RESUMEN
OBJECTIVE: The purpose was to investigate the risk factors for delayed upper gastrointestinal transit (DUGT) in small bowel capsule endoscopy (SBCE) and to improve the efficacy of SBCE. METHODS: The medical records of patients who underwent SBCE in Renji hospital between January 2015 and January 2023 were retrospectively reviewed. Data collection included patient demographics and potential risk factors for DUGT such as indications for the examination, underlying diseases, hospitalization status, anemia, inflammation. Risk factors were analyzed using univariable and multivariable logistic regression models. DUGT was defined as failure of a capsule to pass through the pylorus within 1 h. RESULTS: A total of 1459 patients who underwent SBCE were included in the study. 306 Cases (21%) experienced DUGT and all received conservative observation, medication treatment, endoscopic intervention, and other measures based on specific circumstances. The overall completion rate (CR) of the examination was 95.5% (1394/1459). Logistic regression analysis showed that hospitalization status (p = 0.030), diarrhea (p = 0.017), diabetes (p = 0.027) and cerebrovascular disease (p = 0.038) were significant risk factors for DUGT. CONCLUSIONS: In our study, DUGT of SBCE was associated with hospitalization status, diarrhea, diabetes and cerebrovascular disease. Therefore, for the patients with the above risk factors, we should closely check the capsule status during the examination process, in order to take appropriate intervention measures as soon as possible.
RESUMEN
The cornerstone of antimalarial treatment, artemisinin, has reduced malaria associated morbidity and mortality worldwide. However, Plasmodium falciparum parasites with reduced sensitivity to artemisinin have emerged, and this threatens malaria control and elimination efforts. In this minireview, we describe the initial development of artemisinin as an antimalarial drug, its use both historically and currently, and our current understanding of its mode of action and the mechanisms by which malaria parasites achieve resistance.
Asunto(s)
Antimaláricos/farmacología , Artemisininas/farmacología , Resistencia a Medicamentos , Plasmodium falciparum/efectos de los fármacos , Antimaláricos/uso terapéutico , Artemisininas/uso terapéutico , Resistencia a Medicamentos/genética , Humanos , Malaria Falciparum/tratamiento farmacológico , Mutación , Plasmodium falciparum/genética , Proteínas Protozoarias/genéticaRESUMEN
It has been known that osteoclastogenesis is induced by extracellular acidosis-evoked the rise of intracellular calcium ([Ca(2+)]i), which regulate activation of the transcription factor nuclear factor of activated T cells c1 (NFATc1). However, the acid-sensing ion channels (ASICs) involved remain largely unknown. Here, we show that ASIC1a, ASIC1b, ASIC2a, and ASIC3 are expressed in rat osteoclasts, and only ASIC1a is highly upregulated in response to acidosis. Both the ASIC1a-specific blocker PcTX1 and specific siRNA significantly reduce this increase in acid-induced [Ca(2+)]i and acid-induced nuclear translocation of NFATc1, and inhibit acid-induced osteoclast differentiation and bone resorption. These findings show that ASIC1a-mediated calcium entry plays a critical role in osteoclastogenesis by regulating activation of the NFATc1.