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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nuclear pore complexes (NPCs) are the rate-limiting barriers for the exchange of macromolecules (e.g. transcription factors or mRNA) between the nuclear and cytosolic compartments. NPC conformation determines movement of cargo in either direction and thus controls gene expression. ATP and calcium are known to induce an NPC shape change (increase in height and decrease in diameter) indicating pore contraction. Here we report a CO2-induced shape change which is different to the ATP/calcium response. Experiments were performed on the isolated nuclear envelope of Xenopus laevis oocytes. The nuclear envelope was spread on glass and the native cytoplasmic surface was imaged with atomic force microscopy (AFM). The preparation was scanned in a water-saturated 100% O2 atmosphere at room temperature. Exposure to 5% CO2 (95%O2) led over a time course of minutes to a dramatic NPC shape change (decrease in height and decrease in diameter) indicating pore closure. NPCs turned flat and central channel openings virtually disappeared. The CO2 response was only slowly reversible. We conclude that NPCs apparently collapse in response to CO2, a structural change that could lead to the functional isolation of the cell nucleus.
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PMID:Nuclear pores collapse in response to CO2 imaged with atomic force microscopy. 1065 Sep 75

Milankovitch proposed that summer insolation at mid-latitudes in the Northern Hemisphere directly causes the ice-age climate cycles. This would imply that times of ice-sheet collapse should correspond to peaks in Northern Hemisphere June insolation. But the penultimate deglaciation has proved controversial because June insolation peaks 127 kyr ago whereas several records of past climate suggest that change may have occurred up to 15 kyr earlier. There is a clear signature of the penultimate deglaciation in marine oxygen-isotope records. But dating this event, which is significantly before the 14C age range, has not been possible. Here we date the penultimate deglaciation in a record from the Bahamas using a new U-Th isochron technique. After the necessary corrections for alpha-recoil mobility of 234U and 230Th and a small age correction for sediment mixing, the midpoint age for the penultimate deglaciation is determined to be 135 +/- 2.5 kyr ago. This age is consistent with some coral-based sea-level estimates, but it is difficult to reconcile with June Northern Hemisphere insolation as the trigger for the ice-age cycles. Potential alternative driving mechanisms for the ice-age cycles that are consistent with such an early date for the penultimate deglaciation are either the variability of the tropical ocean-atmosphere system or changes in atmospheric CO2 concentration controlled by a process in the Southern Hemisphere.
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PMID:Evidence from U-Th dating against Northern Hemisphere forcing of the penultimate deglaciation 1071 40

Polar processes can be sensitive indicators of global climate, and the geological features associated with polar ice caps can therefore indicate evolution of climate with time. The polar regions on Mars have distinctive morphologic and climatologic features: thick layered deposits, seasonal CO2 frost caps extending to mid latitudes, and near-polar residual frost deposits that survive the summer. The relationship of the seasonal and residual frost caps to the layered deposits has been poorly constrained, mainly by the limited spatial resolution of the available data. In particular, it has not been known if the residual caps represent simple thin frost cover or substantial geologic features. Here we show that the residual cap on the south pole is a distinct geologic unit with striking collapse and erosional topography; this is very different from the residual cap on the north pole, which grades into the underlying layered materials. These findings indicate that the differences between the caps are substantial (rather than reflecting short-lived differences in frost cover), and so support the idea of long-term asymmetry in the polar climates of Mars.
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PMID:North-south geological differences between the residual polar caps on Mars. 1072 62

Vital capacity (VC) and maximum mouth pressures are often used to monitor respiratory function in motor neuron disease (MND), but require the use of a mouthpiece. Sniff nasal inspiratory pressure (SNIP) is a simple and reliable means of measuring inspiratory muscle strength; it does not involve the use of a mouthpiece and might therefore be better than VC or mouth pressures for assessing patients with bulbar disease. SNIP, maximum inspiratory (MIP) and expiratory mouth pressure (MEP), VC and arterial carbon dioxide tension (Pa,CO2) were measured in 59 consecutive patients attending a specialist MND clinic. Thirty-one had bulbar involvement on clinical grounds. Both SNIP and VC were inversely related to Pa,CO2 in nonbulbar patients only. Neither MIP nor MEP were related to Pa,CO2. The 10 patients with an elevated Pa,CO2 (>6 kPa) had significantly lower SNIP and VC than normocapnic patients. Sniff nasal inspiratory pressure can be used to monitor respiratory function in motor neuron disease. It is quick and easy for patients to perform, but otherwise appears to offer little advantage over vital capacity measurement. Patients with bulbar disease are often poor at performing sniff nasal inspiratory pressure manoeuvres, possibly because of upper airway collapse or inability to close the mouth completely during the manoeuvre.
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PMID:Sniff nasal inspiratory pressure as a marker of respiratory function in motor neuron disease. 1075 49

Congenital vallecular cysts are rare. In this report, four infants having vallecular cysts encountered over a six-year period from 1992 to 1997 were reviewed. All of them presented with upper aerodigestive tract symptoms. Marsupialization was performed in three of them and CO2 laser excision was performed in the fourth patient. There was no recurrence of the cyst in any patient. One of them also had co-existing laryngomalacia. The degree of airway collapse caused by laryngomalacia improved after cyst removal. The laryngomalacia resolved spontaneously. Cyst fluid culture was performed in one of the patients and yielded Staphylococcus aureus but there was no other definite indicator of infection. Staphylococcus aureus could also be isolated in the respiratory tract from two of the other patients.
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PMID:Vallecular cyst: report of four cases--one with co-existing laryngomalacia. 1082 17

Ventilation with decelerating inspiratory flow is known to reduce the dead space fraction and to decrease PaCO2. Constant inspiratory flow with an end-inspiratory pause (EIP) is also known to increase the removal of CO2. The aim of the study was to elucidate the effect of the pause/no-flow period while both the pattern and rate of inspiratory flow was unchanged, and when the lung was ventilated with sufficient PEEP to prevent end-expiratory collapse. Surfactant depleted piglets were assigned to decelerating or constant inspiratory flow with 24 breaths per minute (bpm) or 12 bpm, or to constant flow, without and with an end-inspiratory pause of 25%. By adding an EIP the total time without active inspiratory flow of the respiratory cycle was kept unchanged. Gas exchange, airway pressures, functional residual capacity (using sulfurhexafluoride) and haemodynamics (thermo-dye indicator dilution technique) were measured. Irrespective of ventilatory frequency, PaCO2 was lower and serial dead space reduced with decelerating flow, compared with constant inspiratory flow. With an end-inspiratory pause added to constant inspiratory flow, serial dead space was reduced but did not decrease PaCO2. The results of this study corroborate the assumption that total time without active inspiratory flow is important for arterial CO2-tension.
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PMID:Impact of different inspiratory flow patterns on arterial C02-tension. 1089 50

Clinical studies using transcranial Doppler ultrasonography in patients with mechanical heart valves (MHV) have detected gaseous emboli. The relationship of gaseous emboli release and cavitation on MHV has been a subject of debate in the literature. To study the influence of cavitation and gas content on the formation and growth of stable gas bubbles, a mock circulatory loop, which employed a Medtronic-Hall pyrolytic carbon disk valve in the mitral position, was used. A high-speed video camera allowed observation of cavitation and gas bubble release on the inflow valve surfaces as a function of cavitation intensity and carbon dioxide (CO2) concentration, while an ultrasonic monitoring system scanned the aortic outflow tract to quantify gas bubble production by calculating the gray scale levels of the images. In the absence of cavitation, no stable gas bubbles were formed. When gas bubbles were formed, they were first seen a few milliseconds after and in the vicinity of cavitation collapse. The volume of the gas bubbles detected in the aortic track increased with both increased CO2 and increased cavitation intensity. No correlation was observed between O2 concentration and bubble volume. We conclude that cavitation is an essential precursor to stable gas bubble formation, and CO2, the most soluble blood gas, is the major component of stable gas bubbles.
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PMID:Observation and quantification of gas bubble formation on a mechanical heart valve. 1103 52

Physiological changes of Lactobacillus plantarum (KFRI 815) by high pressure CO2 treatment were investigated to examine the relevance to microbial inactivation. Characteristic properties of the cells measured in this study included salt tolerance, release of UV-absorbing substances, Mg and K ions, proton permeability, glycolysis, H+-ATPase and constitutive enzymes, and dye uptake. The cells treated with high pressure CO2 of 7 MPa at 30 degrees C for 10 min showed the irreversible cellular membrane damages including loss of salt tolerance, leakage of UV-absorbing substances, release of intracellular ions, collapse of proton permeability and uptake of Phloxine B dye. L. plantarum cells after CO2 treatment also exhibited reduced glycolytic activity and inactivation of some constituent enzymes. However, H+-ATPase of the cell membrane maintained its initial specific activity of about 2.50 U/mg protein even though viability of the cells was reduced by several log cycles after high pressure CO2 treatment.
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PMID:Membrane damage and enzyme inactivation of Lactobacillus plantarum by high pressure CO2 treatment. 1120 50

Adenosine (ADO) is a well-known regulator of a variety of physiological functions in the heart. In stress conditions, like hypoxia or ischemia, the concentration of adenosine in the extracellular fluid rises dramatically, mainly through the breakdown of ATP. The degradation of adenosine in the ischemic myocytes induced damage in these cells, but it may simultaneously exert protective effects in the heart by activation of the adenosine receptors. The contribution of ADO to stimulation of protective effects was reported in human and animal hearts, but not in rat hearts. The aim of this study was to evaluate the role of adenosine A1 and A3 receptors (A1R and A3R), in protection of isolated cardiac myocytes of newborn rats from ischemic injury. The hypoxic conditions were simulated by exposure of cultured rat cardiomyocytes (4-5 days in vitro), to an atmosphere of a N2 (95%) and CO2 (5%) mixture, in glucose-free medium for 90 min. The cardiotoxic and cardioprotective effects of ADO ligands were measured by the release of lactate dehydrogenase (LDH) into the medium. Morphological investigation includes immunohistochemistry, image analysis of living and fixed cells and electron microscopy were executed. Pretreatment with the adenosine deaminase considerably increased the hypoxic damage in the cardiomyocytes indicating the importance of extracellular adenosine. Blocking adenosine receptors with selective A1 and A3 receptor antagonists abolished the protective effects of adenosine. A1R and A3R activation during the hypoxic insult delays onset of irreversible cell injury and collapse of mitochondrial membrane potential as assessed using DASPMI fluorochrom. Cardioprotection induced by the A1R agonist, CCPA, was abolished by an A1R antagonist, DPCPX, and was not affected by an A3R antagonist, MRS 1523. Cardioprotection caused by the A3R agonist, Cl-IB-MECA, was antagonized completely by MRS 1523 and only partially by DPCPX. Activation of both A1R and A3R together was more efficient in protection against hypoxia than by each one alone. Our study indicates that activation of either A1 or A3 adenosine receptors in the rat can attenuate myocyte injury during hypoxia. Highly selective A1R and A3R agonists may have potential as cardioprotective agents against ischemia or heart surgery.
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PMID:Cardioprotective effects of adenosine A1 and A3 receptor activation during hypoxia in isolated rat cardiac myocytes. 1126 59

To elucidate the role of serotonin in the maintenance of normal breathing and upper airway (UA) patency in obesity, we studied the effects of systemic administration of ritanserin, a serotonin (5-HT) 2A and 2C receptor antagonist, on ventilation (V E) during room air breathing and during hypoxic (10% O2) and hypercapnic (4% CO2) ventilatory challenges in awake young (6-8 wk) and older (7-8 mo) obese and lean Zucker (Z) rats. Older obese Z rats adopted a more rapid shallow breathing pattern compared with older lean rats. The administration of ritanserin (1 mg/kg intraperitoneally) to older obese rats resulted in a reduction in V E (439 +/- 35 [SD] to 386 +/- 41 ml/kg/min, p < 0.01), a decrease in respiratory rate, a prolongation of inspiratory time, and an increase in V O2 (16.4 +/- 1.7 to 18.2 +/- 1.9 ml/kg(0.75)/min, p < 0.05) during room air breathing. By comparison, it had little effect on ventilation in young lean and obese Z or older lean Z rats. Ritanserin also had no effect on ventilatory responses to either hypoxia or hypercapnia in young or older lean and obese Z rats. The collapsibility of the isolated UA was examined in older Z rats. The pharyngeal critical pressure (Pcrit) of older obese rats was significantly greater than that of lean rats (p < 0.05), indicating that obese rats have more collapsible UA than lean rats. The administration of ritanserin significantly increased Pcrit in older obese rats (-1.6 +/- 0.3 to -0.8 +/- 0.2 cm H2O, p < 0.01) and in lean rats (-3.1 +/- 1.0 to -2.4 +/- 0.6 cm H2O, p < 0.05). We suggest that the 5-HT(2A/2C) receptor subtype plays an important role in the maintenance of UA stability and normal breathing in obesity, and we speculate that older obese Z rats may have augmented serotonergic control of UA dilator muscles as a mechanism to prevent pharyngeal collapse.
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PMID:Serotonergic modulation of ventilation and upper airway stability in obese Zucker rats. 1131 30


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