Emotions in Mormon Canonical Texts

In this study Mormon theology has been brought to interact with the socio-scientific study of emotion. The expressed purpose of this dialogue has been to construct an introductory Latter-day Saint (or LDS) theology of emotion which is both canonically based and scientifically informed. Specifically, this examination has highlighted three widely accepted general outcomes which emerge from the socio-scientific study of emotion, namely the necessity of cognition for their emergence, the personal responsibility attached to their manifestation, and their instrumentality in facilitating various processes of human development and experience. In turn, both the basic theological structure of Mormonism and its unique canonical texts have been examined to determine the extent to which LDS theology is compatible with such a three-fold definition of emotion. As a result it was established that at this basic level of explanation science and Mormon theology undoubtedly share a common perspective. In reaching this conclusion unique LDS texts have been examined with specific reference to their description of six common emotions: hope, fear, joy, sorrow, love, and hate. For each of these emotional phenomena, which have further been classified into three separate groups of emotion types, the extensive report of textual evidence has consistently confirmed an implied presence of the outlined three-fold model of emotion. Furthermore, specific attention to the Mormon theology of Atonement and to its significant role for the LDS framing and regulating of emotions has enlarged this theological examination to include a wider exploration of such areas as epistemology, cosmology, soteriology, and anthropology of Mormonism. In this light, the theological and socio-scientific study of emotions in the LDS social/theological context may benefit from further academic research which could extend in the many possible directions of focus that have been suggested in the conclusion

Increased nitric oxide release by neutrophils of a patient with tyrosinemia type III

Tyrosinemia type III (OMIM 2767 10) is an autosomal recessive disorder caused by the deficiency of 4-hydroxyphenylpyruvate dioxygenase (4-HPD). Few cases have been described with mental retardation or neurological symptoms. Recently it has been demonstrated that 4-HPD participates to nitric oxide (NO) intracellular sequestration in Pseudomonas aeruginosa. 4-HPD is an ubiquitous enzyme with a prominent expression in neutrophils and neurons. In the nervous system NO has been perceived to be a potential neuromodulator although prolonged excessive generation is detrimental. We analyzed NO release by neutrophils of a patient with tyrosinemia type III in order to evaluate a possible influence of 4-HPD deficiency on this process. Our patient, previously described, is a 30-year-old women with persistent tyrosinemia (450-680 mu mol/1) and deficient activity of 4-HPD. At 17 months of age she experienced an acute ataxia and drowsiness lasting for 10 days, but further clinical course showed persistent tyrosinemia with normal growth and psychomotor development. Neutrophils isolated from our patient exhibited a NO release greatly higher in respect to the controls (mean +/- SEM 23.2 +/- 1.8 micromol/10(6) cells vs 3.5 +/- 0.5 micromol/10(6) cells). Clinical findings of tyrosinemia type III include neurological symptoms and mental retardation but no consistent phenotype has emerged. Therefore the pathogenesis of neurological involvement is yet not well understood. Our results suggest that an excessive neutrophils of NO release could reflect the lack of scavenging action of 4-HPD. Considering the prominent expression of this enzyme in neurons, we hypothesize that excessive NO release could participate in neuronal damage explaining the neurological involvement described in patients with tyrosinemia type III. (C) 2008 Elsevier Masson SAS. All rights reserved

Serum brain-type creatine kinase increases in children with osteogenesis imperfecta during neridronate treatment

BACKGROUND: Creatine kinase (Ck) catalyzes the reversible transfer of high-energy phosphate groups between adenosine triphosphate and phosphocreatine. The brain isoform (Ckbb) is greatly induced in mature osteoclasts, playing an important role in bone-resorbing function during osteoclastogenesis. High Ckbb serum level has been found in patients with osteopetrosis and in patients with bisphosphonate (BP)-induced osteopetrosis. BPs are considered the treatment of choice for children with osteogenesis imperfecta (OI), acting as potent inhibitors of bone resorption by suppressing the activity of osteoclasts. METHODS: We determined total serum Ck and isoform activity in 18 prepubertal children with type I OI, before and during treatment with the BP neridronate infusions. RESULTS: Basal serum Ckbb levels were slightly elevated with respect to controls (mean +/- SD = 3.0 +/- 2.7 vs. 2.0 +/- 2.2) and progressively increased after neridronate treatment (t(0) vs. t(4): mean +/- SD = 3.0 +/- 2.7 to 10.8 +/- 8.1), with significant increment after first, second, and fourth infusions (P < 0.01). An inverse correlation was found between serum Ckbb and serum CTx at basal level. CONCLUSION: Our results support previous observations that increased serum Ckbb reflects failure of osteoclasts or, at least, suppression of osteoclasts. Upon considering that BPs are long acting, this information could be useful to prevent the risk of overtreatment after long-term BP exposure in pediatric patients with OI

Tocilizumab for patients with COVID-19 pneumonia. The single-arm TOCIVID-19 prospective trial

BackgroundTocilizumab blocks pro-inflammatory activity of interleukin-6 (IL-6), involved in pathogenesis of pneumonia the most frequent cause of death in COVID-19 patients.MethodsA multicenter, single-arm, hypothesis-driven trial was planned, according to a phase 2 design, to study the effect of tocilizumab on lethality rates at 14 and 30 days (co-primary endpoints, a priori expected rates being 20 and 35%, respectively). A further prospective cohort of patients, consecutively enrolled after the first cohort was accomplished, was used as a secondary validation dataset. The two cohorts were evaluated jointly in an exploratory multivariable logistic regression model to assess prognostic variables on survival.ResultsIn the primary intention-to-treat (ITT) phase 2 population, 180/301 (59.8%) subjects received tocilizumab, and 67 deaths were observed overall. Lethality rates were equal to 18.4% (97.5% CI: 13.6-24.0, P=0.52) and 22.4% (97.5% CI: 17.2-28.3, P<0.001) at 14 and 30 days, respectively. Lethality rates were lower in the validation dataset, that included 920 patients. No signal of specific drug toxicity was reported. In the exploratory multivariable logistic regression analysis, older age and lower PaO2/FiO2 ratio negatively affected survival, while the concurrent use of steroids was associated with greater survival. A statistically significant interaction was found between tocilizumab and respiratory support, suggesting that tocilizumab might be more effective in patients not requiring mechanical respiratory support at baseline.ConclusionsTocilizumab reduced lethality rate at 30 days compared with null hypothesis, without significant toxicity. Possibly, this effect could be limited to patients not requiring mechanical respiratory support at baseline.Registration EudraCT (2020-001110-38); clinicaltrials.gov (NCT04317092)

Correction to: Tocilizumab for patients with COVID-19 pneumonia. The single-arm TOCIVID-19 prospective trial (Journal of Translational Medicine, (2020), 18, 1, (405), 10.1186/s12967-020-02573-9)

Following publication of the original article [1] the authors identified that the collaborators of the TOCIVID-19 investigators, Italy were only available in the supplementary file. The original article has been updated so that the collaborators are correctly acknowledged. For clarity, all collaborators are listed in this correction article