PNI is grossly underreported in CRC and could serve as an independent prognostic factor of outcomes in these patients. PNI should be considered when stratifying CRC patients for adjuvant treatment.
Autism spectrum disorder (ASD) is a term associated with a group of neurodevelopmental disorders. The etiology of ASD is not yet completely understood; however, a disorder in the gut-brain axis is emerging as a prominent factor leading to autism. To identify the taxonomic composition and markers associated with ASD, we compared the fecal microbiota of 30 ASD children diagnosed using Childhood Autism Rating Scale (CARS) score, DSM-5 approved AIIMS-modified INCLEN Diagnostic Tool for Autism Spectrum Disorder (INDT-ASD), and Indian Scale for Assessment of Autism (ISAA) tool, with family-matched 24 healthy children from Indian population using next-generation sequencing (NGS) of 16S rRNA gene amplicon. Our study showed prominent dysbiosis in the gut microbiome of ASD children, with higher relative abundances of families Lactobacillaceae, Bifidobacteraceae, and Veillonellaceae, whereas the gut microbiome of healthy children was dominated by the family Prevotellaceae. Comparative meta-analysis with a publicly available dataset from the US population consisting of 20 ASD and 20 healthy control samples from children of similar age, revealed a significantly high abundance of genus Lactobacillus in ASD children from both the populations. The results reveal the microbial dysbiosis and an association of selected Lactobacillus species with the gut microbiome of ASD children.
BACKGROUND: Colorectal cancer staging criteria do not rely on examination of neuronal tissue. The authors previously demonstrated that perineural invasion is an independent prognostic factor of outcomes in colorectal cancer. For the current study, they hypothesized that neurogenesis occurs in colorectal cancer and portends an aggressive tumor phenotype. METHODS: In total, samples from 236 patients with colorectal cancer were used to create a tissue array and database. Tissue array slides were immunostained for protein gene product 9.5 (PGP9.5) to identify nerve tissue. The correlation between markers of neurogenesis and oncologic outcomes was determined. The effect of colorectal cancer cells on stimulating neurogenesis in vitro was evaluated using a dorsal root ganglia coculture model. RESULTS: Patients whose tumors exhibited high degrees of neurogenesis had 50% reductions in 5‐year overall survival and disease‐free survival compared with patients whose tumors contained no detectable neurogenesis (P = .002 and P = .006, respectively). Patients with stage II disease and high degrees of neurogenesis had greater reductions in 5‐year overall survival and disease‐free survival compared with lymph node‐negative patients with no neurogenesis (P = .002 and P = .008, respectively). Patients with stage II disease and high degrees of neurogenesis had lower 5‐year overall survival and disease‐free survival compared with patients who had stage III disease with no neurogenesis (P = .01 and P = .008, respectively). Colorectal cancer cells stimulated neurogenesis and exhibited evidence of neuroepithelial interactions between nerves and tumor cells in vitro. CONCLUSIONS: Neurogenesis in colorectal cancer appeared to play a critical role in colorectal cancer progression. Furthermore, the current results indicated that neurogenesis functions as an independent predictor of outcomes and may play a role in therapy stratification for patients with lymph node‐negative disease. Cancer 2011;. © 2011 American Cancer Society.
Objective To determine whether adipose tissue functions as a reservoir for HIV-1. Design We examined memory CD4 T cells and HIV DNA in adipose tissue-stromal-vascular-fraction (AT-SVF) of 5 patients (4 ART-treated and 1 untreated). To determine if adipocytes stimulate CD4 T cells and regulate HIV production, primary human adipose cells were co-cultured with HIV-infected CD4 T cells. Methods AT-SVF T cells were studied by flow cytometry, and AT-SVF HIV DNA (Gag and Env) was examined by nested PCR and sequence analyses. CD4 T cell activation and HIV production were measured by flow cytometry and ELISA. Results AT-SVF CD3 T cells were activated (>60% CD69+) memory CD4 and CD8 T cells in uninfected and HIV-infected persons, but the AT-SVF CD4/CD8 ratio was lower in HIV patients. HIV DNA (Gag and Env) was detected in AT-SVF of all 5 patients examined by nested PCR, comparably to other tissues (PBMC, lymph node, or thymus). In co-culture experiments, adipocytes increased CD4 T cell activation and HIV production ∼2-3 fold in synergy with gamma-chain cytokines IL2, IL7, or IL15. These effects were mitigated by neutralizing antibodies against IL6 and integrin-α1β1. Adipocytes also enhanced T cell viability. Conclusions Adipose tissues of ART-treated patients harbor activated memory CD4 T cells and HIV DNA. Adipocytes promote CD4 T cell activation and HIV production in concert with intrinsic adipose factors. Adipose tissue may be an important reservoir for HIV.
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