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A letter to the editor on the detachment of the posterior retina without the macular hole discussing a case report is presented.

The production of syngas (i.e., a mixture of CO and H 2 ) via the electrochemical reduction of CO 2 and water can contribute to the green transition of various industrial sectors. Here we provide a joint academic-industrial perspective on the key technical and economical differences of the concurrent (i.e., CO and H 2 are generated in the same electrolyzer cell) and separated (i.e., CO and H 2 are electrogenerated in different electrolyzers) production of syngas. Using a combination of literature analysis, experimental data, and techno-economic analysis, we demonstrate that the production of synthesis gas is notably less expensive if we operate a CO 2 electrolyzer in a CO-selective mode and combine it with a separate PEM electrolyzer for H 2 generation. We also conclude that by the further decrease of the cost of renewable electricity and the increase of CO 2 emission taxes, such prepared renewable syngas will become cost competitive., Competing Interests: The authors declare the following competing financial interest(s): eChemicles is scaling up its patented CO2 electrolyzer technology to provide an environmentally and economically sustainable alternative to fossil fuel-based chemicals. Air Liquide offers and operates large-scale PEM water electrolysis solutions for the production of low-carbon hydrogen., (© 2023 The Authors. Published by American Chemical Society.)

Background: Transplants cause ischemia-reperfusion (IR) injury that can affect distant organs. Liver is particularly sensitive to IR injury. The present randomized experimental study was designed to investigate a possible protective effect of sevoflurane against liver inflammatory response to lung IR in a lung upper lobe left autotransplant model., Methods: Two groups (sevoflurane and control) of eight swines each were submitted to upper lobe left lung autotransplant. Hypnotic maintenance was performed with sevoflurane 3% or propofol 8 to 10 mg/kg per hr until pneumonectomy was done; then propofol was used for all animals. Blood and liver samples were taken in four different moments: prepneumonectomy, prereperfusion, 10 min postreperfusion and 30 min postreperfusion to measure levels of interleukin (IL)-1β, IL-10, tumor necrosis factor (TNF)-α, monocyte chemotactic protein (MCP)-1, nuclear factor (NF)-κB, C-reactive protein, ferritin and caspase 3. Non-parametric test was used to find statistical meaning., Results: Lung IR markedly increased the expression of TNF-α, IL-1β, MCP-1, NF-κB and caspase activity in control livers compared with basal levels, whereas liver IL-10 expression decreased 10 and 30 min post-reperfusion. Sevoflurane significantly decreased TNF-α, IL-1β, MCP-1, NF-κB liver expression and caspase 3 activity. Sevoflurane also reverted the lung IR-induced decrease in IL-10 expression., Conclusions: The present results indicate that lung IR caused hepatic injury. Sevoflurane attenuated liver injury in a model of upper lobe left lung autotransplant in pigs.

Background: Lung resection surgery is associated with an inflammatory reaction. The use of 1-lung ventilation (OLV) seems to increase the likelihood of this reaction. Different prophylactic and therapeutic measures have been investigated to prevent lung injury secondary to OLV. Lidocaine, a commonly used local anesthetic drug, has antiinflammatory activity. Our main goal in this study was to investigate the effect of IV lidocaine on tumor necrosis factor α (TNF-α) lung expression during lung resection surgery with OLV., Methods: Eighteen pigs underwent left caudal lobectomy. The animals were divided into 3 groups: control, lidocaine, and sham. All animals received general anesthesia. In addition, animals in the lidocaine group received a continuous IV infusion of lidocaine during surgery (1.5 mg/kg/h). Animals in the sham group only underwent thoracotomy. Samples of bronchoalveolar lavage (BAL) fluid and plasma were collected before initiation of OLV, at the end of OLV, at the end of surgery, and 24 hours after surgery. Lung biopsy specimens were collected from the left caudal lobe (baseline) before surgery and from the mediastinal lobe and the left cranial lobe 24 hours after surgery. Samples were flash-frozen and stored to measure levels of the following inflammatory markers: interleukin (IL) 1β, IL-2, IL-10, TNF-α, nuclear factor κB, monocyte chemoattractant protein-1, inducible nitric oxide synthase, and endothelial nitric oxide synthase. Markers of apoptosis (caspase 3, caspase 9, Bad, Bax, and Bcl-2) were also measured. In addition, levels of metalloproteinases and nitric oxide metabolites were determined in BAL fluid and in plasma samples. A nonparametric test was used to examine statistical significance., Results: OLV caused lung damage with increased TNF-α expression in BAL, plasma, and lung samples. Other inflammatory (IL-1β, nuclear factor κB, monocyte chemoattractant protein-1) and apoptosis (caspase 3, caspase 9, and BAX) markers were also increased. With the use of IV lidocaine there was a significant decrease in the levels of TNF-α in the same samples compared with the control group. Lidocaine administration also reduced the inflammatory and apoptotic changes observed in the control group. Hemodynamic values, blood gas values, and airway pressure were similar in all groups., Conclusions: Our results suggest that lidocaine can prevent OLV-induced lung injury through reduced expression of proinflammatory cytokines and lung apoptosis. Administration of lidocaine may help to prevent lung injury during lung surgery with OLV.

Background: Myocardial injury after noncardiac surgery (MINS) was defined as prognostically relevant myocardial injury due to ischemia that occurs during or within 30 days after noncardiac surgery. The study's four objectives were to determine the diagnostic criteria, characteristics, predictors, and 30-day outcomes of MINS., Methods: In this international, prospective cohort study of 15,065 patients aged 45 yr or older who underwent in-patient noncardiac surgery, troponin T was measured during the first 3 postoperative days. Patients with a troponin T level of 0.04 ng/ml or greater (elevated "abnormal" laboratory threshold) were assessed for ischemic features (i.e., ischemic symptoms and electrocardiography findings). Patients adjudicated as having a nonischemic troponin elevation (e.g., sepsis) were excluded. To establish diagnostic criteria for MINS, the authors used Cox regression analyses in which the dependent variable was 30-day mortality (260 deaths) and independent variables included preoperative variables, perioperative complications, and potential MINS diagnostic criteria., Results: An elevated troponin after noncardiac surgery, irrespective of the presence of an ischemic feature, independently predicted 30-day mortality. Therefore, the authors' diagnostic criterion for MINS was a peak troponin T level of 0.03 ng/ml or greater judged due to myocardial ischemia. MINS was an independent predictor of 30-day mortality (adjusted hazard ratio, 3.87; 95% CI, 2.96-5.08) and had the highest population-attributable risk (34.0%, 95% CI, 26.6-41.5) of the perioperative complications. Twelve hundred patients (8.0%) suffered MINS, and 58.2% of these patients would not have fulfilled the universal definition of myocardial infarction. Only 15.8% of patients with MINS experienced an ischemic symptom., Conclusion: Among adults undergoing noncardiac surgery, MINS is common and associated with substantial mortality.

This study tested the hypothesis that the number of CA single sequence repeat (CA-SSR) in the intron 1 of the epidermal growth factor receptor (egfr) gene, which affects transcription efficiency of the gene, is associated with the response to EGFR inhibitors. To this end, we determined the number of CA dinucleotides in the intron 1 of the egfr gene in a panel of 12 head and neck cancer cell lines that lack egfr gene amplification and measured the expression of EGFR (mRNA and protein), as well as response to EGFR inhibition. Cells with lower number of CA dinucleotides in the CA-SSR had higher expression of the EGFR gene and protein and were more sensitive to the inhibitory effects of erlotinib, a small molecule inhibitor of the EGFR tyrosine-kinase. Phenotypic modification by silencing EGFR mRNA expression in a susceptible cell line induced resistance to the drug. The number of CA dinucleotide was equivalent in genomic and tumor DNA obtained from 30 patients with head and neck cancer. In a clinical study in colorectal cancer, subjects with lower number of CA dinucleotide frequently developed skin toxicity, a feature that is related to the antitumor activity of this class of drugs. These results suggest that polymorphic variations in the intron 1 of the egfr gene is associated with response to EGFR inhibitors and may provide an explanation as to why the development of skin toxicity is associated with a favorable outcome in patients treated with these agents.