The pathophysiology of spontaneous coronary artery dissection (SCAD) is heterogeneous, associated with systemic arteriopathies and inflammatory diseases, and often compounded by environmental precipitants, genetics, or stressors. However, the frequency of these associated conditions with SCAD on a population level remains unknown. Therefore, the objective of this analysis was to evaluate heterogeneous phenotypes of SCAD in the United States using data from the Nationwide Inpatient Sample collected from January 1, 2004, to September 31, 2015. Among 66,360 patients diagnosed with SCAD, the mean age was 63.1 ± 13.2 years and 44.2% were women. A total of 3,415 (5.14%) had depression, 670 (1.0%) had rheumatoid arthritis, 640 (0.96%) had anxiety, 545 (0.82%) had a migraine disorder, 440 (0.66%) used steroids, 385 (0.58%) had malignant hypertension, 280 (0.42%) had systemic lupus erythematosus, 250 (0.38%) had cocaine abuse, 215 (0.32%) had hypertensive heart or renal disease, 130 (0.19%) had coronary spasm, 105 (0.16%) had fibromuscular dysplasia, 85 (0.13%) had Crohn's disease, 75 (0.11%) had celiac disease, 60 (0.09%) had adult autosomal dominant polycystic kidney disease, 60 (0.09%) had hormone replacement therapy, 55 (0.08%) had sarcoidosis, 55 (0.08%) had amphetamine abuse, 15 (0.02%) had granulomatosis polyangiitis, 10 (0.02%) had α1-antitrypsin deficiency, 10 (0.02%) had Marfan syndrome, 10 (0.02%) had Ehlers-Danlos syndrome, 10 (0.02%) had Kawasaki disease, 10 (0.02%) had polyarteritis nodosa, and 5 (0.01%) had multiparity. In conclusion, most cases of SCAD had no apparent concomitant arteriopathy, inflammatory disorder, or evident risk factor.

Surveys estimating chronic obstructive pulmonary disease (COPD) prevalence are unevenly distributed in the Americas, which make it difficult to estimate accurately its geographical distribution. The geographic information system inverse distance weighted (IDW) interpolation technique has proved to be an effective tool in spatial distribution estimation of epidemiological variables, even when real data are few or widely spread. We aimed to represent cartographically the COPD prevalence in the Americas by means of a blue to red scale representation of the prevalence data, where different values are represented as different colours, and a population density filtered IDW interpolation mapping, where areas with a population density <0.1 inhabitants/km2 are hidden. We systematically searched for prevalence rates from population surveys of individuals 40 years and older, and a COPD diagnosis confirmed by spirometry. Interpolation maps were obtained for the whole Americas, even from extensive areas lacking real data. Maps showed high prevalence values in the Southeast and Southwest regions of Canada bordering the United States; in several states of the Great Lakes region, and in the lower Missouri, Ohio and Mississippi basins of the United States; in the coastal regions of south-eastern and southern Brazil; Uruguay, and the Argentine Pampas. In general, most of the remaining American regions showed intermediate values of COPD prevalence. IDW interpolation seems to be a suitable tool to visually display estimates of COPD prevalence, and it may be a valuable help to draw attention about the worrying prevalence of this preventable and treatable disease.

In Figure 6 of this article (PDF and HTML) the arrows labelled 'Depolymerization' and 'Polymerization' should be labelled 'Polymerization' and 'Depolymerization', respectively.

Reduction of a disulfide linkage between cysteine residues in proteins, a standard step in the preanalytical preparation of samples in conventional proteomics approach, presents a challenge to characterize S-glutathionylation of proteins. S-glutathionylation of proteins has been reported in medical conditions associated with high oxidative stress. In the present study, we attempted to characterize glutathionylation of CSF proteins in patients with multiple sclerosis which is associated with high oxidative stress. Using the nano-LC/ESI-MS platform, we adopted a modified proteomics approach and a targeted database search to investigate glutathionylation at the residue level of CSF proteins. Compared to patients with Intracranial hypertension, the following CSF proteins: Extracellular Superoxide dismutase (ECSOD) at Cys195, α1-antitrypsin (A1AT) at Cys232, Phospholipid transfer protein (PLTP) at Cys318, Alpha-2-HS-glycoprotein at Cys340, Ectonucleotide pyrophosphate (ENPP-2) at Cys773, Gelsolin at Cys304, Interleukin-18 (IL-18) at Cys38 and Ig heavy chain V III region POM at Cys22 were found to be glutathionylated in patients with multiple sclerosis during a relapse. ECSOD, A1AT, and PLTP were observed to be glutathionylated at the functionally important cysteine residues. In conclusion, in the present study using a modified proteomics approach we have identified and characterized glutathionylation of CSF proteins in patients with multiple sclerosis.

Native α1-antitrypsin (AAT) is a 52-kDa glycoprotein that acts as an antiprotease and is the physiological inhibitor of neutrophil serine proteases. The main function of AAT is to protect the lung from proteolytic damage induced by inflammation. AAT deficiency (AATD) is a codominant autosomal disorder caused by pathogenic mutations in SERPINA1 gene, leading to reduced levels of serum AAT. The deficiency is known to increase the risk of pulmonary emphysema and chronic obstructive pulmonary disease as a consequence of proteolytic imbalance induced by inflammation, associated in many instances with cigarette smoking and other environmental hazards. Currently, the available therapy for lung disease associated with AATD is serum purified human AAT injected into patients on a weekly basis. It would be advantageous to replace serum-derived AAT with a recombinant version which is stable and resistant to oxidation. We have expressed AAT in Escherichia coli as inclusion bodies and developed a highly efficient refolding and purification process. We engineered a series of mutant forms of AAT to achieve enhance thermostability and oxidation resistance. Moreover, we synthesized an active form of AAT via cysteine-pegylation to achieve a markedly extended half-life in vivo. The resulting molecule, which retains comparable activity to the wild-type form, is expected to be an improved therapeutic agent for treating hereditary emphysema. In addition, the molecule may also be used to treat other types of emphysema caused by smoking, cystic fibrosis, pulmonary hypertension, pulmonary fibrosis, and chronic obstructive pulmonary disease.