An Interprofessional Rural Health Education Program

Objectives. To develop, implement, and assess an interprofessional rural health professions program for pharmacy and medical students.Design. A recruitment and admissions process was developed that targeted students likely to practice in rural areas. Pharmacy students participated alongside medical students in completing the Rural Health Professions program curriculum, which included monthly lecture sessions and assignments, and a capstone clinical requirement in the final year.Assessment. Fourteen pharmacy students and 33 medical students were accepted into the program during the first 2 years of the Rural Health Professions program. Approximately 90% of the rural health professions students were originally from rural areas.Conclusions. The rural health professions program is an interprofessional approach to preparing healthcare providers to practice in rural communities.     

Role of inducible nitric oxide synthase in induction of RhoA expression in hearts from diabetic rats

AIMS: Recent studies from our laboratory demonstrated that increased expression of the small GTP-binding protein RhoA and activation of the RhoA/rho kinase (ROCK) pathway play an important role in the contractile dysfunction associated with diabetic cardiomyopathy in hearts from streptozotocin (STZ)-induced diabetic rats. Nitric oxide (NO) has been reported to be a positive regulator of RhoA expression in vascular smooth muscle, and we have previously found that the expression of inducible NO synthase (iNOS) is increased in hearts from STZ-diabetic rats. Therefore, in this study, we investigated the hypothesis that induction of iNOS positively regulates RhoA expression in diabetic rat hearts. METHODS AND RESULTS: To determine whether NO and iNOS could increase RhoA expression in the heart, cardiomyocytes from non-diabetic rats were cultured in the presence of the NO donor sodium nitroprusside (SNP) or lipopolysaccharide (LPS) in the absence and presence of the selective iNOS inhibitor, N(6)-(1-iminoethyl)-l-lysine dihydrochloride (L-NIL). In a second study, 1 week after induction of diabetes with STZ, rats were treated with L-NIL (3 mg/kg/day) for 8 more weeks to determine the effect of iNOS inhibition in vivo on RhoA expression and cardiac contractile function. Expression of iNOS was elevated in cardiomyocytes isolated from diabetic rat hearts. Both SNP and LPS increased RhoA expression in non-diabetic cardiomyocytes. The LPS-induced elevation in RhoA expression was accompanied by an increase in iNOS expression and prevented by L-NIL. Treatment of diabetic rats with L-NIL led to a significant improvement in left ventricular developed pressure and rates of contraction and relaxation concomitant with normalization of total cardiac nitrite levels, RhoA expression, and phosphorylation of the ROCK targets LIM (Lin-11, Isl-1, Mec-3) kinase and ezrin/radixin/moesin. CONCLUSION: These data suggest that iNOS is involved in the increased expression of RhoA in diabetic hearts and that one of the mechanisms by which iNOS inhibition improves cardiac function is by preventing the upregulation of RhoA and its availability for activation.     

Linear growth in relation to the circulating concentrations of insulin-like growth factor I, parathyroid hormone, and 25-hydroxy vitamin D in children with nutritional rickets before and after treatment: endocrine adaptation to vitamin D deficiency

The objective of the study was to determine the degree of linear growth retardation of patients with vitamin D deficiency rickets at presentation and the magnitude of catch-up growth in relation to their calcium (Ca) homeostasis and hormones affecting it before and after treatment. This prospective study recorded the anthropometric data and measured the circulating 25-hydroxy vitamin D (25-OH-D), insulin-like growth factor I (IGF-I), parathyroid hormone, Ca, phosphate, and alkaline phosphatase concentrations in 46 infants and children with nutritional (vitamin D deficiency) rickets before and 6 months or more after treatment with one intramuscular injection of vitamin D3 megadose (300000 IU). Forty normal age- and sex-matched children were included as controls for the auxological data. At presentation, patients' mean age = 13.1 +/- 1.1 months, length standard deviation scores (LSDS) = -1.5 +/- 0.2, and body mass index = 16.3 +/- 0.85. They were significantly shorter and had markedly lower growth velocity standard deviation scores (GVSDS) compared with normal controls (LSDS = 0.25 +/- 0.18 and 0.31 +/- 0.22, respectively). Six months after treatment, the LSDS increased significantly in patients to -0.45 +/- 0.13, with a significantly increased GVSDS (2.76 +/- 0.45) and body mass index (16.9 +/- 0.65). They were still shorter but with significantly higher GVSDS compared with normal controls. Serum Ca and phosphate concentrations increased from 2.07 +/- 0.25 and 1.23 +/- 0.24 mmol/L, respectively, before treatment to 2.44 +/- 0.2 and 1.94 +/- 0.2 mmol/L, respectively, after treatment. Serum alkaline phosphatase and parathyroid hormone concentrations decreased from 1183 +/- 219 U/L and 294 +/- 87 pg/mL, respectively, before treatment to 334 +/- 75 U/L and 35.2 +/- 15.2 pg/mL, respectively, after treatment. The 25-OH-D level increased from 4.5 +/- 0.56 ng/mL before treatment to 44.5 +/- 3.7 ng/mL after treatment. Circulating concentrations of IGF-I increased significantly after treatment (52.2 +/- 18.9 ng/mL) vs before treatment (26.6 +/- 12.8 ng/mL). The 25-OH-D concentrations were correlated significantly with the IGF-I levels before and after treatment (r = 0.603 and r = 0.59, respectively; P < .001). The GVSDS after treatment was correlated with the increase of IGF-I and 25-OH-D levels (r = 0.325 and r= 0.314, respectively; P < .01). These data denote that the accelerated linear growth after treatment of nutritional vitamin D deficiency is mediated through activation of the growth hormone/IGF-I system and suggests an important role of vitamin D as a link between the proliferating cartilage cells of the growth plate and growth hormone/IGF-I secretion. Three different sequential stages of vitamin D deficiency can be recognized according to the clinical/radiological, biochemical, and hormonal data of patients at presentation.