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#36467081   2022/11/17 To Up

Treatment of ADHD: Drugs, psychological therapies, devices, complementary and alternative methods as well as the trends in clinical trials.

Attention-deficit/hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders having a high influence on social interactions. The number of approved treatments and clinical trials for ADHD have increased markedly during the recent decade. This analytical review provides a quantitative overview of the existing pharmacological and non-pharmacological methods of ADHD treatments investigated in clinical trials during 1999-2021. A total of 695 interventional trials were manually assessed from clinicaltrial.gov with the search term « ADHD», and trial data has been used for analysis. A clear majority of the studies investigated non-pharmacological therapies (∼80%), including many behavioral options, such as social skills training, sleep and physical activity interventions, meditation and hypnotherapy. Devices, complementary and other alternative methods of ADHD treatment are also gaining attention. The pharmacological group accounts for ∼20% of all the studies. The most common drug classes include central nervous system stimulants (e.g., methylphenidate hydrochloride, lisdexamfetamine dimesylate, amphetamine sulfate, mixed amphetamine salts, a combination of dexmethylphenidate hydrochloride and serdexmethylphenidate chloride), selective noradrenaline reuptake inhibitors (atomoxetine, viloxazine), and alpha2 adrenergic receptor agonists (guanfacine hydrochloride, clonidine hydrochloride). Several studies investigated antidepressants (e.g., bupropion hydrochloride, vortioxetine), and atypical antipsychotics (e.g., quetiapine, aripiprazole) but these are yet not approved by the FDA for ADHD treatment. We discuss the quantitative trends in clinical trials and provide an overview of the new drug agents and non-pharmacological therapies, drug targets, and novel treatment options.
Victoria A Nazarova, Aleksandr V Sokolov, Vladimir N Chubarev, Vadim V Tarasov, Helgi B Schiöth

2537 related Products with: Treatment of ADHD: Drugs, psychological therapies, devices, complementary and alternative methods as well as the trends in clinical trials.

100 assays1 kit(96 Wells)96 assays1 kit(96 Wells)900 tests96 samples100 assays1 kit20 1 kit(96 Wells)1 kit(96 Wells)100tests

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#36466692   2022/11/17 To Up

Mouse adaptation of H6 avian influenza viruses and their molecular characteristics.

H6 avian influenza viruses (AIVs) not only continue to circulate in both domestic poultry and wild waterfowl, but also have occasionally caused spillovers infections in pigs and humans, posing a potential threat to public health. However, the molecular mechanism of H6 AIV adaptation to mammals remains largely unknown. In this study, two mouse-adapted (MA) H6 AIV strains, named as MA E-Teal/417 and MA GWF-Goose/740, were generated through blind passages in BALB/c mice. The two MA H6 strains replicated more efficiently and showed higher virulence than the corresponding wild type (WT) H6 strains in mice. Genome sequencing revealed that MA E-Teal/417 and MA GWF-Goose/740 carried six amino acid mutations (PB2-T224A/E627K, HA-G124R, NA-F167L/Y356H and M1-M92R), and four amino acid mutations (PB1-K577E, PA-T97I/D514E and HA-T276K), respectively, when compared to the corresponding WT virus. Receptor binding assay showed MA E-Teal/417 had stronger binding activity to α-2,3 SA than WT E-Teal/417. Moreover, the polymerase activity analysis found the RNP polymerase activity of both MA H6 viruses was significantly higher than that of the corresponding WT virus in 293T cells. All these demonstrate that H6 AIV can acquire limit amino acid substitutions to adapt to mammals and increase virulence, highlighting the significance of monitoring such mutations of H6 AIV in the field for alarming the potential of its cross-transmission and pathogenesis in mammals.
Zhimin Wan, Jianxi Gong, Jianjun Sang, Wenjie Jiang, Zhehong Zhao, Mingjun Lian, Ting Tang, Yafeng Li, Qiuqi Kan, Quan Xie, Tuofan Li, Hongxia Shao, Wei Gao, Aijian Qin, Jianqiang Ye

2430 related Products with: Mouse adaptation of H6 avian influenza viruses and their molecular characteristics.

100 100 251 mg0.2 mg50 1 mg0.2 mg1 mg100ug1mg1 mg

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#36462496   2022/11/29 To Up

Virological, pathological, and glycovirological investigations of an Ezo red fox and a tanuki naturally infected with H5N1 high pathogenicity avian influenza viruses in Hokkaido, Japan.

In winter/spring 2021-2022, high pathogenicity avian influenza viruses (HPAIVs) that are genetically closely related to each other were detected worldwide. In a public garden in Sapporo, Hokkaido, Japan, a crow die-off by HPAIV infection occurred from March 29 to May 18, 2022. During the event, H5N1 HPAIVs were isolated from an Ezo red fox (Vulpes vulpes schrencki) and a tanuki (Nyctereutes procyonoides albus) found in the same garden. The fox showed viral meningoencephalitis and moderate virus replication in the upper respiratory tract, whereas the tanuki showed viral conjunctivitis and secondary bacterial infection in the eyes accompanied with visceral larva migrans. Viruses isolated from the fox and the tanuki were genetically closely related to those isolated from crows in the same garden. Various α2-3 sialosides were found in the respiratory tracts of these canid mammals, consistent with HPAIV infections in these animals. This study highlighted the importance of monitoring HPAIV infections in wild carnivore mammals to detect the potential virus spreading in nature.
Takahiro Hiono, Daiki Kobayashi, Atsushi Kobayashi, Tamami Suzuki, Yuki Satake, Rio Harada, Keita Matsuno, Mariko Sashika, Hinako Ban, Maya Kobayashi, Fumihito Takaya, Hiroko Fujita, Norikazu Isoda, Takashi Kimura, Yoshihiro Sakoda

1079 related Products with: Virological, pathological, and glycovirological investigations of an Ezo red fox and a tanuki naturally infected with H5N1 high pathogenicity avian influenza viruses in Hokkaido, Japan.

2550 1mg100 2550 5096T50 10100 25

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#36458566   2022/12/02 To Up

Liquid biomarkers of macrophage dysregulation and circulating spike protein illustrate the biological heterogeneity in patients with post-acute sequelae of COVID-19.

Post-acute sequelae of COVID-19 (PASC) are long-term consequences of SARS-CoV-2 infection that can substantially impair quality of life. Underlying mechanisms ranging from persistent virus to innate and adaptive immune dysregulation have been discussed. Here, we profiled plasma of 181 individuals from the cohort study for digital health research in Germany (DigiHero) including individuals after mild to moderate COVID-19 with or without PASC and uninfected controls. We focused on soluble factors related to monocyte/macrophage biology and on circulating SARS-CoV-2 spike (S1) protein as potential biomarker for persistent viral reservoirs. At a median time of eight months after infection, we found pronounced dysregulation in almost all tested soluble factors including both pro-inflammatory and pro-fibrotic cytokines. These immunological perturbations were remarkably independent of ongoing PASC symptoms per se, but further correlation and regression analyses suggested PASC specific patterns involving CCL2/MCP-1 and IL-8 that either correlated with sCD162, sCD206/MMR, IFN-α2, IL-17A and IL-33, or IL-18 and IL-23. None of the analyzed factors correlated with the detectability or levels of circulating S1 indicating that this represents an independent subset of patients with PASC. This data confirms prior evidence of immune dysregulation and persistence of viral protein in PASC and illustrates its biological heterogeneity that still awaits correlation with clinically defined PASC subtypes. This article is protected by copyright. All rights reserved.
Christoph Schultheiß, Edith Willscher, Lisa Paschold, Cornelia Gottschick, Bianca Klee, Lidia Bosurgi, Jochen Dutzmann, Daniel Sedding, Thomas Frese, Matthias Girndt, Jessica I Höll, Michael Gekle, Rafael Mikolajczyk, Mascha Binder

2388 related Products with: Liquid biomarkers of macrophage dysregulation and circulating spike protein illustrate the biological heterogeneity in patients with post-acute sequelae of COVID-19.

5ug5ug5ug2ug2ug5ug5ug2ug5ug2ug2ug1 Set

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#36458525   2022/12/02 To Up

Effects of dexmedetomidine on pharyngeal swallowing and esophageal motility-A double-blind randomized cross-over study in healthy volunteers.

Sedative agents increase the risk of pulmonary aspiration, where an intact swallowing function is an important defense mechanism. Dexmedetomidine is an α -adrenoceptor agonist widely used during procedural sedation due to beneficial properties with minimal respiratory effects. The effects of dexmedetomidine on pharyngeal swallowing and esophageal motility are not known in detail.
Per Cajander, Taher Omari, Anders Magnuson, Harry Scheinin, Mika Scheinin, Johanna Savilampi

1518 related Products with: Effects of dexmedetomidine on pharyngeal swallowing and esophageal motility-A double-blind randomized cross-over study in healthy volunteers.

100ug

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#36455156   2022/12/01 To Up

Sialosides Containing 7--Acetyl Sialic Acid Are Selective Substrates for Neuraminidases from Influenza A Viruses.

Sialidases or neuraminidases are sialic-acid-cleaving enzymes that are expressed by a broad spectrum of organisms, including pathogens. In nature, sialic acids are monosaccharides with diverse structural variations, but the lack of novel probes has made it difficult to determine how sialic acid modifications impact the recognition by sialidases. Here, we used a chemoenzymatic synthon strategy to generate a set of α2-3- and α2-6-linked sialoside probes that contain 7--acetyl or 7,9-di--acetyl sialic acid as structure mimics for those containing the less stable naturally occurring 7--acetyl- or 7,9-di--acetyl modifications. These probes were used to compare the substrate specificity of several sialidases from different origins. Our results show that 7--acetyl sialic acid was readily cleaved by neuraminidases from H1N1 and H3N2 influenza A viruses, but not by sialidases of human or bacterial origin, thereby indicating that the influenza enzymes possess a distinctive and more promiscuous substrate binding pocket.
Anoopjit Singh Kooner, Yue Yuan, Hai Yu, Hyeog Kang, Laura Klenow, Robert Daniels, Xi Chen

1450 related Products with: Sialosides Containing 7--Acetyl Sialic Acid Are Selective Substrates for Neuraminidases from Influenza A Viruses.

10 mg 1 G10 mg 1 G25 mg50 mg250 mg5 G1 g25 mg100 mg50 mg

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#36454807   2022/12/01 To Up

Brimonidine and timolol concentrations in the human vitreous and aqueous humors after topical instillation of a 0.1% brimonidine tartrate and 0.5% timolol fixed-combination ophthalmic solution: An interventional study.

To evaluate the concentrations of brimonidine and timolol in the vitreous and aqueous humors after instillation of a 0.1% brimonidine tartrate and 0.5% timolol fixed-combination ophthalmic solution.
Yusuke Orii, Eriko Kunikane, Yutaka Yamada, Masakazu Morioka, Kentaro Iwasaki, Shogo Arimura, Akemi Mizuno, Masaru Inatani

1407 related Products with: Brimonidine and timolol concentrations in the human vitreous and aqueous humors after topical instillation of a 0.1% brimonidine tartrate and 0.5% timolol fixed-combination ophthalmic solution: An interventional study.

1000 0.1 mg100ul1 ml200 25 mg1000 tests10 mg100ug200ug 5 G

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#36452458   2022/11/14 To Up

Deficiency in ST6GAL1, one of the two α2,6-sialyltransferases, has only a minor effect on the pathogenesis of prion disease.

Prion diseases are a group of fatal neurodegenerative diseases caused by misfolding of the normal cellular form of the prion protein or PrP, into a disease-associated self-replicating state or PrP. PrP and PrP are posttranslationally modified with N-linked glycans, in which the terminal positions occupied by sialic acids residues are attached to galactose predominantly α2-6 linkages. The sialylation status of PrP is an important determinant of prion disease pathogenesis, as it dictates the rate of prion replication and controls the fate of prions in an organism. The current study tests whether a knockout of ST6Gal1, one of the two mammalian sialyltransferases that catalyze the sialylation of glycans α2-6 linkages, reduces the sialylation status of PrP and alters prion disease pathogenesis. We found that a global knockout of ST6Gal1 in mice significantly reduces the α2-6 sialylation of the brain parenchyma, as determined by staining with agglutinin. However, the sialylation of PrP remained stable and the incubation time to disease increased only modestly in knockout mice (ST6Gal1-KO). A lack of significant changes in the PrP sialylation status and prion pathogenesis is attributed to the redundancy in sialylation and, in particular, the plausible involvement of a second member of the sialyltransferase family that sialylate α2-6 linkages, ST6Gal2.
Natallia Makarava, Elizaveta Katorcha, Jennifer Chen-Yu Chang, Joseph T Y Lau, Ilia V Baskakov

2236 related Products with: Deficiency in ST6GAL1, one of the two α2,6-sialyltransferases, has only a minor effect on the pathogenesis of prion disease.

1100 100ug

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