Chronic hepatitis B infection treatment implicates a long-lasting treatment. M. oleifera extracts contain compounds with antiviral, antioxidant, and antifibrotic properties. In this study, the effect of M. oleifera was evaluated in Huh7 cells expressing either HBV genotypes C or H for the antiviral, antifibrotic, anti-inflammatory, and antioxidative responses. Huh7 cells were treated with an aqueous extract of M. oleifera (leaves) at doses of 0, 30, 45, or 60 μg/mL. The replicative virus and TGF-β1, CTGF, CAT, IFN-β1, and pgRNA expressions were measured by real time. HBsAg and IL-6 titers were determined by ELISA. CTGF, TGF-β1, IFN-β1, and pgRNA expressions decreased with M. oleifera treatment irrespective of the HBV genotype. HBsAg secretion in the supernatant of transfected Huh7 cells with both HBV genotypes was decreased regardless of the dose of M. oleifera. Similar effect was observed in proinflammatory cytokine IL-6, which had a tendency to decrease at 24 hours of treatment. Transfection with both HBV genotypes strongly decreased CAT expression, which is retrieved with M. oleifera treatment. M. oleifera treatment reduced fibrosis markers, IL-6, and HBsAg secretion in HBV genotypes C and H. However, at the level of replication, only HBV-DNA genotype C was slightly reduced with this treatment.

Acute hepatopancreatic necrosis disease (AHPND) was first reported in China in 2009 and afterwards in Mexico in 2013. AHPND is caused by Vibrio parahaemolyticus and affects Penaeus monodon and Litopenaeus vannamei shrimp cultures. The bacterium contains the pirA- and pirB-like genes in 69- to 70-Kb plasmids, which encode the toxins that produce the disease. The aim of this study was to determine whether pirA- and pirB-like genes existed in bacterial genera distinct from Vibrio before the first cases of AHPND were documented in Mexico. Two bacterial isolates were selected from shrimp farms in Nayarit in 2006 and analysed by nested-PCR to determine the presence of pirA- and pirB-like genes. The two isolates chosen did indeed show the presence of these genes, and those findings were confirmed by sequencing. Both strains matched to the bacterial species Micrococcus luteus. Results revealed two important situations: (a) the pirA- and pirB-like genes were present in a bacterial species that has not been reported previously (Micrococcus luteus); and (b) pirA- and pirB-like bacterial genes were present in Mexico before the first AHPND outbreak was reported in China.

Aim Ankylosing spondylitis (AS) pathogenesis has focused on the adaptive immune response; however, innate immune responses may also play a role in the inflammatory response of AS. Dysregulated neutrophil activation can induce tissue damage and contribute to the pathogenesis of immune‐related diseases. Hence, the aim of this study was to assess the effect of immune complexes formed with the p30 of Salmonella typhimurium and anti‐p30 antibodies present in the sera of AS patients and controls in inducing the release of neutrophil extracellular traps (NETs) and the secretion of pro‐inflammatory cytokines. Methods We collected polymorphonuclear leukocytes (PMNs) from healthy donors. The PMNs isolated were stimulated with p30 alone or in immunocomplexes formed with antibodies presents in sera of AS patients or control subjects. Then, the NETs were analyzed by fluorescence microscopy. Concentrations of interleukin (IL)‐6, tumor necrosis factor (TNF)‐α, IL‐1β, IL‐8 and IL‐10, were determined using the Cytometric Bead Array kit. Results Significant difference was observed in the release of NETs between the neutrophils stimulated with p30 + AS (70.52 ± 16.24) those unstimulated neutrophils (9.94 ± 12.12; P = .0095), stimulated with phorbol 12‐myristate 13‐acetate (39.78 ± 14.50; P = .0190), stimulated with control serum (CS) (10.85 ± 5.33; P = .0082) and serum of AS patient (10.28 ± 6.15; P = .0087). The stimulation of neutrophils with p30 alone induced a relatively low production of IL‐6 (64.5 pg/mL), IL‐8 (2658.3 pg/mL), IL‐1β (31.11 pg/mL), and TNF‐α (3.8 pg/mL), compared to p30 + AS and p30 + CS groups. Conclusion Our results show that neutrophils release NETs and pro‐inflammatory cytokines in response to p30 in immunocomplexes. These findings could improve our understanding of the role of innate immunity in the initiation and/or maintenance of inflammatory responses, and in the progression of AS.

The IKZF1 gene is formed by 8 exons and encodes IKAROS, a transcription factor that regulates the expression of genes that control cell cycle progression and cell survival. In general, 15-20% of the patients with preB acute lymphoblastic leukemia (preB ALL) harbor IKZF1 deletions, and the frequency of these deletions increases in BCR-ABL1 or Ph-like subgroups. These deletions have been associated with poor treatment response and the risk of relapse. The aim of this descriptive study was to determine the frequency of IKZF1 deletions and the success of an induction therapy response in Mexican pediatric patients diagnosed with preB ALL in 2 hospitals from 2017 to August 2018. Thirty-six bone marrow samples from patients at the Instituto Nacional de Pediatría in Mexico City and the Centro Estatal de Cancerología in Tepic were analyzed. The IKZF1 deletion was identified by MLPA using the SALSA MLPA P335 ALL-IKZF1 probemix. Deletions of at least 1 IKZF1 exon were observed in 7/34 samples (20.6%): 3 with 1 exon deleted; 1 with 2 exons, 1 with 5 exons, 1 with 6 exons, and 1 patient with a complete IKZF1 deletion. This study was descriptive in nature; we calculated the frequency of the IKZF1 gene deletion in a Mexican pediatric population with preB ALL as 20.6%.

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