Analysis of factors influencing the outpatient workload at Chinese health centres

<p>Abstract</p> <p>Background</p> <p>Although the community health service system is now established in China, the utilisation of the community health service institutions is low due to the lack of a gate-keeping role of the primary health service providers and referrals among the three-tiered health service institutions. In addition to this, patients who can afford to pay, often seek best services in big hospitals to guarantee the quality of care. Thus, the need of guiding the patients to the community health services and increasing the utilisation of the community health service institutions is becoming an urgent problem, which hinders the future development of community health services. This study focuses on the question of how to increase the utilisation of Chinese community health centres (HCs).</p> <p>Methods</p> <p>A cross-sectional Base-line Survey of Chinese City Community Health Service System Building using the multi-staged cluster sampling was conducted to collect data from all HCs in 28 key contact cities. Relevant indicators of totally 1790 HCs were analysed. The statistical methods included ANONVA and logistic regression.</p> <p>Results and Conclusions</p> <p>The analysis suggested several key factors for increasing the outpatient workload (OW) at the HCs: establishing an adequate referral system among the different levels of the health system; enhancing the qualification of health personnel and increasing the compensation by the health insurance for services provided at HCs. Other key factors with a positive effect on the OW included: the government ownership of the HCs, the scale of the institutions, the medical equipment used, the mix of health services provided, and the women in childbearing age in the residence.</p

Assessment of coronary artery disease and calcified coronary plaque burden by computed tomography in patients with and without diabetes mellitus

Purpose: To compare the coronary atherosclerotic burden in patients with and without type-2 diabetes using CT Coronary Angiography (CTCA). Methods and Materials: 147 diabetic (mean age: 65 ± 10 years; male: 89) and 979 nondiabetic patients (mean age: 61 ± 13 years; male: 567) without a history of coronary artery disease (CAD) underwent CTCA. The per-patient number of diseased coronary segments was determined and each diseased segment was classified as showing obstructive lesion (luminal narrowing >50%) or not. Coronary calcium scoring (CCS) was assessed too. Results: Diabetics showed a higher number of diseased segments (4.1 ± 4.2 vs. 2.1 ± 3.0; p 400 (p < 0.001), obstructive CAD (37% vs. 18% of patients; p < 0.0001), and fewer normal coronary arteries (20% vs. 42%; p < 0.0001), as compared to nondiabetics. The percentage of patients with obstructive CAD paralleled increasing CCS in both groups. Diabetics with CCS ≤ 10 had a higher prevalence of coronary plaque (39.6% vs. 24.5%, p = 0.003) and obstructive CAD (12.5% vs. 3.8%, p = 0.01). Among patients with CCS ≤ 10 all diabetics with obstructive CAD had a zero CCS and one patient was asymptomatic. Conclusions: Diabetes was associated with higher coronary plaque burden. The present study demonstrates that the absence of coronary calcification does not exclude obstructive CAD especially in diabetics

MicroRNA Dysregulation in the Spinal Cord following Traumatic Injury

Spinal cord injury (SCI) triggers a multitude of pathophysiological events that are tightly regulated by the expression levels of specific genes. Recent studies suggest that changes in gene expression following neural injury can result from the dysregulation of microRNAs, short non-coding RNA molecules that repress the translation of target mRNA. To understand the mechanisms underlying gene alterations following SCI, we analyzed the microRNA expression patterns at different time points following rat spinal cord injury

Key signalling nodes in mammary gland development and cancer. Mitogen-activated protein kinase signalling in experimental models of breast cancer progression and in mammary gland development

Seven classes of mitogen-activated protein kinase (MAPK) intracellular signalling cascades exist, four of which are implicated in breast disease and function in mammary epithelial cells. These are the extracellular regulated kinase (ERK)1/2 pathway, the ERK5 pathway, the p38 pathway and the c-Jun N-terminal kinase (JNK) pathway. In some forms of human breast cancer and in many experimental models of breast cancer progression, signalling through the ERK1/2 pathway, in particular, has been implicated as being important. We review the influence of ERK1/2 activity on the organised three-dimensional association of mammary epithelial cells, and in models of breast cancer cell invasion. We assess the importance of epidermal growth factor receptor family signalling through ERK1/2 in models of breast cancer progression and the influence of ERK1/2 on its substrate, the oestrogen receptor, in this context. In parallel, we consider the importance of these MAPK-centred signalling cascades during the cycle of mammary gland development. Although less extensively studied, we highlight the instances of signalling through the p38, JNK and ERK5 pathways involved in breast cancer progression and mammary gland development

Child neglect in one-child families from Suzhou City of mainland China

Background The one-child policy introduced in China in 1979 has led to far-reaching changes in socio-demographic characteristics. Under this policy regime, each household has few children. This study aims to describe the prevalence of child neglect in one-child families in China and to examine the correlates of child neglect. Methods A cross-sectional study of 2044 children aged 6 to 9 years and recruited from four primary schools in Suzhou City, China was conducted. Neglect subtypes were determined using a validated indigenous measurement scale reported by parents. Child, parental and family characteristics were obtained by questionnaires and review of social security records. Linear regression analyses were performed to estimate the associations between these factors and the subtypes of child neglect. Results The prevalence of child any neglect was 32.0% in one child families in Suzhou City, China. Supervisory (20.3%) neglect was the most prevalent type of child neglect, followed by emotional (15.2%), physical (11.1%), and educational (6.0%) neglect After simultaneous adjustment to child and family characteristics and the school factor, boys, children with physical health issues and cognitive impairment, younger and unemployed mother, were positively associated with neglect subtypes. We also found that parents with higher education and three-generation families were negatively associated with neglect. Conclusion The rates of child neglect subtypes vary across different regions in China probably due to the different policy implementation and socio-economic levels, with a lower level of physical and educational neglect and a higher level of emotional neglect in this study. The three-generation family structure was correlates of neglect which may be unique in one child families. This indicates that future intervention programs in one-child families should target these factorsBioMed Central open acces

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe