The Effect on Nausea and Vomiting of Structured Education Given to Male Lung Cancer Patients Receiving Chemotherapy.

The objective of this study was to investigate the effect on nausea and vomiting of structured education given to male lung cancer patients receiving chemotherapy. This quasi-experimental research study had pre- and post-tests control groups. The estimated sample size was at least 20 subjects per group. Data were collected in the chest diseases clinic and outpatient chemotherapy unit of a university hospital in Turkey. An education booklet and structured education were given 30 mins for each patient before chemotherapy. In post-test 1, nausea severity was significantly lower in the experimental group than in the control group (mean difference - 2.50, 95% CI - 1.46 to - 0.17, d = 0.82, p = 0.05). This was also the case in post-test 2 (mean difference - 2.10, 95% CI - 1.50 to - 0.21, d = 0.85, p = 0.01). According to this, the sizes of Cohen's d effect were large (0.82 and 0.85 for post-test 1 and post-test 2 respectively). However, vomiting frequency did not differ significantly between the experimental group and the control group in either post-test 1 or post-test 2 (p > 0.05). Structured education given by nurses had a positive effect on the severity of nausea. Nurses may be able to raise nausea management in cancer patients to a better level by education intervention.

Heat shock but not cold shock leads to disturbed intracellular zinc homeostasis.

The heat shock response is a highly conserved process essential for surviving environmental stress, including extremes of temperature. To investigate whether heat shock has an impact on intracellular Zn(2+) homeostasis, cells were subjected to heat shock, and subsequently the intracellular free zinc concentration was investigated. Sublethal heat shock induced a temperature-dependent and transient intracellular Zn(2+) release that was repeatable after 24 h. The free zinc was localized in round-shaped nuclear bodies identified as nucleoli. Metallothionein, the main cellular zinc storing protein, was found to be not functionally essential for this heat-shock-induced effect. No significant oxidative stress within the cells was detected after heat shock. Cold shock and subsequent rewarming did not result in disturbed intracellular zinc homeostasis. These results show that heat shock and cold shock differ with respect to intracellular Zn(2+) release. A role for zinc as signaling ion during fever is conceivable.

Impaired glomerular maturation and lack of VEGF165b in Denys-Drash syndrome.

Individuals with Denys-Drash syndrome (DDS) develop diffuse mesangial sclerosis, ultimately leading to renal failure. The disease is caused by mutations that affect the zinc finger structure of the Wilms' tumor protein (WT1), but the mechanisms whereby these mutations result in glomerulosclerosis remain largely obscure. How WT1 regulates genes is likely to be complex, because it has multiple splice forms, binds both DNA and RNA, and associates with spliceosomes. Herein is described that in DDS podocytes, the ratio of both WT1 +KTS isoforms C to D differs considerably from that of normal child and adult control podocytes and more closely resembles fetal profiles. Aside from the delay in podocyte maturation, DDS glomeruli show swollen endothelial cells, reminiscent of endotheliosis, together with incompletely fused capillary basement membranes; a dramatic decrease in collagen alpha4(IV) and laminin beta2 chains; and the presence of immature or activated mesangial cells that express alpha-smooth muscle actin. Because appropriate vascular endothelial growth factor A (VEGF-A) expression is known to be essential for the development and maintenance of glomerular architecture and function, this article addresses the question of whether VEGF-A expression is deregulated in DDS. The data presented here show that DDS podocytes express high levels of the proangiogenic isoform VEGF165, but completely lack the inhibitory isoform VEGF165b. The VEGF165/VEGF165b ratio in DDS resembles that of fetal S-shaped bodies, rather than that of normal child or adult control subjects. The alteration in VEGF-A expression presented here may provide a mechanistic insight into the pathogenesis of DDS.