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This method presented a satisfactory selectivity, stability, and reproducibility indicating its potential as a promising probe for TBBPA detection.Safe use of genetically modified organisms (GMOs) in biotechnology requires the ability to track the presence of these strains in any environment in which they are applied. For this, introduction of genetic barcodes within the editing site represents a valuable tool for the identification of microbial strains that have undergone genetic modifications. However, it is not known whether these barcodes would have any unexpected effect in the resulting strains or affect the efficiency of the genetic modification. CRISPR/Cas9 has become one of the fastest-growing technologies for genome editing in a range of organisms, including fungi. However, this technology enables the generation of scarless GMOs that are very difficult to distinguish from naturally occurring mutants or other modified organisms. In this study, we address this issue using the industrial workhorse Aspergillus niger as a test case. We applied CRISPR/Cas9 technology to delete the genes encoding the transcriptional regulators XlnR and AraR, involved in the production of plant biomass-degrading enzymes. We generated 20-bp barcoded and non-barcoded ΔxlnR and ΔaraR mutants and analyzed the traceability and fitness of the resulting strains, as well as the efficiency of the genetic modification. Evobrutinib mouse Results showed that both barcoded and non-barcoded mutants can be traced by routine PCR reactions when the specific CRISPR/Cas9 modification is known. Additionally, barcodes neither affected the efficiency of the genetic modification nor the growth or protein production of the resulting strains. These results confirm the suitability of genetic barcodes to trace CRISPR-derived GMOs without affecting the performance of the resulting strains.

The purpose of this study was to (1) test the hypothesis that HTO improves articular cartilage composition in the medial compartment without adversely affecting the lateral compartment and patella, and; (2) explore associations between knee alignment and cartilage composition after surgery.

3T MRI and standing radiographs were obtained from 34 patients before and 1-year after HTO. Articular cartilage was segmented from T2 maps. Mechanical axis angle (MAA), posterior tibial slope, and patellar height were measured from radiographs. Changes in T2 and radiographic measures were assessed using paired t tests, and associations were assessed using Pearson correlation coefficients.

The mean (SD) MAA before and after HTO was – 6.5° (2.4) and 0.6° (3.0), respectively. There was statistically significant shortening [mean (95%CI)] of T2 in the medial femur [- 2.8ms (- 4.2; – 1.3), p < 0.001] and medial tibia [- 2.2ms (- 3.3; – 1.0), p < 0.001], without changes in the lateral femur [- 0.5ms (- 1.6; 0.6), p = 0.3], lateral tibia [0.2ms (- 0.8; 1.1), p = NS], or patella [0.5ms (- 1.0; 2.1), p = NS). Associations between radiographic measures and T2 were low. 23% of the increase in lateral femur T2 was explained by postoperative posterior tibial slope (r = 0.48).

Performing medial opening wedge HTO without overcorrection improves articular cartilage composition in the medial compartment of the knee without compromising the lateral compartment or the patella. Although further research is required, these results suggest HTO is a disease structure-modifying treatment for knee OA.

Performing medial opening wedge HTO without overcorrection improves articular cartilage composition in the medial compartment of the knee without compromising the lateral compartment or the patella. Although further research is required, these results suggest HTO is a disease structure-modifying treatment for knee OA.The lower basin of Coatzacoalcos River is one of the most polluted regions of the southern Gulf of Mexico. Organochlorine compounds, polybrominated diphenyl ethers, polycyclic aromatic hydrocarbons, and heavy metals have been registered in this region. In the present study, genotoxicity was evaluated in the blood of giant toads (Rhinella marina) from Coatzacoalcos’ rural and industrial zones, and compared with laboratory toads. Determination of the frequency of micronucleus and erythrocyte nuclear abnormalities by the light microscope and cell cycle and apoptosis by flow cytometry were used as biomarkers of genotoxicity. We found more variability in micronucleus and more nuclear buds in toads from industrial zones. Also, cell cycle alterations and an increase of apoptosis in erythrocytes were found in toads from rural and industrial zones. Multivariate statistics show that the toads from the industrial zone were more affected than toads from laboratory and rural zones.

Liraglutide controls type 2 diabetes (T2D) and inflammation. Gut microbiota regulates the immune system and causes at least in part type 2 diabetes. We here evaluated whether liraglutide regulates T2D through both gut microbiota and immunity in dysmetabolic mice.

Diet-induced dysmetabolic mice were treated for 14days with intraperitoneal injection of liraglutide (100µg/kg) or with vehicle or Exendin 4 (10µg/kg) as controls. Various metabolic parameters, the intestinal immune cells were characterized and the 16SrDNA gene sequenced from the gut. The causal role of gut microbiota was shown using large spectrum antibiotics and by colonization of germ-free mice with the gut microbiota from treated mice.

Besides, the expected metabolic impacts liraglutide treatment induced a specific gut microbiota specific signature when compared to vehicle or Ex4-treated mice. However, liraglutide only increased glucose-induced insulin secretion, reduced the frequency of Th1 lymphocytes, and increased that of TReg in the intestine. These effects were abolished by a concomitant antibiotic treatment. Colonization of germ-free mice with gut microbiota from liraglutide-treated diabetic mice improved glucose-induced insulin secretion and regulated the intestinal immune system differently from what observed in germ-free mice colonized with microbiota from non-treated diabetic mice.

Altogether, our result demonstrated first the influence of liraglutide on gut microbiota and the intestinal immune system which could at least in part control glucose-induced insulin secretion.

Altogether, our result demonstrated first the influence of liraglutide on gut microbiota and the intestinal immune system which could at least in part control glucose-induced insulin secretion.