Improving access to health care for malaria in Africa: a review of literature on what attracts patients

BACKGROUND: Increasing access to health care services is considered central to improving the health of populations. Existing reviews to understand factors affecting access to health care have focused on attributes of patients and their communities that act as 'barriers' to access, such as education level, financial and cultural factors. This review addresses the need to learn about provider characteristics that encourage patients to attend their health services. METHODS: This literature review aims to describe research that has identified characteristics that clients are looking for in the providers they approach for their health care needs, specifically for malaria in Africa. Keywords of 'malaria' and 'treatment seek*' or 'health seek*' and 'Africa' were searched for in the following databases: Web of Science, IBSS and Medline. Reviews of each paper were undertaken by two members of the team. Factors attracting patients according to each paper were listed and the strength of evidence was assessed by evaluating the methods used and the richness of descriptions of findings. RESULTS: A total of 97 papers fulfilled the inclusion criteria and were included in the review. The review of these papers identified several characteristics that were reported to attract patients to providers of all types, including lower cost of services, close proximity to patients, positive manner of providers, medicines that patients believe will cure them, and timeliness of services. Additional categories of factors were noted to attract patients to either higher or lower-level providers. The strength of evidence reviewed varied, with limitations observed in the use of methods utilizing pre-defined questions and the uncritical use of concepts such as 'quality', 'costs' and 'access'. Although most papers (90%) were published since the year 2000, most categories of attributes had been described in earlier papers. CONCLUSION: This paper argues that improving access to services requires attention to factors that will attract patients, and recommends that public services are improved in the specific aspects identified in this review. It also argues that research into access should expand its lens to consider provider characteristics more broadly, especially using methods that enable open responses. Access must be reconceptualized beyond the notion of barriers to consider attributes of attraction if patients are to receive quality care quickly

Beyond “Big Eaters”: The Versatile Role of Alveolar Macrophages in Health and Disease

Macrophages act as immune scavengers and are important cell types in the homeostasis of various tissues. Given the multiple roles of macrophages, these cells can also be found as tissue resident macrophages tightly integrated into a variety of tissues in which they fulfill crucial and organ-specific functions. The lung harbors at least two macrophage populations: interstitial and alveolar macrophages, which occupy different niches and functions. In this review, we provide the latest insights into the multiple roles of alveolar macrophages while unraveling the distinct factors which can influence the ontogeny and function of these cells. Furthermore, we will highlight pulmonary diseases, which are associated with dysfunctional macrophages, concentrating on congenital diseases as well as pulmonary infections and impairment of immunological pathways. Moreover, we will provide an overview about different treatment approaches targeting macrophage dysfunction. Improved knowledge of the role of macrophages in the onset of pulmonary diseases may provide the basis for new pharmacological and/or cell-based immunotherapies and will extend our understanding to other macrophage-related disorders

Proportional Fair Coding for Wireless Mesh Networks

We consider multi–hop wireless networks carrying unicast flows for multiple users. Each flow has a specified delay deadline, and the lossy wireless links are modelled as binary symmetric channels (BSCs). Since transmission time, also called airtime, on the links is shared amongst flows, increasing the airtime for one flow comes at the cost of reducing the airtime available to other flows sharing the same link. We derive the joint allocation of flow airtimes and coding rates that achieves the proportionally fair throughput allocation. This utility optimisation problem is non–convex, and one of the technical contributions of this paper is to show that the proportional fair utility optimisation can nevertheless be decomposed into a sequence of convex optimisation problems. The solution to this sequence of convex problems is the unique solution to the original non–convex optimisation. Surprisingly, this solution can be written in an explicit form that yields considerable insight into the nature of the proportional fair joint airtime/coding rate allocation. To our knowledge, this is the first time that the utility fair joint allocation of airtime/coding rate has been analysed, and also, one of the first times that utility fairness with delay deadlines has been considered

Additional file 4: Figure S4. of Chemoprotection of murine hematopoietic cells by combined gene transfer of cytidine deaminase (CDD) and multidrug resistance 1 gene (MDR1)

Mock-transduced primary murine hematopoietic cells are susceptible to cytotoxic drug treatment. (A-C) Mock-transduced as well as FACS sorted CTX-R gene-modified lin− hematopoietic progenitor cells were seeded in a clonogenic assays in the absence or presence of cytotoxic drugs [n = 1; data are given as mean (technical duplicates)]. (D-F) Mock-transduced and non-sorted genetically modified lin− cells were treated with cytotoxic drugs in mIL-3/h-GCSF supported suspension culture (n = 2–4; data are given as mean ± SD). (PDF 157 kb

Additional file 1: Figure S1. of Chemoprotection of murine hematopoietic cells by combined gene transfer of cytidine deaminase (CDD) and multidrug resistance 1 gene (MDR1)

Transgene expression of hMDR1 and hCDD in gene-modified 32D cells. Transgene expression of gene-modified cells was analyzed either before or after three day exposure to daunorubicin [50nM], Ara-C [1000nM] or both cytotoxic drugs (daunorunicin/Ara-C: [50nM/1000nM] combination). (A) hMDR1 mRNA expression is shown in LV.SFFV.MDR1 and LV.SFFV.CDD.2A.MDR1 transduced 32D cells (n = 1, technical replicates are shown; data are given relative to untransduced (non-treated) control) and (B) expression of hCDD protein is shown for LV.SFFV.CDD and LV.SFFV.CDD.2A.MDR1 gene-modified cells (n = 1; vinculin used as loading control). (PDF 292 kb

Additional file 5: Table S1. of Chemoprotection of murine hematopoietic cells by combined gene transfer of cytidine deaminase (CDD) and multidrug resistance 1 gene (MDR1)

In vitro selection of primary hematopoietic gene-modified cells. Data for in vitro selection experiments are given as % GFP+ cells (three days post treatment). (DOC 28 kb

Loss of PINK1 impairs stress-induced autophagy and cell survival

The mitochondrial kinase PINK1 and the ubiquitin ligase Parkin are participating in quality control after CCCP- or ROSinduced mitochondrial damage, and their dysfunction is associated with the development and progression of Parkinson’s disease. Furthermore, PINK1 expression is also induced by starvation indicating an additional role for PINK1 in stress response. Therefore, the effects of PINK1 deficiency on the autophago-lysosomal pathway during stress were investigated. Under trophic deprivation SH-SY5Y cells with stable PINK1 knockdown showed downregulation of key autophagic genes, including Beclin, LC3 and LAMP-2. In good agreement, protein levels of LC3-II and LAMP-2 but not of LAMP-1 were reduced in different cell model systems with PINK1 knockdown or knockout after addition of different stressors. This downregulation of autophagic factors caused increased apoptosis, which could be rescued by overexpression of LC3 or PINK1. Taken together, the PINK1-mediated reduction of autophagic key factors during stress resulted in increased cell death, thus defining an additional pathway that could contribute to the progression of Parkinson’s disease in patients with PINK1 mutations

Pulmonary transplantation of alpha-1 antitrypsin (AAT)-transgenic macrophages provides a source of functional human AAT in vivo

Inherited deficiency of the antiprotease alpha-1 antitrypsin (AAT) is associated with liver failure and early-onset emphysema. In mice, in vivo lentiviral transduction of alveolar macrophages (AMs) has been described to yield protective pulmonary AAT levels and ameliorate emphysema development. We here investigated the pulmonary transplantation of macrophages (PMT) transgenic for AAT as a potential therapy for AAT deficiency-associated lung pathology. Employing third-generation SIN-lentiviral vectors expressing the human AAT cDNA from the CAG or Cbx-EF1α promoter, we obtained high-level AAT secretion in a murine AM cell line as well as murine bone marrow-derived macrophages differentiated in vitro (AAT MΦ). Secreted AAT demonstrated a physiologic glycosylation pattern as well as elastase-inhibitory and anti-apoptotic properties. AAT MΦ preserved normal morphology, surface phenotype, and functionality. Furthermore, in vitro generated murine AAT MΦ successfully engrafted in AM-deficient Csf2r