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The article presents an abstract of the study "Caspase-3 and Calpain Activation Following Glucose-Oxygen Deprivation in Mixed Primary Septo-Hippocampal Cell Cultures," by researcher J.K. Newcomb and colleagues, which will be presented at the 30th annual meeting of the American Society for Neurochemistry to be held on March 14-17, 1999 in New Orleans, Louisiana. The study showed that increased duration of oxygen-glucose deprivation is systematically associated with cell injury.

Atmospheric pressure dielectric barrier discharge plasma actuators are experimentally investigated. The temporal force characteristics and dielectric surface charging are determined using interferometry and split electrode techniques. The experiments are conducted at atmospheric pressure in diminishing levels of oxygen content to investigate the effects of oxygen ions. The results show that the force production is dominated by oxygen ions down to a level of 2-5% oxygen content. Temporal force measurements show that the plasma accelerates the air twice during the bias cycle for all oxygen levels, including pure nitrogen. Surface charging measurements show that, for oxygen content levels above 5%, a positive voltage region builds up on the dielectric downstream of the actuator. In the absence of oxygen, no such buildup is observed. The temporal force production characteristics in the pure nitrogen discharge appear to be greatly affected by the dielectric surface charging. Finally, at a 20% oxygen content level, the majority of the force is produced by the actuator while the exposed electrode is negative. When all of the oxygen is removed, the majority of the force is produced while the exposed electrode is positive. [ABSTRACT FROM AUTHOR]

Background Gout patients do not routinely achieve optimal outcomes related in part to suboptimal administration of urate lowering therapy (ULT) including first-line xanthine oxidase inhibitors allopurinol or febuxostat. Studies leading to the approval of febuxostat compared this agent to allopurinol in inappropriately low, fixed doses. We will compare allopurinol with febuxostat in gout using appropriately titrated doses of both agents and a “treat-to-target” strategy congruent with specialty guidelines. Methods We have planned and initiated the Veterans Affairs (VA) Cooperative Study Program (CSP) 594, Comparative Effectiveness in Gout: Allopurinol vs Febuxostat study. This large double-blind, non-inferiority trial will enroll 950 gout patients randomized to receive allopurinol or febuxostat. Patients will be followed for a total of 72 weeks encompassing 3 distinct 24-week study phases. During Phase I (0–24 weeks), participants will undergo gradual dose titration of ULT until achievement of serum uric acid (sUA) <6.0 mg/dL or <5.0 mg/dL if tophi are present. Dose escalation will not be allowed during final three study visits of Phase 2 (24–48 weeks) and during Phase 3 (48–72 weeks). The primary study outcome is the proportion of participants experiencing at least one gout flare during Phase 3. Subsequent to the 72-week study, participants will be followed passively for up to 10 years after the study to assess long-term health outcomes. Conclusion With its completion, the VA Comparative Effectiveness in Gout: Allopurinol vs Febuxostat study will demonstrate the central role of gradual ULT dose escalation and a treat-to-target strategy in gout management. [ABSTRACT FROM AUTHOR]

Abstract: This study investigated the temporal expression and cell subtype distribution of activated caspase-3 following cortical impact-induced traumatic brain injury in rats. The animals were killed and examined for protein expression of the proteolytically active subunit of caspase-3, p18, at intervals from 6 h to 14 days after injury. In addition, we also investigated the effect of caspase-3 activation on proteolysis of the cytoskeletal protein α-spectrin. Increased protein levels of p18 and the caspase-3-specific 120-kDa breakdown product to α-spectrin were seen in the cortex ipsilateral to the injury site from 6 to 72 h after the trauma. Immunohistological examinations revealed increased expression of p18 in neurons, astrocytes, and oligodendrocytes from 6 to 72 h following impact injury. In contrast, no evidence of caspase-3 activation was seen in microglia at all time points investigated. Quantitative analysis of caspase-3-positive cells revealed that the number of caspase-3-positive neurons exceeded the number of caspase-3-positive glia cells from 6 to 72 h after injury. Moreover, concurrent assessment of nuclear histopathology using hematoxylin identified p18-immunopositive cells exhibiting apoptotic-like morphological profiles in the cortex ipsilateral to the injury site. In contrast, no evidence of increased p18 expression or α-spectrin proteolysis was seen in the ipsilateral hippocampus, contralateral cortex, or hippocampus up to 14 days after the impact. Our results are the first to demonstrate the concurrent expression of activated caspase-3 in different CNS cells after traumatic brain injury in the rat. Our findings also suggest a contributory role of activated caspase-3 in neuronal and glial apoptotic degeneration after experimental TBI in vivo. [ABSTRACT FROM AUTHOR]

The article presents an abstract of the study "Proteolytic Mechanisms of Cell Death Following Traumatic Brain Injury." The study reports that cell death pathways are better defined by biochemical mechanisms instead of phenotypic characteristics. The research paper for the study would be presented in the 30th Annual Meeting of the American Society for Neurochemistry, on March 14-17, 1999, in New Orleans, Louisiana.

The article presents an abstract of the study "TNF-α Stimulates Caspase-3 Activation and Apoptotic Cell Death in Primary Septo-Hippocampal Cultures," by researcher X. Zhao and colleagues, which will be presented at the 30th annual meeting of the American Society for Neurochemistry to be held during March 14-17, 1999 in New Orleans, Louisiana. The researchers found that TNF-α instigates caspase-3 activation and apoptotic cell death.

The article presents an abstract of the study "Novel Characteristics of Glutamate Induced Cell Death in Primary Septo-Hippocampal Cultures: Relationship to Calpain and Caspase-3 Activation," which will be presented at the 30th annual meeting of the American Society for Neurochemistry, to be held from March 14-17, 1999 in New Orleans, Louisiana. It was observed that glutamate does not produce phenotypic profiles characteristic of necrotic or apoptotic cell death.