. The hypothesis tested was: Adolescents who receive a social learning intervention (SLI) will show greater improvement in metabolic control of their diabetes than will adolescents who receive only traditional diabetes instruction. Thirty-four adolescents between the ages of 12 and 16 who attended a midwestern camp were randomly divided into two groups. Both groups attended a daily 1-hour teaching session about diabetes. Later each day, the experimental group received an SLI consisting of role modeling to help the subjects circumvent peer pressure. To determine metabolic control, HbA1 values were determined before and 3 1/2 months after the intervention. The control group showed no significant difference in HbA1 values, while the experimental group showed a decrease in metabolic control.     

Inhibition and reversal of platelet-rich arterial thrombus in vivo: direct vs. indirect factor Xa inhibition

BACKGROUND/OBJECTIVE: The efficacy of a direct factor (F)Xa inhibitor, ZK-807834, was compared with indirect inhibition by enoxaparin for inhibition and deaggregation of acute platelet-rich thrombi in a well-characterized porcine carotid injury model. METHODS: A crush injury was performed on a randomly chosen carotid artery and the thrombus allowed to propagate for 30 min. Pigs then received intravenous drug for 35 min: ZK-807834-Dose 1 (40 microg kg(-1) bolus + 1.5 microg kg(-1) min(-1) infusion, n=6); ZK-807834-Dose 2 (20 microg kg(-1) bolus + 0.75 microg kg(-1) min(-1) infusion; n=6); enoxaparin (1 mg kg(-1) bolus; n=6); or saline (n=6). Five minutes after drug initiation, the contralateral artery was injured. Thrombus size was monitored by scintillation detection of autologous 111In-platelets. RESULTS: The prothrombin time ratio was 2.2 +/- 0.1; 1.4 +/- 0.3; 1.2 +/- 0.9 and 1.1 +/- 0.2, respectively. ZK-807834-Dose 1 significantly inhibited carotid platelet deposition (525 +/- 226 x 10(6) cm(-2); P = 0.008), whereas ZK-807834-Dose 2 (2325 +/- 768) and enoxaparin (1236 +/- 383) were not different from saline (2776 +/- 642). Thrombus deaggregation was greatest for animals receiving ZK-807834-Dose 1 (473 +/- 185). Neither ZK-807834-Dose 2 (1588 +/- 480) nor enoxaparin (1618 +/- 686) was different from saline control (2222 +/- 598). CONCLUSIONS: Direct FXa inhibition with ZK-807834, at a prothrombin time ratio of 2.2, effectively inhibits thrombosis and promptly deaggregates thrombi induced by arterial injury. In contrast, indirect FXa inhibition with enoxaparin was ineffective.     

Immunity against the opportunistic fungal pathogen Pneumocystis.

Species of the genus Pneumocystis exist as opportunistic fungal pathogens and are associated with severe pneumonia and pulmonary complications in immunocompromised individuals. Although prophylactic therapy for Pneumocystis has significantly decreased the overall incidence of infection, more than 80% of cases in current patient populations are considered breakthrough cases. In the HIV-infected population, in the years following the initiation of highly active antiretroviral therapy (HAART), significant reductions in the incidence of Pneumocystis infection were observed, although trends over the last several years suggest that the incidence of Pneumocystis has plateaued rather than decreased. Furthermore, with the more prominent usage of immunosuppressive therapies, the frequency of Pneumocystis infection in the HIV-negative population, such as those with hematologic malignancies and those who have undergone transplantation, has risen significantly. Investigating host defense mechanisms against P. carinii has historically been problematic due to the difficulty in achieving continuous in vitro propagation of proliferating Pneumocytis organisms. Nevertheless, clinical and experimental studies have documented that host defense against Pneumocystis involves a concerted effort between innate, cell-mediated (T lymphocyte) and humoral (B lymphocyte) responses. However, the pulmonary environment is a tissue site where heightened inflammatory responses can often lead to inflammation-mediated injury, thereby contributing to the pathogenesis of Pneumocystis infection. Accordingly, clearance of Pneumocystis from the pulmonary environment is dependent on a delicate equilibrium between the inflammatory response and immune-mediated clearance of the organism. Furthermore, innate and adaptive responses against Pneumocystis are strikingly similar to those against other medically-important fungi, thus providing additional evidence that Pneumocystis exists as a fungal organism.     

Developmental Toxicity of Dimethylacetamide by Inhalation in the Rat

Developmental Toxicity of Dimethylacetamide by Inhalation inthe Rat. SOLOMON, H. M., FERENZ, R. L., KENNEDY, G. L., ANDSTAPLES, R. E. (1991). Fundam. Appl. Toxicol. 16, 414–422.Dimethylacetamide (DMAC) is a widely used industrial solvent.It has been reported to be teratogenic when given to rats byinjection or following dermal application. Most of these studiesemployed large single doses and did not examine both the fetaland the maternal response. In this study, groups of pregnantCrl:CD rats were exposed to 32, 100, or 282 ppm DMAC by inhalationfor 6 hr/day from Days 6 through 15 of gestation (day on whichcopulation plug was detected was termed Day 1G). A control groupof chambered pregnant rats was exposed simultaneously to aironly. All female rats were euthanized on Day 21G. At 282 ppm,both maternal weight gain during the exposure period and fetalweight were significantly decreased and accompanied by a significantdose-response trend. These effects were not seen in rats inhalingeither 32 or 100 ppm. Fetal resorptions were not increased inany of the groups exposed to DMAC. Fetal incidences of external,visceral, or skeletal variations and malformations were similarbetween the test and control groups. Therefore, both fetal andmaternal toxicity were noted at 282 ppm and the no-observedadverse-effect level under these experimental conditions was100 ppm for both the dam and the conceptus. DMAC was not demonstratedto produce malformations in the rat fetus even at a level thatwas toxic to the dam.