Mechanical and Chemical Characterisation of TiN and AlTiSiN Coatings on a LPBF Processed IN718 Substrate

Wear-resistant coatings development is progressively increasing steeply due to their advantages when applied to mechanical components subjected to abrasive and destructive environments. Titanium nitride (TiN) coating is typically used to enlarge tools and components’ service life and improve their surface quality. On the other hand, AlTiSiN coating intends to be applied to more aggressive environments such as spatial satellites components exposed to solar radiation, extremely high temperatures, and random particles impact. In this work, specimens of Inconel 718 (IN718) were fabricated via laser powder bed fusion (LPBF), and physical vapour deposition (PVD)-deposited with TiN and AlTiSiN as coatings to mechanically and chemically characterise their surface. In this respect, microhardness testing and chemical analysis via glow discharge optical emission spectroscopy (GDOES) were performed. Later, roughness and wear behaviour analyses were carried out to evaluate the mechanical performance of both coatings and their surface and morphological features. The experimental observations allowed the analysis of both studied coatings by comparing them with the substrate processed via LPBF.     

Amyloid β concentrations and stable isotope labeling kinetics of human plasma specific to central nervous system amyloidosis

Introduction

Cerebrospinal fluid analysis and other measurements of amyloidosis, such as amyloid-binding positron emission tomography studies, are limited by cost and availability. There is a need for a more practical amyloid β (Aβ) biomarker for central nervous system amyloid deposition.

Spatiotemporal activity patterns during respiratory rhythmogenesis in the rat ventrolateral medulla

One of the most important brain rhythms is that which generates involuntary breathing movements. The lower brain stem contains neural circuitry for respiratory rhythm generation in mammals. To date, microsectioning and selective lesioning studies have revealed anatomical regions necessary for respiratory rhythmogenesis. Although respiratory neurons distributed within these regions can be identified by their firing patterns in different phases of the respiratory cycle, conventional electrophysiology techniques have limited the study of spatial organization within this network. Optical imaging techniques offer the potential for monitoring the spatiotemporal activity of large groups of neurons simultaneously. Using high-speed voltage-sensitive dye imaging and spatial correlation analysis in an arterially perfused in situ preparation of the juvenile rat, we determined the spatial distribution of respiratory neuronal activity in a region of the ventrolateral respiratory group containing the pre-B?tzinger complex (pBC) during spontaneous eupneic breathing. While distinctly pre- and postinspiratory-related responses were spatially localizable on length scales less than 100 microm, we found the studied area on whole exhibited a spatial mixture of phase-spanning and postinspiratory-related activity. Additionally, optical recordings revealed significant widespread hyperpolarization, suggesting inhibition in the same region during expiration. This finding is consistent with the hypothesis that inhibitory neurons play a crucial role in the inspiration-expiration phase transition in the pBC. To our knowledge this is the first optical imaging of a near fully intact in situ preparation that exhibits both eupneic respiratory activity and functional reflexes.     

Acute acalculous cholecystitis in children

Acute acalculous cholecystitis(AAC) is the inflammatory disease of the gallbladder in the absence of gallstones. AAC is estimated to represent at least 50% to 70% of all cases of acute cholecystitis during childhood. Although this pathology was originally described in critically ill or post-surgical patients, most pediatric cases have been observed during several infectious diseases. In addition to cases caused by bacterial and parasitic infections, most pediatric reports after 2000 described children developing AAC during viral illnesses(such as Epstein-Barr virus and hepatitis A virus infections). Moreover, some pediatric cases have been associated with several underlying chronic diseases and, in particular, with immune-mediated disorders. Here, we review the epidemiological aspects of pediatric AAC, and we discuss etiology, pathophysiology and clinical management, according to the cases reported in the medical literature.     

Helicobacter pylori upregulates prion protein expression in gastric mucosa： A possible link to prion disease

AIM: Pathological prion protein (PrPSC) is responsible for the development of transmissible spongiform encephalopathies (TSE). While PrPc enters the organism via the oral route, less data is available to know about its uptake and the role of gastrointestinal inflammation on the expression of prion precursor PrPc, which is constitutively expressed in the gastric mucosa. METHODS: We studied PrPc expression in the gastric mucosa of 10 Helicobacter pylori-positive patients before and after successful H pylori eradication compared to non-infected controls using RT-PCR and Western blotting. The effect of central mediators of gastric inflammation, i.e., gastrin, prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) on PrPc expression was analyzed in gastric cell lines. RESULTS: PrPc expression was increased in H pylori-infection compared with non-infected controls and decreased to normal after successful eradication. Gastrin, PGE2, and IL-1β dose-dependently upregulated PrPc in gastric cells, while TNF-α had no effect. CONCLUSION: H pylori infection leads to the upregula-tion of gastric PrPc expression. This can be linked to H pylori induced hypergastrinemia and increased mucosal PGE2 and IL-1β synthesis. H pylori creates a milieu for enhanced propagation of prions in the gastrointestinal tract.     

Efficacy of Tocilizumab Therapy in Different Subtypes of COVID-19 Cytokine Storm Syndrome

Background: Cytokine storm in COVID-19 is heterogenous. There are at least three subtypes: cytokine release syndrome (CRS), macrophage activation syndrome (MAS), and sepsis. Methods: A retrospective study comprising 276 patients with SARS-CoV-2 pneumonia. All patients were tested for ferritin, interleukin-6, D-Dimer, fibrinogen, calcitonin, and C-reactive protein. According to the diagnostic criteria, three groups of patients with different subtypes of cytokine storm syndrome were identified: MAS, CRS or sepsis. In the MAS and CRS groups, treatment results were assessed depending on whether or not tocilizumab was used. Results: MAS was diagnosed in 9.1% of the patients examined, CRS in 81.8%, and sepsis in 9.1%. Median serum ferritin in patients with MAS was significantly higher (5894 vs. 984 vs. 957 ng/mL, p < 0.001) than in those with CRS or sepsis. Hypofibrinogenemia and pancytopenia were also observed in MAS patients. In CRS patients, a higher mortality rate was observed among those who received tocilizumab, 21 vs. 10 patients (p = 0.043), RR = 2.1 (95% CI 1.0–4.3). In MAS patients, tocilizumab decreased the mortality, 13 vs. 6 patients (p = 0.013), RR = 0.50 (95% CI 0.25–0.99). Conclusions: Tocilizumab therapy in patients with COVID-19 and CRS was associated with increased mortality, while in MAS patients, it contributed to reduced mortality.     

Agglutination of Pseudomonas aeruginosa by surfactant protein D

Surfactant protein D (SP-D) is part of the innate host defense system, and may bind and agglutinate invading microorganisms to enhance their removal. The ability of bronchoalveolar lavage (BAL) fluid to agglutinate bacteria and the relationship to its SP-D content are of interest and not yet known. A micromethod on slides was used to assess the agglutination of Pseudomonas aeruginosa by recombinant SP-D and native human BAL fluid. The SP-D-induced agglutination was blocked by calcium depletion, alkaline pH, or the presence of maltose. Twenty-three of 30 BAL fluids from outpatients carrying a chronic tracheostoma clearly agglutinated P. aeruginosa, which was completely inhibited by maltose. The extent of the agglutination correlated weakly to the concentration of SP-D in the BAL fluid, but not to that of SP-A. The functional property, i.e., the agglutination of P. aeruginosa by BAL fluid, was characterized and appeared related in part to the concentration of SP-D. Additional factors, such as the multimeric organization of SP-D, are likely to contribute to the agglutination of microorganisms by BAL or other body fluids. The assay presented will allow the systematic evaluation of small-volume samples for SP-D agglutinating ability from subjects with various lung diseases.     

Oxidative changes of bronchoalveolar proteins in cystic fibrosis

Chronic bacterial infection and severe, polymorphonuclear neutrophil-dominated endobronchial inflammation are characteristic hallmarks of cystic fibrosis (CF) lung disease. The free radicals generated can be deleterious for structure and function of many proteins. The goal of this study was to investigate the degree of oxidation of pulmonary epithelial lining fluid proteins. BAL fluid (BALF) from 55 children with CF and from 11 patients in a control group were investigated by dot-blot assay for content and by two-dimensional electrophoresis and Western blotting for the pattern of distribution of oxidized proteins. The highest level of oxidative stress, as assessed by the level of protein carbonyls, was found in patients with FEV1 < 80% of predicted or with highly elevated neutrophil counts. Compared to control subjects without lung disease, CF patients with normal lung function and CF patients with a normal neutrophil count in their BALF had significantly higher protein carbonyl levels. The extent of protein oxidation was directly related to the neutrophil granulocyte count and inversely to lung function. Our data support the hypothesis that oxidative damage of pulmonary proteins during chronic and excessive neutrophilic endobronchial inflammation may contribute to the decline of lung function in CF patients.