RESUMO
Wild waterfowl serve as a reservoir of some astroviruses. Fecal samples from wild waterfowl collected at Hong Kong's Marshes were tested using pan-astrovirus reverse transcription-PCR. Positive samples underwent subsequent host identification using DNA barcoding. Based on deduced partial sequences, noteworthy samples from three astrovirus groups (mammalian, avian and unclassified astroviruses) were further analyzed by next-generation sequencing. One sample of Avastrovirus 4 clade, MP22-196, had a nearly complete genome identified. The results of ORF2 phylogenetic analysis and genetic distance analysis indicate that Avastrovirus 4 is classified as a distinct subclade within Avastrovirus. MP22-196 has typical astrovirus genome characteristics. The unique characteristics and potential differences of this genome, compared to other avian astrovirus sequences, involve the identification of a modified sgRNA sequence situated near the ORF2 start codon, which precedes the ORF1b stop codon. Additionally, the 3' UTR of MP22-196 is shorter than other avian astroviruses. This study expands our understanding of the Avastrovirus 4 clade.
Assuntos
Infecções por Astroviridae , Aves , Fezes , Variação Genética , Genoma Viral , Filogenia , Animais , Hong Kong , Aves/virologia , Fezes/virologia , Infecções por Astroviridae/veterinária , Infecções por Astroviridae/virologia , Animais Selvagens/virologia , Doenças das Aves/virologia , Sequenciamento de Nucleotídeos em Larga Escala , Avastrovirus/genética , Avastrovirus/classificação , Avastrovirus/isolamento & purificação , RNA Viral/genética , Fases de Leitura Aberta , Astroviridae/genética , Astroviridae/isolamento & purificação , Astroviridae/classificaçãoRESUMO
Many countries have imposed a set of non-pharmaceutical health policy interventions in an effort to slow the spread of the COVID-19 pandemic. The objective of this paper is to examine the effects of the interventions, drawing on evidence from the OECD countries. A special feature here is the mechanism that underlies the impact of the containment policies. To this end, a causal mediation analysis decomposing the total effect into a direct and an indirect effect is conducted. The key finding is a dual cause-effect channel. On the one hand, there is a direct effect of the non-pharmaceutical interventions on the various health variables. Beyond this, a quantitatively dominant indirect impact of non-pharmaceutical interventions operating via voluntary changes in social distancing is shown.
RESUMO
The People's Bank of China (PBoC) has implemented numerous measures to cushion the impacts of the COVID-19 health crisis on the Chinese economy. Since the current monetary policy framework features a multi-instrument mix of liquidity tools and pricing signals, we employ a dynamic-factor modelling approach to derive a composite indicator of China's monetary policy stance. Our quantitative assessment shows that the PBoC's policy response to the outbreak of the COVID-19 pandemic has been swift and decisive. Specifically, our estimates reveal that the PBoC has implemented novel policy measures to ensure that commercial banks maintain liquidity access and credit provision during the COVID-19 crisis.
RESUMO
Buried bumper syndrome (BBS) is an uncommon but serious complication of percutaneous endoscopic ga-strostomy. It involves the internal fixation device, or "bumper", migrating into the gastric wall and subsequent mucosal overgrowth. We described a case series of four patients with BBS treated with a novel endoscopic technique using a HookKnife between June 2016 and February 2017. The HookKnife is a rotating L-shaped cutting wire designed for hooking tissue and pulling it away from the gastric wall towards the lumen. The technique was successful in all four cases with no complications. Each patient was discharged on the day of treatment. The HookKnife is a manoeuvrable, safe and effective device for endoscopic removal of buried bumpers and could avoid surgery in a high risk group of patients. To our knowledge this technique has not been described previously. We suggest that this technique should be added to the treatment algorithms for managing BBS.
Assuntos
Remoção de Dispositivo , Gastrostomia , Endoscopia , Nutrição Enteral , Humanos , Intubação GastrointestinalRESUMO
Conflicting evidence exists whether diabetic myocardium can be protected by ischemic preconditioning (IPC). The phosphatidylinositol 3-kinase (PI3K)-Akt pathway is important in IPC. However, components of this cascade have been found to be defective in diabetes. We hypothesize that IPC in diabetic hearts depends on intact signaling through the PI3K-Akt pathway to reduce myocardial injury. Isolated perfused Wistar (normal) and Goto-Kakizaki (diabetic) rat hearts were subjected to 1) 35 min of regional ischemia and 120 min of reperfusion with infarct size determined; 2) preconditioning (IPC) using 5 min of global ischemia followed by 10 min of reperfusion performed one, two, or three times before prolonged ischemia; or 3) determination of Akt phosphorylation after stabilization or after one and three cycles of IPC. In Wistar rats, one, two, and three cycles of IPC reduced infarct size 44.7 +/- 3.8% (P < 0.05), 31.4 +/- 4.9% (P < 0.01), and 34.3 +/- 6.1% (P < 0.01), respectively, compared with controls (60.7 +/- 4.5%). However, in diabetic rats only three cycles of IPC significantly reduced infarction to 20.8 +/- 2.6% from 46.6 +/- 5.2% in controls (P < 0.01), commensurate with significant Akt phosphorylation after three cycles of IPC. To protect the diabetic myocardium, it appears necessary to increase the IPC stimulus to achieve the threshold for cardioprotection and a critical level of Akt phosphorylation to mediate myocardial protection.
Assuntos
Precondicionamento Isquêmico Miocárdico , Proteínas Serina-Treonina Quinases/metabolismo , Proteínas Proto-Oncogênicas/metabolismo , Animais , Glicemia/análise , Diabetes Mellitus Tipo 2/fisiopatologia , Hemoglobinas Glicadas/análise , Masculino , Isquemia Miocárdica/prevenção & controle , Reperfusão Miocárdica , Fosfatidilinositol 3-Quinases/metabolismo , Fosforilação , Proteínas Proto-Oncogênicas c-akt , Ratos , Ratos WistarRESUMO
Brief intermittent episodes of ischemia and reperfusion, at the onset of reperfusion after a prolonged period of ischemia, confer cardioprotection, a phenomenon termed "ischemic postconditioning" (Postcond). We hypothesized that this phenomenon may just represent a modified form of reperfusion that activates the reperfusion injury salvage kinase (RISK) pathway. Isolated perfused rat hearts were subjected to: (a) 35 minutes of ischemia and 120 minutes of reperfusion, and infarct size was determined by tetrazolium staining; or (b) 35 minutes of ischemia and 7 minutes of reperfusion, and the phosphorylation states of Akt, endothelial NO synthase (eNOS), and p70S6K were determined. Postcond reduced infarct size from 51.2+/-3.4% to 31.5+/-4.1% (P<0.01), an effect comparable with ischemic preconditioning (IPC; 27.5+/-2.3%; P<0.01). Of interest, the combined protective effects of IPC and Postcond were not additive (30.1+/-4.8% with IPC+Postcond; P=NS). Inhibiting phosphatidylinositol 3-kinase (PI3K) at reperfusion using LY or Wortmannin (Wort) during the first 15 minutes of reperfusion completely abolished Postcond-induced protection (31.5+/-4.1% with Postcond versus 51.7+/-4.5% with Postcond+LY, P<0.01; 56.2+/-10.1% with Postcond+ Wort; P<0.01), suggesting that Postcond protects the heart by activating PI3K-Akt. Western blot analysis demonstrated that Postcond induced a significant increase in phosphorylation of Akt, eNOS, and p70S6K in an LY- and Wort-sensitive manner. In conclusion, we show for the first time that ischemic Postcond protects the myocardium by activating the prosurvival kinases PI3K-Akt, eNOS, and p70S6K in accordance with the RISK pathway.
Assuntos
Reperfusão Miocárdica/métodos , Fosfatidilinositol 3-Quinases/fisiologia , Proteínas Serina-Treonina Quinases/fisiologia , Proteínas Proto-Oncogênicas/fisiologia , Transdução de Sinais/fisiologia , Androstadienos/farmacologia , Animais , Cromonas/farmacologia , Inibidores Enzimáticos/farmacologia , Técnicas In Vitro , Canais Iônicos/efeitos dos fármacos , Canais Iônicos/fisiologia , Precondicionamento Isquêmico , Masculino , Proteínas de Transporte da Membrana Mitocondrial , Poro de Transição de Permeabilidade Mitocondrial , Morfolinas/farmacologia , Infarto do Miocárdio/patologia , Isquemia Miocárdica/fisiopatologia , Isquemia Miocárdica/terapia , Óxido Nítrico Sintase/metabolismo , Óxido Nítrico Sintase Tipo III , Inibidores de Fosfoinositídeo-3 Quinase , Fosforilação , Processamento de Proteína Pós-Traducional , Proteínas Proto-Oncogênicas c-akt , Ratos , Ratos Sprague-Dawley , Proteínas Quinases S6 Ribossômicas 70-kDa/metabolismo , WortmaninaRESUMO
Novel treatment approaches, as potential adjunctive therapy to current reperfusion strategies (such as thrombolysis, primary coronary angioplasty, and cardiac surgery), are required to provide further cardioprotection in the setting of an acute myocardial infarction to effect further reductions in morbidity and mortality. In this regard, the activation of prosurvival kinases, such as Akt and Erk1/2 (which we have termed the reperfusion injury salvage kinase [RISK] pathway), at the time of reperfusion, has been demonstrated to confer powerful cardioprotection against myocardial ischemia-reperfusion injury. In this review, we present evidence suggesting that the cardioprotective phenomena of ischemic preconditioning and the recently described ischemic postconditioning exert their cardioprotective effects through the recruitment of the RISK pathway, at the time of reperfusion, and that the protection in these settings is mediated through the inhibition of mitochondrial permeability transition pore (mPTP) opening at this time. Therefore, the pharmacologic manipulation of the RISK pathway at the time of reperfusion may enable one to harness the powerful cardioprotective benefits of both ischemic preconditioning and postconditioning, and provide a novel approach to cardioprotection.
Assuntos
Ativação Enzimática/efeitos dos fármacos , Precondicionamento Isquêmico Miocárdico , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Proteínas Quinases/metabolismo , Animais , Humanos , Canais Iônicos/antagonistas & inibidores , Sistema de Sinalização das MAP Quinases , Mitocôndrias Cardíacas/metabolismo , Proteínas de Transporte da Membrana Mitocondrial , Poro de Transição de Permeabilidade Mitocondrial , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de SinaisRESUMO
Oropharyngeal mucositis is a common and significant complication of cancer chemotherapy and limits the delivery of chemotherapy, affects the quality of life, and increases the cost of care. Oral mucositis caused by cancer chemotherapy is associated with specific agents, but the origin of oral mucositis is poorly understood. These drugs may have direct toxic effects on the rapidly dividing cells of the oral mucosa and on cellular elements of the connective tissue. Microbial flora may play a role in the development of ulcerative mucositis. Chemotherapy may be directly toxic and affect the mucosa by systemic circulation and may be related to secretion of some chemotherapeutic drugs in the saliva, resulting in topical exposure to the oral environment. Other potential mechanisms include reduced saliva volume and change in saliva constituents that may affect epithelial maintenance and repair, the physiology of the oral microflora, and the interaction between the oral flora and the epithelium. Improved understanding of the mechanisms whereby specific chemotherapeutic agents cause mucositis may lead to management approaches that will reduce the incidence and severity of mucositis, improving quality of life and ensuring delivery of the necessary chemotherapy to improve cancer cure rates.
Assuntos
Antineoplásicos/efeitos adversos , Mucosa Bucal/efeitos dos fármacos , Saliva/fisiologia , Estomatite/induzido quimicamente , Animais , Doxorrubicina/efeitos adversos , Humanos , Metotrexato/efeitos adversosRESUMO
We report an innovative use of the Octopus IV cardiac stabilizer in a case of penetrating thoracic injury. In this case, we used the Octopus IV cardiac stabilizer to immobilize the right ventricular outflow tract during the repair of a stab wound. To date, there have been no reports of such an application of the Octopus IV cardiac stabilizer.