No abstract

Among the differential diagnoses that should be considered in acute respiratory failure (ARF) are infectious processes, autoimmune diseases, interstitial pulmonary fibrosis, and pulmonary neoplasia. Timely diagnosis of lung neoplasia is complicated in the early stages. An opportune diagnosis, as well as the specific treatment, decrease mortality. ARF occurs 1 in 500 pregnancies and is most common during the postpartum period. Among the specific etiologies that cause ARF during pregnancy that must be considered are: (1) preeclampsia; (2) embolism of amniotic fluid; (3) peripartum cardiomyopathy; and (4) trophoblastic embolism. The case of a 36-year-old patient with a 33-week pregnancy and ARF is presented. The patient presented dyspnea while exerting moderate effort that progressed to orthopnea and type 1 respiratory insufficiency. Imaging studies showed bilateral alveolar infiltrates and predominantly right areas of consolidation. Blood cultures, a galactomannan assay and IgG antibodies against mycoplasma pneumoniae, were reported as negative. Autoimmune etiology was ruled out through an immunoassay. A percutaneous pulmonary biopsy was performed and an invasive pulmonary adenocarcinoma with lepidic growth pattern (i.e. lepidic pulmonary adenocarcinoma, LPA) result was reported. This etiology is rare and very difficult to recognize in acute respiratory failure cases. After infectious, autoimmune and interstitial lung fibrosis have been excluded the clinician must suspect of lung cancer in a patient with acute respiratory failure and chest imaging compatible with the presence of ground-glass nodular opacities, a solitary nodule or mass with bronchogram, and lung consolidation. In the presence of acute respiratory failure, the suspicion of pulmonary neoplasia in an adult of reproductive age must be timely. Failure to recognize this etiology can lead to fatal results.

IntroductionNonalcoholic fatty liver disease (NAFLD) includes a spectrum of histological findings ranging from simple steatosis (SS) to non‐alcoholic steatohepatitis (NASH). Although often considered the hepatic manifestation of metabolic syndrome (MS), longitudinal studies suggest that NAFLD precedes MS. To date, liver biopsy is the most accurate method to differentiate between SS and NASH. However, recent studies indicate an association between mitochondrial DNA (mtDNA) copy number and NAFLD severity in liver biopsies. If a similar association exists in peripheral blood, mtDNA copy number could represent a non‐invasive alternative for differentiating NAFLD disease stages.Given the above, we analyzed whether mtDNA copy number differs in individuals discordant for NAFLD and MS. We also probed for correlations between liver and peripheral blood mtDNA copy number, in addition to associations between NAFLD and mtDNA copy number.ObjectiveTo analyze whether mtDNA copy number is a useful blood‐based marker of NAFLD severity.Materials and methodsCohort = 73 peripheral blood samples and liver biopsies obtained from patients that were operated for gallstones; individuals were separated into 4 groups: controls (n = 27), NAFLD (n = 14), MS (n = 9) and MS + NAFLD (n = 23). NAFLD severity was determined according to the parameters described by Kleiner; mtDNA copy number was determined by semiquantitative PCR.ResultsWe found no significant differences in mtDNA copy number across the four groups analyzed (i.e. control, NAFLD, MS, MS+NAFLD). However, we did find an association between mtDNA copy number and NAFLD severity. In particular, we found that a significant increase in mtDNA copy number in SS relative to control samples, while mtDNA copy number was significantly reduced in NASH relative to SS.ConclusionAkin to the previously published data of mtDNA copy number in liver biopsies of individuals with NAFLD, we uncovered a dynamic relationship between mtDNA copy number and NAFLD severity in peripheral blood samples. This suggests that mtDNA copy number may be a promising blood‐based biomarker for differentiating between SS and NASH. To address this issue, we are currently probing for correlations between liver and peripheral blood mtDNA copy number.Support or Funding InformationMexican National Council for Science and Technology (CONACyT).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Background: Dyslipidemia and obesity hypercaloric diet-induced lead to kidney damage. We investigated the effect of curcumin on the expression of proteins related to inflammation, fibrosis, fatty acids metabolism, kidney damage, and morphological changes in the kidney of mice hypercaloric diets-fed. Methods: Groups of 5-week-old C57BL/6 mice (n=6) were formed: Control (C), High-fructose diet (F), High-fructose diet and curcumin (F+Cur), High-fat diet (HFD), High-fat diet and curcumin (HFD+Cur), High-fat diet and fructose (HFD+F), High-fat diet, fructose and curcumin (HFD+F+Cur), treated for 16 weeks with 30% (w/v) fructose, 60% (w/w) fat and 0.75% (w/w) curcumin. Kidneys were obtained for histomorphological and Western Blot analysis. Results: Curcumin prevented TNF-α overexpression in the F and HFD+F groups. VLCAD expression was higher in the F, HFD, and HFD+F groups. PPARγ expression was lower in the F+Cur, HFD+Cur, and HFD+F+Cur groups. Curcumin prevented overexpression of CPT1 and KIM1 in the HFD+F and HFD groups. Curcumin prevented morphological lesions, fibrosis, and lipid deposition hypercaloric diet-induced. Conclusion: Chronic consumption of hypercaloric diets causes inflammation, fibrosis, and lipid deposition in the kidney. It is suggested that curcumin differentially modulates kidney injury as a function of the damage induced by the high-fat/high-fructose diet.