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Biomedical subjects

A Xie

Publications and source records attributed to A Xie.

36 records · Page 2Linked to original sources
PubMed1998

[The influences of TBP on the partially saponified DMHPA-heptane systems and the extracted organic phases containing rare earth].

The aggregation states of partially saponified [di-(1-methylheptyl) phosphoric acid] (DMHPA)-tributyl phosphate (TBP) heptane (C7H16) and the extracted organic phases containing rare earth were studied. The result demonstrates that TBP can widen the range of the microemulsion formation in DMHPA-C7H16-NaOH-H2O systems. It also influence the states of the extracted organic phases of DMHPA-RE (III) and the behavior of water clearly. The gel could be formed in DMHPA-TBP-RE (III) systems under proper conditions. FT-IR spectra analysis shows that both DMHPA and TBP may coordinate with RE3+ and the hydrogen bonds of TBP with DMHPA and H2O contribute to the three dimensional network structure of the gels.

English Abstract↗
PubMed1997

Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea.

We hypothesized that reductions in arterial PCO2 (PaCO2) below the apnea threshold play a key role in the pathogenesis of idiopathic central sleep apnea syndrome (ICSAS). If so, we reasoned that raising PaCO2 would abolish apneas in these patients. Accordingly, patients with ICSAS were studied overnight on four occasions during which the fraction of end-tidal CO2 and transcutaneous PCO2 were measured: during room air breathing (N1), alternating room air and CO2 breathing (N2), CO2 breathing all night (N3), and addition of dead space via a face mask all night (N4). Central apneas were invariably preceded by reductions in fraction of end-tidal CO2. Both administration of a CO2-enriched gas mixture and addition of dead space induced 1- to 3-Torr increases in transcutaneous PCO2, which virtually eliminated apneas and hypopneas; they decreased from 43.7 +/- 7.3 apneas and hypopneas/h on N1 to 5.8 +/- 0.9 apneas and hypopneas/h during N3 (P < 0.005), from 43.8 +/- 6.9 apneas and hypopneas/h during room air breathing to 5.9 +/- 2.5 apneas and hypopneas/h of sleep during CO2 inhalation during N2 (P < 0.01), and to 11.6% of the room air level while the patients were breathing through added dead space during N4 (P < 0.005). Because raising PaCO2 through two different means virtually eliminated central sleep apneas, we conclude that central apneas during sleep in ICSA are due to reductions in PaCO2 below the apnea threshold.

Administration, Inhalation↗
PubMed1997

Neural mechanism of the pressor response to obstructive and nonobstructive apnea.

Obstructive and nonobstructive apneas elicit substantial increases in muscle sympathetic nerve activity and arterial pressure. The time course of change in these variables suggests a causal relationship; however, mechanical influences, such as release of negative intrathoracic pressure and reinflation of the lungs, are potential contributors to the arterial pressure rise. To test the hypothesis that apnea-induced pressor responses are neurally mediated, we measured arterial pressure (photoelectric plethysmography), muscle sympathetic nerve activity (peroneal microneurography), arterial O2 saturation (pulse oximeter), and end-tidal CO2 tension (gas analyzer) during sustained Mueller maneuvers, intermittent Mueller maneuvers, and simple breath holds in six healthy humans before, during, and after ganglionic blockade with trimethaphan (3-4 mg/min, titrated to produce complete disappearance of sympathetic bursts from the neurogram). Ganglionic blockade abolished the pressor responses to sustained and intermittent Mueller maneuvers (-4 +/- 1 vs. +15 +/- 3 and 0 +/- 2 vs. +15 +/- 5 mmHg) and breath holds (0 +/- 3 vs. +11 +/- 3, all P < 0.05). We conclude that the acute pressor response to obstructive and nonobstructive voluntary apnea is sympathetically mediated.

Adult↗
PubMed1997

[Study on the properties and microstructure of the gel in the extracted organic phase containing DMHPA-RE(III)].

The content of Na+, RE3+ and the swelling characteristic of dried gel containing DMHPA[di-(1-methylheptyl)phosphoric acid]-RE(III) have been studied by FTIR and ICP/AES spectroscopy methods. The result demonstrates that (1) the mechanism of microemulsion extracting lanthanide ions is complicated and it is difficult to be explained with simple chemical equations, (2) The dried gel can swell, but the aggregation states and microstructure change as the used solvents and its content vary, (3) The far infrared spectroscopy shows that there are ring structures in the gel and differences of the ability in coordination with DMHPA between light and heavy lanthanide ions.

English Abstract↗
PubMed1997

[Study on FTIR spectra of HDEHP and DMHPA in different states].

FTIR spectra of pure di (2-ethylhexyl) phosphoric acid (HDEHP), di (1-methylheptyl) phosphoric acid (DMHPA) and their sodium salts, microemulsions, extracted organic phases containing rare earth were studied. It was seen that the microstructures of the two extractants changed with their different alkyl structures and aggregation states.

English Abstract↗
PubMed1996

Glu46 donates a proton to the 4-hydroxycinnamate anion chromophore during the photocycle of photoactive yellow protein.

Photoactive yellow protein (PYP) is a photoreceptor containing a unique 4-hydroxycinnamic acid (pCA) chromophore. The trans to cis photoisomerization of this chromophore activates a photocycle involving first a short-lived red-shifted intermediate (pR), then a long-lived blue-shifted intermediate (pB), and finally recovery of the original receptor state (pG). The pCA chromophore is deprotonated in pG and protonated in pB, but the proton donor for this process has not yet been identified. Here we report the first FTIR spectroscopic data on pG, pR, and pB. The IR difference signals in the carbonyl stretching region of COOH groups (1700-1800 cm-1) reveal that a buried carboxylic group close to the chromophore (i) is protonated in pG, (ii) develops a stronger hydrogen bonding in pR, and (iii) becomes deprotonated in pB. These signals are unambiguously assigned to Glu46, on the basis of the IR data and the 1.4 A X-ray structure of PYP [Borgstahl et al. (1995) Biochemistry 34, 6278-6287]. Our data demonstrate that in pR Glu46 remains in hydrogen bonding contact with the negatively charged phenolic oxygen of pCA after chromophore photoisomerization. This strongly implies that the chromophore is isomerized to the 7-cis 9-s-trans conformation in pR, resulting from co-isomerization of both the C7 = C8 and C9-C10 bonds. In the pR to pB transition, Glu46 becomes deprotonated, concomitant with chromophore protonation. Therefore, we conclude that Glu46 functions as the proton donor for the protonation of pCA during the PYP photocycle. We propose a molecular mechanism in which intramolecular proton transfer in PYP leads to global protein conformational changes involved in signal transduction.

Bacterial Proteins↗
PubMed1996

Cycle length of periodic breathing in patients with and without heart failure.

Because apnea length during periodic breathing varies according to the preceding increase in ventilation and reduction in PaCO 2, differences in the cycle length of periodic breathing among patients with normal and impaired cardiac function might be explained by the influence of lung-to-carotid body circulatory delay, as reflected by lung-to-ear circulation time (LECT), on hyperpnea length rather than on apnea length. It was therefore hypothesized that circulatory delay is an important determinant of periodic-breathing hyperpnea length but not apnea length. To test this hypothesis, LECT, periodic-breathing cycle length, apnea length, and hyperpnea length were compared in 10 patients with idiopathic central sleep apnea (ICSA), whose cardiac function was normal, as opposed to 10 with Cheyne-Stokes respiration and central sleep apnea (CSR-CSA) in association with congestive heart failure (CHF). As compared with ICSA patients, cycle length was significantly longer in patients with CSR-CSA (37.3 +/- 3.0 s versus 59.0 +/- 4.9 s, p < 0.005). This difference was due to significantly longer hyperpnea length in the CSR-CSA patients (16.7 +/- 2.8 s versus 36.7 +/- 3.4 s, p < 0.001), since apnea length was similar in the two groups. In addition, LECT was longer in the CSR-CSA patients (24.3 +/- 2.0 s versus 10.3 +/- 1.0 s, p < 0.001), and correlated strongly with cycle length (r = 0.88, p < 0.001) and hyperpnea length (r = 0.90, p < 0.001) but not with apnea length. LECT correlated inversely with cardiac output (r = -0.72, p < 0.006), indicating that LECT is a valid measure of circulatory delay. Thus, circulatory delay is an important determinant of hyperpnea length but not of apnea length in patients with ICSA and CSR-CSA.

Cardiac Output↗
PubMed1995

Hypocapnia and increased ventilatory responsiveness in patients with idiopathic central sleep apnea.

We previously demonstrated that central apneas during sleep in patients with idiopathic central sleep apnea (ICSA) are triggered by abrupt hyperventilation. In addition, baseline PCO2 at the time of augmented breaths which triggered central apneas was lower than for augmented breaths which did not trigger apneas. These observations led us to hypothesize that patients with ICSA chronically hyperventilate maintaining their PCO2 close to the threshold for apnea during sleep owing to increased chemical respiratory drive. To test these hypotheses, we recorded transcutaneous PCO2 (PtcCO2) during overnight sleep studies on nine consecutive patients with ICSA and nine sex-, age-, and body-mass-index-matched control subjects. Daytime PaCO2 as well as rebreathing and single breath ventilatory responses to CO2 were also measured. Compared with the control subjects, the patients had significantly lower mean PtcCO2 during sleep (37.8 +/- 1.2 versus 42.7 +/- 10.9 mm Hg, p < 0.01) and lower PaCO2 while awake (35.1 +/- 1.3 versus 38.8 +/- 0.9 mm Hg, p < 0.05). Furthermore, patients with ICSA had significantly higher ventilatory responses to CO2 for both the rebreathing (3.14 +/- 0.34 versus 1.60 +/- 0.32 L/min/mm Hg, p < 0.005) and single breath methods (0.51 +/- 0.10 versus 0.25 +/- 0.04 L/min/mm Hg, p < 0.05). We conclude that: (1) patients with ICSA chronically hyperventilate awake and asleep and (2) chronic hyperventilation is probably related to augmented central and peripheral respiratory drive which predisposes to respiratory control system instability.

Carbon Dioxide↗
PubMed1994

Family of the major cold-shock protein, CspA (CS7.4), of Escherichia coli, whose members show a high sequence similarity with the eukaryotic Y-box binding proteins.

The cspA is a gene of Escherichia coli, whose expression is specifically induced at low temperatures to a level of 13% of total protein synthesis. The CspA protein consisting of 70 amino acid residues has high sequence similarity with eukaryotic Y-box DNA-binding proteins. We found two independent clones from the Kohara miniset phage collection, which hybridized with a DNA fragment containing cspA. DNA sequencing of these clones confirmed that the two genes are highly homologous to cspA. One designated cspB is mapped at 35 min on the E. coli chromosome and encodes a 71-residue protein with 79% identity to CspA, while the other, cspC, is mapped at 40 min and encodes a 69-residue protein with 70% identity. In addition, a DNA sequence upstream of the clpA gene at 19 min published elsewhere contains an open reading frame for a 74-residue protein with 45% identity to CspA. All csp genes were fused in the coding regions with the lacZ gene, and the expression of beta-galactosidase was examined for these hybrid genes upon cold shock. A similar cold-shock induction to cspA was observed for cspB but not cspC and cspD. These results indicate that E. coli has a family of the cspA gene, some of which are induced by cold shock.

Amino Acid Sequence↗
PubMed1994

Interaction of hyperventilation and arousal in the pathogenesis of idiopathic central sleep apnea.

Central apneas during sleep may arise as a result of reduction in PaCO2 below the apnea threshold. We therefore hypothesized that hyperventilation and arousals from sleep interact to cause hypocapnia and subsequent central apneas in patients with idiopathic central sleep apnea (ICSA). Accordingly, the relationships among preapneic ventilation, arousal from sleep, and the onset and duration of subsequent central apneas were examined during Stage 2 non-REM sleep in eight patients with ICSA (mean +/- SEM, 45.4 +/- 4.7 central apneas and hypopneas/h of sleep). During Stage 2 sleep, all episodes of periodic breathing with central apneas were triggered by hyperventilation. Minute ventilation (VI) was greater (6.3 +/- 0.7 versus 5.4 +/- 0.8 L/min, p < 0.05) and mean transcutaneous PCO2 (PtcCO2) was lower (37.8 +/- 1.3 versus 38.9 +/- 1.6 mm Hg, p < 0.05) during periodic breathing than during stable breathing. VI during the ventilatory phase of the periodic breathing cycle increased progressively with increasing grades of associated arousals from Grade 0 (no arousal) (10.3 +/- 1.4 L/min) to Grade 1 (EEG arousal) (12.6 +/- 1.6 L/min) to Grade 2 (movement arousal) (14.1 +/- 1.6 L/min, p < 0.01). There was a corresponding progressive increase in central apnea length following the ventilatory period from no arousal (14.1 +/- 2.0) to EEG arousal (16.4 +/- 1.8) to movement arousal (18.1 +/- 2.0 s, p < 0.01). We conclude that arousals and hyperventilation interact to trigger hypocapnia and central apneas in ICSA.

Aged↗
PubMed1993

Steric constraints in the retinal binding pocket of sensory rhodopsin I.

Steric constraints in the retinal binding pocket of sensory rhodopsin I (SR-I) are analyzed by studying effects of sample temperature and retinal analogs. The flash-induced yield of the earliest detected intermediate S610, which corresponds to the K intermediate in the bacteriorhodopsin (BR) photocycle, decreases below 220 K and reaches zero at 100 K, while K formation is independent of temperature. The reduced S610 formation at low temperatures indicates a more restricted retinal binding pocket in SR-I during primary photochemical events. Introduction of bulky substituents on the retinal polyene chain in four retinal analogs greatly retards or blocks the final step of chromophore binding to the apoprotein of SR-I. Except for the 14-methyl substitution, these modifications exhibit little or no effect on chromophore binding to BR apoprotein. These results corroborate that the retinal polyene chain binding domain in SR-I is more sterically constrained than that of the retinal pocket in BR. Deletion of the beta-ionone ring renders the analog SR-I pigments nonfunctional, as does deletion of the 13-methyl group, but the corresponding BR analogs are both photochemically and physiologically active. In contrast to the corresponding BR analog, photolysis of the analog SR-I reconstituted with 13-desmethylretinal does not produce an S610-like intermediate at room temperature. The above results and the previous findings that protein constraints inhibit the accommodation of a stable 13-cis-retinal configuration in SR-I suggest a model in which the 13-methyl group functions as a fulcrum to permit movement of one or both ends of retinal to overcome an energy barrier against isomerization.

Bacteriorhodopsins↗
PubMed1993

Influence of body position on pressure and airflow generation during hypoxia and hypercapnia in man.

1. Inspiratory oesophageal pressure and ventilatory responses to hyperoxic, progressive hypercapnic rebreathing (HCVR) and isocapnic, progressive hypoxic rebreathing (HVR) were studied in five normal males in both supine and upright seated positions. 2. No significant differences were found in the ventilatory response to hypercapnia between the supine and upright position. The slopes of the relationship between minute ventilation (VI) and the increase of end tidal PCO2 (delta P(ET), CO2) were 3.27 +/- 0.23 and 2.76 +/- 0.24 1 min-1 mmHg-1 supine and upright, respectively. However, the change in oesophageal pressure from the end expiratory level observed during quiet breathing to that at peak inspiration (delta P(oes), I) in relationship to delta P(ET),CO2 was greater supine than upright (1.23 +/- 0.07 versus 0.79 +/- 0.11 cmH2O mmHg-1, P < 0.01). 3. In contrast, during hypoxia-stimulated breathing the slope of the minute ventilation versus oxyhaemoglobin saturation curve (VI-Sa,O2) was flatter supine than upright (1.00 +/- 0.03 versus 1.75 +/- 0.05 l min-1 (percentage fall in Sa,O2)-1, P < 0.0001), but delta P(oes), I in relation to Sa,O2 during hypoxic rebreathing was similar supine and upright (0.38 +/- 0.03 versus 0.40 +/- 0.04 cmH2O (percentage fall in Sa,O2)-1, respectively. 4. It is concluded that body position does not affect the ventilatory response to progressive hyperoxic hypercapnia but does affect the relationship between delta P(oes), I and delta P(ET),CO2. In contrast, body position affects the ventilatory response to isocapnic progressive hypoxia, but does not affect the relationship between delta P(oes), I and Sa,O2.

Adult↗
PubMed1993

Influence of body position on diaphragmatic and scalene activation during hypoxic rebreathing.

We measured electromyographic activity of the diaphragm (EMGdi) and scalene (EMGsc) during isocapnic progressive hypoxic ventilatory responses in five normal males in the supine and upright seated positions. The slope of the regression line relating EMGdi expressed as a percentage of maximum to percent fall in arterial oxyhemoglobin saturation was 93% steeper upright than supine (P < 0.005), whereas the slope of EMGdi activity to minute volume of ventilation was 73% higher upright than supine (P < 0.05). In addition, the slope of EMGsc activity relative to percent fall in arterial oxyhemoglobin saturation and minute ventilation was greater upright than supine (151%, P < 0.001 and 61%, P = 0.056, respectively). Greater EMGsc activity upright than supine was similar to findings during hypercapnic rebreathing. However, the greater EMGdi activity upright than supine stands in contrast to hypercapnic rebreathing where it was previously shown that EMGdi activity was not affected by a change in body position. We conclude that during hypoxic ventilatory responses both EMGdi and EMGsc activities are more pronounced upright than supine. Diaphragmatic activation during progressive hypoxia in response to a change in body position is different from that seen during progressive hypercapnia.

Adult↗
PubMed1992

Reversible steps in the bacteriorhodopsin photocycle.

The absorbance changes that accompany the light-driven proton-pumping cycle of bacteriorhodopsin measured over a broad range of times, wavelengths, temperatures, and pH values have been globally fitted to the kinetic model K in equilibrium with L in equilibrium with X in equilibrium with M in equilibrium with N in equilibrium with O----bR. A remarkably good fit to the data was obtained by optimizing the rate constants at 20 degrees C and the corresponding activation energies at each pH value, together with the extinction coefficients for each intermediate, which were assumed to be independent of both pH and temperature. Back-reactions are included for all but the last step of the cycle and are found to be essential for fitting the data. The rates of these reactions are large, and the analogous irreversible model produced significantly worse fits to the data. Small systematic differences between the fit and the experimental data associated with the X, M, and O intermediates, together with the inability of the model to produce spectra for the X and M intermediates consistent with their assignment as molecular species, indicate that this model must be an incomplete description of the photocycle. We suggest that these problems arise from the presence of additional occupied states that are difficult to distinguish on the basis of their visible absorption spectra alone.

Bacteriorhodopsins↗
PubMed1991

Obstructive sleep apnoea in patients with dilated cardiomyopathy: effects of continuous positive airway pressure.

The combined effects of negative intrathoracic pressure swings during obstructive sleep apnoeas (OSAs) and increased sympathetic nervous system tone associated with hypoxia and sleep arousal may lead to pulmonary oedema or left-ventricular hypertrophy. Therefore, we have done a study of patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy to see whether OSA could contribute to impaired left-ventricular function and to assess nasal continuous positive airway pressure (NCPAP) for treatment. Eight men (aged 29-69 years) took part in the study; all were obese. Left-ventricular ejection fraction (LVEF) was measured while on stable medication and then 4 weeks after the start of nocturnal NCPAP. NCPAP was associated with abolition of OSA (mean [SE] number of apnoeas and hypopnoeas per hour of sleep 54.1 [7.2] and 1.0 [0.4] for pretreatment and NCPAP nights, respectively, p less than 0.0001). Mean (SE) LVEF increased from 37 (4)% pretreatment to 49 (5)% after four weeks' NCPAP therapy (p less than 0.0001). Withdrawal of NCPAP for 1 week in four patients was associated with a reduction in LVEF from 53 (6)% to 45 (5)% (p less than 0.001). OSA may contribute to impaired left-ventricular function in some patients with dilated cardiomyopathy of otherwise unknown origin, and reversal of OSA by NCPAP can lead to significant improvement in LVEF.

Adult↗
PubMed1991

Adaptive changes in visual cell transduction protein levels: effect of light.

Long-term environmental light-mediated changes in visual cell transduction proteins were studied to assess the influence of rearing environment on their levels and their potential effects on intense light-induced retinal damage. The levels of rhodopsin, S-antigen and the alpha subunit of transducin were measured in whole eye detergent extracts, retinal homogenates or rod outer segments isolated from rats reared in weak cyclic light or darkness, and following a change in rearing environment. Rats changed from weak cyclic light to darkness had 22% more rhodopsin per eye than cyclic-light rats after 12-14 days in the new environment. Western trans-blot analysis of retinal proteins from these dark-maintained animals contained 65% higher levels of immunologically detectable alpha transducin; S-antigen levels were approximately 45% lower than in cyclic-light rats. In rats changed from the dark environment to weak cyclic light, rhodopsin levels decreased by 18% during a comparable period; retinal alpha transducin was 35% lower, S-antigen was 30% higher. At various times after the change in rearing environment, some rats were exposed to intense visible light to determine their susceptibility to retinal damage. Two weeks after an 8-hr exposure, cyclic-light reared rats had rhodopsin levels only 10% lower than control (2.1 nmol per eye). However, rhodopsin was 75% lower when cyclic-light rats were maintained in darkness for 2 weeks before intense light. For animals originally reared in darkness, rhodopsin was 78% lower following 8 hr of intense light, whereas only 30% rhodopsin loss occurred in dark-reared rats after previous maintenance for 2 weeks in weak cyclic-light.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗