Biomedical subjects

Y Feng

Publications and source records attributed to Y Feng.

At least 127 records · Page 7Linked to original sources

PubMed2000

Identification of enterohepatic Helicobacter species by restriction fragment-length polymorphism analysis of the 16S rRNA gene.

BACKGROUND: Restriction fragment-length polymorphism (RFLP) analysis of a 1,200-bp polymerase chain reaction-amplified DNA fragment of gene coding for 16S rRNA was used to generate restriction profiles of 11 enterohepatic Helicobacter spp. isolated from various animals and humans. METHODS: The amplicon from each Helicobacter sp. was digested with four restriction endonucleases: Alu I, Hinf I, Hha I, and Dde I. Alu I digestion produced five patterns that were useful for initial differentiation. RESULTS: Most Helicobacter spp. isolated from rodents had the same RFLP profiles by Alu I digestion (except H. rodentium and H. cholecystus), but they had different RFLP profiles by Hha I digestion. Only H. bilis and "H. rappini" mouse isolates could not be readily distinguished by the polymerase chain reaction-RFLP method. However, these two species can be distinguished using H. bilis specific primers. Some of the Helicobacter spp. have an intervening sequence in their 16S rRNA gene, which changes the RFLP patterns; in these cases, sequencing is the preferred method to make an appropriate diagnosis. CONCLUSIONS: The RFLP method used in this study was straightforward and rapid and should prove useful as an adjunct for identification and classification of multiple enterohepatic Helicobacter spp.

Animals↗

PubMed2000

Selenium from high selenium broccoli protects rats from colon cancer.

Colon cancer is the third most common newly diagnosed cancer in the United States and the third most common cause of cancer-related deaths. Previous supplementation studies have demonstrated the efficacy of selenium (Se) for prevention of colon cancer in humans. The metabolism of Se depends on its chemical form, and studies have shown that the chemical form of Se in broccoli does not accumulate in the body as fast as other forms of Se and may be especially beneficial for prevention of cancer. In the first experiment of the present study, Fisher F-344 rats (n = 45) were allotted randomly to torula yeast-based diets supplemented with the following: 1) no Se; 2) 0.1 microg Se/g diet as selenate; 3) 1.0 microg Se/g diet as selenate; 4) 0.1 microg Se/g diet as selenized broccoli (Se concentration of approximately 500 microg/g); or 5) 1.0 microg Se/g diet as selenized broccoli. In Experiment 2, rats (n = 80) were allotted randomly to the same basal diet supplemented with the following: 1) no added Se; 2) 2.0 microg Se/g diet as selenite; 3) 2. 0 microg Se/g diet as selenite + low Se broccoli; and 4) 2.0 microg Se/g diet as selenized broccoli. Rats were fed the diets for 2 wk and injected with a chemical carcinogen (3,2 dimethyl 4-amino biphenyl or dimethyl-hydrazine in Experiment 1 or dimethyl hydrazine in Experiment 2; 2 rats/treatment were used as vehicle controls). Supranutritional amounts of Se supplied as high Se broccoli significantly decreased (P: < 0.05) the incidence of aberrant crypts (AC) and aberrant crypt foci (ACF; preneoplastic lesions indicative of colon cancer) compared with other dietary treatments. Diets were controlled for the presence or absence of broccoli and for the total amount of Se. The reduction in AC and ACF was a function of Se in high Se broccoli and not a result of broccoli alone or Se alone. Adequate dietary Se supplied as high Se broccoli did not accumulate in tissues or increase glutathione peroxidase activity as well as other forms and amounts of Se. Thus, Se from high Se broccoli may be metabolized in a manner that diverts much of the Se into a pool that provides protection against colon cancer.

Analysis of Variance↗

PubMed2000

Desmethyl tirilazad improves neurologic function after hypoxic ischemic brain injury in piglets.

OBJECTIVE: Desmethyl tirilazad is a lipid-soluble free radical quencher. Deferoxamine reduces free radicals by chelating iron and reducing hydroxyl formation. Free radical inhibitors have shown promise in several hypoxic ischemic brain injury models, and we wished to see if this work could be extended to our newborn piglet model. DESIGN: Randomized controlled trial. SUBJECTS: Piglets (0 to 3 days old). INTERVENTION: Carotid snares and arterial and venous catheters were placed under 1.5% isoflurane anesthesia. In Experiment 1, piglets were randomly assigned to receive either 3 mg/kg desmethyl tirilazad or vehicle at -15 and 90 mins. In Experiment 2, piglets were randomly assigned to receive either 20 mg/kg desmethyl tirilazad at -15 mins followed by 8 mg/kg/hr for 90 mins or 100 mg/kg deferoxamine at -15 mins or vehicle. At time 0, both carotid arteries were clamped and blood was withdrawn to reduce the blood pressure to two-thirds normal. At 15 mins, inspired oxygen was reduced to 6%. At 30 mins, the carotid snares were released, the withdrawn blood was reinfused, and the oxygen was switched to 100%. On the third day after the hypoxic ischemic injury, the animals were killed by perfusing their brains with 10% formalin. We tested the timing of lipid peroxidation and inhibition of lipid peroxidation by these agents by freezing the brains of a subset of pigs in liquid nitrogen. MEASUREMENTS: Neurologic examination and brain pathology were scored by blinded observers. Thiobarbituric acid-reactive substance and oxidized and reduced glutathione were measured on frozen brains. MAIN RESULTS: Desmethyl tirilazad (20 mg/kg) and 100 mg/kg deferoxamine inhibit lipid peroxidation. Desmethyl tirilazad (20 mg/kg) improves neurologic exam, but 3 mg/kg Desmethyl tirilazad or 100 mg/kg deferoxamine does not. Neither desmethyl tirilazad nor deferoxamine improves pathologic results. CONCLUSIONS: High-dose desmethyl tirilazad improves neurologic function after hypoxic ischemic brain injury in the newborn piglet.

Animals↗

PubMed2000

DNA adduct levels and intestinal lesions in congenic rapid and slow acetylator syrian hamsters admi food mutagens 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) or 2-amino-3-methylimidazo[4,5-f]quinoline (IQ).

Epidemiological studies indicate that rapid acetylators with a high intake of well-done red meat have an increased risk of colorectal cancer. Arylamine N-acetyltransferase enzymes (E.C. 2.3.1.5) activate carcinogenic heterocyclic amines found in the crust of fried meat via O-acetylation of their N-hydroxylamines to reactive intermediates that bind covalently to DNA and produce mutations. Syrian hamsters as well as humans express two N-acetyltransferase isozymes (NAT1 and NAT2) which differ in substrate specificity and genetic control. Nucleic acid substitutions in the NAT2 gene segregate individuals into rapid, intermediate and slow acetylator phenotypes. In the present paper, we examined the role of the polymorphic NAT2 acetylator genotype in carcinogenesis induced by the food mutagens 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) or 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) by comparing Syrian hamster lines congenic at the NAT2 locus. No differences were found between rapid and slow acetylator congenic hamsters in levels of intestinal PhIP-DNA adducts. In contrast to previous studies in rats, no carcinogen-related induction of the preneoplastic lesions aberrant crypt foci or tumors was found in the intestines of rapid and slow acetylator congenic Syrian hamsters administered PhIP or IQ.

Acetylation↗

PubMed2000

Isolation and characterization of a Helicobacter sp. from the gastric mucosa of dolphins, Lagenorhynchus acutus and Delphinus delphis.

Gastric ulcerations in dolphins have been reported for decades. Some of these lesions were associated with parasitic infections. However, cases of nonparasitic gastric ulcers with no clearly defined etiology also have been reported in wild and captive dolphins. Considerable speculation exists as to whether dolphins have Helicobacter-associated gastritis and peptic ulcer disease. The stomachs of seven stranded Atlantic white-sided dolphins, Lagenorhynchus acutus, and 1 common dolphin, Delphinus delphis, were assessed for the presence of Helicobacter species. Novel Helicobacter species were identified by culture in the gastric mucosa of two of the eight dolphins studied and by PCR in seven of the eight dolphins. The gram-negative organisms were urease, catalase, and oxidase positive. Spiral to fusiform bacteria were detected in gastric mucosa by Warthin Starry staining. Histopathology revealed mild to moderate diffuse lymphoplasmacytic gastritis within the superficial mucosa of the main stomach. The pyloric stomach was less inflamed, and bacteria did not extend deep into the glands. The lesions parallel those observed in Helicobacter pylori-infected humans. Bacteria from two dolphins classified by 16S rRNA analysis clustered with gastric helicobacters and represent a novel Helicobacter sp. most closely related to H. pylori. These findings suggest that a novel Helicobacter sp. may play a role in the etiopathogenesis of gastritis and gastric ulcers in dolphins. To our knowledge this represents the first isolation and characterization of a novel Helicobacter sp. from a marine mammal and emphasizes the wide host distribution and pathogenic potential of this increasingly important genus.

Animals↗

PubMed2000

Helicobacter aurati sp. nov., a urease-positive Helicobacter species cultured from gastrointestinal tissues of Syrian hamsters.

A novel helicobacter with the proposed name Helicobacter aurati (type strain MIT 97-5075c) has been isolated from the inflamed stomachs and ceca of adult Syrian hamsters. The new species is fusiform with multiple bipolar sheathed flagella and periplasmic fibers; it contains urease and gamma-glutamyl transpeptidase. By 16S rRNA sequencing and repetitive element PCR-based DNA fingerprinting, it was found that H. aurati represents a distinct taxon and clusters with Helicobacter muridarum, Helicobacter hepaticus, and Helicobacter sp. MIT 94-022. H. aurati was recovered from hamsters housed in various research and vendor facilities. Further studies are necessary to define its association with disease and other microbiota in hamsters, as well as its impact on research projects involving hamsters. H. aurati (GenBank accession number AF297868) can be used in animal experiments to define the factors that are important for gastric helicobacter pathogenesis.

Animals↗

PubMed2000

Akr1p and the type I casein kinases act prior to the ubiquitination step of yeast endocytosis: Akr1p is required for kinase localization to the plasma membrane.

Ubiquitination of the plasma membrane-localized yeast a-factor receptor (Ste3p) triggers a rapid, ligand-independent endocytosis leading to its vacuolar degradation. This report identifies two mutants that block uptake by blocking ubiquitination, these being mutant either for the ankyrin repeat protein Akr1p or for the redundant type I casein kinases Yck1p and Yck2p. While no obvious defect was seen for wild-type Ste3p phosphorylation in akr1 or yck mutant backgrounds, examination of the Delta320-413 Ste3p deletion mutant phosphorylation did reveal a clear defect in both mutants. The Delta320-413 deletion removes 18 Ser-Thr residues (possible YCK-independent phosphorylation sites) yet retains the 15 Ser-Thr residues of the Ste3p PEST-like ubiquitination-endocytosis signal. Two other phenotypes link akr1 and yck mutants: both are defective in phosphorylation of wild-type alpha-factor receptor, and while both are defective for Ste3p constitutive internalization, both remain partially competent for the Ste3p ligand-dependent uptake mode. Yck1p-Yck2p may be the function responsible in phosphorylation of the PEST-like ubiquitination-endocytosis signal. Akr1p appears to function in localizing Yck1p-Yck2p to the plasma membrane, a localization that depends on prenylation of C-terminal dicysteinyl motifs. In akr1Delta cells, Yck2p is mislocalized, showing a diffuse cytoplasmic localization identical to that seen for a Yck2p mutant that lacks the C-terminal Cys-Cys, indicating a likely Akr1p requirement for the lipid modification of Yck2p, for prenylation, or possibly for palmitoylation.

Acyltransferases↗

PubMed2000

Feedback phosphorylation of the yeast a-factor receptor requires activation of the downstream signaling pathway from G protein through mitogen-activated protein kinase.

The two yeast pheromone receptors, the a and alpha-factor receptors, share many functional similarities: both G protein-coupled receptors couple to the same downstream signal transduction pathway, and both receptors undergo feedback regulation involving increased phosphorylation on their C-terminal domains in response to ligand challenge. The present work, which focuses on the signaling mechanism controlling this feedback phosphorylation, indicates one striking difference. While the alpha-factor-induced phosphorylation of the alpha-factor receptor does not require activation of the downstream G protein-directed signaling pathway (B. Zanolari, S. Raths, B. Singer-Kruger, and H. Riezman, Cell 71:755-763, 1992), the a-factor-induced phosphorylation of the a-factor receptor (Ste3p) clearly does. Induced Ste3p phosphorylation was blocked in cells with disruptions of various components of the pheromone response pathway, indicating a requirement of pathway components extending from the G protein down through the mitogen-activated protein kinase (MAPK). Furthermore, Ste3p phosphorylation can be induced in the absence of the a-factor ligand when the signaling pathway is artificially activated, indicating that the liganded receptor is not required as a substrate for induced phosphorylation. While the activation of signaling is critical for the feedback phosphorylation of Ste3p, pheromone-induced gene transcription, one of the major outcomes of pheromone signaling, appears not to be required. This conclusion is indicated by three results. First, ste12Delta cells differ from cells with disruptions of the upstream signaling elements (e.g., ste4Delta, ste20Delta, ste5Delta, ste11Delta, ste7Delta, or fus3Delta kss1Delta cells) in that they clearly retain some capacity for inducing Ste3p phosphorylation. Second, while activated alleles of STE11 and STE12 induce a strong transcriptional response, they fail to induce a-factor receptor phosphorylation. Third, blocking of new pheromone-induced protein synthesis with cycloheximide fails to block phosphorylation. These findings are discussed within the context of a recently proposed model for pheromone signaling (P. M. Pryciak and F. A. Huntress, Genes Dev. 12:2684-2697, 1998): a key step of this model is the activation of the MAPK Fus3p through the G(betagamma)-dependent relocalization of the Ste5p-MAPK cascade to the plasma membrane. Ste3p phosphorylation may involve activated MAPK Fus3p feeding back upon plasma membrane targets.

Alleles↗

PubMed2000

bFGF increases collateral blood flow in aged rats with femoral artery ligation.

We tested the hypothesis that aged animals are as responsive as the young adult animals in expanding collateral vasculature under a similar treatment of basic fibroblast growth factor (bFGF). Two age groups of male Fischer 344 rats (11 mo old; n = 32, 23 mo old; n = 43) weighing approximately 385 g were subdivided into normal, acute ligation [femoral artery (FA) ligated 3 days before blood flow (BF) measurement] or ligated groups for 16 days and received recombinant human bFGF intra-arterial infusion at doses of 0, 0.5, 5, and 50 microg x kg(-1) x day(-1). BF was determined with (85)Sr- and (141)Ce-labeled microspheres during treadmill running at 15 and 20 m/min at 15% grade. Blood pressure (BP) values were approximately 149 and approximately 163 mmHg (p < 0.05); heart rates were approximately 496 and approximately 512 beats/min in the aged and young adult groups during running, respectively. Maximal collateral BF values were confirmed by no additional BF increase in the calf muscle at the higher speed. Ligation of the FA for 3 days reduced the BF reserve to the calf muscle by approximately 90%. Calf muscle BF was modestly greater (10 ml x min(-1) x 100 g(-1)) by 16 days in the carrier group. bFGF infusion expanded collateral BF in a dose-dependent manner with an increase of 33 and 42 ml x min(-1) x 100 g(-1) (P < 0.001) in the 5 and 50 microg x kg(-1) x day(-1) bFGF groups, respectively. Aged animals showed similar BF improvements as observed with the adult groups in response to ligation surgery and bFGF treatment. Our data indicate that the aged rats (approximately 23 mo old) remain responsive to exogenous bFGF induced in developing collateral-dependent BF as the young adult (approximately 11 mo old) controls. This suggests that the influence of bFGF in expanding collateral BF should not be preempted in the aged group, the population most affected by peripheral arterial insufficiency.

Aging↗

PubMed2000

Efficacy and specificity of bFGF increased collateral flow in experimental peripheral arterial insufficiency.

Angiogenic growth factors could prove to be useful in managing peripheral arterial insufficiency. The present study was designed to evaluate the dose response of basic fibroblast growth factor (bFGF), the efficacy of critical routes and dosing regimens, and the specificity of action in rats with peripheral arterial insufficiency. Bilateral ligation of femoral arteries greatly reduces blood flow capacity to the calf muscles but does not impair resting flow needs. Collateral blood flow to calf muscles was determined 16 days postocclusion, during treadmill running, with (85)Sr and (141)Ce microspheres, in blinded-randomized trials that included intra-arterial and intravenous infusions and subcutaneous injections of recombinant human bFGF. Peak blood flow of 75-80 ml. min(-1). 100 g(-1) for calf muscle was observed at a bFGF dose of 5 microg. kg(-1). day(-1) (ia for 14 days) compared with 50 ml. min(-1). 100 g(-1) for vehicle groups. Similar increases in collateral blood flow were observed with short-term or prolonged and continuous or intermittent delivery of bFGF by any route. Collateral blood flows were similar in corresponding muscles across both limbs. Vascular remodeling induced by bFGF required attendant vascular occlusion, inasmuch as vessels in the normal nonoccluded vascular tree were unresponsive to circulating bFGF. Improvement in collateral blood flow with exogenous bFGF is robust, amenable to short-term administration, and requires vascular occlusion to be effective.

Animals↗

PubMed2000

Screening marine natural products for selective inhibitors of key kynurenine pathway enzymes.

Kynurenine, a metabolite of tryptophan along the 'kynurenine pathway', is at a branch point of the pathway which can lead to the synthesis of both quinolinic acid (QUIN) and kynurenic acid (KYNA). KYNA is an antagonist of glutamate receptors; however, QUIN is a selective agonist of NMDA receptors, and has been shown to act as an excitotoxic agent. A high QUIN/KYNA ratio has been implicated in a variety of neurological diseases in which excitotoxic neuronal cell death is found, e.g. AIDS-related dementia, stroke, etc. Inhibiting the key enzymes of this pathway (i.e. kynureninase and kynurenine 3-hydroxylase) would lower the QUIN/KYNA ratio, which may potentially have neuroprotective effects. We have developed high through-put assays for kynurenine pathway enzymes which allow us to screen extracts from marine organisms for selective enzyme inhibitors. Active metabolites are purified, isolated and identified by HPLC, high-field NMR and mass spectral techniques. Extracts from a sponge of the Aka species were found to contain a selective inhibitor of kynureninase. We have recently purified and identified the active principal as being serotonin sulfate. Related indoleamines, serotonin and 5-hydroxyindoleacetic acids are inactive. This finding may be suggestive of a novel interaction between the serotoninergic and excitatory amino acid pathways.

Animals↗

PubMed2000

Gastritis and intestinal metaplasia in Syrian hamsters infected with Helicobacter aurati and two other microaerobes.

Chronic gastritis and intestinal metaplasia associated with naturally occurring colonization by Helicobacter aurati and two other microaerobic species were observed in Syrian hamsters. Thirty-five hamsters, between 7 and 12 months of age, were evaluated from two research and three commercial facilities. Microaerobic bacteria were cultured from the hamster stomachs. These bacteria included H. aurati, a fusiform, urease-positive species; a second novel helical, urease-negative Helicobacter sp.; as well as a smaller, urease-negative Campylobacter sp. Southern blot analysis detected Helicobacter spp. DNA in the gastric tissues of all 35 hamsters; 15 hamsters also had Campylobacter sp. DNA in their gastric tissues. When examined by light microscopy, argyrophilic bacteria consistent with H. aurati or the second Helicobacter sp. were present in antral sections of 12 out of the 15 hamsters where bacteria were seen, while 9 out of the 15 hamsters had bacteria resembling the Campylobacter sp. The presence of Helicobacter spp. but not the presence of Campylobacter sp. was significantly correlated to gastritis severity (P < 0.0001 for Helicobacter spp., P = 0.6025 for Campylobacter sp.) and intestinal metaplasia, as measured by numbers of goblet cells (P = 0.0239 for Helicobacter spp., P = 0.5525 for Campylobacter sp.). Severely affected hamsters also had Giardia sp. within their metaplastic gastric pits. Hamsters with naturally occurring helicobacter-associated gastritis provide a model for studying the development of intestinal metaplasia and gastric giardiasis in H. pylori-infected humans.

Animals↗

PubMed2000

A designed peptidomimetic agonistic ligand of TrkA nerve growth factor receptors.

A proteolytically stable small molecule beta-turn peptidomimetic, termed D3, was identified as an agonist of the TrkA neurotrophin receptor. D3 binds the Ig-like C2 region of the extracellular domain of TrkA, competes the binding of another TrkA agonist, affords selective trophic protection to TrkA-expressing cell lines and neuronal primary cultures, and induces the differentiation of primary neuronal cultures. These results indicate that a small beta-turn peptidomimetic can activate a tyrosine kinase neurotrophin receptor that normally binds a relatively large protein ligand. Agents such as D3 that bind the extracellular domain of Trk receptors will be useful pharmacological agents to address disorders where Trk receptors play a role, by targeting populations selectively.

Animals↗

PubMed2000

Molecular genetics and epidemiology of the NAT1 and NAT2 acetylation polymorphisms.

The focus of this review is the molecular genetics, including consensus NAT1 and NAT2 nomenclature, and cancer epidemiology of the NAT1 and NAT2 acetylation polymorphisms. Two N-acetyltransferase isozymes, NAT1 and NAT2, are polymorphic and catalyze both N-acetylation (usually deactivation) and O-acetylation (usually activation) of aromatic and heterocyclic amine carcinogens. Epidemiological studies suggest that the NAT1 and NAT2 acetylation polymorphisms modify risk of developing urinary bladder, colorectal, breast, head and neck, lung, and possibly prostate cancers. Associations between slow NAT2 acetylator genotypes and urinary bladder cancer and between rapid NAT2 acetylator genotypes and colorectal cancer are the most consistently reported. The individual risks associated with NAT1 and/or NAT2 acetylator genotypes are small, but they increase when considered in conjunction with other susceptibility genes and/or aromatic and heterocyclic amine carcinogen exposures. Because of the relatively high frequency of some NAT1 and NAT2 genotypes in the population, the attributable cancer risk may be high. The effect of NAT1 and NAT2 genotype on cancer risk varies with organ site, probably reflecting tissue-specific expression of NAT1 and NAT2. Ethnic differences exist in NAT1 and NAT2 genotype frequencies that may be a factor in cancer incidence. Large-scale molecular epidemiological studies that investigate the role of NAT1 and NAT2 genotypes and/or phenotypes together with other genetic susceptibility gene polymorphisms and biomarkers of carcinogen exposure are necessary to expand our current understanding of the role of NAT1 and NAT2 acetylation polymorphisms in cancer risk.

Acetylation↗

PubMed2000

[Radiation-induced apoptosis and p53, bcl-2 gene expression products in QGY-7703 cell line in vitro].

OBJECTIVE: To investigate the dose response and time course of radiation-induced apoptosis and gene expression products of p53, bcl-2 genes in human hepatocarcinoma cell line QGY-7703 in vitro. METHODS: Apoptosis was induced by radiation and quantitated by Flow Cytometry. The oncoproteins of p53 and bcl-2 genes after radiation were detected immunocytochemically on cell cytospinned slides. The data were analyzed with Sony Mias-300 Spato Immage Analyzer. RESULTS: The percentage of apoptosis in unradiation QGY-7703 was 4. 79%. After radiation, the apoptotic fraction increased with incubation time and radiation dose. Both gene expression products increased with incubation time and reached plateau at 6h post-radiation. CONCLUSION: After radiation, the response and time course of radiation-induced apoptosis in QGY-7703 cell line are similar to those of p53, bcl-2 oncoproteins. The later proceeds by the apoptosis peak about 6 h. The results suggest that p53 and bcl-2 genes are the regulating factors partially in radiation-induced apoptosis of QGY-7703 cell line.

Apoptosis↗

PubMed2000

Effects of diltiazem on down-regulation of lymphocyte beta-adrenoceptors in patients with chronic congestive heart failure.

AIM: To determine whether diltiazem could reverse down-regulation of lymphocyte beta-adrenoceptor (beta-AR) in patients with chronic congestive heart failure (CHF). METHODS: Before and after the treatment with diltiazem in CHF patients, lymphocyte beta-AR density was measured with [3H]dihydroalprenolol radioligand binding assay, levels of free cytosolic calcium ([Ca2+]i) in platelets were estimated with fluorescent indicator Fura 2-AM, plasma norepinephrine (NE) levels were measured with 125I-radioimmunoassay. RESULTS: Lymphocyte beta-AR density was lower and [Ca2+]i in platelets was significantly higher in CHF patients than those in control. Plasma NE levels were higher in CHF patients than those in control. Diltiazem therapy reduced [Ca2+]i in platelets and increased lymphocyte beta-AR density in CHF patients without significant change of plasma NE concentration. CONCLUSIONS: Diltiazem partly reversed down-regulation of lymphocyte beta-AR density in CHF patients, and this effect was not related to the level of plasma NE, and might be attributed to intracellular [Ca2+]i decrease.

Blood Platelets↗

PubMed2000

Development and laboratory evaluation of a new toothbrush with a novel brush head design.

Despite many developments in manual toothbrush design, plaque removal at the back of the mouth and at approximal surfaces remains inadequate, yet it is at these sites in particular that plaque accumulates and leads to the development of gingival disease. Improved oral hygiene can be achieved by better brushing technique and by increasing brushing time, but a change in behavior patterns is almost impossible to achieve for the majority of individuals. What is required is a brush head design that maximizes plaque removal, regardless of how the user brushes. As a result of a detailed investigation into the action of bistles during brushing, the Oral-B CrossAction toothbrush has been developed. It incorporates bristles angled at 16 degrees in a unique CrissCross design arranged along the horizontal axis of the toothbrush. Laboratory studies have demonstrated that this development significantly enhances interproximal penetration and cleaning effectiveness when compared with an identical brush head with vertical rather than angled bristles. Laboratory comparisons with more than 80 leading manual toothbrushes from around the world demonstrate a consistent, significant advantage for the new CrossAction toothbrush, both with respect to interproximal penetration and cleaning effectiveness. These results suggest that the CrossAction toothbrush has the potential to remove greater amounts of plaque, especially from the approximal surfaces, than conventional toothbrushes incorporating vertical bristles or more traditional tuft designs.

Adult↗

PubMed2000

[Aluminum forms in acid sulfate soils].

With the method of sequential extraction, the extractable noncrystalline aluminum in Acid Sulfate Soils was fractionized into exchangeable Al (ExAl), absorbed inorganic hydroxy-Al(HyAl), organic complexed Al(OrAl), Fe oxide bound Al (DCBAl), interlayered Al(InAl) and noncrystalline aluminosilicate(NcAl) with average of 1.79, 2.51, 4.17, 4.14, 4.31 and 8.66 g Al2O3.kg-1, respectively. In actual Acid Sulfate Soils, the amount of different forms Al followed the order of NcAl > OrAl > InAl > DCBAl > ExAl > HyAl, but in potential acid sulfate soils, NcAl > InAl > DCBAl > HyAl > OrAl > ExAl. The average of the total extractable noncrystalline Al was 35.57 g Al2O3.kg-1, which covered 25.04% of the total amount of Al in Acid Sulfate Soils. The characteristic of extractable noncrystalline Al in Acid Sulfate Soils was the high proportion of active aluminum, such as ExAl, HyAl and OrAl. All forms of Al were closely related to the corresponding properties and ecological characteristics of Acid Sulfate Soils. The strong acid environment of actual Acid Sulfate Soils induced over-released Al, which transformed to active Al and resulted in Al toxicity.

Aluminum↗