Behavioural drivers of child feeding during and after illness in the Democratic Republic of the Congo: results from a qualitative study through the lens of behavioural science.

OBJECTIVE: For young children experiencing an illness, adequate nutrition is critical for recovery and to prevent malnutrition, yet many children do not receive the recommended quantities of food during illness and recuperation. Our research applied a behavioural science lens to identify drivers of feeding behaviours, including barriers inhibiting caregivers from following the feeding guidelines. DESIGN: In 2021, we conducted qualitative research informed by the behavioural design process. Data from in-depth interviews and observations were analysed for themes. SETTING: Research was conducted in South Kivu, Democratic Republic of the Congo. PARTICIPANTS: Research participants included caregivers of young children, other family members, health workers and other community members. RESULTS: Five key findings about behavioural drivers emerged: (1) poverty and scarcity impose practical constraints and a cognitive and emotional burden on caregivers; (2) health providers are distracted and discouraged from counselling on feeding during sick visits; (3) a focus on quality and hesitations about quantity obscure benefits of feeding greater amounts of available foods; (4) perceptions of inappropriate foods limit caregivers' choices; and (5) deference to a child's limited appetite leads to missed opportunities to encourage them to eat. CONCLUSIONS: Each of these behavioural drivers is triggered by one or more addressable features in caregivers' and health workers' environment, suggesting concrete opportunities for programmes to support caregivers and health workers to improve feeding of young children during illness and recovery. In other settings where these features of the environment are similar, the insights and programming implications are likely to translate.

Edible Sword Bean Extract Induces Apoptosis in Cancer Cells In Vitro and Inhibits Ascites and Solid Tumor Development In Vivo.

Antitumor potential of edible sword bean (Canavalia gladiata (L.)) extract has been evaluated against Daltons lymphoma ascites (DLA) using in vitro and in vivo studies. Methanolic extraction was carried out and in vitro studies were performed against both DLA and A549, lung cancer cell lines. The results revealed that sword bean extract inhibited cell growth and induced apoptosis as evidenced by cytotoxic assay, Hoechst 33342 staining and acridine orange/ethidium bromide dual staining. In vivo studies performed on DLA induced solid as well as ascitic tumors models showed administration of sword bean extract (10 mg/kg B.wt.) could significantly inhibit ascitic and solid tumor development in mice. Therefore, our overall results revealed that C. gladiata treatment could significantly inhibit tumor development and induce apoptosis in tumor cells.

Framed, Interactive Theory-Driven Texting: Effects of Message Framing on Health Behavior Change for Weight Loss.

More approaches to support weight control are needed, especially among racial minorities who shoulder a disproportionate obesity burden. Using an approach influenced by regulatory fit theory, we conducted a 28-day, 4-arm experimental trial with 89 obese adults recruited from urban, predominantly African American churches to ascertain the efficacy of framed text messages to motivate behaviors conducive to weight loss. Participants were assigned to receive message framing that was matched versus mismatched to their motivational orientation. Results were mixed overall; however, matched texts elicited greater motivation to change eating and exercise behavior, suggesting promise in using motivational approaches to tailor messages.

Continuing with " a heavy heart" - consequences of maternal death in rural Kenya.

BACKGROUND: This study analyzes the consequences of maternal death to households in Western Kenya, specifically, neonatal and infant survival, childcare and schooling, disruption of daily household activities, the emotional burden on household members, and coping mechanisms. METHODS: The study is a combination of qualitative analysis with matched and unmatched quantitative analysis using surveillance and survey data. Between September 2011 and March 2013 all households in the study area with a maternal death were surveyed. Data were collected on the demographic characteristics of the deceased woman; household socio-economic status; a history of the pregnancy that led to the death; schooling experiences of surviving school-age children; and disruption to household functioning due to the maternal death. These data were supplemented by in-depth and focus group discussions. Quantitative data on neonatal and infant survival from a demographic surveillance system in the study area were also used. Descriptive and bivariate analyses were conducted with the quantitative data, and qualitative data were analyzed through text analysis using NVivo. RESULTS: More than three-quarters of deceased women performed most household tasks when healthy. After the maternal death, the responsibility for these tasks fell primarily on the deceased's husbands, mothers, and mothers-in-law. Two-thirds of the individuals from households that suffered a maternal death had to shift into another household. Most children had to move away, mostly to their grandmother's home. About 37% of live births to women who died of maternal causes survived till age 1 year, compared to 65% of live births to a matched sample of women who died of non-maternal causes and 93% of live births to surviving women. Older, surviving children missed school or did not have enough time for schoolwork, because of increased housework or because the loss of household income due to the maternal death meant school fees could not be paid. Respondents expressed grief, frustration, anger and a sense of loss. Generous family and community support during the funeral and mourning periods was followed by little support thereafter. CONCLUSION: The detrimental consequences of a maternal death ripple out from the woman's spouse and children to the entire household, and across generations.

Evaluating a youth-designed sexual and reproductive health mass and social media campaign in Côte d'Ivoire: triangulation of three independent evaluations.

Merci Mon Héros (MMH) is a youth-designed multi-media campaign seeking to improve sexual and reproductive health and family planning (SRH/FP) outcomes among youth living in nine francophone countries. A mixed methods approach was implemented to assess the MMH campaign progress and impact in Côte d'Ivoire. Three data sources were triangulated to evaluate the campaign: social media listening (October 2019-January 2021); a quantitative cross-sectional monitoring survey (September 2020) with 412 youth (aged 16-24) and 597 adults (aged 25-49); and a qualitative study using a Most Significant Change approach (March 2021), including a total of 24 focus group discussions with youth (aged 15-24) and adults (aged 25+) exposed to the MMH campaign. Data from all three studies were analysed independently and then brought together through a triangulation workshop where the study team compared findings to achieve convergence in evaluation results. Social listening results showed topic-specific online conversations related to MMH campaign spiked significantly during the two-week period after topic-specific campaign posts (p < .05), suggesting potential campaign impact. Survey results showed both adults and youth were more likely to have spoken with someone about FP in the past five months if exposed to the campaign (p < 0.01). Qualitative findings support the campaign's effect on shifting attitudes and behavioural uptake of intergenerational communication among adults and youth. This evaluation shows evidence of MMH's strong potential for impact in encouraging communication and the need to focus efforts on strategies to strengthen supportive adults' communication competencies and redefine what it means to act in support of SRH/FP for youth.

Regulatory Components of Oxidative Stress and Inflammation and Their Complex Interplay in Carcinogenesis.

Cancer progression is closely linked to oxidative stress (OS) inflammation. OS is caused by an imbalance between the amount of reactive oxygen species produced and antioxidants present in the body. Excess ROS either oxidizes biomolecules or activates the signaling cascade, resulting in inflammation. Immune cells secrete cytokines and chemokines when inflammation is activated. These signaling molecules attract a wide range of immune cells to the site of infection or oxidative stress. Similarly, increased ROS production by immune cells at the inflamed site causes oxidative stress in the affected area. A review on the role of oxidative stress and inflammation in cancer-related literature was conducted to obtain data. All of the information gathered was focused on the current state of oxidative stress and inflammation in various cancers. After gathering all relevant information, a narrative review was created to provide a detailed note on oxidative stress and inflammation in cancer. Proliferation, differentiation, angiogenesis, migration, invasion, metabolic changes, and evasion of programmed cell death are all aided by OS and inflammation in cancer. Imbalance between reactive oxygen species (ROS) and antioxidants lead to oxidative stress that damages macromolecules (nucleic acids, lipids and proteins). It causes breakdown of the biological signaling cascade. Prolonged oxidative stress causes inflammation by activating transcription factors (NF-κB, p53, HIF-1α, PPAR-γ, Nrf2, AP-1) that alter the expression of many other genes and proteins, including growth factors, tumor-suppressor genes, oncogenes, and pro-inflammatory cytokines, resulting in cancer cell survival. The present review article examines the complex relationship between OS and inflammation in certain types of cancer (colorectal, breast, lung, bladder, and gastric cancer).

Role and regulation of autophagy in cancer.

Autophagy is an intracellular self-degradative mechanism which responds to cellular conditions like stress or starvation and plays a key role in regulating cell metabolism, energy homeostasis, starvation adaptation, development and cell death. Numerous studies have stipulated the participation of autophagy in cancer, but the role of autophagy either as tumor suppressor or tumor promoter is not clearly understood. However, mechanisms by which autophagy promotes cancer involves a diverse range of modifications of autophagy associated proteins such as ATGs, Beclin-1, mTOR, p53, KRAS etc. and autophagy pathways like mTOR, PI3K, MAPK, EGFR, HIF and NFκB. Furthermore, several researches have highlighted a context-dependent, cell type and stage-dependent regulation of autophagy in cancer. Alongside this, the interaction between tumor cells and their microenvironment including hypoxia has a great potential in modulating autophagy response in favour to substantiate cancer cell metabolism, self-proliferation and metastasis. In this review article, we highlight the mechanism of autophagy and their contribution to cancer cell proliferation and development. In addition, we discuss about tumor microenvironment interaction and their consequence on selective autophagy pathways and the involvement of autophagy in various tumor types and their therapeutic interventions concentrated on exploiting autophagy as a potential target to improve cancer therapy.

Modulation of multiple cellular signalling pathways as targets for anti-inflammatory and anti-tumorigenesis action of Scopoletin.

OBJECTIVES: Scopoletin (6-methoxy-7-hydroxycoumarin) is a naturally occurring coumarin belonging to the category of secondary metabolites. Coumarins are commonly found in several herbs and play a prominent role in the defense mechanism of plants. Beneficial effects of scopoletin including antioxidant, anti-diabetic, hepatoprotective, neuroprotective and anti-microbial activity induced via numerous intracellular signalling mechanisms have been widely studied. However, anti-inflammation and anti-tumorigenesis properties of scopoletin are not well documented in the literature. Therefore, the primary focus of the present review was to highlight the plethora of research pertaining to the signalling mechanisms associated with the prevention of the progression of disease condition by scopoletin. KEY FINDINGS: Multiple signalling pathways like nuclear erythroid factor-2 (NEF2)-related factor-2 (NRF-2), apoptosis/p53 signalling, nuclear factor-κB (NF-κB) signalling, autophagy signalling, hypoxia signalling, signal transducer and activator of transcription-3 (STAT3) signalling, Wnt-ß signalling, Notch signalling are coupled with the anti-inflammation and anti-tumorigenesis potential of scopoletin. SUMMARY: Understanding crucial targets in these molecular signalling pathways may support the role of scopoletin as a promising naturally derived bioactive compound for the treatment of several diseases.

Process evaluation of Baltimore Healthy Stores: a pilot health intervention program with supermarkets and corner stores in Baltimore City.

Reduced access to affordable healthy foods is linked to higher rates of chronic diseases in low-income urban settings. The authors conduct a feasibility study of an environmental intervention (Baltimore Healthy Stores) in seven corner stores owned by Korean Americans and two supermarkets in low-income East Baltimore. The goal is to increase the availability of healthy food options and to promote them at the point of purchase. The process evaluation is conducted largely by external evaluators. Participating stores stock promoted foods, and print materials are displayed with moderate to high fidelity. Interactive consumer taste tests are implemented with high reach and dose. Materials developed specifically for Korean American corner store owners are implemented with moderate to high fidelity and dose. Results indicate that small food store-based intervention programs are feasible to implement and are a viable means of increasing healthy food availability and a good location for point-of-purchase promotions in low-income urban settings.

NF-κB inhibitors in treatment and prevention of lung cancer.

Intracellular signalling pathways have provided excellent resource for drug development particularly in the development of cancer therapeutics. A wide variety of malignancies common in human exhibit aberrant NF-κB constitutive expression which results in tumorigenic processes and cancer survival in a variety of solid tumour, including pancreatic cancer, lung, cervical, prostate, breast and gastric carcinoma. Numerous evidences indicate that NF-κB signalling mechanism is mainly involved in the progression of several cancers which may intensify an enhanced knowledge on its role in disease particularly lung tumorigenesis. This has led to tremendous research in designing a variety of NF-κB antagonists with enhanced clinical applications through different approaches the most common being suppression of IκB kinase (IKK) beta activity. Many NF-κB inhibitors for lung cancer are now under clinical trials. Preliminary results of clinical trials for several of these agents include small-molecule inhibitors and monoclonal antibodies. A few combinatorial treatment therapies are currently under investigation in the clinics and have shown promise, particularly NF-κB inhibition associated with lung cancer.

Autophagy markers as mediators of lung injury-implication for therapeutic intervention.

Lung injury is characterized by inflammatory processes demonstrated as loss of function of the pulmonary capillary endothelial and alveolar epithelial cells. Autophagy is an intracellular digestion system that work as an inducible adaptive response to lung injury which is a resultant of exposure to various stress agents like hypoxia, ischemia-reperfusion and xenobiotics which may be manifested as acute lung injury (ALI), acute respiratory distress syndrome (ARDS), chronic lung injury (CLI), bronchopulmonary dysplasia (BPD), chronic obstructive pulmonary disease (COPD), asthma, ventilator-induced lung injury (VILI), ventilator-associated lung injury (VALI), pulmonary fibrosis (PF), cystic fibrosis (CF) and radiation-induced lung injury (RILI). Numerous regulators like LC3B-II, Beclin 1, p62, HIF1/BNIP3 and mTOR play pivotal role in autophagy induction during lung injury possibly for progression/inhibition of the disease state. The present review focuses on the critical autophagic mediators and their potential cross talk with the lung injury pathophysiology thereby bringing to limelight the possible therapeutic interventions.

Oxidative stress responsive transcription factors in cellular signalling transduction mechanisms.

Oxidative stress results from the imbalances in the development of reactive oxygen species (ROS) and antioxidants defence system resulting in tissue injury. A key issue resulting in the modulation of ROS is that it alters hosts molecular, structural and functional properties which is accomplished via various signalling pathways which either activate or inhibit numerous transcription factors (TFs). Some of the regulators include Nuclear erythroid-2 related factors (Nrf-2), CCAAT/enhancer-binding protein delta (CEBPD), Activator Protein-1 (AP-1), Hypoxia-inducible factor 1(HIF-1), Nuclear factor κB (NF-κB), Specificity Protein-1 (SP-1) and Forkhead Box class O (FoxO) transcription factors. The expression of these transcription factors are dependent upon the stress signal and are sometimes interlinked. They are highly specific having their own regulation cellular events. Depending upon the transcription factors and better knowledge on the type of the oxidative stress help researchers develop safe, novel targets which can serve as efficient therapeutic targets for several disease conditions.

Ki-67 protein as a tumour proliferation marker.

Newer treatment strategy based on proliferative nuclear marker Ki-67 targeted therapy holds promise for prioritized/personalized treatment options with regard to improved survival and outcome in patients with renal cancer. Over the past decade, the importance of Ki-67 in prognosis of breast cancer has been widely studied, however very few studies and literatures are available in the context of renal cancer which has an increasing incidence internationally. The focus of this present review is to fill the gaps pertaining to its prognosis and management with newly understood mechanisms of targeted interventions. Recent breakthrough discoveries have highlighted the correlation of Ki-67 expression to stage and metastatic potential in renal tumours. A better understanding of molecular structure and different protein domains along with its regulation will provide evidence for precise target thereby controlling the proliferation rate correlated with decrease in the Ki-67 protein levels. Therapies targeting Ki-67 is still in the preclinical stage, besides its diagnostic and/or prognostic significance, a better understanding of targeted strategical studies is required for extrapolation to the clinical use. Current understanding of the associated molecular pathways and the precise role of Ki-67 could streamline the basis for predicting renal cancer outcome.

Pulmonary injury associated with radiation therapy - Assessment, complications and therapeutic targets.

Pulmonary injury is more common in patients undergoing radiation therapy for lungs and other thoracic malignancies. Recently with the use of most-advanced technologies powerful doses of radiation can be delivered directly to tumor site with exquisite precision. The awareness of technical and clinical parameters that influence the chance of radiation induced lung injury is important to guide patient selection and toxicity minimization strategies. At the cellular level, radiation activates free radical production, leading to DNA damage, apoptosis, cell cycle changes, and reduced cell survival. Preclinical research shows the potential for therapies targeting transforming growth factor-ß (TGF-B), Toll like receptor (TLRs), Tumour necrosis factor-alpha (TNF-alpha), Interferon gamma (IFN-γ) and so on that may restore lung function. At present Amifostine (WR-2721) is the only approved broad spectrum radioprotector in use for patients undergoing radiation therapy. Newer techniques also offer the opportunity to identify new biomarkers and new targets for interventions to prevent or ameliorate these late effects of lung damage.