Project description:Objectives: To identify gene expression changes in acne flare-up patients, thereby exploring the mechanisms of acne flare-up after treatment. Methods: 11 acne patients and 3 healthy people were divided into 4 groups (group1: 4 with flare-up, group2: 4 with improvement, group3: 3 without obvious changes, group4: healthy control). Peripheral blood of patients before and after isotretinoin or minocycline were collected. RNA-seq were used to detect the gene expression. We applied data in self-contrast and intergroup comparisons. Results: In the self-contrast of group1, 22 upregulated genes were involved in Toll-like receptor signaling pathway and inflammatory response. Comparing group1 and group3 before treatment, 1778 upregulated genes enriched in Th17 cell differentiation, while 57 downregulated genes enriched in defensive response to organism. Conclusions: The gene expression profiles of acne flare-up patients changed. Inflammatory, immune responses played a prominent role in acne flare-up process and relatively weak defensive response to microbes, comedogenesis might be risk factors.
Project description:We performed scRNAseq of PBMCs from three idiopathic multicentric Castleman Disease (iMCD) patients with paired flare and remission samples
Project description:‘Big tau’, a longer isoform of tau is expressed in peripheral nervous system (PNS) and specific regions of the central nervous system (CNS). Big tau distribution across the human nervous system and pathophysiological role remains largely unknown. Here, using mass spectrometry, we demonstrate the big tau protein results from the insertion of exon 4a-long in the human MAPT sequence. We observed a central-to-peripheral gradient of big tau expression, lowest in the cortical brain region, followed by the cerebellum, then spinal cord, with the highest level in the human sciatic nerve (PNS). Interestingly, brain regions overlapping with relatively lower big tau are more susceptible to neurofibrillary tangle (NFT) formation. Furthermore, we found that CSF big tau levels did not change with CSF Aβ abnormalities in AD, unlike the CNS tau isoform, which increased significantly with concomitant Aβ and cognitive abnormalities. Our findings provide new insights into the basic biology of big tau in humans, crucial for understanding its pathophysiological functions.
Project description:This project aims to characterize the distribution of “big tau,” a longer tau isoform expressed in the peripheral nervous system (PNS) and select central nervous system (CNS) regions, and to examine its relationship with aging and neurodegeneration. We performed mass spectrometric sequencing of big tau sequence and mapped its distribution across the human nervous system. Postmortem samples included brains from Alzheimer’s disease (AD), disease controls, and amyotrophic lateral sclerosis (ALS); spinal cord from young controls, disease controls and ALS; and peripheral nerves. Big and small tau levels were also quantified in the cerebrospinal fluid (CSF) from young normal controls, amyloid positive and amyloid negative participants. To reinforce the presence of big tau in the brain, iso-seq was performed on post-mortem brain tissue samples.
