Biomedical subjects

Yun Jiang

Publications and source records attributed to Yun Jiang.

24 records · Page 2Linked to original sources

PubMed2003

Lipophilic G-quadruplexes are self-assembled ion pair receptors, and the bound anion modulates the kinetic stability of these complexes.

With an eye toward the eventual selective modification of noncovalent structures, we used ESI-MS, X-ray crystallography, and NMR spectroscopy to study the anion's influence on the structure and dynamics of self-assembled ion pair receptors formed from guanosine G 1. We compared five complexes of formula (G 1)(16).2Ba(2+).4A(-) containing different organic anions: 2,4,6-trinitrophenolate (2), 2,6-dinitrophenolate (3), 4-methyl-2,6-dinitrophenolate (4), 4-methoxy-2,6-dinitrophenolate (5), and 2,5-dinitrophenolate (6). Crystallography reveals that anion-nucleobase hydrogen bond geometry is sensitive to both phenolate basicity and structure. For the 2,6-substituted anions 2-5, progressive shortening of anion-nucleobase hydrogen bonds is correlated with increased phenolate basicity. Lipophilic G-quadruplexes with different anions also have much different kinetic stabilities in CD(2)Cl(2) solution. Proton NMR shows that free 6 exchanges faster with G-quadruplex-bound anion than do the 2,6-dinitrophenolates 2-5. The increased lability of 6 is probably because, unlike the 2,6-dinitrophenolates, this anion cannot effectively chelate separate G(8).M(2+) octamers via anion-nucleobase hydrogen bonds. In addition to these structural effects, the anion's basicity modulates the anion exchange rate between its free and bound states. 2D EXSY NMR shows that 3 and 5 exchange about 7 times slower than the less basic picrate (2). The use of 3, a relatively basic dinitrophenolate that hydrogen bonds with the amino groups of the two "inner" G(4)-quartets, resulted in extraordinary kinetic stabilization of the G-quadruplex in CD(2)Cl(2). Thus, no isomerization product (G 1)(8).Ba(2+).(G 1)(8).Sr(2+).4(3) was observed even 2 months after the separate G-quadruplexes (G 1)(16).2Ba(2+).4(3) and (G 1)(16).2Sr(2+).4(3) were combined in CD(2)Cl(2). In sharp contrast, G-quadruplexes containing the isomeric 6 anion have isomerization half-lives of approximately t(1/2) = 30 min under identical conditions. All the evidence indicates that the structure and electronics of the organic anions, bound to the assembly's periphery, are crucial for controlling the kinetic stability of these cation-filled G-quadruplexes.

Anions↗

PubMed2003

A highly efficient and automated method of purifying and desalting PCR products for analysis by electrospray ionization mass spectrometry.

In this work we present a rapid and fully automated method to purify and desalt PCR products prior to analysis by electrospray ionization mass spectrometry. The protocol employs a commercial pipette tip packed with an anion-exchange resin and comprises four primary steps: tip pretreatment, sample loading, rinsing, and sample elution. This tip-based purification/desalting protocol has two distinct advantages over previously published methods. First, the protocol can be performed either manually (1-12 samples at a time), using a standard p10 manual pipette, or in a fully automated microtiter plate format (96 samples at a time) employing standard laboratory robotics. Additionally, the entire protocol from crude PCR product to an "electrosprayable" analyte solution requires only 10 microl of crude product and takes less than 20 min. Using capillary gel electrophoresis, we demonstrate an overall recovery efficiency of approximately 80% and demonstrate the exquisite desalting efficiency with high-performance electrospray ionization Fourier transform ion cyclotron resonance mass spectrometry. Using an internal mass standard we demonstrate sub-ppm mass measurement error which provides an unambiguous base composition for a 120-mer PCR product.

Bacillus subtilis↗

PubMed2003

[Toxic effects of ammonium perchlorate on thyroid of rats].

OBJECTIVE: To study the effects of toxicity of ammonium perchlorate (AP) on thyroid of rats. METHODS: Eighty-eight Wistar rats were treated orally with different dosages of AP. Three treated groups received 129, 257, 514 mg.kg(-1).d(-1) of AP respectively and one control group drunk water for 13 weeks. Another 3 groups received 1.2, 46.5, 465.0 mg.kg(-1).d(-1) of AP respectively and one control group drunk water for 36 weeks. The behavior and change of body weight in rats were observed. The levels of thyroid hormones in serum were measured and the pathological changes of thyroid tissue were observed as well. RESULTS: There were no differences in behavior and change of body weight between different AP exposure time. When the rats were treated with AP 514 mg for 13 weeks, free triiodothyronine (FT3, 2.48 pmol/L), free thyroxin (FT4, 13.33 pmol/L) were lower than those in control group (3.24, 20.92 pmol/L respectively, P<0.05). Thyroid-stimulating hormone (TSH, 0.375 mIU/L), thyroglobulin (TG, 3.37 microg/L) were higher than those in control group (0.29 mIU/L, 2.00 microg/L respectively, P<0.05). When the rats were treated with AP 465 mg for 36 weeks, FT3 (2.65 pmol/L) was lower than that in control group (4.97 pmol/L, P<0.01). FT4 in 46.5, 465 mg groups (10.63, 2.17 pmol/L respectively) were lower than that in control group (15.74 pmol/L, P<0.05, P<0.01). TSH in 465 mg group (0.34 mIU/L) was higher than that in control group (0.14 mIU/L, P<0.05). Histopathologic examination showed that follicle proliferation, no colloid in follicle, gore, follicular diminishing or atresia were found in 46.5, 465 mg groups with a dose-effect relationship. CONCLUSIONS: The toxic effects of AP on the growth of rats were not found, but those on the thyroid of rats were found significantly. Thyroid is the target organ of AP. It is considered that none effect dose of AP for rat thyroid may be 1.2 mg.kg(-1).d(-1), its threshold dose may be 46.5 mg.kg(-1).d(-1).

Animals↗

PubMed2002

Growth hormone increases circulating neutrophil activation and provokes lung microvascular injury in septic peritonitis rats.

BACKGROUND: Growth hormone (GH) has been shown to increase mortality in critical illness, illustrating the need for better understanding of GH treatment. The neutrophil is a key mediator in producing organ injury following shock and trauma and is regulated by GH. Therefore, the purpose of the present study was to examine the effects of GH on circulating neutrophil activation and subsequent lung injury induced by sepsis in rats. MATERIALS AND METHODS: Sepsis was induced in male Wistar rats via cecal ligation and puncture (CLP). Recombinant human growth hormone (1 IU/kg) was given subcutaneously right after CLP with an additional injection at 12 h after CLP. CD11b expression and an oxidative burst of neutrophils were detected using flow cytometric analysis. Lung myeloperoxidase activity was determined as an index of tissue neutrophil accumulation. Lung microvascular injury was assessed by quantitating extravasation of Evan's blue dye into lung parenchyma. RESULTS: Growth hormone significantly increased sepsis-induced expression of CD11b and sepsis-induced circulating neutrophil activation. Also growth hormone increased neutrophil accumulation in lungs induced by sepsis. Lung microvascular injury was aggravated by growth hormone treatment in septic rats. CONCLUSIONS: It is worthwhile to rethink GH administration in critical illness and further studies are required to determine the safety and clinical benefits of GH administration in critical illness.

Animals↗

PubMed2002

DQ 65-79, a peptide derived from HLA class II, induces I kappa B expression.

A synthetic peptide corresponding to residues 65-79 of the alpha helix of the alpha-chain of the class II HLA molecule DQA03011 (DQ 65-79) inhibits the proliferation of human T lymphocytes in an allele nonrestricted manner. By using microarray technology, we found that expression of 29 genes was increased or decreased in a human CTL cell line after treatment with DQ 65-79. This study focuses on one of these genes, IkappaB-alpha, whose expression is increased by DQ 65-79. IkappaB proteins, including IkappaB-alpha and IkappaB-beta, are increased in T cells treated with DQ 65-79. Nuclear translocation of the NF-kappaB subunits p65 and p50 is decreased in T cells after treatment with DQ 65-79, while elevated levels of p65 and p50 are present in cytosol. DQ 65-79 inhibits the degradation of IkappaB-alpha mRNA and inhibits the activity of IkappaB kinase. These findings indicate that the DQ 65-79 peptide increases the level of IkappaB proteins, thereby preventing nuclear translocation of the transcription factor, NF-kappaB, and inhibiting T cell proliferation.

Amino Acid Sequence↗

PubMed2002

Growth hormone increases lung NF-kappaB activation and lung microvascular injury induced by lipopolysaccharide in rats.

The purpose of this study was to examine the effects of growth hormone (GH) on nuclear factor kappa B (NF-kappaB) activation and organ injury induced by lipopolysaccharide (LPS) in rats. Male Wistar rats were divided into 6 groups treated with saline, LPS (5 mg/kg), LPS plus GH (0.5, 1.0, 2.0 mg/kg), or GH (2.0 mg/kg) alone for 2 or 4 hr. NF-kappaB activity and I-kappaB level in lung, lung accumulation of neutrophils, and lung microvascular injury were measured. LPS-challenged rats had increased NF-kappaB activity and decreased I-kappaB level in lung, compared to controls. GH dramatically enhanced NF-kappaB activation and I-kappaB degradation induced by LPS challenge. LPS plus GH treatment increased lung accumulation of neutrophils, compared with LPS treatment. Also, subsequently, GH treatment increased lung microvascular injury induced by LPS. These findings suggest that treatment with GH is harmful, instead of beneficial, to LPS-induced organ injury. Increased NF-kappaB activation may be a critical in vivo mechanism that mediates GH action on LPS-induced organ injury. Thus, it is appropriate to rethink GH administration in critical illnesses; further studies are required to evaluate the safety and clinical benefits of GH administration in such conditions.

Animals↗