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#32783419   // To Up

Quiescence and Subsequent Anterior Chamber Inflammation in Adalimumab-treated Pediatric Noninfectious Uveitis.

To evaluate the effect of adalimumab in pediatric uveitis and subsequent changes in anterior chamber inflammation following the inactivation of uveitis.
Sooyeon Choe, Jang Won Heo, Baek Lok Oh

2501 related Products with: Quiescence and Subsequent Anterior Chamber Inflammation in Adalimumab-treated Pediatric Noninfectious Uveitis.

16-22 Sample Kit4 Sample Kit128 Sample Kit4 Membranes/Box16 Arrays/Slide8 Sample Kit1-8 Sample Kit4 Sample Kit4 Arrays/Slide8 Sample Kit

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#32783409   2020/08/12 To Up

Expression and function of lncRNA MALAT1 in gestational diabetes mellitus.

Gestational diabetes mellitus (GDM) severely threatens maternal and fetal health. Long non-coding RNA (lncRNA) participates in the regulation of various cellular processes.
Yan Zhang, Liping Qu, Huijie Ni, Yuping Wang, Lei Li, Xiaowei Yang, Xiao Wang, Yuanyuan Hou

1150 related Products with: Expression and function of lncRNA MALAT1 in gestational diabetes mellitus.

50 UG300 units100 μg1 Set100 μg1 Set100 μg1 Set

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#32783381   2020/08/12 To Up

Chidamide acts on the histone deacetylase-mediated miR-34a/Bcl-2 axis to regulate NB4 cell line proliferation and apoptosis.

Acute promyelocytic leukemia (APL), a biologically and clinically distinct variant of acute myelogenous leukemia, is characterized by the fusion of the N-terminus of promyelocytic leukemia protein to the C terminus of retinoic acid receptor alpha, mostly due to chromosomal translocation t(15;17). Chidamide, a synthetic analogue of MS-275 identified from a group of benzamide-type compounds, has been found to have efficient anticancer activity in basic and clinical research studies. However, the concrete role and underlying mechanism of Chidamide in the treatment of APL has not been well characterized. Our data demonstrate that Chidamide inhibited the expression of histone deacetylase (HDAC) to induce apoptosis and suppress proliferation in NB4 cells. Mechanistically, Chidamide increases the expression of miR-34a by suppressing HDAC. Furthermore, B-cell lymphoma-2 (Bcl-2) is a direct target of miR-34a, the expression of which is regulated by miR-34a. Functionally, Chidamide inhibits cell proliferation and promotes apoptosis through miR-34a/Bcl-2. Chidamide exerts its anticancer effect via the HDAC-mediated miR-34a/Bcl-2 axis, providing potential targets for APL therapy.
Jie Peng, Shu-Jun Li, Xiao Fu, Yi Liu, Xie-Lan Zhao

2618 related Products with: Chidamide acts on the histone deacetylase-mediated miR-34a/Bcl-2 axis to regulate NB4 cell line proliferation and apoptosis.

2500 Tests2500 assays2 x 10^6 cells2500 assays~2x10(6) cells1 kit10 plates

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#32783373   2020/08/11 To Up

Protective effects of P2X R antagonist in sepsis-induced acute lung injury in mice via regulation of circ_0001679 and circ_0001212 and downstream Pln, Cdh2, and Nprl3 expression.

Sepsis induces pulmonary P2X receptor (P2X R) expression, and P2X R-knockout reduced lung inflammation in mice. This study investigated expression of circular RNA (circRNA) and messenger RNA (mRNA) in sepsis-induced acute lung injury (ALI) treated with a P2X R antagonist.
Zijun Zou, Qin Wang, Minggen Zhou, Weichao Li, Yikai Zheng, Fanyi Li, Shengcai Zheng, Zhijie He

2465 related Products with: Protective effects of P2X R antagonist in sepsis-induced acute lung injury in mice via regulation of circ_0001679 and circ_0001212 and downstream Pln, Cdh2, and Nprl3 expression.

300 units5mg1000 100ug1 ml

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#32783328   2020/08/12 To Up

Occlusion Heightened by Metal Crown Cementation is Aggressive for Periodontal Tissues.

To investigate the effect of experimental traumatic occlusion (ETO) induced by metal crowns on alveolar bone loss.
Henrique Ballassini Abdalla, Juliana Trindade Clemente-Napimoga, Carlos Antônio Trindade-da-Silva, Luciane Jorge Alves, Roberta da Silva Prats, Alexandre Youssef, Paulo César Vieira Dos Santos, Wilkens Aurélio Buarque E Silva, Frederico Andrade E Silva, Marcelo Henrique Napimoga

2222 related Products with: Occlusion Heightened by Metal Crown Cementation is Aggressive for Periodontal Tissues.

0.1 ml100ug Lyophilized100ug25 µg25 μg1 g100μg0.1 mg0.1ml (1mg/ml)0.25 mg25 μg1 ml

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#32783288   2020/08/11 To Up

Characterization of putative regulatory isoforms of porcine tumor necrosis factor receptor 2 in endothelial cells.

Tumor necrosis factor α (TNFα) and its receptors contribute to rejection of transplanted cells and organs. To elucidate how TNFα affects xenograft rejection, we previously cloned the cDNA of pig TNF-receptor 2 (pTNFR2) and found four isoforms: one comprising the full receptor with four cysteine-rich domains (CRD), a shorter variant (pTNFR2ΔE7-10) encoding for a soluble isoform, another lacking exon 4 (pTNFR2ΔE4) displaying only 3 CRD and poor ligand binding, and the smallest one generated by the two alternative splicings. All isoforms contained the pre-ligand assembly domain (PLAD) responsible for receptor trimerization. We now investigated their roles by structural, expression, and subcellular localization studies. Structural in silico analyses identified four amino acids potentially involved in TNFα binding and lacking in pTNFR2ΔE4. Quantitative RT-PCR determined regulated expression affecting the two pTNFR2 alternative splicings in cytokine-stimulated porcine aortic endothelial cells (PAEC). Particularly, human IL-1α and TNFα produced a strong mRNA upregulation of all isoforms, being the full receptor the predominant one. However, expression of pTNFR2 on PAEC did not correlate with mRNA and decreased after 24-hour exposure to IL-1α or TNFα. Notably, confocal microscopy confirmed the presence of pTNFR2 inside and on the plasma membrane, whereas pTNFR2ΔE4 located only intracellularly. Most interestingly, FRET analyses showed that membrane-bound isoforms pTNFR2 and pTNFR2ΔE4 colocalized intracellularly and associated through the PLAD. Our data show that pTNFR2ΔE4 bind and may retain the full receptor intracellularly. This mechanism has not been described in other species and represents a particularity that may affect the pathophysiology of pig xenografts.
Mireia Uribe-Herranz, Sebastián G Kuguel, Kelly Casós, Cristina Costa

2764 related Products with: Characterization of putative regulatory isoforms of porcine tumor necrosis factor receptor 2 in endothelial cells.

0.1 mg1 mg96T5ug5ug20ug1.00 flask100 96T/Kit 10 ug200ul10ug

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#32783189   2020/08/12 To Up

Autosomal dominant neuronal ceroid lipofuscinosis - clinical features and molecular basis.

The Neuronal Ceroid Lipofuscinoses (NCLs) are at least 13 distinct progressive neurodegenerative disorders unified by the accumulation of lysosomal auto-fluorescent material called lipofuscin. The only form that occurs via autosomal-dominant inheritance exhibits adult onset and is sometimes referred to as Parry type NCL. The manifestations may include behavioral symptoms followed by seizures, ataxia, dementia, and early death. Mutations in the gene DNAJC5 that codes for the presynaptic co-chaperone cysteine string protein-α (CSPα) were recently reported in sporadic adult-onset cases and in families with dominant inheritance. The mutant CSPα protein may lead to disease progression by both loss and gain of function mechanisms. Iron chelation therapy may be considered as a possible pharmaceutical intervention based on our recent mechanism-based proposal of CSPα oligomerization via ectopic Fe-S cluster-binding, summarized in this review.
Nima Naseri, Manu Sharma, Milen Velinov

2793 related Products with: Autosomal dominant neuronal ceroid lipofuscinosis - clinical features and molecular basis.

100ug100 mg96T1000 tests

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#32783154   2020/08/11 To Up

Cranberry extract-based formulations for preventing bacterial biofilms.

Generating formulations for the delivery of a mixture of natural compounds extracted from natural sources is a challenge because of unknown active and inactive ingredients and possible interactions between them. As one example, natural cranberry extracts have been proposed for the prevention of biofilm formation on dental pellicle or teeth. However, such extracts may contain phenolic acids, flavonol glycosides along with other constituents like coumaroyl iridoid glycosides, flavonoids, alpha-linolenic acid, n-6 (or n-3) fatty acids, and crude fiber. Due to the presence of a variety of compounds, determining which molecules (and how many molecules) are essential for preventing biofilm growth is nontrivial to ascertain. Therefore, a formulation that could contain natural, unrefined, cranberry extract (with all its constituent compounds) at high loading would be ideal. Accordingly, we have generated several candidate formulations including poly(lactic-co-glycolic) acid (PLGA)-based microencapsulation of cranberry extract (CE15) as well as formulations including stearic acid along with polyvinylpyrrolidone (PVP) or Ethyl lauroyl arginate (LAE) complexed with cranberry extracts (CE15). We found that stearic acid in combination with PVP or LAE as excipients led to higher loading of the active and inactive compounds in CE15 as compared with a PLGA microencapsulation and also sustained release of CE15 in a tunable manner. Using this method, we have been able to generate two successful formulations (one preventative based, one treatment based) that effectively inhibit biofilm growth when incubated with saliva. In addition to cranberry extract, this technique could also be a promising candidate for other natural extracts to form controlled release systems.Graphical abstract.
Ashlee C Greene, Abhinav P Acharya, Sang B Lee, Riccardo Gottardi, Erin Zaleski, Steven R Little

1322 related Products with: Cranberry extract-based formulations for preventing bacterial biofilms.

0.2 mg 5 GTwo 96-Well Microplate Ki 1 G1 ml0.1 mg1,000 tests1 mg10 ml2x96 well plate

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