Sponge-like CoNi Catalysts Synthesized by Combustion of Reactive Solutions: Stability and Performance for CO2 Hydrogenation

Active and stable catalysts are essential for effective hydrogenation of gaseous CO₂ into valuable chemicals. This work focuses on the structural and catalytic features of single metals, i.e., Co and Ni, as well as bimetallic CoNi alloy catalysts synthesized via combustion of reactive sol-gels. Different characterization methods were used for studying the relationships between the structure, composition, and catalytic activity of the fabricated materials. All catalysts exhibited highly porous sponge-like microstructure. The outermost surfaces of the CoNi alloys were more saturated with Co, while a stoichiometric Co/Ni ratio was observed for the particle’s bulk. Catalytic properties of the as-synthesized powders were studied in the CO₂ hydrogenation reaction at 300 °C for over 80 h of time on stream. All the catalysts demonstrated exceptional selectivity with respect to CH₄ formation. However, the combination of elemental Co and Ni in a single phase resulted in a synergistic effect in bulk alloy catalysts, with activity twofold to threefold that of single-metal catalysts. The activity and stability of the CoNi₃ catalyst were higher than those previously reported for Ni-based catalysts. The reasons for this behavior are discussed.     

Control of graft‐versus‐host disease with rabbit anti‐thymocyte globulin,rituximab, and bortezomib in TCRαβ/CD19‐depleted graft transplantation for leukemia in children: a single‐center retrospective analysis of two GVHD‐prophylaxis regimens

Both acute GVHD and chronic GVHD remain the leading cause of morbidity and death after allogeneic HSCT. We conducted a retrospective analysis comparing two GVHD‐prophylaxis regimens: 35 patients received “Regimen 1” (horse ATG, tacrolimus, and methotrexate) and 46 “Regimen 2” (rabbit ATG, rituximab, and peritransplant bortezomib). All 81 patients with a median age of 9 (0.6‐23) years with ALL (n = 31) or AML (n = 50) in complete remission received TCRαβ/CD19‐depleted transplants between May 2012 and October 2016, from 40 HLA‐matched unrelated and 41 haploidentical donors. After a median follow‐up of 3.9 years, the CI of acute GVHD II‐IV was 15% (95% CI: 7‐30) in the “Regimen 2” group and 34% (95% CI: ?54) in the “Regimen 1” group, P = .05. “Regimen 2” was also more effective in the prevention of chronic GVHD; the CI at 1 year after HSCT was 7% (95% CI: 2‐19) vs 31% (95% CI: 19‐51), P = .005. The CI of relapse at 3 years adjusted for the GVHD‐prophylaxis regimen groups 31% (95% CI: 19‐51) for the “Regimen 1” vs 21% (95% CI: 11‐37) for the “Regimen 2”, P = .3. The retrospective observation suggests that the use of the rATG, rituximab, and bortezomib was associated with significantly lower rate of GVHD without the loss of anti‐leukemic activity.     

9,10-Phenanthrenequinone induces DNA deletions and forward mutations via oxidative mechanisms in the yeast Saccharomyces cerevisiae.

The estimated cancer risk from diesel exhaust particles (DEP) in the air is approximately 70% of the cancer risk from all air pollutants. DEP is comprised of a complex mixture of chemicals whose carcinogenic potential has not been adequately assessed. The polycyclic aromatic hydrocarbon quinone 9,10-phenanthrenequinone (9,10 PQ) is a major component of DEP and a suspect genotoxic agent for DEP induced DNA damage. 9,10 PQ undergoes redox cycling to produce reactive oxygen species that can lead to oxidative DNA damage. We used two systems in the yeast Saccharomyces cerevisiae to examine possible differential genotoxicity of 9,10 PQ. The DEL assay measures intra-chromosomal homologous recombination leading to DNA deletions and the CAN assay measures forward mutations leading to canavanine resistance. Cells were exposed to 9,10 PQ aerobically and anaerobically followed by DNA damage assessment. The results indicate that 9,10 PQ induces DNA deletions and point mutations in the presence of oxygen while exhibiting negligible effects anaerobically. In contrast to the cytotoxicity observed aerobically, the anaerobic effects of 9,10 PQ seem to be cytostatic in nature, reducing growth without affecting cell viability. Thus, 9,10 PQ requires oxygen for genotoxicity while different toxicities exhibited aerobically and anaerobically suggest multiple mechanisms of action.     

Social reactions to Valium and Prozac: A cultural lag perspective of drug diffusion and adoption

BackgroundIn the sociological context, the concept of cultural lag holds that material technologies advance more rapidly than social guidelines for their use. The result can be social conflict including liability accusations and product stigmatization that have characterized several new drugs which were widely accepted initially but then publicly criticized in the lay and scientific press.ObjectivesThe objective was to illustrate the utility of the concept of cultural lag to technology commercialization by applying cultural lag to the social and professional environments surrounding the diffusion of the “minor tranquilizers” Librium and Valium in the United States from the 1950s to the 1970s, and the antidepressant Prozac from 1987 to 2005. The intention is to develop a perspective from which to view patterns of social acceptance followed by critique that may occur when technological advances are introduced to the marketplace.MethodsThis study systematically reviews academic, medical, and lay literature regarding the diffusion of the “minor tranquilizers” Librium and Valium in the United States from the 1950s to the 1970s, and the antidepressant Prozac from 1987 to 2005.ResultsThe minor tranquilizers and Prozac both reveal similar patterns of initial widespread public endorsement, followed by growing public criticism and recommendations for more restrictive usage guidelines.ConclusionsCultural lag provides a perspective from which to anticipate, view, and avoid controversies that develop from new technologies in general and pharmaceutical technologies in particular. Market demands for rapid introduction must be balanced by public education. This requires proactive encouragement of lay and professional discussions and the establishment of marketing guidelines that aid development of social consensus regarding appropriate usage.     

Atropine aggravates signs and symptoms of Takotsubo cardiomyopathy

We present a novel case of Takotsubo cardiomyopathy, associated with worsening chest pain and T-wave inversions on electrocardiogram after atropine use. Our patient was an 82-year-old woman who complained of substernal chest discomfort of 5 hours duration. Atropine 0.5 mg was administered intravenously by the emergency medical service for symptomatic bradycardia. The patient subsequently complained of worsening chest pain and developed new T-wave inversions on the electrocardiogram. Cardiac catheterization was diagnostic and revealed normal coronary arteries but akinesis of the apical segment. Although the pathogenesis of Takotsubo cardiomyopathy is not completely understood, catecholamine-mediated myocardial stunning due to enhanced sympathetic activity is the most widely accepted underlying mechanism. The withdrawal of parasympathetic drive in such cases should exacerbate sympathetic activity, leading to the genesis or worsening of disease activity. The role of atropine in relation to Takotsubo cardiomyopathy has been questioned before. However, it was always in the setting of general anesthesia induction, at which time atropine had been used for reversal of symptomatic bradycardia; consequently, determining the exact role of atropine in the disease process was difficult. Our patient received only atropine and therefore illustrated its capacity to worsen signs and symptoms of Takotsubo Cardiomyopathy. Because patients with Takotsubo cardiomyopathy may present with recurrent chest pain, we would recommend caution against the use of atropine for symptomatic bradycardia in such patients in the emergency department. Transcutaneous pacemaker should be preferred.