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Ying Li

Publications and source records attributed to Ying Li.

At least 91 records · Page 5Linked to original sources

Characteristics of antiaromatic ring pi multi-hydrogen bonds in (H2O)n-C4H4 (n = 1, 2) complexes.

By counterpoise-corrected optimization method, the six antiaromatic ring pi multi-hydrogen bond structures with diversiform shapes for (H2O)n-C4H4 (n = 1,2) have been obtained at the MP2/aug-cc-pVDZ level. At the CCSD(T)/aug-cc-pVDZ level, the interaction energy obtained mainly depends on the numbers of H2O and fold numbers of the pi multi-hydrogen bond. The interaction energy order is -2.342 (1a with pi mono-hydrogen) < -2.777 (1b with pi bi-hydrogen) << -4.683 (2a with pi bi-hydrogen) < -4.734 (2b with pi tri-hydrogen) < -4.782 (2c with pi tri-hydrogen) < -5.009 kcal/mol (2d with pi tetra-hydrogen bond). Strangely, why is the interaction energy of the pi bi-hydrogen bond in 1b close to that of the pi mono-hydrogen bond in 1a (their difference is only 15.7%)? The reason is that a pi-type H-bond (as an accompanying interaction) between two lone pairs of the O-atom and a near pair of H-atoms of C4H4 exists shoulder by shoulder in structures 1a, 2a, 2b, and 2c and contributes to the interaction energy. Another accompanying interaction, a repulsive interaction between the pi H-bond (using the H-atom(s) of H2O) and the near pair of H-atoms of C4H4, is also found. For the structures and interaction energies, the pi-type H-bond produces four effects: bending the strong pi H-bond, attracting the pair of H-atoms of C4H4 so that they deviate from the C4 ring plane, showing the interaction energy contribution, and bringing the larger electron correlation contribution. The repulsive interaction also produces four effects: pushing the pair of H-atoms of C4H4 so that they deviate from its ring plane, elongating the distance of the pi H-bond, promoting the formation of pi-type H-bond, and slightly influencing the interaction energy. In the present paper, one C=C bond with two H2O (over and below the ring plane) forms a pi H-bond link in two ways: a strong-weak pi H-bond link and a strong-strong pi H-bond link. The stability contribution of the former is more favorable than the latter. One H2O forms a pi H-bond with C4H4 in two ways. One strong pi H-bond part (over or below the ring plane) always is accompanied by another H-bond part. The accompanying part is either a weak pi H-bond or pi-type H-bond.

Computer Simulation↗

State-dependent gating of sensory inputs by zona incerta.

We have previously shown that the GABAergic nucleus zona incerta (ZI) suppresses vibrissae-evoked responses in the posterior medial (POm) thalamus of the rodent somatosensory system. We proposed that this inhibitory incerto-thalamic pathway regulates POm responses during different behavioral states. Here we tested the hypothesis that the cholinergic reticular activating system, implicated in regulating states of arousal, modulates ZI activity. We show that stimulation of brain stem cholinergic nuclei (laterodorsal tegmental and pedunculopontine tegmental) results in suppression of spontaneous firing of ZI neurons. Iontophoretic application of the cholinergic agonist carbachol to ZI neurons suppresses both their spontaneous firing and their vibrissae-evoked responses. We also found that carbachol application to an in vitro slice preparation suppresses spontaneous firing of neurons in the ventral sector of ZI (ZIv). Finally, we demonstrate that the majority of ZIv neurons contain parvalbumin and project to POm. Based on these results, we present the state-dependent gating hypothesis, which states that differing behavioral states-regulated by the brain stem cholinergic system-modulate ZI activity, thereby regulating the response properties of higher-order nuclei such as POm.

Animals↗

Current controlled spin reversal of nanomagnets with giant uniaxial anisotropy.

Since a giant magnetic anisotropy of 9 meV per atom has been realized on a Pt surface, we use the kinetic Monte Carlo method to study the spin dynamics of a nanomagnet that is made by putting a line of such adatoms on a thin metallic strip so that the fixed spins are coupled very weakly and a spin-polarized current can be injected into the strip. There is a magnetization hysteresis versus the current because of the giant anisotropy. The hysteresis loop is diminished exponentially with the temperature increasing. The magnetization can be controlled by injecting a spin-polarized current.

Journal Article↗

ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding.

L-selectin directs neutrophils to sites of inflammation, and upon their activation, surface expression of the receptor is rapidly down-regulated by ectodomain shedding. Tumor necrosis factor-alpha-converting enzyme (TACE, or ADAM17) is a sheddase of L-selectin; however, Adam17 gene targeting (ADAM17(DeltaZn/DeltaZn)) in mice is perinatal lethal and its role in L-selectin shedding by mature neutrophils has not been determined. This was addressed here by using radiation-chimeric mice reconstituted with ADAM17(DeltaZn/DeltaZn) fetal liver cells. ADAM17-deficient neutrophils, monocytes, and lymphocytes failed to shed L-selectin in response to PMA, as did neutrophils infiltrating the inflamed peritoneum. In addition, the absence of functional ADAM17 resulted in significantly increased levels of L-selectin surface expression by peripheral-blood leukocytes, indicating the sheddase also plays a role in the constitutive cleavage of L-selectin. Interestingly, not all manners of L-selectin turnover required ADAM17. Plasma L-selectin levels were similar between ADAM17(DeltaZn/DeltaZn)-chimeric and control mice, as was the shedding of L-selectin by neutrophils undergoing spontaneous apoptosis. The latter process, however, was diminished by a metalloprotease inhibitor, indicating the role of a sheddase other than ADAM17. Together, our data reveal that L-selectin's surface density on neutrophils is regulated by ADAM17, but homeostatic L-selectin cleavage is not.

ADAM Proteins↗

RETRACTED: Investigation on photocatalytic degradation of ethyl violet dyestuff using visible light in the presence of ordinary rutile TiO2 catalyst doped with upconversion luminescence agent.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. After careful investigations the editors have found that information in the paper is not reliable. Figure 4 appears similar to Figure 2 from another publication of the same authors in Dyes and Pigments 75 (2007) 335-343 https://doi.org/10.1016/j.dyepig.2006.06.007 which it is not describing the particles discussed in this Water Research paper. Although this article was published earlier than the Dyes and Pigments article, the Editor decided to retract this article given concerns about the reliability of the data.

Catalysis↗

In vitro release and in vivo absorption in beagle dogs of meloxicam from Eudragit FS 30 D-coated pellets.

The objective of this study was to develop meloxicam-loaded colon-specific pellets coated with Eudragit FS 30 D and further evaluate their in vitro release and in vivo absorption in beagle dogs. Meloxicam-loaded cores (drug loading, 4.8%, w/w) were prepared by layering drug-binder (HPMC)-solubilizer (beta-cyclodextrin) solution onto nonpareils (710-850 microm) and then coated with a copolymer of methyl acrylate, methyl methacrylate and methacrylic acid (Eudragit FS 30 D). The obtained pellets with 15% (w/w) coating level had a spherical form and a smooth surface with coating thickness approximately 28 microm. The in vitro drug release from the pellets was pH-dependent with sufficient gastric resistance (pH 1.2: no release; pH 6.8: 6%; pH 7.0: 52%; pH 7.2: 100%; pH 7.4: 100%, after 3 h incubation). In vivo study was carried out using pentagastrin-pretreated beagle dogs. The onset of meloxicam absorption from the coated pellets with 15% (w/w) Eudragit FS 30 D (3.0+/-0.8 h) was significantly delayed (p<0.05) compared to that from the uncoated drug-layered cores (0.6+/-0.3 h). The area under the meloxicam plasma concentration-time curve (AUC(0-->96)(h) was not significantly different between the two preparations (p>0.05), although AUC(0-->96)(h) obtained after oral administration of coated pellets (142.5+/-59.6 microg h/ml) was lower than that obtained after administration of uncoated drug-layered cores (180.8+/-61.9 microg h/ml). These results suggested that meloxicam could be delivered to the colon with 15% (w/w) coating level of Eudragit FS 30 D and this polymer coating had no significant influence on the relative bioavailability of meloxicam of the pellets.

Animals↗

Investigation on the sonocatalytic degradation of parathion in the presence of nanometer rutile titanium dioxide (TiO2) catalyst.

The nanometer rutile titanium dioxide (TiO2) powder was adopted to act as the sonocatalyst after treatment of high-temperature activation and the ultrasound of low power was used as an irradiation source to induce heat-treated TiO2 powder performing sonocatalytic degradation of parathion. Although there are many factors influencing sonocatalytic degradation of parathion, the experimental results demonstrate that the optimal degradation condition of parathion can be obtained when the experimental conditions such as initial concentration of 50 mg/L parathion, addition amount of 1000 mg/L nanometer rutile TiO2, ultrasonic of 30-50 kHz frequency and 50 W output power, acidity of pH 10.0 and temperature of 20 degrees C are adopted. The degradation ratio of parathion surpassed 90% within 120 min ultrasonic irradiation in these optimal experiment conditions. The total degradation process of parathion has been monitored by UV-vis spectra and ion chromatography. At last, the parathions in aqueous solution are completely degraded and become some simple inorganic ions such as NO3(-), PO4(3-), SO4(2-), etc. In addition, the sonocatalytic activities of reused TiO2 catalysts were also studied and found to decline gradually along with the reused times. In this paper, the research on sonocatalytic degradation kinetics was also been performed and found to follow pseudo first-order reaction. All experiments indicated that the sonocatalytic method in the presence of nanometer rutile TiO2 powder was an advisable choice for the treatments of non- or low-transparent organic wastewaters in future.

Catalysis↗

Novel superalkali superhalogen compounds (Li3)+(SH)- (SH=LiF2, BeF3, and BF4) with aromaticity: new electrides and alkalides.

Optimized structures, with all real frequencies, of superalkali superhalides (Li(3))(+)(SH)(-) (SH=LiF(2), BeF(3), and BF(4)), are obtained, for the first time, at the B3LYP/aug-cc-pVDZ and MP2/aug-cc-pVDZ computational levels. These superalkali superhalides possess three characteristics that are significantly different from normal alkali halides. 1) They have a variety of structures, which come from five bonding mode types: edge-face, edge-edge, face-face, face-edge, and staggered face-edge. We find that the bonding mode type closely correlates with the Li(3)-SH bond energy. 2) The valence electrons on the Li(3) ring are pushed out by the (SH)(-) anion, and become excess electrons, conferring alkalide or electride characteristics on these Li(3)-SH species, depending on the bonding mode type. 3) The highest occupied molecular orbital of each Li(3)-SH species is a doubly occupied delocalized sigma bonding orbital on the Li(3) ring, which indicates its aromaticity. It is noticeable that the maximum negative nucleus-independent chemical shift value (about -10 ppm) moves out from the center of the Li(3) ring, owing to repulsion by the SH(-) anion. We find that these superalkali superhalides are not only complicated "supermolecules", but are also a new type of alkalide or electride, with aromaticity.

Journal Article↗

Gene expression profiling of microglia infected by a highly neurovirulent murine leukemia virus: implications for neuropathogenesis.

BACKGROUND: Certain murine leukemia viruses (MLVs) are capable of inducing progressive spongiform motor neuron disease in susceptible mice upon infection of the central nervous system (CNS). The major CNS parenchymal target of these neurovirulent retroviruses (NVs) are the microglia, whose infection is largely coincident with neuropathological changes. Despite this close association, the role of microglial infection in disease induction is still unknown. In this paper, we investigate the interaction of the highly virulent MLV, FrCasE, with microglia ex vivo to evaluate whether infection induces specific changes that could account for neurodegeneration. Specifically, we compared microglia infected with FrCasE, a related non-neurovirulent virus (NN) F43/Fr57E, or mock-infected, both at a basic virological level, and at the level of cellular gene expression using quantitative real time RT-PCR (qRT-PCR) and Afffymetrix 430A mouse gene chips. RESULTS: Basic virological comparison of NN, NV, and mock-infected microglia in culture did not reveal differences in virus expression that provided insight into neuropathogenesis. Therefore, microglial analysis was extended to ER stress gene induction based on previous experiments demonstrating ER stress induction in NV-infected mouse brains and cultured fibroblasts. Analysis of message levels for the ER stress genes BiP (grp78), CHOP (Gadd153), calreticulin, and grp58 in cultured microglia, and BiP and CHOP in microglia enriched fractions from infected mouse brains, indicated that FrCasE infection did not induce these ER stress genes either in vitro or in vivo. To broadly identify physiological changes resulting from NV infection of microglia in vitro, we undertook a gene array screen of more than 14,000 well-characterized murine genes and expressed sequence tags (ESTs). This analysis revealed only a small set of gene expression changes between infected and uninfected cells (<18). Remarkably, gene array comparison of NN- and NV-infected microglia revealed only 3 apparent gene expression differences. Validation experiments for these genes by Taqman real-time RT-PCR indicated that only single Ig IL-1 receptor related protein (SIGIRR) transcript was consistently altered in culture; however, SIGIRR changes were not observed in enriched microglial fractions from infected brains. CONCLUSION: The results from this study indicate that infection of microglia by the highly neurovirulent virus, FrCasE, does not induce overt physiological changes in this cell type when assessed ex vivo. In particular, NV does not induce microglial ER stress and thus, FrCasE-associated CNS ER stress likely results from NV interactions with another cell type or from neurodegeneration directly. The lack of NV-induced microglial gene expression changes suggests that FrCasE either affects properties unique to microglia in situ, alters the expression of microglial genes not represented in this survey, or affects microglial cellular processes at a post-transcriptional level. Alternatively, NV-infected microglia may simply serve as an unaffected conduit for persistent dissemination of virus to other neural cells where they produce acute neuropathogenic effects.

3T3 Cells↗

[Histopathologic study of the ethmoid bone in chronic sinusitis].

OBJECTIVE: To investigate the histopathologic study of the ethmoid bone in chronic sinusitis (CRS) and the role of bone pathology in the pathogenesis of CRS. METHODS: Specimens of mucosa of ethmoid sinus with bone were collected during operation from 40 patients with CRS, 25 males and 15 females, aged 44.8, and specimens of mucosa of ethmoid sinus were collected from 16 patients with other otorhinolaryngologic diseases, 9 males and 7 females, aged 40.9 during operation. The specimens underwent HE, tartrate-resistant acid phosphatase, alkaline phosphatase, and Van Gieson staining so as to obtain the scores of nasal mucosa inflammation, pathology of mucoperiosteum and bone, and activity of bone remodeling. RESULTS: The average score of mucosal inflammation of the CRS group was 2.30 +/- 0.88, significantly higher than that of the control group (1.38 +/- 0.81, P = 0.004). The score of mucoperiosteum and bone pathology of the CRS group was 1.65 +/- 0.84, significantly higher than that of the control group (1.00 +/- 0.73, P = 0.004). The score of bone remodeling activity of the CRS group was 2.15 +/- 0.74, significantly higher than that of the control group (1.56 +/- 0.63, P = 0.007). In the CRS patients, the score of mucosal inflammation was not significantly correlated with the mucoperiosteum and bone pathology (R = 0.047, P = 0.772), and the activity of bone remodeling (R = 0.021, P = 0.897). CONCLUSION: The ethmoid bone of CRS patients shows marked fibrosis, bone remodeling, structure of woven bone, and pathologic changes similar to those of chronic osteomyelitis, especially bone absorption, new bone formation, etc.

Acid Phosphatase↗

Generation of anti-tumor immunity using mammalian heat shock protein 70 DNA vaccines for cancer immunotherapy.

In this study, we explored the protective anti-tumor potency of mouse (self) Hsp70 or Hsp110-based DNA vaccination approach targeting a tumor-associated antigen, human papilloma virus (HPV) type 16 E7 protein. Linkage of E7 to the N-terminus of the mouse Hsp70 not only elicits an E7-specific cytotoxic T cell (CTL) response, but also protects mice against challenge with E7 expressing tumors. CD8+ T-cells are crucial in both priming and effector phases for the induction of tumor immunity, whereas CD4+ T-cells and NK cells do not appear to play a major role. Furthermore, the ATP-binding domain deletion mutant Hsp70(382-641), when fused to E7, was immunologically effective, suggesting that the peptide-binding region, not the ATPase domain of Hsp70, is required for the vaccine activity of the E7-Hsp70 DNA. This study demonstrates that autologous Hsp70 is highly potent in enhancing antigen-specific immune responses. Functional domain mapping and orientation of the E7 and Hsp70 in the fusion gene may have clinical implications for the design and optimization of Hsp70-based DNA vaccines.

Animals↗

The new fluorescence enhancement system Tb-N-(2-pyridinyl) ketoacetamide-Et(3)N-Zn and its application.

A sensitive fluorescence enhancement system was developed for the determination of terbium. The fluorescence intensity of the Tb-N-(2-pyridinyl) ketoacetamide (PKAA) system was greatly enhanced by the addition of triethylamine (Et(3)N) and zinc nitrate in the methanol solution. The excitation and emission wavelengths were 329 and 546 nm, respectively. Under optimal conditions, the fluorescence intensities varied linearly with the concentration of Tb(3+) in the range of 7.5 x 10(-8)-8.2 x 10(-6)M with a detection limit of 6.4 x 10(-8)M. The interferences of some rare earth ions were described. This method was applied to the determination of trace amounts of terbium (III) in a synthetic rare earth oxide and a high purity Y(2)O(3) matrix. The mechanism of fluorescence enhancement was also studied.

Acetamides↗

Aristolochic acid I-induced DNA damage and cell cycle arrest in renal tubular epithelial cells in vitro.

DNA damage is a critical event preceding cellular apoptosis or necrosis. This study was carried out to investigate the effect of aristolochic acid I (AAI) on DNA damage and cell cycle in porcine proximal tubular epithelial cell lines (LLC-PK1 cells). LLC-PK1 cells were stimulated with AAI at the concentrations of 80, 320, and 1,280 ng/ml for 24 h. DNA damage was examined by comet assay and the cell cycle was assayed by flow cytometry (FCM), cellular apoptosis and lysis were examined simultaneously. Cellular nuclear changes were observed by electron microscopy and the expression of wild-type p53 protein and mRNA were measured by FCM and RT-PCR. We found that AAI-induced DNA damage prior to apoptosis and lysis in LLC-PK1 cells in a dose-dependent manner (P<0.01). The percentage of cells in the G2/M phase that were treated with AAI (320 and 1,280 ng/ml) for 24 h increased significantly (P<0.01). Electron micrographs showed the nuclear abnormalities in AAI-treated cells. The expression of p53 protein and mRNA did not change in the AAI-treated cells. AAI may cause DNA damage and cell cycle arrest in LLC-PK1 cells through a wild-type p53-independent pathway, prior to apoptosis or necrosis. This study on the molecular mechanism of AAI-induced toxicity may explain why tubular epithelial cells present limited proliferation and regeneration abilities in the clinical presentation of AAI-associated nephrotoxicity.

Animals↗

[Preliminary screening and identification of a peptide that binds specifically to gastric cancers cells with high metastasis to peritoneum].

OBJECTIVE: To screen and identify peptides that binds specifically to gastric cancers cells with high metastasis to peritoneum so as to find appropriate vectors for targeting therapy for cancer. METHODS: Human gastric cancer cells of the line GC9811 and those with high metastasis to peritoneum of the line GC9811-P were co-incubated with the 12-mer bacteriophage random peptide library. After 3 round of repeated screening, phage clones were collected. Forty internalized phage single-stranded DNA that specifically binding to the GC98112-P cells were sequenced. GC9811 and GC9811-P cells were co-inoculated with 5 peptides with the N end marked with fluorescein isothiocyanate (FITC) and 1 un-related peptide not binding to GC9811 and GC9811-P cells. Fluorescence microscopy, ELISA, and flow cytometry were used to detect the binding activity. BALB/cnu/nu mice were inoculated intraperitoneally with GC9811 and GC9811-P cells and then randomly divided into. 2 equal groups: experimental group, inoculated with the peptide PIII-FITC and control group (inoculated with un-related peptide PC-FITC. Forty-eight hours later the mice were killed and the peritoneum and tumor masses in different organs were collected and under fluorescence microscopy. RESULTS: DNA sequencing showed that 45% (18/45) of the isolated phages displayed repeated sequence SMSIASPYIALE, and SMSI was defined as a conservative motif. Obvious fluorescence was seen in the GC9811-P cells co-incubated with PIII-FITC and weak fluorescence was seen in the GC9811 cells co-incubated with PIII-FITC. Un-marked un-related peptide PC and PIII-FITC did not influenced the fluorescence staining of the GC9811-P cells, however, no fluorescence could be seen in the GC9811-P cells co-incubated with un-marked PIII and PIII-FITC. The fluorescence positive cell rate was 5.9% in the GC9811 cells co-incubated with PIII-FITC, and was 90.2% in the GC9811-P cells co-incubated with PIII-FITC. The fluorescence positive cell rates of the GC9811 cells and GC9811-P cells co-incubated with PC-FITC were 10.1% and 9.9% respectively 10.1% and 9.9% respectively. The fluorescence strength of the GC9811-P cells co-incubated with PIII-FITC was significantly greater than that of the GC9811-P cells co-incubated with PC-FTIC at any time-point and dose (all P < 0.01), and increased along with the increase of co-incubation time and dose of PIII-FITC. The peritoneal tumor tissues caused by the GC9811-P cells of the mice showed strong fluorescence and those caused by GC9811 cells only showed very weak fluorescence. Weak fluorescence could be seen in the tumor masses in the lymph nodes, liver, and muscle of the mice inoculated with GC9811-P cells and was not seen in the tissues of the mice inoculated with GC9811 cells. CONCLUSION: The sequence SMSIASPYIALE that specifically binds to human gastric cancer cells with high metastasis has been screened that has the potential to be used as a marker and targeting vector in diagnosis and treatment of gastric cancer.

Amino Acid Sequence↗

Flow injection analysis-Rayleigh light scattering detection for online determination of protein in human serum sample.

A flow injection analysis (FIA) system combined with Rayleigh light scattering (RLS) detection is developed for the sensitive and rapid determination of protein concentration in human serum sample. This method is based on the weak intensity of RLS of Eriochrome Black T (EBT, 2-hydroxy-1-(1-hydroxy-2-naphthylazo)-6-nitronaphthalene-4-sulfonic acid sodium salt), which can be enhanced by the addition of protein in weakly acidic solution. The effects of pH and interfering species on the determination of protein were examined. Calibrations for protein, based on RLS intensity, were linear in the concentration ranges of 7-36 microg/ml for human serum album (HSA) and 8-44 microg/ml for bovine serum album (BSA). The detection limits of the method were found to be 0.882 and 2.507 microg/ml for HSA and BSA, respectively. A relative standard deviation of 0.76% (n=5) was obtained with 20 microg/ml HSA standard solution. The FIA-RLS method was more stable than the general RLS method, and the average RSD value of FIA-RLS was less than that of the general RLS. The sample rate was determined to be 90 samples per hour.

Animals↗

Ghrelin acts on the dorsal vagal complex to stimulate pancreatic protein secretion.

Ghrelin receptors are present in the central nervous system. We hypothesized that ghrelin released from the stomach acts as an endocrine substance and stimulates brain stem vagovagal circuitry to evoke pancreatic secretion. In an in vivo anesthetized rat model, an intravenous infusion of ghrelin at doses of 5, 10, and 25 nmol increased pancreatic protein secretion from a basal level of 125 +/- 6 to 186 +/- 8, 295 +/- 12, and 356 +/- 11 mg/h, respectively. Pretreatment with atropine or hexamethonium or an acute vagotomy, but not a perivagal application of capsaicin, completely abolished pancreatic protein secretion responses to ghrelin. In conscious rats, an intravenous infusion of ghrelin at a dose of 10 nmol resulted in a 2.2-fold increase in pancreatic protein secretion over basal volume. Selective ablation of the area postrema abolished pancreatic protein secretion stimulated by intravenous infusion of ghrelin but did not alter the increase in pancreatic protein secretion evoked by diversion of bile-pancreatic juice. Immunohistochemical staining showed a marked increase in the number of c-Fos-expressing neurons in the area postrema, nucleus of the solitary tract, and dorsal motor nucleus of the vagus after an intravenous infusion of ghrelin in sham-lesioned rats; selective ablation of the area postrema eliminated this increase. In conclusion, ghrelin stimulates pancreatic secretion via a vagal cholinergic efferent pathway. Circulating ghrelin gains access to the brain stem vagovagal circuitry via the area postrema, which represents the primary target on which peripheral ghrelin may act as an endocrine substance to stimulate pancreatic secretion.

Animals↗

Characterization of solvated electrons in hydrogen cyanide clusters: (HCN)n- (n=3, 4).

Theoretical studies of the solvated electrons (HCN)n- (n=3, 4) reveal a variety of electron trapping possibilities in the (HCN)n (n=3, 4) clusters. Two isomers for (HCN)3- and four isomers for (HCN)4- are obtained at the MP2aug-cc-pVDZ+dBF (diffusive bond functions) level of theory. In view of vertical electron detachment energies (VDEs) at the CCSD(T) level, the excess electron always "prefers" locating in the center of the system, i.e., the isomer with higher coordination number shows larger VDE value. However, the most stable isomers of the solvated electron state (HCN)3- and (HCN)4- are found to be the linear Cinfinitynu and Dinfinityh structures, respectively, but not the fullyl symmetric structures which have the largest VDE values.

Journal Article↗

Increased heat shock protein 70 expression in the pancreas of rats with endotoxic shock.

AIM: To investigate the ultra-structural changes and heat shock protein 70 (HSP70) expression in the pancreas of rats with endotoxic shock and to detect their possible relationship. METHODS: A total of 33 Wistar rats were randomly divided into three groups: control group (given normal saline), small dose lipopolysaccharide (LPS) group (given LPS 5 mg/kg) and large dose LPS group (given LPS 10 mg/kg). Pancreas was explanted to detect the ultra-structural changes by TEM and the HSP70 expression by immunohistochemistry and Western blot. RESULTS: Rats given small doses of LPS showed swelling and loss of mitochondrial cristae of acinar cells and increased number of autophagic vacuoles in the cytoplasm of acinar cells. Rats given large doses of LPS showed swelling, vacuolization, and obvious myeloid changes of mitochondrial cristae of acinar cells, increased number of autophagic vacuoles in the cytoplasm of acinar cells. HSP70 expression was increased compared to the control group (P<0.05). CONCLUSION: Small doses of LPS may induce stronger expression of HSP70, promote autophagocytosis and ameliorate ultra-structural injuries.

Animals↗