Environmental fluctuations, such as salinity, impose serious challenges to marine animal survival. Neuropeptides, signaling molecules involved in the regulation process, and the dynamic changes of their full complement in the stress response have yet to be investigated. Here, a MALDI-MS-based stable isotope labeling quantitation strategy was used to investigate the relationship between neuropeptide expression and adaptability of Carcinus maenas to various salinity levels, including high (60 p.p.t.) and low (0 p.p.t.) salinity, in both the crustacean pericardial organ (PO) and brain. Moreover, a high salinity stress time course study was conducted. MS imaging (MSI) of neuropeptide localization in Carcinus maenas PO was also performed. As a result of salinity stress, multiple neuropeptide families exhibited changes in their relative abundances, including RFamides (e.g. APQGNFLRFamide), RYamides (e.g. SSFRVGGSRYamide), B type-allatostatins (AST-B) (e.g. VPNDWAHFRGSWamide), and orcokinins (e.g. NFDEIDRSSFGFV). The MSI data revealed distribution differences in several neuropeptides (e.g. SGFYANRYamide) between color morphs, but salinity stress appeared to not have a major effect on the localization of the neuropeptides.

a b s t r a c tThe covalent attachment of heme to mitochondrial cytochrome c is catalysed by holocytochrome c synthase (HCCS, also called heme lyase). How HCCS functions and recognises the substrate apocytochrome is unknown. Here we have examined HCCS recognition of a chimeric substrate comprising a short mitochondrial cytochrome c N-terminal region with the C-terminal sequence, including the CXXCH heme-binding motif, of a bacterial cytochrome c that is not otherwise processed by HCCS. Heme attachment to the chimera demonstrates the importance of the N-terminal region of the cytochrome. A series of variants of a mitochondrial cytochrome c with amino acid replacements in the N-terminal region have narrowed down the specificity determinants, providing insight into HCCS substrate recognition.

BACKGROUND Preventable readmission has become a national focus. It is clear that surgical patients present specific challenges to those interested in preventing readmission. Little is known about this outcome in the emergent population. We are interested in determining if there are readily available data variables to predict risk of readmission. The surgical Apgar score (SAS) is calculated from objective intraoperative variables and has been shown to be predictive of postoperative mortality in the nonemergent setting. The objectives of this study were to characterize 30-day readmissions in emergent general surgery and to determine whether certain variables were associated with readmissions. We hypothesized that the SAS correlates with the risk for readmission in emergency general surgery patients. PATIENTS AND METHODS Variables of interest were obtained from a retrospective analysis of the American College of Surgeons’ National Surgical Quality Improvement Program database at an academic institution, paired with the electronic medical record. We identified adult general surgery patients who underwent an emergency procedure from 2006 to 2012. Univariate analysis identified factors associated with 30-day readmission. Factors with p < 0.1 were included in the multivariate analysis to reveal potential risk factors. SPSS version 20 was used for the statistical analysis, with p < 0.05 considered to be significant on multivariate analysis. RESULTS As compared with nonemergency surgery patients, emergency surgery patients had a higher readmission rate (11.1% vs. 15.2%, p = 0.004). The SAS (odds ratio, 3.297; 95% confidence interval, 1.074–10.121; p = 0.037) and the combined variable of the American Society of Anesthesiologists Physical Status Classification and length of stay (odds ratio, 4.370; 95% confidence interval, 2.251–8.486; p < 0.001) were associated with elevated risk for readmission in emergency general surgery patients. CONCLUSION We have identified readily available measures that allow for the stratification of patients into low- and high-risk groups for 30-day readmission. The stratification of patients will enable the study of prospective interventions designed to decrease unplanned readmissions in emergency surgery patients. LEVEL OF EVIDENCE Prognostic study, level II.

Context Patients with aggrecan (ACAN) deficiency present with dominantly inherited short stature, often with advanced skeletal maturation and premature growth cessation. There is a paucity of information on the effects of growth-promoting interventions. Objective The aim of this study was to evaluate the efficacy and safety of recombinant human growth hormone (rhGH) therapy on linear growth in children with ACAN deficiency. Design and Setting Open-label, single-arm, prospective study at Cincinnati Children’s Hospital Medical Center. Patients Ten treatment-naïve patients were recruited. Inclusion criteria were: a confirmed heterozygous mutation in ACAN, age ≥ 2 years, pre-pubertal, bone age (BA) ≥ chronological age (CA), and normal IGF-I concentration. Intervention Treatment with rhGH (50 mcg/kg/day) over one year. Main Outcome Measure(s) Main outcomes measured were height velocity (HV) and change in (Δ) height SD (HtSDS). Results Ten patients (six females) were enrolled with median CA of 5.6 yrs (range 2.4 to 9.7). Baseline median HtSDS was -2.5 (range -4.3 to -1.1). Median baseline BA was 6.9 yrs (range 2.5 to 10.0), with median BA/CA of 1.2 (range 0.9 to 1.5). Median pre-treatment HV was 5.2 cm/y (range 3.8 to 7.1), increased to 8.3 cm/y (range 7.3 to 11.2) after one year of therapy (p=0.004). Median ΔHtSDS after one year was +0.62 (range +0.35 to +1.39) (p=0.002). Skeletal maturation did not advance inappropriately (median Δ BA/CA -0.1, p=0.09). No adverse events related to rhGH were observed. Conclusion Treatment with rhGH improved linear growth in a cohort of patients with short stature due to ACAN deficiency.