The carbon footprint of cataract surgery in Spain.

BACKGROUND AND PURPOSE: Climate change is one of the most important threats to human health nowadays. The healthcare industry produces a significant part of greenhouse gases (GHG) emissions. The aim of this study is to assess direct and indirect GHG emissions due to cataract surgery in Spain to identify opportunities for improving. METHODS: This observational case series study estimates and analyses the carbon footprint of a single cataract surgery using phacoemulsification in Ávila Hospital. ISO standard 14064 was applied. RESULTS: The carbon footprint of a single cataract surgery in Ávila Hospital was 86.62kg CO2eq. Medical and pharmaceutical equipment were responsible for 85% of GHG emissions. CONCLUSIONS: Collaboration between pharmaceuticals and ophthalmologists is important to improve the environmental impact of cataract surgery. Future research is needed to introduce changes that do not compromise patient and surgeon safety. Green surgery models could play an encouraging role in the new global health scene.

Inducers of heme oxygenase-1.

Heme oxygenase-1 (HO-1) is an inducible rate-limiting enzyme which catalyzes group heme into carbon monoxide, iron and bilirubin. In the recent years, HO-1 expression has been reported as an important protective endogenous mechanism against physical, chemical and biological stress. In this regard, induction of this enzyme has shown beneficial effects in several pathologic conditions, such as inflammatory processes, atherosclerosis, carcinogenesis, ischemia-reperfusion systems or degenerative diseases. Complex intracellular signalling cascades mediate the expression of HO-1 in response to external stimuli, Transcription factors, as nuclear factor E2-related factor-2, activator protein-1, and nuclear factor-kappa B, and some of their upstream kinases, mitogen-activated protein kinases, phosphatidylinositol 3-kinase, or protein kinases A, C are responsible of the HO-1 gene expression. The purpose of this article is to review the increasing number of natural and synthetic molecules reported to induce HO-1 as additive mechanism responsible for their therapeutic effects; experimental and pathological conditions as well as possible signalling mechanism involved in HO-1 expression by this compounds are described. Controlled upregulation of this enzyme, or its catalytic activity, has shown antioxidant, anti-proliferative, anti-apoptotic and anti-inflammatory properties. For this reason, pharmacologic modulation of HO-1 system may represent an effective and cooperative strategy to intervene in several pathologic conditions.

Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis.

OBJECTIVE: CO-releasing molecules (CO-RMs) are a novel class of anti-inflammatory agents. We have examined the possible therapeutic effects of CORM-3 in collagen-induced arthritis (CIA). METHODS: Arthritis was induced in DBA-1/J mice by type II collagen. Animals were treated with CORM-3 (5 and 10 mg/kg/day, intraperitoneally) or the inactive compound iCORM-3 (10 mg/kg/day, intraperitoneally) unable to release CO, from days 22 to 31. Production of anti-type II collagen antibodies, cytokines and cartilage olimeric matrix protein (COMP) was evaluated by enzyme-linked immunosorbent assay, and prostaglandin E(2) (PGE(2)) by radioimmunoassay. Localisation of cyclooxygenase-2 (COX-2), haem oxygenase-1 (HO-1), intercellular adhesion molecule-1 (ICAM-1) and receptor activator of nuclear factor kappaB ligand (RANKL) was examined by immunohistochemistry. RESULTS: Therapeutic administration of CORM-3 suppressed clinical and histopathological manifestations of disease. The levels of PGE(2), interleukin (IL)1beta, IL2, IL6, IL10 and tumour necrosis factor (TNF)alpha in joint tissues were inhibited by CORM-3. By contrast, CORM-3 augmented IL4. Anti-type II collagen antibodies and COMP levels in serum were reduced by CORM-3. Treatment with CORM-3 decreased cellular infiltration, joint inflammation and destruction, as well as the expression of COX-2, ICAM-1 and RANKL, whereas HO-1 increased. These beneficial effects were due to CO release, as iCORM-3 was ineffective. CONCLUSION: This study reveals the antiarthritic properties of CORM-3 in the CIA model and supports the notion that CO-RMs could be developed as a novel strategy for the treatment of inflammatory and arthritic conditions.

Effects of heme oxygenase-1 inducers on established rat adjuvant arthritis.

Heme oxygenase-1 (HO-1) activity can inhibit inflammatory and immune responses. We have examined the influence of HO-1 induction on the established rat adjuvant arthritis model of chronic inflammation. Therapeutic administration of cobalt protoporphyrin IX (CoPP; 5 mg/kg/day i.p.) from day 17 to 23 significantly reduced the inflammatory response, with partial inhibition of hind paw edema and the production of some inflammatory mediators such as nitric oxide metabolites and tumor necrosis factor-alpha, although joint erosion was observed. Hemin administration (26 mg/kg/day i.p.) during the same time period was ineffective on these parameters. Western blot analysis of hind paw homogenates revealed a weaker induction of HO-1 by this compound in comparison with CoPP. Our data indicate that pharmacological HO-1 induction after the establishment of adjuvant arthritis partially reduced the inflammatory response but it was not sufficient to control joint erosion in our experimental conditions.

[Autoimmune hepatitis and anti-Ro antibodies. Is there a link?]. / Hepatitis autoinmune y anticuerpos anti-Ro positivos. ¿Alguna relación?

Antinuclear antibodies (ANA) are considered to be markers of autoimmune disease. Several specific reactivities of ANA are known, among them the Ro (SS-a) complex. Although the presence of anti-Ro antibodies is widely known in systemic connective tissue diseases such as lupus erythematous or Sjögren's syndrome, few studies have attempted to link this finding with autoimmune hepatitis (AIH). We present a case of acute AIH in a 55-year-old woman who tested positive for anti-Ro 60 kD antibodies. The Ro (SS-A) antigen is a complex ribonucleoprotein whose structure is still the subject of debate. Two fractions, of 50 and 60 kD, have been identified. A review of the literature revealed frequencies of 21-34% for anti-Ro 52 kD and of 9-13-6% for anti-Ro 60 kD in AIH. Although no relationship has been demonstrated between this complex and the etiopathogenic mechanisms or clinical patterns of AIH, we propose that multicenter investigations with large series should be performed before the possible involvement of anti-Ro antibodies in these diseases is definitively ruled out.