Reciprocal learning and chronic care model implementation in primary care: results from a new scale of learning in primary care

<p>Abstract</p> <p>Background</p> <p>Efforts to improve the care of patients with chronic disease in primary care settings have been mixed. Application of a complex adaptive systems framework suggests that this may be because implementation efforts often focus on education or decision support of individual providers, and not on the dynamic system as a whole. We believe that learning among clinic group members is a particularly important attribute of a primary care clinic that has not yet been well-studied in the health care literature, but may be related to the ability of primary care practices to improve the care they deliver.</p> <p>To better understand learning in primary care settings by developing a scale of learning in primary care clinics based on the literature related to learning across disciplines, and to examine the association between scale responses and chronic care model implementation as measured by the Assessment of Chronic Illness Care (ACIC) scale.</p> <p>Methods</p> <p>Development of a scale of learning in primary care setting and administration of the learning and ACIC scales to primary care clinic members as part of the baseline assessment in the ABC Intervention Study. All clinic clinicians and staff in forty small primary care clinics in South Texas participated in the survey.</p> <p>Results</p> <p>We developed a twenty-two item learning scale, and identified a five-item subscale measuring the construct of reciprocal learning (Cronbach alpha 0.79). Reciprocal learning was significantly associated with ACIC total and sub-scale scores, even after adjustment for clustering effects.</p> <p>Conclusions</p> <p>Reciprocal learning appears to be an important attribute of learning in primary care clinics, and its presence relates to the degree of chronic care model implementation. Interventions to improve reciprocal learning among clinic members may lead to improved care of patients with chronic disease and may be relevant to improving overall clinic performance.</p

Bacteria Modulate the CD8+ T Cell Epitope Repertoire of Host Cytosol-Exposed Proteins to Manipulate the Host Immune Response

The main adaptive immune response to bacteria is mediated by B cells and CD4+ T-cells. However, some bacterial proteins reach the cytosol of host cells and are exposed to the host CD8+ T-cells response. Both gram-negative and gram-positive bacteria can translocate proteins to the cytosol through type III and IV secretion and ESX-1 systems, respectively. The translocated proteins are often essential for the bacterium survival. Once injected, these proteins can be degraded and presented on MHC-I molecules to CD8+ T-cells. The CD8+ T-cells, in turn, can induce cell death and destroy the bacteria's habitat. In viruses, escape mutations arise to avoid this detection. The accumulation of escape mutations in bacteria has never been systematically studied. We show for the first time that such mutations are systematically present in most bacteria tested. We combine multiple bioinformatic algorithms to compute CD8+ T-cell epitope libraries of bacteria with secretion systems that translocate proteins to the host cytosol. In all bacteria tested, proteins not translocated to the cytosol show no escape mutations in their CD8+ T-cell epitopes. However, proteins translocated to the cytosol show clear escape mutations and have low epitope densities for most tested HLA alleles. The low epitope densities suggest that bacteria, like viruses, are evolutionarily selected to ensure their survival in the presence of CD8+ T-cells. In contrast with most other translocated proteins examined, Pseudomonas aeruginosa's ExoU, which ultimately induces host cell death, was found to have high epitope density. This finding suggests a novel mechanism for the manipulation of CD8+ T-cells by pathogens. The ExoU effector may have evolved to maintain high epitope density enabling it to efficiently induce CD8+ T-cell mediated cell death. These results were tested using multiple epitope prediction algorithms, and were found to be consistent for most proteins tested

Assessing the impact of low level laser therapy (LLLT) on biological systems: a review

PURPOSE: Low level laser therapy (LLLT) in the visible to near infrared spectral band (390-1100 nm) is absorption of laser light at the electronic level, without generation of heat. It may be applied in a wide range of treatments including wound healing, inflammation and pain reduction. Despite its potential beneficial impacts, the use of lasers for therapeutic purposes still remains controversial in mainstream medicine. Whilst taking into account the physical characteristics of different qualities of lasers, this review aims to provide a comprehensive account of the current literature available in the field pertaining to their potential impact at cellular and molecular levels elucidating mechanistic interactions in different mammalian models. The review also aims to focus on the integral approach of the optimal characteristics of LLLT that suit a biological system target to produce the beneficial effect at the cellular and molecular levels. METHODS: Recent research articles were reviewed that explored the interaction of lasers (coherent sources) and LEDs (incoherent sources) at the molecular and cellular levels. RESULTS: It is envisaged that underlying mechanisms of beneficial impact of lasers to patients involves biological processes at the cellular and molecular levels. The biological impact or effects of LLLT at the cellular and molecular level could include cellular viability, proliferation rate, as well as DNA integrity and the repair of damaged DNA. This review summarizes the available information in the literature pertaining to cellular and molecular effects of lasers. CONCLUSIONS: It is suggested that a change in approach is required to understand how to exploit the potential therapeutic modality of lasers whilst minimizing its possible detrimental effects

Integrating the prevention of mother-to-child transmission of HIV into primary healthcare services after AIDS denialism in South Africa: perspectives of experts and health care workers - a qualitative study

Integrating Prevention of Mother-to-Child Transmission (PMTCT) programmes into routine health services under complex socio-political and health system conditions is a priority and a challenge. The successful rollout of PMTCT in sub-Saharan Africa has decreased Human Immunodeficiency Virus (HIV), reduced child mortality and improved maternal health. In South Africa, PMTCT is now integrated into existing primary health care (PHC) services and this experience could serve as a relevant example for integrating other programmes into comprehensive primary care. This study explored the perspectives of both experts or key informants and frontline health workers (FHCWs) in South Africa on PMTCT integration into PHC in the context of post-AIDS denialism using a Complex Adaptive Systems framework. METHODS: A total of 20 in-depth semi-structured interviews were conducted; 10 with experts including national and international health systems and HIV/PMTCT policy makers and researchers, and 10 FHCWs including clinic managers, nurses and midwives. All interviews were conducted in person, audio-recorded and transcribed

Extracellular matrix formation enhances the ability of streptococcus pneumoniae to cause invasive disease

Extent: 17p.During infection, pneumococci exist mainly in sessile biofilms rather than in planktonic form, except during sepsis. However, relatively little is known about how biofilms contribute to pneumococcal pathogenesis. Here, we carried out a biofilm assay on opaque and transparent variants of a clinical serotype 19F strain WCH159. After 4 days incubation, scanning electron microscopy revealed that opaque biofilm bacteria produced an extracellular matrix, whereas the transparent variant did not. The opaque biofilm-derived bacteria translocated from the nasopharynx to the lungs and brain of mice, and showed 100- fold greater in vitro adherence to A549 cells than transparent bacteria. Microarray analysis of planktonic and sessile bacteria from transparent and opaque variants showed differential gene expression in two operons: the lic operon, which is involved in choline uptake, and in the two-component system, ciaRH. Mutants of these genes did not form an extracellular matrix, could not translocate from the nasopharynx to the lungs or the brain, and adhered poorly to A549 cells. We conclude that only the opaque phenotype is able to form extracellular matrix, and that the lic operon and ciaRH contribute to this process. We propose that during infection, extracellular matrix formation enhances the ability of pneumococci to cause invasive disease.Claudia Trappetti, Abiodun D. Ogunniyi, Marco R. Oggioni and James C. Pato

The secretin receptor antagonist (SCT 5-27) reduces biliary hyperplasia and liver fibrosis in an animal model of primary sclerosing cholangitis

Secretin (SCT) is trophic and profibrotic hormone produced by the S cells of the duodenum as well as cholangiocytes. The SCT/secretin receptor (SR) axis stimulates biliary proliferation in normal and cholestatic mice following bile duct ligation (BDL). We have shown that SCT down-regulates the expression of the miRNAs, miR-125b and let-7a, which target the expression of VEGF-A and NGF, respectively, that are proliferative factors that stimulate biliary proliferation during cholestasis. The AIM of our study was to evaluate the effect of inhibition of the SCT/SR axis with Sec 5-27 on biliary proliferation and liver fibrosis in the Mdr2-/- mouse model of primary sclerosing cholangitis (PSC). PSC is a disease characterized by inflammation of cholangiocytes that leads to scar formation and duct obstruction with subsequent cirrhosis and liver failure. Methods: Our studies were performed in: (i) wild-type (WT) mice; and (ii) 12-wk old Mdr2-/- mice treated with saline or SCT 5-27 (10 μg/kg WT/day) by osmotic minipumps for 1 wk. Then, biliary proliferation and intrahepatic bile duct mass (IBDM) were evaluated by immunohistochemistry for PCNA and CK-19, respectively. Liver fibrosis was determined by: (i) Sirius red staining in liver sections; and (ii) qPCR for the profibrotic markers collagen 1, fibronectin, TGFβ1, alpha-SMA, MMP2, MMP9, TIMP- 1, TIMP-2 in total liver and purified cholangiocytes from the in vivo treatment groups. The expression levels of miR-125b, let-7a, VEGF-A and NGF in total liver and cholangiocytes were evaluated by qPCR. The serum levels of transaminases were evaluated. Serum and cholangiocyte supernatant levels of TGFβ1 (a key factor for the activation of hepatic stellate cells) were evaluated by ELISA. Results: In Mdr2-/- mice there enhanced biliary proliferation, IBDM and liver fibrosis compared to WT mice. There was a significant reduction in biliary proliferation, IBDM, liver fibrosis and mRNA expression of the aforementioned profibrotic markers in Mdr2-/- mice that were treated with SCT 5-27 compared to saline-treated Mdr2-/- mice. There was a significant reduction in the levels of serum transaminases as well as serum and cholangiocyte supernatant levels of TGFβ1 in Mdr2-/- mice treated with SCT 5-27 compared to controls. We also observed a significant increase in miR- 125b and let-7a in the Mdr2-/- mice treated with SCT 5-27 compared to control mice, which corresponded to decreased mRNA expression of the biliary proliferative factors VEGF-A and NGF. Conclusion: Inhibition of the SCT/SR axis with the SR antagonist may represent a novel therapeutic approach for modulating biliary proliferation and liver fibrosis during cholestasis