Publications by authors named "Jianhu Zhang"

Currently, the phylogenetic relationships of Linnaeus (1753) remain unclear. This study presents the first report on the complete chloroplast genome of , which is a quadripartite structure with a length of 153,002 bp and containing a large single copy (LSC, 84,225 bp) region, a small single copy (SSC, 18,407 bp) region, a pair of inverted repeats (IR, 25,185 bp) regions. A total of 134 genes are identified, including 87 protein-coding genes, 8 rRNA genes, 37 tRNA genes, and 2 pseudogenes.

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Parkinson's disease (PD), Alzheimer's disease (AD) are common neurodegenerative disease, while mild cognitive impairment (MCI) may be happened in the early stage of AD or PD. Blood biomarkers are considered to be less invasive, less cost and more convenient, and there is tremendous potential for the diagnosis and prediction of neurodegenerative diseases. As a recently mentioned field, artificial intelligence (AI) is often applied in biology and shows excellent results.

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1,3,5-Trinitro-1,3,5-triazinane (RDX) has attracted considerable attention in energy-related fields. However, the safety performance of RDX needs to be improved in terms of various external stimuli. Herein, such issues of RDX could be well balanced through hydrothermal assembly with the assistance of insensitive 1,3,5-triamino-2,4,6-trinitrobenzene (TATB) in a low content of 10 wt% (named RT co-particles).

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The energy release performance of energetic compounds like 3-nitro-1,2,4-trizole-5-one (NTO) and 5,5'-bistetrazole-1,1'-diolate (TKX-50) are indispensable in propellent formulations. However, thermal decomposition behavior is impeded by unfavorable catalysts. Presently, ultrathin porous MoS nanosheets (pMoS) are considered as high-performance catalysts for NTO and TKX-50 decomposition.

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There are no obvious clinical signs and symptoms in the early stages of Alzheimer's disease (AD), and most patients usually have mild cognitive impairment (MCI) before diagnosis. Therefore, early diagnosis of AD is very critical. This paper mainly discusses the blood biomarkers of AD patients and uses machine learning methods to study the changes of blood transcriptome during the development of AD and to search for potential blood biomarkers for AD.

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The mechanical properties of composites are highly dependent on the interfacial interaction. In the present work, inspired by marine mussel, the adhesion between energetic crystals of 1,3,5-triamino-2,4,6-trinitrobenzene (TATB) and polymer binders was improved. Three types of linear polymeric agents of glycidyl azide polymer (GAP), polyethylene glycol (PEG), and polytetramethylene ether glycol (PTMEG) were grafted onto TATB particles bridged through polydopamine (PDA) films.

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Cyclin-dependent kinase 9 (CDK9) transcriptionally regulates several proteins and cellular pathways central to radiation induced tissue injury. We investigated a role of BAY1143572, a new highly specific CDK9 inhibitor, as a sensitizer to radiation in esophageal adenocarcinoma. synergy between the CDK9 inhibitor and radiation was evaluated by clonogenic assay.

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A novel core@double-shell (CDS) 1,3,5,7-tetranitro-1,3,5,7-tetrazocane (HMX) based energetic composite was constructed with an inner nano-1,3,5-triamino-2,4,6-trinitrobenzene (nano-TATB) shell and outer polydopamine (PDA) shell fabricated via a facile ultrasonic method and a simple immersion method, respectively. The inner nano-TATB shell was chosen to reduce the sensitivity of HMX while maintaining explosion performance; the outer PDA shell was adopted to enhance the interfacial interaction between explosive crystals and polymer binder. The uniform PDA coating resulted in the increased β-δ phase transition temperature of HMX from 197.

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Purpose: HSP90 inhibition is well known to sensitize cancer cells to radiation. However, it is currently unknown whether additional radiosensitization could occur in the more clinically relevant setting of chemoradiation (CRT). We used the potent HSP90 inhibitor ganetespib to determine whether it can enhance CRT effects in NSCLC.

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Sunitinib malate is a multitargeted receptor tyrosine kinase inhibitor used in the treatment of human malignancies. A substantial number of sunitinib-treated patients develop cardiac dysfunction, but the mechanism of sunitinib-induced cardiotoxicity is poorly understood. We show that mice treated with sunitinib develop cardiac and coronary microvascular dysfunction and exhibit an impaired cardiac response to stress.

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We consider a three-stage game where a public firm and a private firm choose R&D, location, and price, under the assumption that R&D spillovers rely on their locations. We show that, in equilibrium, whether the public firm engages in innovation more aggressively than the private firm depends on the degree of spillovers. Moreover, firms' equilibrium locations exhibit neither maximal nor minimal differentiation.

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Mesenchymal stem cells (MSCs) may be useful for treating a variety of disease states associated with vascular instability including traumatic brain injury (TBI). A soluble factor, tissue inhibitor of matrix metalloproteinase-3 (TIMP3), produced by MSCs is shown to recapitulate the beneficial effects of MSCs on endothelial function and to ameliorate the effects of a compromised blood-brain barrier (BBB) due to TBI. Intravenous administration of recombinant TIMP3 inhibited BBB permeability caused by TBI, whereas attenuation of TIMP3 expression in intravenously administered MSCs blocked the beneficial effects of the MSCs on BBB permeability and stability.

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The platelet derived growth factor receptor (PDGFR) is an important target for novel anti-cancer therapeutics, but agents targeting PDGFR have been associated with cardiotoxicity. Cardiomyocyte PDGFR-β signaling in pressure-overloaded hearts induces compensatory angiogenesis via a paracrine-signaling cascade. Tight regulation of receptor tyrosine kinases in response to ligand stimulation is a critical part of any such cascade.

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PDGFR is an important target for novel anticancer therapeutics because it is overexpressed in a wide variety of malignancies. Recently, however, several anticancer drugs that inhibit PDGFR signaling have been associated with clinical heart failure. Understanding this effect of PDGFR inhibitors has been difficult because the role of PDGFR signaling in the heart remains largely unexplored.

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Background: The authors sought to determine the incidence and severity of cardiovascular toxicity caused by imatinib mesylate in gastrointestinal stromal tumor (GIST) and other sarcoma patients, and to explore cardiotoxicity caused by imatinib mesylate using cell culture and in vitro models.

Methods: To determine the incidence and significance of serious cardiac adverse events in GIST and other sarcoma patients receiving imatinib mesylate, the authors performed a retrospective analysis of 219 consecutive patients treated with imatinib mesylate. In vitro studies of imatinib mesylate on cultured cardiomyocytes and biochemical studies of cardiac lysates from mice treated with imatinib mesylate were performed to define the potential cardiotoxic effects of imatinib mesylate.

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Background: Repetitive deformation stimulates proliferation in human Caco2 intestinal epithelial cells by way of an ERK1/2-dependent pathway. We examined the effects of cytoskeletal perturbation on deformation-induced signaling in Caco2 cells.

Methods: The Caco2 cell cytoskeleton was disrupted with either cytochalasin D, phalloidin, colchicine, or paclitaxel.

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Background & Aims: Complex deformation during normal digestion due to peristalsis or villous motility may be trophic for the intestinal mucosa. Because tissue fibronectin is increased in inflammatory states that may accompany mucosal injury, we evaluated the effects of cyclic mechanical strain and fibronectin on intestinal epithelial monolayer wound closure in Caco-2 and IEC-6 intestinal epithelial cells.

Methods: Wounds created in intestinal epithelial monolayers were subjected to cyclic deformation.

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Mucosal healing requires migration and proliferation. Most studies of focal adhesion kinase (FAK), a protein that regulates motility, proliferation, and apoptosis, have focused on rapid phosphorylation. We reported lower FAK protein levels in motile Caco-2 colon cancer cells and postulated that this reduction in FAK available for activation might impact cell migration and mucosal healing.

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Emerging evidence suggests that both human stem cells and mature stromal cells can play an important role in the development and growth of human malignancies. In contrast to these tumor-promoting properties, we observed that in an in vivo model of Kaposi's sarcoma (KS), intravenously (i.v.

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Diverse repetitive forces deform the intestinal epithelium and basement membrane. Such repetitive deformation induces intestinal epithelial proliferation, differentiation, and intracellular signaling. Although at least some deformation-induced signals probably involve integrins, the matrix-dependence of these signals is poorly understood.

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Repetitive mechanical deformation may stimulate intestinal epithelial proliferation. Because the extracellular matrix modulates static intestinal epithelial biology, we examined whether matrix proteins influence intestinal epithelial responses to deformation. Human Caco-2BBE cells and nontransformed human enterocytes (HIPEC) were subjected to 10% average cyclic strain at 10 cycles/min on flexible membranes precoated with matrix proteins without or with plasma fibronectin or functional anti-integrin antibodies in the medium.

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Docosahexaenoic acid (DHA) and butyrate favorably modulate colonocyte proliferation and apoptosis. In order to elucidate how oncogenic Ras modulates responses to these chemopreventive nutrients, we incubated isogenic non-transformed and Ras malignant transformed mouse colon cells with butyrate and DHA or linoleic acid (LA). Combining DHA with 1mM butyrate decreased proliferation relative to LA or no PUFA treatment in both cell lines.

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