169 research outputs found

    Strategies of human resource management in China's community health service institutions: a case study in Guangzhou

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    Human resource is the first factor for development. For community-based health services, the rational allocation and full utilization of their human resources are important guarantees to meet people’s growing demands for the health service. This research takes community health service institutions in Guangzhou as an example.By semi-structured interviews with 15 key insiders from community health service centers and field survey conducted among 328 medical staff, this research aims to find the quality of human resource allocation, recruiting and staffing, training and development, performance management, salary and welfare of community health service institutions. Through a combination of theories of human resource management and advanced experience of human resource management in community health service institutions at home and abroad, this research aims to put forward a strategy, which fits the China's national conditions, for human resource management in community health service institutions. The results can provide a theoretical basis for the human resource development planning of Chinese community health service institutions.According to the survey results: in regard to staff allocation, the current human resource quantity in Guangzhou community health service centers basically meets the document requirement. However, the structures of gender, education background and professional title are facing imbalance, thus the quality of human resource remains to be improved. In regard to staff recruitment, system of employment under contract is basically fulfilled and generally recognized by staff. But owing to the limitation of the current management system for human resources, it is hard to recruit and retain in-need talents. In regard to staff training, most of the Guangzhou community health service centers have developed cooperation in training with other institutions including Class III Grade I hospitals or medical associations. However, the single training content, slow knowledge update and relatively fragmented training still fail to meet the diversified human resource demands in community health service institutions.In regard to performance management, though a performance appraisal mechanism has been basically established, it has not been well systemized due to a lack of an objective, scientific assessment index system.Seeing that Guangzhou community health service centers are facing a lot of problems, such as human resources being short of quantity and quality, talents introduction mechanism and incentive mechanism being yet undeveloped, training and development of human resources being monotonous and fruitless, performance assessment being formalistic, this research proposes the five following targeted suggestions to solve the problems: first, continue to deepen the medical and health system reform; second, draw up rational human resources planning; third, optimize the mode of community health talents introduction; forth, build a systematic training and development system; fifth, develop a scientific performance appraisal and salary system.Os recursos humanos são o primeiro fator importantedo desenvolvimento. A disposição adquadaeaplena utilização de recursos humanos nos serviços de saúde da comunidade é uma garantia importante para atender à crescente demanda por serviços de saúde dos habitantes. Este estudo terá como exemploosserviçosde saúde dascomunidades deGuangzhou, através de entrevistas no local com 15 informantes-chave doscentros de serviços de saúde dascomunidades, e de investigações de 328 profissionais médicos, combinado com as teorias de gestão de recursos humanos nacionais e internacionais e as experiências avançadas de gestão de recursos humanos das instituições de serviços de saúde da comunidade, obtendo informações sobre as vantagens e desvantagens na disposição, recrutamento, formação, gestão de desempenho, remuneração e nos subsídios dos recursos humanos em organizações de serviços de saúde da comunidade, e explorandouma estratégia de gestão de recursos humanos para instituições de saúde da comunidade que atende às condições nacionais da China e fornecer uma base teórica para o programa de desenvolvimento dos serviços de saúde da comunidade da China.Os resultados da pesquisa mostram que,em termos de disposição do pessoal médico, a quantidade do pessoal que se destina aos serviços de saúde da comunidade de Guangzhou satisfaz os requisitos elementares para os recursos humanos, no entanto, existem diferenças estruturais de sexo, educação e de títulos profissionais, etc., poranto, a qualidade dos recursos humanos ainda está sujeito a mais melhoramento. Por outro lado, em relação à introdução de talentos, o sistema de recrutamento foi realizado e tem sido amplamente reconhecido pelos médicos, no entanto, devidoàs limitações do sistema de gestão do pessoal médico, mantém difícil introduzir e reter os talentos necessários. No que diz respeito à formação do pessoal médico, a maior parte deles já tinham estabelecido as relações de cooperação comos hospitais do nível 3A e as assiciações da área, mas os conteúdos da formação são uniformes e fragmantários, a atualização do conhecimento também é atrasada, por consequência, ainda não consegue atender aos requisitos dos recursos humanos dos serviços de saúde da comunidade. Toca à gestão de desempenho, o mecanismo de avaliação de desempenho já foi estabelecido, mas não tem um conjunto de indicadores científicos e objetivos para a avaliação do desempenho, portanto, o grau de sistematicidade do mecanismo de avaliação de desempenho ainda está sujeito ao mais aprefeiçoamento

    Nanoparticles Containing Anti-inflammatory Agents as Chemotherapy Adjuvants II: Role of Plasma Esterases in Drug Release

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    The pre-administration of the anti-inflammatory drugs dexamethasone (DEX) and cortisone acetate reduces toxicity and enhances efficacy of anticancer agents in murine models and in human clinical trials (1–5). We previously reported on the formulation of the lipophilic dexamethasone palmitate ester (DEX-P) in nanoparticles (NPs) employing a microemulsion template engineering technique to achieve tumor-specific delivery of dexamethasone (6). The nanoparticles exhibited significantly enhanced stealth properties as indicated by reduced macrophage uptake and decreased adsorption of opsonin proteins in in vitro assays (6). Unexpectedly, preliminary biodistribution studies of NPs containing [3H]-DEX-P in tumor-bearing mice showed that the radiolabel was cleared from the circulation rapidly and exhibited high liver uptake. Our previous in vitro release studies demonstrated that rapid release of the radiolabel from the NPs was observed when 10% mouse plasma was used as the medium, while nominal release was observed in phosphate-buffered saline (PBS) buffer (6). Esterolysis of NP-associated DEX-P was presumed to be the main cause for the rapid drug release in plasma, as most of the released radioactivity was in the form of DEX and not DEX-P. High degradation rates of ester prodrugs in rodent plasma has been attributed to increased esterase activity, while only minimal degradation in human plasma has been observed (7–9). Based on our observation of the release of [3H]-DEX from NPs in mouse plasma, we studied the release of DEX from nanoparticles in various plasma sources as a guide for the design of future in vivo experiments

    High Payload Dual Therapeutic-Imaging Nanocarriers for Triggered Tumor Delivery

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    The in vitro and in vivo characterization of an optimized formulation of nanoparticles (NPs) loaded with a high content of dexamethasone palmitate (DEX-P), a chemotherapeutic adjuvant that decreases interstitial fluid pressure in tumors, and 111In, a signaling agent, is described. These NPs are uniform in size and composition. Single photon emission computed tomography imaging demonstrates significant tumor uptake of 111In-labeled DEX-P NPs in tumor-bearing mice. As with many nanoparticle-based drug delivery systems, significant liver accumulation is observed. Assessment of liver histology and blood tests show no apparent hepatic or renal toxicity of the DEX-P NPs. Conversion of DEX-P to DEX occurs when DEX-P NPs are incubated with mouse plasma, human tumor homogenate and ascites from tumor bearing mice, but not with human plasma. This conversion is slower in plasma from Es1e(−/−)/SCID mice, a potential alternative animal model that better mimics humans; however, plasma from these mice are not completely devoid of esterase activity. The difference between blood and tumor esterase activity in humans facilitates the delivery of DEX-P NPs to tumors and the release of dexamethasone by an esterase trigger

    Enzyme-Nanoporous Gold Biocomposite: Excellent Biocatalyst with Improved Biocatalytic Performance and Stability

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    Background: Applications involving biomolecules, such as enzymes, antibodies, and other proteins as well as whole cells, are often hampered by their unstable nature at extremely high temperature and in organic solvents. Methodology/Principal Findings: We constructed enzyme-NPG biocomposites by assembling various enzymes onto the surface of nanoporous gold (NPG), which showed much enhanced biocatalytic performance and stability. Various enzymes with different molecular sizes were successfully tethered onto NPG, and the loadings were 3.6, 3.1 and 0.8 mg g 21 for lipase, catalase and horseradish peroxidase, respectively. The enzyme-NPG biocomposites exhibited remarkable catalytic activities which were fully comparable to those of free enzymes. They also presented enhanced stability, with 74, 78 and 53 % of enzymatic activity retained after 20 successive batch reactions. Moreover, these novel biocomposites possessed significantly enhanced reaction durability under various thermal and in organic solvent systems. In a sample transesterification reaction, a high conversion rate was readily achieved by using the lipase-NPG biocomposite. Conclusion/Significance: These nano-biocomposite materials hold great potential in applications such as biosensing, molecular electronics, catalysis, and controlled delivery

    Overcoming Wnt–β-catenin dependent anticancer therapy resistance in leukaemia stem cells

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    Leukaemia stem cells (LSCs) underlie cancer therapy resistance but targeting these cells remains difficult. The Wnt–β-catenin and PI3K–Akt pathways cooperate to promote tumorigenesis and resistance to therapy. In a mouse model in which both pathways are activated in stem and progenitor cells, LSCs expanded under chemotherapy-induced stress. Since Akt can activate β-catenin, inhibiting this interaction might target therapy-resistant LSCs. High-throughput screening identified doxorubicin (DXR) as an inhibitor of the Akt–β-catenin interaction at low doses. Here we repurposed DXR as a targeted inhibitor rather than a broadly cytotoxic chemotherapy. Targeted DXR reduced Akt-activated β-catenin levels in chemoresistant LSCs and reduced LSC tumorigenic activity. Mechanistically, β-catenin binds multiple immune-checkpoint gene loci, and targeted DXR treatment inhibited expression of multiple immune checkpoints specifically in LSCs, including PD-L1, TIM3 and CD24. Overall, LSCs exhibit distinct properties of immune resistance that are reduced by inhibiting Akt-activated β-catenin. These findings suggest a strategy for overcoming cancer therapy resistance and immune escape

    Activation of Thromboxane A2 Receptor (TP) Increases the Expression of Monocyte Chemoattractant Protein -1 (MCP-1)/Chemokine (C-C motif) Ligand 2 (CCL2) and Recruits Macrophages to Promote Invasion of Lung Cancer Cells

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    Thromboxane synthase (TXAS) and thromboxane A2 receptor (TP), two critical components for thromboxane A2 (TXA2) signaling, have been suggested to be involved in cancer invasion and metastasis. However, the mechanisms by which TXA2 promotes these processes are still unclear. Here we show that TXA2 mimetic, I-BOP, induced monocyte chemoattractant protein -1(MCP-1)/chemokine (C-C motif) ligand 2 (CCL2) expression at both mRNA and protein levels in human lung adenocarcinoma A549 cells stably over-expressing TP receptor α isoform (A549-TPα). The induction of MCP-1 was also found in other lung cancer cells H157 and H460 that express relatively high levels of endogenous TP. Using specific inhibitors of several signaling molecules and promoter/luciferase assay, we identified that transcription factor SP1 mediates I-BOP-induced MCP-1 expression. Furthermore, supernatants from I-BOP-treated A549-TPα cells enhanced MCP-1-dependent migration of RAW 264.7 macrophages. Moreover, co-culture of A549 cells with RAW 264.7 macrophages induced expression of MMPs, VEGF and MCP-1 genes, and increased the invasive potential in A549 cells. These findings suggest that TXA2 may stimulate invasion of cancer cells through MCP-1-mediated macrophage recruitment

    MUC1 Contributes to BPDE-Induced Human Bronchial Epithelial Cell Transformation through Facilitating EGFR Activation

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    Although it is well known that epidermal growth factor receptor (EGFR) is involved in lung cancer progression, whether EGFR contributes to lung epithelial cell transformation is less clear. Mucin 1 (MUC1 in human and Muc1 in animals), a glycoprotein component of airway mucus, is overexpressed in lung tumors; however, its role and underlying mechanisms in early stage lung carcinogenesis is still elusive. This study provides strong evidence demonstrating that EGFR and MUC1 are involved in bronchial epithelial cell transformation. Knockdown of MUC1 expression significantly reduced transformation of immortalized human bronchial epithelial cells induced by benzo[a]pyrene diol epoxide (BPDE), the active form of the cigarette smoke (CS) carcinogen benzo(a)pyrene (BaP)s. BPDE exposure robustly activated a pathway consisting of EGFR, Akt and ERK, and blocking this pathway significantly increased BPDE-induced cell death and inhibited cell transformation. Suppression of MUC1 expression resulted in EGFR destabilization and inhibition of the BPDE-induced activation of Akt and ERK and increase of cytotoxicity. These results strongly suggest an important role for EGFR in BPDE-induced transformation, and substantiate that MUC1 is involved in lung cancer development, at least partly through mediating carcinogen-induced activation of the EGFR-mediated cell survival pathway that facilitates cell transformation

    Suppression of Methylation-Mediated Transcriptional Gene Silencing by βC1-SAHH Protein Interaction during Geminivirus-Betasatellite Infection

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    DNA methylation is a fundamental epigenetic modification that regulates gene expression and represses endogenous transposons and invading DNA viruses. As a counter-defense, the geminiviruses encode proteins that inhibit methylation and transcriptional gene silencing (TGS). Some geminiviruses have acquired a betasatellite called DNA β. This study presents evidence that suppression of methylation-mediated TGS by the sole betasatellite-encoded protein, βC1, is crucial to the association of Tomato yellow leaf curl China virus (TYLCCNV) with its betasatellite (TYLCCNB). We show that TYLCCNB complements Beet curly top virus (BCTV) L2- mutants deficient for methylation inhibition and TGS suppression, and that cytosine methylation levels in BCTV and TYLCCNV genomes, as well as the host genome, are substantially reduced by TYLCCNB or βC1 expression. We also demonstrate that while TYLCCNB or βC1 expression can reverse TGS, TYLCCNV by itself is ineffective. Thus its AC2/AL2 protein, known to have suppression activity in other geminiviruses, is likely a natural mutant in this respect. A yeast two-hybrid screen of candidate proteins, followed by bimolecular fluorescence complementation analysis, revealed that βC1 interacts with S-adenosyl homocysteine hydrolase (SAHH), a methyl cycle enzyme required for TGS. We further demonstrate that βC1 protein inhibits SAHH activity in vitro. That βC1 and other geminivirus proteins target the methyl cycle suggests that limiting its product, S-adenosyl methionine, may be a common viral strategy for methylation interference. We propose that inhibition of methylation and TGS by βC1 stabilizes geminivirus/betasatellite complexes
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