BACKGROUND The relationship of PaO2 and PaCO2 levels with outcome after cardiac arrest (CA) is controversial. Few studies have analysed both PaO2 and PaCO2 in this setting and the overall exposure to different PaO2 and PaCO2 levels has not been taken into account. METHODS We reviewed blood gas data obtained within the first 24 h from all comatose adult patients who were admitted to the intensive care unit after successful resuscitation from CA. Exposure times to different PaO2 and PaCO2 thresholds were reported as areas under the curve (AUC) and the time above these thresholds was then calculated. The primary outcome measure was neurological outcome assessed using the Cerebral Performance Category (CPC) score at 3 months. An unfavourable outcome was defined as a CPC of 3-5 and a favourable outcome as a CPC of 1-2. RESULTS A total of 356 patients were studied, with a median number of 9 [6-11] blood gas measurements within the first 24 h after admission. The highest and lowest PaO2 and PaCO2 were similar in patients with unfavourable and favourable neurological outcomes. There were no differences in the AUCs or times over different thresholds of PaO2 and PaCO2 in the two groups. In a multivariable analysis, high blood lactate concentrations on admission, presence of shock and a non-shockable initial rhythm were significantly associated with unfavourable outcome. CONCLUSIONS There was no association between exposure to various levels of PaO2 and PaCO2 and neurological outcome after cardiac arrest. BACKGROUND Long-term assessment of global functional outcomes in cardiac arrest (CA) survivors allows for evaluation of acute care practices and referral to rehabilitation services. Given that many post-CA patients are lost to follow-up (LTFU), we explored whether these patients are systematically different from those who complete follow-up based on demographic, resuscitation and outcome characteristics. METHODS We conducted a prospective cohort study of 168 English-speaking CA survivors between 9/25/2016 and 5/31/2018. We measured demographic data and global functional outcomes using Modified Rankin Scale (mRS), and Cerebral Performance Category (CPC) in-person at hospital discharge, and via telephone at 3-, 6-months, and 1-year. We compared patients LTFU (e.g., failure to contact or refused to follow-up) with those contacted. Patients who were hospitalized, in a rehabilitation facility, missed by the research team, or dead were considered not eligible for follow-up.  https://www.selleckchem.com/products/Irinotecan-Hcl-Trihydrate-Campto.html  RESULTS Of the 116 patients eligible for follow-up at 3-months, the majority completed follow-up (n = 69; 59.5%) and 47 (40.5%) were LTFU. Conversely, at 6-months and 1-year, fewer subjects were assessed (42% and 47%) compared to those who were LTFU (58% and 53%), respectively. At 3-months, LTFU patients were younger, unmarried, and had longer ICU stay. At 6-months and 1-year, LTFU patients were primarily male, had a non-shockable primary rhythm, and non-cardiac arrest etiologies. CONCLUSIONS Over one-third of patients are LTFU during the first year after CA, and differences emerged for demographics and characteristics of the event. Future research should account for the informative, non-random distribution of patients LTFU. BACKGROUND Ventricular fibrillation (VF) waveform analyses are considered a reliable proxy for OHCA characteristics in out-of-hospital cardiac arrest (OHCA), but patient characteristics such as cardiovascular medication use might also be associated with changes in VF waveform measures. OBJECTIVES To assess associations between cardiovascular medication use and amplitude spectrum area (AMSA) of VF, while correcting for the presence of cardiovascular disease (CVD), CVD risk factors, and OHCA characteristics. METHODS We included 990 VF patients from an OHCA registry in the Netherlands, with available information on medical history and cardiovascular medication use. Associations between cardiovascular medication use and AMSA were tested in a multivariate linear regression model, adjusting for CVD, CVD risk factors, and OHCA characteristics. Model performance was shown using R-square and R-change. We also calculated whether medication use was associated with faster dissolution of AMSA to lower values with increasing time delay. RESULTS In the multivariate analysis, when corrected for CVD, CVD risk factors and OHCA characteristics, only potassium-sparing agents were associated with a lower AMSA when compared to patients using other cardiovascular medications (OR 0.46 [95% CI 0.10-0.81]; P  0.05). Only a small part of the variance in AMSA could be explained by medication use (R-square 0.003- 0.026). Adding OHCA characteristics to the model resulted in the largest R square change (0.09-0.15). CONCLUSIONS It is unlikely that there is a strong and clinically relevant independent pharmacologic effect of cardiovascular medication use on AMSA. In OHCA, AMSA might be used as patient management tool without considering cardiovascular medication use. Musculoskeletal diseases and disorders, including osteoporosis and rheumatoid arthritis are diseases that threaten a healthy life expectancy, and in order to extend the healthy life expectancy of elderly people, it is important to prevent bone and joint diseases and disorders. We previously reported that alymphoplasia (aly/aly) mice, which have a loss-of-function mutation in the Nik gene involved in the processing of p100 to p52 in the alternative NF-κB pathway, show mild osteopetrosis with a decrease in the osteoclast number, suggesting that the alternative NF-κB pathway is a potential drug target for ameliorating bone diseases. Recently, the novel NF-κB-inducing kinase (NIK)-specific inhibitor compound 33 (Cpd33) was developed, and we examined its effect on osteoclastic bone resorption in vitro and in vivo. Cpd33 inhibited the receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis accompanied by a decrease in the expression of nfatc1, dc-stamp, and cathepsin K, markers of osteoclast differentiation, without affecting the cell viability, in a dose-dependent manner. Cdp33 specifically suppressed the RANKL-induced processing of p100 to p52 but not the phosphorylation of p65 or the degradation or resynthesis of IκBα in osteoclast precursors. Cpd33 also suppressed the bone-resorbing activity in mature osteoclasts. Furthermore, Cdp33 treatment prevented bone loss by suppressing the osteoclast formation without affecting the osteoblastic bone formation in ovariectomized mice. Taken together, NIK inhibitors may be a new option for patients with a reduced response to conventional pharmacotherapy or who have serious side effects.