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Jing Zhao

Publications and source records attributed to Jing Zhao.

At least 19 recordsLinked to original sources

Multi-omics characterization of flavor profile differences in the Longissimus thoracis between Angus and Hereford cattle.

BACKGROUND: Angus and Hereford cattle are premier breeds widely used in genetic improvement and crossbreeding programs to enhance meat quality, yet the flavor differences between them remain poorly understood. RESULTS: In this study, we performed an integrated analysis using headspace solid-phase microextraction coupled with gas chromatography-mass spectrometry (HS-SPME-GC-MS)-based volatile metabolomics, lipidomics, and untargeted metabolomics to characterize the flavor profiles of the Longissimus thoracis (LT) muscle from both breeds and to identify potential precursor substances underlying flavor formation. In total, we identified 76 differential volatile organic compounds (VOCs) among the 493 candidate VOCs. By combing relative odor activity value (ROAV) and sensory attribute annotation, 2,3-butanedione which may contribute to the creamy aroma was revealed as the core differential VOC between the two breeds. This finding was robustly validated across SHAP (Shapley additive explanations) analysis, KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment, and flavor annotation. Lipidomic analysis revealed 689 differential lipids primarily belonging to classes such as phosphatidylcholine, triglycerides, and phosphatidylethanolamine. Correlation analysis further linked these lipid profiles to flavor, showing that fatty acids (FAs) including FA(19:0), FA(18:2 + O), FA(14:1), FA(16:1), and FA(14:0) were significantly correlated with 2,3-butanedione. Notably, the unsaturated fatty acids (UFAs) in the Longissimus thoracis (LT) of Hereford cattle exhibited higher double bond content compared to Angus cattle, suggesting a greater potential for rich flavor development. Untargeted metabolomics revealed that nine of the 9474 metabolites were significantly correlated with both 2,3-butanedione and FAs, including norepinephrine, l-beta-aspartyl-l-leucine, and artemetin. CONCLUSIONS: Overall, our research has identified differential flavor compounds and potential precursor substances between Angus cattle and Hereford cattle, providing targeted guidance for breed improvement. © 2026 Society of Chemical Industry.

2,3‐butanedione↗

LDLR Variant Classification Through Activity-Normalized Prime Editing Screening.

BACKGROUND: Inherited variants in the LDL (low-density lipoprotein) receptor (LDLR) gene are the most common cause of familial hypercholesterolemia, significantly increasing coronary artery disease risk. Early identification of pathogenic LDLR variants enables prompt lipid-lowering therapy and cascade testing of at-risk relatives; however, most LDLR variants observed in the population have uncertain or absent clinical classifications, leaving many patients without actionable information. METHODS: We developed the first activity-normalized prime editing screening pipeline to measure the impact of 5184 LDLR coding variants on LDL-cholesterol (LDL-C) uptake. Each prime editing guide RNA is paired with a genotypic outcome reporter to correct for variable editing efficiency, overcoming a key limitation of previous pooled genome editing screens. A statistical framework further improves variant effect estimates by jointly analyzing all missense variants at each amino acid position. RESULTS: We show that prime editing of the reporter construct correlates with endogenous variant installation frequency, validating the activity normalization approach. The resulting scores capture a continuous spectrum of functional effects, robustly separate pathogenic versus benign ClinVar variants, and show concordance with LDL-C levels in UK Biobank participants. We calibrate functional evidence strengths to the ACMG/AMP variant interpretation framework, enabling integration into a clinical variant classification workflow. By combining functional, computational, population, and contextual evidence, 322 of 434 LDLR variants currently classified as variants of uncertain significance, conflicting, or absent from ClinVar appear to meet evidence thresholds for reclassification and can be prioritized for expert review, substantially expanding the pool of actionable variant classifications. The screen also reveals a cluster of gain-of-function variants in LDLR class A repeat 5, at least some of which enhance LDL-C uptake through increased apolipoprotein B interaction, with implications for therapeutic genome editing. Last, prime editing uniquely detects splice-altering coding variants missed by cDNA-based screens and pathogenicity predictors, revealing an advantage of endogenous variant installation. CONCLUSIONS: Altogether, activity-normalized prime editing provides a scalable framework for LDLR variant classification that substantially expands the proportion of variants with evidence for genetic diagnosis and reveals novel biology with therapeutic relevance.

CRISPR screening↗

Efficacy of transcranial alternating current stimulation for musculoskeletal pain and sleep quality: a systematic review and meta-analysis.

BACKGROUND: Transcranial alternating current stimulation (tACS) is a non-invasive neuromodulation technique, emerging as a potential therapeutic option for musculoskeletal pain management. OBJECTIVE: To comprehensively evaluate the efficacy and safety of tACS for alleviating pain and improving sleep quality in adults with musculoskeletal pain. METHODS: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs). Seven major databases and other sources were searched from inception until April 2026. Two reviewers independently screened studies, extracted data, and assessed risk of bias. A random-effects model was used to pool standardized mean differences (SMDs). The certainty of evidence was evaluated using the Grading of Recommendation Assessment, Development, and Evaluation framework. RESULTS: Six RCTs involving 232 participants were included. Meta-analysis showed that tACS could significantly reduce pain intensity compared to control (SMD = -0.355, 95% CI: -0.625 to -0.084, p = 0.010, I² = 28.7%). However, no significant improvement was found for sleep quality (SMD = 0.004, 95% CI: -0.310-0.317, p = 0.982, I² = 0.0%). Adverse effects were mild and transient, comparable to sham stimulation. The overall certainty of evidence was rated as low for both pain and sleep quality outcomes. CONCLUSION: Current evidence suggests that tACS may be beneficial for musculoskeletal pain; however, the available evidence remains limited and should be interpreted cautiously. The effect of tACS on sleep quality remains uncertain because of the limited number of available studies. Future well-designed RCTs with standardized outcome measures, condition-specific stimulation protocols, and longer follow-up are required to establish the efficacy and long-term safety of tACS.

Humans↗

Oro-esophageal feeding for tracheostomized patients with severe traumatic brain injury: a randomized controlled trial.

BACKGROUND: This study reports the clinical effects of intermittent oro-esophageal tube feeding (IOE) versus nasogastric tube feeding (NGT) on nutritional status, aspiration pneumonia, decannulation, and level of consciousness in tracheostomized patients with severe traumatic brain injury (sTBI). METHODS: A randomized controlled trial was conducted between March 2024 and October 2025 in China and included tracheostomized patients with sTBI. Participants were randomized 1:1 to the intervention and control groups for 28-day interventions. IOE or NGT was used for nutritional supports, respectively. The primary outcome was nutritional status, including hemoglobin, albumin, prealbumin and body mass index. The secondary outcomes included aspiration pneumonia, decannulation, and level of consciousness assessed using the Glasgow Coma Scale (GCS). Generalized linear mixed-effects models, generalized estimating equations, and Cox regression were used for data analyze. RESULTS: A total of 104 participants were included in the analysis. After intervention, significant interaction effects were observed in hemoglobin (&#x3b2;&#x2009;=&#x2009;5.272, 95% CI: 2.707, 7.837), albumin (&#x3b2;&#x2009;=&#x2009;3.675, 95% CI: 1.854, 5.496), prealbumin (&#x3b2;&#x2009;=&#x2009;11.835, 95% CI: 6.623, 17.047), body mass index (&#x3b2;&#x2009;=&#x2009;1.719, 95% CI: 0.868, 2.569), the GCS (&#x3b2;&#x2009;=&#x2009;0.981, 95% CI: 0.572, 1.390), and aspiration pneumonia (OR= 0.304, 95% CI: 0.133, 0.693). The Cox model revealed that group significantly influenced the decannulation outcomes [HR (95% CI) =5.556 (3.197, 9.657), p&#x2009;<&#x2009;0.001]. CONCLUSIONS: In tracheostomized patients with sTBI who received routine treatment, IOE is more conducive to decannulation and the improvement in nutritional status, aspiration pneumonia, and level of consciousness than NGT. CLINICAL TRIAL REGISTRATION: Prospectively registered at ClinicalTrials.gov (NCT06328985, 03/18/2024, clinicaltrials.gov/study/NCT06328985).

Humans↗

Third-generation whole-genome sequencing reveals the role of CNTNAP2 as a tumor suppressor gene in high-risk neuroblastomas.

BACKGROUND: Neuroblastoma is a common and aggressive pediatric sympathetic nervous system tumor. Genomic structural variants (SVs) contribute substantially to neuroblastoma, yet remain under-characterized in high-risk neuroblastomas. We aimed to elucidate neuroblastoma pathogenesis using third-generation whole-genome sequence high-risk cases to identify driver aberrations and explore potential therapeutic strategies. METHODS: We analyzed third-generation whole-genome sequencing data of 20 high-risk neuroblastoma samples and combined the findings with those obtained from the analysis of clinical samples, in vitro models, and public datasets. RESULTS: The contactin-associated protein-like 2 (CNTNAP2) gene was observed to be frequently aberrated because of structural variants in high-risk neuroblastoma samples. CNTNAP2 expression was significantly correlated with favorable histology and could be used to predict prognosis using clinical samples and neuroblastoma datasets. Overexpression and knockdown experiments and transcriptomic analysis revealed that CNTNAP2 was primarily involved in neuronal differentiation and axon guidance pathways; moreover, CNTNAP2 was required for neuroblastoma differentiation and affected cancer stemness. Immunoprecipitation and mass spectrometry revealed that CNTNAP2 interacted with cytoskeletal proteins like drebrin 1 (DBN1) and myosin-heavy chain 9 (MYH9). CNTNAP2 dynamically reorganises actin and microtubules for DBN1-mediated neuronal differentiation. CNTNAP2 also reduces CTNNB1 transcription and &#x3b2;-catenin pathway activation by inhibiting MYH9 nuclear translocation. CNTNAP2 overexpression in neuroblastoma cell lines resulted in cell cycle arrest, decreased cell proliferation and metastasis. CONCLUSIONS: The recurrent loss of CNTNAP2 in neuroblastoma contributes to an aggressive phenotype by impairing neuronal differentiation and increasing cancer stemness. These findings may serve as a foundation for developing therapeutic strategies to overcome barriers to differentiation.

Humans↗

Clinical characteristics and genetic analysis of four pediatric patients with Kleefstra syndrome.

BACKGROUND: Kleefstra syndrome spectrum (KLEFS) is an autosomal dominant disorder that can lead to intellectual disability and autism spectrum disorders. KLEFS encompasses Kleefstra syndrome-1 (KLEFS1) and Kleefstra syndrome-2 (KLEFS2), with KLEFS1 accounting for more than 75%. However, limited information is available regarding KLEFS2. KLEFS1 is caused by a subtelomeric chromosomal abnormality resulting in either deletion at the end of the long arm of chromosome 9, which contains the EHMT1 gene, or by variants in the EHMT1 gene and the KMT2C gene that cause KLEFS2. METHODS: This study was a retrospective analysis of clinical data from four patients with KLEFS. Exome sequencing (ES) and Sanger sequencing techniques were used to identify and validate the candidate variants, facilitating the analysis of genotype&#x2012;phenotype correlations of the EHMT1 and KMT2C genes. Protein structure modeling was performed to evaluate the effects of the variants on the protein's three-dimensional structure. In addition, real-time quantitative reverse transcription&#x2012;polymerase chain reaction (RT&#x2012;qPCR) and western blotting were used to examine the protein and mRNA levels of the KMT2C gene. RESULTS: Two patients with KLEFS1 were identified: one with a novel variant (c.2382&#x2009;+&#x2009;1G&#x2009;>&#x2009;T) and the other with a previously reported variant (c.2426&#xa0;C&#x2009;>&#x2009;T, p.Pro809Leu) in the EHMT1 gene. A De novo deletion at the end of the long arm of chromosome 9 was also reported. Furthermore, a patient with KLEFS2 was identified with a novel variant in the KMT2C gene (c.568&#xa0;C&#x2009;>&#x2009;T, p.Arg190Ter). The RT&#x2012;qPCR and western blot results revealed that the expression of the KMT2C gene was downregulated in the KLEFS2 sample. CONCLUSION: This study contributes to the understanding of both KLEFS1 and KLEFS2 by identifying novel variants in EHMT1 and KMT2C genes, thereby expanding the variant spectrum. Additionally, we provide the first evidence of how a KMT2C variant leads to decreased gene and protein expression, enhancing our understanding of the molecular mechanisms underlying KLEFS2. Based on these findings, children exhibiting developmental delay, hypotonia, distinctive facial features, and other neurodevelopmental abnormalities should be considered for ES to ensure early intervention and treatment.

Child↗

Tissue specificity of senescent cell accumulation during physiologic and accelerated aging of mice.

Senescent cells accumulate with age in vertebrates and promote aging largely through their senescence-associated secretory phenotype (SASP). Many types of stress induce senescence, including genotoxic stress. ERCC1-XPF is a DNA repair endonuclease required for multiple DNA repair mechanisms that protect the nuclear genome. Humans or mice with reduced expression of this enzyme age rapidly due to increased levels of spontaneous, genotoxic stress. Here, we asked whether this corresponds to an increased level of senescent cells. p16Ink4a and p21Cip1 mRNA were increased ~15-fold in peripheral lymphocytes from 4- to 5-month-old Ercc1-/&#x2206; and 2.5-year-old wild-type (WT) mice, suggesting that these animals exhibit a similar biological age. p16Ink4a and p21Cip1 mRNA were elevated in 10 of 13 tissues analyzed from 4- to 5-month-old Ercc1-/&#x2206; mice, indicating where endogenous DNA damage drives senescence in vivo. Aged WT mice had similar increases of p16Ink4a and p21Cip1 mRNA in the same 10 tissues as the mutant mice. Senescence-associated &#x3b2;-galactosidase activity and p21Cip1 protein also were increased in tissues of the progeroid and aged mice, while Lamin B1 mRNA and protein levels were diminished. In Ercc1-/&#x394; mice with a p16Ink4a luciferase reporter, bioluminescence rose steadily with age, particularly in lung, thymus, and pancreas. These data illustrate where senescence occurs with natural and accelerated aging in mice and the relative extent of senescence among tissues. Interestingly, senescence was greater in male mice until the end of life. The similarities between Ercc1-/&#x2206; and aged WT&#xa0;mice support the conclusion that the DNA repair-deficient mice accurately model the&#xa0;age-related accumulation of senescent cells, albeit six-times faster.

Aging↗

Suppressing phosphatidylcholine-specific phospholipase C and elevating ROS level, NADPH oxidase activity and Rb level induced neuronal differentiation in mesenchymal stem cells.

In the previous research, we found that D609 (tricyclodecan-9-yl-xanthogenate) could induce human marrow stromal cell (hMSC) differentiation to neuron-like cells. In this study, to understand the possible mechanism, we sequentially investigated the changes of phosphatidylcholine-specific phospholipase C (PC-PLC) activity, the expression of Rb, the intracellular reactive oxygen species (ROS) levels, NADPH oxidase and superoxide dismutase (SOD) activities when D609 induced neuronal differentiation in rat mesenchymal stem cells (MSCs). The results showed that D609 obviously inhibited the activity of PC-PLC when it induced neuronal differentiation in rat MSCs. Simultaneously, ROS level and the activity of NADPH oxidase increased significantly, but the MnSOD and Cu/ZnSOD activities were not altered. Furthermore, the level of Rb protein was evidently elevated. Our data suggested that PC-PLC mediated neuronal differentiation of rat MSCs by elevating NADPH oxidase activity, ROS level, and up-regulating the expression of Rb protein.

Animals↗

Low-carbon energy policy and ambient air pollution in Shanghai, China: a health-based economic assessment.

Energy and related health issues are of growing concern worldwide today. To investigate the potential public health and economic impact of ambient air pollution under various low-carbon energy scenarios in Shanghai, we estimated the exposure level of Shanghai residents to air pollution under various planned scenarios, and assessed the public health impact using concentration-response functions derived from available epidemiologic studies. We then estimated the corresponding economic values of the health effects based on unit values for each health outcome. Our results show that ambient air pollution in relation to low-carbon energy scenarios could have a significant impact on the future health status of Shanghai residents, both in physical and monetary terms. Compared with the base case scenario, implementation of various low-carbon energy scenarios could prevent 2804-8249 and 9870-23,100 PM10-related avoidable deaths (mid-value) in 2010 and 2020, respectively. It could also decrease incidence of several relevant diseases. The corresponding economic benefits could reach 507.31-1492.33 and 2642.45-6192.11 million U.S. dollars (mid-value) in 2010 and 2020, respectively. These findings illustrate that a low-carbon energy policy will not only decrease the emission of greenhouse gases, but also play an active role in the reduction of air pollutant emissions, improvement of air quality, and promotion of public health. Our estimates can provide useful information to local decision-makers for further cost-benefit analysis.

Air Pollutants↗

Microsurgical anatomy of the superior orbital fissure.

The microanatomy of the superior orbital fissure (SOF) was studied in 96 sides of cadaver specimens. The SOF is a narrow bony cleft that lies at the apex of the orbit between the greater and lesser wings of the sphenoid. Through this fissure, many important structures enter the orbit from the middle cranial fossa including the third, fourth, sixth cranial nerves, and the ophthalmic branch of the fifth nerve. In addition, the superior opthalmamic vein exits the orbit to drain into the cavernous sinus via the SOF. The fissure can be divided into three anatomical regions by the annulus of Zinn (common annular tendon): the lateral, central, and inferior regions. The lateral wall of the SOF can also be divided between the upper and lower segments, and the angle between them was measured to be 144.27 degrees +/- 20.03 degrees . Defining these regions is useful in describing the course and placement of the nerves and vasculature in the SOF. Managing lesions at the orbital apex requires an extensive knowledge of the cranial base and the intracranial and extracranial relationships of the anatomical structures coursing through the SOF. The goal of this study was to describe the microanatomy of the SOF region in detail and to provide a reference for surgical procedures involving the orbital apex.

Cavernous Sinus↗

Antiretroviral activity, pharmacokinetics, and tolerability of MK-0518, a novel inhibitor of HIV-1 integrase, dosed as monotherapy for 10 days in treatment-naive HIV-1-infected individuals.

BACKGROUND: MK-0518 is a novel HIV-1 integrase strand transfer inhibitor with potent in vitro activity against HIV-1 (95% inhibitory concentration [IC95] = 33 nM in 50% human serum) and good bioavailability in uninfected subjects. This study explored the antiretroviral activity and safety of MK-0518 versus placebo for 10 days as monotherapy in antiretroviral therapy-naive HIV-1-infected patients with plasma HIV-1 RNA levels of at least 5000 copies/mL and CD4 T-cell counts of at least 100 cells/mm. METHODS: This was a multicenter, double-blind, randomized, placebo-controlled 2-part study, with the first part using MK-0518 in 1 of 4 doses (100, 200, 400, and 600 mg) versus placebo (randomized 1:1:1:1:1) given twice daily for 10 days of monotherapy. Patients were monitored for safety, pharmacokinetic parameters, and antiretroviral effect. RESULTS: Thirty-five patients were enrolled (6-8 patients per treatment group) and completed 10 days of therapy; the mean baseline log10 HIV RNA level ranged from 4.5 to 5.0 copies/mL in each group. On day 10, the mean decrease from baseline in the log10 HIV RNA level was -0.2 copies/mL for the placebo group and -1.9, -2.0, -1.7 and -2.2 log10 copies/mL for the MK-0518 100-, 200-, 400-, and 600-mg treatment groups, respectively. All dose groups had superior antiretroviral activity compared with placebo (P < 0.001 for comparison of each dose with placebo). At least 50% of patients in each MK-0518 dose group achieved an HIV RNA level <400 copies/mL by day 10. Mean trough MK-0518 concentrations at each dose exceeded the IC95 of 33 nM. Study therapy was generally well tolerated. The most common adverse experiences were headache and dizziness; these were similar between active and control groups. There were no discontinuations because of adverse experiences and no serious adverse experiences. CONCLUSIONS: MK-0518 showed potent antiretroviral activity as short-term monotherapy and was generally well tolerated at all doses. Based on these results, part 2 of the study, a dose-ranging 48-week trial of MK-0518 versus efavirenz in a combination regimen, has been initiated.

Adult↗

Safrole oxide induces neuronal apoptosis through inhibition of integrin beta4/SOD activity and elevation of ROS/NADPH oxidase activity.

Neuronal apoptosis is a very important event in the development of the central nervous system (CNS), but the underlying mechanisms remain to be elucidated. We have previously shown that safrole oxide, a small molecule, induces integrin beta4 expression and promotes apoptosis in vascular endothelial cells. In this study, the effects of safrole oxide on cell growth and apoptosis have been examined in primary cultures of mouse neurons. Safrole oxide was found to significantly inhibit neuronal cell growth and to induce apoptosis. The inhibitory and apoptotic activities of safrole oxide followed a dose- and time-dependent manner. Interestingly, the expression of integrin beta4 was significantly inhibited with safrole oxide treatment. Furthermore, safrole oxide dramatically increases the level of intracellular reactive oxygen species (ROS) and the activity of NADPH oxidase. Moreover, manganese-dependent superoxide dismutase (MnSOD) activity was decreased significantly with safrole oxide treatment. Our study thus demonstrates that safrole oxide induces neuronal apoptosis through integrin beta4, ROS, NADPH, and MnSOD.

Animals↗

Cell membranes and liposomes dissociate C-reactive protein (CRP) to form a new, biologically active structural intermediate: mCRP(m).

Emerging evidence indicates that C-reactive protein (CRP) has at least two conformationally distinct isoforms, i.e., pentameric CRP (pCRP) and monomeric CRP (mCRP or CRP subunit). Both CRP isoforms are proposed to play roles in inflammation and may participate in the pathogenesis of cardiovascular disease. However, the origin of mCRP in situ and the interplay between the two CRP isoforms under physiological/pathological circumstances remain elusive. Herein, by probing conformational alteration, neoepitope expression, and direct visualization using electron-microscopy, we have shown that calcium-dependent binding of pCRP to membranes, including liposomes and cell membranes, led to a rapid but partial structural change, producing molecules that express CRP subunit antigenicity but with retained native pentameric conformation. This hybrid molecule is herein termed mCRP(m). The formation of mCRP(m) was associated with significantly enhanced complement fixation. mCRP(m) can further detach from membrane to form the well-recognized mCRP isoform converted in solution (mCRP(s)) and exert potent stimulatory effects on endothelial cells. The membrane-induced pCRP dissociation not only provides a physiologically relevant scenario for mCRP formation but may represent an important mechanism for regulating CRP function.

Animals↗

Dexamethasone alters bronchoalveolar lavage fluid proteome in a mouse asthma model.

BACKGROUND: Glucocorticoid is the most effective anti-inflammatory agent for asthma. The spectrum of protein targets that can be regulated by glucocorticoid in asthma is not fully understood. The present study tried to identify novel protein targets of dexamethasone in allergic airway inflammation by analyzing the proteome of mouse bronchoalveolar lavage (BAL) fluid. METHODS: BALB/c mice sensitized and challenged with ovalbumin (OVA) showed increased pulmonary inflammatory cell infiltration, airway mucus production and serum OVA-specific IgE level. Dexamethasone inhibited all these allergic airway inflammation endpoints. BAL fluid proteins were resolved by two-dimensional gel electrophoresis and identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. RESULTS: The levels of 26 BAL fluid proteins were found to be markedly altered by dexamethasone. A family of chitinases (Ym1, Ym2 and acidic mammalian chitinase, AMCase), lungkine, gob-5, surfactant protein D and polymeric immunoglobulin receptor have been found for the first time to be downregulated by dexamethasone in allergic airways. The downregulatory effects were confirmed by immunoblotting and RT-PCR analyses. Dexamethasone was also shown to significantly inhibit lavage fluid chitinase bioactivity. In addition, dexamethasone promoted airway expression of vitamin D-binding protein, heptoglobin and alpha(1)-antitrypsin. CONCLUSIONS: Among all these newly identified protein targets of dexamethasone, AMCase and gob-5 have been shown to be pro-inflammatory in asthma. Downregulation of AMCase and gob-5 may be considered as two novel anti-inflammatory actions of glucocorticoid in asthma.

Animals↗

DNA-binding and cleavage studies of novel binuclear copper(II) complex with 1,1'-dimethyl-2,2'-biimidazole ligand.

DNA-binding properties of novel binulear copper(II) complex [Cu(2)(Dmbiim)(4)(H(2)O)(2)](ClO(4))(4).6H(2)O, where Dmbiim = 1,1'-Dimethyl-2,2'-biimidazole are investigated using electronic absorption spectroscopy, fluorescence spectroscopy, viscosity measurement and voltammetry. The results show that the copper(II) complex interacts with DNA through minor groove binding. The interaction between the complex and DNA has also been investigated by gel electrophoresis, interestingly, we found that the copper(II) complex can cleave circular plasmid pBR322 DNA efficiently in the presence of AH(2) (ascorbic acid) at pH 8.0 and 37 degrees C.

Base Sequence↗

A novel butyrolactone derivative inhibited apoptosis and depressed integrin beta4 expression in vascular endothelial cells.

To understand the effects of a novel butyrolactone derivative, 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one (3BDO), on the apoptosis of vascular endothelial cells (VECs), we exposed 3BDO (20-60 microg/ml) to VECs deprived of serum and FGF-2 for 24 and 48 h, respectively. The results showed that 3BDO (20-60 microg/ml) increased VEC viability and inhibited VEC apoptosis induced by deprivation of serum and FGF-2 in a very weak dose-dependent manner. During this process, integrin beta4 expression was depressed, but the level of reactive oxygen species (ROS) was not changed. The data suggested that 3BDO (20-60 microg/ml) could inhibit VEC apoptosis and suppress integrin beta4 expression, but it could not depress the ROS level induced by deprivation of serum and FGF-2.

4-Butyrolactone↗

Development of a monoclonal antibody-based enzyme-linked immunosorbent assay for the analysis of glycyrrhizic acid.

Glycyrrhizic acid (GL) is a major active compound of licorice. The specific monoclonal antibody (MAb) (designated as 8F8A8H42H7) against GL was produced with the immunogen GL-BSA conjugate. The dissociation constant (Kd) value of the MAb was approximately 9.96x10(-10) M. The cross reactivity of the MAb with glycyrrhetic acid was approximately 2.6%. The conventional indirect competitive enzyme-linked immunosorbent assay (icELISA) and simplified icELISA adapted with a modified procedure were established using the MAb. The IC50 value and the detect range by the conventional icELISA were 1.1 ng mL-1 and 0.2-5.1 ng mL-1, respectively. The IC50 value and the detect range by the simplified icELISA were 5.3 ng mL-1 and 1.2-23.8 ng mL-1, respectively. The two icELISA formats were used to analyze GL contents in the roots of wild licorice and different parts of cultivated licorice (Glycyrrhiza uralensis Fisch). The results obtained with the two icELISAs agreed well with those of the HPLC analysis. The correlation coefficient was more than 0.98 between HPLC and the two icELISAs. The two icELISAs were shown to be appropriate, simple, and effective for the quality control of raw licorice root materials.

Animals↗