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Biomedical subjects

M Ma

Publications and source records attributed to M Ma.

At least 37 records · Page 2Linked to original sources
PubMed2001

Loss of E-cadherin expression in gastric intestinal metaplasia and later stage p53 altered expression in gastric carcinogenesis.

Gastric cancers are commonly subdivided into intestinal and diffuse subtypes on a morphologic basis, supported by corollary evidence of differences at the pathogenetic and molecular levels. Chronic atrophic gastritis with intestinal metaplasia is a common precursor lesion for the intestinal type of carcinoma. To identify early molecular changes, in this study we have examined 13 surgical specimens both for the expression of E-cadherin, p53 and beta-catenin by immunohistochemistry and for methylation of the CDH1 promoter (E-cadherin) by bisulfite genomic sequencing of laser capture microdissected samples. Each specimen examined contained areas of normal (nonmetaplastic) gastric mucosa, as well as areas of intestinal metaplasia and/or carcinoma. Reduced or absent E-cadherin and partial to complete methylation of one to multiple CpG sites examined in the CDH1 promoter were observed in all of the metaplasia samples. Thus, the methylation status of the CDH1 promoter and expression of E-cadherin together provide strong evidence that loss of E-cadherin is an early event in intestinal type gastric carcinogenesis. In contrast, expression of p53, assumed to be mutant p53, was generally not detected (except for isolated cells) until the carcinoma stage in tissues from these patients. These results suggest that mutation of p53 is a late event in intestinal type gastric cancer. The level of beta-catenin expression did not appear to change between normal, metaplastic and carcinoma cells of intestinal type, and no nuclear staining was visible in any of the tissues. These results suggest that the Wnt signaling pathway is not upregulated in this type of cancer.

Adenocarcinoma↗
PubMed2001

A prospective survey of patients after cessation of patient-controlled analgesia.

UNLABELLED: Cessation of IV patient-controlled analgesia (PCA) in the postoperative period is often an arbitrary clinical decision. We conducted a prospective survey of patients 24 h after cessation of IV PCA morphine to determine whether they wished to be restarted on PCA, and to evaluate factors affecting this decision. One hundred and fifteen patients were surveyed over a 3-mo period. Thirty-eight patients (33%) wished to restart PCA. The most common reason was the expectation that IV PCA would be more effective. Age, sex, type of surgery, duration of PCA use, side effects, pain scores, and reasons for cessation of PCA did not affect the decision. The reasons given by those who did not wish to restart PCA were minimal pain (51.9%), inconvenient PCA machine (15.6%), ineffective analgesia by IV PCA (11.7%), side effects during PCA (11.7%), and wishing to tolerate pain (7.8%). PCA morphine consumption in the 24-h period before cessation of PCA (mean [SD]) was larger in patients wishing to restart PCA than in those who did not (21.1 [14.8] mg vs 15.1 [15.1] mg; P < 0.05). In conclusion, the clinical decisions to cease IV PCA do not predict patient acceptance of and satisfaction with the decision and with subsequent pain treatment. Morphine consumption may predict a patient's acceptance of ceasing PCA. IMPLICATIONS: We surveyed patients 24 h after cessation of IV patient-controlled analgesia (PCA). This survey revealed that the usual clinical reasons to stop IV PCA might not be the most appropriate. Patients have different reasons why they wish to restart or not restart IV PCA. The cessation of PCA should be individualized.

Adult↗
PubMed2001

Cardiovascular responsivity to stress in adolescents with and without persistently elevated blood pressure.

OBJECTIVES: The goal of this study was to compare the cardiovascular responses to behavioural stressors of three groups of adolescents who differed in blood pressure status across assessments. DESIGN: Casual blood pressure of adolescents who were identified as having elevated blood pressure during a school screen was re-evaluated in the laboratory. The adolescents were classified into two groups: (i) those with consistently elevated blood pressure across school and laboratory assessments and (i) those with labile blood pressure whose blood pressure in the laboratory was below 130/80 mmHg. A comparison group of adolescents with consistently normal blood pressure was also included. METHODS: Cardiovascular parameters were assessed during rest and during two behavioural stressors, the evaluated speaking task and the mirror tracing task. RESULTS: Adolescents with elevated blood pressure were more vascularly responsive across stressors than adolescents with labile blood pressure, who, in turn, were more reactive than adolescents with normal blood pressure. CONCLUSIONS: These results suggest that vascular reactivity to behavioural stressors may be useful in predicting risk of hypertension because of its sensitivity in distinguishing adolescents with consistently elevated blood pressure from those with labile blood pressure and those with normal blood pressure.

Adolescent↗
PubMed2001

Inhibition of progression of heart failure and expression of TGF-beta 1 mRNA in rats with heart failure by the ACE inhibitor quinapril.

The cardioprotective effects of quinapril, an angiotensin-converting enzyme inhibitor, were studied in a rat model of heart failure. Twenty-six rats were divided into two groups: one given 20 mg/kg/day quinapril (n = 11), and controls given 0.5% methylcellulose (n = 15). After oral administration for 1 month, quinapril reduced heart weight (from 1.28+/-0.05 to 0.87+/-0.02 g; p < 0.05) without changing body weight. Quinapril lowered left ventricular end-diastolic pressure (from 14.1+/-2.0 to 6.6+/-1.5 mmHg; p < 0.05) and central venous pressure (from 2.7+/-0.9 to 0.7+/-0.4 mmHg), and increased +/- dP/dt (from +2409+/-50 to +3569+/-169 mmHg/s, and from -2318+/-235 to -3960+/-203 mmHg/s; both p < 0.01). The area of myocardial fibrosis was markedly reduced by quinapril (6+/-3%) as compared with controls (29+/-6%; p < 0.01). Expression of transforming growth factor (TGF)-beta1 mRNA was markedly increased in controls as compared with age-matched normal rats. The increase in level of TGF-beta1 mRNA was significantly suppressed by quinapril (from 17.1+/-6.2 to 9.00+/-2.40; p < 0.05). These observations indicated that quinapril has cardioprotective effects on heart failure, and that the beneficial effects may be partly explained by attenuation of fibrotic response through suppression of TGF-beta1 mRNA expression.

Administration, Oral↗
PubMed2001

Bisoprolol improves survival in rats with heart failure.

The cardioprotective effects of bisoprolol were studied in a rat model of severe heart failure induced by autoimmune myocarditis. Twenty-eight days after immunization, Lewis rats were divided into four groups: 0.1 mg/kg/day bisoprolol (Group 0.1), 1.0 mg/kg/day bisoprolol (Group 1) and 10 mg/kg/day bisoprolol (Group 10), and vehicle (0.5% methylcellulose; Group V) (all groups, n = 13). After oral administration for 1 month, heart weight, mean blood pressure, heart rate, central venous pressure, peak left ventricular pressure, left ventricular end-diastolic pressure, +/- dP/dt, and area of fibrosis were measured. Although bisoprolol reduced heart rate (399+/-11/min in Group V, 382+/-10/min in Group 0.1, 348+/-8/min in Group 1 and 302+/-9/min in Group 10) and increased survival (62% in Group V, 69% in Group 0.1, and 100% in Group 1 and Group 10) in a dose-dependent manner, this drug did not change heart weight, the area of myocardial fibrosis or hemodynamic parameters. These observations suggested that bisoprolol may improve survival independently of its effect on left ventricular function by reducing sudden death in patients with severe heart failure.

Adrenergic beta-Antagonists↗
PubMed2001

[Large-capacity expanded cytoline-induced killer cells and its cytotoxic activity].

This study was conducted to establish the large-capacity culture methd of cytokine-induced killer (CIK) cells for clinical therapy and assess its effect on the fuction of cell-mediated immunity following autologous CIK cells reinfusion. Autologus CIK cells were expanded in 1000 ml culture-bag and reinfused back. The MTT method was used to test the cytotoxic activity of CIK cells before and after reinfusion. The results showed that the total amount of autologous CIK cells reinfusion exceeded 1.6 x 10(10) with the use of the culture method of large-capacity. The PBMNC from patients treated by CIK cells showed significant increase in cytotoxic activity, no side effects were observed, and therefore the large-capacity culture method of CIK cells is a simle and safe therapy for treating the minimum residue of diseases.

Adult↗
PubMed2001

Transgenic mice with overexpression of human scavenger receptor A on endothelial cells.

OBJECTIVES: To establish a new transgenic mouse model for determining the function and role of human scavenger receptor A (SR-A) in atherosclerosis in vivo. METHODS: Human scavenger receptor minigene-driven mouse tie-1 promoter was constructed and confirmed by endonuclease digestion and sequence analysis. Transgenic mice were generated via the microinjection method. PCR and Southern blot were used to screen the positive transgenic mice. RT-PCR and immunohistochemical analysis were used to detect the level and location of human SR-AI expression in transgenic mice. The activity of human SR-AI was determined by morphologic observation of aortic endothelial cells of transgenic mice under transmission electron microscopy. RESULTS: The electrophoresis assay showed the expected 4 fragments of 0.9 kb, 1.1 kb, 1.2 kb and 4.2 kb in the Sma I digest and 2 fragments of 0.8 kb and 6.7 kb in Bgl II digest of plasmids pTie-1/hSR-A. The fragment sequence of tie-1 promoter and human SR-A cDNA in plasmids pTie-1/hSR-A was correct and no ATG before the translation initiation sites of human SR-A was found by sequence analysis. 561 injected and surviving embryos with the purified human SR-A minigene were implanted into the oviducts of 19 ICR pseudopregnant mice. Among the 54 surviving pups from 13 foster mothers, 7 were identified by PCR and Southern blot analysis. The results of RT-PCR and immunohistochemical analysis showed human SR-A was specifically expressed on vascular endothelial cells of the aorta and renal artery, as well as hepatic sinusoidal endothelial cells in transgenic mice. Transmission electron microscope (TEM) of aorta of transgenic mice showed that a large number of vesicles, multivesicle bodies and swollen mitochondria filled the plasma of endothelial cells. CONCLUSIONS: A transgenic mouse model with overexpression of human SR-A in endothelial cells was successfully established. The transgene was integrated and transmitted into the chromosome of transgenic mice. Tie-1 promoter controlled the transgene to express in endothelial cells in mice. Pinocytic activity of aortic endothelial cells in transgenic mice was higher than that of C57BL/6J mice. Our studies will provide a new transgenic model for investigation of atherosclerosis and functions of human SR-A.

Animals↗
PubMed2001

[Mutagenic activity of organic pollutants extracted from waters in Guanting Reservoir and Yongding River].

Water samples collected from Guanting Reservoir and Yongding River in July 1999 were examined by Ames test to evaluate the mutagenic activity of organic pollutants. The samples have been concentrated by using XAD-2 resin filled columns. In the test with strain TA98, direct mutagenic effects (-S9) were observed in water extracted from Bridge No.8 and Yanchi at the dosage of 0.8 L/plate, indicating the existence of direct frame shift mutagens. The mutagenic effects disappeared after addition of S9, indicating no pro-mutagen in the samples. In the test with strain TA100, direct base pair substitute mutagenic effect was observed only in the sample from Bridge No. 8 at the dosage of 0.4 L/plate. When adding S9, suspicious positive reaction could exist at the dosage of 0.8 L/plate. The results demonstrated that the water in Yongding River has been heavily polluted by mutagens, for which further studies should be carried out to identify the sources and types of these mutagens.

Animals↗
PubMed2001

[Cloning and sequence analysis of the phytase phyA gene of Aspergillus niger N25].

The phyA encoding phytase of Aspergillus niger N25 was amplified by the polymerase chain reaction (PCR) with primers designed according to the sequences of the phyA in GenBank. The amplified fragment was cloned and sequenced. The results show that: the coding region is 1506 bp in size, includes a 102 bp intron, and encodes a peptide of 476 amino acid residues, in which there is a signal peptide with 19 amino acids and a mature peptide of 448 amino acids. Comparison of this sequence with the phyA of the natural A. niger NRRL3135 (GenBank Accession: M94550), the most highly secreting-phytase strain, shows that the nucleotide homology is as high as 96.746%, and the amino acid homology comes up to 97.64%. The phyA of A. niger N25 strain in this paper is appropriate to be used to construct the phytase gene-engineering bacteria.

6-Phytase↗
PubMed2000

Functional mosaic organization of mouse olfactory receptor neurons.

In contrast to rapid progress in the molecular biology of olfaction, there are few physiological data to characterize the odor response properties of different populations of olfactory receptor neurons (ORNs) and their spatial distributions across the epithelium, which is essential for understanding the coding mechanisms underlying odor discrimination and recognition. We have tested the hypothesis that the ORNs are arranged in a functional mosaic, using an intact epithelial preparation from the mouse, in which odor responses of many ORNs in situ can be monitored simultaneously with calcium imaging techniques. ORNs responding to a given odor were widely distributed across epithelium and intermingled with ORNs responding to other odors. Tight clusters of ORNs responding to the same odor were observed. For a given odor, more ORNs were recruited when the concentration was increased. ORNs were able to distinguish between pairs of enantiomers by showing distinct but somewhat overlapping patterns. The results provide evidence regarding the response spectra of ORNs in situ, supporting the combinatorial coding of odor quality and intensity by different ORN subsets.

Animals↗
PubMed2000

Speciation of key arsenic metabolic intermediates in human urine.

Biomethylation is the major human metabolic pathway for inorganic arsenic, and the speciation of arsenic metabolites is essential to a better understanding of arsenic metabolism and health effects. Here we describe a technique for the speciation of arsenic in human urine and demonstrate its application to the discovery of key arsenic metabolic intermediates, monomethylarsonous acid (MMAIII) and dimethylarsinous acid (DMAIII), in human urine. The study provides a direct evidence in support of the proposed arsenic methylation pathway in the human. The finding of MMAIII and DMAIII in human urine, along with recent studies showing the high toxicity of these arsenicals, suggests that the usual belief of arsenic detoxification by methylation needs to be reconsidered. The arsenic speciation technique is based on ion pair chromatographic separation of arsenic species on a 3-micron particle size column at 50 degrees C followed by hydride generation atomic fluorescence detection. Speciation of MMAIII, DMAIII, arsenite (AsIII), arsenate (AsV), monomethylarsonic acid (MMAV), and dimethylarsinic acid (DMAV) in urine samples is complete in 6 min with detection limits of 0.5-2 micrograms/L. There is no need for any sample pretreatment. The capability of rapid analysis of trace levels of arsenic species, which resulted in the findings of the key metabolic intermediates, makes the technique useful for routine arsenic speciation analysis required for toxicological and epidemiological studies.

Arsenic↗
PubMed2000

Orbitally degenerate spin-1 model for insulating V2O3

Motivated by recent neutron, x-ray absorption, and resonant scattering experiments, we revisit the electronic structure of V2O3. We propose a model in which S = 1 V3+ ions are coupled in the vertical V-V pairs forming twofold orbitally degenerate configurations with S = 2. Ferro-orbital ordering of the V-V pairs gives a description which is consistent with all experiments in the antiferromagnetic insulating phase.

Journal Article↗
PubMed2000

DMPS-arsenic challenge test. II. Modulation of arsenic species, including monomethylarsonous acid (MMA(III)), excreted in human urine.

The administration of sodium 2,3-dimercapto-1-propane sulfonate (DMPS) to humans chronically exposed to inorganic arsenic in their drinking water resulted in the increased urinary excretion of arsenic, the appearance and identification of monomethylarsonous acid (MMA(III)) in their urine, and a large decrease in the concentration and percentage of urinary dimethylarsinic acid (DMA). This is the first time that MMA(III) has been detected in the urine. In vitro biochemical experiments were then designed and performed to understand the urinary appearance of MMA(III) and decrease of DMA. The DMPS-MMA(III) complex was not active as a substrate for the MMA(III) methyltransferase. The experimental results support the hypothesis that DMPS competes with endogenous ligands for MMA(III), forming a DMPS-MMA complex that is readily excreted in the urine and points out the need for studying the biochemical toxicology of MMA(III). It should be emphasized that MMA(III) was excreted in the urine only after DMPS administration. The results of these studies raise many questions about the potential central role of MMA(III) in the toxicity of inorganic arsenic and to the potential involvement of MMA(III) in the little-understood etiology of hyperkeratosis, hyperpigmentation, and cancer that can result from chronic inorganic arsenic exposure.

Adult↗
PubMed2000

Effects of Manduca diuresin on neonates of the tobacco hornworm, Manduca sexta.

Manduca diuresin (MD), a 30 amino acid peptide, was isolated and identified from the type IIb median neurosecretory cells in the brain of adult Manduca sexta (Blackburn et al., Biochem. Biophys. Res. Commun., 181, 927-932, 1991). The synthetic hormone stimulates water loss in the adult moth both in vitro using isolated Malphigian tubule preparations and in vivo using decapitated adult moths as bioassay animals (Blackburn and Ma, Arch. Insect Biochem. Physiol., 27, 3-10, 1994). In the present study, MD was shown to have adverse physiological effects on neonates of Manduca sexta when fed synthetic hormone-treated leaf discs. With a sustained diet of MD-treated discs, neonates exhibited symptoms of reduced food consumption and marginal weight increases. In addition to slowed growth and reduced developmental rates, a high percentage of these neonates failed to molt into second instar larvae and death usually followed shortly thereafter. This is a first report that a synthetic insect neuropeptide has shown detrimental effect on insect larvae by ingestion. The possibility of utilizing this peptide in plant protection is discussed.

Animals↗
PubMed2000

Occurrence of monomethylarsonous acid in urine of humans exposed to inorganic arsenic.

Monomethylarsonous acid (MMA(III)) has been detected for the first time in the urine of some humans exposed to inorganic arsenic in their drinking water. Our experiments have dealt with subjects in Romania who have been exposed to 2.8, 29, 84, or 161 microg of As/L in their drinking water. In the latter two groups, MMA(III) was 11 and 7% of the urinary arsenic while the monomethylarsonic acid (MMA(V)) was 14 and 13%, respectively. Of our 58 subjects, 17% had MMA(III) in their urine. MMA(III) was not found in urine of any members of the group with the lowest level of As exposure. If the lowest-level As exposure group is excluded, 23% of our subjects had MMA(III) in their urine. Our results indicate that (a) future studies concerning urinary arsenic profiles of arsenic-exposed humans must determine MMA(III) concentrations, (b) previous studies of urinary profiles dealing with humans exposed to arsenic need to be re-examined and re-evaluated, and (c) since MMA(III) is more toxic than inorganic arsenite, a re-examination is needed of the two hypotheses which hold that methylation is a detoxication process for inorganic arsenite and that inorganic arsenite is the major cause of the toxicity and carcinogenicity of inorganic arsenic.

Adolescent↗
PubMed2000

Intracellular mRNA cleavage induced through activation of RNase P by nuclease-resistant external guide sequences.

Most antisense oligonucleotide experiments are performed with molecules containing RNase H-competent backbones. However, RNase H may cleave nontargeted mRNAs bound to only partially complementary oligonucleotides. Decreasing such "irrelevant cleavage" would be of critical importance to the ability of the antisense biotechnology to provide accurate assessment of gene function. RNase P is a ubiquitous endogenous cellular ribozyme whose function is to cleave the 5' terminus of precursor tRNAs to generate the mature tRNA. To recruit RNase P, complementary oligonucleotides called external guide sequences (EGS), which mimic structural features of precursor tRNA, were incorporated into an antisense 2'-O-methyl oligoribonucleotide targeted to the 3' region of the PKC-alpha mRNA. In T24 human bladder carcinoma cells, these EGSs, but not control sequences, were highly effective in downregulating PKC-alpha protein and mRNA expression. Furthermore, the downregulation is dependent on the presence of, and base sequence in, the T-loop. Similar observations were made with an EGS targeted to the bcl-xL mRNA.

3' Untranslated Regions↗