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Biomedical subjects

Jing Zhang

Publications and source records attributed to Jing Zhang.

At least 109 records · Page 6Linked to original sources

UV Raman spectroscopic study on TiO2. I. Phase transformation at the surface and in the bulk.

Phase transformation of TiO2 from anatase to rutile is studied by UV Raman spectroscopy excited by 325 and 244 nm lasers, visible Raman spectroscopy excited by 532 nm laser, X-ray diffraction (XRD), and transmission electron microscopy (TEM). UV Raman spectroscopy is found to be more sensitive to the surface region of TiO2 than visible Raman spectroscopy and XRD because TiO2 strongly absorbs UV light. The anatase phase is detected by UV Raman spectroscopy for the sample calcined at higher temperatures than when it is detected by visible Raman spectroscopy and XRD. The inconsistency in the results from the above three techniques suggests that the anatase phase of TiO2 at the surface region can remain at relatively higher calcination temperatures than that in the bulk during the phase transformation. The TEM results show that small particles agglomerate into big particles when the TiO2 sample is calcined at elevated temperatures and the agglomeration of the TiO2 particles is along with the phase transformation from anatase to rutile. It is suggested that the rutile phase starts to form at the interfaces between the anatase particles in the agglomerated TiO2 particles; namely, the anatase phase in the inner region of the agglomerated TiO2 particles turns out to change into the rutile phase more easily than that in the outer surface region of the agglomerated TiO2 particles. When the anatase particles of TiO2 are covered with highly dispersed La2O3, the phase transformation in both the bulk and surface regions is significantly retarded, owing to avoiding direct contact of the anatase particles and occupying the surface defect sites of the anatase particles by La2O3.

Hot Temperature↗

C-reactive protein induced expression of adhesion molecules in cultured cerebral microvascular endothelial cells.

Ischemic stroke can trigger an acute phase response resulting in a rise of plasma concentration of C-reactive protein (CRP). Clinical data about the relationship between CRP and prognosis suggest that CRP might be involved in the pathogenesis of cerebral ischemia. In the present work, a significant increase of circulating level of CRP was observed in an vivo rat brain ischemia model of middle cerebral artery occlusion. To determine the possible effects of CRP on brain microvessel endothelium, we performed a dose-dependent experiment in mouse brain microvascular endothelial cells (bEnd.3 cells) with emphasis on its relation to cell adhesions molecules. Incubation with CRP (1-75 mg/L) for 24 h significantly increased Lactate dehydrogenase (LDH) leakage from bEnd.3 cells (P<0.01) in a dose-dependent manner, and induced significant up-regulations of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions analyzed by Western blotting (P<0.01). In contrast to earlier report, CRP also induced significant increase in ICAM-1 expression in the absence of serum (P<0.01). In conclusion, the present results suggest that CRP may be involved directly in the development of inflammation in response to cerebral ischemia.

Animals↗

Intermedin1-53 activates L-arginine/nitric oxide synthase/nitric oxide pathway in rat aortas.

Intermedin (IMD), a novel member of the calcitonin/calcitonin gene-related peptide (CGRP) family, has similar or more potent vasodilatory and hypotensive actions than adrenomedullin (ADM) and CGRP. The present study was designed to observe the effects of synthetic rat IMD1-53 on L-arginine (L-Arg) cellular transport, nitric oxide synthase (NOS) activity, and nitric oxide (NO) production in the isolated rat aortic ring to illustrate its direct effect on the L-Arg/NOS/NO pathway in vasculature. IMD1-53 significantly increased NO production and cNOS activity in rat aortas and was more potent than equivalent ADM. But the peptides of both IMD and ADM had no effect on inducible NOS expression and activity. Otherwise, IMD1-53 induced a concentration-dependent increase in [3H]L-Arg transport and its effect was more potent than that of an equivalent concentration of ADM. Semiquantitative RT-PCR revealed that IMD1-53 significantly increased cationic amino acid transport (CAT)-1 and CAT-2B mRNA expression, and its effect was similar to that of ADM. All these results suggest that IMD1-53 might regulate vessel function homeostasis via upregulating the L-Arg/NOS/NO pathway.

Adrenomedullin↗

Extracellular TNFR1 release requires the calcium-dependent formation of a nucleobindin 2-ARTS-1 complex.

Extracellular tumor necrosis factor (TNF) receptors function as TNF-binding proteins that modulate TNF activity. In human vascular endothelial cells (HUVEC), extracellular TNFR1 (type I TNF receptor, TNFRSF1A) is generated by two mechanisms, proteolytic cleavage of soluble TNFR1 ectodomains and the release of full-length 55-kDa TNFR1 in the membranes of exosome-like vesicles. TNFR1 release from HUVEC is known to involve the association between ARTS-1 (aminopeptidase regulator of TNFR1 shedding), an integral membrane aminopeptidase, and TNFR1. The goal of this study was to identify ARTS-1 binding partners that modulate TNFR1 release to the extracellular space. A yeast two-hybrid screen of a human placenta cDNA library showed that NUCB2 (nucleobindin 2), via its helix-loop-helix domains, binds the ARTS-1 extracellular domain. The association between endogenous ARTS-1 and NUCB2 in HUVEC was demonstrated by co-immunoprecipitation experiments, which showed the formation of a calcium-dependent NUCB2.ARTS-1 complex that associated with a subset of total cellular TNFR1. Confocal microscopy experiments demonstrated that this association involved a distinct population of NUCB2-containing intracytoplasmic vesicles. RNA interference was utilized to specifically knock down NUCB2 and ARTS-1 expression, which demonstrated that both are required for the constitutive release of a full-length 55-kDa TNFR1 within exosome-like vesicles as well as the inducible proteolytic cleavage of soluble TNFR1 ectodomains. We propose that calcium-dependent NUCB2.ARTS-1 complexes, which associate with TNFR1 prior to its commitment to pathways that result in either the constitutive release of TNFR1 exosome-like vesicles or the inducible proteolytic cleavage of TNFR1 ectodomains, play an important role in mediating TNFR1 release to the extracellular compartment.

Aminopeptidases↗

Characterization of an anti-thioredoxin monoclonal antibody.

An anti-E. coli thioredoxin monoclonal antibody, IMM-3C6, which showed high specificity to thioredoxin as assessed by indirect ELISA, was generated using hybridoma technology. The affinity constant of IMM-3C6 to thioredoxin was 0.40 x 10(9) M: (-1) and its sensitivity to thioredoxin fusion protein in dot blotting was 50 ng. In sandwich ELISA, it detected thioredoxin fusion protein between 16 and 150 ng/ml. By using IMM-3C6 as the ligand, thioredoxin fusion protein was successfully purified by affinity chromatography. IMM-3C6 was confirmed to be a useful tool for immunoassay and purification of thioredoxin fusion proteins.

Animals↗

Molecular characterization of a bacterial consortium enriched from an oilfield that degrades phenanthrene.

Characterization of functional and phylogenetic genes was carried out on a bacterial consortium, enriched from a water treatment system of an oilfield, that could use phenanthrene as the sole carbon source. The mixed culture degraded 130 mg phenanthrene l(-1) in 16 days, which is significantly faster than previously reported pure cultures. The existence of catabolic genes (nahAc, C23O) in the mixed culture was quantitated by most probable number PCR. The plasmid encoding phenanthrene catabolic genes increased relative to the chromosome genes. Heterogeneous bacteria were present according to both PCR denaturing gradient gel electrophoresis and cloning methods, suggesting the possible existence of cooperation between different biochemical PAH-transforming pathways.

Bacteria↗

Isolation and characterization of a pseudomonas oleovorans degrading the chloroacetamide herbicide acetochlor.

To date, no pure bacterial cultures that could degrade acetochlor have been described. In this study, one strain of microorganism capable of degrading acetochlor, designated as LCa2, was isolated from acetochlor-contaminated soil. The strain LCa2 is Pseudomonas oleovorans according to the criteria of Bergey's manual of determinative bacteriology and sequence analysis of the partial 16S rRNA gene. Optimum growth temperature and pH were 35 degrees C and 8.0, respectively. The strain could degrade 98.03% of acetochlor treated at a concentration of 7.6 mg l(-1) after 7 days of incubation and could tolerate 200 mg l(-1) of acetochlor. When the acetochlor concentration became higher, the degradation cycle became longer. The acetochlor biodegradation products were identified by GC-MS based on mass spectral data and fragmentation patterns. The main plausible degradative pathways involved dechlorination, hydroxylation, N-dealkylation, C-dealkylation and dehydrogenation.

Herbicides↗

Pacing the gut in motility disorders.

Similar to cardiac pacing, gastrointestinal (GI) pacing is an attractive idea and may become a promising therapy, as the GI organs, like the heart, have their own natural pacemakers. Over the past 10 years, electrical stimulation of the gut has received increasing attention among researchers and clinicians. Several clinical studies have shown that gastric electrical stimulation (GES) with short pulses is able to reduce nausea and vomiting in patients with gastroparesis and that GES with long pulses is able to pace the intrinsic gastric slow waves and thus normalize gastric dysrhythmia. However, possible placebo effects cannot be ruled out, although recent animal studies have revealed various peripheral and central mechanisms involved with GES. Electrical stimulation of the small intestine, colon, or anal sphincter also has been reported for the treatment of dumping syndrome, constipation, and fecal incontinency. Similarly, there is a lack of placebo-controlled studies. In our opinion, pacing of the gut has great potential for the treatment of various GI motor disorders. However, none of the commercially available devices is designed for pacing the gut. The lack of well-suited devices and the invasive nature of gut pacing slow down the progress and clinical applications of gut pacing.

Journal Article↗

Lymphatic vessel density as a prognostic indicator for patients with stage I cervical carcinoma.

Lymphatic vessel density (LVD) was recently considered important for spread of several malignant tumors. However, there are no reports describing the situation in cervical carcinoma. The purpose of this study was to investigate whether LVD could serve as a risk factor for nodal metastasis and recurrence of cervical carcinoma in 147 cases of stage I patients. Other questions were if depth of invasion, proliferation rate, and tumor size could be used as predictive markers for Chinese patients with cervical carcinoma. The lymphatics were determined by immunohistochemistry with the antibody to LYVE-1, a specific lymphatic endothelium marker, and average LVD was calculated. Double immunohistochemistry and double immunofluorescence staining for LYVE-1/CD34 were used to distinguish between lymphatic and blood vessels. The results showed that average LVD in cervical carcinoma was statistically associated with inflammatory cell infiltration of carcinoma tissues, but not associated with other pathological parameters. Average LVD of the cases with nodal metastasis or recurrence was significantly higher than the cases without metastasis and recurrence in both stage IA and stage IB cervical carcinomas. The correlation between both depth of invasion and tumor size with nodal metastasis and recurrence of cervical carcinoma was also statistically significant. Ki-67 labeling index was found to be correlated with the recurrence of disease, but not to be correlated with nodal metastasis. We concluded that for the patients with stage I cervical carcinoma, increased LVD could serve as a high-risk factor for nodal metastasis and recurrence. Depth of invasion and tumor size could also be useful indicators.

Biomarkers, Tumor↗

Excitatory effects of gastric electrical stimulation on gastric distension responsive neurons in ventromedial hypothalamus (VMH) in rats.

INTRODUCTION: Gastric electrical stimulation (GES) has been used for the treatment of obesity with unclear central mechanisms. The purpose of this study was to investigate the effects of GES on the neuronal activity in the ventromedial hypothalamus (VMH). METHODS: Extracellular potentials of single neurons in VMH were recorded in 52 anesthetized rats. Neurons were classified as gastric distension-excitatory (GD-E) neurons or GD-inhibitory (GD-I) neurons. GES with four sets of parameters was applied for comparison. RESULTS: Eighty two neurons out of 96 (85.41%) in VMH responded to gastric distension (GD). 37.8% were GD-E neurons and 51(62.2%) were GD-I neurons. 55.0%, 17.6%, 77.8%, 14.3% of GD-E neurons were excited by four sets of parameters: GES1 (standard), GES2 (reduced pulse numbers), GES3 (increased pulse width) and GES4 (reduced frequency), respectively. More GD-E neurons were excited by GES3 (P < 0.05 versus GES2 or GES4) and by GES1 (P < 0.02 versus GES2 or GES4). Among the GD-I neurons, 63.6, 37.9, 73.3, and 51.9% neurons were excited by GES1-4, respectively. CONCLUSION: GES with parameters used for treating obesity excites GD-responsive neurons in VMH. The excitatory effect of GES is related to the strength of stimulation, including pulse frequency and width as well as pulse train on-time.

Action Potentials↗

Liquid chromatography with tandem mass spectrometry-based proteomic discovery in aging and Alzheimer's disease.

Systems biology offers enormous potential to understand the complexity of human brain aging and neurodegenerative diseases. Proteomics has an important role in these investigations because of its unique strengths and because of the potential central pathogenic contribution of pathological protein to several of these diseases. Here we have reviewed the methods and presented some examples of liquid chromatography-electrospray ionization-tandem mass spectrometry-based proteomics, with and without quantification using isotope-coded affinity tags, in the investigation of aging and Alzheimer's disease. As protocols and methods for improved quantitative high-throughput proteomics constantly improve, this approach will likely continue to provide deeper insight into human brain aging and neurodegenerative diseases.

Aging↗

Identification of glycoproteins in human cerebrospinal fluid with a complementary proteomic approach.

Biomarkers are pressingly needed to assist with the clinical diagnosis of neurodegenerative diseases and/or the monitoring of disease progression. Glycoproteins are enriched in bodily fluids such as human cerebrospinal fluid (CSF), an ideal source for discovering biomarkers due to its proximity to the central nervous system (CNS), and consequently can serve as diagnostic and/or therapeutic markers for CNS diseases. We report here an in-depth identification of glycoproteins in human CSF using a complementary proteomic approach which integrated hydrazide chemistry and lectin affinity column for glycoprotein enrichment, followed by multidimensional chromatography separation and tandem mass spectrometric analysis. Using stringent criteria, a total of 216 glycoproteins, including many low-abundance proteins, was identified with high confidence. Approximately one-third of these proteins was already known to be relevant to the CNS structurally or functionally. This investigation, for the first time, not only categorized many glycoproteins in human CSF but also expanded the existing overall CSF protein database.

Adult↗

Reverse gastric pacing reduces food intake without inducing symptoms in dogs.

OBJECTIVE: To investigate the therapeutic potential of reverse gastric pacing (RGP) for obesity by studying the effects of RGP on food intake and symptoms in dogs. MATERIAL AND METHODS: The study was performed in 9 dogs in 3 sessions (control, strong RGP and moderate RGP). Gastric myoelectrical activity and food intake were measured in each session. RGP was performed using serosal electrodes implanted in the distal stomach at the physiological frequency of the intrinsic gastric myoelectrical activity with a pulse width of 550-950 ms. The amplitude of the stimulus was set at a level maximally tolerable by the animals in the strong RGP session and 50% of the maximum level in the moderate session. RESULTS: 1) Compared with the control, strong RGP (p<0.001) and moderate RGP (p<0.01) significantly reduced the amount of food intake by 62.9% and 31.7%, respectively (p<0.05, ANOVA). 2) Whereas strong RGP induced significant symptoms, moderate RGP did not induce any significant symptoms in comparison with the control session. 3) The regularity and coupling of gastric myoelectrical activity were significantly impaired with both strong RGP and moderate RGP in the fasting state. CONCLUSIONS: RGP impairs intrinsic gastric myoelectrical activity and substantially and acutely reduces food intake. The reduced food intake and freedom from symptoms resulting from moderate RGP are indicative of the therapeutic potential of RGP in obesity.

Animals↗

Preparation of tissue-specific monoclonal antibodies using purified endothelial membrane proteins from biotinylated pulmonary vasculature of rhesus monkey.

In the present study, we perfused the rhesus lung vascular bed in situ with sulfo-NHS-LC-Biotin to biotinylate its luminal surface membrane proteins. After homogenization, dialysis, and affinity chromatography, biotinylated endothelial membrane proteins were successfully isolated and characterized as enriched endothelial membrane proteins with no contamination of intracellular proteins. When they were used as immunogens to develop monoclonal antibodies (MAbs), three MAbs--TX111, TX112, and TX113--were obtained. Among them, TX111 was demonstrated to specifically bind to rhesus lung tissue by Western blotting and enzymelinked immunosorbent assay (ELISA)--that is, positively stained capillary endothelium of rhesus lung. The molecular weight of the corresponding antigen for TX111 was approximately 70 kDa under reducing conditions. TX111 also reacted with human lung homogenate, but not with rat lung homogenate. These results suggest that (1) the biotinylation method is applicable for isolating endothelial proteins in situ from large animals; (2) anti-human protein MAbs are likely to be obtained using monkey proteins; and (3) TX111 is potentially useful for pulmonary vascular targeting.

Animals↗

A study of the diagnostic utility of HLA typing, CSF hypocretin-1 measurements, and MSLT testing for the diagnosis of narcolepsy in 163 Korean patients with unexplained excessive daytime sleepiness.

STUDY OBJECTIVE: To study DQB1*0602 status and hypocretin-1 levels in the cerebrospinal fluid (CSF) in a cohort of patients with hypersomnolence and to test International Classification of Sleep Disorders-2 (ICSD-2) criteria for hypersomnia of central origin. DESIGN: Retrospective case series. PATIENTS AND SETTING: One hundred sixty-three consecutive patients with unexplained sleepiness and 282 controls recruited at St. Vincent's Hospital, Korea. The gold standard for diagnosis was ICSD-2 criteria. Patients and controls completed the Stanford Sleep Inventory, and agreed to HLA typing. Polysomnography (87%), Multiple Sleep Latency Test (MSLT) (96%), and CSF hypocretin-1 measurements (53%) were conducted in patients. MEASUREMENTS AND RESULTS: Most patients (80%) could be classified using the ICSD-2. The 33 patients who could not be classified were without cataplexy (4 with low CSF hypocretin-1). These could not be included because of sleep apnea (apnea-hypopnea index > or = 5/h, 84%) and/or because sleep prior to MSLT was less than 6 hours (27%). Narcolepsy with cataplexy cases were 92% HLA positive with low hypocretin-1. Cataplexy at interview was predicted by validated Stanford Sleep Inventory questions regarding cataplexy triggers. In contrast, cataplexy-like events were frequently reported in all groups, including controls. Cases with narcolepsy without cataplexy were frequently men (73%) and heterogeneous biologically (36% HLA positive, 40% with low CSF hypocretin-1). None of the controls had low CSF hypocretin-1, whereas 13% were HLA positive. CONCLUSION: The ICSD-2 was easily applicable in cases with typical cataplexy. In these cases, the MSLT and further evaluations were almost always positive and may thus not always be needed. Many patients without cataplexy were difficult to classify because of difficulties in interpreting the MSLT in the presence of sleep apnea or reduced sleep.

Adult↗

CSF versus serum leptin in narcolepsy: is there an effect of hypocretin deficiency?

STUDY OBJECTIVE: To determine if hypocretin deficiency is associated with abnormally low serum leptin levels, a putative cause of increased body mass index in narcoleptics. DESIGN: Cross-sectional controlled study. PARTICIPANTS: Three hundred seventy subjects, including 111 healthy controls, 93 narcoleptic subjects with hypocretin deficiency (cerebrospinal fluid [CSF] hypocretin-1 levels < 110 pg/mL), 72 narcoleptic subjects with normal hypocretin levels, and 89 subjects with other sleep disorders INTERVENTION: After completing the Stanford Sleepiness Inventory, participants underwent spinal taps and blood sampling for measurement of CSF leptin and hypocretin-1 levels, HLA DQB1*0602 phenotyping, and serum leptin and C-reactive protein levels. RESULTS: Serum leptin levels were similar in narcoleptic subjects, whether hypocretin-deficient (13.2 +/- 1.7 ng/mL, mean +/- SEM) or not (13.0 +/- 1.8 ng/mL), controls (10.1 +/- 1.1 ng/mL) and subjects with other sleep disorders (11.5 +/- 1.6 ng/mL). Similarly, the CSF leptin levels and the CSF: serum leptin ratios (an indicator of brain leptin uptake) were not different between groups. Serum and CSF leptin levels were higher in women and in subjects with higher body mass indexes. Leptin brain uptake decreased in women, in the aged, and in more-obese subjects. In contrast with a presumed inhibitory effect of leptin on hypocretin-containing cells, CSF leptin levels tended to correlate positively with CSF hypocretin-1 levels. C-reactive protein was higher (4.2 +/- 0.9 mg/L) in narcoleptic subjects with hypocretin deficiency than in controls (1.4 +/- 0.3 mg/L, p = .0055), a difference still significant after adjustment on confounding factors. DISCUSSION: Our data do not support a role for leptin in mediating increased body mass index in narcolepsy. A moderate but selective increase in C-reactive protein in hypocretin-1 deficient subjects should prompt research on inflammation in narcolepsy.

Adult↗

Toll-like receptor 3 agonist poly(I:C)-induced antiviral response in human corneal epithelial cells.

The objective of this study was to examine the expression of Toll-like receptor 3 (TLR3) by human corneal epithelial cells (HCECs) and to determine whether exposure to the TLR3 agonist polyinosinic-polycytidylic acid [poly(I:C)] induces an antiviral response in these cells. Fluorescence-activated cell sorter (FACS) analysis revealed TLR3 to be constitutively expressed and distributed intracellularly in HCECs. Stimulation of HCECs with the TLR3 agonist poly(I:C) induced the activation of nuclear factor (NF)-kappaB and production of the proinflammatory cytokine interleukin (IL)-6 and the chemokine IL-8. Upon exposure to poly(I:C), HCECs initiated a potent antiviral response resulting in an increase of interferon (IFN)-beta mRNA expression (7-fold). Poly(I:C) stimulation also up-regulated mRNA expression of the antiviral chemokine IFN-gamma inducible protein 10 (IP10), myxovirus resistance gene A and 2',5'-oligoadenylate synthetase (5-, 10- and 9-fold, respectively), and secretion of IP10. These responses were also induced by exogenously added type 1 IFNs, but could not be blocked by pretreatment of the cells with anti-TLR3 monoclonal antibody, suggesting that the receptor was not expressed on the cell surface. Furthermore, incubation of HCECs with an endosomal acidification inhibitor, chloroquine, markedly inhibited poly(I:C)-mediated IFN-beta expression in HCECs. These results suggest that corneal epithelial cells are important sentinels of the corneal innate immune system against viral infection, and that stimulation of TLR3 can induce the expression of key proinflammatory cytokines and chemokines and antiviral genes that help in the defence of the cornea against viral infection.

2',5'-Oligoadenylate Synthetase↗