Biomedical subjects

Hong Ding

Publications and source records attributed to Hong Ding.

At least 19 recordsLinked to original sources

PubMed2025

Effects of nitrogen allocation and photosynthetic proteins response in peanut leaves on photosynthesis under conditions of water scarcity and nitrogen deficiency.

Leaf nitrogen allocation and photosynthetic proteins response can affect net photosynthetic rate (Pn), ultimately influencing crop yield under diverse environmental stresses. However, the internal relationship between Pn with leaf nitrogen allocation and photosynthetic proteins response under nitrogen or water scarcity in peanut (Arachis hypogaea L.) remains elusive. Here, comprehensive physiological property and proteomic analyses of peanut were conducted, revealing that both nitrogen and water scarcity remarkably impeded leaf growth and reduced Pn. Nitrogen deficiency significantly reduced the total nitrogen content per unit leaf area (Narea), chlorophyll content, and Pn, whereas drought stress caused a greater decline in photosynthetic nitrogen use efficiency (PNUE). The allocation of leaf nitrogen to photosynthetic components, including the carboxylation system and electron transport system in leaves, was significantly reduced when subjected to individual or combined deficiency. Proteomic analyses exhibited that several key photosynthetic proteins underwent a decrease under both single and combined water and nitrogen deficiency conditions. Thereby, Pn may decline due to the disruption of nitrogen allocation and down-regulated expression of photosynthetic proteins under these stress conditions. Our findings establish a benchmark for future research exploring the roles of leaf nitrogen allocation and photosynthetic proteins in the plant's response to nitrogen or water deficiency.

Nitrogen↗

PubMed2025

Colorectal Liver Metastasis Pathomics Model: Integrating Single-Cell and Spatial Transcriptome Analysis With Pathomics for Predicting Liver Metastasis in Colorectal Cancer.

The liver is the primary target organ for hematologic metastasis of colorectal cancer (CRC), and CRC liver metastasis (CRLM) often precludes radical resection, making it the leading cause of death in patients with CRC. To improve the identification and prediction of liver metastasis risk, we identified a cell type of liver metastasis--triggering malignant cells (LMTMCs) through integrating single-cell RNA sequencing and spatial transcriptome analysis. Multiomics cell communication analysis indicated that the interaction between fibroblasts and LMTMCs through the COL1A1-CD44/SDC4 and LAMA4-CD44 signaling axes could promote CRLM. By applying the one-class logistic regression algorithm, we developed a CRLM scoring system in the bulk RNA-sequencing data according to the abundance of LMTMCs in each individual. Using the grouping labels derived from the CRLM scoring system in the bulk data and the corresponding whole-slide images without any manual annotations at the region or pixel level, processed via slide-level weakly supervised learning, a deep-learning model based on the ResNet18 architecture, called Colorectal Liver Metastasis Pathomics Model, was developed to predict the risk of liver metastasis in patients with CRC. The Colorectal Liver Metastasis Pathomics Model achieved an area under the curve of 0.84 at the internal test set of The Cancer Genome Atlas-CRC histology images. In the external independent validation sets, namely the Affiliated Hospital of Southwest Medical University and the Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University cohorts, the areas under the curve were 0.89 and 0.72, respectively, indicating effective classification performances. This study provided new insights and tools for the early identification of CRLM and demonstrated the potential of combining multiomics with deep learning-based pathomics in cancer research.

Humans↗

PubMed2006

Pharmacological characteristics of endothelium-derived hyperpolarizing factor-mediated relaxation of small mesenteric arteries from db/db mice.

Endothelial dysfunction is considered as a major risk factor of cardiovascular complications of type I and type II diabetes. Our previous studies have demonstrated that endothelial dysfunction in the small mesenteric arteries from 12-16 week old type II diabetic mice was associated with decreased bio-availability of nitric oxide whereas endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation was preserved. The objective of the present study was to characterize EDHF-mediated relaxations of small mesenteric arteries from db/db mice. A depolarizing concentration of KCl or tetraethylammonium (TEA, 10 mM) significantly inhibited the EDHF-mediated relaxation to acetylcholine and bradykinin in small mesenteric arteries from both db/+ and db/db mice. Charybdotoxin or iberiotoxin alone and a combination of ouabain and barium significantly reduced the maximal relaxation to acetylcholine in small mesenteric arteries from db/db mice and charybdotoxin or iberiotoxin either alone or in combination with apamin reduced the sensitivity to the EDHF-mediated component of the relaxation response to bradykinin. 17-octadecynoic acid, but not catalase, significantly reduced the sensitivity to EDHF-mediated responses to bradykinin in db/db mice; 17-octadecynoic acid had no effect on acetylcholine-mediated relaxations. No differences were, however, detected for mRNA expression levels of calcium-activated potassium channels or connexins 37, 40, 43 and 45. Collectively, these data suggest that bradykinin-induced, EDHF-dependent relaxation in small mesenteric arteries from db/db mice is mediated via cytochrome P450 product that activates the large conductance calcium-activated potassium (BK(Ca) or Slo) channel, whereas the acetylcholine-induced, EDHF-mediated relaxation involves neither cytochrome P450 product nor hydrogen peroxide.

Acetylcholine↗

PubMed2006

Protein tyrosine phosphatase 1B regulates TGF beta 1-induced Smad2 activation through PI3 kinase-dependent pathway.

Insulin is known to modulate transforming growth factor-beta (TGFbeta) signaling. In this report, by using the IN Cell Analyzer 1000, the fluorescence cell imaging instrument, we demonstrated that protein tyrosine phosphatase 1B (PTP1B) could regulate TGFbeta1-induced Smad2 activation in a PI3 kinase-dependent manner. By using the CHO cells stably expressing EGFP-Smad2, we showed that TGFbeta1 effectively stimulated Smad2 nuclear translocation in CHO cells. When pretreated with insulin, TGFbeta1-induced Smad2 nuclear entry was dramatically decreased. Furthermore, both the PI3K inhibitor LY294002 and the dominant negative AKT (DN-AKT) abolished the inhibitory effects of insulin, demonstrating that the inhibition of Smad2 activation by insulin was PI3K/AKT dependent. Since PTP1B negatively modulates insulin signaling, we further addressed the effects of PTP1B on insulin-mediated inhibition of Smad2 activation. Our data showed that overexpression of PTP1B effectively attenuated insulin-induced inhibition of Smad2 stimulation. Moreover, the PTP1B inhibitor, 3-(3,5-dibromo-4-hydroxy-benzoyl)-2-ethyl-benzofuran-6-sulfonicacid-(4-(thiazol-2-ylsulfamyl)-phenyl)-amide (Compound-2), recovered insulin inhibition of Smad2 activation. In conclusion, our data revealed the insulin inhibitory effects on TGFbeta1-induced Smad2 activation and the regulation role of PTP1B in the inhibition events.

Animals↗

PubMed2006

Comparing the effect of ATRA, 4-HPR, and CD437 in bladder cancer cells.

Clinical trials have explored the use of natural and synthetic retinoids for the prevention of bladder cancer recurrence. Natural retinoids have been shown to inhibit bladder cancer growth. Here, we compared the effects of natural and synthetic retinoids in bladder cancer cells. Bladder cancer cell lines were treated with all-trans-retinoid acid (ATRA), N-4-hydroxyphenyl-retinamide (4-HPR) and 6-[3-(1-adamantyl)-4 hydroxyphenyl]-2-naphthalene carboxylic acid (CD437). Their effects on cell growth, apoptosis, cell cycle, gene expression, and retinoid acid receptors (RARs) and the JWA-retinoid response gene were assessed. Most of the bladder cancer cells were resistant to ATRA (1 and 10 microM). 4-HPR inhibited cell growth by 90% at 10 microM; however, CD437 showed the same effect at 1 microM. 4-HPR and CD437 increased G1 and decreased S phase. The three retinoids differentially affected p53, RARs, and JWA. Only CD437 increased Caspase 3 expression. The results demonstrated that 4-HPR and CD437 were more potent growth inhibitors and apoptosis inducers than ATRA. However, 4-HPR was effective at a concentration at least 10 microM. The in vitro results suggested the higher dose of 4-HPR in chemoprevention trial be considered.

Antineoplastic Agents↗

PubMed2006

Intravesical N-(4-hydroxyphenyl) retinamide and adriamycin induces apoptosis in bladder cancer.

The objective of this study was to evaluate the intravesical application of N-(4-hydroxyphenyl) retinamide (4-HPR) and adriamycin (ADM), as a treatment modality in a an animal model of chemically-induced bladder cancer. Bladder cancer developed in 50.0% of female Wistar rats, 4-6 weeks after intravesical application of the chemical carcinogen, N-methyl-N-nitrosourea (MNU). There was no significant difference in side effects induced by local versus systemic 4-HPR. Although tumor growth was inhibited by 4-HPR and ADM alone, tumor size was lower when both agents were used together. Apoptosis occurred at a higher rate in the combination group than when 4-HPR or ADM was used alone. The results suggest that intravesical use of 4-HPR and ADM may increase their efficacy in treatment of bladder cancer.

Administration, Intravesical↗

PubMed2006

[Regulation effect of d-alpha-tocopherol on the expression of hexokinase induced by high glucose in cultured human peritoneal mesothelium cells].

OBJECTIVE: To investigate the effect of d-alpha-tocopherol on the expression of hexokinase (HK) induced by high glucose in cultured human peritoneal mesothelium cell (HPMC). METHODS: Specimens of human omentum were obtained from consenting patient undergoing elective abdominal surgery. HPMC were isolated and subcultured by enzymatic disaggregation. Morphology and immunocytochemical method were used for identification. HPMC were divided into normal glucose group (0.1% glucose, equal to 5.5 mmol/L), high glucose group (0.5%, 1.0%, 1.5%, 2.5%, 4.25% glucose) and d-alpha-tocopherol group. After 24 h, standard G6PDH-coupled assay, temperature sensitive essay were used to detect the activity of total HK and its isozyme. Immunocytochemical staining was used for observation the intracellular location of HKII. Western blotting was used to analyze the protein expression of HKII and RT-PCR was used to detect the mRNA expression of HKII. The net glucose utilization was assayed by glucose disappearance from medium by hexokinase method. RESULTS: Primary cultured HPMC reacted positively for cytokeratin and vimentin and had numerous surface microvilli under electron microscope. High glucose induced HK activity in a dose-dependent manner and increased HKII isoform selectively. At concentration of 1.5%, 2.5% and 4.25% glucose for 24 h, the relative activity of total HK were 115.4%, 129.1% and 155.2%, respectively comparing with normal control (P < 0.05), and selectively increased HKII isoform expression. D-alpha-tocopherol blocked the activity of total HK and HKII induced by glucose. The relative activity of total HK inhibited by d-alpha-tocopherol was 82.1% (P = 0.001). After incubated with d-alpha-tocopherol, the net glucose utilization were decreased from (25.3 +/- 3.9) mmol/L to (17.3 +/- 2.1) mmol/L (P = 0.018). HKII stained light brown in cytoplasm of HPMC in normal group, accompanying with the increased concentration of glucose, the staining of HKII became strong and accumulated to nuclear. D-alpha-tocopherol made it thinning. The protein and mRNA expression of HKII were accorded with its activity. CONCLUSION: D-alpha-tocopherol inhibited the expression of HKII in activity, protein and mRNA induced by high glucose and decreased the net glucose utilization, which might become a method to improve ultrafiltration in peritoneal dialysis.

Cell Line↗

PubMed2006

Quantitative characterization of 15-deoxy-delta(12,14)-prostaglandin J2 in regulating EGFPSmad2 translocation in CHO cells through PPARgamma/TGFbeta/Smad2 pathway.

Smad2 is an important factor in TGFbeta/Smad2 signal transduction pathway with ability for signal propagation, it could translocate from cytoplasm to nucleus after the TGFbeta receptor-mediated phosphorylation. 15-deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2), a natural agonist of the peroxisome proliferator-activated receptor gamma (PPARgamma), is found recently to be able to function in the regulation of Smad2 activity. However, no quantification data have been yet reported, and it still keeps suspenseful whether or not 15d-PGJ2 could regulate Smad2 activity by depending on PPARgamma through PPAR gamma/TGFbeta/ Smad2 pathway. In this work, by analyzing the EGFP-Smad2 location in CHO cells according to the Nucleus Trafficking Analysis Module based on IN Cell Analyzer 1000 platform, TGFbeta stimulated EGFP-Smad2 translocation regulated by 15d-PGJ2 was quantitatively investigated. The results showed that TGFbeta could induce EGFP-Smad2 translocation from cytoplasm to nucleus by EC50 of 8.83 pM, and 15d-PGJ2 could impede the TGFbeta-stimulated Smad2 translocation by IC50 of 0.68 microM. Moreover, GW9662, a PPARgamma antagonist, could attenuate such a 15d-PGJ2 inhibitory activity by almost one order of magnitude. This result thereby implies that 15d-PGJ2 might inhibit Smad2 translocation through PPARgamma/TGFbeta/Smad2 pathway. Further investigation discovered that different from the case for 15d-PGJ2, rosiglitazone, another PPARgamma agonist, could enhance Smad2 translocation to nucleus, suggesting that rosiglitazone and 15d-PGJ(2) might take different modes in the activation of PPARgamma within the signaling pathway.

Anilides↗

PubMed2006

HIV protease inhibitors activate the unfolded protein response and disrupt lipid metabolism in primary hepatocytes.

Treatment of human immunodeficiency virus (HIV)-infected patients with HIV protease inhibitors (PIs) has been associated with serious lipid disturbances. However, the incidence and degree of impaired lipid metabolism observed in the clinic vary considerably between individual HIV PIs. Our previous studies demonstrated that HIV PIs differ in their ability to increase the levels of transcriptionally active sterol regulatory element-binding proteins (SREBPs), activate the unfolded protein response (UPR), induce apoptosis, and promote foam cell formation in macrophages. In the present study, we examined the effects of three HIV PIs, including amprenavir, atazanavir, and ritonavir, on the UPR activation and the expression of key genes involved in lipid metabolism in primary rodent hepatocytes. Both atazanavir and ritonavir activated the UPR, induced apoptosis, and increased nuclear SREBP levels, but amprenavir had no significant effect at the same concentrations. In rat primary hepatocytes, cholesterol 7alpha-hydroxylase (CYP7A1) mRNA levels were significantly decreased by atazanavir (38%) and ritonavir (56%) but increased by amprenavir (90%); 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase mRNA levels were increased by amprenavir (23%) but not by ritonavir and atazanavir; low-density lipoprotein receptor mRNA was increased by atazanavir (20%) but not by amprenavir and ritonavir. Similar results were obtained in mouse primary hepatocytes. Atazanavir and ritonavir also decreased CYP7A1 protein levels and bile acid biosynthesis, while amprenavir had no significant effect. The current results may help provide a better understanding of the cellular mechanisms of HIV PI-induced dyslipidemia and also provide useful information to help predict clinical adverse effects in the development of new HIV PIs.

Acyl Coenzyme A↗

PubMed2006

Discovery and structure-activity relationship of antagonists of B-cell lymphoma 2 family proteins with chemopotentiation activity in vitro and in vivo.

Development of a rationally designed potentiator of cancer chemotherapy, via inhibition of Bcl-X(L) function, is described. Lead compounds generated by NMR screening and directed parallel synthesis displayed sub-microM binding but were strongly deactivated in the presence of serum. The dominant component of serum deactivation was identified as domain III of human serum albumin (HSA); NMR solution structures of inhibitors bound to both Bcl-X(L) and HSA domain III indicated two potential optimization sites for separation of affinities. Modifications at both sites resulted in compounds with improved Bcl-X(L) binding and greatly increased activity in the presence of human serum, culminating in 73R, which bound to Bcl-X(L) with a K(i) of 0.8 nM. In a cellular assay 73R reversed the protection afforded by Bcl-X(L) overexpression against cytokine deprivation in FL5.12 cells with an EC(50) of 0.47 microM. 73R showed little effect on the viability of the human non small cell lung cancer cell line A549. However, consistent with the proposed mechanism, 73R potentiated the activity of paclitaxel and UV irradiation in vitro and potentiated the antitumor efficacy of paclitaxel in a mouse xenograft model.

Aniline Compounds↗

PubMed2006

Simple high-performance liquid chromatographic method for the determination of tetramethylpyrazine phosphate in very small volumes of dog plasma: application to a pharmacokinetic study.

A rapid and sensitive high-performance liquid chromatographic (HPLC) method is developed for the determination of tetramethylpyrazine phosphate, an antiplatelet aggregation agent, in 100 microL of dog plasma. Sample preparations are carried out by deproteinization with an internal standard (carbamazepine) solution in acetonitrile. An aliquot of the supernatant (20 microL) is directly injected into an HPLC apparatus with methanol-phosphate buffer (0.01M, pH 3.0) (62:38, v/v) as the mobile phase at a flow rate of 1.0 mL/min. Separation is performed with a C18 column at 30 degrees C. The peak is detected using a UV detector set at 279 nm. The capacity factors are 1.48 for tetramethylpyrazine phosphate and 2.09 for carbamazepine, with a total run time of 10 min. The calibration curve is linear in the 0.2-50-microg/mL range. The limit of detection is 0.05 microg/mL. Mean recoveries are 92.6-98.1%. The within- and between-day variation coefficients are less than 4.9% and 7.5%, respectively. The present method has been successfully used to provide pharmacokinetic data after oral administration of tetramethylpyrazine phosphate pulsincap capsules and immediate-release tablets to dogs.

Animals↗

PubMed2006

[Investigation of the in vivo desintegration and transit behavior of tetramethylpyrazine phosphate pulsincap capsule in the gastrointestinal tract of dogs by gamma scintigraphy].

This study aims to investigate whether a self-made novel pulsatile drug delivery system--razine phosphate pulsincap capsule-will achieve a pulsatile drug release in vivo and to study the drug release sites. A gamma scintigraphic study was conducted to assess the in vivo transit and release behavior of the pulsincap capsule with a drug tablet containing 99mTc-labeled diethylenetriamine pentaacetic acid (DTPA) in the gastrointestinal (GI) tract of dog. The results revealed that after a time interval (lag time), the drug tablet began to disintegrate and then released at the pylorus of stomach or in the small intestine of dogs with a relatively rapid release rate, which was consistent with the expected pulsed release pattern. The in vivo lag time of the pulsincap capsule in dog was shortened with the decrease of erodible plugs(EP) weight. Thus we can achieve a desirable lag time to meet the chronotherapeutic requirements by adjusting the weight of EP.

Animals↗

PubMed2006

[Study on the Chinese herbal formula for treatment of vaginitis and the antimicrobial activity in murine models].

OBJECTIVE: To study on the various proportions of Radix Sophorae Flavescentis, Cortex Phellodendri, Fructus Cnidii and pericarp of Zanthoxylum bungeanum Maxim in the formulas, whose antimicrobial effects on E. coli, S. aureus, P. aeruginosa and C. albicans under different pH values were compared in vitro. METHODS: According to Chinese ancient proved recipe, the K-B method and plate diluting method were adopted to measure antimicrobial activity, and orthogonal design to ascertain the herbal formula in vitro. Finally, murine models were established to test the antimicrobial activity in vivo through vaginal membrane irritancy experiment, negative rate of pathogeny and pathological grade of vaginal membrane. RESULTS: The results suggested that formulas with different proportions of the herbs had diverse antimicrobial activities, and the effect was shown to be most obvious when one milliliter drug contains 100 microl Fructus Cnidii-pericarp of Zanthoxylum bungeanum (2:1) co-extracted volatile oil and 50 microl Radix Sophorae Flavescentis and Cortex Phenodendri ethanol extraction respectively under pH6. The antimicrobial effect of the formula, which hardly had any membrane irritancy, was better than Jie Eryin in vitro and vivo. CONCLUSION: The fromula has few components and better effect, and adaptation to the pH value of vaginitis. It is a promising alternative for gynecological diseases.

Alkaloids↗

PubMed2005

Two- to three-dimensional crossover in the electronic structure of (Bi, Pb)2(Sr, La)2CuO(6+delta) from angle-resolved photoemission spectroscopy.

The hole-concentration (x) dependence of the three-dimensional energy-momentum dispersion in (Bi, Pb)2(Sr, La)2CuO(6+delta) has been investigated by angle-resolved photoemission spectroscopy. For a heavily overdoped sample of T(c) < or = 0.5 K, an energy dispersion of approximately 10 meV in width is observed in the vicinity of the (pi, 0) point with varying momentum along the c axis (k(z)). This k(z) dispersion is zero for underdoped, optimally doped, and slightly overdoped samples up to a doping level corresponding to T(c) = 22 k. At higher doping levels we observe significant dispersion of the order of 10 meV (sample with T(c) < or = 0.5 K). This is clear evidence that at a doping value corresponding to T(c) = 22 K, a crossover from two- to three-dimensional electronic structure occurs.

Journal Article↗

PubMed2005

[Proportion of proinsulin two minutes after arginine stimulation: a pilot study].

OBJECTIVE: To seek an easy way to evaluate islet beta cell function. METHODS: 214 residents of Shanghai, aged 20-70, all of Han nationality, were divided into 3 groups according the 1999 WHO standard: 39 in the normal glucose tolerance (NGT) group, aged 52 years +/- 6 years, with the BMI of 22.3 kg/m(2) +/- 0.4 kg/m(2); 29 in the impaired glucose tolerance (IGT) group, aged 54 years +/- 9 years, with the BMI of 24.4 kg/m(2) +/- 0.6 kg/m(2); and 146 in the T2DM group, that was subdivided into 2 subgroups: 43 in the newly diagnosed T2DM (NT2DM) group, aged 52 years +/- 9 years, with the BMI of 24.4 kg/m(2) +/- 0.5 kg/m(2), and 103 in the previously diagnosed T2DM (PT2DM) group, aged 57 years +/- 9 years, with the BMI of 23.5 kg/m(2) +/- 0.3 kg/m(2). Arginine at the dose of 10% 50 ml was injected intravenously in fasting situation. Two, four, and six minutes after blood samples were collected from a needle indwelling in the contralateral vein to examine the levels of plasma glucose (PG), true insulin (TI), and proinsulin (PI). RESULTS: (1) The TI and TI/PG levels of all groups peaked 2 minutes after arginine stimulation and then gradually decreased, however, the levels 6 minutes after stimulation were still higher than the baseline values. The peak values of TI and TI/PG were arranged from high to low in the order of IGT, NGT, NT2DM and PT2DM. The peak values of NT2DM and PT2DM groups were significantly lower than those of the NGT and IGT groups (all P < 0.01). The peak values of the NT2DM group were significantly higher than those of the PT2DM group (both P < 0.01). (2) The PI value of the IGT, NT2DM and PT2DM groups peaked 2 minutes after the stimulation and then gradually decreased with the peak values significantly higher than that of the NGT group (all P < 0.05). The fasting PI/TI and PI/(TI + PI) of the NGT group were all significantly lower than those of the IGT group (both P < 0.05). (3) The changes of PI/TI in each groups manifested almost the mirror image of TI/PG mentioned above, and the lowest PI/TI levels were observed 2 minutes after stimulation. The similar changes of PI/(TI + PI) were found. The lowest points of groups 2 minutes after stimulation was arranged from low to high in the order of NGT, IGT, NT2DM and PT2DM. CONCLUSION: The PI/TI and PI/(TI + PI) values 2 minutes after arginine stimulation may be used as predictors for beta cell function in clinical practice.

Adult↗

PubMed2005

Electron correlation and fermi surface topology of NaxCoO2.

The electronic structure of NaxCoO2 revealed by recent photoemission experiments shows important deviations from band theory predictions. The six small Fermi surface pockets predicted by local-density approximation calculations have not been observed as the associated e'(g) band fails to cross the Fermi level for a wide range of sodium doping concentration x. In addition, significant bandwidth renormalizations of the t(2g) complex have been observed. We show that these discrepancies are due to strong electronic correlations by studying the multiorbital Hubbard model in the Hartree-Fock and strong-coupling Gutzwiller approximation. The quasiparticle dispersion and the Fermi surface topology obtained in the presence of strong local Coulomb repulsion are in good agreement with experiments.

Journal Article↗

PubMed2005

Endothelial dysfunction in Type 2 diabetes correlates with deregulated expression of the tail-anchored membrane protein SLMAP.

The Type 2 diabetic db/db mouse experiences vascular dysfunction typified by changes in the contraction and relaxation profiles of small mesenteric arteries (SMAs). Contractions of SMAs from the db/db mouse to the alpha1-adrenoceptor agonist phenylephrine (PE) were significantly enhanced, and acetylcholine (ACh)-induced relaxations were significantly depressed. Drug treatment of db/db mice with a nonthiazolidinedione peroxisome prolifetor-activated receptor-gamma agonist and insulin sensitizing agent 2-[2-(4-phenoxy-2-propylphenoxy)ethyl]indole-5-acetic acid (COOH) completely prevented the changes in endothelium-dependent relaxation, but, with the discontinuation of therapy, endothelial dysfunction returned. Dysfunctional SMAs were found to specifically upregulate the expression of a 35-kDa isoform of sarcolemmal membrane-associated protein (SLMAP), which is a component of the excitation-contraction coupling apparatus and implicated in the regulation of membrane function in muscle cells. Real-time PCR revealed high SLMAP mRNA levels in the db/db microvasculature, which were markedly downregulated during COOH treatment but elevated again when drug therapy was discontinued. These data reveal that the microvasculature in db/db mice undergoes significant changes in vascular function with the endothelial component of vascular dysfunction specifically correlating with the overexpression of SLMAP. Thus changes in SLMAP expression may be an important indicator for microvascular disease associated with Type 2 diabetes.

Acetates↗

PubMed2005

Preparation of micro-biosensor and its application in monitoring in vivo change of dopamine.

The self-made high sensitivity and selectivity micro-biosensor was applied to monitor the change of dopamine in cerebral nucleus in rats in vivo. The micro-biosensor was prepared and used to detect dopamine level in vitro and monitor the dynamic change of dopamine in different cerebral nucleus in vivo. The results showed the lowest concentration of dopamine that could be detected by the biosensor was 32.5 nmol/L. Its positive peak was significantly different from that of AA, 5-HTP and E. The biosensor could keep working for monitoring the dopamine concentration in the cerebral tissue for more than 10 h. It was concluded that the microsensor has high sensitivity and selectivity to dopamine and can be used to dynamically monitor the change of dopamine in vivo.

Animals↗