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Socio-economic determinants of health (SDoH) include various nonmedical factors in the socio-economic sphere with a potentially significant impact on health outcomes. Their effects manifest through several mediators/moderators (behavioral characteristics, physical environment, psychosocial circumstances, access to care, and biological factors). Various critical covariates (age, gender/sex, race/ethnicity, culture/acculturation, and disability status) also interact. Analyzing the effects of these factors is challenging due to their enormous complexity. Although the significance of SDoH for cardiovascular diseases is well documented, research regarding their impact on peripheral artery disease (PAD) occurrence and care is less well documented. This narrative review explores to what extent SDoH are multifaceted in PAD and how they are associated with its occurrence and care. Additionally, methodological issues that may hamper this effort are addressed. Finally, the most important question, whether this association may contribute to reasonable interventions aimed at SDoH, is analyzed. This endeavor requires attention to the social context, a whole systems approach, multilevel-thinking, and a broader alliance that reaches out to more stakeholders outside the medical sphere. More research is needed to justify the power in this concept to improve PAD-related outcomes like lower extremity amputations. At the present time, some evidence, reasonable consideration, and intuitive reasoning support the implementation of various interventions in SDoH in this field.

The SARS-CoV-2 infection (COVID-19) is causing an ongoing pandemic and potentially fatal disease. Development of coagulopathy with thrombotic complications such as deep vein thrombosis and pulmonary embolism are emerging as factors for progression to severe disease and death. Also, a markedly increased level of D-dimer, a protein product of fibrin degradation, has been associated to mortality. Furthermore, activation of immune response due to virus infection may led to uncontrolled severe inflammation with damage to host cells and induction of endotheliitis and cellular apoptosis and pyroptosis. The use of low molecular weight heparin in early stage of the disease could prevent vascular complications and reduce the progression to severe stage of the disease. Aim of this paper was to summarize current evidence about vascular involvement in COVID-19 disease and potential antithrombotic therapy.

Studies suggest that high dose NSAID use may be associated with a reversible impairment of cognition in the elderly. Prolonged NSAID use, on the other hand, may prevent the decline in cognition associated with aging. However, it has yet to be to be definitively determined whether this protection arises from an anti-inflammatory effect that modifies pathways involved in Alzheimer's dementia, or is mediated by a platelet effect that decreases the risk of cerebrovascular disease. Further large-scale, randomised, controlled trials using NSAIDs are needed before patients can be advised that the known risks of NSAIDs are outweighed by their potential long term benefits on cognition. While clinicians await the results of such studies, they should continue to be alert to the possibility of acute CNS adverse effects in their elderly patients who are receiving NSAIDs and to prescribe the minimum dose that is necessary to control pain and inflammation.

Nephritis strain-associated protein (NSAP), a streptokinase produced by strains of streptococci isolated from patients with acute glomerulonephritis, is believed to be a specific antigen which participates in the production of glomerular injury. In order to investigate the mechanisms by which NSAP induces damage we have examined its potential to activate complement in vitro and to bind to isolated human glomeruli. NSAP, both alone and in combination with specific antibody, caused depletion of complement in normal human serum as measured by total haemolytic complement activity and generation of the complement breakdown products. C3a and C4a. Furthermore, Scatchard analysis showed that NSAP bound tightly to human glomeruli (Ka of 400 +/- 240 x 10(6) M) when compared to non-nephritic streptokinase (Ka of 7.3 +/- 4.1 x 10(6) M) and fully cationized human serum albumin (Ka of 0.6 +/- 0.04 x 10(6) M). These findings are consistent with the hypothesis that the deposition of streptococcal antigens within the glomerulus may precede the fixation of complement and specific antibody.

We have set up a vascular database based upon an IBM personal computer in the vascular unit at Repatriation General Hospital, Concord, using 'Dataease'. This is commercially available software that allows the development of a database by users with little or no programming knowledge. The database is menu driven and designed to record details of admissions, indications for surgery, operations, complications and follow-up and has been set up as a prospective project from 1 January 1989 after a pilot study in 1988. Currently, interns, residents and registrars enter data directly onto the computer, providing an excellent teaching and review medium. Unit audit is easy as the program is completely menu driven and there are more than 100 customized reports written, ranging from providing simple complication details to complex reports deriving graft cumulative patency rates. This system also provides for 'instant' discharge letters which have markedly improved communication with the general practitioner.

Clinical, operative and pathological findings in a series of 18 patients with aldosterone producing adrenal cortical adenomas are reviewed. All patients presented with hypertension and hypokalaemia. The main challenges in preoperative diagnosis were to differentiate primary aldosteronism from other causes of hypokalaemia, such as diuretic therapy, to establish the presence of a discrete adenoma and to localize the tumour to the left or right adrenal gland. A high rate of success was achieved in predicting a surgical diagnosis of aldosterone-producing adenoma. This was attributed to thorough biochemical evaluation of the underlying metabolic state by measurement of renal potassium handling and by determining the responses of the renin-aldosterone axis to changes in sodium balance. Preoperative tumour localization, using adrenal phlebography or scintiscanning, was accomplished in only eight cases. Our experience suggests that the transabdominal approach is preferable for cases in which a unilateral lesion is not clearly identified by imaging techniques.

A method of reducing endotoxin contamination in protein-containing solutions is described here using a combination of polymyxin B-Sepharose 4B (PB-Seph 4B) affinity binding and endotoxin-protein dissociation with the dialyzable surfactant, octyl-beta-D-glucopyranoside (OBDG). Using the limulus amoebocyte lysate (LAL) assay to detect endotoxin, greater than 1000-fold reduction of endotoxin reactivity could be accomplished from a contaminated commercial preparation of bovine catalase. Importantly, this occurred with only a 24% protein loss and an 11% loss of catalase enzymatic activity after treatment. The treated catalase appeared to be largely endotoxin-free since it no longer elicited a pyrogenic response in rabbits or primed for intravascular coagulation of the generalized Shwartzman reaction. Of interest, OBDG treatment of Salmonella minnesota Re595 lipopolysaccharide enhanced its ability to bind to serum high density lipoproteins which might contribute to decreased in vivo toxicity. In quantitative studies using radiolabeled endotoxin, the OBDG was shown to be capable of dissociating protein-bound endotoxin thereby facilitating its binding to the PB-Seph 4B adduct. The technique was also useful in removing radiolabeled endotoxin added to human IgG. The methodology described here would be expected to have general usefulness in reducing endotoxin contamination of macromolecular solutions that can bind and retain endotoxin.

We have isolated 64 different missense mutations at 36 out of 53 residue positions in the Arc repressor of bacteriophage P22. Many of the mutant proteins with substitutions in the C-terminal 40 residues of Arc have reduced intracellular levels and probably have altered structures or stabilities. Mutations in the N-terminal ten residues of Arc cause large decreases in operator DNA binding affinity without affecting the ability of Arc to fold into a stable three-dimensional structure. We argue that these N-terminal residues are important for operator recognition but that they are not part of a conventional helix-turn-helix DNA binding structure. These results suggest that Arc may use a new mechanism for sequence specific DNA binding.