Nursing Care Aesthetic in Iran: A Phenomenological Study

Background: Despite the emphasis of contemporary nursing theories on the belief that nursing is a science and an art in care, published studies show that only the nursing science has developed. Many experts believe that by recognizing and perceiving this concept, the clinical field can develop aesthetic knowledge in nursing and education of students. Objectives: The purpose of this study was to explain clients and nurses perspective of nursing care aesthetics. Patients and Methods: Using an interpretive phenomenology, 12 clients and 14 nurses were interviewed. Participants in this study were purposefully selected and their experiences were analyzed using Van Manen’s hermeneutic phenomenological framework. Results: Emerged themes were as follows: subjective description, overt spirituality, opening desperate impasse, sense of unity, continue to shine, and painful pass and pleasing. According the participants experiences, nursing care aesthetics includes subjective description of spiritual and desirable caring behaviors combined with sense of unity and sympathy between the nurse and the patients, which leads to opening in desperate impasse with creating the feeling of satisfaction and peace in the patient. It is a shining of clinical capabilities and an action beyond what should be combined with a decorating care that leads to a pleasant ending against the pain and suffering of the others for the nurse. Conclusions: Many caring behaviors associate with aesthetic experience for both patients and nurses and despite two different views, findings of this study showed that these experiences were similar in most cases. The aesthetics of nursing care was defined as what reflects the holistic nature of nursing with an emphasis on spirituality and skill. Results of this study are effective in identification of the values existed in nurse caring behaviors and developing of profession by instruction, implementation, and evaluation them

Nursing Students' Competencies in Evidence-Based Practice and Its Related Factors

Background: Evidence-Based Practice (EBP) is one of the nursing professional roles that can lead them to provide the best and more effective care. However, no studies are available on nursing students’ competencies in EBP. Objectives: This study aimed to investigate the nursing students’ knowledge, attitude and intention to implement EBP and its related factors in two nursing and midwifery faculties in Tehran, Iran. Materials and Methods: In this cross-sectional study, 170 undergraduate nursing students were selected from two faculties of nursing and midwifery in Tehran, Iran. A census sampling method was applied and they were all before graduation in 2013. The Rubin and Parrish questionnaire was used to assess the students’ knowledge, attitude and intention to implement EBP as well as factors affecting the implementation of EBP. Students completed the instrument through self-report. Descriptive statistics, Independent sample t-test and Pearson correlation coefficient were used to analyze the data. Results: The students mean scores of knowledge, attitude and intention to implement EBP was 31.08 ± 5.77, 50.40 ± 9.58, 36.01 ± 4.64, respectively. The students’ age was inversely correlated with their scores of knowledge, attitude and intention to use EBP (P < 0.05). However, the students’ GPA was in direct association with their knowledge, attitude and intention to implement EBP (P < 0.05). No significant differences were observed between the males and females mean scores in the three subscales. However, significant differences were found between the students mean scores in the two subscales of knowledge and attitudes toward EBP in terms of familiarity with statistics and research methods (P < 0.05). Neither familiarity with research methods nor familiarity with EBP could significantly affect the students’ intention to implement EBP. Conclusions: The present study showed that nursing students have not a high mean score in the three subscales of knowledge, attitude and intention to implement EBP. It is essential for faculties and nurse managers not only to focus on education of EBP, but also to support nurses and nursing students to implement it in the process patient care

Distinct Genetic Alterations in Colorectal Cancer

Colon cancer (CRC) development often includes chromosomal instability (CIN) leading to amplifications and deletions of large DNA segments. Epidemiological, clinical, and cytogenetic studies showed that there are considerable differences between CRC tumors from African Americans (AAs) and Caucasian patients. In this study, we determined genomic copy number aberrations in sporadic CRC tumors from AAs, in order to investigate possible explanations for the observed disparities.We applied genome-wide array comparative genome hybridization (aCGH) using a 105k chip to identify copy number aberrations in samples from 15 AAs. In addition, we did a population comparative analysis with aCGH data in Caucasians as well as with a widely publicized list of colon cancer genes (CAN genes). There was an average of 20 aberrations per patient with more amplifications than deletions. Analysis of DNA copy number of frequently altered chromosomes revealed that deletions occurred primarily in chromosomes 4, 8 and 18. Chromosomal duplications occurred in more than 50% of cases on chromosomes 7, 8, 13, 20 and X. The CIN profile showed some differences when compared to Caucasian alterations. as the most frequently amplified genes. The observed CIN may play a distinctive role in CRC in AAs

Helicobacter pylori-induced gastric cancer is orchestrated by MRCK beta-mediated Siah2 phosphorylation

Background Helicobacter pylori-mediated gastric carcinogenesis is initiated by a plethora of signaling events in the infected gastric epithelial cells (GECs). The E3 ubiquitin ligase seven in absentia homolog 2 (Siah2) is induced in GECs in response to H. pylori infection. Posttranslational modifications of Siah2 orchestrate its function as well as stability. The aim of this study was to evaluate Siah2 phosphorylation status under the influence of H. pylori infection and its impact in gastric cancer progression. Methods H. pylori-infected various GECs, gastric tissues from H. pylori-infected GC patients and H. felis-infected C57BL/6 mice were evaluated for Siah2 phosphorylation by western blotting or immunofluorescence microscopy. Coimmunoprecipitation assay followed by mass spectrometry were performed to identify the kinases interacting with Siah2. Phosphorylation sites of Siah2 were identified by using various plasmid constructs generated by site-directed mutagenesis. Proteasome inhibitor MG132 was used to investigate proteasome degradation events. The importance of Siah2 phosphorylation on tumorigenicity of infected cells were detected by using phosphorylation-null mutant and wild type Siah2 stably-transfected cells followed by clonogenicity assay, cell proliferation assay, anchorage-independent growth and transwell invasion assay. Results Siah2 was phosphorylated in H. pylori-infected GECs as well as in metastatic GC tissues at residues serine(6) (Ser(6)) and threonine(279) (Thr(279)). Phosphorylation of Siah2 was mediated by MRCK beta, a Ser/Thr protein kinase. MRCK beta was consistently expressed in uninfected GECs and noncancer gastric tissues but its level decreased in infected GECs as well as in metastatic tissues which had enhanced Siah2 expression. Infected murine gastric tissues showed similar results. MRCK beta could phosphorylate Siah2 but itself got ubiquitinated from this interaction leading to the proteasomal degradation of MRCK beta and use of proteasomal inhibitor MG132 could rescue MRCK beta from Siah2-mediated degradation. Ser(6) and Thr(279) phosphorylated-Siah2 was more stable and tumorigenic than its non-phosphorylated counterpart as revealed by the proliferation, invasion, migration abilities and anchorage-independent growth of stable-transfected cells. Conclusions Increased level of Ser(6) and Thr(279)-phosphorylated-Siah2 and downregulated MRCK beta were prominent histological characteristics of Helicobacter-infected gastric epithelium and metastatic human GC. MRCK beta-dependent Siah2 phosphorylation stabilized Siah2 which promoted anchorage-independent survival and proliferative potential of GECs. Phospho-null mutants of Siah2 (S6A and T279A) showed abated tumorigenicity.Peer reviewe

Distinct High-Profile Methylated Genes in Colorectal Cancer

Background: Mutations and promoters ’ methylation of a set of candidate cancer genes (CAN genes) are associated with progression of colorectal cancer (CRC). We hypothesized that these genes ’ promoters are inactivated through epigenetic silencing and may show a different profile in high-risk populations. We investigated the status of CAN gene methylation and CHD5 protein expression in African American CRC tissue microarrays (TMA) using immunohistochemical staining. Methodology/Principal Findings: The promoter methylation status of the CAN genes was studied by methylation-specific PCR (MSP) in 51 Iranians (a white population) and 51 African Americans (AA). Microsatellite instability (MSI) was analyzed as well. The differential frequency of methylation for each gene was tested by chi-square analysis between the two groups based on matched age and sex. CHD5 protein expression was evaluated in moderate to well differentiated and poorly differentiated carcinomas compared to matched normal tissue using TMA. In addition, the correlation between these epigenetic biomarkers and various clinicopathological factors, including, age, location, and stage of the disease were analyzed. Seventy-seven and 34 % of tumors were distal in Iranian and African American patients, respectively. In both populations, the percentage of methylation was.65 % for SYNE1, MMP2, APC2, GPNMB, EVL, PTPRD, and STARD8, whereas methylation was,50 % for LGR6, RET, CD109, and RNF. The difference in methylation between the two populations was statistically significant for CHD5, ICAM5 and GPNMB. Thirty-one percent AA tumors showed MSI-H, compared to 28 % i

Neutron Decay from Giant Resonances and the Isobaric Analog State in 120-Sb Populated in 120-Sn(3-He,t)120-Sb(n)119-Sb Charge Exchange

This research was sponsored by the National Science Foundation Grant NSF PHY-931478

MicroRNA-211 Expression Promotes Colorectal Cancer Cell Growth In Vitro and In Vivo by Targeting Tumor Suppressor CHD5

Background: Chromodomain-helicase-DNA-binding protein 5 (CHD5) is a newly identified tumor suppressor that is frequently downregulated in a variety of human cancers. Our previous work revealed that the low expression of CHD5 in colorectal cancer is correlated with CHD5 promoter CpG island hypermethylation. In this study, we investigated the effect of microRNA-211 (miR-211)-regulated CHD5 expression on colorectal tumorigenesis. Methodology/Principal Findings: miR-211 was predicted to target CHD5 by TargetScan software analysis. A stably expressing exogenous miR-211 colorectal cancer cell line (HCT-116 miR-211) was generated using lentiviral transduction and used as a model for in vitro and in vivo studies. The expression level of miR-211 in HCT-116 miR-211 cells was upregulated by 16-fold compared to vector control cells (HCT-116 vector). Exogenous miR-211 directly binds to the 39-untranslated region (39-UTR) of CHD5 mRNA, resulting in a 50 % decrease in CHD5 protein level in HCT-116 miR-211 cells. The levels of cell proliferation, tumor growth, and cell migration of HCT-116 miR-211 cells were significantly higher than HCT-116 vector cells under both in vitro and in vivo conditions, as determined using the methods of MTT, colony formation, flow cytometry, scratch assay, and tumor xenografts, respectively. In addition, we found that enforced expression of miR-211 in HCT-116 cells was able to alter p53 pathway-associated regulatory proteins, such as MDM2, Bcl-2, Bcl-xL, and Bax. Conclusion/Significance: Our results demonstrate that CHD5 is a direct target of miR-211 regulation. Enforced expression o

Case-Control Study of Vitamin D, dickkopf homolog 1 (DKK1) Gene Methylation, VDR Gene Polymorphism and the Risk of Colon Adenoma in African Americans

There are sparse data on genetic, epigenetic and vitamin D exposure in African Americans (AA) with colon polyp. Consequently, we evaluated serum 25(OH) D levels, vitamin D receptor (VDR) polymorphisms and the methylation status of the tumor suppressor gene dickkopf homolog 1 (DKK1) as risk factors for colon polyp in this population.The case-control study consisted of 93 patients with colon polyp (cases) and 187 healthy individuals (controls) at Howard University Hospital. Serum levels of 25(OH)D (including D3, D2, and total) were measured by liquid chromatography-mass spectrometry. DNA analysis focused on 49 single nucleotide polymorphisms (SNPs) in the VDR gene. Promoter methylation analysis of DKK1 was also performed. The resulting data were processed in unadjusted and multivariable logistic regression analyses.Cases and controls differed in vitamin D status (D(3)<50 nmol/L: Median of 35.5 in cases vs. 36.8 in controls nmol/L; P = 0.05). Low levels of 25(OH)D(3) (<50 nmol/L) were observed in 86% of cases and 68% of controls and it was associated with higher risks of colon polyp (odds ratio of 2.7, 95% confidence interval 1.3-3.4). The SNP analysis showed no association between 46 VDR polymorphisms and colon polyp. The promoter of the DKK1 gene was unmethylated in 96% of the samples.We found an inverse association between serum 25(OH)D(3) and colon polyp in AAs. VDR SNPs and DKK1 methylation were not associated with colon polyp. Vitamin D levels may in part explain the higher incidence of polyp in AAs

Impact of BRAF, MLH1 on the incidence of microsatellite instability high colorectal cancer in populations based study

We have identified an alternative pathway of tumorigenesis in sporadic colon cancer, involving microsatellite instability due to mismatched repair methylation, which may be driven by mutations in the BRAF gene (V600E). Colorectal cancer (CRC) is the most common cancer in the world, and African Americans show a higher incidence than other populations in the United States. We analyzed sporadic CRCs in Omani (of African origin, N = 61), Iranian (of Caucasian origin, N = 53) and African American (N = 95) patients for microsatellite instability, expression status of mismatched repair genes (hMLH1, hMSH2) and presence of the BRAF (V600E) mutation. In the Omani group, all tumors with BRAF mutations were located in the left side of the colon, and for African Americans, 88% [7] of tumors with BRAF mutations were found in the right side of the colon. In African Americans, 31% of tumors displayed microsatellite instability at two or more markers (MSI-H), while this rate was 26% and 13% for tumors in the Iranian and Omani groups, respectively. A majority of these MSI-H tumors were located in the proximal colon (right side) in African American and Iranian subjects, whereas most were located in the distal colon (left side) in Omani subjects. Defects in hMLH1 gene expression were found in 77% of MSI-H tumors in both African Americans and Iranians and in 38% of tumors in Omanis. BRAF mutations were observed in all subjects: 10% of tumors in African Americans (8/82), 2% of tumors in Iranians (1/53), and 19% of tumors in Omanis (11/59). Our findings suggest that CRC occurs at a younger age in Omani and Iranian patients, and these groups showed a lower occurrence of MSI-H than did African American patients. Our multivariate model suggests an important and significant role of hMLH1 expression and BRAF mutation in MSI-H CRC in these populations. The high occurrence of MSI-H tumors in African Americans may have significant implications for treatment, since patients with MSI-H lesions display a different response to chemotherapeutic agents such as 5-fluorouracil

Semiempirical Shell Model Masses with Magic Number Z=126 for Translead Elements with N smaller or equal to 126

A semiempirical shell model mass equation based on magic number Z=126 and applicable to translead elements with N smaller or equal to 126 is presented. For alpha decay energies the equation is shown to have a high predictive power and an rms deviation from the data of about 100 keV. The rms deviations for masses and other mass differences are between about 200 and 300 keV.Comment: 8 pages including 3 figures and 3 table