DISC POLYETH 1.0 CM PK 10
- Known as:
- DISC POLYETH 1.0 CM PK 10
- Catalog number:
- 31050-250
- Product Quantity:
- Case of 10
- Category:
- -
- Supplier:
- COREX
- Gene target:
- DISC POLYETH 1.0 10
Related genes to: DISC POLYETH 1.0 CM PK 10
- Gene:
- DISC2 NIH gene
- Name:
- disrupted in schizophrenia 2
- Previous symbol:
- -
- Synonyms:
- DISC1-AS1, DISC1OS, NCRNA00015
- Chromosome:
- 1q42.1
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2000-01-20
- Date modifiied:
- 2018-05-16
Related products to: DISC POLYETH 1.0 CM PK 10
Related articles to: DISC POLYETH 1.0 CM PK 10
- Presynaptic congenital myasthenic syndromes (CMS) encompass a large number of rare neurologic disorders caused by impaired release of acetylcholine (ACh) from motor nerve terminals. There are two main groups of presynaptic CMS: one in which the amount of ACh in synaptic vesicles (SV) is diminished and another in which the mechanism of synaptic vesicle release is impaired. The latter is often referred to as a congenital Lambert-Eaton myasthenic syndrome (LEMS). Presynaptic CMS, like other forms of CMS, is primarily characterized by muscle weakness and fatigue, but is often associated with additional manifestations of central and autonomic nervous system involvement, including episodic apneas, cognitive delay, seizures, and gastrointestinal complications. The most common causes of presynaptic CMS are recessive and dominant mutations in genes encoding proteins participating in the mechanisms of ACh synthesis and SV release. However, at times gene mutations can result in more complex pathogenic mechanisms. The most effective treatment of these conditions is prevention of potentially fatal episodes of apnea and other respiratory complications resulting from bulbar weakness. Pharmacologic treatments are also useful; however, in many cases the response is incomplete, and in other mild cases there is improvement with age that obviates the need for pharmacologic interventions. Preclinical studies in animal models of presynaptic CMS using targeted gene therapies are promising but these new therapies will not be available in the near future. - Source: PubMed
Publication date: 2026/07/01
Maselli Ricardo A - - Source: PubMed
Publication date: 2026/04/20
Molokanova ElenaSavchenko AlexVerkhratsky Alexei - We evaluated human embryonic stem cell-derived mesenchymal stem cells (ES-MSCs) on collagen scaffolds for meniscus-like neotissue formation and ex vivo repair of human osteoarthritic (OA) meniscal defects. Collagen type I fibrous scaffolds were pneumatospun, and laminate scaffolds were fabricated from electrospun PLA/collagen; crosslinked; heparin conjugated; fibronectin coated; functionalized with TGFβ1, TGFβ3, or PDGFbb; seeded with ES-MSCs; and cultured for 4 weeks, followed by in vitro assessment or ex vivo implantation into 3.5 mm human meniscus defects for 5 weeks. Pneumatospinning generated highly porous scaffolds that supported uniform cell infiltration, while laminate scaffolds demonstrated interlocking fiber interfaces and enhanced mechanical properties. TGFβ1 and TGFβ3 immobilization enhanced scaffold bioactivity, defined as growth factor-mediated increases in meniscus-like matrix deposition, collagen fiber organization, and meniscogenic gene expression, by significantly increasing safranin O staining, collagen type II deposition, collagen fiber polarization, and ACAN expression. TGFβ3 additionally increased COL1A1 expression and pushout shear modulus; TGFβ1 increased peak pushout stress, indicating superior ex vivo mechanical integration. Laminate scaffolds resulted in extensive cell infiltration, robust neotissue formation (elastic modulus ~2.4 MPa), and improved ex vivo tissue integration when functionalized with TGFβ3. The data indicated that ES-MSC-seeded, heparin-conjugated, TGFβ-immobilized pneumatospun/electrospun collagen-PLA scaffolds support meniscogenic differentiation and biomechanical integration, with repair of focal meniscal defects and potential for partial meniscus replacement. - Source: PubMed
Publication date: 2026/03/09
Grogan Shawn PDorthé Erik WWilliams Austin BGlembotski Nicholas ED'Lima Darryl D - Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by the uncontrolled expansion of undifferentiated myeloid precursors in the bone marrow. Hypomethylating agents (HMAs) such as azacitidine and decitabine can reverse abnormal DNA methylation, promote leukemic cell differentiation, and enhance immune recognition, yet relapse and therapeutic resistance remain major challenges. In this study, we found that long-term, low-dose HMA treatment upregulated CD70, NK receptor ligands, and CD1d on AML tumor cells, rendering them more susceptible to chimeric antigen receptor (CAR)-engineered invariant natural killer T (CAR-NKT) cell-mediated cytotoxicity. To exploit these features, we generated two types of CD70-targeting CAR-NKT cells: cord blood hematopoietic stem and progenitor cell (HSPC)-derived allogeneic CAR70-NKT (CAR70-NKT) cells and peripheral blood mononuclear cell (PBMC)-derived CAR70-NKT (CAR70-NKT) cells. Both CAR70-NKT cell products exhibited potent cytotoxicity against AML cells and synergized with HMAs, while CAR70-NKT cells demonstrated superior antitumor efficacy, multi-target recognition, and sustained expansion. In multiple xenograft models, CAR70-NKT cells effectively killed AML tumors without inducing graft-versus-host disease, cytokine release syndrome, or long-term organ toxicity. These findings highlight CAR70-NKT cells as a safe and powerful off-the-shelf immunotherapy that can synergize with HMAs to improve treatment outcomes for patients with AML. - Source: PubMed
Publication date: 2026/03/26
Li Yan-RuideShen XinyuanChen YuningZhu YichenHuang JieOliai CaspianYang Lili - Invariant natural killer T (iNKT) cells are a unique subset of T lymphocytes with allogeneic potential and strong solid tumour-homing capacity, making them attractive for cancer immunotherapy. Unlike conventional T cells, iNKT cells recognize lipid antigens presented by the non-polymorphic CD1d molecule. Chimaeric antigen receptor (CAR)-redirected iNKT (CAR-iNKT) cells have shown promise; however, their clinical efficacy is limited by insufficient activation and poor long-term persistence within the tumour microenvironment. Here we describe the iNKT cell-targeted microparticle recruitment and activation system (iMRAS), a biomimetic platform engineered to locally recruit, activate and expand CAR-iNKT cells in vivo. Acting as an in vivo 'charging station', iMRAS provides chemotactic and activating cues that enhance CAR-iNKT cell functionality, improving persistence and tumour control in preclinical lymphoma and melanoma models. Through its biomimetic design and localized immunostimulatory effects, iMRAS helps overcome the limitations of current therapies for solid tumours, establishing a robust platform for advancing CAR-iNKT cell-based cancer immunotherapy. - Source: PubMed
Publication date: 2026/03/17
Li Yan-RuideNan HaochenLiu ZeyangFang YingZhu YichenLyu ZibaiShao ZhengyaoZhu EnboZhang BoYang YouchengShen XinyuanChen YuningHsiai TzungYang LiliLi Song