Breastfeeding promotion and support services in local community health centers

This study had a two-fold goal. First, to document services relating to breastfeeding promotion and support in CLSCs and, second, to examine the links between the delivery of such services and certain organizational and environmental factors. The data were collected in 1999 by means of a self-administered questionnaire sent to all CLSCs in Quebec. The responses indicated that breastfeeding is most often systematically addressed at prenatal meetings and through integrated perinatal programs. CLSCs belonging to a multipurpose establishment are more apt to integrate the issue of breastfeeding into perinatal activities; in addition, many of them offer breastfeeding activities considered innovative, although the average for this kind of activities is fairly low (33%). In addition, CLSCs that collaborate more closely with community organizations and those that spend more on perinatal programs are the ones that most often offer "innovative" breastfeeding activities.     

In vitro reactivation of acetylcholinesterase inhibited by cyclosarin using bisquaternary pyridinium aldoximes K005, K033, K027 AND K048

We have tested four new bisquaternary pyridinium acetylcholinesterase (AChE; EC 3.1.1.7) reactivators - K005 (1,3-bis(2-hydroxyiminomethylpyridinium) propane dibromide), K033 (1,4-bis(2-hydroxyiminomethylpyridinium) butane dibromide), K027 (1 -(4-hydroxyiminomethylpyridinium)-3-(4-carbamoylpyridinium) propane dibromide) and K048 (1-(4-hydroxyiminomethylpyridinium)-4-(4-carbamoylpyridinium) butane dibromide) as the potential reactivators of AChE inhibited by cyclosarin. Their reactivation potencies were studied using standard in vitro reactivation test. Rat brain homogenate was used as the source of the enzyme. Oxime K033 seems to be the most potent reactivator of cyclosarin-inhibited AChE. Its reactivation potency is significantly higher than the efficacy of all other tested AChE reactivators.     

Diet-induced obesity delays cardiovascular recovery from stress in spontaneously hypertensive rats

OBJECTIVE: Blood pressure (BP) and heart rate (HR) responses to stress are significant predictors of cardiovascular morbidity and mortality. Because obesity is a major risk factor for cardiovascular disease, we examined whether diet-induced obesity alters the BP and HR responses to stress and whether these alterations are associated with augmented cardiovascular morbidity in the rat. RESEARCH METHODS AND PROCEDURES: Adult male spontaneously hypertensive rats were fed either a normal diet or high-fat diet (HFD) for 12 weeks. At weeks 0 and 12, body weight was measured, and BP and HR were recorded by radiotelemetry throughout three consecutive day and night periods and in response to 30-minute immobilization stress. At the end of the 12-week intervention, the rats were sacrificed, and their organs and sera were collected. RESULTS: With the intervention, HFD rats showed a significantly greater increase in body weight (as expected) and circulating leptin and free fatty acid levels compared with normal diet rats. In addition, they showed similar increases in BP and HR elevations during stress but significantly slower BP and HR decreases after stress. These HFD-induced delays in stress recovery were associated with BP and HR elevations during the night (behaviorally active) period and with augmentations in cardiac mass. DISCUSSION: The results of this study indicate that, in spontaneously hypertensive rats, dietary obesity delays cardiovascular recovery from stress, and, in parallel, it promotes the development of nocturnal hypertension as well as cardiac hypertrophy. This suggests that dietary obesity may significantly potentiate the impact of daily stressful experiences on the cardiovascular system.     

Predictors of initiation into prostitution among female street youths

Prostitution among female street youths represents an important risk factor for several health problems. Little is known about the incidence and determinants of prostitution in this vulnerable population, and no data have been previously reported based on a longitudinal follow-up study. The objective of this study was to determine predictors of initiation into prostitution among female street youths. Female youths aged 14 to 25 years were enrolled in the Montreal Street Youth Cohort. They completed a baseline and at least one follow-up questionnaire between January 1995 and March 2000. Girls who reported never having engaged in prostitution at baseline were followed prospectively to estimate the incidence and predictors of prostitution. Of the 330 female street youths enrolled as of September 2000 in the cohort, 148 reported no history of involvement in prostitution at baseline and completed at least one follow-up questionnaire. Of these 148 girls, 33 became involved in prostitution over the course of the study (mean follow-up 2.4 years), resulting in an incidence rate of 11.1/100 person-years. Multivariate Cox regression analysis revealed having a female sex partner (adjusted hazard ratio [AHR] 3.8; 95% confidence interval [CI] 1.6–9.1) was an independent predictor of initiation into prostitution after controlling for having been on the street at age 15 years or younger (AHR 1.8, 95% CI 0.9–3.8), using acid or phecyclidine (PCP; AHR 2.0, 95% CI 0.9–4.6), using heroin (AHR 1.9, 95% CI 0.7–5.5), the use of drugs greater than twice perweek (AHR 1.9, 95% CI 0.9–4.2), and injection drug use (AHR 0.8, 95% CI 0.3–2.4). The incidence of prostitution in female street youths was elevated. Having a female sex partner was a strong predictor of initiating involvement in prostitution.     

Parental social determinants of risk for intentional injury: a cross-sectional study of Swedish adolescents

OBJECTIVES: We investigated the effect of family social and economic circumstances on intentional injury among adolescents. METHODS: We conducted a cross-sectional register study of youths aged 10 to 19 years who lived in Sweden between 1990 and 1994. We used socioeconomic status, number of parents in the household (1- or 2-parent home), receipt of welfare benefits, parental country of birth, and population density as exposures and compiled relative risks and population-attributable risks (PARs) for self-inflicted and interpersonal violence-related injury. RESULTS: For both genders and for both injury types, receipt of welfare benefits showed the largest crude and net relative risks and the highest PARs. The socioeconomic status-related PAR for self-inflicted injury and the PAR related to number of parents in the household for interpersonal violence-related injury also were high. CONCLUSIONS: Intentional-injury prevention and victim treatment need to be tailored to household social circumstances.     

Falls and Fall-Related Injuries Among the Elderly: A Survey of Residential-Care Facilities in a Swedish Municipality

Injurious falls among the elderly are an increasing public-health problem in Sweden. One group particularly vulnerable to falls consists of elderly people living in residential-care facilities. The purpose of this study was to investigate the extent to which falls lead to injury within a defined population of elderly people in institutionalized care. All the elderly persons living in residential-care facilities in an urban Swedish municipality during the year 1997 (n = 469 institutional places). Falls and fall-related injuries were registered over a one-year period. Data were gathered by personnel at the time of the falls, using a form specifically designed for surveillance purposes. Of the 865 falls reported during the study period, 375 were among men, with an average age of 82 years, and 490 among women, with an average age of 85 years. Men were subject to falling to a greater extent than women. The most common location was the individual's own bedroom. Injuries were incurred in approximately one in four falls, and the head was the body part most frequently injured. Only 24 falls (2.8%) resulted in a fracture, of which 18 were hip fractures. Although elderly people living in residential-care facilities fall fairly often, serious injuries, in the form of fractures, are incurred to a relatively limited extent.     

Rosiglitazone increases extravasation of macromolecules and endothelial nitric oxide synthase in skeletal muscles of the fructose-fed rat model

Reduced extravasation of macromolecules in skeletal muscle has recently been documented in the fructose-fed rat model, corroborating a hypothesis that a functional obliteration of muscle regional microcirculation might lead to hypertension and restrict access of nutrients and hormones to their target cells. The goal of this study was to assess the impact of a treatment with rosiglitazone on the reduced muscle vasopermeability observed previously in the fructose-fed rat model. Fructose-fed Sprague-Dawley rats were gavaged with rosiglitazone (10 micromol kg(-1) per day; n = 21) or the vehicle only (n = 19) for 3 consecutive weeks before assessing the extravasation of Evans Blue (EB) dye in vivo in distinct muscle groups. Relative to control group, rosiglitazone reduced mean arterial blood pressure (Delta = -16.7%, P < 0.001), plasma insulin (Delta= -39.1%, P < 0.05) and plasma triglyceride (Delta= -32.8 %, P < 0.01) concentrations in a significant manner. Plasma VEGF concentrations were significantly lower in the rosiglitazone-treated animals compared to the control animals (32.7 +/- 0.8 pg ml(-1) versus 46.1 +/- 1.2 pg ml(-1), P < 0.001). While no changes were observed in the lungs or the kidneys, fructose-fed rats treated with rosiglitazone had a 30-50% increase (P < 0.005) in the extravasation of EB regardless of the skeletal muscle group studied (rectus femoris, soleus, gastrocnemius lateralis, vastus lateralis and tibialis cranalis). In homogenates of skeletal muscles (vastus lateralis) of fructose-fed rats, rosiglitazone resulted in a significant increase in NO synthase (NOS) activity (Delta = +41.9 %, P < 0.003) as well as endothelial NOS immunoreactive mass (Delta = +37.8 %, P < 0.01) compared to the control animals. There was no change in the immunoreactive level of the nNOS isoform, the most abundant muscle isoform, or in the immunoreactive levels of VEGF. In conclusion, rosiglitazone appears to restore a vascular dysfunction previously documented in the skeletal muscle microcirculation, as evidenced by improved skeletal muscle vasopermeability and upregulation of the muscle endothelium-NO system in the fructose-fed rat model. These effects on muscle per se might also result in a partial improvement of the insulin resistance phenomenon by improving the distribution of nutrients and insulin to skeletal muscle. This effect appears to be independent of circulating levels of VEGF since changes in plasma concentrations of this permeability factor were lower in the rosiglitazone-treated group.     

The effect of tryptophan depletion on the action of haloperidol in MK-801-treated rats

We investigated the effect of tryptophan depletion (tryptophan-free mixture) on locomotor activity in an animal model of schizophrenia, induced by acute administration of 5R,10S-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine hydrogen maleate (MK-801), and the influence of the tryptophan-free mixture on the action of the typical antipsychotic haloperidol. Male rats were pre-treated with haloperidol 60 min after receiving the tryptophan-free mixture (or water). We measured total distance travelled in an open field during a 90-min period. Administration of the tryptophan-free mixture resulted in decreased levels of tryptophan, serotonin and its metabolite 5-hydroxyindolacetic acid in the frontal cortex. Serotonin depletion increased the total distance travelled by MK-801-treated rats, modified the inhibitory effect of haloperidol and normalized the locomotor activity pattern in the model of schizophrenia-like behaviour. The effect of the tryptophan-free mixture combined with the classical antipsychotic haloperidol in MK-801-treated rats indicates the possibly important role of the serotonergic system in the action of antipsychotics.     

Loss of neural cell adhesion molecule induces tumor metastasis by up-regulating lymphangiogenesis

Reduced expression of neural cell adhesion molecule (NCAM) has been implicated in the progression to tumor malignancy in cancer patients. Previously, we have shown that the loss of NCAM function causes the formation of lymph node metastasis in a transgenic mouse model of pancreatic beta cell carcinogenesis (Rip1Tag2). Here we show that tumors of NCAM-deficient Rip1Tag2 transgenic mice exhibit up-regulated expression of the lymphangiogenic factors vascular endothelial growth factor (VEGF)-C and -D (17% in wild-type versus 60% in NCAM-deficient Rip1Tag2 mice) and, with it, increased lymphangiogenesis (0% in wild-type versus 19% in NCAM-deficient Rip1Tag2 mice). Repression of VEGF-C and -D function by adenoviral expression of a soluble form of their cognate receptor, VEGF receptor-3, results in reduced tumor lymphangiogenesis (56% versus 28% in control versus treated mice) and lymph node metastasis (36% versus 8% in control versus treated mice). The results indicate that the loss of NCAM function causes lymph node metastasis via VEGF-C- and VEGF-D-mediated lymphangiogenesis. These results also establish Rip1Tag2;NCAM-deficient mice as a unique model for stochastic, endogenous tumor lymphangiogenesis and lymph node metastasis in immunocompetent mice.     

Increased baclofen-stimulated G protein coupling and deactivation in rat brain cortex during development

The number and affinity of GABA(B) receptors (assayed by the specific antagonist [(3)H]CGP54626A) was unchanged when compared in carefully washed cerebrocortical membranes from young (12-day-old) and adult (90-day-old) rats. In contrast, high-affinity GTPase activity, both basal and baclofen-stimulated was significantly higher (by 45% and 56%, respectively) in adult than in young rats. Similar results were obtained by concomitant determination of agonist (baclofen)-stimulated GTP gamma S binding. Under standard conditions, baclofen-stimulated GTPase activity was further considerably enhanced by exogenously added regulator of G protein function, RGS1, but not by RGS16. RGS16 was able to affect agonist-stimulated GTPase activity only in the presence of markedly increase substrate (GTP) concentrations. RGS1 alone slightly increased GTPase activity in adult rats, but neither RGS1 nor RGS16 influenced GTPase activity in membrane preparations isolated from young animals. These findings indicate increasing functional activity of trimeric G protein(s) involved in GABAergic transmission in the developing rat brain cortex and suggest a high potential of RGS1 in regulation of high-affinity GTPase activity.