Evaluating the Effectiveness of Mobile Health in Breast Cancer Care: A Systematic Review.

Breast cancer is affecting millions of people worldwide. If not appropriately handled, the side effects of different modalities of cancer treatment can negatively impact patients' quality of life and cause treatment interruptions. In recent years, mobile health (mHealth) interventions have shown promising opportunities to support breast cancer care. Numerous studies implemented mobile health interventions aiming to support patients with breast cancer, for example, through physical activity promotion or educational content. Nonetheless, current literature reveals that real-world evidence for the actual benefits remains unclear. In this systematic review, we focus on analyzing the methodology used in recent studies to determine the effects of mHealth applications and wearable devices on the outcome of patients with breast cancer. We followed the PRISMA guideline for the selection, analysis, and reporting of relevant studies found in the databases of Medline, Scopus, Web of Science, and Cochrane Library. A total of 276 unique records were identified, and 20 studies met the inclusion criteria. Study quality was assessed with the Effective Public Health Practice Project (EPHPP) Quality Assessment Tool for Quantitative Studies. While many of the studies used standardized questionnaires as patient-reported outcome measures, there was minimal use of objective measurements, such as activity sensors. Adoption, drop-out rates, and usage behavior of users of the mobile health intervention were often not reported. Future work should clearly define the focus and desired outcome of mHealth interventions and select outcome measures accordingly. Greater transparency facilitates the interpretation of results and conclusions about the real-world evidence of mobile health in breast cancer care.

No evidence of the unfolded protein response in the placenta of two rodent models of preeclampsia and intrauterine growth restriction.

In humans, intrauterine growth restriction (IUGR) and preeclampsia (PE) are associated with induction of the unfolded protein response (UPR) and increased placental endoplasmic reticulum (ER) stress. Especially in PE, oxidative stress occurs relative to the severity of maternal vascular underperfusion (MVU) of the placental bed. On the premise that understanding the mechanisms of placental dysfunction could lead to targeted therapeutic options for human IUGR and PE, we investigated the roles of the placental UPR and oxidative stress in two rodent models of these human gestational pathologies. We employed a rat IUGR model of gestational maternal protein restriction, as well as an endothelial nitric oxide synthase knockout mouse model (eNOS-/-) of PE/IUGR. Placental expression of UPR members was analyzed via qRT-PCR (Grp78, Calnexin, Perk, Chop, Atf6, and Ern1), immunohistochemistry, and Western blotting (Calnexin, ATF6, GRP78, CHOP, phospho-eIF2α, and phospho-IRE1). Oxidative stress was determined via Western blotting (3-nitrotyrosine and 4-hydroxy-2-nonenal). Both animal models showed a significant reduction of fetal and placental weight. These effects did not induce placental UPR. In contrast to human data, results from our rodent models suggest retention of placental plasticity in the setting of ER stress under an adverse gestational environment. Oxidative stress was significantly increased only in female IUGR rat placentas, suggesting a sexually dimorphic response to maternal malnutrition. Our study advances understanding of the involvement of the placental UPR in IUGR and PE. Moreover, it emphasizes the appropriate choice of animal models researching various aspects of these pregnancy complications.

Renal Chemerin Expression is Induced in Models of Hypertensive Nephropathy and Glomerulonephritis and Correlates with Markers of Inflammation and Fibrosis.

Chemerin and its receptor, chemokine-like receptor 1 (CmklR1), are associated with chemotaxis, inflammation, and endothelial function, especially in metabolic syndrome, coronary heart disease, and hypertension. In humans, circulating chemerin levels and renal function show an inverse relation. So far, little is known about the potential role of chemerin in hypertensive nephropathy and renal inflammation. Therefore, we determined systemic and renal chemerin levels in 2-kidney-1-clip (2k1c) hypertensive and Thy1.1 nephritic rats, respectively, to explore the correlation between chemerin and markers of renal inflammation and fibrosis. Immunohistochemistry revealed a model-specific induction of chemerin expression at the corresponding site of renal damage (tubular vs. glomerular). In both models, renal expression of chemerin (RT-PCR, Western blot) was increased and correlated positively with markers of inflammation and fibrosis. In contrast, circulating chemerin levels remained unchanged. Taken together, these findings demonstrate that renal chemerin expression is associated with processes of inflammation and fibrosis-related to renal damage. However, its use as circulating biomarker of renal inflammation seems to be limited in our rat models.

Expression of Retinoid Acid Receptor-Responsive Genes in Rodent Models of Placental Pathology.

In humans, retinoic acid receptor responders (RARRES) have been shown to be altered in third trimester placentas complicated by the pathologies preeclampsia (PE) and PE with intrauterine growth restriction (IUGR). Currently, little is known about the role of placental Rarres in rodents. Therefore, we examined the localization and expression of Rarres1 and 2 in placentas obtained from a Wistar rat model of isocaloric maternal protein restriction (E18.5, IUGR-like features) and from an eNOS-knockout mouse model (E15 and E18.5, PE-like features). In both rodent models, Rarres1 and 2 were mainly localized in the placental spongiotrophoblast and giant cells. Their placental expression, as well as the expression of the Rarres2 receptor chemokine-like receptor 1 (CmklR1), was largely unaltered at the examined gestational ages in both animal models. Our results have shown that RARRES1 and 2 may have different expression and roles in human and rodent placentas, thereby underlining immanent limitations of comparative interspecies placentology. Further functional studies are required to elucidate the potential involvement of these proteins in early placentogenesis.