Evolution of microstructure and crystallographic texture during dissimilar friction stir welding of duplex stainless steel to low carbon-manganese structural steel

Electron backscattered diffraction (EBSD) was used to analyze the evolution of microstructure and crystallographic texture during friction stir welding of dissimilar type 2205 duplex stainless steel (DSS) to type S275 low carbon-manganese structural steel. The results of microstructural analyses show that the temperature in the center of stirred zone reached temperatures between Ac 1 and Ac 3 during welding, resulting in a minor ferrite-to-austenite phase transformation in the S275 steel, and no changes in the fractions of ferrite and austenite in the DSS. Temperatures in the thermomechanically affected and shoulder-affected zones of both materials, in particular toward the root of the weld, did not exceed the Ac 1 of S275 steel. The shear generated by the friction between the material and the rotating probe occurred in austenitic/ferritic phase field of the S275 and DSS. In the former, the transformed austenite regions of the microstructure were transformed to acicular ferrite, on cooling, while the dual-phase austenitic/ferritic structure of the latter was retained. Studying the development of crystallographic textures with regard to shear flow lines generated by the probe tool showed the dominance of simple shear components across the whole weld in both materials. The ferrite texture in S275 steel was dominated by D 1, D 2, E, E¯ , and F, where the fraction of acicular ferrite formed on cooling showed a negligible deviation from the texture for the ideal shear texture components of bcc metals. The ferrite texture in DSS was dominated by D 1, D 2, I, I¯ , and F, and that of austenite was dominated by the A, A¯ , B, and B¯ of the ideal shear texture components for bcc and fcc metals, respectively. While D 1, D 2, and F components of the ideal shear texture are common between the ferrite in S275 steel and that of dual-phase DSS, the preferential partitioning of strain into the ferrite phase of DSS led to the development of I and I¯ components in DSS, as opposed to E and E¯ in the S275 steel. The formations of fine and ultrafine equiaxed grains were observed in different regions of both materials that are believed to be due to strain-induced continuous dynamic recrystallization (CDRX) in ferrite of both DSS and S275 steel, and discontinuous dynamic recrystallization (DDRX) in austenite phase of DSS

Positron-emitting radioligands for imaging neuroleptic receptors

A series of /sup 18/F-labeled butyrophenones (benperidol, haloperidol, spiroperidol and N-methylspiroperidol) were evaluated in baboons and rats with respect to potential utility as radioligands for studying neuroleptic receptors in the living human brain by positron emission tomography. These compounds were administered to baboons, and the radioactivity distributions to the striatum, and to the cerebellum were determined by PET at times up to 8 hours after isotope injection. 4 refs. (DT

Helicobacter pylori activates and expands Lgr5(+) stem cells through direct colonization of the gastric glands

BACKGROUND & AIMS: Helicobacter pylori infection is the main risk factor for gastric cancer. We characterized the interactions of H pylori with gastric epithelial progenitor and stem cells in humans and mice and investigated how these interactions contribute to H pylori-induced pathology. METHODS: We used quantitative confocal microscopy and 3-dimensional reconstruction of entire gastric glands to determine the localizations of H pylori in stomach tissues from humans and infected mice. Using lineage tracing to mark cells derived from leucine-rich repeat-containing G-protein coupled receptor 5-positive (Lgr5(+)) stem cells (Lgr5-eGFP-IRESCreERT2/ Rosa26-TdTomato mice) and in situ hybridization, we analyzed gastric stem cell responses to infection. Isogenic H pylori mutants were used to determine the role of specific virulence factors in stem cell activation and pathology. RESULTS: H pylori grow as distinct bacterial microcolonies deep in the stomach glands and interact directly with gastric progenitor and stem cells in tissues from mice and humans. These gland-associated bacteria activate stem cells, increasing the number of stem cells, accelerating Lgr5(+) stem cell proliferation, and up-regulating expression of stem cell-related genes. Mutant bacteria with defects in chemotaxis that are able to colonize the stomach surface but not the antral glands in mice do not activate stem cells. In addition, bacteria that are unable to inject the contact-dependent virulence factor CagA into the epithelium colonized stomach glands in mice, but did not activate stem cells or produce hyperplasia to the same extent as wild-type H pylori. CONCLUSIONS: H pylori colonize and manipulate the progenitor and stem cell compartments, which alters turnover kinetics and glandular hyperplasia. Bacterial ability to alter the stem cells has important implications for gastrointestinal stem cell biology and H pylori-induced gastric pathology

Suppression of GSK3β by ERK mediates lipopolysaccharide induced cell migration in macrophage through β-catenin signaling

We investigate the role of β-catenin signaling in the response of macrophage to lipopolysaccharide (LPS) using RAW264.7 cells. LPS rapidly stimulated cytosolic β-catenin accumulation. β-catenin-mediated transcription was showed to be required for LPS induced gene expression and cell migration. Mechanically, ERK activation-primed GSK3β inactivation by Akt was demonstrated to mediate the LPS induced β-catenin accumulation. Overall, our findings suggest that suppression of GSK3β by ERK stimulates β-catenin signaling therefore contributes to LPS induced cell migration in macrophage activation

Clinical impact of COVID-19 on patients with cancer (CCC19): a cohort study.

Data on patients with COVID-19 who have cancer are lacking. Here we characterise the outcomes of a cohort of patients with cancer and COVID-19 and identify potential prognostic factors for mortality and severe illness. In this cohort study, we collected de-identified data on patients with active or previous malignancy, aged 18 years and older, with confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection from the USA, Canada, and Spain from the COVID-19 and Cancer Consortium (CCC19) database for whom baseline data were added between March 17 and April 16, 2020. We collected data on baseline clinical conditions, medications, cancer diagnosis and treatment, and COVID-19 disease course. The primary endpoint was all-cause mortality within 30 days of diagnosis of COVID-19. We assessed the association between the outcome and potential prognostic variables using logistic regression analyses, partially adjusted for age, sex, smoking status, and obesity. This study is registered with ClinicalTrials.gov, NCT04354701, and is ongoing. Of 1035 records entered into the CCC19 database during the study period, 928 patients met inclusion criteria for our analysis. Median age was 66 years (IQR 57-76), 279 (30%) were aged 75 years or older, and 468 (50%) patients were male. The most prevalent malignancies were breast (191 [21%]) and prostate (152 [16%]). 366 (39%) patients were on active anticancer treatment, and 396 (43%) had active (measurable) cancer. At analysis (May 7, 2020), 121 (13%) patients had died. In logistic regression analysis, independent factors associated with increased 30-day mortality, after partial adjustment, were: increased age (per 10 years; partially adjusted odds ratio 1·84, 95% CI 1·53-2·21), male sex (1·63, 1·07-2·48), smoking status (former smoker vs never smoked: 1·60, 1·03-2·47), number of comorbidities (two vs none: 4·50, 1·33-15·28), Eastern Cooperative Oncology Group performance status of 2 or higher (status of 2 vs 0 or 1: 3·89, 2·11-7·18), active cancer (progressing vs remission: 5·20, 2·77-9·77), and receipt of azithromycin plus hydroxychloroquine (vs treatment with neither: 2·93, 1·79-4·79; confounding by indication cannot be excluded). Compared with residence in the US-Northeast, residence in Canada (0·24, 0·07-0·84) or the US-Midwest (0·50, 0·28-0·90) were associated with decreased 30-day all-cause mortality. Race and ethnicity, obesity status, cancer type, type of anticancer therapy, and recent surgery were not associated with mortality. Among patients with cancer and COVID-19, 30-day all-cause mortality was high and associated with general risk factors and risk factors unique to patients with cancer. Longer follow-up is needed to better understand the effect of COVID-19 on outcomes in patients with cancer, including the ability to continue specific cancer treatments. American Cancer Society, National Institutes of Health, and Hope Foundation for Cancer Research