Assessing management training needs: a study in the Punjab health services,Pakistan

Pakistan's public sector is organized in a federal system with many management and planning functions devolved to the 4 provincial governments. Provincial health secretariats lead on most policy and planning decisions for health services. The provinces employ health personnel, although the national Public Service Commission controls some key aspects of human resources management. Reporting the findings of a training needs assessment (TNA) for health personnel in the provincial health services of Punjab, the authors show how TNA can be used systematically to improve the quality of health professional training. They also discuss the extent to which better training could contribute to improved health management capacity in Pakistan, and describe the context and problems of Pakistan's health services, focusing upon management capacity, and the methods and results of a training needs assessment conducted to address the problems. A final section covers the usefulness of the TNA method in Pakistan and its applicability to other countries. Moreover, the implications of decentralization and the problems of preparing training plans in the absence of decentralized structures are discussed.     

Decreased incidence of arterial thrombosis using heparin-bonded intraaortic balloons

BACKGROUND: This experimental study sought to determine whether heparin-bonding of intraaortic balloons (IAB) would decrease the incidence of arterial thrombosis in the absence of systemic heparinization. METHODS: In 25 adult pigs, a 9F, 40-mL IAB was inserted into the femoral artery and positioned just below the takeoff of the left subclavian artery for 9 hours. Five animals received systemic heparin, 10 animals had no heparin, and another 10 animals received no heparin but the IAB was heparin-bonded (Duraflo II). Thrombus formation was assessed using a numerical scoring system (0 = no thrombosis to 3 = thrombus >5 cm or evidence of luminal compromise). RESULTS: Animals receiving heparin and heparin-bonded IAB had no thrombus formation around the IAB (mean +/- SE; 0 +/- 0.00 heparin versus 1.55 +/- 0.29 no heparin versus 0 +/- 0.00 heparin-bonded; p < 0.005), at the insertion site (0 +/- 0.00 heparin versus 1.55 +/- 0.29 no heparin versus 0 +/- 0.0 heparin-bonded; p < 0.005), and in the distal femoral artery (0 +/- 0.00 heparin versus 2.00 +/- 0.23 no heparin versus 0 +/- 0.00 heparin-bonded; p < 0.005). CONCLUSIONS: Heparin-bonding of the IAB significantly decreases thrombus formation in the absence of systemic heparinization.     

Microcirculatory basis for nonuniform flow delivery with intravenous nitroprusside.

BACKGROUND: The purpose of this study was to determine the effects of systemic infusions of nitroglycerin and sodium nitroprusside on flow distribution and wall shear stress in the microcirculation. METHODS: With university approval, the cremaster muscle of 28 anesthetized (70 mg/kg pentobarbital given intraperitoneally) hamsters (Harlan Sprague Dawley: Syrian; weight, 121+/-11 g [mean +/- SDD) was observed using in vivo fluorescence microscopy. Arteriolar diameter, erythrocyte flux, and velocity were measured for a feed arteriole and its sequential branches. Observations were made during control (mean arterial pressure, 88+/-4 mm Hg) and after 30 min of intravenous delivery of sodium nitroprusside or nitroglycerin, titrated to decrease mean arterial pressure by 20 mm Hg. RESULTS: Sodium nitroprusside significantly dilated select upstream portions of the network (23+/-2.6 to 29+/-2.6 microm); no arterioles were dilated with nitroglycerin. Erythrocyte flux into the feed (i.e., inflow into the arteriolar network) and into the sequential branches (i.e., distribution within the network) were evaluated. With nitroglycerin, inflow decreased significantly from 1,560+/-335 to 855+/-171 cells/s, and flux into the branches decreased evenly. With sodium nitroprusside, inflow increased significantly to 2,600+/-918 cells/s, yet cells were "stolen" from upstream branches (a decrease from 425+/-67 to 309+/-87 cells/s in the first branch). Excess flow passed into a downstream "thorough-fare channel," significantly increasing flux from 347+/-111 to 761+/-246 cells/s. Wall shear stress decreased uniformly with nitroglycerin infusion, with a decrease in the feed from 8.8+/-2.5 to 6+/-1.7 dyn/cm2. With sodium nitroprusside, variable changes occurred that were location specific within the network. For instance, at the inflow point to the network, wall shear stress changed from 8.3+/-2.5 to 4.2+/-3.3 dyn/cm2. CONCLUSIONS: Nitroglycerin infusion promoted homogeneity of flow. Sodium nitroprusside significantly increased the heterogeneity of flow within this arteriolar network; an anatomic location for steal induced by sodium nitroprusside is identified.     

Pharmacologic study of muscarinic receptor subtypes and arteriolar dilations: a comparison of conducted and local responses

Arteriolar relaxation caused by the application of muscarinic agonists is mediated by multiple factors. One factor causes dilation only at the point of drug microapplication (local response), and a second factor causes responses remote (500 microm away) from the site of application (conducted response). This study was performed to determine if different muscarinic subtypes mediate the two responses. Arterioles of anesthetized hamster cheek pouch were studied with videomicroscopy. Muscarinic antagonists methscopolamine, scopolamine, pirenzepine, 4-DAMP (4-diphenylacetoxy-N-methylpiperidine methiodide), and AFDX-116 [(11-2[[2-[(diethylamino)methyl]-1-piperidinyl]acetyl]-5, 11-dihydro-6H-pyrido [2,3-b][1,4]benzodiazepin-6-one)] were cumulatively applied, and the K(B) for each antagonist was determined for the local and conducted responses caused by methacholine microapplication (10(-4) M, 5 s). The pK(B) (local, conducted) were not significantly different for the two responses when using scopolamine (10.5, 10.4). When the antagonist AFDX-116 (5.6, 6.3), selective for muscarinic receptor (m2) subtype was applied, the K(B) was greater for the conducted response. The pK(B) was greater, however, for the local response when the m1 subtype-selective pirenzepine (7.7, 6.9) or m3 subtype-selective 4-DAMP (10.1, 9.8) was applied. Thus the antagonist pK(B) ratio for on the local and conducted responses depends on the subtype selectivity of the antagonist. These data strongly suggest that different receptors are involved in the two responses.     

Osteoarthritic changes in the biochemical composition of thumb carpometacarpal joint cartilage and correlation with biomechanical properties

The biochemical composition and biomechanical properties of articular cartilage from 53 human thumb carpometacarpal (CMC) joints from cadavers aged 20 to 79 years were measured and studied in normal, mildly fibrillated, and advanced osteoarthritic (OA) joints. Statistical analyses were performed to determine the correlations between the compositional measures and biomechanical properties. For these CMC joint tissues we found that water content increased, proteoglycan content decreased, and collagen content per dry weight remained unaltered with progression of OA degeneration. We also found that with disease progression, as defined by an OA staging score, the aggregate modulus (ie, compressive stiffness) decreased, along with an unexpected moderate decrease in permeability. This latter finding appears to be specific to CMC cartilage degeneration since articular cartilage from knees and hips generally demonstrates an increase in permeability with water content and OA score. Correlations between biochemical composition and biomechanical properties were found to be stronger in joints with OA than in joints without OA. This finding suggests that OA changes in biochemical composition, relative to baseline normal values, directly affect the biomechanical properties of cartilage, even though the baseline compositional values themselves do not directly determine the magnitude of the biomechanical properties in normal tissue.     

The efficacy of the ketogenic diet-1998: a prospective evaluation of intervention in 150 children

OBJECTIVE: The ketogenic diet is a high-fat, low-protein, low-carbohydrate diet developed in the 1920s for the treatment of children with difficult to control seizures. Despite advances in both the pharmacotherapy and the surgery of epilepsy, many children continue to have difficult-to-control seizures. This prospective study sought to determine the ketogenic diet's effectiveness and tolerability in children refractory to today's medications. METHODS: One hundred fifty consecutive children, ages 1 to 16 years, virtually all of whom continued to have more than two seizures per week despite adequate therapy with at least two anticonvulsant medications, were prospectively enrolled in this study, treated with the ketogenic diet, and followed for a minimum of 1 year. Seizure frequency was tabulated from patients' daily seizure calendars and seizure reduction calculated as percentage of baseline frequency. Adverse events and reasons for diet discontinuation were recorded. RESULTS: The children (mean age, 5.3 years), averaged 410 seizures per month before the diet, despite an exposure to a mean of 6.2 antiepileptic medications. Three months after diet initiation, 83% of those starting remained on the diet and 34% had >90% decrease in seizures. At 6 months, 71% still remained on the diet and 32% had a >90% decrease in seizures. At 1 year, 55% remained on the diet and 27% had a >90% decrease in seizure frequency. Most of those discontinuing the diet did so because it was either insufficiently effective or too restrictive. Seven percent stopped because of intercurrent illness. CONCLUSIONS: The ketogenic diet should be considered as alternative therapy for children with difficult-to-control seizures. It is more effective than many of the new anticonvulsant medications and is well tolerated by children and families when it is effective.     

Improving the Power of an Efficacy Study of a Social and Emotional Learning Program: Application of Generalizability Theory to the Measurement of Classroom-Level Outcomes

Social and emotional learning programs are designed to improve the quality of social interactions in schools and classrooms in order to positively affect students’ social, emotional, and academic development. The statistical power of group randomized trials to detect effects of social and emotional learning programs and other preventive interventions on setting-level outcomes is influenced by the reliability of the outcome measure. In this paper, we apply generalizability theory to an observational measure of the quality of classroom interactions that is an outcome in a study of the efficacy of a social and emotional learning program called The Recognizing, Understanding, Labeling, Expressing, and Regulating emotions Approach. We estimate multiple sources of error variance in the setting-level outcome and identify observation procedures to use in the efficacy study that most efficiently reduce these sources of error. We then discuss the implications of using different observation procedures on both the statistical power and the monetary costs of conducting the efficacy study.     

CDw60 glycolipid antigens of human leukocytes: structural characterization and cellular distribution

Monoclonal CDw60 antibodies recognize glycolipid antigens with restricted surface expression on human leukocytes. They allow us to define new functional subpopulations of T lymphocytes and are able to induce costimulatory signals. In this report, we describe the molecular composition of CDw60 glycolipid antigens derived from different human leukocyte subpopulations. The glycolipids were isolated and their structures were identified by immunochemical methods. All molecules containing the CDw60 determinant were found in the disialoganglioside fraction. They were O-acetylated derivatives of the gangliosides II3 (Neu5Ac)2-LacCer (GD3), IV3 (Neu5Ac)2-nLc4Cer (DSPG), and VI3 (Neu5Ac)2- nLc6Cer (DSnHC), respectively. The most common CDw60 glycolipid antigen in human leukocytes was 9-O-acetyl GD3. In a comparison of various cell types, the highest concentration of 9-O-acetyl GD3 on a per cell basis was determined in granulocytes and in blood T lymphocytes, whereas B lymphocytes, thymus cells, and monocytes contained considerably smaller amounts of this molecule. Polar CDw60 antigens such as 9-O-acetyl DSPG and 9-O-acetyl DSnHC were only detected in granulocytes.     

Phospholipase A2 levels in acute chest syndrome of sickle cell disease

Acute chest syndrome (ACS) is associated with significant morbidity and is the leading cause of death in patients with sickle cell disease (SCD). Recent reports suggest that bone marrow fat embolism can be detected in many cases of severe ACS. Secretory phospholipase A2 (sPLA2) is an important inflammatory mediator and liberates free fatty acids, which are felt to be responsible for the acute lung injury of the fat embolism syndrome. We measured SPLA2 levels in 35 SCD patients during 20 admissions for ACS, 10 admissions for vaso-occlusive crisis, and during 12 clinic visits when patients were at the steady state. Eleven non-SCD patients with pneumonia were also evaluated. To determine if there was a relationship between sPLA2 and the severity of ACS we correlated SPLA2 levels with the clinical course of the patient. In comparison with normal controls (mean = 3.1 +/- 1.1 ng/mL), the non- SCD patients with pneumonia (mean = 68.6 +/- 82.9 ng/mL) and all three SCD patient groups had an elevation of SPLA2 (steady state mean = 10.0 +/- 8.4 ng/mL; vaso-occlusive crisis mean = 23.7 +/- 40.5 ng/mL; ACS mean = 336 +/- 209 ng/mL). In patients with ACS sPLA2 levels were 100- fold greater than normal control values, 35 times greater than values in SCD patients at baseline, and five times greater than non-SCD patients with pneumonia. The degree of SPLA2 elevation in ACS correlated with three different measures of clinical severity and, in patients followed sequentially, the rise in SPLA2 coincided with the onset of ACS. The dramatic elevation of SPLA2 in patients with ACS but not in patients with vaso-occlusive crisis or non-SCD patients with pneumonia and the correlation between levels of SPLA2 and clinical severity suggest a role for SPLA2 in the diagnosis and, perhaps, in the pathophysiology of patients with ACS.