The functions of adequate communication in the neonatal care unit: A systematic review and meta-synthesis of qualitative research

ObjectiveTo assess the main functions of parent-provider communication in the neonatal (intensive) care unit (NICU) and determine what adequate communication entails according to both parents and health professionals.MethodsA systematic review and meta-synthesis of qualitative research. PubMed, Ebsco/PsycINFO, Wiley/Cochrane Library, Ebsco/CINAHL, Clarivate Analytics/Web of Science Core Collection, and Elsevier/Scopus were searched in October-November 2019 for records on interpersonal communication between parents and providers in neonatal care. Title/abstract screening and full-text analysis were conducted by multiple, independent coders. Data from included articles were analyzed using deductive and inductive thematic analysis.Results43 records were included. Thematic analysis of data resulted in the development of the NICU Communication Framework, including four functions of communication (1. building/maintaining relationships, 2. exchanging information, 3. (sharing) decision-making, 4. enabling parent self-management) and five factors that contribute to adequate communication across these functions (topic, aims, location, route, design) and, thereby, to tailored parent-provider communication.ConclusionThe NICU Communication Framework fits with the goals of Family Integrated Care to encourage parent participation in infants’ care. This framework forms a first step towards the conceptualization of (adequate) communication in NICU settings.Practice implicationsFindings can be used to improve NICU communication in practice, in particular through the mnemonic TAILORED.     

Sehverschlecherung bei seltener Netzhautveränderung

A combined hamartoma of the retinal pigment epithelium and the retina is a rare alteration of the ocular fundus. Knowledge of this mostly benign clinical picture is important to be able to differentiate it from malignant tumors such as choroidal melanoma. Occurrence in parallel with phacomatoses is known although it is not present in every case.     

Point mutations in the conserved box 1 region inactivate the human granulocyte colony-stimulating factor receptor for growth signal transduction and tyrosine phosphorylation of p75c-rel

The human granulocyte colony-stimulating factor receptor (hG-CSFR) belongs to the cytokine receptor superfamily. As with other members of this family, the cytoplasmic domain of hG-CSFR lacks intrinsic tyrosine kinase activity. To identify critical regions mediating growth signal transduction by hG-CSFR, deletions or site-directed amino acid substitutions were introduced into the cytoplasmic domain of hG-CSFR, and the mutant cDNAs were transfected into the murine interleukin-3 (IL- 3)-dependent Ba/F3 and FDCP cell lines. Truncation of the carboxy- terminal end of the receptor to the membrane-proximal 53 amino acids of the cytoplasmic domain, which retained the conserved Box 1 and Box 2 sequence motifs, decreased the ability of hG-CSFR to transduce G-CSF- mediated growth signals without an associated loss in receptor binding affinity. Substitution of proline by alanine at amino acid positions 639 and 641 within Box 1 completely abolished the G-CSF-mediated growth signal. Rapid induction of tyrosine phosphorylation of several cellular proteins, including a 75-kD protein (p75) identified as c-rel, was an early event associated with transduction of proliferative signals by hG- CSFR in Ba/F3 transfectants. Mutant receptors containing Pro-to-Ala substitutions that inactivated the receptor for mitogenic activity also inactivated the receptor for tyrosine-specific phosphorylation of p75. These results show that the conserved Box 1 sequence motif (amino acids 634 to 641) is critical for mitogenesis and activation of cellular tyrosine kinases by hG-CSFR.     

Follicular variant of papillary thyroid carcinoma: genome-wide appraisal of a controversial entity

The majority of thyroid tumors are classified as papillary (papillary thyroid carcinomas; PTCs) or follicular neoplasms (follicular thyroid adenomas and carcinomas; FTA/FTC) based on nuclear features and the cellular growth pattern. However, classification of the follicular variant of papillary thyroid carcinoma (FVPTC) remains an issue of debate. These tumors contain a predominantly follicular growth pattern but display nuclear features and overall clinical behavior consistent with PTC. In this study, we used comparative genomic hybridization (CGH) to compare the global chromosomal aberrations in FVPTC to the PTC of classical variant (classical PTC) and FTA/FTC. In addition, we assessed the presence of peroxisome proliferator-activated receptor-gamma (PPARG) alteration, a genetic event specific to FTA/FTC, using Southern blot and immunohistochemistry analyses. In sharp contrast to the findings in classical PTC (4% of cases), CGH analysis demonstrated that both FVPTC (59% of cases) and FTA/FTC (36% of cases) were commonly characterized by aneuploidy (P = 0.0002). Moreover, the pattern of chromosomal aberrations (gains at chromosome arms 2q, 4q, 5q, 6q, 8q, and 13q and deletions at 1p, 9q, 16q, 17q, 19q, and 22q) in the follicular variant of PTC closely resembled that of FTA/FTC. Aberrations in PPARG were uniquely detected in FVPTC and FTA/FTC. Our findings suggest a stronger relationship between the FVPTC and FTA/FTC than previously appreciated and support further consideration of the current classification of thyroid neoplasms.     

Evaluation of activatory and inhibitory natural killer cell receptors in non-segmental vitiligo: a flow cytometric study

Background Recent observations established the role of altered cellular immunity and autoimmune hypothesis in the pathogenesis of vitiligo. There have been several reports discussing T‐cell and natural killer (NK) cell populations, but NK cell receptors were not evaluated in vitiligo. Objective The purpose of this investigation was to assess the role of T and NK cells as well as activatory and inhibitory NK cell receptor alterations in the pathogenesis of vitiligo and whether any aberrations were correlated with clinical findings of the disease. Patients/methods Fifty‐three patients with non‐segmental vitiligo and 45 age‐ and sex‐matched healthy controls were enrolled in the study. The percentages of lymphocytes, granulocytes, monocytes and CD3, CD4, CD8, CD14, CD16, CD56, CD45, CD45RA, CD54RO, CD28, CD80, CD94, CD158a, KIR3DL‐1 receptors as well as CD94, CD158a, KIR3DL‐1 receptors on CD16⁺ cells were detected by using flow cytometry. The patient and control groups were compared in terms of the results of flow cytometric analysis, and the results were assessed regarding the type and activity of vitiligo. Results The percentages of CD16⁺CD56⁺, CD3⁺CD16⁺CD56⁺, CD8⁺ and CD45RO⁺ cells were significantly increased in vitiligo group compared with the controls. No difference was detected between the patients and control groups in percentages of CD3⁺, CD4⁺, CD3^?CD16⁺CD56⁺, CD28⁺, CD45⁺, CD45RA⁺, CD94⁺, CD158a⁺ and KIR3DL‐1⁺ cells. The percentage of CD16⁺CD158a⁺ cells was significantly decreased in a randomized selected group of vitiligo patients. There were no differences in percentage expression of studied cell surface antigens between patients in the active or stable period. CD3⁺ cells were significantly increased in generalized form, and CD45RO⁺ cells were significantly increased in acral/acrofacial form when compared with the other types of vitiligo. Conclusions These results indicate further evidence for T and NK cell abnormalities in non‐segmental vitiligo. The present data show that NK cell activation may be responsible in the pathogenesis of vitiligo in conformity with decreased inhibitory and increased activatory NK cell receptors.     

MUC1 plays a role in tumor maintenance in aggressive thyroid carcinomas

BACKGROUND: We recently identified MUC1 as a target driving selection for 1q21 amplification and validated it as an independent marker of aggressive behavior in thyroid cancer (TC). The aims of this study were to determine whether TC cell lines retain MUC1 expression patterns that are seen in primary tumors, assess the role of MUC1 in tumor maintenance, and develop a virally delivered anti-MUC1 RNA interference (RNAi) that is effective in decreasing MUC1 expression in vitro. METHODS: Fifteen TC cell lines were screened for MUC1 protein expression. Cell lines with varying MUC1 protein levels were treated with anti-MUC1 monoclonal antibody to assess cell viability. A recombinant retroviral short hairpin RNAi delivery system against MUC1 was developed. Efficacy and optimal dosing of short hairpin RNA against MUC1 was determined. RESULTS: MUC1 expression patterns in TC cell lines were found to be similar to that seen in primary tumors. Treatment with anti-MUC1 antibody resulted in a significant decrease in cell viability in MUC1 over-expressing cell lines. MUC1-779 RNAi construct showed excellent infection efficiency and reproducible silencing. CONCLUSION: These data offer functional evidence that implicates MUC1 over-expression as a key molecular event in the pathogenesis of aggressive TC. Retrovirally delivered anti-MUC1 RNAi is effective in silencing MUC1 and merits further investigation to establish therapeutic efficacy and safety in anticipation of potential clinical application.