Type I programmed cell death (PCD) or apoptosis is critical for cellular self-destruction for a variety of processes such as development or the prevention of oncogenic transformation. Alternative forms, including type II (autophagy) and type III (necrotic) represent the other major types of PCD that also serve to trigger cell death. PCD must be tightly controlled since disregulated cell death is involved in the development of a large number of different pathologies. To counter the multitude of processes that are capable of triggering death, cells have devised a large number of cellular processes that serve to prevent inappropriate or premature PCD. These cell survival strategies involve a myriad of coordinated and systematic physiological and genetic changes that serve to ward off death. Here we will discuss the different strategies that are used to prevent cell death and focus on illustrating that although anti-apoptosis and cellular survival serve to counteract PCD, they are nevertheless mechanistically distinct from the processes that regulate cell death.
In this study, we develop a method for calculating electric vehicle lithium-ion battery pack performance and cost. To begin, we construct a model allowing for calculation of cell performance and material cost using a bottom-up approach starting with real-world material costs. It thus provides a supplement to existing models, which often begin with fixed cathode active material (CAM) prices that do not reflect raw metal price fluctuations. We collect and display data from the London Metal Exchange to show that such metal prices, in this case specifically cobalt and nickel, do indeed fluctuate and cannot be assumed to remain static or decrease consistently. We input this data into our model, which allows for a visualization of the effects of these metal price fluctuations on the prices of the CAMs. CAMs analyzed include various lithium transition metal oxide-type layered oxide (NMC and NCA) technologies, as well as cubic spinel oxide (LMO), high voltage spinel oxide (LNMO), and lithium metal phosphate (LFP). The calculated CAM costs are combined with additional cell component costs in order to calculate full cell costs, which are in turn scaled up to full battery pack costs. Economies of scale are accounted for separately for each cost fraction.
Immune-driven dry eye disease primarily affects women; the cause for this sex-specific prevalence is unknown. PMN have distinct phenotypes that drive inflammation but also regulate lymphocytes and are the rate-limiting cell for generating anti-inflammatory lipoxin A4 (LXA4). Estrogen regulates the LXA4 circuit to induce delayed female-specific wound healing in the cornea. However, the role of PMN in dry eye disease remains unexplored. We discovered a LXA4-producing tissue-PMN population in the corneal limbus, lacrimal glands and cervical lymph nodes of healthy male and female mice. These tissue-PMN, unlike inflammatory-PMN, expressed a highly amplified LXA4 circuit and were sex-specifically regulated during immune-driven dry eye disease. Desiccating stress in females, unlike in males, triggered a remarkable decrease in lymph node PMN and LXA4 formation that remained depressed during dry eye disease. Depressed lymph node PMN and LXA4 in females correlated with an increase in T effector cells (TH1 and TH17), a decrease in regulatory T cells (Treg) and increased dry eye pathogenesis. Antibody depletion of tissue-PMN abrogated LXA4 formation in lymph nodes, caused a marked increase in TH1 and TH17 and decrease in Treg cells. To establish an immune regulatory role for PMN-derived LXA4 in dry eye females were treated with LXA4. LXA4 treatment markedly inhibited TH1 and TH17 and amplified Treg cells in draining lymph nodes, while reducing dry eye pathogenesis. These results identify female-specific regulation of LXA4-producing tissue-PMN as a potential key factor in aberrant T effector cell activation and initiation of immune-driven dry eye disease.
The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are precursors to immune regulatory and specialized pro-resolving mediators (SPM) of inflammation termed resolvins, maresins, and protectins. Evidence for lipid mediator formation in vivo can be gained through evaluation of their 5-lipoxygenase (LOX) and 15-LOX metabolic pathway precursors and downstream metabolites. We performed a secondary blood sample analysis from 60 participants in the Mothers, Omega-3, and Mental Health study to determine whether SPM and SPM precursors are augmented by dietary EPA- and DHA-rich fish oil supplementation compared to soy oil placebo. We also aimed to study whether SPM and their precursors differ in early and late pregnancy or between maternal and umbilical cord blood. We found that compared to placebo supplementation, EPA- and DHA-rich fish oil supplementation increased SPM precursor 17-hydroxy docosahexaenoic acid (17-HDHA) concentrations in maternal and umbilical cord blood (P = 0.02). We found that the D-series resolvin pathway marker 17-HDHA increased significantly between enrollment and late pregnancy (P = 0.049). Levels of both 14-HDHA, a maresin pathway marker, and 17-HDHA were significantly greater in umbilical cord blood than in maternal blood (P < 0.001, both).
Study Design. A retrospective cohort study. Objective. The aim of this study was to determine the difference in 30-day readmission, reoperation, and morbidity for patients undergoing either posterior or anterior lumbar interbody fusion. Summary of Background Data. Despite increasing utilization of lumbar interbody fusion to treat spinal pathology, few studies compare outcomes by surgical approach, particularly using large nationally represented cohorts. Methods. Patients who underwent lumbar interbody fusion were identified using the NSQIP database. Rates of readmission, reoperation, morbidity, and associated predictors were compared between posterior/transforaminal (PLIF/TLIF) and anterior/lateral (ALIF/LLIF) lumbar interbody fusion using multivariate regression. Bonferroni-adjusted alpha-levels were utilized whereby variables were significant if their P values were less than the alpha-level or trending if their P values were between 0.05 and the alpha-level. Results. We identified 26,336 patients. PLIF/TLIF had greater operative time (P = 0.015), transfusion (P < 0.001), UTI (P = 0.008), and stroke/CVA (P = 0.026), but lower prolonged ventilation (P < 0.001) and DVT (P = 0.002) rates than ALIF/LLIF. PLIF/TLIF independently predicted greater morbidity on multivariate analysis (odds ratio: 1.155, P = 0.0019). In both groups, experiencing a complication and, in PLIF/TLIF, ASA-class ≥3 predicted readmission (P < 0.001). Increased age trended toward readmission in ALIF/LLIF (P = 0.003); increased white cell count (P = 0.003), dyspnea (P = 0.030), and COPD (P = 0.005) trended in PLIF/TLIF. In both groups, increased hospital stay and wound/site-related complication predicted reoperation (P < 0.001). Adjunctive posterolateral fusion predicted reduced reoperation in ALIF/LLIF (P = 0.0018). ASA-class ≥3 (P = 0.016) and age (P = 0.021) trended toward reoperation in PLIF/TLIF and ALIF/LLIF, respectively. In both groups, age, hospital stay, reduced hematocrit, dyspnea, ASA-class ≥3, posterolateral fusion, and revision surgery and, in PLIF/TLIF, bleeding disorder predicted morbidity (P < 0.001). Female sex (P = 0.010), diabetes (P = 0.042), COPD (P = 0.011), and disseminated cancer (P = 0.032) trended toward morbidity in PLIF/TLIF; obesity trended in PLIF/TLIF (P = 0.0022) and ALIF/LLIF (P = 0.020). Conclusion. PLIF/TLIF was associated with a 15.5% increased odds of morbidity; readmission and reoperation were similar between approaches. Older age, higher ASA-class, and specific comorbidities predicted poorer 30-day outcomes, while procedural-related factors predicted only morbidity. These findings can guide surgical approach given specific factors. Level of Evidence: 3
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