An ecological and theoretical deconstruction of a school-based obesity prevention program in Mexico

BACKGROUND: Ecological intervention programs are recommended to prevent overweight and obesity in children. The National Institute of Public Health (INSP) in Mexico implemented a successful ecological intervention program to promote healthy lifestyle behaviors in school age children. This study assessed the integration of ecological principles and Social Cognitive Theory (SCT) constructs in this effective school-based obesity prevention program implemented in 15 elementary schools in Mexico City. METHODS: Two coders applied the Intervention Analysis Procedure (IAP) to “map” the program’s integration of ecological principles. A checklist gauged the use of SCT theory in program activities. RESULTS: Thirty-two distinct intervention strategies were implemented in one setting (i.e., school) to engage four different target-groups (students, parents, school representatives, government) across two domains (Nutrition and Physical Activity). Overall, 47.5% of the strategies targeted the school infrastructure and/or personnel; 37.5% of strategies targeted a key political actor, the Public Education Secretariat while fewer strategies targeted parents (12.5%) and children (3%). More strategies were implemented in the Nutrition domain (69%) than Physical Activity (31%). The most frequently used SCT construct within both intervention domains was Reciprocal Determinism (e.g., where changes to the environment influence changes in behavior and these behavioral changes influence further changes to the environment); no significant differences were observed in the use of SCT constructs across domains. CONCLUSIONS: Findings provide insight into a promising combination of strategies and theoretical constructs that can be used to implement a school-based obesity prevention program. Strategies emphasized school-level infrastructure/personnel change and strong political engagement and were most commonly underpinned by Reciprocal Determinism for both Nutrition and Physical Activity

Molecular Characterization of Borrelia persica, the Agent of Tick Borne Relapsing Fever in Israel and the Palestinian Authority

The identification of the Tick Borne Relapsing Fever (TBRF) agent in Israel and the Palestinian Authority relies on the morphology and the association of Borrelia persica with its vector Ornithodoros tholozani. Molecular based data on B. persica are very scarce as the organism is still non-cultivable. In this study, we were able to sequence three complete 16S rRNA genes, 12 partial flaB genes, 18 partial glpQ genes, 16 rrs-ileT intergenic spacers (IGS) from nine ticks and ten human blood samples originating from the West Bank and Israel. In one sample we sequenced 7231 contiguous base pairs that covered completely the region from the 5′end of the 16S rRNA gene to the 5′end of the 23S rRNA gene comprising the whole 16S rRNA (rrs), and the following genes: Ala tRNA (alaT), Ile tRNA (ileT), adenylosuccinate lyase (purB), adenylosuccinate synthetase (purA), methylpurine-DNA glycosylase (mag), hypoxanthine-guanine phosphoribosyltransferase (hpt), an hydrolase (HAD superfamily) and a 135 bp 5′ fragment of the 23S rRNA (rrlA) genes. Phylogenic sequence analysis defined all the Borrelia isolates from O. tholozani and from human TBRF cases in Israel and the West Bank as B. persica that clustered between the African and the New World TBRF species. Gene organization of the intergenic spacer between the 16S rRNA and the 23S rRNA was similar to that of other TBRF Borrelia species and different from the Lyme disease Borrelia species. Variants of B. persica were found among the different genes of the different isolates even in the same sampling area

A Case of Canine Borreliosis in Iran Caused by Borrelia persica

Tick-borne relapsing fever is an endemic disease in Iran, with most cases attributed to infection by B. persica, which is transmitted by Ornithodoros tholozani soft ticks. Here, we report spirochetemia in blood of a puppy residing in Tehran, Iran. The causative species was identified by use of highly discriminative IGS sequencing; the 489 bp IGS sequence obtained in our study showed 99% identity (100% coverage) when compared with Borrelia persica sequences derived from clinical cases or from Ornithodoros tholozani ticks. Our IGS sequence also showed 99% similarity over 414 bp (85% coverage) with a strain from a domestic dog, and 96% over 328 bp (69% coverage) with a strain from a domestic cat. Pet-keeping in cosmopolitan cities like Tehran has become increasingly popular in recent years. Animals are often transported into the city in cages or cardboard boxes that might also harbour minute tick larvae and/or early stages of the nymphs bringing them into the urban environment. This may pose a threat to household members who buy and keep these puppies and as a result may come into close contact with infected ticks

Effects of Dietary Restriction on Cancer Development and Progression

The effects of caloric restriction on tumor growth and progression are known for over a century. Indeed, fasting has been practiced for millennia, but just recently has emerged the protective role that it may exert toward cells. Fasting cycles are able to reprogram the cellular metabolism, by inducing protection against oxidative stress and prolonging cellular longevity. The reduction of calorie intake as well as short- or long-term fasting has been shown to protect against chronic and degenerative diseases, such as diabetes, cardiovascular pathologies, and cancer. In vitro and in vivo preclinical models showed that different restriction dietary regimens may be effective against cancer onset and progression, by enhancing therapy response and reducing its toxic side effects. Fasting-mediated beneficial effects seem to be due to the reduction of inflammatory response and downregulation of nutrient-related signaling pathways able to modulate cell proliferation and apoptosis. In this chapter, we will discuss the most significant studies present in literature regarding the molecular mechanisms by which dietary restriction may contribute to prevent cancer onset, reduce its progression, and positively affect the response to the treatments

Food environment research in low- and middle-income countries: a systematic scoping review

Food environment research is increasingly gaining prominence in low- and middle-income countries (LMICs). However, in the absence of a systematic review of the literature, little is known about the emerging body of evidence from these settings. This systematic scoping review aims to address this gap. A systematic search of 6 databases was conducted in December 2017 and retrieved 920 records. In total, 70 peer-reviewed articles met the eligibility criteria and were included. Collectively, articles spanned 22 LMICs, including upper-middle-income countries (n = 49, 70%) and lower-middle-income countries (n = 18, 26%). No articles included low-income countries. Articles featured quantitative (n = 45, 64%), qualitative (n = 17, 24%), and mixed-method designs (n = 11, 8%). Studies analyzed the food environment at national, community, school, and household scales. Twenty-three articles (55%) assessed associations between food environment exposures and outcomes of interest, including diets (n = 14), nutrition status (n = 13), and health (n = 1). Food availability was associated with dietary outcomes at the community and school scales across multiple LMICs, although associations varied by vendor type. Evidence regarding associations between the food environment and nutrition and health outcomes was inconclusive. The paucity of evidence from high-quality studies is a severe limitation, highlighting the critical need for improved study designs and standardized methods and metrics. Future food environment research must address low-income and lower-middle-income countries, and include the full spectrum of dietary, nutrition, and health outcomes. Improving the quality of food environment research will be critical to the design of feasible, appropriate, and effective interventions to improve public health nutrition in LMICs

Senolytics and senostatics as adjuvant tumour therapy

Cell senescence is a driver of ageing, frailty, age-associated disease and functional decline. In oncology, tumour cell senescence may contribute to the effect of adjuvant therapies, as it blocks tumour growth. However, this is frequently incomplete, and tumour cells that recover from senescence may gain a more stem-like state with increased proliferative potential. This might be exaggerated by the induction of senescence in the surrounding niche cells. Finally, senescence will spread through bystander effects, possibly overwhelming the capacity of the immune system to ablate senescent cells. This induces a persistent system-wide senescent cell accumulation, which we hypothesize is the cause for the premature frailty, multi-morbidity and increased mortality in cancer survivors. Senolytics, drugs that selectively kill senescent cells, have been developed recently and have been proposed as second-line adjuvant tumour therapy. Similarly, by blocking accelerated senescence following therapy, senolytics might prevent and potentially even revert premature frailty in cancer survivors. Adjuvant senostatic interventions, which suppress senescence-associated bystander signalling, might also have therapeutic potential. This becomes pertinent because treatments that are senostatic in vitro (e.g. dietary restriction mimetics) persistently reduce numbers of senescent cells in vivo, i.e. act as net senolytics in immunocompetent hosts

Chemotherapy-Induced Late Transgenerational Effects in Mice

To our knowledge, there is no report on long-term reproductive and developmental side effects in the offspring of mothers treated with a widely used chemotherapeutic drug such as doxorubicin (DXR), and neither is there information on transmission of any detrimental effects to several filial generations. Therefore, the purpose of the present paper was to examine the long-term effects of a single intraperitoneal injection of DXR on the reproductive and behavioral performance of adult female mice and their progeny. C57BL/6 female mice (generation zero; G0) were treated with either a single intraperitoneal injection of DXR (G0-DXR) or saline (G0-CON). Data were collected on multiple reproductive parameters and behavioral analysis for anxiety, despair and depression. In addition, the reproductive capacity and health of the subsequent six generations were evaluated. G0-DXR females developed despair-like behaviors; delivery complications; decreased primordial follicle pool; and early lost of reproductive capacity. Surprisingly, the DXR-induced effects in oocytes were transmitted transgenerationally; the most striking effects being observed in G4 and G6, constituting: increased rates of neonatal death; physical malformations; chromosomal abnormalities (particularly deletions on chromosome 10); and death of mothers due to delivery complications. None of these effects were seen in control females of the same generations. Long-term effects of DXR in female mice and their offspring can be attributed to genetic alterations or cell-killing events in oocytes or, presumably, to toxicosis in non-ovarian tissues. Results from the rodent model emphasize the need for retrospective and long-term prospective studies of survivors of cancer treatment and their offspring

Intermittent calorie restriction largely counteracts the adverse health effects of a moderate-fat diet in aging C57BL/6J mice

Scope: Calorie restriction (CR) has been shown to extend life- and health-span in model species. For most humans, a life-long CR diet is too arduous to adhere to. The aim of this study was to explore whether weekly intermittent CR can 1) provide long-term beneficial effects and 2) counteract diet-induced obesity in male aging mice. Methods and results: In this study we have exposed C57Bl/6J mice for 24 months to an intermittent (INT) diet, alternating weekly between CR of a control diet and ad libitum moderate-fat (MF) feeding. This weekly intermittent CR significantly counteracted the adverse effects of the MF diet on mortality, body weight and liver health markers in male 24-month-old mice. Hepatic gene expression profiles of INT-exposed animals appeared much more comparable to CR than to MF-exposed mice. At 12 months of age, a subgroup of MF-exposed mice was transferred to the INT diet. Gene expression profiles in the liver of the 24-month-old diet switch mice were highly similar to the INT-exposed mice. However, a small subset of genes was consistently changed by the MF diet during the first phase of life. Conclusion: Weekly intermittent CR largely, but not completely, reversed adverse effects caused by a MF diet