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Practical eminence and experience-based recommendations for use of TNF-α inhibitors in sarcoidosis.

In severe refractory sarcoidosis cases not responding to conventional immunosuppressive treatment, the third-line tumor necrosis factor-alpha (TNF-α) inhibitors infliximab and adalimumab might be an alternative. However, appropriate studies to guide the clinician are lacking. The aim of this study was to establish practical recommendations for the use of TNF-α inhibitors in the management of refractory sarcoidosis patients.

METHODS: Based on a literature search and the opinion of sarcoidosis experts worldwide, the recommendations were established. Studies conducted in sarcoidosis were supplemented with data obtained from relevant studies in other inflammatory diseases. A Delphi method of polling, using an online survey addressing 12 clinical questions, was performed amongst 20 of the world's leading sarcoidologists to investigate consensus in case of inadequate data to determine an objective answer.

RESULTS: Of the 256 papers found, 101 were included. Randomized controlled trial studies about the use of TNF-α inhibitors in sarcoidosis are limited. Ninety-five percent (19 of 20) of the sarcoidologists contacted, completed the questionnaire (Europe 68%, North America 32%). Nine recommendations were formulated concerning general aspects of TNF-α inhibitor use; Specific sarcoidosis related items, including indications, starting and maintenance dosage, interval of treatment, treatment duration, and discontinuation regimen of infliximab and adalimumab, were addressed.

CONCLUSION: Based on earlier studies and consensus amongst world's leading sarcoidologists, practical recommendations for the use of TNF-α inhibitors in sarcoidosis were established. These recommendations, with emphasis on indications, dosage and discontinuation regimens, have been developed to support the clinician in the management of refractory sarcoidosis patients.

Treatment for Pulmonary Arterial Hypertension-Associated Right Ventricular Dysfunction.

Pulmonary arterial hypertension (PAH) includes a heterogeneous group of diseases characterized by pulmonary vasoconstriction and remodeling of the lung circulation. Although PAH is a disease of the lungs, patients with PAH frequently die of right heart failure. Indeed, it has been increasingly recognized that patient survival depends on the adaptive response of the right ventricle to the changes in the lung circulation. Many PAH specific drugs can affect the function of right ventricle, however whether these drug effects are direct or indirect remains incompletely understood.

In this review, we sought to recapitulate some of the known effects of standard PAH treatments on the heart, as well as to explore potentially new additional therapies to directly treat right ventricular failure.

Talc pleurodesis in pleuropulmonary diseases treatment.

Aim To determine the efficiency and safety of talc pleurodesis in treating the malignant pleural effusion and recurrent spontaneous pneumothorax.

Methods The study included 54 patients with malignant pleural effusion and recurrent spontaneous pneumothorax, who underwent talc pleurodesis using the "talc slurry" method of pleural talc obliteration.

Results : Pleurodesis was successful in 52 (96%) patients. The average duration of thoracic drainage was 4.4 days. Procedure complications included higher body temperature, pneumonia and pleural effusion separation. All of the patients had satisfying radiological findings at the point of discharge and three months later. There was no death outcome related to the procedure of pleurodesis itself.

Conclusion Our study has proved the efficiency and simplicity oftalc pleurodesis in treating symptomatic malignant pleural effusions and cases with recurrent spontaneous pneumothorax. Appropriate patient selection and compliance with surgical principles during the procedure make this method safe, efficient and successful in treating pleuropulmonal diseases.Large particle talc should be used for pleurodesis because of the minimum risk of complications.

A computational study of the Warburg effect identifies metabolic targets inhibiting cancer migration.

Over the last decade, the field of cancer metabolism has mainly focused on studying the role of tumorigenic metabolic rewiring in supporting cancer proliferation.

Here, we perform the first genome-scale computational study of the metabolic underpinnings of cancer migration. We build genome-scale metabolic models of the NCI-60 cell lines that capture the Warburg effect (aerobic glycolysis) typically occurring in cancer cells. The extent of the Warburg effect in each of these cell line models is quantified by the ratio of glycolytic to oxidative ATP flux (AFR), which is found to be highly positively associated with cancer cell migration. We hence predicted that targeting genes that mitigate the Warburg effect by reducing the AFR may specifically inhibit cancer migration.

By testing the anti-migratory effects of silencing such 17 top predicted genes in four breast and lung cancer cell lines, we find that up to 13 of these novel predictions significantly attenuate cell migration either in all or one cell line only, while having almost no effect on cell proliferation. Furthermore, in accordance with the predictions, a significant reduction is observed in the ratio between experimentally measured ECAR and OCR levels following these perturbations.

Inhibiting anti-migratory targets is a promising future avenue in treating cancer since it may decrease cytotoxic-related side effects that plague current anti-proliferative treatments. Furthermore, it may reduce cytotoxic-related clonal selection of more aggressive cancer cells and the likelihood of emerging resistance.

Airborne dissemination of transmissible bacterial species in cystic fibrosis

bacteriaDelivery of multidisciplinary care by experienced teams in specialist units has conferred considerable benefits in care for individuals with cystic fibrosis (CF), with significant improvements in clinical outcome and survival figures. However, one particular concern of congregating patients at specialist CF centres is the potential for cross-infection.

Over the past decade, the emergence and spread of clonal (transmissible) Pseudomonas aeruginosa strains among patients with CF has become an international problem.

Case series suggest that initial infection with clonal P. aeruginosa strains may be more difficult to eradicate,4 and in cohort studies chronic infection is associated with worse clinical outcomes.

The mechanism of spread of P. aeruginosa between patients with CF is unresolved. Potential routes include direct or indirect contact, droplet spread of relatively large infectious particles that travel short distances or airborne spread of...

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