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Blood transfusion can have detrimental effects on the pulmonary system leading to lung injury and respiratory decompensation with subsequent increased morbidity and mortality in surgical and critically ill patients. How much of this effect is carried from a lung donor to transplant recipient is not fully understood, raising questions regarding transplant-suitability of lungs from transfused donors.

United Network for Organ Sharing data were reviewed. Lung transplants from adult donors and known donor transfusion status were included while multiorgan transplants and retransplants were excluded. Recipient mortality was evaluated based on donor and recipient characteristics using a Kaplan-Meier survival estimate, Cox proportional hazards, and logistic regression models. We further assessed whether recipient mortality risk modified the donor transfusion effect.

From March 1996 to June 2017, 20,294 transplants were identified. Outcome analysis based on transfusion status showed non-significant difference in one-year mortality (P=.214). Ninety-day recipient-mortality was significantly higher with transfusion of >10 units (U) versus 1-10U or no transfusion (8.5%, 6.1%, and 6.0%, respectively, P=.005). Multivariable analysis showed increased 90-day mortality with transfusion of >10U compared to no transfusion (odds ratio 1.62, P<.001), while 1-10U showed no difference (odds ratio 1.07, P=.390). When stratified by recipient transplant risk, transfusion of >10U was associated with increased mortality even with the lowest-risk recipients, while transfusion of 1-10U showed no mortality-increase even in the highest-risk recipients.

Donor transfusion of >10U of blood was associated with increased 90-day recipient-mortality even in low-risk transplants. This risk should be considered when evaluating donor lungs.
10U of blood was associated with increased 90-day recipient-mortality even in low-risk transplants. This risk should be considered when evaluating donor lungs.
Robotic surgery is an alternative to traditional and minimally invasive cardiac procedures. However, the adaption of robotics in congenital cardiac surgery has remained limited. We analyzed the early outcomes of our single-center experience in robotically assisted congenital cardiac surgery.

From May 2013 to February 2020, 242 robotic operations were done for secundum atrial septal defects (74.7%), sinus venous atrial septal defects (16.1%), partial anomalous pulmonary venous connections (10.7%), widely-patent foramen ovale (3.7%), ostium primum defects (2.5%), unroofed coronary sinus (1.2%), partial atrioventricular canal defects (2.5%), residual septal defects after failed percutaneous closure (1.2%) ventricular septal defect (0.4%), Cor triatriatum sinister (0.4%), subvalvular aortic stenosis (0.4%), common atrium (0.4%), and double-chambered right ventricle (0.4%) using the da Vinci system.

There was no mortality. Mean age was 30.9±12.1 years, and 132 (54.5%) patients were female. Thirty (12.3%) patent and adult patients.Descending necrotizing mediastinitis is a life-threatening disease that extends into the pretracheal, perivascular, retrovisceral, and/or prevertebral spaces, generally sparing the esophagus. We report a case of deep neck abscess complicated by phlegmonous esophagitis and mediastinitis. The patient was successfully treated with antibiotics and surgery, combining transcervical and bilateral thoracoscopic transthoracic mediastinal drainage. However, a pseudo-lumen with a large amount of pus remained in the esophagus. The septum between the true and the pseudo-lumen was cut endoscopically, following which the patient recovered well without any complications.As a potential drug, 2-nitrobenzaldehyde-thiosemicarbazone (2-TSC), a thiosemicarbazone derived from the terpene R-(+)-limonene, was studied through calorimetric and spectroscopic techniques. Differential Scanning Calorimetry (DSC) data showed that 2-TSC causes structural changes in a 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DMPC) membrane, strongly decreasing the cooperativity of the bilayer gel-fluid thermal transition. Optical absorption spectroscopy showed that 2-TSC is more soluble in ethanol and lipids than in water medium, and that the drug displays different structures in the different environments. Though 2-TSC displays no fluorescence, time resolved fluorescence showed that the drug is an effective quencher of the fluorescent probe 6-dodecanoyl-2-dimethylaminonaphthalene (Laurdan). As it is well accepted that Laurdan is positioned into the bilayer close to the membrane surface, that is possibly the localization of 2-TSC in a bilayer. Electron spin resonance (ESR) of the probe 1-palmitoyl-2-stearoyl-(14-doxyl)-sn-glycero-3-phosphocholine (14-PCSL) revealed that 2-TSC is inserted into the hydrocarbon part of the bilayer, fluidizing the lipid bilayer gel phase and rigidifying or organizing the bilayer fluid phase. Similar effects are found for other lipophilic molecules, including cholesterol. These results are useful to improve the understanding of the processes that govern the interaction of thiosemicarbazones with cell membranes, related to the activity of the drugs and their cytotoxicity.Niosomes, as a kind of drug delivery system, is widely used for the topical delivery of lipophilic drugs. Optimization of niosomes plays an essential role in enhancing their therapeutic efficiencies. This study aims to prepare an optimized niosomal formulation of simvastatin (nSIM), a lipophilic member of statins, through the experiment (Response Surface methodology). Optimized niosomes were characterized in size, polydispersity index (PDI), entrapment efficiency (EE), stability, releasing pattern, and antimicrobial activity. The different molar ratio of surfactant and cholesterol were applied to prepare various formulation of simvastatin loaded niosome. Mean particle size and size distribution were analyzed by dynamic light scattering. Antibacterial activity was determined by MIC and MBC tests against Staphylococcus aureus and Escherichia coli. The release rate of simvastatin from noisome nanoparticles was studied by the Franz diffusion cell method. The release pattern was studied through zero order, first order, Higuchi, Korsmeyer-Peppas, and Hixson-Crowell kinetics models. Optimized niosomes were obtained by span 80, drug to cholesterol ratio of 0.4 with 7 min sonication time. Mean particle size, PDI, zeta potential, and entrapment efficiency (EE%) of optimized nSIM were obtained about 168 nm, 0.34, -32.40, and 96 %, respectively. The niosomes significantly decreased the drug's releasing rate and enhanced antibacterial activity against S. aureus and E. Coli. It was found that the release pattern of drug followed the Higuchi kinetic model which means drug release is by diffusion. Overall, our findings indicated that the prepared simvastatin loaded niosomes showed good stability and biological properties than free drug. Our study suggests that niosomal formulation could be considered as a promising strategy for the delivery of poor water-soluble drugs that enhance antibacterial activity.The upregulation of co-inhibitory checkpoint receptors/ligands that inactivate antitumor T-cells, the enhancement of Tregs-mediated trogocytosis that contribute delayed maturation of antigen presenting cell (APC), and the high Tregs/CD+8 ratio that maintained low threshold of CD+8 cells in the tumor microenvironment (TME); all represent the nuances in the immune evasive strategies of pancreatic ductal adenocarcinoma (PDAC). PDAC is the most aggressive type of pancreatic cancers characterized by poor prognosis and extremely low survivability. Over the years, fraternity of scientists have developed therapeutic agents that can bolster the capacity of the antitumor immunity, usually via the inhibition of immune checkpoints. While this immune checkpoint inhibition therapy represents one major jab from immunity to PDAC, this cancer remains highly resistant due to the acme of desmoplasia in its TME. In this review, we discuss the mechanisms of various checkpoint receptors/ligands axes that are relevant to the fitness of PDAC in its oncogenic ring. These checkpoints include PD-1, CTLA-4, ICOS, TIM-3, TIGIT, BTLA, BTN3A, and VISTA. In addition, we provided evidences that are relevant to the understanding of immune checkpoint inhibition, with extensive outline of immune checkpoint inhibitors that are critical to the treatment of PDAC. Finally, we discuss recently known intricacies of PDAC-mediated immunosuppression, and current advances in treatment options. Having realized that the overall scenario between PDAC and antitumor immunity is like the throwing of jabs in a ring, we therefore discuss future directions and prospect that can knock out PDAC in favor of immunity and humanity.The synthesis and NMR structure analysis of a group of oxygenated steroids containing isoxazole, dihydrofuran, tetrahydrofuran rings or enamino carbonyl fragment in the side chain have been fulfilled. The prepared compounds were tested toward several enzymes (human cytochrome P450s CYP17, CYP19, CYP51 and CYP51 of pathogenic fungus Candida glabrata) as their potential inhibitors. A number steroids show a high level affinity (micro- and submicromole) for the enzyme-ligand complexes of the tested compounds with human CYP51, CYP19 and CYP51 of C. glabrata.Recently, a new subgroup of T cells, named peripheral helper T (Tph) cells, has been implicated in autoimmune pathogenesis. An imbalance of Tph cell subsets influences the severity of immune-related diseases. However, the characteristics and roles of Tph cell subsets in psoriasis remain unknown. Programmed cell death 1-positive, chemokine C-X-C receptor (CXCR) 5-negative Tph cells can be divided into 3 subgroups based on differential expression of chemokine CXCR3 and chemokine C-C receptor (CCR) 6. CXCR3+CCR6- Tph cells are classified as Tph1, CXCR3-CCR6- Tph cells are classified as Tph2, and CXCR3-CCR6+ Tph cells are classified as Tph17. In this study, conditions of circulating Tph cell subsets and CD4+CXCR5+ follicular helper T (Tfh) cells in 27 patients with psoriasis and 13 healthy individuals were detected by flow cytometry. The level of plasma chemokine C-X-C ligand (CXCL) 13 was measured by enzyme-linked immunosorbent assay. The correlations between the above indexes and disease severity were explored. In the peripheral blood of patients with psoriasis, Tph17 cells had an activated, proliferative phenotype; the quantity of the cells correlated with disease severity. TTNPB in vitro Plasma CXCL13 levels were elevated in psoriasis and associated with disease severity and the frequency of Tph17 cells. CD4+CXCR5+ Tfh cells were increased in patients and positively correlated with disease severity, the frequency of Tph17 cells, and plasma CXCL13 levels. Our results suggest that Tph17 cells and the CXCL13/CXCR5 axis may be involved in the pathogenesis of psoriasis and represent new immunotherapeutic targets for treating psoriasis.Rheumatic fever (RF) and chronic rheumatic heart disease (RHD) are complications of oropharyngeal infection caused by Streptococcus pyogenes. Despite the importance of the complement system against infections and autoimmunity diseases, studies on the role of the lectin pathway in RF and RHD are scarce. Thus, our aim was to evaluate the association of ficolin-3 serum levels, FCN3 polymorphisms and haplotypes with the susceptibility to RF and RHD. We investigated 179 patients with a history of RF (126 RHD and 53 RF only) and 170 healthy blood donors as control group. Ficolin-3 serum concentrations were measured using enzyme-linked immunosorbent assay (ELISA). Three FCN3 single nucleotide polymorphisms (SNPs rs532781899, rs28362807 and rs4494157) were genotyped through the sequence-specific PCR method. Lower ficolin-3 serum levels were observed in RF patients when compared to controls (12.81 μg/mL vs. 18.14 μg/mL respectively, p  less then  0.0001, OR 1.22 [1.12-1.34]), and in RHD in comparison to RF only (RFo) (12.
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