Ensuring the success of local public health workforce assessments: using a participatory-based research approach with a rural population.

OBJECTIVES: To investigate a process for comprehensive rural public health workforce data collection, and apply this process to a competency and training needs assessment of local health department (LHD) workers in the state of Kansas, USA. STUDY DESIGN: Participatory research methods were used to determine an appropriate process for data collection. Survey instruments included the Council on Linkages public health core competencies and Columbia University public health emergency preparedness competencies. METHODS: LHD workers collaborated with the state health department to develop and pre-test training for LHD directors about the nature and purpose of the survey, as well as instructions for distributing it to their staff members. The final survey instrument included demographics, a workforce competency assessment, and an assessment of training interests, motivators and barriers. Surveys were stratified by occupational type, with employees in professional roles asked to report on additional competencies. RESULTS: All 1501 Kansas LHD employees received the needs assessment survey, and 1141 (76%) were returned. Respondents reported greater mean 'importance to job' than ability across competency domains, indicating potential training needs. Across occupational types, primary training motivators were increased competency and personal satisfaction. Barriers included lack of time, cost and family commitments. CONCLUSIONS: Using participatory research methods, the state of Kansas was able to achieve a high response rate from LHD workers. This process can serve as a model for other rural communities and organizations with limited resources. In addition, the survey results provide information about competency-oriented knowledge and training gaps of sectors of the local public health workforce, which can be used to develop training in a targeted fashion.

Effects of electrical stimulation on lymphatic flow and limb volume in the rat.

BACKGROUND AND PURPOSE: The mechanism by which electrical stimulation affects edema has not been elucidated. The purpose of this study was to determine whether subcontraction high-voltage stimulation (SC-HVS) (ie, electrical stimulation that did not elicit a visible contraction) applied to the right hind limbs of rats would (1) alter the rate of lymphatic uptake of injected albumin labeled with Evans blue dye (AL-EBD) and (2) affect experimentally induced edema. SUBJECTS AND METHODS: The paws of 28 anesthetized Sprague-Dawley rats (mean weight = 263 g, SD = 48 g) were injected with AL-EBD. The experimental group (n = 13) received 1 hour of SC-HVS, and the control group (n = 15) received sham treatment consisting of the same treatment administered to the experimental group but without the SC-HVS. Blood samples and volume measurements were obtained at intervals over a 7-hour period. RESULTS: Analysis of variance and post hoc testing indicated that higher amounts of AL-EBD were taken up by the lymph of the experimental group animals as compared with the control group animals at each time period following the treatment. The experimental group's AL-EBD reached significance immediately after treatment, whereas the control group required an additional 4 hours. There was no significant reduction in limb volume in either group. CONCLUSION AND DISCUSSION: The SC-HVS significantly increased the uptake of AL-EBD by lymphatic vessels, but it did not cause a significant decrease in the induced edema. The results of this study indicate that SC-HVS has the potential to reduce edema by increasing lymphatic uptake of proteins.

Decreased activation of skeletal muscle glycogen synthase by mixed-meal ingestion in NIDDM.

Glycogen synthase (GS) catalyzes the formation of glycogen in human skeletal muscle, the tissue responsible for disposal of a significant portion of an oral carbohydrate load. Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by fasting and postprandial hyperglycemia in conjunction with reduced rates of insulin-stimulated glucose disposal and storage in peripheral tissues, including muscle. Our objectives in this study were to determine whether ingestion of a mixed meal activates GS in control nondiabetic subjects and whether meal-related GS activation is reduced in NIDDM. To accomplish this, mixed formula meals were administered to 11 NIDDM and 9 age- and weight-matched nondiabetic control subjects. Plasma glucose and insulin values were measured before and for 90 min after meal ingestion. Skeletal muscle biopsies were performed just before and 90 min after meal ingestion for measurement of GS activity. Compared with control subjects, NIDDM subjects had significantly higher postprandial hyperglycemia and reduced postprandial hyperinsulinemia. GS was activated by meal ingestion in control subjects to a significantly greater extent than in NIDDM subjects. In NIDDM subjects, activation of GS was inversely correlated with fasting plasma glucose (r = .69, P less than .05). Therefore, NIDDM is characterized by reduced activation of a key step in the process of muscle glycogen repletion after a meal. Reduced activation of GS by a mixed meal in NIDDM may contribute to the reduced glucose disposal after a meal, thus contributing to the hyperglycemia observed in these subjects.

Effects of insulin infusion on human skeletal muscle pyruvate dehydrogenase, phosphofructokinase, and glycogen synthase. Evidence for their role in oxidative and nonoxidative glucose metabolism.

To determine whether activation by insulin of glycogen synthase (GS), phosphofructokinase (PFK), or pyruvate dehydrogenase (PDH) in skeletal muscle regulates intracellular glucose metabolism, subjects were studied basally and during euglycemic insulin infusions of 12, 30, and 240 mU/m2 X min. Glucose disposal, oxidative and nonoxidative glucose metabolism were determined. GS, PFK, and PDH were assayed in skeletal muscle under each condition. Glucose disposal rates were 2.37 +/- 0.11, 3.15 +/- 0.19, 6.71 +/- 0.44, and 11.7 +/- 1.73 mg/kg X min; glucose oxidation rates were 1.96 +/- 0.18, 2.81 +/- 0.28, 4.43 +/- 0.32, and 5.22 +/- 0.52. Nonoxidative glucose metabolism was 0.39 +/- 0.13, 0.34 +/- 0.26, 2.28 +/- 0.40, and 6.52 +/- 1.21 mg/kg X min. Both the proportion of active GS and the proportion of active PDH were increased by hyperinsulinemia. PFK activity was unaffected. Activation of GS was correlated with nonoxidative glucose metabolism, while activation of PDH was correlated with glucose oxidation. Sensitivity to insulin of GS was similar to that of nonoxidative glucose metabolism, while the sensitivity to insulin of PDH was similar to that of glucose oxidation. Therefore, the activation of these enzymes in muscle may regulate nonoxidative and oxidative glucose metabolism.