Middleton Grantham (kendosunday24)

Real-time fMRI neurofeedback (rtfMRI-nf) left amygdala (LA) training is a promising intervention for major depressive disorder (MDD). We have previously proposed that rtfMRI-nf LA training may reverse depression-associated regional impairments in neuroplasticity and restore information flow within emotion-regulating neural circuits. Inflammatory cytokines as well as the neuroactive metabolites of an immunoregulatory pathway, i.e. the kynurenine pathway (KP), have previously been implicated in neuroplasticity. Therefore, in this proof-of-principle study, we investigated the association between rtfMRI-nf LA training and circulating inflammatory mediators and KP metabolites. Based on our previous work, the primary variable of interest was the ratio of the NMDA-receptor antagonist, kynurenic acid to the NMDA receptor agonist, quinolinic acid (KynA/QA), a putative neuroprotective index. We tested two main hypotheses. i. Whether rtfMRI-nf acutely modulates KynA/QA, and ii. whether baseline KynA/QA predicts responsewhether the increase in KynA/3HK and KynA/QA is specific to rtfMRI-nf or whether it is a non-specific correlate of the resolution of depressive symptoms. Similarly, replication studies are needed to determine whether KynA/QA has clinical utility as a treatment response biomarker. About 10-15% children develop frequent acute otitis media (AOM) confirmed by tympanocentesis. These children are designated sOP (stringently defined otitis-prone) because all AOM episodes have been microbiologically confirmed. The cause of otitis-proneness in sOP children is multi-factorial, including frequent otopathogen nasopharyngeal (NP) colonization and deficiency in innate and adaptive immune responses. A largely unexplored contributor to otitis proneness is NP microbiome composition. Since the microbiome modulates otopathogen NP colonization and immune responses, we hypothesized that the NP microbiome composition in sOP children might be dysregulated. We performed 16S rRNA sequencing to analyze microbiome composition in 157 NP samples from 28 sOP and 68 AOM-free children when they were 6 months or 12 months old and healthy. Bioinformatic approaches were employed to examine the composition difference between the two populations and its correlation with changes in levels of inflammatory cytokines. A different global microbiome profile and reduced alpha diversity was observed in the NP microbiome of sOP children when 6 months old, compared with that from AOM-free children of the same age. This difference was resolved when groups were compared at 12 months old. We found 4 bacterial genera-Bacillus, Veillonella, Gemella, and Prevotella-correlated with higher levels of pro-inflammatory cytokines in the NP. Those 4 bacterial genera were in lower abundance in sOP compared to AOM-free children. Dysbiosis occurs in the NP microbiome of sOP children at an early age even when they were healthy. This dysbiosis correlates with a lower inflammatory state in the NP of these children. Dysbiosis occurs in the NP microbiome of sOP children at an early age even when they were healthy. This dysbiosis correlates with a lower inflammatory state in the NP of these children.Paneth-like cells (PLCs) are different from Paneth cells (PCs) and contain Paneth-like granules, which have been reported in non-neoplastic conditions and in neoplasms of various organs. PLCs have been reported in clear cell renal cell carcinoma (CCRCC), but not in non-CCRCC, including acquired cystic disease-associated renal cell carcinoma (ACD-RCC). We analyzed clinicopathological features of 24 acquired cystic disease-associated renal cell carcinoma (ACD-RCC) with PLCs (ACD-RCCP+) and compared with those of 23 ACD-RCCs without PLCs (ACD-RCCP-). Approximately half of ACD-RCCs had PLCs and that almost all kidneys harboring ACD-RCC had cysts with PLCs. selleck chemicals The fact that many ACD-RCCs and the cysts had PLCs is further evidence that