Feeding inequality: food insecurity,social status and college student health

A growing but limited body of research has identified the college student population as one that is particularly vulnerable to food insecurity. Early estimates of food insecurity prevalence among college students range from 14 to 60 per cent. The present study utilises original survey data collected from a random sample (n = 300) of college students enrolled at an urban university in the Midwest region of the United States of America (USA). This study examines the impact of food insecurity on health outcomes and the mediation of this relationship by subjective social status among college students. Ordinary least squares (OLS) and logistic regression analyses find that food insecurity is related to worse self-rated, physical and mental health among college students, and Sobel-Goodman tests find that subjective social status plays a significant mediating role in the relationship between food insecurity and health among college students. The implications of these findings in a university context are discussed using a psychosocial framework and insights from the stress process model. In doing so, I discuss food insecurity among college students with an emphasis on the social significance of food and food insecurity.     

Differential roles of neurokinin 1 and neurokinin 2 receptors in the development and maintenance of heat hyperalgesia induced by acute inflammation

1. Following induction of acute inflammation by intraarticular injection of kaolin and carrageenan into the knee joint in rats, there was a significant decrease in the withdrawal latency to radiant heat applied to the paw (i.e. heat hyperalgesia), an increased joint circumference and increased joint temperature.
2. A neurokinin₁ (NK₁) receptor antagonist (CP-99,994, 10 mM) had no effect on the paw withdrawal latency when it was administered spinally through a microdialysis fibre before the induction of inflammation. Pretreatment with a NK₂ receptor antagonist (SR48968, 1 mM) administered spinally through the microdialysis fibre prevented the heat hyperalgesia from developing in the early stages of the inflammation.
3. Post-treatment through the microdialysis fibre with the NK₁ receptor antagonist (0.0110 mM) was effective in reversing the heat hyperalgesia. In contrast, post-treatment spinally with the NK₂ receptor antagonist (0.011 mM) had no effect on the heat hyperalgesia. The inactive stereoisomers of the NK₁ receptor antagonist, CP100,263, or the NK₂ receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the heat hyperalgesia.
4. Pretreatment systemically with the NK₁ receptor antagonist (30 mg kg⁻¹) had no effect on the heat hyperalgesia or pain-related behaviour ratings where 0 is none and 5 is non weight bearing and complete avoidance of limb contact. Pretreatment with a NK₂ receptor antagonist (10 mg kg⁻¹) systemically prevented the heat hyperalgesia and pain-related behaviour ratings from developing in the early stages of the inflammation. The inactive stereoisomers of NK₁ receptor antagonist, CP100,263, or the NK₂ receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the heat hyperalgesia.
5. Post-treatment systemically with either the NK₁ (0.130 mg kg⁻¹) or the NK₂ (0.110 mg kg⁻¹) receptor antagonist resulted in a dose-dependent reversal of the heat hyperalgesia. Pain-related behaviour ratings were reduced by post-treatment only with the NK₁ receptor antagonist. The inactive stereoisomers of the NK₁ receptor antagonist, CP100,263, or the NK₂ receptor antagonist, SR48965, administered at the same doses, had no effect on the behavioural responses.
6. Direct pretreatment of the knee joint with either the NK₁ (30 mg) or the NK₂ (10 mg) receptor antagonist prevented the heat hyperalgesia from developing without affecting joint swelling. The inactive stereoisomers of the NK₁ receptor antagonist, CP100,263, or the NK₂ receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the heat hyperalgesia.
7. There appears to be a differential role for the spinal tachykinin receptors in the development and maintenance of the heat hyperalgesia associated with acute joint inflammation. The NK₂ receptors appear to be activated early in the development of the heat hyperalgesia and NK₁ receptors are involved in the maintenance of the heat hyperalgesia.
8. Peripherally, both NK₁ and NK₂ receptors are involved in the development of heat hyperalgesia and pain-related behaviour ratings induced by acute inflammation.

     

Age and the onset of desaturation in apnoeic children

Most patients undergoing general anaesthesia are apnoeic during laryngoscopy and tracheal intubation. This study determined the time until the onset of desaturation following preoxygenation in apnoeic infants, children, and adolescents. Fifty ASA physical status I patients, 2 days to 18 yr of age, were studied. The patients were stratified into one of five groups according to age: Group I, 0–6 mo; Group II, 7–23 mo; Group III 2–5 yr; Group IV, 6–10 yr; and Group V, 11–18 yr. Following induction of anaesthesia with halothane via mask or intravenous barbiturates, the ability of the anaesthetist to ventilate the lungs via the mask was ascertained and paralysis was accomplished with vecuronium 0.1 mg · kg^?1. Manual mask ventilation was maintained with oxygen and halothane. When end-tidal N₂ decreased below 3% (minimum time two minutes), the face mask was removed. The time between the removal of the face mask and a decrease in oxygen saturation (SpO₂ from 99–100% to 90% was measured. Manual ventilation was then resumed and the trachea intubated. Desaturation started earlier in infants than in two-to five-year-old children (96.5 ± 12.7 sec vs 160.4 ± 30.7 sec, P < 0.0001). Children became desaturated faster than adolescents (160.4 ± 30.7 vs 382.4 ± 79.9 sec, P < 0.0001). The time required to reach 90% saturation correlated well with age by linear regression analysis (r² = 0.88, P < 0.0001). We conclude that the time to onset of desaturation following pre-oxygenation with mask ventilation increases with age in healthy apnoeic children. Adolescents can tolerate apnoea for longer than children, and infants exhibit desaturation faster than children.     

Soybean isoflavones, genistein and genistin, inhibit rat myoblast proliferation, fusion and myotube protein synthesis.

The isoflavones, genistein and genistin, are cytotoxic in vitro (e.g. , inhibition of cell proliferation), due in part to inhibition of protein tyrosine kinase and DNA topoisomerase activities. Normal cell functions associated with these enzymatic activities could potentially be impaired in animals through ingestion of soybean products. In this study, cultured rat myogenic cells (L8) were used to determine whether genistein or genistin influences myoblast proliferation and fusion, and myotube protein synthesis and degradation. Genistein or genistin was dissolved in dimethylsulfoxide and included in the culture medium at 0, 1, 10 or 100 micromol/L. Myoblast proliferation was measured by methyl-3H-thymidine incorporation over 48 h. Myoblast differentiation was evaluated by the number of nuclei in multinucleated myotubes. Myotube protein synthesis was measured by 2-h 3H-amino acid incorporation into the myosin and total protein pools after acute (2 h) or chronic (24 h) exposure to similar treatments; protein degradation was measured by measuring radioactivity in protein pools following a time course of protein breakdown after myotube proteins were prelabeled with 3H-amino acids. Genistein or genistin strongly inhibited in vitro myoblast proliferation (P < 0.001) and fusion (P < 0.001) in a dose-dependent manner with effective genistein concentration as low as 1 micromol/L. Genistein or genistin inhibited protein accretion in myotubes (P < 0.001). Decreased protein accretion is largely a result of inhibition on cellular (myofibrillar) protein synthesis rate. No adverse effect on protein degradation was observed. Results suggest that if sufficient circulating concentrations are reached in tissues of animals consuming soy products, genistein/genistin can potentially affect normal muscle growth and development.     

Unique presentation of Crohn's disease during treatment of Hodgkin's disease

Although Hodgkin's disease and Crohn's disease are associated with abnormalities in cell-mediated immunity, their co-existence in an individual patient is uncommon. To our knowledge, this is the first report of the clinical presentation of Crohn's disease during treatment for Hodgkin's disease. The basic immunologic mechanisms underlying these two pathologic states as well as chemotherapy-related effects are postulated as potential etiologic mechanisms for the codevelopment of these diseases. A brief review of the literature and basic immunologic defects associated with Crohn's disease and Hodgkin's disease are presented.     

Effects of Extracorporeal Shock Wave Lithotripsy to One Kidney on Bilateral Glomerular Filtration Rate and PAH Clearance in Minipigs

Purpose

This study examined the acute time course of effects of extracorporeal shock wave lithotripsy (ESWL)¹ on renal hemodynamics in anesthetized minipigs with and without pretreatment with verapamil.

Materials and Methods

We applied ESWL (2000 shocks, 24 kV, unmodified Dornier HM3), to the right kidneys of isoflurane-anesthetized female pigs. Urine flow and renal hemodynamics were monitored from each kidney via ureteral balloon catheters. Arterial blood pressure and bilateral urine flow, glomerular filtration rate (GFR, inulin clearance) and renal plasma flow (RPF, para-aminohippurate clearance) were monitored for 45 minutes before ESWL, and at 1, 4 and 24 hours after ESWL.

Results

Treatment with ESWL consistently caused unilateral hematuria and subcapsular renal hematomas in the shocked kidneys and significantly reduced GFR and RPF in those kidneys at 1 and 4 hours after ESWL. Urine flow was reduced through 24 hours in the shocked kidneys. Renal plasma flow, but not GFR, was significantly reduced in the contralateral (unshocked) kidneys at 1 and 4 hours after ESWL to the other kidneys. Verapamil blunted the ESWL-induced reductions of urine flow, GFR and RPF in the shocked kidneys and eliminated the reduction of RPF in the unshocked kidneys.

Conclusions

These experiments demonstrate that ESWL to 1 kidney acutely impaired hemodynamics in both kidneys and that verapamil attenuated the response in the shocked kidneys and eliminated it in the contralateral unshocked kidneys.