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The ribosome content was markedly reduced when illumination (at 28 C) was repeatedly interrupted; an opposite trend was observed with continuous light as the temperature was decreased.
Chest wall diameters measured by magnetometers were used to indicate a lung volume reference for repeated interrupted partial flow-volume curves (IPFVC's) and IPFVC's, and total respiratory conductances were measured before and after bronchodilation in normals. With posture rigidly controlled, subjects matched the magnetometer display on an X-Y oscilloscope to a previously marked point on the screen. Seven subjects performed six inspiratory capacities (IC's) from the reference point, completely reposturing before each maneuver. For a mean IC of 2.25 liters the standard deviation was 5.5%. IPFVC's were performed through a valve system triggering open at 60 cmH2O and shutting after 1 liter of expiration. Ten subjects each performed five sets of IPFVC's volume-referenced by magnetometers and the pooled flow variability was 5% or 0.15 l/s. Respiratory conductances by forced oscillations and IPFVC's were measured in five normal subjects before and after inhaled isoproterenol. In each subject the flow increase was always greater than the conductance increase (about 2.5:1.0) for P less than 0.05. We conclude that magnetometers may be used in normals to volume-reference IPFVC's with excellent reproducibility.
An in vitro perfused carotid body preparation was developed to study its chemosensory responses to physiological and pharmacological stimuli. The carotid bifurcation with the carotid body was vascularly isolated and excised from pentobarbital sodium-anesthetized cats. The CB was perfused in a chamber by gravity (80 Torr) with modified Tyrode's solution (N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-NaOH at pH 7.40) equilibrated at a given Po2 and superfused with the same medium at (Po2 of 20 Torr). The temperature was maintained at 35.5 +/- 0.5 degrees C. The frequency of chemosensory discharges (CD) was recorded from the whole carotid sinus nerve (n = 24), and the responses were tested by repeated interruptions of perfusate flow (SF), perfusion with hypoxic medium, and injections of nicotine and cyanide (0.1 nmol to 1 mumol) and hypercapnic medium. During hyperoxic perfusion, SF resulted in a sigmoidal increase in CD, reaching a maximum that was 23.6 +/- 4.4-fold greater than the basal activity. Restoration of flow returned CD promptly to basal values. After normoxic perfusion, SF led to a similar maximal activity more rapidly, but the duration was shorter. Reduction of the perfusate PO2 (Po2 from 450 Torr to 150, 30, and less than 10 Torr) caused a nonlinear increase in CD. CO2 stimuli (PCo2 38-110 Torr) resulted in a linear increase in CD. Nicotine or cyanide increased CD in a dose-dependent manner. The preparation retained its initial responsiveness for 2-3 h, making extensive experimental studies feasible.(ABSTRACT TRUNCATED AT 250 WORDS)
Ventilation (V) decreases during sleep while upper airway resistance (UAR) increases. A number of studies have suggested that in normal healthy individuals the changes in the two variables are reciprocal. Other findings, however, suggest that the relationship between V and UAR may change as non-rapid-eye-movement (NREM) sleep progresses such that most of the change in V occurs early during the sleep period, whereas the most marked changes in UAR occur later during established NREM sleep. However, no study has examined the progressive development of changes in both V and UAR over the NREM sleep period. This study examined V and UAR over one NREM sleep period in two groups of healthy young male subjects: a "slow-wave sleep (SWS) group" (n = 8) in which the subjects obtained the full range of NREM sleep stages from wakefulness to stage 4 NREM sleep and a "no-SWS group" (n = 5) in which the subjects did not attain SWS but spent a prolonged period in stage 2 NREM sleep that was repeatedly interrupted by arousals. Results showed that the most marked changes in V occurred early during the sleep period in association with relatively small increases in UAR. Once NREM sleep became established, further attenuation of V was minimal despite marked and progressive increases in UAR. The progressive increase in UAR occurred in association with increasing delta (0.4- to 3.0-Hz) electroencephalographic activity and did not occur in the no-SWS group. We interpret these findings to indicate that factors in addition to UAR contribute to the reduction in V early in sleep onset, whereas later, during NREM sleep, compensatory mechanisms are activated to allow for maintenance of V in the context of larger increases in UAR.
A simple shield made of a folded silastic sheet is described for the protection of the externalized portion of a permanent biliary cannula in rats. Advantages of this shield are its light weight, flexibility, transparency, and ease of resealing for repeated interruption of hepatobiliary circulation. Since the shield is positioned around rather than being a segment of the cannula, a single length of tubing can be used.
Chronic stress can trigger several pathologies including mood disorders for which no clear diagnostic molecular markers have been established yet. Attractive biomarker sources are extracellular vesicles (EVs). Evs are released by cells in health and disease and contain genetic material, proteins and lipids characteristic of the cell state. Here we show that Evs recovered from the blood of animals exposed to a repeated interrupted stress protocol (RIS) have a different protein profile compared to those obtained from control animals. Proteomic analysis indicated that proteins differentially present in bulk serum Evs from stressed animals were implicated in metabolic and inflammatory pathways and several of them were previously related to psychiatric disorders. Interestingly, these serum Evs carry brain-enriched proteins including the stress-responsive neuronal protein M6a. Then, we used an in-utero electroporation strategy to selectively overexpress M6a-GFP in brain neurons and found that M6a-GFP could also be detected in bulk serum Evs suggesting a neuronal origin. Finally, to determine if these Evs could have functional consequences, we administered Evs from control and RIS animals intranasally to naïve mice. Animals receiving stress EVs showed changes in behavior and brain M6a levels similar to those observed in physically stressed animals. Such changes could therefore be attributed, or at least in part, to EV protein transfer. Altogether these findings show that EVs may participate in stress signaling and propose proteins carried by EVs as a valuable source of biomarkers for stress-induced diseases.
The ciliate Stentor coeruleus exhibits photodispersal, that is, these cells swim away from light sources and collect in dimly lighted areas. We imaged and reconstructed the tracks of 48 Stentor to determine which swimming behaviors produced their photodispersal. We observed that their photodispersal is not due to a change in their swimming speed but rather to a change in the frequency with which they reorient their swimming direction. Therefore, their photodispersal must be due to either (1) a gradual reorientation of the organism's swimming direction determined by the direction of the light beam (phototaxis) or (2) multiple randomly directed reorientations in swimming direction that occur less frequently when the cell is swimming away from the light source (biased random walk). Sixteen (19%) of the 83 observed forward swimming tracks lasting three or more seconds exhibited a gradual bending away from the light source consistent with a phototaxis. However, most tracks were interrupted repeatedly by abrupt reorientations resulting from ciliary reversals and "smooth turns" that caused cells to reorient through 5.4 times as many degrees as were needed to direct them away from the light source. When cells were swimming away from the light source, their probability of reorienting was reduced and photodispersal resulted.
The effect of repeated interruption of FI responding by short S(Delta) presentations on the pattern of increasing frequency of responding through the interval has been studied. Although the S(Delta) profoundly changed the pattern of responding during their presentation, the general scalloped pattern of FI responding survived. The implication of these findings for understanding the role of chaining of responses in FI patterns is discussed. It is suggested that chaining is not a necessary condition for the scalloped pattern.
Massage is known to produce a reduction in spinal reflex excitability. However, the mechanisms subserving this phenomenon have yet to be elucidated. This study was undertaken to determine the role of superficial cutaneoreceptors overlying the triceps surae during the application of a massage. Twelve neurologically healthy volunteers were subjected to an interrupted repeated measures design consisting of eight conditions. Each condition was comprised of eleven H-reflex recordings obtained from the right soleus muscle. Six conditions served to establish baseline control levels, while the remaining two conditions consisted of reflex recordings obtained simultaneous to the application of the massage. During the first massage condition, subjects were at rest while a three minute petrissage was applied to the right triceps surae muscle group. The second massage condition was always preceded by the application of a topical anaesthetic to abolish the sensation to touch and pin-prick to the skin area that was to be massaged. It was expected that the cutaneous afferents would not play any major role in the changes associated with the application of the massage. H-reflex amplitudes recorded during each massage condition (1.20 mV +/- 0.30 SEM, 1.05 mV +/- 0.23 SEM, respectively) were significantly reduced (F7.77 = 26.048, p < 0.01) in contrast to all control conditions (range: 2.21 to 2.63 mV). However, no difference was observed between the two massage conditions. The inhibitory effects of massage on the soleus H-reflex do not appear to originate from mechanical stimulation of cutaneous mechanoreceptors. It seems more likely that deep mechanoreceptors are involved.
The sleep apnea syndrome (SAS), which is defined by more than 5 apneas or hypopneas per hour of sleep (9), is quite a frequent affection which concerns 1.4 to 10% of general population (1.7). The major daytime complaints of the SAS are daytime sleepiness, memory and attention disorders, headaches and asthenia especially in the morning, and sexual impotence (9). The nocturnal manifestations are dominated by sonorous and generally long standing snoring, increased by dorsal decubitus and intake of alcohol, with repeated interruptions by respiratory arrests. These manifestations are always noted but rarely spontaneously reported. The sleep, non refreshing, is agitated and perturbed by numerous awakenings. The findings of the clinical examination are poor: obesity is found in 2/3 of the cases and arterial hypertension in 1/2 of the cases (20). Polygraphic recording during sleep only permits an absolute diagnosis. This frequent affection is a real problem of public health because of its numerous complications (3, 10, 12, 13, 18, 21). Symptoms of depression are often found when a patient with a SAS is examined and conversely, symptoms which evoke a SAS can be found in the clinical examination of depressed patients. We decided so to study the thymic and anxious status of 24 patients investigated for a SAS and submitted to a polygraphic recording during sleep. Four clinical parameters were studied: DSM III-R diagnosis criteria, Montgomery and Asberg Depression Rating Scale (MADRS), Hamilton Anxiety Rating Scale (HARS) and thymasthenia rating scale of Lecrubier, Payan and Puech. We also reported Total Sleep Time (TST = 6.5 +/- 1.5), Apnea Hypopnea Index (AHI = 26.7 +/- 21.6), number (2.1 +/- 2.8/h) and duration (174.2 +/- 150.8 s/h) of hypoxic events. Results showed that among 24 patients, 8 were depressed according to DSM III-R diagnosis criteria and had MADRS > 25, 22 were anxious, 11 had a major anxiety (HARS > 15) and 15 presented thymasthenia (SET > 15). Significative correlations existed between anxiety and depression (r = 0.82; p < 0.0001), depression and thymasthenia (r = 0.77; p < 0.0001) and thymasthenia and anxiety (r = 0.75; p < 0.0001). Among the 8 depressed patients a correlation existed between AHI and depression (r = 0.72; p = 0.04), but no correlation was found between depression and hypoxic events. These results were comparable to those of Guilleminault (10), Reynolds (21), Kales (12), Bliwise (3), Klonoff (13) and Millman (18) who studied relations between SAS and depression. The evaluation of thymasthenia gave a more precise typology of the depressive state associated to SAS: the type of the mood disorder is more "blunted" and "anhedonic" than "sorrowful", particularly characterised by asthenia, lack of energy, reduction of interests (leisures, libido, work), loss of initiative, difficulties to organise tasks, fall of performances and reduction of pleasure usually felt in pleasant events (15). The physic symptomatology dominated the psychic one. The sleep disorganization, more than metabolic consequences of apneas, could be involved in this associated depressive state. Other neuropsychiatric troubles can be associated to the SAS. In fact, cognitive troubles (2, 8, 14, 16, 19, 22, 24) and personality disorders (12, 18) have been described. Our data confirm previous observations suggesting a frequent association between SAS, depression, fatigue and anxiety. Clinicians should consequently be aware that a depression with severe complaints of fatigue should deserve an investigation oriented towards SAS. Conversely, when a SAS is diagnosed, it is necessary to look for a possible depression in order to set up the most appropriate treatment. The frequency of SAS, like depression's one, increases with age. Prescription and consummation of sedative psychotropic drugs increase too with age. Since respiratory depressant effects of these drugs have been clearly demonstrated, it is important to evoke SAS when depressive and/or anxious states are diagnosed and not to aggravate it. An efficacious treatment of SAS can also cure the associated depressive state, but this one can persist. It is necessary, in this case, to select a non sedative antidepressant.
Of the various therapeutic modalities available to treat ectopic atrial tachycardia, radiofrequency catheter ablation has shown excellent results. It is usually possible to localize the earliest site of endocardial activation by conventional or newer three-dimensional mapping techniques. We report a case of ectopic atrial tachycardia, wherein the tachycardia was being repeatedly interrupted by mechanical trauma. Finally, with the help of P wave pace mapping, the tachycardia was localized near the posterolateral part of the mitral annulus, and successfully ablated. This report demonstrates the utility of P wave pace mapping in ectopic atrial tachycardia.
Oral diadochokinetic abilities in 6 patients with ataxic dysarthria (ATAXICs), 6 with spastic dysarthria (SPASTICs), 3 with parkinsonism (PARKINs), and 6 normal subjects (NORMALs) were investigated using repetition of monosyllable /pa/ and "on-off phonation test" in which they had been requested to repeat interrupted vowel /a/ as fast as possible. Oscillographic as well as photographic records of the speech acoustic signal were obtained to analyse interval for a syllable, which consisted of voiced and unvoiced intervals, and peak-value of voiced interval. The results were as follows: 1) ATAXICs and SPASTICs showed prolonged interval for a syllable, yet that of PARKINs was within normal range, when tested either in /a/ or in /pa/. 2) Standard deviation and coefficient of variation for intervals of syllable and those of peak-values in voiced interval could not distinguish their characteristics among ATAXICs, SPASTICs, and PARKINs. 3) In "on-off phonation test", ATAXICs showed prolonged unvoiced intervals, while SPASTICs did prolonged voiced intervals. Results suggested that hypotonic laryngeal muscles in ATAXICs might result in prolongation of unvoiced interval, but that prolonged voiced interval related to biased hypertonus of laryngeal adductor. It is concluded that "on-off phonation test" could, with reasonable sensitivity, reflect the phonatory dynamics of laryngeal muscles in dysarthric patients.
The detection of regional myocardial dysfunction due to acute ischemic event has been limited almost entirely to experimental animal models. In human subjects, it has been limited to the observations during spontaneously-occurring or exercise-induced ischemic events. Recently, percutaneous transluminal coronary angioplasty (PTCA) provides an opportunity to study such dysfunction as the result of repeated interruptions of coronary blood flow. Echocardiograms and electrocardiograms were simultaneously recorded immediately before, during, and after 21 episodes of complete interruptions of coronary blood flow by PTCA in 11 patients. No patient had asynergy of the left ventricle either by two-dimensional echocardiography (2DE) or angiography. All patients had isolated single coronary artery stenosis including the left anterior descending artery in nine, left circumflex artery in one and right coronary artery in one. Recordings of M-mode and 2DE were successfully obtained in 10 patients. After balloon inflation, regional asynergy in the distribution of the instrumented coronary artery appeared in all 10 patients. Hypokinesis developed 9 +/- 3 (means +/- SD) sec after balloon inflation and progressed rapidly to akinesis or dyskinesis. At the same time, decreased systolic thickening of the left ventricular wall appeared in some patients in relation to the development of regional asynergy. However, systolic thinning of the left ventricular wall was not noted in all. The regional asynergy preceded ischemic electrocardiographic changes and had no relation to chest pain. Left ventricular wall motion began to normalize 12 +/- 3 sec after balloon deflation. Thereafter, transient hyperkinesis of the left ventricle developed. The first ischemic electrocardiographic change was a negative U wave which appeared 13 +/- 7 sec after coronary occlusion and remained 3 to 4 sec. Tall T waves were recorded at 28 +/- 12 sec and significant ST elevations developed 31 +/- 11 sec, after balloon inflation. These electrocardiographic changes invariably occurred only after the onset of wall motion abnormalities. Normalization of T waves was recognized at 17 +/- 16 sec and ST segment deviation were no longer present at 18 +/- 10 sec, after reperfusion. These electrocardiographic changes also preceded normalization of regional myocardial dysfunction. In conclusion, left ventricular wall motion abnormalities after coronary occlusion invariably precede the electrocardiographic changes, and begin to normalize after reperfusion prior to the electrocardiographic recovery.
The dental-phobic patient is rarely motivated to seek treatment. When this type of patient does, it is difficult to perform the dental work without repeated interruptions due to the high anxiety being displayed. Many dental phobics are actually agoraphobic, and this further complicates the matter. The agoraphobic dental patient mislabels any physiologic changes that are experienced as a prelude to disaster, or horrific consequences, and something there is no control over. This type of patient looks to depend on "safe" places (like home) and "safe" people (like spouses and doctors). The physiologic changes that are perceived may be induced pharmacologically (for example, numbness and tingling from the lidocaine, imbalanced blood gases due to hyperventilation), physically (for example, tilt of the dental chair, pressure in the mouth), or cognitively (autonomic excitation due to negative thoughts). The inability to mitigate the physiologic changes or symptoms confirms the patient's irrational belief that disaster is inevitable. Two basic considerations must be given priority when treating agoraphobic dental patients. These are: (1) providing them with a sense of being in control of the situation and/or their symptoms, and (2) training them to relabel or reinterpret their symptoms objectively as nervousness, or some simple and explainable physiologic change that should be present. Therefore, teaching agoraphobic dental patients cognitive-behavioral procedures such as relaxation and cognitive-restructuring techniques works quite well. Both will help to prevent, or reduce to a manageable level, the symptoms, and result in successful dental work.
A new approach to the treatment of chronic nonspecific pulmonary diseases is proposed: helium-oxygen therapy combined with repeated interrupted hypoxic stimuli. Helium inclusion into hypoxic gas mixture leads to reduced air density. Gas mixture containing 10-15% of oxygen is more effective at the level of alveolocapillary membrane. When conducted in normal atmospheric pressure, the method involved no complications and produced positive responses in coronary heart disease, hypertension, alimentary diseases. The mixture of helium with oxygen (85-90% of helium, 10-15% oxygen) in combination with impulse normobaric hypoxia has been tried in 25 chronics with obstructive bronchitis and bronchial asthma. The results were indicative of the treatment efficacy: bronchial permeability improved in 67% of the cases, forced vital capacity of the lungs increased, inspiratory reserve volume grew, dyspnea and cough diminished, sputum discharge improved, general tonicity and performance status changed positively. Six-month follow-up evidenced positive shifts too.
UNLABELLED: The series "Illness and Vehicular Traffic", published by the German Federal Ministry for Transportation, has set forth the following guidelines on the subject of driving for patients with cardiac rhythm disorders: "Anyone suffering from disorders of cardiac rhythm which might, on occasion, lead to the repeated interruption of oxygen supply to the brain and thus cause disturbances in consciousness or even loss of consciousness, must be considered unsuitable for driving a motor vehicle of any class." While these guidelines are essentially indisputable, it remains unclear how they affect patients with an implantable cardioverter/defibrillator (ICD). The issue is further complicated by the fact that these patients, as a rule, suffer from malignant and life-threatening cardiac rhythm disorders, often owing to a severe cardiac disorder (primarily coronary heart disease and cardiomyopathy). It was the purpose of a recent study to investigate how medical permission to drive in ICD patients is handled in various European countries. A specifically designed questionnaire was addressed to 46 European National Delegates of the Working Groups on Cardiac Pacing in order to determine their present practices and criteria utilized when advising driving restrictions to patients (pts) after ICD implantation. RESULTS: Of the 39 (83%) respondents, 22 (56%) cardiologists advised all pts to abstain from driving. Permanent driving abstinence was advised by 13 (33%) of the responding cardiologists, while temporary driving abstinence for periods of 3 to 18 months (mean 9 +/- 4 months) was recommended by 26 (67%) physicians. Criteria for subsequently advising a longer period of driving abstinence were: presyncope by 15 (38%), syncope by 13 (33%) and multiple shocks by 2 (5%) cardiologists. Despite medical advice not to drive, about one-third of pts resume driving. About half of the pts resumed driving after 6 months, with the vast majority driving 12 months after ICD implantation. Two pts experienced ICD discharges while driving, but no motor vehicle accident occurred. One patient had a motor vehicle collision with a fatal outcome which was not caused by loss of consciousness or ICD discharge. CONCLUSIONS: 1) Fatal accidents of ICD discharges while driving are a rare finding in ICD pts. 2) About half of the physicians always advise their pts to cease driving for a period of 9 +/- 4 months. Despite this medical advice pts resume driving 6 months after ICD implantation. 3) Criteria used in advising driving abstinence are not uniform among physicians. In symptomatic bradyarrhythmias the driving privilege may be reinstated after pacemaker implantation provided that symptoms resulting from the interruption of the oxygen supply to the brain have not recurred.
A 69-year-old female patient with renal failure developed heparin-induced thrombocytopenia type II (HIT II) two months after starting haemodialysis therapy with heparin as anticoagulant and a 6-week course of thromboembolism prophylaxis with enoxaparin sodium. The platelet count dropped by 50% as compared with initial values and ex vivo platelet aggregation induced by heparin antibodies (HIPA-test) was detected. Haemodialysis therapy was complicated by a massive thrombosis of dialyzer and ensuing repeated interruptions of treatment. After confirmation of the diagnosis of HIT II haemodialysis therapy was continued with hirudin as anticoagulant. Polysulfone dialyzers and an intravenous bolus of 0.14 mg/kg of recombinant hirudin (r-hirudin) achieved efficient haemodialysis therapy of 4.5 hours, with a minimum therapeutic blood level of hirudin of 0.5 micrograms/mL. More than 50 regular haemodialysis with hirudin anticoagulation were performed without additional problems. The ecarin clotting time (ECT) was used as bedside method to monitor blood levels and for dosage adjustments of hirudin. After the 34th haemodialysis, the frequency (previously 3-4 haemodialyses sessions/week) was reduced to 2 sessions/week. The creatinine clearance increased continuously from initially 2.6 to 10.4 ml/min after the 13th week of hirudin-anticoagulated haemodialysis and the platelet count normalized. In conclusion, we report the first long-term administration of r-hirudin to a patient on regular haemodialysis therapy complicated by heparin-induced thrombocytopenia. The use of hirudin as anticoagulant along with dialyzers impermeable to hirudin offers a novel alternative means of anticoagulation and, even in patients with HIT, enables performing an efficient haemodialysis therapy. Hirudin dosage must be individually adjusted by using bedside drug monitoring of plasma concentrations.
Spinocerebellar ataxia type 2 (SCA2), one of the hereditary human neurodegenerative disorders, is caused by the expansion of the CAG tandem repeats in the translated sequence of the SCA2 gene. In a normal population the CAG repeat is polymorphic not only in length but also in the number and localization of its CAA interruptions. The aim of this study was to determine the structure of the repeat region in the normal and mutant SCA2 transcripts and to reveal the structural basis of its normal function and dysfunction. We show here that the properties of the CAA interruptions are major determinants of the CAG repeat folding in the normal SCA2 transcripts. We also show that the uninterrupted repeats in mutant transcripts form slippery hairpins, whose length is further reduced by the base pairing of the repeat portion with a specific flanking sequence. The structural organization of the repeat interruption systems present in other human transcripts, such as SCA1, TBP, FOXP2, and MAML2, are also discussed.