Hypertension treatment capacity in India by increased workforce, greater task-sharing, and extended prescription period: a modelling study

Background: The worldwide control rate for hypertension is dismal. An inadequate number of physicians to treat patients with hypertension is one key obstacle. Innovative health system approaches such as delegation of basic tasks to non-physician health workers (task-sharing) might alleviate this problem. Massive scale up of population-wide hypertension management is especially important for low- and middle-income countries such as India. Methods: Using constrained optimization models, we estimated the hypertension treatment capacity and salary costs of staff involved in hypertension care within the public health system of India and simulated the potential effects of (1) an increased workforce, (2) greater task-sharing among health workers, and (3) extended average prescription periods that reduce treatment visit frequency (e.g., quarterly instead of monthly). Findings: Currently, only an estimated 8% (95% uncertainty interval 7%–10%) of ∼245 million adults with hypertension can be treated by physician-led services in the Indian public health system (assuming the current number of health workers, no greater task-sharing, and monthly visits for prescriptions). Without task-sharing and with continued monthly visits for prescriptions, the least costly workforce expansion to treat 70% of adults with hypertension would require ∼1.6 (1.0–2.5) million additional staff (all non-physicians), with ∼INR 200 billion (≈USD 2.7 billion) in additional annual salary costs. Implementing task-sharing among health workers (without increasing the overall time on hypertension care) or allowing a 3-month prescription period was estimated to allow the current workforce to treat ∼25% of patients. Joint implementation of task-sharing and a longer prescription period could treat ∼70% of patients with hypertension in India. Interpretation: The combination of greater task-sharing and extended prescription periods could substantially increase the hypertension treatment capacity in India without any expansion of the current workforce in the public health system. By contrast, workforce expansion alone would require considerable, additional human and financial resources. Funding: Resolve to Save Lives, an initiative of Vital Strategies, was funded by grants from Bloomberg Philanthropies; the Bill and Melinda Gates Foundation; and Gates Philanthropy Partners (funded with support from the Chan Zuckerberg Foundation)

Localization and potential role of matrix metalloproteinase-1 and tissue inhibitors of metalloproteinase-1 and -2 in different phases of bronchopulmonary dysplasia

Bronchopulmonary dysplasia (BPD) can evolve in prematurely born infants who require mechanical ventilation because of hyaline membrane disease (HMD). The development of BPD can be divided in an acute, a regenerative, a transitional, and a chronic phase. During these different phases, extensive remodeling of the lung parenchyma with re-epithelialization of the alveoli and formation of fibrosis occurs. Matrix metalloproteinase-1 (MMP-1) is an enzyme that is involved in re-epithelialization processes, and dysregulation of MMP-1 activity contributes to fibrosis. Localization of MMP-1 and its inhibitors, tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2, were investigated in lung tissue obtained from infants who died during different phases of BPD development. In all studied cases (n = 50) type-II pneumocytes were found to be immunoreactive for MMP-1, TIMP-1, and TIMP-2. During the acute and regenerative phase of BPD, type-II pneumocytes re-epithelialize the injured alveoli. This may suggest that MMP-1 and its inhibitors, expressed by type-II pneumocytes, play a role in the re-epithelialization process after acute lung injury. Although MMP-1 staining intensity remained constant in type-II pneumocytes during BPD development, TIMP-1 increased during the chronic fibrotic phase. This relative elevation of TIMP-1 compared with MMP-1 is indicative for reduced collagenolytic activity by type-II pneumocytes in chronic BPD and may contribute to fibrosis. Fibrotic foci in chronic BPD contained fibroblasts immunoreactive for MMP-1 and TIMP-1 and -2. This may indicate that decreased collagen turnover by fibroblasts contributes to fibrosis in BPD development

Systematic Review Protocol : Optimizing Endoscopic Management of Neonatal Piriform Fossa Sinus Tract with Neck Cystic Mass : a scoping review

Medicine, Faculty ofMedicine, Department ofUnreviewedFacultyResearche

Assessing the reliability of the modified Gartland classification system for extension-type supracondylar humerus fractures.

PurposeThe Gartland extension-type supracondylar humerus (SCH) fracture is the most common paediatric elbow fracture. Treatment options range from nonoperative treatment (taping or casting) to operative treatments (closed reduction and percutaneous pinning or open reduction). Classification variability between surgeons is a potential contributing factor to existing controversy over treatment options for type II SCH fractures. This study investigated levels of agreement in extension-type SCH fracture classification using the modified Gartland classification system.MethodsA retrospective review was conducted on 60 patients aged between two and 12 years who had sustained an extension-type SCH fracture and received operative or nonoperative treatment at a tertiary children's hospital. Baseline radiographs were provided, and surgeons were asked to classify the fractures as type I, IIA, IIB or III according to the modified Gartland classification. Respondents were then asked to complete a second round of classifications using reshuffled radiographs. Weighted kappa values were calculated to assess interobserver and intraobserver levels of agreement.ResultsIn all, 21 paediatric orthopaedic surgeons responded to the survey and 15 completed a second round of ratings. Interobserver agreement for classification based on the Gartland criteria between surgeons was substantial with a kappa of 0.679 (95% confidence interval (CI) 0.501 to 0.873). Intraobserver agreement was substantial with a kappa of 0.796, (95% CI 0.628 to 0.864).ConclusionRadiographic classification of extension-type SCH fractures demonstrated substantial agreement both between and within surgeon raters. Therefore, classification variability may not be a major contributing factor to the treatment controversy for type II SCH fractures and treatment variability may be due to differences in surgeon preferences.Level of evidenceIII

Impairment of rat postnatal lung alveolar development by glucocorticoids: involvement of the p21CIP1 and p27KIP1 cyclin-dependent kinase inhibitors

It has been shown that glucocorticoids accelerate lung development by limiting alveolar formation resulting from a premature maturation of the alveolar septa. Based on these data, the aim of the present work was to analyze the influence of dexamethasone on cell cycle control mechanisms during postnatal lung development. Cell proliferation is regulated by a network of signaling pathways that converge to the key regulator of cell cycle machinery: the cyclin-dependent kinase (CDK) system. The activity of the various cyclin/CDK complexes can be modulated by the levels of the cyclins and their CDKs, and by expression of specific CDK inhibitors (CKIs). In the present study, newborn rats were given a 4-d treatment with dexamethasone (0.1-0.01 microg/g body weight dexamethasone sodium phosphate daily on d 1-4), or saline. Morphologically, the treatment caused a significant thinning of the septa and an acceleration of lung maturation on d 4. Study of cyclin/CDK system at d 1-36 documented a transient down-regulation of cyclin/CDK complex activities at d 4 in the dexamethasone-treated animals. Analysis of the mechanisms involved suggested a role for the CKIs p21CIP1 and p27KIP1. Indeed, we observed an increase in p21CIP1 and p27KIP1 protein levels on d 4 in the dexamethasone-treated animals. By contrast, no variations in either cyclin and CDK expression, or cyclin/CDK complex formation could be documented. We conclude that glucocorticoids may accelerate lung maturation by influencing cell cycle control mechanisms, mainly through impairment of G1 cyclin/CDK complex activation