Household income differences in food sources and food items purchased

<p>Abstract</p> <p>Background</p> <p>The present study examined income-related household food purchases among a sample of 90 households from the community.</p> <p>Methods</p> <p>Annotated food purchase receipts were collected for a four-week period by the primary household shopper. Receipt food source and foods items were classified into specific categories, and food quantities in ounces were recorded by research staff. For home sources, a limited number of food/beverage categories were recorded. For eating out sources, all food/beverage items were recorded. Median monthly per person dollars spent and per person ounces purchased were computed. Food sources and food categories were examined by household income tertile.</p> <p>Subjects and Setting</p> <p>A community-based sample of 90 households.</p> <p>Results</p> <p>Higher income households spent significantly more dollars per person per month from both home and eating out sources compared with lower income households ($163 versus$100, p < .001). Compared with lower income households, higher income households spent significantly more home source dollars on both fruits/vegetables (21.5 versus 10.2, p < .001) and sweets/snacks (17.3 versus 8.3, p < .001), but did not differ on home dollars spent on sugar sweetened beverages (2.0 versus 1.7, p < .46). The proportion of home beverages that were sugar sweetened beverages was significantly higher among lower income households (45% versus 26%, p < .01). Within eating out sources, lower income households spent a significantly greater percent of dollars per person at carry out places (54% versus 37%, p < .01). No income differences were observed for dollars spent at discount grocery stores, small grocery stores or convenience stores.</p> <p>Conclusions</p> <p>Higher income households spent more money on both healthy and less healthy foods from a wide range of sources. Lower income households spent a larger proportion of their eating out dollars at carry out places, and a larger proportion of their home beverage purchases were sugar sweetened beverages.</p

Cellular-Defined Microenvironmental Internalization of Exosomes

The extracellular environment exhibits a potent effect on cellular growth and development. Exosomes secreted into this milieu carry functional proteins and nucleic acids from the cell of origin to recipient cells, facilitating intercellular communication. This interaction is particularly influential in the tumor microenvironment, transporting oncogenes and oncoproteins within a tumor and to distant sites. The mechanisms by which cells internalize exosomes vary greatly and the factors dictating this process are still unknown. Most cancers show evidence of exosomal transfer of material, but differences in cell type can dictate the effectiveness and extent of the process. Improving therapeutics requires addressing specific cellular functions, illustrating the need to better understand the forces involved in exosome-cell interactions. This review summarizes what is known about the different types of cells that play a role in exosome internalization

A p34cdc2 survival checkpoint in cancer

AbstractA checkpoint surveying the entry into mitosis responds to defects in spindle microtubule assembly/stability. This has been used to trigger apoptosis in cancer cells, but how the spindle checkpoint couples to the cell survival machinery has remained elusive. Here, we report that microtubule stabilization engenders a survival pathway that depends on elevated activity of p34cdc2 kinase and increased expression of the apoptosis inhibitor and mitotic regulator, survivin. Pharmacologic, genetic, or molecular ablation of p34cdc2 kinase after microtubule stabilization resulted in massive apoptosis independent of p53, suppression of tumor growth, and indefinite survival without toxicity in mice. By ablating this survival checkpoint, inhibitors of p34cdc2 kinase could safely improve the efficacy of microtubule-stabilizing agents used to treat common cancers

Annotated receipts capture household food purchases from a broad range of sources

<p>Abstract</p> <p>Background</p> <p>Accurate measurement of household food purchase behavior (HFPB) is important for understanding its association with household characteristics, individual dietary intake and neighborhood food retail outlets. However, little research has been done to develop measures of HFPB. The main objective of this paper is to describe the development of a measure of HFPB using annotated food purchase receipts.</p> <p>Methods</p> <p>Households collected and annotated food purchase receipts for a four-week period as part of the baseline assessment of a household nutrition intervention. Receipts were collected from all food sources, including grocery stores and restaurants. Households (n = 90) were recruited from the community as part of an obesity prevention intervention conducted in 2007–2008 in Minneapolis, Minnesota, USA. Household primary shoppers were trained to follow a standardized receipt collection and annotation protocol. Annotated receipts were mailed weekly to research staff. Staff coded the receipt data and entered it into a database. Total food dollars, proportion of food dollars, and ounces of food purchased were examined for different food sources and food categories. Descriptive statistics and correlations are presented.</p> <p>Results</p> <p>A total of 2,483 receipts were returned by 90 households. Home sources comprised 45% of receipts and eating-out sources 55%. Eating-out entrees were proportionally the largest single food category based on counts (16.6%) and dollars ($106 per month). Two-week expenditures were highly correlated (r = 0.83) with four-week expenditures.</p> <p>Conclusion</p> <p>Receipt data provided important quantitative information about HFPB from a wide range of sources and food categories. Two weeks may be adequate to reliably characterize HFPB using annotated receipts.</p

Dynamic changes to survivin subcellular localization are initiated by DNA damage

Subcellular distribution of the apoptosis inhibitor survivin and its ability to relocalize as a result of cell cycle phase or therapeutic insult has led to the hypothesis that these subcellular pools may coincide with different survivin functions. The PIK kinases (ATM, ATR and DNA-PK) phosphorylate a variety of effector substrates that propagate DNA damage signals, resulting in various biological outputs. Here we demonstrate that subcellular repartitioning of survivin in MCF-7 cells as a result of UV light-mediated DNA damage is dependent upon DNA damage-sensing proteins as treatment with the pan PIK kinase inhibitor wortmannin repartitioned survivin in the mitochondria and diminished it from the cytosol and nucleus. Mitochondrial redistribution of survivin, such as was recorded after wortmannin treatment, occurred in cells lacking any one of the three DNA damage sensing protein kinases: DNA-PK, ATM or ATR. However, failed survivin redistribution from the mitochondria in response to low-dose UV occurred only in the cells lacking ATM, implying that ATM may be the primary kinase involved in this process. Taken together, this data implicates survivian’s subcellular distribution is a dynamic physiological process that appears responsive to UV light-initiated DNA damage and that its distribution may be responsible for its multifunctionality

Suppression of survivin phosphorylation on Thr34 by flavopiridol enhances tumor cell apoptosis

Survivin is a member of the inhibitor of apoptosis gene family that is expressed in most human cancers and may facilitate evasion from apoptosis and aberrant mitotic progression. Here, exposure of breast carcinoma MCF-7 or cervical carcinoma HeLa cells to anticancer agents, including Adriamycin, Taxol, or UVB resulted in a 4-5-fold increased survivin expression. Changes in survivin levels after anticancer treatment did not involve modulation of survivin mRNA expression and were independent of de novo gene transcription. Conversely, inhibition of survivin phosphorylation on Thr(34) by the cyclin-dependent kinase inhibitor flavopiridol resulted in loss of survivin expression, and nonphosphorylatable survivin Thr(34)--\u3eAla exhibited accelerated clearance as compared with wild-type survivin. Sequential ablation of survivin phosphorylation on Thr(34) enhanced tumor cell apoptosis induced by anticancer agents independently of p53 and suppressed tumor growth without toxicity in a breast cancer xenograft model in vivo. These data suggest that Thr(34) phosphorylation critically regulates survivin levels in tumor cells and that sequential ablation of p34(cdc2) kinase activity may remove the survivin viability checkpoint and enhance apoptosis in tumor cells

miRNA signatures underlie chemoresistance in the gemcitabine-resistant pancreatic ductal adenocarcinoma cell line MIA PaCa-2 GR

Introduction: Chemotherapy resistance remains a significant challenge in the treatment of pancreatic adenocarcinoma (PDAC), particularly in relation to gemcitabine (Gem), a commonly used chemotherapeutic agent. MicroRNAs (miRNAs) are known to influence cancer progression and chemoresistance. This study investigates the association between miRNA expression profiles and gemcitabine resistance in PDAC.Methods: The miRNA expression profiles of a gemcitabine-sensitive (GS) PDAC cell line, MIA PaCa-2, and its gemcitabine-resistant (GR) progeny, MIA PaCa-2 GR, were analyzed. miRNA sequencing (miRNA-seq) was employed to identify miRNAs expressed in these cell lines. Differential expression analysis was performed, and Ingenuity Pathway Analysis (IPA) was utilized to elucidate the biological functions of the differentially expressed miRNAs.Results: A total of 1867 miRNAs were detected across both cell lines. Among these, 97 (5.2%) miRNAs showed significant differential expression between the GR and GS cell lines, with 65 (3.5%) miRNAs upregulated and 32 (1.7%) miRNAs downregulated in the GR line. The most notably altered miRNAs were implicated in key biological processes such as cell proliferation, migration, invasion, chemosensitization, alternative splicing, apoptosis, and angiogenesis. A subset of these miRNAs was further analyzed in patient samples to identify potential markers for recurrent tumors.Discussion: The differential miRNA expression profiles identified in this study highlight the complex regulatory roles of miRNAs in gemcitabine resistance in PDAC. These findings suggest potential targets for improving prognosis and tailoring treatment strategies in PDAC patients, particularly those showing resistance to gemcitabine. Future research should focus on validating these miRNAs as biomarkers for resistance and exploring their therapeutic potential in overcoming chemoresistance

Docetaxel-induced prostate cancer cell death involves concomitant activation of caspase and lysosomal pathways and is attenuated by LEDGF/p75

<p>Abstract</p> <p>Background</p> <p>Hormone-refractory prostate cancer (HRPC) is characterized by poor response to chemotherapy and high mortality, particularly among African American men when compared to other racial/ethnic groups. It is generally accepted that docetaxel, the standard of care for chemotherapy of HRPC, primarily exerts tumor cell death by inducing mitotic catastrophe and caspase-dependent apoptosis following inhibition of microtubule depolymerization. However, there is a gap in our knowledge of mechanistic events underlying docetaxel-induced caspase-independent cell death, and the genes that antagonize this process. This knowledge is important for circumventing HRPC chemoresistance and reducing disparities in prostate cancer mortality.</p> <p>Results</p> <p>We investigated mechanistic events associated with docetaxel-induced death in HRPC cell lines using various approaches that distinguish caspase-dependent from caspase-independent cell death. Docetaxel induced both mitotic catastrophe and caspase-dependent apoptosis at various concentrations. However, caspase activity was not essential for docetaxel-induced cytotoxicity since cell death associated with lysosomal membrane permeabilization still occurred in the presence of caspase inhibitors. Partial inhibition of docetaxel-induced cytotoxicity was observed after inhibition of cathepsin B, but not inhibition of cathepsins D and L, suggesting that docetaxel induces caspase-independent, lysosomal cell death. Simultaneous inhibition of caspases and cathepsin B dramatically reduced docetaxel-induced cell death. Ectopic expression of lens epithelium-derived growth factor p75 (LEDGF/p75), a stress survival autoantigen and transcription co-activator, attenuated docetaxel-induced lysosomal destabilization and cell death. Interestingly, LEDGF/p75 overexpression did not protect cells against DTX-induced mitotic catastrophe, and against apoptosis induced by tumor necrosis factor related apoptosis inducing ligand (TRAIL), suggesting selectivity in its pro-survival activity.</p> <p>Conclusion</p> <p>These results underscore the ability of docetaxel to induce concomitantly caspase-dependent and independent death pathways in prostate cancer cells. The results also point to LEDGF/p75 as a potential contributor to cellular resistance to docetaxel-induced lysosomal destabilization and cell death, and an attractive candidate for molecular targeting in HRPC.</p

Where eagles soar: Fine-resolution tracking reveals the spatiotemporal use of differential soaring modes in a large raptor

Unlike smaller raptors, which can readily use flapping flight, large raptors are mainly restricted to soaring flight due to energetic constraints. Soaring comprises of two main strategies: thermal and orographic soaring. These soaring strategies are driven by discrete uplift sources determined by the underlying topography and meteorological conditions in an area. High‐resolution GPS tracking of raptor flight allows the identification of these flight strategies and interpretation of the spatiotemporal occurrence of thermal and orographic soaring. In this study, we develop methods to identify soaring flight behaviors from high‐resolution GPS tracking data of Verreaux’s eagle Aquila verreauxii and analyze these data to understand the conditions that promote the use of thermal and orographic soaring. We use these findings to predict the use of soaring flight both spatially (across the landscape) and temporally (throughout the year) in two topographically contrasting regions in South Africa. We found that topography is important in determining the occurrence of soaring flight and that thermal soaring occurs in relatively flat areas which are likely to have good thermal uplift availability. The predicted use of orographic soaring was predominately determined by terrain slope. Contrary to our expectations, the topography and meteorology of eagle territories in the Sandveld promoted the use of soaring flight to a greater extent than in territories in the more mountainous Cederberg region. Spatiotemporal mapping of predicted flight behaviors can broaden our understanding of how large raptors like the Verreaux’s eagle use their habitat and how that links to energetics (as the preferential use of areas that maximize net energy gain is expected), reproductive success, and ultimately population dynamics. Understanding the fine‐scale landscape use and environmental drivers of raptor flight can also help to predict and mitigate potential detrimental effects of anthropogenic developments, such as mortality via collision with wind turbines.Publisher PDFPeer reviewe