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2.
Malar J ; 22(1): 305, 2023 Oct 10.
Artículo en Inglés | MEDLINE | ID: mdl-37817161

RESUMEN

BACKGROUND: Cooperation between China and Africa is deepening, and business, trade, and people-to-people exchanges are growing closer together, especially in the infrastructure construction field. At the same time, malaria has become a serious health concern for Chinese construction workers in Africa, who are at increased risk of infection and complications due to lack of immunity and exposure to high-transmission environments. One of the biggest challenges in fighting malaria is their lack of knowledge and misinterpretations about the disease, which can impact their need for interventions, adherence to treatments, and health services. This study aims to determine the perception and interpretation of malaria among Chinese construction workers in sub-Saharan Africa. METHODS: Semi-structured interviews were conducted with 20 Chinese construction workers in sub-Saharan Africa. Some early respondents initially made contact through two Chinese construction companies in Africa, while the rest of the participants were engaged via a snowball method by the early participants. NVivo10, a qualitative research data management software and a thematic approach, was used to analyze the data and create themes. In order to achieve the general study goals, an inductive content analysis was applied. RESULTS: The study classified participants' perceptions and interpretations of malaria into four categories: flu-like malaria, the rumors of malaria, the hard-to-explain confusion about malaria, and the special interpretation of malaria. CONCLUSION: Malaria poses major health issues to Chinese construction workers in sub-Saharan Africa who lack immunity and live in an environment of high transmission. Their dearth of awareness and misunderstanding of malaria impacts their prevention and treatment behaviors and health outcomes. This study adopts qualitative methods to examine their perceptions and interpretations of malaria, which can serve as a source for future health management strategies.


Asunto(s)
Industria de la Construcción , Malaria , Humanos , Pueblos del Este de Asia , África del Sur del Sahara , Malaria/prevención & control , Investigación Cualitativa , Percepción
3.
J Vasc Surg ; 67(3): 899-908.e1, 2018 03.
Artículo en Inglés | MEDLINE | ID: mdl-28024851

RESUMEN

OBJECTIVE: It is known that T lymphocytes are activated in human abdominal aortic aneurysms (AAAs). γδT cells, as a subset of T cells, play a role in many inflammation-related diseases. However, whether γδT cells participate in the formation of AAA remains unknown. In this study, we explored the role of γδT cells in AAA lesions. METHODS AND RESULTS: Using the porcine pancreatic elastase-induced AAA model, we found that knock out of γδT cells significantly attenuated AAA formation. To elucidate how γδT cells contribute to AAA, microarray analysis was performed, which found that the phosphoinositide 3-kinase/AKT signaling pathway was activated in elastase-perfused γδT knockout (γδT KO) mice. By studying differentially expressed genes involved in phosphoinositide 3-kinase signaling, we found that proliferation-related genes (Sos1, Mtor, Myc) were upregulated whereas apoptosis-related genes (Pten, Bcl1, Bad) were downregulated in elastase-perfused γδT KO mice. Furthermore, histopathologic analysis showed increased PCNA+ and decreased TUNEL+ cells in elastase-perfused γδT KO mice compared with wild-type mice. In addition, inflammatory cytokines including interleukin-1ß, Mcp-1, and tumor necrosis factor-α were downregulated in the aneurysm tissues of elastase-perfused γδT KO mice. CONCLUSIONS: These data reveal a pathogenic role of γδT cells in the experimental AAA model, likely through mechanisms regulating cell proliferation and mediating inflammatory response. Thus, targeting of γδT cells may offer a potential therapeutic method for aortic aneurysms.


Asunto(s)
Aorta Abdominal/enzimología , Aneurisma de la Aorta Abdominal/prevención & control , Linfocitos Intraepiteliales/inmunología , Fosfatidilinositol 3-Quinasa/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Receptores de Antígenos de Linfocitos T gamma-delta/deficiencia , Transducción de Señal , Animales , Aorta Abdominal/inmunología , Aorta Abdominal/patología , Aneurisma de la Aorta Abdominal/enzimología , Aneurisma de la Aorta Abdominal/inmunología , Aneurisma de la Aorta Abdominal/patología , Apoptosis , Proteínas Reguladoras de la Apoptosis/genética , Proteínas Reguladoras de la Apoptosis/metabolismo , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Proliferación Celular , Dilatación Patológica , Modelos Animales de Enfermedad , Predisposición Genética a la Enfermedad , Mediadores de Inflamación/metabolismo , Masculino , Ratones Endogámicos C57BL , Ratones Noqueados , Elastasa Pancreática , Fenotipo , Receptores de Antígenos de Linfocitos T gamma-delta/genética , Remodelación Vascular
4.
Cardiovasc Res ; 109(2): 249-59, 2016 Feb 01.
Artículo en Inglés | MEDLINE | ID: mdl-26614777

RESUMEN

AIMS: IL-12p35 is a pro-inflammatory cytokine that participates in a variety of inflammatory diseases. This study aimed to determine whether IL-12 regulates cardiac injury and repair following acute myocardial infarction (AMI) and investigate the underlying mechanisms. METHODS AND RESULTS: Mice with AMI showed a marked increase in IL-12p35 expression of ischaemic cardiac tissues. IL-12 was mainly produced by CD11b(+) monocytes. Cardiac functions were significantly improved in IL-12p35 knockout (p35-KO) mice compared with wild-type (WT) littermates in response to AMI. IL-12p35 deficiency attenuated the infarct scar and hypertrophy compared with WT mice. RNA transcriptome sequencing and quantitative RT-PCR analysis of CD11b(+) monocytes isolated from WT and p35-KO ischaemic hearts revealed a distinct transcriptional profile in p35-KO CD11b(+) monocytes, displaying pro-angiogenesis and anti-inflammation properties. Angiogenesis was enhanced in p35-KO mice with AMI and hindlimb ischaemia. Moreover, tube formation assay and Matrigel plug analysis demonstrated that IL-12 inhibition of angiogenesis was dependent on monocytes. IL-12p35 deficiency inhibited inflammation by reducing chemokine production and monocyte infiltration into the heart. Finally, administration of an IL-12p35-neutralizing antibody limited AMI-induced inflammatory cell infiltration into the heart and improved angiogenesis and cardiac function. CONCLUSIONS: Deficiency of IL-12p35 limited AMI-induced cardiac injury by promoting pro-angiogenesis and anti-inflammatory functions of monocytes.


Asunto(s)
Inflamación/metabolismo , Subunidad p35 de la Interleucina-12/metabolismo , Monocitos/metabolismo , Infarto del Miocardio/genética , Infarto del Miocardio/metabolismo , Neovascularización Patológica/metabolismo , Animales , Modelos Animales de Enfermedad , Subunidad p35 de la Interleucina-12/deficiencia , Ratones Noqueados , Neovascularización Patológica/genética
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