Indolent T cell lymphoproliferative disorder of the gastrointestinal tract: an uncommon case with lymph node involvement and the classic Hodgkin's lymphoma.

Here we describe an unusual case of an indolent CD8+ T-cell lymphoproliferative disorder in the gastrointestinal tract (ITCLD-GT) accompanied by neck lymph node infiltration and new onset of classic Hodgkin's lymphoma after two years follow-up. Previously, this 42-year-old Asian man suffered from diarrhea and abdominal pain for two years. Intestinal biopsies showed a group of small to intermediate-sized lymphocytes which were monomorphic as well as arranged in a nodular pattern with no clear boundary and were diagnosed as ITCLD-GT. He did not receive chemotherapy or have any disease progression in the gastrointestinal tract (GIT) during the follow-up until a development of neck lymphadenopathy, which led to an eventual mixed cellularity type of Hodgkin's lymphoma, one type of classic HL diagnosis. Interestingly, besides the Hodgkin's cells, the same pathological T-cells in the GIT were present in the Hodgkin's lymphoma lesions. These two pathological T cells in GIT and neck lymph node had the identical histopathological and molecular abnormalities that confirmed the abenteric distant infiltration of ITCLD-GT to the neck lymph node in this patient. This is the first case of ITCLD-GT that has a definite distant lymph node invasion. ITCLD-GT usually has a relatively good prognosis but patients with ITCLD-GT may have abenteric distant infiltration. Thus, long-term follow-up and further study of the underlying mechanisms of this process are necessary.

Down regulation of miR-218, miR-124, and miR-144 relates to Parkinson's disease via activating NF-κB signaling.

Parkinson's disease (PD) is a neurological degenerative disorder that is partially induced by inflammation in the neural system. To explore the roles of disordered microRNAs in the development of PD, we screened 10 miRNAs in the brain samples of 15 postmortem PD patients and 10 postmortem healthy controls by qRT-PCR. The direct targets of miRNAs were predicted by informatics tools and further confirmed by dual luciferase assay and immunoblotting. The function of miRNAs in regulating NF-κB/p65 translocation was examined by immunoblotting, and the overactivation of NF-κB signaling was examined by ELISA. The relationship between dysregulated miRNAs and cytokines was analyzed by correlation analysis. Three miRNAs were found to be reduced in the brains of patients with PD. KPNB1, KPNA3, and KPNA4 were identified as direct targets of miR-218, miR-124, and miR-144. Additionally, KPNA3 was identified as a direct target of miR-124, and KPNA4 was a direct target of both miR-124 and miR-218. The p65 translocation from the cytoplasm to the nucleus was repressed by miR-124, miR-218, and miR-144 in the SH-SY5Y cells. The NF-κB signaling pathway was overactivated after miRNA inhibitor transfection. The upregulation of KPNB1, KPNA3, and KPNA4 in the brain samples of PD patients was confirmed by immunoblotting, and negative correlations were found between dysregulated miRNAs and cytokines. In conclusion, we identified that the downregulation of miR-218, miR-124, and miR-144 in the brain was related to PD via activation of NF-κB signaling, helping to unveil the role played by dysregulated miRNAs in the pathogenesis of PD and provide new potential targets for PD treatment.