Elective Cancer Surgery in COVID-19-Free Surgical Pathways During the SARS-CoV-2 Pandemic: An International, Multicenter, Comparative Cohort Study.

PURPOSE: As cancer surgery restarts after the first COVID-19 wave, health care providers urgently require data to determine where elective surgery is best performed. This study aimed to determine whether COVID-19-free surgical pathways were associated with lower postoperative pulmonary complication rates compared with hospitals with no defined pathway. PATIENTS AND METHODS: This international, multicenter cohort study included patients who underwent elective surgery for 10 solid cancer types without preoperative suspicion of SARS-CoV-2. Participating hospitals included patients from local emergence of SARS-CoV-2 until April 19, 2020. At the time of surgery, hospitals were defined as having a COVID-19-free surgical pathway (complete segregation of the operating theater, critical care, and inpatient ward areas) or no defined pathway (incomplete or no segregation, areas shared with patients with COVID-19). The primary outcome was 30-day postoperative pulmonary complications (pneumonia, acute respiratory distress syndrome, unexpected ventilation). RESULTS: Of 9,171 patients from 447 hospitals in 55 countries, 2,481 were operated on in COVID-19-free surgical pathways. Patients who underwent surgery within COVID-19-free surgical pathways were younger with fewer comorbidities than those in hospitals with no defined pathway but with similar proportions of major surgery. After adjustment, pulmonary complication rates were lower with COVID-19-free surgical pathways (2.2% v 4.9%; adjusted odds ratio [aOR], 0.62; 95% CI, 0.44 to 0.86). This was consistent in sensitivity analyses for low-risk patients (American Society of Anesthesiologists grade 1/2), propensity score-matched models, and patients with negative SARS-CoV-2 preoperative tests. The postoperative SARS-CoV-2 infection rate was also lower in COVID-19-free surgical pathways (2.1% v 3.6%; aOR, 0.53; 95% CI, 0.36 to 0.76). CONCLUSION: Within available resources, dedicated COVID-19-free surgical pathways should be established to provide safe elective cancer surgery during current and before future SARS-CoV-2 outbreaks

Elective cancer surgery in COVID-19-free surgical pathways during the SARS-CoV-2 pandemic: An international, multicenter, comparative cohort study

PURPOSE As cancer surgery restarts after the first COVID-19 wave, health care providers urgently require data to determine where elective surgery is best performed. This study aimed to determine whether COVID-19–free surgical pathways were associated with lower postoperative pulmonary complication rates compared with hospitals with no defined pathway. PATIENTS AND METHODS This international, multicenter cohort study included patients who underwent elective surgery for 10 solid cancer types without preoperative suspicion of SARS-CoV-2. Participating hospitals included patients from local emergence of SARS-CoV-2 until April 19, 2020. At the time of surgery, hospitals were defined as having a COVID-19–free surgical pathway (complete segregation of the operating theater, critical care, and inpatient ward areas) or no defined pathway (incomplete or no segregation, areas shared with patients with COVID-19). The primary outcome was 30-day postoperative pulmonary complications (pneumonia, acute respiratory distress syndrome, unexpected ventilation). RESULTS Of 9,171 patients from 447 hospitals in 55 countries, 2,481 were operated on in COVID-19–free surgical pathways. Patients who underwent surgery within COVID-19–free surgical pathways were younger with fewer comorbidities than those in hospitals with no defined pathway but with similar proportions of major surgery. After adjustment, pulmonary complication rates were lower with COVID-19–free surgical pathways (2.2% v 4.9%; adjusted odds ratio [aOR], 0.62; 95% CI, 0.44 to 0.86). This was consistent in sensitivity analyses for low-risk patients (American Society of Anesthesiologists grade 1/2), propensity score–matched models, and patients with negative SARS-CoV-2 preoperative tests. The postoperative SARS-CoV-2 infection rate was also lower in COVID-19–free surgical pathways (2.1% v 3.6%; aOR, 0.53; 95% CI, 0.36 to 0.76). CONCLUSION Within available resources, dedicated COVID-19–free surgical pathways should be established to provide safe elective cancer surgery during current and before future SARS-CoV-2 outbreaks

Primary and acquired resistance of Mycobacterium tuberculosis in western Mexico

Resistance of Mycobacterium tuberculosis to antimycobacterial agents is a worldwide problem. The proposite of this study was to analyze the current resistance patterns of patients with initial episodes, as well as relapses, due to M. tuberculosis in western Mexico. From January 1993 to February 1999 a total of 237 strains of M. tuberculosis (120 from initial cases and 117 from relapse cases) were analyzed. Two hundred and four (86%) strains were isolated from the lower respiratory tract, and 33 strains (14%) from extrapulmonary sites. Twenty-three percent of M. tuberculosis isolated from patients with initial episodes were resistant to both isoniazid and rifampin, and 52% of M. tuberculosis isolated from relapse cases were also resistant to both isoniazid and rifampin

Primary and acquired resistance of Mycobacterium tuberculosis in western Mexico

Resistance of Mycobacterium tuberculosis to antimycobacterial agents is a worldwide problem. The proposite of this study was to analyze the current resistance patterns of patients with initial episodes, as well as relapses, due to M. tuberculosis in western Mexico. From January 1993 to February 1999 a total of 237 strains of M. tuberculosis (120 from initial cases and 117 from relapse cases) were analyzed. Two hundred and four (86%) strains were isolated from the lower respiratory tract, and 33 strains (14%) from extrapulmonary sites. Twenty-three percent of M. tuberculosis isolated from patients with initial episodes were resistant to both isoniazid and rifampin, and 52% of M. tuberculosis isolated from relapse cases were also resistant to both isoniazid and rifampin

Tumor necrosis factor ? down-regulates expression of the ?1(I) collagen gene in rat hepatic stellate cells through a p20C/EBP?- and C/EBP?-dependent mechanism

Tumor necrosis factor ? (TNF-?) is one of the key cytokines of the acute phase response and of many inflammatory processes. This cytokine has several antifibrogenic actions and down-regulates the expression of the type I collagen genes and induces the expression of metalloproteinases. Because TNF-? directly antagonizes some fibrogenic actions of transforming growth factor ?1 (TGF-?1), we considered it important to map the cis-acting regulatory element of the ?1(I) collagen (col1a1) promoter involved in TNF- ? responsiveness in hepatic stellate cells (HSC), to investigate the transcription factors that bind to it, and to establish possible mechanisms by which TNF-? downregulates its expression. In this article, we show the presence of a functional TNF-?-responsive element (TaRE) in the -378 to -345 region of the col1a1 promoter. This element colocalizes with a previously reported TGF-?1-responsive element. We further demonstrate that TNF-? induces nuclear translocation and binding of transcriptional complexes containing p20C/EBP?, p35C/EBP?, and C/EBP? to this sequence of the promoter. Transient overexpression of C/EBP? or p20C/EBP?, the natural dominant negative form of C/EBP? in HSC, down-regulated activity of a CAT reporter vector driven by -412 to +110 of the col1a1 promoter. Taken together, these data suggest that the -378 to -340 region of the col1a1 promoter is the site of convergence of different stimuli that ultimately modulate col1a1 gene transcription

Tumor necrosis factor α down-regulates expression of the α1(I) collagen gene in rat hepatic stellate cells through a p20C/EBPβ- and C/EBPδ-dependent mechanism

Tumor necrosis factor α (TNF-α) is one of the key cytokines of the acute phase response and of many inflammatory processes. This cytokine has several antifibrogenic actions and down-regulates the expression of the type I collagen genes and induces the expression of metalloproteinases. Because TNF-α directly antagonizes some fibrogenic actions of transforming growth factor β1 (TGF-β1), we considered it important to map the cis-acting regulatory element of the α1(I) collagen (col1a1) promoter involved in TNF- α responsiveness in hepatic stellate cells (HSC), to investigate the transcription factors that bind to it, and to establish possible mechanisms by which TNF-α downregulates its expression. In this article, we show the presence of a functional TNF-α-responsive element (TaRE) in the -378 to -345 region of the col1a1 promoter. This element colocalizes with a previously reported TGF-β1-responsive element. We further demonstrate that TNF-α induces nuclear translocation and binding of transcriptional complexes containing p20C/EBPβ, p35C/EBPβ, and C/EBPδ to this sequence of the promoter. Transient overexpression of C/EBPδ or p20C/EBPβ, the natural dominant negative form of C/EBPβ in HSC, down-regulated activity of a CAT reporter vector driven by -412 to +110 of the col1a1 promoter. Taken together, these data suggest that the -378 to -340 region of the col1a1 promoter is the site of convergence of different stimuli that ultimately modulate col1a1 gene transcription

Renal dysfunction as a consequence of acute liver damage by bile duct ligation in cirrhotic rats

Renal failure is a common complication in patients with alcohol-induced cirrhosis who undergo a superimposed severe alcoholic hepatitis. Aim: Our aim was to evaluate renal dysfunction established as a consequence of acute liver damage (ALD) induced by bile duct ligation (BDL) in cirrhotic rats. Hepatic and renal functional assays were performed. Results: Hiperbilirubinemia and increased alanine aminotransferase and aspartate aminotransferase (p < 0.05) in rats with BDL were observed since the first day of bile obstruction in cirrhotic rats. Urinary volume and urinary sodium concentration showed a significant reduction (p < 0.05) on days 3 and 5 after BDL. Plasma renin activity, plasma renin concentration, serum creatinine, and BUN values increased (p < 0.05) from day 1 to day 7 after BDL. Glomerular filtration rate was substantially decreased from day 1 to day 7. Histological changes became apparent since day 3 after BDL in which glomeruli with mesangial hipercellularity took place in the absence of tubular necrosis; with portal inflammation and proliferation of biliar conduits. Results of the present work demonstrate that ALD induced by BDL in cirrhotic rats produces changes in renal function. In conclusion, this experimental model demonstrates that an ALD of variable etiology, either surgical or induced by CCl4, can cause important damage that eventually results in renal function deterioration. This experimental model may be suitable, to study the physiopathology of this syndrome, as well as for the evaluation of different pharmacological therapies. � 2006 Elsevier GmbH. All rights reserved

De novo synthesis and accumulation of apoplastic proteins in leaves of heavy metal-exposed barley seedlings

Blinda A, Koch B, Ramanjulu S, Dietz K-J. De novo synthesis and accumulation of apoplastic proteins in leaves of heavy metal-exposed barley seedlings. Plant Cell & Environment. 1997;20(8):969-981.The leaf apoplast is a site of preferential accumulation of heavy metals in the shoot when barley seedlings are grown in the presence of cadmium, nickel or zinc in hydroponic medium. It was shown recently that apoplastic protein content increased concomitantly in plants grown in the presence of high Zn (Brune et al. 1994, Journal Experimental Botany 45, 1189), Here it is demonstrated that apoplastic proteins increase to an even greater extent in Ni-treated plants, and that the response is intermediate for Cd-treated plants, The paper focuses on possible causes for the increase in apoplastic proteins, (1) Synthesis of cell wall proteins was studied by in vivo pulse labelling of leaf proteins with S-35 methionine followed by extraction of extracellular polypeptides, Depending on growth conditions and leaf age, 1--6% of the protein synthesized de novo in the leaf was allocated to the extractable protein fraction of the leaf apoplast, Under control conditions, labelling reached its maximum after 2 h; labelling continued to rise in Ni-treated plants, where the maximum level of final labelling was reached only after several hours, Labelling decreased with leaf age and increased proportionally with Ni concentration in the nutrient solution, (2) Autolysis experiments on extracted apoplastic proteins and in situ digestion of infiltrated ovalbumin revealed a low proteolytic activity in the apoplast which was not altered in heavy metal-treated leaves, (3) Following a sudden application of Ni to the growth medium, protein content and peroxidase activity increased with a 48 h delay and approached the level obtained for continuously Ni-treated plants, even in previonsly fully expanded leaf tissue. It is concluded that altered cell wall structure is probably not involved in increasing the extraction yield of apoplastic proteins, (4) The increase in extractable apoplastic proteins was also not due to inhibited ionical or covalent immobilization of proteins in the cell wall matrix of heavy metal-challenged plants, (5) Northern blotting revealed heavy metal-induced upregulation of mRNA levels of selected apoplastic proteins. Taken together, the data provide evidence for a transcriptional or translational level of regulation as the main cause of the strong response of apoplastic proteins to heavy metal stress