When working is not enough: food insecurity in the Canadian labour force.

OBJECTIVE: Food insecurity, lack of access to food due to financial constraints, is highly associated with poor health outcomes. Households dependent on social assistance are at increased risk of experiencing food insecurity, but food insecurity has also been reported in households reporting their main source of income from employment/wages (working households). The objective of the present study was to examine the correlates of food insecurity among households reliant on employment income. DESIGN: Working households reporting food insecurity were studied through analysis of the Canadian Community Health Survey, 2007-2008, employing descriptive statistics and logistic regression. Food insecurity was measured using the Household Food Security Survey Module; all provinces participated. SETTING: Canada. SUBJECTS: Canadian households where main income was derived through labour force participation. Social assistance recipients were excluded. RESULTS: For the period 2007-2008, 4% of working households reported food insecurity. Canadian households reliant on primary earners with less education and lower incomes were significantly more likely to experience food insecurity; these differences were accentuated across some industry sectors. Residence in Quebec was protective. Working households experiencing food insecurity were more likely to include earners reporting multiples jobs and higher job stress. Visible minority workers with comparable education levels experienced higher rates of food insecurity than European-origin workers. CONCLUSIONS: Reliance on employment income does not eliminate food insecurity for a significant proportion of households, and disproportionately so for households with racialized minority workers. Increases in work stress may increase the susceptibility to poor health outcomes of workers residing in households reporting food insecurity.

Coping with child hunger in Canada: have household strategies changed over a decade?

OBJECTIVE: To determine if household coping strategies for child hunger in Canada have changed over a decade (1996-2007). METHODS: We applied t-tests to data derived from Cycle 2 (1996-1997; n=8165) and Cycle 7 (2006-2007; n=15,961) of the National Longitudinal Survey of Children and Youth (NLSCY) to determine changes in household coping strategies for child hunger. Data were restricted to households with children aged 2-9 years, allowing for cross-sectional analysis of two independent samples. Logistic regression was employed to estimate the odds of reporting child hunger for socio-demographic characteristics and the odds of using different coping strategies. RESULTS: The national prevalence of child hunger fell from 1.5% in 1997 to 0.7% in 2007 (p<0.001). The determinants of child hunger (increased child age and household size, lack of home ownership, low household income, lone-parent status, family dysfunction) and hunger frequency (regular versus occasional) were similar in both NLSCY cycles. Utilization of food banks and other community resources as a method of coping with child hunger remained static despite an increase in national food banks/affiliated agencies in Canada (2,141 in 1998 to 3,540 in 2007). In contrast, there was an increased reliance on reducing household food variety, an internal coping mechanism, to manage child hunger (17.6% Cycle 2 to 35.1% Cycle 7; p=0.03). CONCLUSION: Community outreach programs between 1997 and 2007 had little impact on coping strategies utilized by households facing child hunger. Our results indicate that current initiatives fail to reach these families.

Optically sectioned fluorescence endomicroscopy with hybrid-illumination imaging through a flexible fiber bundle.

We present an endomicroscope apparatus that exhibits out-of-focus background rejection based on wide-field illumination through a flexible imaging fiber bundle. Our technique, called HiLo microscopy, involves acquiring two images, one with grid-pattern illumination and another with standard uniform illumination. An evaluation of the image contrast with grid-pattern illumination provides an optically sectioned image with low resolution. This is complemented with high-resolution information from the uniform illumination image, leading to a full-resolution image that is optically sectioned. HiLo endomicroscope movies are presented of fluorescently labeled rat colonic mucosa.

Microscale sample preparation for PCR of C. difficile infected stool.

In this paper, we describe the design of a microfluidic sample preparation chip for human stool samples infected with Clostridium difficile. We established a polymerase chain reaction able to distinguish C. difficile in the presence of several other organisms found in the normal intestinal flora. A protocol for on-chip extraction of nucleic acids from clinical samples is described that can detect target DNA down to 5.0x10(-3) ng of template. The assay and sample preparation chip were then validated using known positive and known negative clinical samples. The work presented has potential applications in both the developed and developing world.

Glucose-dependent insulinotropic polypeptide (GIP) stimulates transepithelial glucose transport.

The purpose of this study was to characterize the effects of glucose-dependent insulinotropic peptide (GIP) on small intestinal glucose transport in vitro. Stripped proximal jejunum from fasted mice was mounted in Ussing chambers. The serosal side was bathed in Regular Ringer solution containing 5 mmol/l glucose, and the mucosal side, with solution containing 10 mmol/l 3-O-methyl glucose (3OMG). Intercellular cyclic adenosine monophosphate (cAMP), mucosa-to-serosa fluxes of 3OMG (J(ms)(3OMG)), and short-circuit current (I(SC)) were measured in the presence and absence of GIP. GIP increased cAMP by 2.5-fold in isolated enterocytes, consistent with a direct effect of GIP on these epithelial cells. GIP also increased I(SC) and J(ms)(3OMG) by 68 and 53%, respectively, indicating that the increase in J(ms)(3OMG) was primarily electrogenic, with a small electroneutral component. The stimulatory effect of GIP on J(ms)(3OMG) was concentration dependent. In addition, 1,000 nmol/l and 10 nmol/l GIP increased J(ms)(3OMG) by 70 and 30% over control, respectively, consistent with receptor activation. Phlorizin (20 mumol/l), an inhibitor of Na(+)-glucose cotransporter (SGLT-1), abolished the increase in I(SC) and decreased J(ms)(3OMG) by approximately 65%. These results indicate that stimulation of SGLT-1 activity by GIP partially accounts for the increase in J(ms)(30MG). These studies are the first to demonstrate direct stimulation of intestinal glucose transport by GIP independent of its insulinotropic properties. GIP stimulates cellular accumulation of cAMP and thereby upregulates glucose transport. The GIP-induced increase in glucose transport appears to be mediated, at least in part, by SGLT-1.

ATP induces guinea pig gallbladder smooth muscle excitability via the P2Y4 receptor and COX-1 activity.

The purpose of this study was to elucidate the mechanisms by which ATP increases guinea pig gallbladder smooth muscle (GBSM) excitability. We evaluated changes in membrane potential and action potential (AP) frequency in GBSM by use of intracellular recording. Application of ATP (100 microM) caused membrane depolarization and a significant increase in AP frequency that were not sensitive to block by tetrodotoxin (0.5 microM). The nonselective P2 antagonist, suramin (100 microM), blocked the excitatory response, resulting in decreased AP frequency in the presence of ATP. The excitatory response to ATP was not altered by pyridoxal-phosphate-6-azophenyl-2,4-disulfonic acid (30 microM), a nonselective P2X antagonist. UTP also caused membrane depolarization and increased AP frequency, with a similar dose-response relationship as ATP. RT-PCR demonstrated that the P2Y(4), but not P2Y(2), receptor subtype is expressed in guinea pig gallbladder muscularis. ATP induced excitation was blocked by indomethacin (10 microM) and the cyclooxygenase (COX)-1 inhibitor SC-560 (300 nM), but not the COX-2 inhibitor nimesulide (500 nM). These data suggest that ATP stimulates P2Y(4) receptors within the gallbladder muscularis and, in turn, stimulate prostanoid production via COX-1 leading to increased excitability of GBSM.

Role of mitochondria in spontaneous rhythmic activity and intracellular calcium waves in the guinea pig gallbladder smooth muscle.

Mitochondrial Ca(2+) handling has been implicated in spontaneous rhythmic activity in smooth muscle and interstitial cells of Cajal. In this investigation we evaluated the effect of mitochondrial inhibitors on spontaneous action potentials (APs), Ca(2+) flashes, and Ca(2+) waves in gallbladder smooth muscle (GBSM). Disruption of the mitochondrial membrane potential with carbonyl cyanide 3-chlorophenylhydrazone, carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone, rotenone, and antimycin A significantly reduced or eliminated APs, Ca(2+) flashes, and Ca(2+) waves in GBSM. Blockade of ATP production with oligomycin did not alter APs or Ca(2+) flashes but significantly reduced Ca(2+) wave frequency. Inhibition of mitochondrial Ca(2+) uptake and Ca(2+) release with Ru360 and CGP-37157, respectively, reduced the frequency of Ca(2+) flashes and Ca(2+) waves in GBSM. Similar to oligomycin, cyclosporin A did not alter AP and Ca(2+) flash frequency but significantly reduced Ca(2+) wave activity. These data suggest that mitochondrial Ca(2+) handling is necessary for the generation of spontaneous electrical activity and may therefore play an important role in gallbladder tone and motility.

Expression and distribution of TTX-sensitive sodium channel alpha subunits in the enteric nervous system.

The expression and distribution of TTX-sensitive voltage-gated sodium channel (VGSC) alpha subunits in the enteric nervous system (ENS) has not been described. Using RT-PCR, expression of Na(v)1.2, Na(v)1.3, Na(v)1.6, and Na(v)1.7 mRNA was detected in small and large intestinal preparations from guinea pigs. Expression of Na(v)1.1 mRNA as well as Na(v)1.1-like immunoreactivity (-li) were not observed in any intestinal region investigated. Na(v)1.2-li was primarily observed within the soma of the majority of myenteric and submucosal neurons, although faint immunoreactivity was occasionally observed in ganglionic and internodal fibers. Na(v)1.3-li was observed in dendrites, soma, and axons in a small group of myenteric neurons, as well as in numerous myenteric internodal fibers; immunoreactivity was rarely observed in the submucosal plexus. Na(v)1.6-li was primarily observed in the initial axonal segment of colonic myenteric neurons. Na(v)1.7-li was observed in dorsal root ganglia neurons but not in the myenteric plexus of the small and large intestine. In the ileum, 37% of Na(v)1.2-li cell bodies colocalized with calbindin-li while colocalization with calretinin-li was rare. In contrast, 22% of Na(v)1.3-li cell bodies colocalized with calretinin-li but colocalization with calbindin-li was not observed. In the colon, both Na(v)1.2-li and Na(v)1.3-li cell bodies frequently colocalized with either calretinin-li or calbindin-li. Na(v)1.2-li cell bodies also colocalized with the majority of NeuN-li cells in the small and large intestine. These data suggest that Na(v)1.1 may not be highly expressed in the ENS, but that Na(v)1.2, Na(v)1.3, and Na(v)1.6, and possibly Na(v)1.7, have broadly important and distinct functions in the ENS.