Archive for the 'Acne Treatment' Category

Understanding uptake of continuous quality improvement in Indigenous primary health care: lessons from a multi-site case study of the Audit and Best Practice for Chronic Disease project

Friday, March 12th, 2010

Background:
Experimentation with continuous quality improvement (CQI) processes is well underway in Indigenous Australian primary health care. To date, little research into how health organizations take up, support and embed these complex innovations is available on which services can draw to inform implementation. In this paper we examine the practices and processes in the policy and organisational contexts and aim to explore the ways in which they interact to support and/or hinder services’ participation in a large scale Indigenous primary health care CQI program.
Methods:
We took a theory driven approach, drawing on literature on the theory and effectiveness of CQI systems and the Greenhalgh diffusion of innovation framework. Data included routinely collected regional and service profile data; uptake of tools and progress through the first CQI cycle, and data collected quarterly from hub coordinators on their perceptions of barriers and enablers. A total of 48 interviews were also conducted with key people involved in the development, dissemination and implementation of ABCD. We compiled the various data, conducted thematic analyses and developed an in-depth narrative account of the processes of uptake and diffusion into services.
Results:
Uptake of CQI was a complex and messy process that happened in fits and starts, was often characterised by conflicts and tensions and was iterative, reactive and transformational. Despite initial enthusiasm, the mixed successes during the first cycle were associated with the interaction of features of the environment, the service, the quality improvement process and the stakeholders, which operated to produce a set of circumstances that either inhibited or enabled the process of change. Organisations had different levels of capacity to mobilize resources that could shift the balance toward supporting implementation. Different forms of leadership and organisational linkages were critical to success. The Greenhalgh framework provided a useful starting point for investigation but we believe is more a descriptive than explanatory model. As such, it has limitations in the extent to which it could assist us in understanding the interactions of the practices and processes that we observed at different levels of the system.
Conclusions:
Taking up CQI involved engaging multiple stakeholders in new relationships that could support services to construct shared meaning and purpose, operationalise key concepts and tools, and develop and embed new practices into services systems and routines. Promoting quality improvement requires a system approach and organization-wide commitment. At the organization level, a formal high-level mandate, leadership at all levels and resources to support implementation are needed. At the broader system level, governance arrangements that can fulfil a number of policy objectives related to articulating the linkages between CQI and other aspects of the regulatory, financing and performance frameworks within the health system would help articulate a role and vision for quality improvement.

Pancreatic adenocarcinoma in type 2 progressive familial intrahepatic cholestasis

Friday, March 12th, 2010

Background:
BSEP disease results from mutations in ABCB11, which encodes the bile salt export pump (BSEP). BSEP disease is associated with an increased risk of hepatobiliary cancer.Case Presentation: A 36 year old woman with BSEP disease developed pancreatic adenocarcinoma at age 36. She had been treated with a biliary diversion at age 18. A 1.7 x 1.3 cm mass was detected in the pancreas on abdominal CT scan. A 2 cm mass lesion was found at the neck and proximal body of the pancreas. Pathology demonstrated a grade 2-3 adenocarcinoma with invasion into the peripancreatic fat.
Conclusions:
Clinicians should be aware of the possibility of pancreatic adenocarcinoma in patients with BSEP disease.

RRM1 single nucleotide polymorphism -37C->A correlates with progression-free survival in NSCLC patients after gemcitabine-based chemotherapy

Friday, March 12th, 2010

Background:
The ribonucleotide reductase M1 (RRM1) gene encodes the regulatory subunit of ribonucleotide reductase, the molecular target of gemcitabine. The overexpression of RRM1 mRNA in tumor tissues is reported to be associated with gemcitabine resistance. Thus, single nucleotide polymorphisms (SNPs) of the RRM1 gene are potential biomarkers of the response to gemcitabine chemotherapy. We investigated whether RRM1 expression in peripheral blood mononuclear cells (PBMCs) or SNPs were associated with clinical outcome after gemcitabine-based chemotherapy in advanced non-small cell lung cancer (NSCLC) patients.
Methods:
PBMC samples were obtained from 62 stage IIIB and IV patients treated with gemcitabine-based chemotherapy. RRM1 mRNA expression levels were assessed by real-time PCR. Three RRM1 SNPs, 37C->A, 2455A->G, and 2464G->A, were assessed by direct sequencing.
Results:
RRM1 expression was detectable in 57 PBMC samples, and SNPs were sequenced in 56 samples. The overall response rate to gemcitabine was 18%; there was no significant association between RRM1 mRNA expression and response rate (P = 0.56). The median progression-free survival (PFS) was 23.3 weeks in the lower expression group and 26.9 weeks in the higher expression group (P = 0.659). For the 37C->A polymorphism, the median PFS was 30.7 weeks in the C( )37A group, 24.7 weeks in the A( )37A group, and 23.3 weeks in the C( )37C group (P = 0.043). No significant difference in PFS was observed for the SNP 2455->G or 2464G->A.
Conclusions:
The RRM1 polymorphism 37C->A correlated with PFS in NSCLC patients treated with gemcitabine-based chemotherapy. No significant correlation was found between PBMC RRM1 mRNA expression and the efficacy of gemcitabine.

Oral health status of adults in Southern Vietnam – a cross-sectional epidemiological study

Friday, March 12th, 2010

Background:
Before strategies or protocols for oral health care can be advised at population level, epidemiological information on tooth decay patterns and its effects on oral function are indispensable. The aim of this study was to investigate influences of socio-demographic variables on the prevalence of decayed, missing, filled (DMF) and sound teeth (St) and to determine the relative risk of teeth in different dental regions for D, M, and F, of adults living in urban and rural areas in Southern Vietnam.
Methods:
Cross-sectional DMF and St data of 2965 dentate subjects aged 20 to 95 living in urban and rural areas in three provinces were collected by means of a self-administered questionnaire and an oral examination. The sample was stratified by age, gender, residence and province.
Results:
The percentage of subjects having missing teeth was high for all ages while it was low for subjects with decayed and filled teeth. The mean number of missing teeth increased gradually by age from approximately 1 in each jaw at the age of 20 to 8 at the age of 80. The number of decayed teeth was relative low at all ages, being highest in molars at young ages. The mean number of filled teeth was extremely low at all ages in all dental regions. Every additional year of age gives a significantly lower chance for decay, a higher chance for missing, and a lower chance for filled teeth. Molars had a significantly higher risk for decay, missing and filled than premolars and anterior teeth. Females had significantly higher risk for decayed and filled teeth, and less chance for missing teeth than males. Urban subjects presented lower risk for decay, but approximately 4 times greater chance for having fillings than rural subjects. Low socio-economic status (SES) significantly increased the chance for missing anterior and molar teeth; subjects with high SES had more often fillings.
Conclusions:
The majority of adults of Southern Vietnam presented a reduced dentition. The combination of low numbers of filled teeth and relative high numbers of decayed and missing teeth indicates that the main treatment for decay is extraction. Molars are more at risk for being decayed or missing than premolars and anterior teeth.

Overexpression of the JmjC histone demethylase KDM5B in human carcinogenesis: involvement in the proliferation of cancer cells through the E2F/RB pathway

Friday, March 12th, 2010

Background:
Although an increasing number of histone demethylases have been identified and biochemically characterized, their biological functions largely remain uncharacterized, particularly in the context of human diseases such as cancer. We investigated the role of KDM5B, a JmjC histone demethylase, in human carcinogenesis. Quantitative RT-PCR and microarray analysis were used to examine the expression profiles of histone demethylases in clinical tissue samples. We also examined the functional effects of KDM5B on the growth of cancer cell lines treated with small interfering RNAs (siRNAs). Downstream genes and signal cascades induced by KDM5B expression were identified from Affymetrix Gene Chip experiments, and validated by real-time PCR and reporter assays. Cell cycle-dependent characteristics of KDM5B were identified by immunofluorescence and FACS.
Results:
Quantitative RT-PCR analysis confirmed that expression levels of KDM5B are significantly higher in human bladder cancer tissues than in their corresponding non-neoplastic bladder tissues (P < 0.0001). The expression profile analysis of clinical tissues also revealed up-regulation of KDM5B in various kinds of malignancies. Transfection of KDM5B-specific siRNA into various bladder and lung cancer cell lines significantly suppressed the proliferation of cancer cells and increased the number of cells in sub-G1 phase. Microarray expression analysis indicated that E2F1 and E2F2 are downstream genes in the KDM5B pathway.
Conclusions:
Inhibition of KDM5B may affect apoptosis and reduce growth of cancer cells. Further studies will explore the pan-cancer therapeutic potential of KDM5B inhibition.