Private health care in low-income and middle-income countries is very extensive and very heterogeneous, ranging from itinerant medicine sellers, through millions of independent practitioners-both unlicensed and licensed-to corporate hospital chains and large private insurers. Policies for universal health coverage (UHC) must address this complex private sector. However, no agreed measures exist to assess the scale and scope of the private health sector in these countries, and policy makers tasked with managing and regulating mixed health systems struggle to identify the key features of their private sectors. In this report, we propose a set of metrics, drawn from existing data that can form a starting point for policy makers to identify the structure and dynamics of private provision in their particular mixed health systems; that is, to identify the consequences of specific structures, the drivers of change, and levers available to improve efficiency and outcomes. The central message is that private sectors cannot be understood except within their context of mixed health systems since private and public sectors interact. We develop an illustrative and partial country typology, using the metrics and other country information, to illustrate how the scale and operation of the public sector can shape the private sector's structure and behaviour, and vice versa.

The use of cerium compounds as diesel fuel catalyst results in the emission of cerium oxide nanoparticles (CeO2) in the exhaust. This study characterized the potential effects of CeO2 exposure on lung toxicity. Male Sprague Dawley rats were exposed to CeO2 by a single intratracheal instillation at 0.15, 0.5, 1, 3.5 or 7 mg/kg body weight. At 1 day after exposure, CeO2 significantly reduced NO production, but increased IL-12 production, by alveolar macrophages (AM) in response to ex vivo lipopolysacchride (LPS) challenge, and caused AM apoptosis, through activation of caspases 9 and 3. CeO2 exposure markedly increased suppressor of cytokine signaling-1 at 1-day and elevated arginase-1 at 28-day post exposure in lung cells, while osteopontin was significantly elevated in lung tissue at both time points. CeO2 induced inflammation, cytotoxicity, air/blood barrier damage, and phospholipidosis with enlarged AM. Thus, CeO2 induced lung inflammation and injury in lungs which may lead to fibrosis.

BackgroundDuring the spring of 2009, a pandemic influenza A (H1N1) virus emerged and spread globally. We describe the clinical characteristics and factors associated with the death of patients who were hospitalized with 2009 H1N1 influenza pneumonia in Shenyang, China, from November to December 2009.MethodsWe carried out a retrospective chart review of 68 patients who were hospitalized with pneumonia and confirmed to have 2009 H1N1 virus infection by a real time RT-PCR assay of respiratory specimens.ResultsOf the 68 patients we studied, 30 (44%) were admitted to an intensive care unit and 10 (14.7%) died. The median age of patients was 41 years (range, 18-66), and only one patient was over 65 years of age. The male to female ratio was 2.78:1 (50:18). Of the 68 patients, 23 (34%) had at least one underlying medical condition, 9 (13%) had a cigarette index ≥400 and 22 (32%) were obese. All patients underwent chest radiography on admission and the findings were consistent with pneumonia in all cases. All patients were treated with oseltamivir and treatment was initiated at a median time of seven days after the onset of illness. The laboratory test results indicated lymphopenia, hypoproteinemia and elevated lactic dehydrogenase and C reactive protein levels. Of the 68 patients, 33 (52%) showed a reduction in CD4 T cell counts. Of the 58 patients who survived, 31 (53%) had lymphopenia and 27 recovered from this condition after five days. Of the 10 patients who died, nine (90%) had lymphopenia and only two patients recovered from this condition after five days. Obesity and recovery from lymphopenia after five days were factors associated with death, as determined by multivariate logistic-regression analysis (obesity, odds ratio = 23.06; lymphocytopenia reversion, odds ration = 28.69).ConclusionsDuring the evaluation period in Shenyang, China, 2009 H1N1 influenza caused severe illness requiring hospitalization in 68 patients, 10 (14.7%) of which died. Many of these patients were considered healthy adults and few were elderly (65 years or older). Obesity and lymphopenia, which was not restored after five days of treatment, were factors associated with poor outcomes of 2009 H1N1 influenza infection.

Lung cancer is the most common cancer worldwide, accounting for 1.3 million cancer deaths annually. Despite extensive studies over the past decade, the detailed mechanism about the initiation and development of the lung cancer is still elusive. In the present report, we showed that overexpression of mdig is a common feature of the non-small cell lung cancer. Gene silencing or overexpression of mdig revealed that mdig is involved in demethylation of tri-methyl lysine 9 on histone H3, leading to an increase in ribosomal RNA expression. The transcriptional regulation of ribosomal RNA gene by mdig is achieved through abrogating tri-methyl lysine 9 on histone H3 and enhancing RNA polymerase I occupancy in the promoter region of the ribosomal RNA gene as demonstrated by chromatin immunoprecipitation. The pronounced expression of mdig in lung cancer tissues but not normal lung tissues, thus, suggests that mdig possesses oncogenic property through antagonizing tri-methyl lysine 9 on histone H3 and promoting ribosomal RNA synthesis.