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Biomedical subjects

J Ma

Publications and source records attributed to J Ma.

At least 235 records · Page 13Linked to original sources
PubMed2000

Daily head-up tilt, standing or centrifugation can prevent vasoreactivity changes in arteries of simulated weightless rats.

Artificial gravity will be considered for long-duration spaceflight missions. Recent studies have shown that continuous exposure to gravity does not appear necessary to prevent the adverse effects of weightlessness, instead intermittent exposure may suffice. Vernikos et al reported that 1 G intermittent exposures with and without walking exercise was effective in preventing physiologic deconditioning with 4-d, -6 degrees bedrest, and standing at 1 G was most effective in preventing orthostatic intolerance. Our previous work has demonstrated differential adaptational changes in structure, function, and innervation state of arterial vasculature in different body regions of rat during simulated weightlessness and further suggested that these changes might be one of the most important mechanisms accounting for postflight orthostatic intolerance. We therefore designed the present study involving a comprehensive evaluation of the effect of intermittent G exposure in preventing the differential functional changes of the arteries at the end of 3-wk head-down tail suspension in rats to answer the following questions: (1) do intermittent G exposure have counteracting effect in preventing differential functional changes in arterial vasculature with tail-suspension? (2) among the treatments used in the present study, i.e., head-up tilt (HUT), standing (STD), and centrifugation (CEN), what kind of exposure is more effective? (3) how much time in daily 1 G exposure is needed to maintain the normal (1 G) vascular responsiveness?

Adaptation, Physiological↗
PubMed2000

Vasoconstrictor responsiveness of hind body vascular beds is diminished in tail-suspended rats.

It is well known that the mechanisms of occurrence of orthostatic intolerance induced by exposure to microgravity deal with multiple factors including alterations of arteries. In the previous works, the diminished contractile responsiveness of abdominal aorta and hind body medium-sized conduit arteries, mesenteric artery and femoral artery, were observed in tail-suspended rats, and the data showed that the femoral artery have subjected to the greatest changes. These results suggested that the vasoreactivity of resistance vessels might be affected by the real or simulated microgravity. Since the arterioles are the main site of peripheral resistance and of its regulation. Therefore, changes in responsiveness of arteriolar network, especially in the lower/hind body region, would be of primary importance in the genesis of postflight orthostatic intolerance. The aim of the present work was to examine whether simulated weightlessness may lead to an impairment in vasoconstrictor responsiveness in hind body vascular beds.

Animals↗
PubMed2000

[Transposition of expanded cervical-shoulder skin flaps for the repair of cicatricial contracture deformity of neck].

OBJECTIVE: To evaluate the efficacy of expanded cervical-shoulder skin flap in the treatment of cicatricial contracture deformity of neck, and improve the method for the repair of soft tissue defect of neck. METHOD: 12 patients with cicatricial contracture of neck were treated by pre-expanded cervical-shoulder skin flap and then transposition for the reconstruction of the defect after cervical scar resection. RESULT: All the 24 flaps were survived. Postoperative follow-up for 6 months to one year showed that the cervico-mandibular function and the external appearance of the flaps were satisfactory without swelling and contracture. CONCLUSION: Pre-expanded cervical-shoulder skin flap is available for the treatment of cicatricial contracture deformity of neck.

Adolescent↗
PubMed2000

[Erythroid differentiation denucleation factor: a family of erythroid regulators for mammalian erythroid terminal differentiation/tumor suppression and the cloning of their related genes].

The role of regulation of erythroid differentiation denucleation factor(EDDF) on mammalian erythroid differentiation and myeloma cell malignancy as well as cloning of their stage related genes were serially studied. Through a series of cybrid and hybridization experiments between mammalian erythroid cells and erythroleukemia or non-erythroid myeloma cells, we have demonstrated a novel family of erythroid regulators(EDDFs) in the mammalian differentiating erythroblasts which with an active peak occurred concomitantly with marked decreases in DNA, RNA and the nuclear anchoring vimentin-IF, but increased in hemoglobin synthesis in cytoplasm prior to the denucleation process during terminal differentiation. The results of cell fusion experiments verified that the supplement of regulators(EDDFs) was critical to the recovery of the originally lost features of terminal differentiation and the reversion of malignant phenotype of tumor cells. Here we showed that the erythroid regulator family EDDFs were essential regulators for the sequential expression of stage related genes of erythroid terminal differentiation, and for the redifferentiation of tumor cells to express the originally inactive globe genes, repressed the oncogenes, and vimentin-IF system, thus initiated nuclear condensation and denucleation. The EDDF gene family consisted of MEDDF, HEDDF-1, HEDRF-1, HEDRF-2 and HCNBP-1 were cloned. All were novel cDNA sequences that have been searched and registered in GenBank. They expressed varying in a stage specific manner, and acted on corresponding genes of terminal differentiation.

Activins↗
PubMed2000

[Simultaneous determination of iron, cobalt and nickel in oil by multiwavelength linear regression spectrophotometry].

A method for simultaneous determination of iron, cobalt and nickel, using multiwavelength linear regression spectrophotometry, is proposed. Since there were no interferences caused by cobolt and nickel complexes at the peak of iron complex compound formed with 5-Br-PADAP at 750 nm, the content of iron was determined by working-curve method at 750 nm. Cobalt and nickel were simultaneously determined by multiwavelength linear regression method over the range 550-600 nm. The method was applied to the analysis of iron, cobalt and nickel in synthetic mixtures and oil samples with satisfactory results. The recovery was 97.5%-104.3% and the RSD% was 1.4%-3.8%.

English Abstract↗
PubMed1999

A negatively charged region of the skeletal muscle ryanodine receptor is involved in Ca(2+)-dependent regulation of the Ca(2+) release channel.

The ryanodine receptor/Ca(2+) release channels from skeletal (RyR1) and cardiac (RyR2) muscle cells exhibit different inactivation profiles by cytosolic Ca(2+). D3 is one of the divergent regions between RyR1 (amino acids (aa) 1872-1923) and RyR2 (aa 1852-1890) and may contain putative binding site(s) for Ca(2+)-dependent inactivation of RyR. To test this possibility, we have deleted the D3 region from RyR1 (DeltaD3-RyR1), residues 1038-3355 from RyR2 (Delta(1038-3355)-RyR2) and inserted the skeletal D3 into Delta(1038-3355)-RyR2 to generate sD3-RyR2. The channels formed by DeltaD3-RyR1 and Delta(1038-3355)-RyR2 are resistant to inactivation by mM [Ca(2+)], whereas the chimeric sD3-RyR2 channel exhibits significant inactivation at mM [Ca(2+)]. The DeltaD3-RyR1 channel retains its sensitivity to activation by caffeine, but is resistant to inactivation by Mg(2+). The data suggest that the skeletal D3 region is involved in the Ca(2+)-dependent regulation of the RyR1 channel.

Amino Acid Sequence↗
PubMed1999

Glutamate-89 in subunit II of cytochrome bo3 from Escherichia coli is required for the function of the heme-copper oxidase.

Recent electrostatics calculations on the cytochrome c oxidase from Paracoccus denitrificans revealed an unexpected coupling between the redox state of the heme-copper center and the state of protonation of a glutamic acid (E78II) that is 25 A away in subunit II of the oxidase. Examination of more than 300 sequences of the homologous subunit in other heme-copper oxidases shows that this residue is virtually totally conserved and is in a cluster of very highly conserved residues at the "negative" end (bacterial cytoplasm or mitochondrial matrix) of the second transmembrane helix. The functional importance of several residues in this cluster (E89II, W93II, T94II, and P96II) was examined by site-directed mutagenesis of the corresponding region of the cytochrome bo(3) quinol oxidase from Escherichia coli (where E89II is the equivalent of residue E78II of the P. denitrificans oxidase). Substitution of E89II with either alanine or glutamine resulted in reducing the rate of turnover to about 43 or 10% of the wild-type value, respectively, whereas E89D has only about 60% of the activity of the control oxidase. The quinol oxidase activity of the W93V mutant is also reduced to about 30% of that of the wild-type oxidase. Spectroscopic studies with the purified E89A and E89Q mutants indicate no perturbation of the heme-copper center. The data suggest that E89II (E. coli numbering) is critical for the function of the heme copper oxidases. The proximity to K362 suggests that this glutamic acid residue may regulate proton entry or transit through the K-channel. This hypothesis is supported by the finding that the degree of oxidation of the low-spin heme b is greater in the steady state using hydrogen peroxide as an oxidant in place of dioxygen for the E89Q mutant. Thus, it appears that the inhibition resulting from the E89II mutation is due to a block in the reduction of the heme-copper binuclear center, expected for K-channel mutants.

Alanine↗
PubMed1999

A(2A) adenosine receptor deficiency attenuates brain injury induced by transient focal ischemia in mice.

Extracellular adenosine critically modulates ischemic brain injury, at least in part through activation of the A(1) adenosine receptor. However, the role played by the A(2A) receptor has been obscured by intrinsic limitations of A(2A) adenosinergic agents. To overcome these pharmacological limitations, we explored the consequences of deleting the A(2A) adenosine receptor on brain damage after transient focal ischemia. Cerebral morphology, as well as vascular and physiological measures (before, during, and after ischemia) did not differ between A(2A) receptor knock-out and wild-type littermates. The volume of cerebral infarction, as well as the associated neurological deficit induced by transient filament occlusion of the middle cerebral artery, were significantly attenuated in A(2A) receptor knock-out mice. This neuroprotective phenotype of A(2A) receptor-deficient mice was observed in different genetic backgrounds, confirming A(2A) receptor disruption as its cause. Together with complimentary pharmacological studies, these data suggest that A(2A) receptors play a prominent role in the development of ischemic injury within brain and demonstrate the potential for anatomical and functional neuroprotection against stroke by A(2A) receptor antagonists.

Aging↗
PubMed1999

Beta-carotene supplementation for patients with low baseline levels and decreased risks of total and prostate carcinoma.

BACKGROUND: The Physicians' Health Study was a randomized, double-blind, placebo-controlled trial using a 2x2 factorial design including supplementation with beta-carotene (50 mg every other day) in the primary prevention of cancer among 22,071 U.S. male physicians ages 40-84 years at randomization. Before randomization, the authors collected baseline blood specimens to determine whether any benefit was greater among or confined to those with low baseline levels of beta-carotene. METHODS: Baseline blood samples were collected from 14,916 participants. These samples were assayed, according to a nested case-control design, from 1439 men subsequently diagnosed with cancer over 12 years of follow-up (631 with prostate carcinoma) and 2204 controls matched by age and smoking habits. RESULTS: Men in the lowest quartile for plasma beta-carotene at baseline had a marginally significant (P = 0.07) increased risk of cancer compared with those in the highest quartile (relative risk [RR] = 1.30, 95% confidence interval [CI], 0.98-1.74). Men in the lowest quartile assigned at random to beta-carotene supplementation had a possible but nonsignificant decrease in overall cancer risk (RR = 0.83, 95% CI, 0.63-1.09) compared with those assigned to placebo. This was primarily due to a significant reduction in the risk of prostate carcinoma (RR = 0.68, 95% CI, 0. 46-0.99) in this group. After the first 2 years of follow-up were excluded, the results were virtually unchanged. CONCLUSIONS: These prespecified subgroup analyses appeared to support the idea that beta-carotene supplementation may reduce risk of prostate carcinoma among those with low baseline levels. Further follow-up of this population will help determine whether these findings are valid.

Adult↗
PubMed1999

Function of the second nucleotide-binding fold in the CFTR chloride channel.

To test the role of nucleotide-binding fold (NBF) 2 and its interaction with the regulatory (R) domain in the function of the cystic fibrosis transmembrane conductance regulator (CFTR) channel, we used three deletion mutants of CFTR: DeltaR(708-835), DeltaNBF2(1185-1349) and DeltaR-DeltaNBF2. In lipid bilayers, DeltaNBF2 channel activity is ATP- and cAMP-dependent protein kinase (PKA)-dependent, but unlike wild-type (wt) CFTR, it displays a reduced activity and insensitivity to 5'-adenylylimidodiphosphate (AMP-PNP). Both DeltaR and DeltaR-DeltaNBF2 channels are PKA-independent, but DeltaR activity is reduced whereas DeltaR-DeltaNBF2 activity is increased. Deletion of NBF2 from CFTR affects protein trafficking and channel gating kinetics. The data suggest that NBF2 could have inhibitory and stimulatory roles in CFTR activity by interaction with NBF1 directly or indirectly via the R domain.

Adenosine Triphosphate↗
PubMed1999

l-Deprenyl, blocking apoptosis and regulating gene expression in cultured retinal neurons.

Apoptosis is the final pathway of many forms of retinal degeneration. E1A-NR3 is an immortalized retinal cell line that manifests specific phenotypes of retinal neurons. The present study induced apoptosis in these cells by two ischemic assaults, serum deprivation and hypoxia. The results demonstrated that both the assaults decreased viable cell numbers significantly by inducing apoptosis, as revealed by viable cell count, DNA fragmentation analysis, and in situ labeling of apoptotic cells by the TdT-mediated dUTP-biotin nick end-labeling (TUNEL) method. l-Deprenyl is known to be a monoamine oxidase inhibitor, and it was found recently to have neurotrophic activities. We set out to determine the protective effect of l-deprenyl on retinal cells and delineate its mechanism independent of monoamine oxidase inhibition. At concentrations as low as 0.0001 and 0.001 microM, l-deprenyl significantly increased the numbers of surviving cells under serum-free and hypoxic conditions, respectively. This effect appeared to be dependent upon the l-deprenyl concentration within the range of 0.001 to 10 microM. The neurotrophic activity was via blocking apoptosis, as l-deprenyl decreased the fragmented DNA and the numbers of positively stained apoptotic cells under serum-free or hypoxic conditions. Using mRNA differential display, nine mRNAs were identified and confirmed by northern blot analysis to have altered expression levels at 8 hr of exposure to hypoxia. Five of them do not match any existing sequences in GenBank, whereas the other four represent known genes including c-jun, heat-shock protein hsp70, phosphoglycerate kinase (PGK), and calpactin I heavy chain. All of the four mRNAs were increased significantly by hypoxia. The c-jun, PGK, and calpactin mRNAs, but not hsp70, also were increased by serum withdrawal. l-Deprenyl partially reversed the increase in c-jun and hsp70 mRNA levels, but not in PGK and calpactin. These results suggest that l-deprenyl blocks apoptosis induced by hypoxia as well as by growth factor withdrawal and regulates the expression of apoptosis-related genes.

Animals↗
PubMed1999

Plasma fatty acid composition and 6-year incidence of hypertension in middle-aged adults: the Atherosclerosis Risk in Communities (ARIC) Study.

The association of baseline fatty acid composition in plasma cholesterol esters with 6-year incidence of hypertension was examined in middle-aged Minneapolis participants of the Atherosclerosis Risk in Communities (ARIC) Study (1987-1995). Compared with those who were never hypertensive (n = 1,975), incident hypertensives (n = 413) had statistically significantly higher baseline levels of palmitic (16:0) and palmitoleic (16:1n7) acids but lower levels of linoleic (18:2n6) acid and the polyunsaturated/saturated fatty acids ratio (P/S ratio). Among polyunsaturated fatty acids, levels of dihomo-gamma-linolenic (20:3n6) and arachidonic (20:4n6) acids were statistically significantly higher in incident hypertensives, compared with normotensives. After adjustment for age, sex, body mass index, waist/hip ratio, smoking status, ethanol intake, education level, physical activity, and baseline systolic blood pressure in separate models, the odds ratio estimates of incident hypertension for an interquartile increment of a fatty acid in cholesterol esters were 1.26 (95% confidence interval (CI): 1.05, 1.51) for 16:0, 1.11 (95% CI: 0.96, 1.28) for 16:1n7, 1.01 (95% CI: 0.85, 1.21) for 20:3n6, 1.14 (95% CI: 1.03, 1.27) for 20:5n3, 0.81 (95% CI: 0.68, 0.96) for 18:2n6, and 0.83 (95% CI: 0.70, 0.99) for the P/S ratio. The authors conclude that reduced levels of linoleic acid and the P/S ratio and elevated levels of palmitic and arachidonic acids are associated with a higher risk of hypertension.

Arteriosclerosis↗
PubMed1999

Cloning and expression analysis of a novel WD repeat gene, WDR3, mapping to 1p12-p13.

WD repeat proteins are components of multiprotein complexes that are involved in a wide spectrum of cellular activities, such as cell cycle progression, signal transduction, apoptosis, and gene regulation. These proteins are characterized by repeat units bracketed by Gly-His and Trp-Asp (GH-WD). We report here the isolation of a new member of the WD repeat gene family, WDR3, which encodes a putative 943-amino-acid nuclear protein consisting of 10 WD repeat modules. WDR3 is widely expressed in hematopoietic cell lines and in nonhematopoietic tissues. Fluorescence in situ hybridization mapped WDR3 to human chromosome 1p12-p13, a region that is affected by chromosomal rearrangements in a number of hematologic malignancies and solid tumors.

Amino Acid Sequence↗
PubMed1999

Medial septum mediates the increase in post-ictal behaviors and hippocampal gamma waves after an electrically induced seizure.

Hippocampal EEG and behavior of freely moving rats were studied before and after a hippocampal afterdischarge (AD), with or without reversible inactivation of the medial septum (MS) by muscimol. Muscimol suppressed the normal hippocampal EEG, including theta (5-10 Hz) and gamma (30-70 Hz) waves. After a hippocampal AD, hippocampal gamma waves were decreased for about 2 min and then increased at 3-10 min, while power of EEG of <30 Hz was decreased at </=3 min and showed no increase after an AD. Muscimol injection in the MS before the AD blocked the post-ictal increase of the gamma waves. In rats injected with vehicle in the MS, post-ictal increase in gamma waves was accompanied by an increase in horizontal locomotion, rearings, face washes, and wet dog shakes. In rats injected with muscimol in the MS before the AD, both the post-ictal increase in gamma waves and behaviors were completely suppressed. Muscimol injection in the MS after the AD significantly suppressed both gamma waves and post-ictal behaviors, as compared to vehicle-injected rats, but to a lesser degree than rats injected with muscimol in the MS before the AD. Hippocampal AD duration was not significantly affected by muscimol injection in the MS. We conclude that the MS is responsible for the maintenance of the normal and the post-ictal gamma waves. We suggest that the post-ictal gamma waves in the hippocampus may drive post-ictal behaviors, and in previous studies, we showed that this may occur through the nucleus accumbens.

Animals↗
PubMed1999

Molecular cloning, enzymatic characterization, developmental expression, and cellular localization of a mouse cytochrome P450 highly expressed in kidney.

A cDNA encoding a new cytochrome P450 was isolated from a mouse liver library. Sequence analysis reveals that this 1,886-base pair cDNA encodes a 501-amino acid polypeptide that is 69-74% identical to CYP2J subfamily P450s and is designated CYP2J5. Recombinant CYP2J5 was co-expressed with NADPH-cytochrome P450 oxidoreductase in Sf9 cells using a baculovirus system. Microsomal fractions of CYP2J5/NADPH-cytochrome P450 oxidoreductase-transfected cells metabolize arachidonic acid to 14,15-, 11,12-, and 8, 9-epoxyeicosatrienoic acids and 11- and 15-hydroxyeicosatetraenoic acids (catalytic turnover, 4.5 nmol of product/nmol of cytochrome P450/min at 37 degrees C); thus CYP2J5 is enzymologically distinct. Northern analysis reveals that CYP2J5 transcripts are most abundant in mouse kidney and present at lower levels in liver. Immunoblotting using a polyclonal antibody against a CYP2J5-specific peptide detects a protein with the same electrophoretic mobility as recombinant CYP2J5 most abundantly in mouse kidney microsomes. CYP2J5 is regulated during development in a tissue-specific fashion. In the kidney, CYP2J5 is present before birth and reaches maximal levels at 2-4 weeks of age. In the liver, CYP2J5 is absent prenatally and during the early postnatal period, first appears at 1 week, and then remains relatively constant. Immunohistochemical staining of kidney sections with anti-human CYP2J2 IgG reveals that CYP2J protein(s) are present primarily in the proximal tubules and collecting ducts, sites where the epoxyeicosatrienoic acids are known to modulate fluid/electrolyte transport and mediate hormonal action. In situ hybridization confirms abundant CYP2J5 mRNA within tubules of the renal cortex and outer medulla. Epoxyeicosatrienoic acids are endogenous constituents of mouse kidney thus providing direct evidence for the in vivo metabolism of arachidonic acid by the mouse renal epoxygenase(s). Based on these data, we conclude that CYP2J5 is an enzymologically distinct, developmentally regulated, protein that is localized to specific nephron segments and contributes to the oxidation of endogenous renal arachidonic acid pools. In light of the well documented effects of epoxyeicosatrienoic acids in modulating renal tubular transport processes, we postulate that CYP2J5 products play important functional roles in the kidney.

Amino Acid Sequence↗