Our iPSC culture system is a potent tool for investigating the molecular and cellular foundation underlying chimpanzee early neural development and better understanding of human brain evolution. A hexanucleotide repeat expansion in chromosome 9 open reading frame 72 (C9orf72) gene causes a heterogeneous neurodegenerative disorder that includes amyotrophic lateral sclerosis (ALS), frontotemporal degeneration (FTD), and parkinsonism. Here, we used the Sendai virus delivery system to generate induced pluripotent stem cells (iPSCs) from peripheral blood mononuclear cells of a male patient with an increased hexanucleotide repeat expansion in C9orf72. The resulting iPSCs exhibited pluripotency, confirmed by immunofluorescent staining for pluripotency markers, and differentiated into three germ layers in vivo. This cellular model will provide a useful platform for further pathophysiological studies of C9orf72-related neurodegeneration. IPSC line RCPCMi004-A was generated from skin fibroblasts collected from a male patient with early onset Parkinson’s disease. The patient carries a heterozygous deletion of the exon 2 of PARK2 gene. The reprogramming of fibroblasts was performed with Sendai viruses containing Oct-4, Sox-2, Klf-4 and c-Myc. Pluripotency was confirmed by immunofluorescence, RT-PCR, and formation of embryoid bodies. The RCPCMi004-A cell line carries the same deletion in PARK2 gene. The RCPCMi004-A cell line can be used to model Parkinson’s disease in vitro. As a cell prepares to divide, its genetic material changes dramatically in both form and function. During interphase, a dynamic interplay between DNA compartmentalization and transcription functions to program cell identity. During mitosis, this purpose is put on hold and instead chromosomes function to facilitate their accurate segregation to daughter cells. Vorinostat cell line Chromatin loops are rearranged, stacked, and compressed to form X-shaped chromosomes that are neatly aligned at the center of the mitotic spindle and ready to withstand the forces of anaphase. Many factors that contribute to mitotic chromosome assembly have now been identified, but how the plethora of molecular mechanisms operate in concert to give rise to the distinct form and physical properties of mitotic chromosomes at the cellular scale remains under active investigation. In this review, we discuss recent work that addresses a major challenge for the field How to connect the molecular-level activities to large-scale changes in whole-chromosome architecture that determine mitotic chromosome size, shape, and function. The occurrence and characteristics of Clostridioides (previously Clostridium) difficile and Clostridium perfringens in the feces of diarrheic and non-diarrheic cats was investigated. Apparently healthy animals were more likely to be positive for C. perfringens type A (p = 0.009). Two isolates (0.7%), one each from a diarrheic and an apparently healthy cat, were positive for the enterotoxin-encoding gene but negative for the NetF-encoding gene. Six toxigenic C. difficile isolates were isolated, all RT106 and ST42, which is commonly reported in humans with C. difficile infection. CNS myelination process involves proliferation and differentiation of oligodendrocyte progenitor cells (OPCs). Defective myelination causes onset of neurological disorders. Bisphenol-A (BPA), a component of plastic items, exerts adverse effects on human health. Our previous studies indicated that BPA impairs neurogenesis and myelination process stimulating cognitive dysfunctions. But, the underlying mechanism(s) of BPA induced de-myelination and probable neuroprotection by curcumin remains elusive. We found that curcumin protected BPA mediated adverse effects on oligosphere growth kinetics. Curcumin significantly improved proliferation and differentiation of OPCs upon BPA exposure both in-vitro and in-vivo. Curcumin enhanced the mRNA expression and protein levels of myelination markers in BPA treated rat hippocampus. Curcumin improved myelination potential via increasing β-III tubulin-/MBP+ cells (neuron-oligodendrocyte co-culture) and augmented fluoromyelin intensity and neurofilament/MBP+ neurons in vivo. In silico docking studies suggested Notch pathway genes (Notch-1, Hes-1 and Mib-1) as potential targets of BPA and curcumin. Curcumin reversed BPA mediated myelination inhibition via increasing the Notch pathway gene expression. Genetic and pharmacological Notch pathway inhibition by DAPT and Notch-1 siRNA exhibited decreased curcumin mediated neuroprotection. Curcumin improved BPA mediated myelin sheath degeneration and neurobehavioral impairments. Altogether, results suggest that curcumin protected BPA induced de-myelination and behavioural deficits through Notch pathway activation. In the early stages of carcinogenesis cells confront two key suppressive checkpoints; senescence and telomere crisis. Telomere crisis is characterized by massive chromosomal instability and cell death. The genetic instability initiated during crisis leaves detectable scars on cancer genomes, the full scope of which is only just beginning to be appreciated. In particular, the dramatic genome reshuffling phenomenon chromothripsis has been mechanistically linked to the resolution of DNA bridges formed by dicentric chromosomes, and by the shattering of DNA inside micronuclei. Furthermore, an intriguing connection to innate immune signaling has begun to position telomere crisis as a crucial stage not only in the evolution of the cancer genome, but also in the interaction between the genome and the immune system. We screened the RFC1 intronic AAGGG repeat expansions in late-onset ataxia cases, MSA patients and controls. The data suggested that no biallelic repeat expansion carrier was found in our cohort and the heterozygous intronic AAGGG repeat expansions may not lead to an increased risk of late-onset ataxia or MSA. Emerging evidence has manifested the critical effect of abnormally expressed circular RNAs (circRNAs) on the initiation and progression of non-small cell lung cancer (NSCLC). Although circRNA circCCDC66 has been revealed to elicit facilitating impact on cell growth and metastasis in colon cancer, the potential biological function and regulatory mechanism of it in NSCLC still require to be explored. In this study, circCCDC66 in NSCLC cells was highly expressed. Downregulation of circCCDC66 impaired cell proliferation, migration and invasion whereas boosted cell apoptosis in NSCLC. Data from molecular mechanism assays testified that circCCDC66 bound with miR-33a-5p in NSCLC cells. And miR-33a-5p inhibition could rescue the suppressive effect of circCCDC66 knockdown on NSCLC progression. In addition, karyopherin subunit alpha 4 (KPNA4) in NSCLC cells was proofed to be directly targeted by miR-33a-5p. Moreover, through rescued-function assays, we observed that upregulating KPNA4 expression could countervail the restraining function of silenced circCCDC66 on NSCLC progression.