Dictyocaulus arnfieldi (Cobbold, 1884): análise comparativa da ocorrência em eqüinos, muares e asininos

Para estudo da ocorrência da infecção por Dictyocaulus arnfieldi, em alguns Estados brasileiros, foram examinados os pulmões de 20 asininos, 22 muares e 44 eqüinos procedentes dos seguintes Estados: Maranhão, Piauí, Ceará, Rio Grande do Norte, Paraíba, Pernambuco, Bahia, Minas Gerais e Goiás. Foram registradas as ocorrências de 65%, 22,72% e 4,54%, respectivamente, para asininos, muares e eqüinos; as intensidades médias de 34,3, 36,5 e 2,0 vermes para asininos, muares e eqüinos e as relações macho/fêmea de 1: 1,82 e de 1: 1,41 D. arnfieldi em asininos e muares.To study Dictyocaulus arnfieldi occurrence, the authors analysed the lungs of 20 donkeys, 22 mules and 44 horses from the following Brazilian States: Maranhão, Piauí, Ceará, Rio Grande do Norte, Paraíba, Pernambuco, Bahia,Minas Gerais and Goiás. The prevalence of the infection was 65% in donkeys, 22.72% in mules and 4.54% in horses, with the mean intensity of 34.3 worms in the donkeys, 36.5 in the mules and 2.0 in the horses. The authors reportedthe D. arnfieldi Male/Female ratios which are: 1: 1.82 in donkeys and 1: 4.41 in mules

The Impact of Donor Risk Index, Recipients’ and Operative Characteristics on Post Liver Transplant One-Year Graft Failure: A Cohort Analysis

Background and Aims: The donor risk index (DRI) quantifies donor-related characteristics potentially associated with increased risk of early graft failure. We aimed to assess the impact of the DRI, recipient and perioperative factors on post liver transplant (LT) outcomes. Methods: This was a singlecenter retrospective cohort study including all adult (≥18 years) patients who underwent LT from 01/2019 to 12/2019 at Curry Cabral Hospital, Lisbon, Portugal. Primary endpoint was 1-year graft failure post LT. Associations were studied with logistic regression. Results: A total of 131 cadaveric donor LT procedures were performed in 116 recipients. Recipients’ median (IQR) age was 57 (47–64) years and 101/131 (77.1%) were males. Cirrhosis was the underlying etiology in 95/131 (81.2%) transplants. Based on 8 predefined donors’ characteristics, median (IQR) DRI was 1.96 (1.67–2.16). Following adjustment for MELDNa score pre LT and SOFA score (adjusted odds ratio [aOR], 95% confidence interval [CI] = 0.91 [0.56–1.47]) or lactate (aOR [95% CI] = 2.76 [0.71–10.7]) upon intensive care unit (ICU) admission post LT, DRI was not associated with 1-year graft failure. However, higher SOFA score (aOR [95% CI] = 1.20 [1.05–1.37]) or lactate (aOR [95% CI] = 1.27 [1.10–1.46]) upon ICU admission post LT were independently associated with higher odds of 1-year graft failure. Conclusions: In a recent cohort of patients who underwent LT, DRI, despite being high, was not associated with 1-year graft failure, but SOFA score or lactate upon ICU admission post LT were.info:eu-repo/semantics/publishedVersio

ABO-Incompatible Liver Transplantation in Acute Liver Failure: A Single Portuguese Center Study

INTRODUCTION: ABO-incompatible liver transplantation (ABOi LT) is considered to be a rescue option in emergency transplantation. Herein, we have reported our experience with ABOi LT including long-term survival and major complications in these situations. PATIENT AND METHODS: ABOi LT was performed in cases of severe hepatic failure with imminent death. The standard immunosuppression consisted of basiliximab, corticosteroids, tacrolimus, and mycophenolate mofetil. Pretransplantation patients with anti-ABO titers above 16 underwent plasmapheresis. If the titer was above 128, intravenous immunoglobulin (IVIG) was added at the end of plasmapheresis. The therapeutic approach was based on the clinical situation, hepatic function, and titer evolution. A rapid increase in titer required five consecutive plasmapheresis sessions followed by administration of IVIG, and at the end of the fifth session, rituximab. RESULTS: From January 2009 to July 2012, 10 patients, including 4 men and 6 women of mean age 47.8 years (range, 29 to 64 years), underwent ABOi LT. At a mean follow-up of 19.6 months (range, 2 days to 39 months), 5 patients are alive including 4 with their original grafts. One patient was retransplanted at 9 months. Major complications were infections, which were responsible for 3 deaths due to multiorgan septic failure (2 during the first month); rejection episodes (4 biopsy-proven of humoral rejections in 3 patients and 1 cellular rejection) and biliary. CONCLUSION: The use of ABOi LT as a life-saving procedure is justifiable in emergencies when no other donor is available. With careful recipient selection close monitoring of hemagglutinins and specific immunosuppression we have obtained acceptable outcomes

Loxosceles gaucho Venom-Induced Acute Kidney Injury – In Vivo and In Vitro Studies

Loxosceles (recluse or brown spider) is the most important spider genus causing human envenomation. In Brazil Loxosceles spiders were responsible for approximately 7,000 cases of spider envenomation per year. The brown spider accidents may cause late cutaneous necrosis at the bite site, intravascular hemolysis, rhabdomyolysis, coagulation system changes and acute kidney injury (AKI). Even patients with mild cutaneous lesion may develop severe hemolysis and AKI, which is the main cause of death after these accidents. The mechanisms causing kidney injury are poorly understood. In this manuscript we described a consistent rodent model of Loxosceles gaucho venom-induced AKI and studied some of the possible mechanisms of the renal lesion. The results of this research showed that kidney injury may occur independently of the cutaneous lesion and without changes in the systemic blood pressure. Kidney dysfunction occurred likely due to intra-renal vasoconstriction and rhabdomyolysis, although a direct toxic effect of the venom on the proximal tubules cannot be ruled out

The thromboxane receptor antagonist NTP42 promotes beneficial adaptation and preserves cardiac function in experimental models of right heart overload

BackgroundPulmonary arterial hypertension (PAH) is a progressive disease characterized by increased pulmonary artery pressure leading to right ventricular (RV) failure. While current PAH therapies improve patient outlook, they show limited benefit in attenuating RV dysfunction. Recent investigations demonstrated that the thromboxane (TX) A2 receptor (TP) antagonist NTP42 attenuates experimental PAH across key hemodynamic parameters in the lungs and heart. This study aimed to validate the efficacy of NTP42:KVA4, a novel oral formulation of NTP42 in clinical development, in preclinical models of PAH while also, critically, investigating its direct effects on RV dysfunction.MethodsThe effects of NTP42:KVA4 were evaluated in the monocrotaline (MCT) and pulmonary artery banding (PAB) models of PAH and RV dysfunction, respectively, and when compared with leading standard-of-care (SOC) PAH drugs. In addition, the expression of the TP, the target for NTP42, was investigated in cardiac tissue from several other related disease models, and from subjects with PAH and dilated cardiomyopathy (DCM).ResultsIn the MCT-PAH model, NTP42:KVA4 alleviated disease-induced changes in cardiopulmonary hemodynamics, pulmonary vascular remodeling, inflammation, and fibrosis, to a similar or greater extent than the PAH SOCs tested. In the PAB model, NTP42:KVA4 improved RV geometries and contractility, normalized RV stiffness, and significantly increased RV ejection fraction. In both models, NTP42:KVA4 promoted beneficial RV adaptation, decreasing cellular hypertrophy, and increasing vascularization. Notably, elevated expression of the TP target was observed both in RV tissue from these and related disease models, and in clinical RV specimens of PAH and DCM.ConclusionThis study shows that, through antagonism of TP signaling, NTP42:KVA4 attenuates experimental PAH pathophysiology, not only alleviating pulmonary pathologies but also reducing RV remodeling, promoting beneficial hypertrophy, and improving cardiac function. The findings suggest a direct cardioprotective effect for NTP42:KVA4, and its potential to be a disease-modifying therapy in PAH and other cardiac conditions