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Biomedical subjects

X Chu

Publications and source records attributed to X Chu.

At least 19 recordsLinked to original sources

Experimental evidence of fragile-to-strong dynamic crossover in DNA hydration water.

We used high-resolution quasielastic neutron scattering spectroscopy to study the single-particle dynamics of water molecules on the surface of hydrated DNA samples. Both H(2)O and D(2)O hydrated samples were measured. The contribution of scattering from DNA is subtracted out by taking the difference of the signals between the two samples. The measurement was made at a series of temperatures from 270 down to 185 K. The relaxing-cage model was used to analyze the quasielastic spectra. This allowed us to extract a Q-independent average translational relaxation time of water molecules as a function of temperature. We observe clear evidence of a fragile-to-strong dynamic crossover (FSC) at T(L)=222+/-2 K by plotting log versus T. The coincidence of the dynamic transition temperature T(c) of DNA, signaling the onset of anharmonic molecular motion, and the FSC temperature T(L) of the hydration water suggests that the change of mobility of the hydration water molecules across T(L) drives the dynamic transition in DNA.

DNA↗

Time-resolved measurement of dissipation-induced decoherence in a Josephson junction.

We determined the dissipation-induced decoherence time (DIDT) of a superconducting Josephson tunnel junction by time-resolved measurements of its escape dynamics. Double-exponential behavior of the time-dependent escape probability was observed, suggesting the occurrence of a two-level decay-tunneling process in which energy relaxation from the excited to the ground level significantly affects the escape dynamics of the system. The observation of temporal double-exponential dependence enables direct measurements of the DIDT, a property critical to the study of quantum dynamics and the realization of macroscopic quantum coherence and quantum computing. We found that the DIDT was tau(d) > 11 micros at T = 0.55 K, demonstrating good prospects for implementing quantum computing with Josephson devices.

Journal Article↗

Drug inhibition of Gly-Sar uptake and hPepT1 localization using hPepT1-GFP fusion protein.

An hPepT1-GFP fusion construct was made to study drug inhibition of dipeptide uptake and apical, basolateral, or subcellular hPepT1 localization. The hPepT1 stop codon was mutated by polymerase chain reaction and was subsequently cloned into the pEGFP-N1 vector. The hPepT1-GFP fusion construct was then transfected into Caco-2 and HeLa cells, and drug inhibition was studied by inhibiting 3H-Gly-Sar uptake. Western blot analysis was used to determine hPepT1-GFP expression levels and confocal microscopy was used to examine the localization. Both anti-hPepT1 antibody and anti-GFP antibody recognized a 120-kd hPepT1-GFP fusion protein in the transfected cells. The 3H-Gly-Sar uptake in transfected HeLa cells was enhanced more than 20 times compared with the control. Valacyclovir (5 mmol/L) was able to completely inhibit 3H-Gly-Sar uptake in these transfected cells. Confocal microscopy showed that the hPepT1-GFP mainly localized in the Caco-2 cell apical membrane, but was present throughout the entire HeLa cell membranes. The hPepT1-GFP fusion protein was not found in either early endosome or lysosome of Caco-2 cells under normal conditions; however, it was detected in some subsets of lysosomes and early endosomes in phorbol 12-myristate 13-acetate (PMA)-treated Caco-2 cells.

Acyclovir↗

[Radiographic study of the development of the permanent teeth].

OBJECTIVE: To study the development of permanent teeth by radiographic methods. METHODS: The permanent teeth development of children ranging from 4-17 years was evaluated from 1709 panoramic radiographs by the Nolla's method. Each tooth was graded from 0 to 10 stage. The average developmental stage for girls and boys were calculated. RESULTS: The average developmental stage and development curves for girls and boys were obtained respectively. For the completion of crown and root development, girls are more advanced than boys by an average of 0.3 and 0.6 years. CONCLUSIONS: Girls are ahead of boys for the development of the permanent teeth. The norms of the maturation of permanent teeth can be used to evaluated the development of the individual teeth.

Adolescent↗

Decreased +gz tolerance following lower body positive pressure: simulated push-pull effect.

OBJECTIVE: The purpose of this study was to attempt to simulate the push-pull maneuver on a single-axis human centrifuge using lower body positive pressure (LBPP), and to observe the effect of the push-pull maneuver on +Gz tolerance. METHODS: Six volunteers participated in the experiment. They were subjected to LBPP of up to 300 mm Hg for 1 min. Blood pressure (BP) and heart rate (HR) were monitored before, during and after LBPP. Immediately after LBPP, +Gz tolerance was measured on a human centrifuge. RESULTS: During LBPP, systolic BP (SBP) and diastolic BP (DBP) increased significantly, mean arterial pressure (MAP) increased but not significantly, and HR decreased significantly. After LBPP, SBP and MAP decreased significantly, while DBP and HR decreased but not significantly. In all subjects, +Gz tolerance decreased after LBPP. The decreased value was 0.70 +/- 0.06 G, maximum 1.0 G and minimum 0.5 G. CONCLUSION: The push-pull maneuver can be simulated on a single-axis human centrifuge using LBPP. The physiologic effects of LBPP were similar to those of -Gz. We observed that +Gz tolerance decreased after LBPP, which confirmed the push-pull effect from the experiment.

Acceleration↗

Genomic organization of mouse and human erythrocyte tropomodulin genes encoding the pointed end capping protein for the actin filaments.

Erythrocyte tropomodulin (E-Tmod), a globular protein of 359 residues, is highly expressed in the erythrocyte, heart and skeletal muscle. By binding to the N-terminus of tropomyosin (TM) and actin, E-Tmod blocks the elongation and depolymerization of the actin filaments at the pointed end. In erythrocytes, the E-Tmod/TM complex contributes to the formation of the short actin protofilament, which in turn defines the geometry of the membrane skeleton. In juvenile mice, over-expression of E-Tmod is associated with dilated cardiomyopathy. We have previously cloned the human E-Tmod cDNA, identified its TM-binding region, and mapped its gene to chromosome 9q22. Through genomic library screening and PCR-based genomic walking we have now cloned the mouse E-Tmod gene, whose coding region spans approximately 60kb containing nine exons and eight introns. The human E-Tmod gene obtained by PCR has an identical exon-intron organization. In sanpodo, a Tmod homologue in Drosophila, the exon boundaries are also conserved except that exons 2-5 and 6-7 are 'fused' and alternative splicing of two additional 5' exons and the 3' exons may give rise to several sanpodo isoforms. In a Tmod-like gene of C. elegans, exons 2-3 are 'fused', boundaries of exons 1, 7, 8, and 9 are conserved and exon/intron junctions of exons 4, 5 and 6 are shifted by a few residues. Analyses of 15 Tmod members from six species show no insertions or deletions of residues in the region of exons 6 and 7. A 5' rapid amplification of cDNA ends reveals that mouse E-Tmod transcripts obtained from embryonic stem cells, skeletal muscle and heart, but not smooth muscle, contain an additional 86bp untranslated cDNA sequence further upstream from exon 1. Thus, alternative promoters may provide a possible mechanism for tissue-specific expression and regulation of E-Tmod. This study is the first to report the exon organization of E-Tmod genes, which allows their regulation, manipulation, and disease relevance to be further investigated.

5' Untranslated Regions↗

Ordered assembly of roX RNAs into MSL complexes on the dosage-compensated X chromosome in Drosophila.

BACKGROUND: In the male Drosophila, the X chromosome is transcriptionally upregulated to achieve dosage compensation, in a process that depends on association of the MSL proteins with the X chromosome. A role for non-coding RNAs has been suggested in recent studies. The roX1 and roX2 RNAs are male-specific, non-coding RNAs that are produced by, and also found associated with, the dosage-compensated male X chromosome. Whether roX RNAs are physically part of the MSL complex has not been resolved. RESULTS: We found that roX RNAs colocalize with the MSL proteins and are highly unstable unless the MSL complex is coexpressed, suggesting a physical interaction. We were able to immunoprecipitate roX2 RNA from male tissue-culture cells with antibodies to the proteins Msl1 and Mle, consistent with an integral association with MSL complexes. Localization of roX1 and roX2 RNAs in mutants indicated an order of MSL-complex assembly in which roX2 RNA is incorporated early in a process requiring the Mle helicase. We also found that the roX2 gene, like roX1, is a nucleation site for MSL complex spreading into flanking chromatin in cis. CONCLUSIONS: Our results support a model in which MSL proteins assemble at specific chromatin entry sites (including the roX1 and roX2 genes); the roX RNAs join the complex at their sites of synthesis; and complete complexes spread in cis to dosage compensate most genes on the X chromosome.

Animals↗

Cerebral blood flow velocity by transcranial Doppler during a vertical-rotating table simulation of the push-pull effect.

BACKGROUND: The push-pull effect (PPE) has been suspected of causing many aircraft accidents. The perfusion and then withdrawal of cerebral blood during the PPE may change the state of the cerebral blood vessel. HYPOTHESIS: During head-down tilt (HDT) cerebral vasoconstriction occurs in response to the elevated perfusion pressure to maintain cerebral blood flow, and during subsequent head-up tilt (HUT) the increased resistance of the cerebral blood vessel recovers slowly. METHODS: Ten healthy male non-pilots were exposed to the following protocol using a rotating-table to simulate the push-pull maneuver: HUT (+1 Gz) for 1 min followed by transition to HDT (-1 Gz) 10 s followed by transition to HUT (+1 Gz) 1 min. Cerebral blood flow velocity and pulsatility indices in the left middle cerebral artery were continually measured with a transcranial Doppler (TCD) instrument. RESULTS: Mean blood flow velocity (Vm) increased significantly by 10%, during the first 5 s of HDT, recovered to baseline during HDT 5 10 s, and remained unchanged during subsequent HUT. Systolic blood flow velocity (Vs) increased by 9% during HDT 5-10 s and 11% during HUT 0-5 s. Diastolic blood flow velocity (Vd) decreased by -9% during HDT 5-10 s, and -22% during HUT 0-5 s. Vs-Vd increased by 26% during HDT 5 10 s, and 41%, during HUT 0-5 s. Pulsatile indices (PI) and resistance index (RI) increased by 26%) and 15% during HDT 5-10 s, and by 40% and 27% during HUT 0-5 s, respectively. Vs, Vs-Vd, PI, and RI remained at the higher level, and Vd remained at the lower level to HDT 15-20 s. CONCLUSIONS: The results indicate that cerebral vasoconstriction occurred to prevent brain over-perfusion during HDT. During HUT, the elevated resistance of the cerebral vessel remained at the higher level for about 20 s, and may have worsened the cerebral perfusion from exposure to +Gz. This may be one of the mechanisms of PPE.

Adaptation, Physiological↗

The protection against +Gz afforded by pressure breathing with different pressure schedules.

OBJECTIVE: System of pressure breathing for +Gz (PBG) has been incorporated into service in the high performance fighter aircraft, but there were significant differences among PBG pressure schedules used in different countries. The purpose of this study was to define an optimal pressure schedule in PBG system. METHOD: Five male subjects wearing GZ-2 anti-G suit and medium-sized bladder vest, plus PBG with 1.6, 2.4, and 3.2 kPa/G pressure schedules, respectively, were exposed to rapid onset (3.0 G/s) centrifuge +Gz runs. +Gz protection of PBG with each of the three pressure schedules were measured and the subjective ratings were collected. RESULT: The +Gz protection afforded by PBG with 1.60, 2.40, and 3.20 kPa/G pressure schedules were 2.00 +/- 0.31, 2.54 +/- 0.32, and 2.44 +/- 0.31 G, respectively. Subjective ratings showed that the PBG with 2.40 kPa/G pressure schedule was better than the other two. CONCLUSION: Our data suggest that a PBG pressure schedule of 2.4 kPa/G in PBG system is optimal. It not only assures the anti-G performance of PBG, but also reduces its side effects.

Acceleration↗

[Data analysis of 492 times centrifuge examination].

Objective. To sum up the experiences and to find the regularity of centrifuge examinations. Method. The data of nine years of centrifuge examination (from 1988 to 1996) of pilots who suffered from black out or LOC frequently were analyzed. Result. There were totally 492 times centrifuge examinations. First centrifuge examination included 229 pilots, 49 qualified, 180 unqualified. Second centrifuge examination included 263 pilots, 50 qualified, 213 unqualified. The pilots were all male. The average age of first centrifuge examination was 29.27 +/- 4.87 years. Average flying time was 1015.24 +/- 131.89 h. 68.7% of their plane was JJ-6 or above. Conclusion. Most pilots undergoing centrifuge examination these nine years were 26-35 year old, and had flown for 601-1200 h. The planes they flew are mostly high-performance fighter aircraft. Close attention must be paid to pilots under similar condition by the flight surgeon. It is recommended that the special equipment of G-tolerance training should be added to the fighter aircraft units.

Acceleration↗

[Effect of intravascular laser irradiation of blood and traditional Chinese medical therapy on immune function in senile cerebral infarction patients of kidney deficiency type].

OBJECTIVE: To observe the effect of intravascular laser irradiation of blood (ILIB) therapy on cellular immunity, change of T-lymphocyte subsets and humoral immunity in senile cerebral infarction patients of Kidney deficiency type. METHODS: Seventy-five patients were divided randomly into the ILIB group and the control group treated by conventional medicine (CM). Serum CD3, CD4, CD8, IgG, IgA, IgM, C3 and C4 levels of patients were determined before and after treatment for self-control and comparing between various groups and that of normal control. RESULTS: Before treatment, in patients of both groups, the levels of CD3, CD4, CD4/CD8, C3 were all lower than normal levels significantly, C4 and IgM higher than normal (P < 0.05, P < 0.01), the level of IgG lowered in patients inclined to Kidney-Yang deficiency and raised in those inclined to Kidney-Yin deficiency (P < 0.01). After treatment, in the ILIB group, CD3, CD4 and CD4/CD8 raised significantly (P < 0.05, P < 0.01), IgG and C3 varied towards normal control (P < 0.01, P < 0.05), and C4 lowered but without significance. In the control group, the indexes changed also toward normal but without significance except the change of IgG (P < 0.05). As for IgA and IgM, marked changes were not found in both groups in comparison between before and after treatment. CONCLUSION: ILIB therapy could bi-directionally regulate cellular and humoral immunity in senile cerebral infarction patients of Kidney deficiency type, which was similar to the function in supplementing Qi and invigorating Kidney of Chinese herbal medicine.

Aged↗

[Effects of rotating-table simulated "push-pull maneuver" on cerebral circulation function].

OBJECTIVE: To investigate the change and regulation of cerebral circulation during rotating-table simulated push-pull maneuver. METHOD: A special rotating-table was used to simulate the push-pull maneuver. 10 healthy adults were subjected to a series of "head-up stand (+1Gz) 1 min head-down stand (-1Gz) 10 s and head-up stand (+1Gz) 1 min" changes. Cerebral blood flow velocity and pulsatility indices in the left middle cerebral artery were constantly measured with a TC2020TCD using Transcranial Doppler [correction of Transcanial Dopplor] instrument. RESULT: During 10 s head-down stand (-1Gz) systolic velocity (Vs) increased, diastolic velocity (Vd) decreased, and the pulsatility indices (PI and RI) increased significantly in the left middle cerebral artery. During subsequent head-up stand (+1Gz), these changes didn't resume immediately and maintained for at least 20 s. CONCLUSION: This result implied that the push-pull maneuver increased the resistance of the cerebral vessels, which might be one of the mechanisms of the push-pull effect.

Adult↗

[Content analysis on gardenoside in grown and ungrown fruits of Gardenia from different habitats].

This paper reported content analysis on gardenoside in grown fruits of Gardenia from different habitats and ungrown fruits of Gardenia jasminoides and G. jasminoides f. longicarpa. The results were as follows: (1) The content of gardenoside in G. jasminoides from indigenous region of Jiangxi was higher than other habitats; (2) The content of gardenoside in G. jasminoides f. longicarpa was the highest; (3) The content of gardenoside in fruits of growth period of G. jasminoides and G. jasminoides f. longicarpa had two peak stages.

Chromatography, High Pressure Liquid↗

Inhibition of cardiovascular activity following microinjection of novel opioid-like neuropeptide nociceptin (orphanin FQ) into the rat rostral ventrolateral medulla.

Nociceptin (orphanin FQ), the newly discovered endogenous ligand for the novel opioid receptor-like 1 receptor, has been initially found to participate in pain modulation. In this study, centrally mediated cardiovascular actions of this peptide were investigated in the alpha-chloralose/urethane-anesthetized rats. We found that bilateral injection of nociceptin (10 nmol) into the rostral ventrolateral medulla (RVLM), wherein injection of excitatory amino acid dl-homocysteic acid (3 nmol) induced typical pressor responses, significantly reduced arterial blood pressure and heart rate by -32% and -15%, respectively. Reduction of blood pressure and heart rate in response to intra-RVLM injection of nociceptin was dose-dependent with a threshold dose being 3 nmol. Pretreatment with the selective nociceptin receptor antagonist, [Phe1psi(CH2-NH)Gly2]NC(1-13)NH2 (10 nmol), into the RVLM abolished the nociceptin-induced cardiovascular inhibition. In contrast, non-selective opioid receptor antagonist, naloxone (10 nmol), did not modify the hypotension and bradycardia induced by nociceptin, even though naloxone at the same dose prevented reduction of blood pressure and heart rate induced by intra-RVLM injection of methionine-enkephalin (3 nmol). Both [Phe1psi(CH2-NH)Gly2]NC(1-13)NH2 and naloxone injection alone had no significant effect on baseline blood pressure and heart rate. These data suggest that the newly discovered opioid-like neuropeptide nociceptin in the CNS exert powerful influence on hemodynamic activity by affecting the RVLM neurons. This influence is inhibitory in nature, which may not be active in normal physiological conditions. Moreover, the cardiovascular effects of nociceptin were mediated by activation of specific nociceptin receptors rather than typical naloxone-sensitive opioid receptors.

Animals↗

The nociceptin receptor-mediated inhibition of the rat rostral ventrolateral medulla neurons in vitro.

The recently available antagonist selective for novel nociceptin receptor, [Phe1 psi(CH2-NH)Gly2]NC(1-13)NH2, was utilized in this study to verify specificity of nociceptin receptor in mediating the nociceptin-induced inhibition of electrical activity of neurons in the rostral ventrolateral medulla of rat brain slices. Perfusion of nociceptin (10 nM) considerably reduced spontaneously firing frequency of the medullary neurons. Co-perfusion of [Phe1 psi(CH2-NH)Gly2]NC(1-13)NH2 (10 microM) completely blocked the nociceptin-induced depression of the neuronal activity. Blocking effect of [Phe1 psi(CH2-NH)Gly2]NC(1-13)NH2 was concentration-dependent. However, the nociceptin antagonist did not modify basal, and opioid peptide enkephalin-depressed, firing rates of the neurons. In contrast to [Phe1 psi(CH2-NH)Gly2]NC(1-13)NH2, the non-selective opioid receptor antagonist naloxone (10 microM) failed to affect the nociceptin inhibition even though naloxone at a lower concentration (1 microM) readily blocked enkephalin-induced depression of the neuronal activity. These data indicate that the nociceptin-induced inhibition of spontaneous discharge of the rostral ventrolateral medulla neurons is specifically mediated by [Phe1 psi(CH2-NH)Gly2]NC(1-13)NH2-sensitive nociceptin receptors distinct from typical naloxone-sensitive opioid receptors.

Animals↗

In vitro alteration of macrophage phenotype and function by serum lipids.

Diabetes (type I and type II) affects approximately 13 million people in the United States. Delayed and incomplete healing of wounds can be a major problem for diabetic patients. Macrophages are an important cell in the complex process of wound repair representing the major source of cytokines throughout the wound-healing process. Cytokines mediate many of the cellular responses critical to timely wound repair. It has been suggested that diabetes impairs wound healing through disruption of local cytokine production. Our previous in vivo studies in rats demonstrated that diabetes-induced and diet-induced hyperlipidemia cause changes in macrophage phenotype and function (Iacopino 1995; Doxey et al. 1998), suggesting that alterations in macrophage cytokine profiles represent the cellular/molecular mechanism responsible for delayed wound healing. The purpose of this study was to investigate how monocyte maturation/differentiation and cytokine production were altered by serum lipids in an in vitro system using human cells. Commercially prepared purified human monocytes were cultured and exposed to serum lipids. Phenotypic analysis of differentiated macrophages was then performed by flow cytometry and fluorescent microscopy using surface antigens specific for various macrophage subsets. Selected cytokines in conditioned medium were assayed using commercial human enzyme-linked immunosorbent assay (ELISA) kits. We demonstrate that serum lipids cause an increase in monocytic differentiation leading to an inflammatory macrophage phenotype rather than a reparative/proliferative phenotype. We also show that serum lipids cause a generalized decrease in macrophage cytokine production using interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), platelet-derived growth factor (PDGF), and transforming growth factor beta 1 (TGF-beta 1) as marker cytokines. Our present in vitro results using human cells confirm our previous in vivo studies in the rat and support the hypothesis that diabetes-induced hyperlipidemia alters the monocyte differentiation process resulting in changes of macrophage subsets and cytokine release at the wound site, ultimately impairing the wound-healing process.

Animals↗