Publications by authors named "Jianqiang Ding"

Bacterial-infected wound repair has become a significant public health concern. This study developed a novel 3D-printed piezocatalytic SF-MA/PEGDA/Ag@BT (SPAB) hydrogels were fabricated by using digital light processing. These hydrogels exhibited high consistency, mechanical properties and good biocompatibility.

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Treatment of diabetic wounds is a major clinical issue. Diabetic wound dressings have higher requirements for anti-oxidant, antibacterial and wound monitoring properties compared to conventional wound dressings. In this study, a novel tannic acid (TA)/quaternized carboxymethyl chitosan (QCMCS)/oxidized sodium alginate (OSA)@carbon quantum dots (CQD) (TA/QCMCS/OSA@CQD) hydrogels for promoting diabetic wound healing and real-time monitoring have been developed.

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Objective: To comprehensively analyze that how liver injury in patients with metabolic syndrome is affected by coronavirus disease 2019 (COVID-19) and provide clinical reference to their prevention and treatment.

Background: The current COVID-19 pandemic poses a major threat to human life and health. Metabolic syndrome is also a major global health problem, and evidence suggests that patients with metabolic syndrome are at an increased risk of COVID-19 complications.

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Background: This study aimed to investigate the clinicopathological significance of sine oculis homeobox homolog 1 (SIX1) and eyes absent 1 (EYA1) in patients with chronic hepatitis B (CHB) and other liver diseases.

Methods: SIX1 and EYA1 levels were detected in human serum and liver tissues by enzyme linked immunosorbent assay (ELISA) and immunofluorescent staining method, respectively.

Results: The serum SIX1 and EYA1 levels in 313 CHB patients were 7.

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Objective: α-1 antitrypsin deficiency (AATD) is an inherited liver disease characterized by the "Z" mutations, which can cause pulmonary emphysema and liver fibrosis. Transplantation of the organ (i.e.

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Duchenne muscular dystrophy (DMD) is a fatal X-linked genetic disease of the neuromuscular system and is the most serious type of muscular dystrophy in humans. The disease is characterized by progressive muscular atrophy and a poor prognosis. The incidence rate is 1/3500, and symptoms appear at age of 5 years-old.

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FibroScan is used to determine liver stiffness and controlled attenuation parameter (referred to as CAP) scores in patients, including those with chronic hepatitis B (CHB). We used FibroScan to detect the incidence of fatty liver and fibrosis in CHB patients, and to assess the correlation of FibroScan measurements with blood chemistry tests. CHB patients enrolled in this study were divided independently for three separate analyses (of fibrosis, cirrhosis, and fatty liver) based on FibroScan results.

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Background: The 2019 coronavirus disease (COVID-19) was first identified in Wuhan, Hubei, China in December 2019, caused by a novel coronavirus (SARS-CoV-2). There is a need to study the clinical features of patients in a hospital near Wuhan.

Objective: To identify clinical features of patients with COVID-19 in a tertiary hospital near Wuhan.

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An increasing body of evidence supports the association of immune genes with tumorigenesis and prognosis of breast cancer (BC). This research aims at exploring potential regulatory mechanisms and identifying immunogenic prognostic markers for BC, which were used to construct a prognostic signature for disease-free survival (DFS) of BC based on artificial intelligence algorithms. Differentially expressed immune genes were identified between normal tissues and tumor tissues.

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The transcription factor Six1 is essential for induction of sensory cell fate and formation of auditory sensory epithelium, but how it activates gene expression programs to generate distinct cell-types remains unknown. Here, we perform genome-wide characterization of Six1 binding at different stages of auditory sensory epithelium development and find that Six1-binding to cis-regulatory elements changes dramatically at cell-state transitions. Intriguingly, Six1 pre-occupies enhancers of cell-type-specific regulators and effectors before their expression.

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Background: The current study aimed to construct competing endogenous RNA (ceRNA) regulation network and develop two precision medicine predictive tools for colorectal cancer (CRC).

Methods: Differentially expressed (DE) analyses were performed between CRC tissues and normal tissues. A ceRNA regulation network was constructed based on DElncRNAs, DEmiRNAs, and DEmRNAs.

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Background: Hepatocellular carcinoma (HCC) is a serious threat to public health due to its poor prognosis. The current study aimed to develop and validate a prognostic nomogram to predict the overall survival of HCC patients.

Methods: The model cohort consisted of 24,991 mRNA expression data points from 348 HCC patients.

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The aim of the present study is to construct a competitive endogenous RNA (ceRNA) regulatory network by using differentially expressed long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and mRNAs in patients with hepatocellular carcinoma (HCC), and to construct a prognostic model for predicting overall survival (OS) of HCC patients. Differentially expressed lncRNAs, miRNAs, and mRNAs were explored between HCC tissues and normal liver tissues. A prognostic model was built for predicting OS of HCC patients and receiver operating characteristic curves were used to evaluate the performance of the prognostic model.

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Although several types of somatic cells have been reprogrammed into induced pluripotent stem cells (iPSCs) and then differentiated to hepatocyte-like cells (iHeps), the method for generating such cells from renal tubular epithelial cells shed in human urine and transplanting them into animal livers has not been described systematically. We report reprogramming of human urinary epithelial cells into iPSCs and subsequent hepatic differentiation, followed by a detailed characterization of the newly generated iHeps. The epithelial cells were reprogrammed into iPSCs by delivering the pluripotency factors OCT3/4, SOX2, KLF4, and MYC using methods that do not involve transgene integration, such as nucleofection of episomal (oriP/EBNA-1) plasmids or infection with recombinant Sendai viruses.

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BACKGROUND VKORC1 is reported to be capable of treating several diseases with thrombotic risk, such as cardiac valve replacement. Some single-nucleotide polymorphisms (SNPs) in VKORC1 are documented to be associated with clinical differences in warfarin maintenance dose. This study explored the correlations of VKORC1-1639 G/A, 1173 C/T and 497 T/G genetic polymorphisms with warfarin maintenance dose requirement in patients undergoing cardiac valve replacement.

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Objective: In this study, we investigated two VKORC1 gene polymorphisms, -1639G/A and 1173C/T, for effects on warfarin maintenance dosage in valvular heart disease (VHD) patients after cardiac valve replacement (CVR).

Methods: A total of 219 VHD patients receiving warfarin therapy after CVR surgery were recruited to this study between June 2010 and December 2013. Basic clinical data, prothrombin time, warfarin maintenance dose, and blood samples were collected from all patients.

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Background And Aims: Preparative hepatic irradiation (HIR), together with mitotic stimulation of hepatocytes, permits extensive hepatic repopulation by transplanted hepatocytes in rats and mice. However, whole liver HIR is associated with radiation-induced liver disease (RILD), which limits its potential therapeutic application. In clinical experience, restricting HIR to a fraction of the liver reduces the susceptibility to RILD.

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α1-Antitrypsin deficiency is an inherited condition that causes liver disease and emphysema. The normal function of this protein, which is synthesized by the liver, is to inhibit neutrophil elastase, a protease that degrades connective tissue of the lung. In the classical form of the disease, inefficient secretion of a mutant α1-antitrypsin protein (AAT-Z) results in its accumulation within hepatocytes and reduced protease inhibitor activity, resulting in liver injury and pulmonary emphysema.

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We have prepared a series of TiO2 nanoparticles for antibacterial applications. These TiO2 nanoparticles were prepared by the hydrolysis precipitation method with Ti(OBu)4, silver nitrate and ammonia. Crystal structure, particle size, interfacial structure and UV-visible light response of the prepared nanoparticles were characterized by X-ray diffraction measurements (XRD), Transmission electron microscopy (TEM), Fourier-transform infrared spectroscopy (FTIR) and UV-Vis diffuse reflectance spectroscopy (UV-Vis-DRs).

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An iodine and boron co-doped TiO2 photocatalyst was prepared by the hydrolyzation-precipitation method. X-ray diffraction (XRD), ultraviolet-visible diffuse reflectance spectroscopy (UV-Vis DRS), and X-ray photoelectron spectroscopy (XPS) were applied to characterize the crystalline structure, light absorbing ability, and the chemical state of iodine and boron in the photocatalysts. The results of photocatalytic degradation of methyl orange demonstrated that the I-B-TiO2 catalyst prepared at 400 degrees C for 3 h exhibited the highest photocatalytic activity with a methyl orange degradation ratio of 61% under visible-light (lambda > or = 420 nm) irradiation for 120 min.

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Although the role of NF-kappaB in the pathogenesis of sepsis and septic shock has been extensively studied, little is known about the causative contribution of endothelial-intrinsic NF-kappaB to these pathological processes. In this study, we used transgenic (TG) mice (on FVB genetic background) that conditionally overexpress the NF-kappaB inhibitor, mutant I-kappaBalpha, selectively on endothelium and their transgene-negative littermates (wild type (WT)) to define the causative role of endothelial-specific NF-kappaB signaling in septic shock and septic vascular dysfunction. In WT mice, LPS challenge caused systemic hypotension, a significantly blunted vasoconstrictor response to norepinephrine, and an impaired endothelium-dependent vasodilator response to acetylcholine, concomitant with a markedly increased aortic inducible NO synthase expression, significantly elevated plasma and aortic levels of nitrite/nitrate, increased aortic TNF-alpha expression, and decreased aortic endothelial NO synthase (eNOS) expression.

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To define the roles of endothelial-intrinsic nuclear factor kappaB (NF-kappaB) activity in host defense and multiple organ injury in response to sepsis, we generated double transgenic (TG) mice (EC-rtTA/I-kappaB alpha mt) that conditionally overexpress a degradation-resistant form of the NF-kappaB inhibitor I-kappaB alpha (I-kappaB alpha mt) selectively on vascular endothelium. The EC-rtTA/I-kappaB alpha mt mice had no basal, but a relatively high level of doxycycline-inducible, I-kappaB alpha mt expression. I-kappaB alpha mt expression was detected in endothelial cells, but not in fibroblasts, macrophages, and whole blood cells, confirming that transgene expression was restricted to the endothelium.

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Surfactant protein-A enhances the phagocytosis and killing of many pathogens, although studying this effect in an assortment of models and different experimental protocols has sometimes yielded conflicting results. In this report, using the human THP-1 cell line as the primary phagocytic cell, we systematically examined several models where microspheres, Staphylococcus aureus and Escherichia coli were used for targets. We found that SP-A derived from human lavage appeared to enhance phagocytosis by two different mechanisms; by SP-A binding of the target to enhance its recognition and subsequent phagocytosis and by a direct SP-A stimulatory effect on the phagocyte itself.

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