Biomedical subjects

Hui Chen

Publications and source records attributed to Hui Chen.

At least 37 records · Page 2Linked to original sources

PubMed2007

Inhibition of human betaine-homocysteine methyltransferase expression by S-adenosylmethionine and methylthioadenosine.

BHMT (betaine-homocysteine methyltransferase) remethylates homocysteine to form methionine. SAM (S-adenosylmethionine) inhibits BHMT activity, but whether SAM modulates BHMT gene expression is unknown. Transcriptional regulation of the human BHMT is also unknown. The present study examined regulation of the human BHMT gene by SAM and its metabolite, MTA (5'-methylthioadenosine). To facilitate these studies, we cloned the 2.7 kb 5'-flanking region of the human BHMT gene (GenBank accession number AY325901). Both SAM and MTA treatment of HepG2 cells resulted in a dose- and time-dependent decrease in BHMT mRNA levels, which paralleled their effects on the BHMT promoter activity. Maximal suppression was observed with the BHMT promoter construct -347/+33, which contains a number of NF-kappaB (nuclear factor kappaB) binding sites. SAM and MTA treatment increased NF-kappaB nuclear binding and NF-kappaB-driven luciferase activities, and increased nuclear binding activity of multiple histone deacetylase co-repressors to the NF-kappaB sites. Overexpression of p50 and p65 decreased BHMT promoter activity, while blocking NF-kappaB activation increased BHMT expression and promoter activity, and prevented SAM but not MTA's ability to inhibit BHMT expression. The NF-kappaB binding site at -301 is responsible, at least in part, for this effect. Lower BHMT expression can impair homocysteine metabolism, which can induce ER (endoplasmic reticulum) stress. Indeed, MTA treatment resulted in increased expression ER stress markers. In conclusion, SAM and MTA down-regulate BHMT expression in HepG2 cells in part by inducing NF-kappaB, which acts as a repressor for the human BHMT gene. While SAM's mechanism is NF-kappaB-dependent, MTA has both NF-kappaB-dependent and -independent mechanisms.

Adenosine↗

PubMed2006

Proteasome substrate degradation requires association plus extended peptide.

To determine the minimum requirements for substrate recognition and processing by proteasomes, the functional elements of a ubiquitin-independent degradation tag were dissected. The 37-residue C-terminus of ornithine decarboxylase (cODC) is a native degron, which also functions when appended to diverse proteins. Mutating the cysteine 441 residue within cODC impaired its proteasome association in the context of ornithine decarboxylase and prevented the turnover of GFP-cODC in yeast cells. Degradation of GFP-cODC with C441 mutations was restored by providing an alternate proteasome association element via fusion to the Rpn10 proteasome subunit. However, Rpn10-GFP was stable, unless extended by cODC or other peptides of similar size. In vitro reconstitution experiments confirmed the requirement for both proteasome tethering and a loosely structured region. Therefore, cODC and degradation tags in general must serve two functions: proteasome association and a site, consisting of an extended peptide region, used for initiating insertion into the protease.

Animals↗

PubMed2006

CASPT2//CASSCF study on the photolysis mechanism of 2,3-diazabicyclo[2.1.1]hex-2-ene: alpha C-N versus beta C-C cleavage.

A CASPT2//CASSCF study has been carried out to investigate the mechanism of the photolysis of 2,3-diazabicyclo[2.1.1]hex-2-ene under direct irradiation and triplet-sensitized irradiation. By exploring the detailed potential energy surfaces and surface crossing points for several low-lying excited states, we have been able to provide a tentative description on the photophysical and photochemical processes of this compound. According to our calculations, on the S(1) surface one C-N bond is broken first to generate the diazenyl biradicals, which then result in the photoproduct bicyclobutane through a concerted C-N cleavage and C-C coupling process. The intersystem crossing (ISC) from the S(1) state to the triplet state was found to be quite efficient, which could account for two other photoproducts (butadiene and 1,2-diazabicyclo[3.1.0]hex-2-ene) on direct irradiation. On the T(1) surface, the C-C bond cleavage could readily take place to generate the triplet hydrazonyl biradical. One deactivation path of this intermediate is to convert into the corresponding singlet biradical by an ISC process. Then this biradical undergoes a barrierless C-N bond formation to form the photoproduct 1,2-diazabicyclo[3.1.0]hex-2-ene. Another path of the triplet hydrazonyl biradical is to form the intermediate 2-allyl-diazomethane through a C-N cleavage. This intermediate will break another C-N bond to produce a terminal carbene species, which is easily converted into butadiene and bicyclobutane by 1,2-hydrogen shift reaction and addition to C=C double bond, respectively.

Journal Article↗

PubMed2006

Theoretical study on the excitation energies of six tautomers of guanine: evidence for the assignment of the rare tautomers.

The CASPT2//CASSCF method with the 6-31G basis set and an active space up to (16,12) was used to calculate the excitation energies for six tautomers of guanine. Our calculations provide further support on the recent reassignment of the near-UV resonant two-photon ionization (R2PI) spectrum, in which two rare tautomers of the 7H-oxo-imino form were proposed to replace the previously assigned 7H/9H-oxo-amino tautomers. The adiabatic excitation energies of the 7H-oxo-imino tautomers are calculated to be 0.3-0.5 eV higher than those of the 7H/9H-oxo-amino tautomers. Our calculations also indicate that the missing most stable tautomers (7H/9H-oxo-amino tautomers) in the R2PI experiment is possibly due to the existence of an ultrafast nonradiative deactivation process in the excited-state of these two tautomers.

Guanine↗

PubMed2006

Ghrelin has novel vascular actions that mimic PI 3-kinase-dependent actions of insulin to stimulate production of NO from endothelial cells.

Ghrelin is an orexigenic peptide hormone secreted by the stomach. In patients with metabolic syndrome and low ghrelin levels, intra-arterial ghrelin administration acutely improves their endothelial dysfunction. Therefore, we hypothesized that ghrelin activates endothelial nitric oxide synthase (eNOS) in vascular endothelium, resulting in increased production of nitric oxide (NO) using signaling pathways shared in common with the insulin receptor. Similar to insulin, ghrelin acutely stimulated increased production of NO in bovine aortic endothelial cells (BAEC) in primary culture (assessed using NO-specific fluorescent dye 4,5-diaminofluorescein) in a time- and dose-dependent manner. Production of NO in response to ghrelin (100 nM, 10 min) in human aortic endothelial cells was blocked by pretreatment of cells with NG-nitro-L-arginine methyl ester (nitric oxide synthase inhibitor), wortmannin [phosphatidylinositol (PI) 3-kinase inhibitor], or (D-Lys3)-GHRP-6 (selective antagonist of ghrelin receptor GHSR-1a), as well as by knockdown of GHSR-1a using small-interfering (si) RNA (but not by mitogen/extracellular signal-regulated kinase inhibitor PD-98059). Moreover, ghrelin stimulated increased phosphorylation of Akt (Ser473) and eNOS (Akt phosphorylation site Ser1179) that was inhibitable by knockdown of GHSR-1a using siRNA or by pretreatment of cells with wortmannin but not with PD-98059. Ghrelin also stimulated phosphorylation of mitogen-activated protein (MAP) kinase in BAEC. However, unlike insulin, ghrelin did not stimulate MAP kinase-dependent secretion of the vasoconstrictor endothelin-1 from BAEC. We conclude that ghrelin has novel vascular actions to acutely stimulate production of NO in endothelium using a signaling pathway that involves GHSR-1a, PI 3-kinase, Akt, and eNOS. Our findings may be relevant to developing novel therapeutic strategies to treat diabetes and related diseases characterized by reciprocal relationships between endothelial dysfunction and insulin resistance.

Animals↗

PubMed2006

Microendoscopic discectomy for lumbar disc herniation: surgical technique and outcome in 873 consecutive cases.

STUDY DESIGN: A retrospective review involving 873 consecutive cases of lumbar disc herniation treated by microendoscopic discectomy (MED) was conducted and a mean 28-month follow-up was performed. OBJECTIVE: The purpose of this study was to describe the MED technique for lumbar disc herniation and report long-time outcome and complications. SUMMARY OF BACKGROUND DATA: The conception of MED was introduced in 1997. Long-time outcome has not been described. METHOD: A total of 873 consecutive patients with lumbar disc herniation were treated with the METRx system. Oswestry Disability Index (ODI) was used to quantify pain relief. The degree of pain and disability was also measured by visual analog scale (VAS) and modified MacNab criteria. A control group of 358 patients treated with standard open discectomy was used for comparison. RESULTS: There was significant improvement in the mean preoperative and postoperative VAS and ODI score for the MED and open groups, and there was no statistical difference of the pain improvement between the two groups. For the MED group, average length of hospital stay was 4.8 days; mean time to return to work or normal activities was 15 days; average operative blood loss per level was 44 mL. These were significantly less than open group. CONCLUSIONS: MED is an effective microendoscopic system with fine long-term outcome in treating lumbar disc herniation. The endoscopic approach allows smaller incisions and less tissue trauma, compared with standard open microdiscectomy. Strict adherence to well-defined preoperative selection criteria could ensure optimal postoperative outcome.

Adult↗

PubMed2006

Coincidence of actin filaments and talin is required to activate vinculin.

Vinculin regulates cell adhesion by strengthening contacts between extracellular matrix and the cytoskeleton. Binding of the integrin ligand, talin, to the head domain of vinculin and F-actin to its tail domain is a potential mechanism for this function, but vinculin is autoinhibited by intramolecular interactions between its head and tail domain and must be activated to bind talin and actin. Because autoinhibition of vinculin occurs by synergism between two head and tail interfaces, one hypothesis is that activation could occur by two ligands that coordinately disrupt both interfaces. To test this idea we use a fluorescence resonance energy transfer probe that reports directly on activation of vinculin. Neither talin rod, VBS3 (a talin peptide that mimics a postulated activated state of talin), nor F-actin alone can activate vinculin. But in the presence of F-actin either talin rod or VBS3 induces dose-dependent activation of vinculin. The activation data are supported by solution phase binding studies, which show that talin rod or VBS3 fails to bind vinculin, whereas the same two ligands bind tightly to vinculin head domain (K(d) approximately 100 nM). These data strongly support a combinatorial mechanism of vinculin activation; moreover, they are inconsistent with a model in which talin or activated talin is sufficient to activate vinculin. Combinatorial activation implies that at cell adhesion sites vinculin is a coincidence detector awaiting simultaneous signals from talin and actin polymerization to unleash its scaffolding activity.

Actins↗

PubMed2006

[Identification of the differentially expressed genes between primary breast cancer and paired lymph node metastasis through combining mRNA differential display and gene microarray].

OBJECTIVE: To identify and clone the genes related to breast cancer metastasis through comparing the mRNA expression profiling between primary breast cancer and paired lymph node metastasis. METHODS: First, primary breast cancer cells and paired lymph node metastasis tissues were used to identify their differentially expressed genes by using mRNA differential display, and fragments of differentially expressed genes were obtained by gel cutting and cloning to pGEM-T vector, then sequencing and blasting with the GenBank for their homologous genes. Then, the obtained genes were validated by using reverse dot blot hybridization and gene microarray. Finally, the mRNA expression levels in the 7 breast cancer cell lines with different metastasis behaviors were detected by real-time RT-PCR. RESULTS: The mRNA expression profiling of the metastatic breast cancers in lymph node was similar to that of their primary cancers. 16 differentially expressed gene fragments were obtained from mRNA differential display; four of them were found to be unknown genes, and had been accepted by the GenBank, with the accession numbers BG518428, BG518429, BM005520, and BM005521. Of the other 12 genes, 8 were known genes, and 4 were genes with known sequences but unknown functions. The kinesin-like DNA binding protein (KNSL4) and dihydropyrimidine dehydrogenase (DYPD) were down-regulated in the metastatic tissues in comparison with the paired primary tissues, which was identified by both radioactivity-labeled reverse dot blot hybridization and fluorescence-labeled gene microarray hybridization. KNSL4 mRNA expression had a down-regulation trend with increasing metastatic ability of breast cancer cell lines. CONCLUSIONS: The gene expression profiling of the lymph node metastasis is almost similar to that of their primary breast cancer, indicating that the metastatic cancer cells in lymph node are the subclone with higher metastasis ability of the primary cancer cells, and that some differentially expressed genes between them may be involved in the change of metastasis phenotype. KNSL4 and DYPD are potential metastasis-related genes, and KNSL4 mRNA expression is correlated with metastasis behaviors of the breast cancer cell lines, suggesting that KNSL4 may play an important role in the metastasis process of breast cancer.

Breast Neoplasms↗

PubMed2006

Neural stem cells: isolation and differentiation into cholinergic neurons.

This investigation aimed to isolate neural stem cells from neonatal hippocampus and induce them to differentiate into cholinergic neurons. The isolated neural stem cells were incubated in serum-free Dulbecco's modified Eagle medium/F12 medium added with 20 ng/ml basic fibroblast growth factor and B27. The cell line isolated from the hippocampal formation of neonatal rats expressed nestin and had the potency to form clones and differentiate into neurons, astrocytes and oligodendrocytes. Embryonic chick skeletal muscle extract was used to induce the differentiation of the neural stem cells into cholinergic neurons. Immunocytochemistry was used to detect the choline acetyltransferase antigen of cholinergic neurons for confirmation. The results showed that embryonic chick skeletal muscle extract could induce isolated neural stem cell to differentiate into a significantly larger number of cholinergic neurons than controls.

Animals↗

PubMed2006

Periodontal parameters and platelet-activating factor levels in serum and gingival crevicular fluid in a Chinese population.

AIM: Platelet-activating factor (PAF) is a potent proinflammatory mediator and has been implicated in cardiovascular pathophysiology. The present clinical study assessed the relation between the severity of periodontal disease and PAF levels in gingival crevicular fluid (GCF) and serum. METHODS: A total of 60 non-smoking subjects (21 periodontitis, 19 gingivitis patients and 20 healthy individuals) were included. Probing depth, attachment level, bleeding on probing, plaque index and sulphide levels were recorded at six sites of each tooth. GCF and blood samples were collected from all individuals, and PAF levels were investigated by enzyme-linked immunoabsorbent assay. RESULTS: The periodontitis group showed significantly higher PAF levels in the serum (329.3+/-287.3 pg/ml) and GCF (21.8+/-7.0 pg/sample) compared with the gingivitis group (138.0+/-77.9 pg/ml, 13.8+/-3.6 pg/sample) and with healthy controls (68.9+/-42.8 pg/ml, 2.4+/-2.7 pg/sample). The differences between patients and controls were statistically significant (p<or=0.05). Positive correlations were observed between PAF levels in GCF and serum and for PAF levels and clinical parameters. CONCLUSION: The present findings suggest a role of PAF in the pathogenesis of periodontitis. Based on the observed close correlation of GCF and serum PAF levels, future studies are warranted to test the hypothesis of a possible link between periodontitis and adverse systemic events mediated by PAF.

Adult↗

PubMed2006

Is the CCK2 receptor essential for normal regulation of body weight and adiposity?

Cholecystokinin (CCK) is a gastrointestinal satiety signal released from the duodenum to terminate feeding, via CCK1 receptors. CCK2 receptors are considered to be involved in anxiety. CCK2 receptor knockout mice have increased body weight and food intake. Little is known regarding the effects of CCK2 receptor deficiency on adipose distribution and hypothalamic feeding regulators such as neuropeptide Y (NPY), a powerful stimulator of feeding. Adult (10 week) CCK2 receptor knockout and wild-type mice were anaesthetized and killed by decapitation. Brain sections, organs and fat tissue were dissected. Plasma leptin, insulin and brain NPY content were measured by radioimmunoassay. Female CCK2 receptor knockout mice weighed more than control mice (22.0 +/- 0.2 vs. 19.9 +/- 0.4 g, P < 0.05), with this difference being less marked in male mice (26.4 +/- 0.4 vs. 25.6 +/- 0.6 g). Fat masses in all locations sampled were significantly smaller in CCK2 receptor knockout mice of both genders (P < 0.05), resulting in lower plasma leptin and insulin levels. NPY concentrations were significantly increased in arcuate nucleus and anterior hypothalamus in both male and female CCK2 receptor knockout mice, and total hypothalamic NPY content was increased by 7 and 9% in males and females, respectively (P < 0.05). CCK2 receptor deletion was associated with increased body weight and hypothalamic NPY content, but reduced fat masses and plasma leptin and insulin. Increased NPY might contribute to increased food intake in CCK2 receptor knockout mice. Further work needs to focus on the metabolic changes.

Adiposity↗

PubMed2006

Perinatal invasive malignant diseases: a review of twenty-five cases in South China.

Malignant neoplastic diseases (MND) are unusual complications during perinatal period and compose a dilemma for both patients and the health practitioners. Little is known about the information in Chinese suffering perinatal MND. Analyzing medical records and questionnaire, information on a series of 25 patients with a diagnosis of perinatal MND was collected from 3 medical centers between 1992 and 2004. Among all the 25 patients, 10 selected termination of the pregnancies and the other 15 continued their pregnancies until labor voluntarily, both groups obtain anti-malignancies therapies during the perinatal period. The two groups were not statistically different for the age of pregnancy, gravid and parity number, interval weeks between symptoms emergence and diagnosis of invasive malignant disease, as well as the occurrence rates of major side effects induced by malignant therapies. No statistical differences in overall survival and disease-free survival between the two groups, including the age of pregnancy, gravid and parity number, obstetric bleeding rates, neonatal distress rates, neonatal weight and puerperal morbidity rates. The patients' neonates all show no serious complications. In conclusion, pregnancy may not affect the course of MND, and termination of pregnancy may not benefit the maternal-fetal conditions, in a macroscopical point of view.

Adult↗

PubMed2006

Selective labeling and isolation of functional classes of interstitial cells of Cajal of human and murine small intestine.

Specific functions of interstitial cells of Cajal (ICC) have been linked to distinct classes that differ by morphology and distribution. In the small intestine, slow wave-generating ICC are located in the myenteric region (ICC-MY), whereas ICC that mediate neuromuscular neurotransmission occur either throughout the circular muscle layer (intramuscular ICC, ICC-IM) or in association with the deep muscular plexus (ICC-DMP). Selective isolation of ICC to characterize specific properties has been difficult. Recently, neurokinin-1 receptors have been detected in murine ICC-DMP and neurons but not in ICC-MY. Here we identified and isolated ICC-DMP/IM by receptor-mediated internalization of fluorescent substance P and Kit immunofluorescence. Specificity of labeling was verified by confocal microscopy. Mouse and human ICC-DMP/IM were detected in suspension by fluorescent microscopy and harvested for RT-PCR with micropipettes. The isolated cells expressed Kit but not markers for neurons, smooth muscle, or antigen-presenting cells. ICC-DMP expressed neurokinin-1 receptor, M(2) and M(3) muscarinic receptors, P2Y(1) and P2Y(4) purinergic receptors, VIP receptor 2, soluble guanylate cyclase-1 subunits, and protein kinase G. L- or T-type Ca(2+) channels were not detected in these cells. ICC-MY and ICC-DMP were simultaneously detected and enumerated by flow cytometry and sorted to purity by fluorescence-activated cell sorting. In summary, functional classes of ICC have distinct molecular identities that can be used to selectively identify and harvest these cells with, for example, receptor-mediated uptake of substance P and Kit immunofluorescence. ICC-DMP express neurotransmitter receptors and signaling intermediate molecules that are consistent with their role in neuromuscular neurotransmission.

Animals↗

PubMed2006

The research of molecular and ionic mechanisms in vagally mediated atrial fibrillation in canine.

BACKGROUND: The reentrant mechanism of vagally mediated AF is not clearly elucidated. METHODS AND RESULTS: After vagal stimulation, thirty dogs were divided AF group (AF could be induced) and control group (AF could not be induced). Western blot and patch clamp were used to determine M(2) receptor and I(K,ACh) in left atrial appendage (LAA), right atrial appendage (RAA), left atrium (LA), right atrium (RA), pulmonary veins (PVs) and superior vena cava (SVC). In control group, the densities of M(2) receptor and I(K,ACh) in LAA, RAA and LA were higher than that in RA, PVs and SVC. However, there was no significant difference in LAA, RAA and LA. In AF group, the densities of M(2) receptor and I(K,ACh) in LAA, RAA and LA were higher than that in RA, PVs and SVC. Furthermore, the densities of the M(2) and I(K,ACh) in LAA and RAA were higher than that in LA. CONCLUSIONS: Atrial appendage perhaps play an important role in initiation of cholinergic AF. However, PVs and SVC less often play an important role in vagotonic paroxysmal AF.

Animals↗

PubMed2006

BMP4 activation and secretion are negatively regulated by an intracellular gremlin-BMP4 interaction.

Bone morphogenetic protein 4 (BMP4) is a potent growth factor that is involved in many important biological processes. Regulation of the level of secreted mature BMP4 determines the biological effects of BMP4 on cells in the local microenvironment. Previous studies suggested that Gremlin, a member of DAN family proteins, antagonizes BMP4 activity by sequestering extracellular BMP4. Herein, we report a novel intracellular regulatory mechanism by which Gremlin interacts with BMP4 precursor, prevents secretion of mature BMP4, and therefore inhibits BMP4 activity more efficiently. Furthermore, we also defined a 30-amino acid peptide sequence within the Gremlin DAN domain that is essential for BMP4 interaction. This novel Gremlin-mediated BMP4 posttranslational regulatory mechanism implies that the level of BMP4 mRNA expression does not truly reflect BMP4 activity when Gremlin and BMP4 are coexpressed within the same cell. Similar regulatory mechanisms may be utilized by other DAN family proteins.

Amino Acid Sequence↗

PubMed2006

Blockage of epidermal growth factor receptor by quinazoline tyrosine kinase inhibitors suppresses growth of human hepatocellular carcinoma.

Epidermal growth factor receptor (EGFR) is highly expressed in many human tumors including hepatocellular carcinoma (HCC). Therefore, inhibition of EGF receptors could be a potential target for anticancer therapy. In this study, we investigated the effects of two EGFR tyrosine kinase inhibitors, PD153035 and its analogue 4-[[3-chloro-4-fluorophenyl]amino]-6,7-dimethoxyquinazoline hydrochloride (ANAPD) on human HCC cell lines by cell proliferation assay, flow cytometry and Western blot. Our results demonstrated that both EGFR inhibitors inhibited tumor cell growth in a dose-dependent manner, but ANAPD was more potent than PD153035. These specific inhibitors not only blocked EGF-stimulated EGFR autophosphorylation but also targeted EGFR signaling including MAPK and Akt pathways. Furthermore, EGFR inhibitors induced a delay in cell cycle progression and a G(1) arrest together with a partial G(2)/M block. EGFR inhibitors also induced tumor cells to undergo apoptosis. In conclusion, this study demonstrated that both PD153035 and ANAPD inhibit tumor cell growth in HCC through inhibition of EGFR signaling pathway, and ANAPD is a more potent inhibitor than PD153035. This suggested that blockage of EGF receptors may provide an effective therapeutic approach for human HCC and ANAPD could be a potential drug candidate for the treatment of HCC.

Apoptosis↗

PubMed2006

Syntheses and structural characterizations of 24-membered dimetal (Mn, Ni, Fe) macrocyclic complexes and the C-S bond formation between acetylacetone and a mercapto N-heterocycle.

An organic ligand 2,5-di(3-pentanedionylthio)-1,3,4-thiadiazole (H2L) reacts with metal (Mn, Ni, Fe) salts, resulting in 24-membered dimetal macrocyclic complexes [MnL(H2O)(dmso)](2).2dmso, [NiL(H2O)(dmf)](2).2dmf, [MnL(dmf)2]2 and [Fe2L2(solvent)2(SO4)] (solvent=dmso; H2O ; dmf). Di-manganese macrocyclic complexes [MnL(dmf)(dmso)]2 and [MnL(H2O)2](2).6H2O can also be obtained directly by aerobic assembly reaction of MnCl2, dipotassium 1,3,4-thiadiazole-2,5-dithiolate (K2tdadt) and acetylacetone (H2acac) in various solvents, accompanying a C-S bond formation between acetylacetone and the mercapto N-heterocycle. Disulfide has been considered as the intermediate in the assembly reaction. Meanwhile an assembly reaction including MnCl2, 2-mercaptobenzimidazole and H2acac has produced an organic compound 2-(3-pentanedionylthio)benzimidazole with a new C-S bond. These dimetal complexes have similar macrocyclic structures, in which solvent molecules and sulfate coordinate to the octahedral metal in trans-configuration, whereas a pair of water molecules are located in octahedral cis-positions for owing to a small steric effect. A host cavity of sufficiently large size exists in the macrocyclic structure to trap the solvent molecules and the sulfate anion. The IR spectra have been used to assign the solvent molecules trapped and the sulfate anion which is shown as a bridged bidentate ligand. Thermal analyses show the stability of the macrocyclic backbone below 200 degrees C and gradual release processes of the trapped solvent molecules. Decomposition and oxidation of the dimetal macrocycle backbone occur at 300-500 degrees C, resulting in a metal sulfate. Further decomposition led to metal oxide at 500-600 degrees C.

Journal Article↗

PubMed2006

Formation of actin-ADF/cofilin rods transiently retards decline of mitochondrial potential and ATP in stressed neurons.

When neurons in culture are transiently stressed by inhibition of ATP synthesis, they rapidly form within their neurites rodlike actin inclusions that disappear when the insult is removed. Oxidative stress, excitotoxic insults, and amyloid beta-peptide oligomers also induce rods. Immunostaining of neurites indicates that these rods also contain the majority of the actin filament dynamizing proteins, actin-depolymerizing factor (ADF) and cofilin (AC). If the rods reappear within 24 h after the stress is removed, the neurite degenerates distal to the rod but with no increase in neuronal death. Here, rods were generated in cultured rat E18 hippocampal cells by overexpression of a green fluorescent protein chimera of AC. Surprisingly, we have found that, for a short period (approximately 60 min) immediately after initial rod formation, the loss of mitochondrial membrane potential (Delta Psi(m)) and ATP in neurites with rods is slower than in neurites without them. The Delta Psi(m) was monitored with the fluorescent dye tetramethylrhodamine methyl ester, and ATP was monitored with the fluorescent ion indicator mag-fura 2. Actin in rods is less dynamic than is filamentous actin in other cytoskeletal structures. Because Delta Psi(m) depends on cellular ATP and because ATP hydrolysis associated with actin filament turnover is responsible for a large fraction of neuronal energy consumption (approximately 50%), the formation of rods transiently protects neurites by slowing filament turnover and its associated ATP hydrolysis.

Actins↗