An Interventional Study on the Effects of Pressure Ulcer Education on Jordanian Registered Nurses’ Knowledge and Practice

AbstractBACKGROUND: Pressure ulcers (PUs) are health problems that resulted in human suffering, pain, disfigurement, loss of productive time, and financial burden. Despite the fact that PU is largely preventable (Elliott, McKinley & Fox, 2008) and recent advances in health care, PU rates are significantly increased in health care facilities (EPUAP, 2009). PURPOSE: The current study examined the effects of pressure ulcer education program on nurses’ knowledge, practices, attitudes and intentions towards PU prevention and treatment. METHODS: Interventional approach using before-after test design was used. Two hundred and twenty nurses were randomly selected from eight hospitals in Jordan. Nurses’ knowledge and practice about PU was measured by PU knowledge and practice test based on EPUAP guidelines and Beeckman et al. (2011), while attitudes and intentions were measured using scales. RESULTS: The study revealed that nurses’ knowledge, practices, attitudes and intentions were improved towards PU prevention and treatment. Demographic variables such as gender and years of experience were influential in relation to nurses’ knowledge, practices, attitudes and intentions towards PU prevention and treatment. Results also showed lack of accurate information about PU management among nurses and positive nurses’ attitudes toward PU prevention and treatment. CONCLUSION: A PU education program is a powerful tool for nurses. It provides an opportunity to improve understanding of PU, keep abreast of current knowledge on PU, and eliminate patient's suffering. Additionally, PU education programs can help nurses to acquire professional attitudes that will enable them to improve quality of nursing care

Dietary alterations modulate the microRNA 29/30 and IGF-1/AKT signaling axis in breast Cancer liver metastasis.

Background: Metastatic cancer is incurable and understanding the molecular underpinnings is crucial to improving survival for our patients. The IGF-1/Akt signaling pathway is often impaired in cancer leading to its progression and metastases. Diet modification is known to alter the IGF-1/Akt pathway and affect the expression of microRNA involved in tumor initiation, growth and metastases. Liver metastases are one of the most common type of metastases in breast and colon cancer. In the present study, we looked at the effect of diet modification on the expression of microRNA in normal liver and liver with breast cancer metastases using in vivo model. Methodology: 6-month-old C57BL/6 J mice were put on either an ad libitum (AL) diet, or 40% calorie restricted (CR) diet or were fasted for 24 h (FA) before sacrifice. MicroRNA array analysis, western blot and qRT-PCR were performed using liver tissue to compare the treatment groups. A breast cancer model was also used to study the changes in microRNA expression in liver of a group of BALB/c mice orthotopically injected with 4 T1 cells in the mammary fat pad, put on either an AL or 30% CR diet. Liver and primary tumor tissues were used to perform qRT-PCR to compare the treatment groups. Results: MicroRNA array analysis showed significant changes in miRNA expression in both CR and FA conditions in normal liver. Expression of miR-29 and miR-30 family members was increased in both CR and FA. Western blot analysis of the normal liver tissue showed that CR and FA downregulated the IGF-1/Akt pathway and qRT-PCR showed that the expression of miR-29b, miR-29c, miR-30a and miR-30b were increased with CR and FA. Liver tissue collected from mice in the breast cancer model showed an increase in expression of miR-29b, miR-29c and miR-30b while tumor tissue showed increased expression of miR-29c, miR-30a and miR-30b. Discussion: Members of the miR-29 family are known to target and suppress IGF-1, while members of the miR-30 family are known to target and suppress both IGF-1 and IGF-1R. In the present study, we observe that calorie restriction increased the expression of miR-29 and miR-30 in both the normal liver as well as the liver with breast cancer metastases. These findings suggest that dietary alterations may play a role in the treatment of liver metastasis, which should be evaluated further

Obligatory role for phosphatidylinositol 4,5-bisphosphate in activation of native TRPC1 store-operated channels in vascular myocytes

In the present study the effect of phosphatidylinositol 4,5-bisphosphate (PIP2) was studied on a native TRPC1 store-operated channel (SOC) in freshly dispersed rabbit portal vein myocytes. Application of diC8-PIP2, a water soluble form of PIP2, to quiescent inside-out patches evoked single channel currents with a unitary conductance of 1.9 pS. DiC8-PIP2-evoked channel currents were inhibited by anti-TRPC1 antibodies and these characteristics are identical to SOCs evoked by cyclopiazonic acid (CPA) and BAPTA-AM. SOCs stimulated by CPA, BAPTA-AM and the phorbol ester phorbol 12,13-dibutyrate (PDBu) were reduced by anti-PIP2 antibodies and by depletion of tissue PIP2 levels by pre-treatment of preparations with wortmannin and LY294002. However, these reagents did not alter the ability of PIP2 to activate SOCs in inside-out patches. Co-immunoprecipitation techniques demonstrated association between TRPC1 and PIP2 at rest, which was greatly decreased by wortmannin and LY294002. Pre-treatment of cells with PDBu, which activates protein kinase C (PKC), augmented SOC activation by PIP2 whereas the PKC inhibitor chelerythrine decreased SOC stimulation by PIP2. Co-immunoprecipitation experiments provide evidence that PKC-dependent phosphorylation of TRPC1 occurs constitutively and was increased by CPA and PDBu but decreased by chelerythrine. These novel results show that PIP2 can activate TRPC1 SOCs in native vascular myocytes and plays an important role in SOC activation by CPA, BAPTA-AM and PDBu. Moreover, the permissive role of PIP2 in SOC activation requires PKC-dependent phosphorylation of TRPC1

Activation of native TRPC1/C5/C6 channels by endothelin-1 is mediated by both PIP3 and PIP2 in rabbit coronary artery myocytes

We investigate activation mechanisms of native TRPC1/C5/C6 channels (termed TRPC1 channels) by stimulation of endothelin-1 (ET-1) receptor subtypes in freshly dispersed rabbit coronary artery myocytes using single channel recording and immunoprecipitation techniques. ET-1 evoked non-selective cation channel currents with a unitary conductance of 2.6 pS which were not inhibited by either ET(A) or ET(B) receptor antagonists, respectively BQ-123 and BQ788, when administered separately. However, in the presence of both antagonists, ET-1-evoked channel activity was abolished indicating that both ET(A) and ET(B) receptor stimulation activate this conductance. Stimulation of both ET(A) and ET(B) receptors evoked channel activity which was inhibited by the protein kinase C (PKC) inhibitor chelerythrine and by anti-TRPC1 antibodies indicating that activation of both receptor subtypes causes TRPC1 channel activation by a PKC-dependent mechanism. ET(A) receptor-mediated TRPC1 channel activity was selectively inhibited by phosphoinositol-3-kinase (PI-3-kinase) inhibitors wortmannin (50 nm) and PI-828 and by antibodies raised against phosphoinositol-3,4,5-trisphosphate (PIP(3)), the product of PI-3-kinase-mediated phosphorylation of phosphatidylinositol 4,5-bisphosphate (PIP(2)). Moreover, exogenous application of diC8-PIP(3) stimulated PKC-dependent TRPC1 channel activity. These results indicate that stimulation of ET(A) receptors evokes PKC-dependent TRPC1 channel activity through activation of PI-3-kinase and generation of PIP(3). In contrast, ET(B) receptor-mediated TRPC1 channel activity was inhibited by the PI-phospholipase C (PI-PLC) inhibitor U73122. 1-Oleoyl-2-acetyl-sn-glycerol (OAG), an analogue of diacylglycerol (DAG), which is a product of PI-PLC, also activated PKC-dependent TRPC1 channel activity. OAG-induced TRPC1 channel activity was inhibited by anti-phosphoinositol-4,5-bisphosphate (PIP(2)) antibodies and high concentrations of wortmannin (20 μm) which depleted tissue PIP(2) levels. In addition exogenous application of diC8-PIP(2) activated PKC-dependent TRPC1 channel activity. These data indicate that stimulation of ET(B) receptors evokes PKC-dependent TRPC1 activity through PI-PLC-mediated generation of DAG and requires a permissive role of PIP(2). In conclusion, we provide the first evidence that stimulation of ET(A) and ET(B) receptors activate native PKC-dependent TRPC1 channels through two distinct phospholipids pathways involving a novel action of PIP(3), in addition to PIP(2), in rabbit coronary artery myocytes

Kinetic and inhibition studies on human Jumonji-C (JmjC) domain-containing protein 5

Jumonji-C (JmjC) domain-containing protein 5 (JMJD5) is a human 2-oxoglutarate (2OG) and Fe(II)-dependent oxygenase which catalyses the post-translational C3 hydroxylation of arginyl-residues and which is linked to the circadian rhythm and to cancer biology through as yet unidentified mechanisms. We report robust solid phase extraction coupled to mass spectrometry (SPE-MS)-based JMJD5 assays which enable kinetic and high-throughput inhibition studies. The kinetic studies reveal that some synthetic 2OG derivatives, notably including a 2OG derivative with a cyclic carbon backbone (i.e. (1R)-3-(carboxycarbonyl)cyclopentane-1-carboxylic acid), are efficient alternative cosubstrates of JMJD5 and of factor inhibiting hypoxia-inducible transcription factor HIF-α (FIH), but not of the Jumonji-C (JmjC) histone Nε-methyl lysine demethylase KDM4E, apparently reflecting the closer structural similarity of JMJD5 and FIH. The JMJD5 inhibition assays were validated by investigating the effect of reported 2OG oxygenase inhibitors on JMJD5 catalysis; the results reveal that broad-spectrum 2OG oxygenase inhibitors are also efficient JMJD5 inhibitors (e.g. N-oxalylglycine, pyridine-2,4-dicarboxylic acid, ebselen) whereas most 2OG oxygenase inhibitors that are in clinical use (e.g. roxadustat) do not inhibit JMJD5. The SPE-MS assays will help enable the development of efficient and selective JMJD5 inhibitors for investigating the biochemical functions of JMJD5 in cellular studies

Essential Role of Sperm-Specific PLC-Zeta in Egg Activation and Male Factor Infertility: An Update.

Sperm-specific phospholipase C zeta (PLCζ) is widely considered to be the physiological stimulus responsible for generating calcium (Ca) oscillations that induce egg activation and early embryonic development during mammalian fertilization. In the mammalian testis, PLCζ expression is detected at spermiogenesis following elongated spermatid differentiation. Sperm-delivered PLCζ induces Ca release via the inositol 1,4,5-trisphosphate (InsP) signaling pathway. PLCζ is the smallest known mammalian PLC isoform identified to date, with the simplest domain organization. However, the distinctive biochemical properties of PLCζ compared with other PLC isoforms contribute to its unique potency in stimulating cytosolic Ca oscillations within mammalian eggs. Moreover, studies describing PLCζ "knockout" mouse phenotypes confirm the supreme importance of PLCζ at egg activation and monospermic fertilization in mice. Importantly, a number of clinical reports have highlighted the crucial importance of PLCζ in human fertilization by associating PLCζ deficiencies with certain forms of male factor infertility. Herein, we give an update on recent advances that have refined our understanding of how sperm PLCζ triggers Ca oscillations and egg activation in mammals, while also discussing the nature of a potential "alternative" sperm factor. We summarise PLCζ localization in mammalian sperm, and the direct links observed between defective PLCζ protein in sperm and documented cases of male infertility. Finally, we postulate how this sperm protein can be used as a potential diagnostic marker, and also as a powerful therapeutic agent for treatment of certain types of male infertility due to egg activation failure or even in more general cases of male subfertility.Qatar University student grant QUST-1-CMED-2020-3. Healthcare Research Fellowship Award (HF-14-16) made by Health and Care Research Wales (HCRW). National Science, Technology, and Innovation plan (NSTIP) project grant (15-MED4186-20) awarded by the King Abdulaziz City for Science and Technology (KACST)

Pea aphid winged and wingless males exhibit reproductive, gene expression, and lipid metabolism differences

Alternative, intraspecific phenotypes offer an opportunity to identify the mechanistic basis of differences asso- ciated with distinctive life history strategies. Wing dimorphic insects, in which both flight-capable and flight- incapable individuals occur in the same population, are particularly well-studied in terms of why and how the morphs trade offflight for reproduction. Yet despite a wealth of studies examining the differences between fe- male morphs, little is known about male differences, which could arise from different causes than those acting on females. Here we examined reproductive, gene expression, and biochemical differences between pea aphid ( Acyrthosiphon pisum ) winged and wingless males. We find that winged males are competitively superior in one- on-one mating circumstances, but wingless males reach reproductive maturity faster and have larger testes. We suggest that males tradeoffincreased local matings with concurrent possible inbreeding for outbreeding and in- creased ability to find mates. At the mechanistic level, differential gene expression between the morphs revealed a possible role for activin and insulin signaling in morph differences; it also highlighted genes not previously identified as being functionally important in wing polymorphism, such as genes likely involved in sperm produc- tion. Further, we find that winged males have higher lipid levels, consistent with their use as flight fuel, but we find no consistent patterns of different levels of activity among five enzymes associated with lipid biosynthesis. Overall, our analyses provide evidence that winged versus wingless males exhibit differences at the reproductive, gene expression, and biochemical levels, expanding the field’s understanding of the functional aspects of morph differences

Characterisation of CD154+ T cells following ex vivo allergen stimulation illustrates distinct T cell responses to seasonal and perennial allergens in allergic and non-allergic individuals

Background Allergic sensitisation has been ascribed to a dysregulated relationship between allergen-specific Th1, Th2 and regulatory T cells. We sought to utilise our short-term CD154 detection method to further analyse the relationship between these T cell subsets and investigate differences between seasonal and perennial allergens. Using peripheral blood samples from grass-allergic, cat-allergic and healthy non-atopic subjects, we compared the frequencies and phenotype of CD154-positive T helper cells following stimulation with seasonal (grass) and perennial (cat dander) allergens. Results We identified a higher frequency of CD154+ T cells in grass-allergic individuals compared to healthy controls; this difference was not evident following stimulation with cat allergen. Activated Th1, Th2 and Tr1-like cells, that co-express IFNγ, IL4 and IL10, respectively, were identified in varying proportions in grass-allergic, cat-allergic and non-allergic individuals. We confirmed a close correlation between Th1, Th2 and Tr1-like cell frequency in non-allergic volunteers, such that the three parameters increased together to maintain a low Th2: Th1 ratio. This relationship was dysregulated in grass-allergic individuals with no correlation between the T cell subsets and a higher Th2: Th1 ratio. We confirmed previous reports of a late-differentiated T cell phenotype in response to seasonal allergens compared to early-differentiated T cell responses to perennial allergens. Conclusions The findings confirm our existing work illustrating an important balance between Th1, Th2 and Tr1-like responses to allergens in health, where Th2 responses are frequently observed, but balanced by Th1 and regulatory responses. We confirm previous tetramer-based reports of phenotypic differences in T cells responding to seasonal and perennial allergens

CIRCULAR TEST STRUCTURES FOR DETERMINING THE SPECIFIC CONTACT RESISTANCE OF OHMIC CONTACTS

Though the transport of charge carriers across a metal-semiconductor ohmic interface is a complex process in the realm of electron wave mechanics, such an interface is practically characterised by its specific contact resistance. Error correction has been a major concern in regard to specific contact resistance test structures and investigations by finite element modeling demonstrate that test structures utilising circular contacts can be more reliable than those designed to have square shaped contacts as test contacts become necessarily smaller. Finite element modeling software NASTRAN can be used effectively for designing and modeling ohmic contact test structures and can be used to show that circular contacts are efficient in minimising error in determining specific contact resistance from such test structures. Full semiconductor modeling software is expensive and for ohmic contact investigations is not required when the approach used is to investigate test structures considering the ohmic interface as effectively resistive

The Secret Life of Articles: From Download Metrics to Downstream Impact

Traditional citation and download metrics have long been the standard by which we measure the use and value of scholarly articles. However, these methods neglect the usage and real‐world impact of newer technologies to access, store, and share downloaded scholarly articles. This session’s speakers will share the results of interviews, focus groups, and an international survey with 1,000 scholars to investigate the ways in which they now access, store, share, and use downloaded scholarly articles. By identifying and measuring what traditional metrics fail to examine, the Beyond Downloads project attempts to capture a more complete picture of the use and value of scholarly articles, which is critical for librarians, publishers, and vendors to understand in developing scholarly tools and services. Complete usage can no longer be measured by traditional means alone. The speakers will discuss the findings of their research and the implications for metrics that take into account scholars’ changing access, reading, and sharing behaviors