The impact of intense nursing care in improving anxiety, depression, and quality of life in patients with liver cancer: A systematic review and meta-analysis.

BACKGROUND: Liver resection is a major, serious, and very delicate operation that should be done only by specialized, well-skilled, and experienced surgeons. However, the role of nurses, which has often been under-estimated, is also crucial for the success of the intervention or surgery. Intensive nursing care involves high quality nursing modes to achieve the expected goals of treatment smoothly and with less complications. In this analysis, we aimed to show the impact of intense nursing care in improving anxiety, depression, and quality of life in patients with intervention for liver cancers. METHODS: Data sources included EMBASE, MEDLINE, Web of Science, the Cochrane central, Google scholar, and http://www.ClinicalTrials.gov. Three authors independently extracted data from the selected original studies. The statistical analysis was carried out by the Cochrane based RevMan software. For dichotomous data, the number of events and the total number of participants were required and for the continuous data, mean, standard deviation as well as the total number of participants were required in the input for analysis. Odds ratios (OR) with 95% confidence intervals (CI) were used to represent the data following assessment. RESULTS: A total of 1205 participants with liver cancer enrolled between the years 2010 to 2018 were included in this analysis whereby 667 participants were assigned to an intensive nursing care. Our current analysis showed that most of the patients who were assigned to an intense nursing intervention were significantly very satisfied with their quality of life (OR: 4.07, 95% CI: 1.45 - 11.45; P = .008). However, a minor number of patients with liver cancer who were not assigned to intense nursing care were significantly dissatisfied with their quality of life with OR: 0.18, 95% CI: 0.04 - 0.77; P = .02. This analysis also showed that self-rating anxiety score (SAS) and self-rating depression score (SDS) were significantly in favor of the participants with intense nursing care with OR: - 7.66, 95% CI: [(-9.66) - (-5.66)]; P = .00001 and OR: -7.87, 95% CI: [(-8.43) - (-7.26)]; P = .00001 respectively. In addition, physical function (OR: 13.56, 95% CI: 12.39 - 14.74; P = .00001), and total activity score (OR: 16.58, 95% CI: 13.51 - 19.65; P = .00001) were also significantly in favor of an intense nursing care. CONCLUSIONS: Our current analysis showed that intense nursing care significantly improved anxiety, depression, and quality of life following interventions in patients with liver cancers. Most of the patients with liver cancers who were assigned to an intense nursing care were very satisfied with their quality of life. However, this hypothesis should further be confirmed in larger nursing related studies based on patients with liver cancers.

Myosin 16 levels fluctuate during the cell cycle and are downregulated in response to DNA replication stress.

Myosins comprise a highly conserved superfamily of eukaryotic actin-dependent motor proteins implicated in a large repertoire of functions in both the cytoplasm and the nucleus. Class XVI myosin, MYO16, reveals expression in most somatic as well as meiotic cells with prominent localization in the nucleus, excepting the nucleolus; however, the role(s) of Myo16 in the nucleus remain unknown. In this report, we investigated Myo16 abundance during transit through the cell cycle. Immunolocalization, immunoblot, flow cytometric and quantitative RT-PCR studies performed in Rat2 cells indicate that Myo16 mRNA and protein abundance are cell cycle regulated: in the unperturbed cell cycle, each rises to peak levels in late G1 and thereon through S-phase and each decays as cells enter M-phase. Notably, RNA interference-induced Myo16 depletion results in altered cell cycle distribution as well as in large-scale cell death. In response to DNA replication stress (impaired replication fork progression as a consequence of DNA damage, lack of sufficient deoxynucleotides, or inhibition of DNA polymerases), Myo16 protein shows substantial loss. Attenuation of replication stress (aphidicolin or hydroxyurea) is followed by a recovery of Myo16 expression and resumption of S-phase progression. Collectively, these observations suggest that Myo16 may play a regulatory role in cell cycle progression.

Myosin16b: The COOH-tail region directs localization to the nucleus and overexpression delays S-phase progression.

Rat Myo16a and Myo16b comprise the founding members of class XVI myosin and are characterized by an N-terminal ankyrin repeat domain thought to mediate an association with protein phosphatase 1 catalytic subunits 1alpha and 1gamma. Myo16b is the principal isoform and reveals predominant expression in developing neural tissue. Here, we use COS-7 cells as a model system to develop an understanding of Myo16b function. We find that Myo16b displays predominant localization in the nucleus of cells transitioning through interphase, but is not associated with processes of mitosis. Using a panel of EGFP-Myo16b-expression plasmids in transient transfection studies, we identified the COOH-terminal residues 1616-1912 as necessary and solely sufficient to target Myo16b to the nucleus. We show that the Myo16b-tail region directs localization to a nuclear compartment containing profilin and polymerized actin, which appears to form a three-dimensional meshwork through the depth of the nucleus. Further, we demonstrate that this compartment localizes within euchromatic regions of the genome and contains proliferating cell nuclear antigen (PCNA) and cyclin A, both markers of S-phase of the cell cycle. Cells transiently expressing Myo16b or Myo16b-tail region show limited incorporation of BrdU, delayed progression through S-phase of the cell cycle, and curtailed cellular proliferation.

Caveolin-1 expression is maintained in rat and human astroglioma cell lines.

Caveolin-1 is the principal structural and functional component of caveolae, a plasmalemmal compartment that has been proposed to sequester lipid and protein components that participate in transmembrane signal transduction processes. Multiple studies reveal a reduction in the expression level of caveolin-1 mRNA and protein in many carcinomas as well as transformed cells. The human caveolin-1 gene is localized to a suspected tumor suppressor locus (7q31.1). Collectively, these data have been taken to imply that caveolin-1 may function in a tumor suppressor capacity. To determine if a reduction in the expression level of caveolin-1 mRNA and protein accompanied the transformation of astrocytes, we undertook studies of two transformed rat astroglial cell lines, C6 and DI TNC(1), as well as several cell lines derived from human glioblastoma tumors: T98G, U87MG, U118MG, U138MG, and U373MG. Ultrastructural, immunolocalization, immunoblot, and Northern blot analyses demonstrated that caveolin-1 message and protein were expressed in all rat and human glioma cells. The localization pattern, buoyant density, and detergent-insolubility property of caveolin-1 protein were indistinguishable from that determined for nontransformed type 1 astrocytes in culture. Nucleotide sequence analyses of caveolin-1 cDNAs indicate that mutations are not present in the caveolin-1 sequence in any of the glioma cell types. Taken together with previous analyses, these data indicate that, at least for astrocytes, the process of transformation in and of itself is not solely sufficient to reduce the level of caveolin-1 expression, and that caveolin-1 expression in and of itself is not solely sufficient to prevent the acquisition of a transformed phenotype.