Cancer patients and telenursing interventions in Italy. a systematic review

Objective: The use of digital technologies could improve patients’ quality of care, satisfaction, and health-related outcomes in cancer patients. This paper aims to explore the use of digital technologies in nursing management of cancer patients in Italy. Patients and Methods: A systematic literature review was performed. PubMed, Excerpta Medica dataBASE (Embase), Cumulative Index to Nursing and Allied Health Literature (CINAHL), and Cochrane Library databases were consulted from September 1, 2021, to January 31, 2022. Key terms for Telenurs-ing/Telemedicine and cancer in Italy were used. The quality of each study was assessed through the Grading of Recommendations, Assessment, Development, and Evaluations method. Results: 131 articles were found and 5 were included: two randomized-clinical-trial protocols aimed to explore the impact of medication management apps on patients’ quality of life; one validation trial suggested good reliability in the therapeutic adherence of patients on chemotherapy but limited sensitivity in detecting related adverse events; two observational studies described the validation of telephone triage prehospitalization programs performed by nurses during the pandemic. Conclusions: The use of digital technologies in nursing management of cancer patients is in-frequent in Italy, however, increased during the pandemic. Further studies are needed to evaluate the impact and effectiveness of the use of digital technologies in nursing management in cancer patients

How to improve educational behaviors for caregivers and patients having Central Venous Access Device (CVAD). a scoping review

Objective: Central venous access devices (CVADs) are essential to the modern management of patients with hematological malignancies and solid tumors. Educational programs play a crucial role in promoting appropriate patient actions to support patient safety during hospitalization and homecare. This review aimed to identify literature concerning educational interventions to promote patients’ actions to overcome CVAD-related problems and improve self-monitoring and self-management. Materials and Methods: Documentary evaluation of international databases, such as PubMed, CINAHL, Scopus and Cochrane. Searching for data on population, context and concept regarding CVAD self-management. The extracted data was subject to thematic analysis. The following scoping reviews were developed using the five-stage framework outlined by Arksey and O’Malley, and advanced by Levac and colleagues. Results: Of the 2802 articles identified, 19 research articles were selected in this review. Educational programs have been shown to improve CVAD self management, to decrease stress and anxiety related to their use, and to reduce the onset of complications. In addition, nurses have proven to be the professional reference figure for educational interventions. Conclusions: The results of the study lead to the conclusion that programs aimed at improving selfcare and reducing the onset of complications in patients living with chronic and debilitating diseases should be made available to a larger portion of individuals. Both generic and specific programs are needed, in the different contexts of home and hospital, for the short and long term, in order to ameliorate participants’ abilities. The results of this study should, therefore, encourage health professionals to plan, carry out, and evaluate the establishment of educational programs with patient participation

Cancer patients and telenursing interventions in Italy: a systematic review

OBJECTIVE: The use of digital technologies could improve patients’ quality of care, satisfaction, and health-related outcomes in cancer patients. This paper aims to explore the use of digital technologies in nursing management of cancer patients in Italy. PATIENTS AND METHODS: A systematic literature review was performed. PubMed, Excerpta Medica dataBASE (Embase), Cumulative Index to Nursing and Allied Health Literature (CINAHL), and Cochrane Library databases were consulted from September 1, 2021, to January 31, 2022. Key terms for Telenursing/Telemedicine and cancer in Italy were used. The quality of each study was assessed through the Grading of Recommendations, Assessment, Development, and Evaluations method. RESULTS: 131 articles were found and 5 were included: two randomized-clinical-trial protocols aimed to explore the impact of medication management apps on patients' quality of life; one validation trial suggested good reliability in the therapeutic adherence of patients on chemotherapy but limited sensitivity in detecting related adverse events; two observational studies described the validation of telephone triage prehospitalization programs performed by nurses during the pandemic. CONCLUSIONS: The use of digital technologies in nursing management of cancer patients is infrequent, however, increased during the pandemic. Further studies are needed to evaluate the impact and effectiveness of the use of digital technologies in nursing management in cancer patients

A Mouse Model of Heritable Cerebrovascular Disease

The study of animal models of heritable cerebrovascular diseases can improve our understanding of disease mechanisms, identify candidate genes for related human disorders, and provide experimental models for preclinical trials. Here we describe a spontaneous mouse mutation that results in reproducible, adult-onset, progressive, focal ischemia in the brain. The pathology is not the result of hemorrhage, embolism, or an anatomical abnormality in the cerebral vasculature. The mutation maps as a single site recessive locus to mouse Chromosome 9 at 105 Mb, a region of shared synteny with human chromosome 3q22. The genetic interval, defined by recombination mapping, contains seven protein-coding genes and one processed transcript, none of which are changed in their expression level, splicing, or sequence in affected mice. Targeted resequencing of the entire interval did not reveal any provocative changes; thus, the causative molecular lesion has not been identified

High disease impact of myotonic dystrophy type 2 on physical and mental functioning

The aim of the study was to investigate health status in patients with myotonic dystrophy type 2 (DM2) and determine its relationship to pain and fatigue. Data on health status (SF-36), pain (MPQ) and fatigue (CIS-fatigue) were collected for the Dutch DM2 population (n = 32). Results were compared with those of sex- and age-matched adult-onset myotonic dystrophy type 1 (DM1) patients. In addition, we compared the obtained scores on health status of the DM2 group with normative data of the Dutch general population (n = 1742). Compared to DM1, the SF-36 score for bodily pain was significantly (p = 0.04) lower in DM2, indicating more body pain in DM2. DM2 did not differ from DM1 on any other SF-36 scales. In comparison to the Dutch population, DM2 patients reported lower scores (indicating worse clinical condition) on the physical functioning, role functioning-physical, bodily pain, general health, vitality, social functioning, and role functioning-emotional scales (p < 0.01 on all scales). The difference was most profound for the physical functioning scale. In the DM2 group the severity of pain was significantly correlated with SF-36 scores for bodily pain (p = 0.003). Fatigue was significantly correlated with the SF-36 scores for role functioning-physical (p = 0.001), general health (p = 0.02), and vitality (p = 0.02). The impact of DM2 on a patients’ physical, psychological and social functioning is significant and as high as in adult-onset DM1 patients. From the perspective of health-related quality of life, DM2 should not be considered a benign disease. Management of DM2 patients should include screening for pain and fatigue. Symptomatic treatment of pain and fatigue may decrease disease impact and help improve health status in DM2, even if the disease itself cannot be treated

Micro-CT imaging reveals<i> Mekk3 </i>heterozygosity prevents cerebral cavernous malformations in <i>Ccm2</i>-deficient mice

Mutations in CCM1 (aka KRIT1), CCM2, or CCM3 (aka PDCD10) gene cause cerebral cavernous malformation in humans. Mouse models of CCM disease have been established by deleting Ccm genes in postnatal animals. These mouse models provide invaluable tools to investigate molecular mechanism and therapeutic approaches for CCM disease. However, the full value of these animal models is limited by the lack of an accurate and quantitative method to assess lesion burden and progression. In the present study we have established a refined and detailed contrast enhanced X-ray micro-CT method to measure CCM lesion burden in mouse brains. As this study utilized a voxel dimension of 9.5μm (leading to a minimum feature size of approximately 25μm), it is therefore sufficient to measure CCM lesion volume and number globally and accurately, and provide high-resolution 3-D mapping of CCM lesions in mouse brains. Using this method, we found loss of Ccm1 or Ccm2 in neonatal endothelium confers CCM lesions in the mouse hindbrain with similar total volume and number. This quantitative approach also demonstrated a rescue of CCM lesions with simultaneous deletion of one allele of Mekk3. This method would enhance the value of the established mouse models to study the molecular basis and potential therapies for CCM and other cerebrovascular diseases

Deregulated MicroRNAs in Myotonic Dystrophy Type 2

Myotonic Dystrophy Type-2 (DM2) is an autosomal dominant disease caused by the expansion of a CCTG tetraplet repeat. It is a multisystemic disorder, affecting skeletal muscles, the heart, the eye, the central nervous system and the endocrine system. Since microRNA (miRNA) expression is disrupted in Myotonic Dystrophy Type-1 and many other myopathies, miRNAs deregulation was studied in skeletal muscle biopsies of 13 DM2 patients and 13 controls. Eleven miRNAs were deregulated: 9 displayed higher levels compared to controls (miR-34a-5p, miR-34b-3p, miR-34c-5p, miR-146b-5p, miR-208a, miR-221-3p and miR-381), while 4 were decreased (miR-125b-5p, miR-193a-3p, miR-193b-3p and miR-378a-3p). To explore the relevance of DM2 miRNA deregulation, the predicted interactions between miRNA and mRNA were investigated. Global gene expression was analyzed in DM2 and controls and bioinformatic analysis identified more than 1,000 miRNA/mRNA interactions. Pathway and function analysis highlighted the involvement of the miRNA-deregulated mRNAs in multiple aspects of DM2 pathophysiology. In conclusion, the observed miRNA dysregulations may contribute to DM2 pathogenetic mechanisms

Cardiac troponins: from myocardial infarction to chronic disease.

Elucidation of the physiologically distinct subunits of troponin in 1973 greatly facilitated our understanding of cardiac contraction. Although troponins are expressed in both skeletal and cardiac muscle, there are isoforms of troponin I/T expressed selectively in the heart. By exploiting cardiac-restricted epitopes within these proteins, one of the most successful diagnostic tests to-date has been developed: cardiac troponin (cTn) assays. For the past decade, cTn has been regarded as the gold-standard marker for acute myocardial necrosis: the pathological hallmark of acute myocardial infarction (AMI). Whilst cTn is the cornerstone for ruling-out AMI in patients presenting with a suspected acute coronary syndrome (ACS), elevated cTn is frequently observed in those without clinical signs indicative of AMI, often reflecting myocardial injury of 'unknown origin'. cTn is commonly elevated in acute non-ACS conditions, as well as in chronic diseases. It is unclear why these elevations occur; yet they cannot be ignored as cTn levels in chronically unwell patients are directly correlated to prognosis. Paradoxically, improvements in assay sensitivity have meant more differential diagnoses have to be considered due to decreased specificity, since cTn is now more easily detected in these non-ACS conditions. It is important to be aware cTn is highly specific for myocardial injury, which could be attributable to a myriad of underlying causes, emphasising the notion that cTn is an organ-specific, not disease-specific biomarker. Furthermore, the ability to detect increased cTn using high-sensitivity assays following extreme exercise is disconcerting. It has been suggested troponin release can occur without cardiomyocyte necrosis, contradicting conventional dogma, emphasising a need to understand the mechanisms of such release. This review discusses basic troponin biology, the physiology behind its detection in serum, its use in the diagnosis of AMI, and some key concepts and experimental evidence as to why cTn can be elevated in chronic diseases

Long Tract of Untranslated CAG Repeats Is Deleterious in Transgenic Mice

The most frequent trinucleotide repeat found in human disorders is the CAG sequence. Expansion of CAG repeats is mostly found in coding regions and is thought to cause diseases through a protein mechanism. Recently, expanded CAG repeats were shown to induce toxicity at the RNA level in Drosophila and C. elegans. These findings raise the possibility that CAG repeats may trigger RNA-mediated pathogenesis in mammals. Here, we demonstrate that transgenic mice expressing EGFP transcripts with long CAG repeats in the 3′ untranslated region develop pathogenic features. Expression of the transgene was directed to the muscle in order to compare the resulting phenotype to that caused by the CUG expansion, as occurs in myotonic dystrophy. Transgenic mice expressing 200, but not those expressing 0 or 23 CAG repeats, showed alterations in muscle morphology, histochemistry and electrophysiology, as well as abnormal behavioral phenotypes. Expression of the expanded CAG repeats in testes resulted in reduced fertility due to defective sperm motility. The production of EGFP protein was significantly reduced by the 200 CAG repeats, and no polyglutamine-containing product was detected, which argues against a protein mechanism. Moreover, nuclear RNA foci were detected for the long CAG repeats. These data support the notion that expanded CAG repeat RNA can cause deleterious effects in mammals. They also suggest the possible involvement of an RNA mechanism in human diseases with long CAG repeats