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#32272498   2020/04/09 To Up

NFE2L2/KEAP1 mutations correlate with higher TMB value/PD-L1 expression and potentiate improved clinical outcome with immunotherapy.

Abnormalities in the KEPA1-NRF2 pathway have a role in cancer progression, metastasis, and resistance to chemo-/radio-therapies. Persistent activation of NRF2 associates with poor prognosis across different cancer types. However, the beneficial therapeutic strategy to harness this pathway in cancer remains unclear. This study aimed to investigate the clinical outcome with immunotherapy in NFE2L2/KEAP1 mutant population.
Xian Xu, Yang Yang, Xiaoyan Liu, Na Cao, Peng Zhang, Songhui Zhao, Donglin Chen, Li Li, Yong He, Xiaowei Dong, Kai Wang, Hanqing Lin, Naiquan Mao, Lingxiang Liu

1879 related Products with: NFE2L2/KEAP1 mutations correlate with higher TMB value/PD-L1 expression and potentiate improved clinical outcome with immunotherapy.

0.1 mg500 mg

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#32272486   2020/04/09 To Up

Proteomic changes during experimental de- and remyelination in the corpus callosum.

In the cuprizone model of multiple sclerosis, de- and remyelination can be studied without major interference from the adaptive immune responses. Since previous proteomic studies did not focus on the corpus callosum, where cuprizone causes the most pronounced demyelination, we performed a bottom up proteomic analysis on this brain region.
Gabor T Szilagyi, Arkadiusz M Nawrocki, Krisztian Eros, Janos Schmidt, Katalin Fekete, Maria L Elkjaer, Kirsten H Hyrlov, Martin R Larsen, Zsolt Illes, Ferenc Gallyas

1654 related Products with: Proteomic changes during experimental de- and remyelination in the corpus callosum.

11 Set

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#32272483   2020/04/09 To Up

Cerebrospinal fluid endocannabinoid levels in Gilles de la Tourette syndrome.

Gilles de la Tourette syndrome (TS) is a complex neurodevelopmental disorder characterized by the presence of motor and vocal tics as well as psychiatric comorbidities such as attention-deficit/hyperactivity disorder (ADHD), obsessive-compulsive disorder (OCD), depression, and anxiety. The underlying cause of the disease is still unknown, but several lines of evidence suggest a paramount role of the dopaminergic system. Based on the clinical observation that cannabis-based medicine including cannabis and delta-9-tetrahydrocannabinol (THC, dronabinol) may improve TS, alternatively, an involvement of the endocannabinoid system (ECS) has been suggested. In this study we measured cerebrospinal fluid (CSF) levels of the two most important endocannabinoids "N"-arachidonoylethanolamine (AEA, anandamide) and 2-arachidonoylglycerol (2-AG), the endocannabinoid-like molecule palmitoyl ethanolamide (PEA), and the lipid arachidonic acid (AA) in a sample of adult patients with TS (n = 20) compared with controls (n = 19) using liquid-liquid lipid extraction and simultaneous quantification by liquid chromatography multiple reaction monitoring (LC/MRM). CSF levels of AEA (p = 0.0018), 2-AG (p = 0.0003), PEA (p = 0.02), and AA (p < 0.0001) were significantly increased in TS compared with controls. Levels of 2-AG correlated with the severity of comorbid ADHD (p < 0.01). This is the first study, demonstrating alterations in the ECS suggesting an involvement of this system in the pathophysiology of TS. It can be speculated that elevated endocannabinoid levels either represent secondary changes in order to compensate for alterations in other neurotransmitter systems such as the dopaminergic system, are simply an epiphenomenon or, alternatively, represent the primary cause of TS.
Kirsten R Müller-Vahl, Laura Bindila, Beat Lutz, Frank Musshoff, Thomas Skripuletz, Charlotte Baumgaertel, Kurt-Wolfram Sühs

1741 related Products with: Cerebrospinal fluid endocannabinoid levels in Gilles de la Tourette syndrome.

3 mg100 μg10mg100ug Lyophilized20 100

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#32272441   2020/03/25 To Up

Antioxidant Berberine-Derivative Inhibits Multifaceted Amyloid Toxicity.

Multiple lines of evidence indicate that amyloid beta (Aβ) peptide is responsible for the pathological devastation caused in Alzheimer's disease (AD). Aβ aggregation species predominantly contribute to multifaceted toxicity observed in neuronal cells including generation of reactive oxygen species (ROS), mitochondrial dysfunction, interfering with synaptic signaling, and activation of premature apoptosis. Herein, we report a natural product berberine-derived (Ber-D) multifunctional inhibitor to ameliorate in cellulo multifaceted toxicity of AD. The structural attributes of polyphenolic Ber-D have contributed to its efficient Cu chelation and arresting the redox cycle to prevent the generation of ROS and rescue biomacromolecules from oxidative damage. Ber-D inhibits metal-dependent and -independent Aβ aggregation, which is supported by in silico studies. Ber-D treatment averts mitochondrial dysfunction and corresponding neuronal toxicity contributing to premature apoptosis. These key multifunctional attributes make Ber-D a potential therapeutic candidate to ameliorate multifaceted Aβ toxicity in AD.
Kolla Rajasekhar, Sourav Samanta, Vardhaman Bagoband, N Arul Murugan, Thimmaiah Govindaraju

1850 related Products with: Antioxidant Berberine-Derivative Inhibits Multifaceted Amyloid Toxicity.

100 ul100ug Lyophilized100ug Lyophilized100μg100ug100ug 1 kit(s) 100ul100ug Lyophilized100ug Lyophilized96 tests250ul

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#32272434   2020/03/17 To Up

Characterizing false-positive fluorescence in situ hybridization results by mate-pair sequencing in a patient with chronic myeloid leukemia and progression to myeloid blast crisis.

Traditional cytogenetic testing methodologies, including conventional chromosome analysis and fluorescence in situ hybridization (FISH), are invaluable for the detection or recurrent genetic abnormalities in various hematologic malignancies. However, technological advances, including a novel next-generation sequencing technique termed mate-pair sequencing (MPseq), continue to revolutionize the field of cytogenetics by enabling the characterization of structural variants at a significantly higher resolution compared to traditional methodologies. To illustrate the power of MPseq, we present a 27-year-old male diagnosed with chronic myeloid leukemia in myeloid blast crisis with multiple chromosomal abnormalities observed in all 20 metaphases from a peripheral blood specimen, including t(9;22)(q34;q11.2) and t(4;11)(q12;p15). Suspicious of a novel NUP98/PDGFRA fusion [t(4;11)(q12;p15)], break-apart FISH probe sets for the PDGFRA (4q12) and NUP98 (11p15.4) gene regions were performed and were both positive in approximately 86% of 200 interphase nuclei. However, subsequent MPseq testing revealed breakpoints located within the NUP98 gene and within an intergenic region (4q12) located between the CHIC2 and PDGFRA genes, indicating this 4;11 translocation does not result in the predicted NUP98/PDGFRA gene fusion as inferred from FISH and conventional chromosome results. This case demonstrates the clinical utility of MPseq, particularly for characterizing novel gene fusion events which may ultimately identify a false-positive FISH result.
Jaime L Lopes, Matthew Webley, Beth A Pitel, Kathryn E Pearce, James B Smadbeck, Sarah H Johnson, George Vasmatzis, William R Sukov, Patricia T Greipp, Nicole L Hoppman, Rhett P Ketterling, Linda B Baughn, Laura Finn, Jess F Peterson

1168 related Products with: Characterizing false-positive fluorescence in situ hybridization results by mate-pair sequencing in a patient with chronic myeloid leukemia and progression to myeloid blast crisis.

1 kit1 kit1 Set1 Set1 Set1 Set1 Set1 Set1 Set1 Set1 Set

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#32272430   2020/03/27 To Up

Crowding in humans is unlike that in convolutional neural networks.

Object recognition is a primary function of the human visual system. It has recently been claimed that the highly successful ability to recognise objects in a set of emergent computer vision systems-Deep Convolutional Neural Networks (DCNNs)-can form a useful guide to recognition in humans. To test this assertion, we systematically evaluated visual crowding, a dramatic breakdown of recognition in clutter, in DCNNs and compared their performance to extant research in humans. We examined crowding in three architectures of DCNNs with the same methodology as that used among humans. We manipulated multiple stimulus factors including inter-letter spacing, letter colour, size, and flanker location to assess the extent and shape of crowding in DCNNs. We found that crowding followed a predictable pattern across architectures that was different from that in humans. Some characteristic hallmarks of human crowding, such as invariance to size, the effect of target-flanker similarity, and confusions between target and flanker identities, were completely missing, minimised or even reversed. These data show that DCNNs, while proficient in object recognition, likely achieve this competence through a set of mechanisms that are distinct from those in humans. They are not necessarily equivalent models of human or primate object recognition and caution must be exercised when inferring mechanisms derived from their operation.
Ben Lonnqvist, Alasdair D F Clarke, Ramakrishna Chakravarthi

1171 related Products with: Crowding in humans is unlike that in convolutional neural networks.

100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized50ul (1mg/ml)100 ul100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized

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