Managing depression in general practice.
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Biomedical subjects
Publications and source records attributed to R Lane.
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1. We have validated a method for the continuous display and 'on-line' measurement of total pulmonary resistance in man, using a hybrid digital/analog computer. 2. The basic variables, which are measured by standard techniques, are flow rate of the mouth (V) and oesophageal pressure (Poes), and these are the only analog inputs necessary to the computer. 3. Resistance (RL,cont) is calculated continuously as: RL,cont = (Poes-V/C)/V where V is tidal volume and C is the dynamic compliance. RL,cont is continuously displayed as an analog signal on an oscilloscope. 4. Changes in resistance, measured by this method over a wide range of values in three subjects, showed an almost exact correlation with those measured by a standard method (Mead-Whittenberger).
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1. A previous study showed that when combined with exercise in normal subjects, hypercapnic and hypoxic ventilatory stimuli did not have a specific effect on the intensity of the sensation of breathlessness in addition to their stimulation of ventilation. The aim of the present study was to assess the significance of another reflex ventilatory stimulus, metabolic acidosis, in the genesis of this sensation. 2. Six subjects performed progressive exercise tests (mean workload, 103 W; range, 88-125 W) with normal acid-base status. Following NH4Cl-induced metabolic acidosis (mean change in base excess, -3.6 mmol l-1; range, -0.3 to -6.8 mmol l-1) exercise was repeated (mean workload, 91 W; range, 53-116 W) such that the combined ventilatory stimulation resulted in levels of ventilation (mean maximum, 65 l min-1) 'matched' to those resulting from exercise alone. A third, 'matched ventilation', exercise test was performed during metabolic acidosis but with end-tidal PCO2 controlled to a normal level (mean workload, 56 W; range, 17-103 W). Breathlessness was assessed using a visual analogue scale (VAS). 3. Progressive hypercapnic ventilatory stimulation was given before (mean maximum end-tidal PCO2 (PET,CO2), 61 mmHg) and during metabolic acidosis (mean maximum PET,CO2, 57 mmHg) to achieve the same peak level of ventilation (mean maximum, 59 l min-1). Breathlessness was assessed with the VAS. 4. As ventilation increased during a test, there were no statistically significant differences in the increasing breathlessness scores with metabolic acidosis compared to control, for either exercise (mean VAS, 22 mm vs. 24 mm) or progressive hypercapnia (mean peak VAS, 31 mm vs. 32 mm). 5. These results do not support the idea that metabolic acidosis is associated with a change in the relationship between the intensity of breathlessness and ventilation; this is similar to results found with other reflex ventilatory stimuli. 6. These findings are consistent with the hypothesis that the degree of reflex ventilatory activation is an important determinant of the intensity of the sensation of breathlessness in healthy humans, irrespective of the exact nature of ventilatory stimulus.
Familial amyotrophic lateral sclerosis (FALS) has recently been shown to be linked to chromosome 21 markers in a subset of families. However, we were unable to show linkage between FALS and chromosome 21 markers which flank the putative FALS locus in UK families.
This report describes a digitally controlled system for use in auditory physiology in which signal generation and data acquisition are under the control of a single microcomputer. The system is designed to generate the complex waveforms required in neuroethological studies, and is able to generate these signals at frequencies of up to 160 kHz with a resolution of 1 Hz. The system is built around a commercially available digital hardware system, and augmented with custom components to enhance operation speed, precision and flexibility.
An understanding of clinical pathology is extremely important for the pet avian clinician. The basics are often poorly understood by the busy practitioner. This article has served as a review for clinicians wanting the basics but having neither the time nor the resources to examine large volumes of material. This information has been designed to enable the veterinarian to understand better the limitations of the tests and the difficulties encountered by the avian technician in performing the tests so important in clinical avian practice.
1. The sensation of breathlessness increases when ventilation is reflexly stimulated but it is not clear whether different stimuli have specific effects in the genesis of this sensation. 2. Our aim was to compare subjective assessments of the intensity of breathlessness at the same levels of ventilation induced by different combinations of reflex ventilatory stimuli. 3. Against a background of progressive exercise (maximum workload 170 W) in 'blinded' normal naive subjects, normoxic hypercapnia (maximum end-tidal CO2, PET, CO2, 56 mmHg) or isocapnic hypoxia (minimum O2 saturation 88%) was induced to achieve levels of ventilation (maximum 60 l min-1) 'matched' with those resulting from a higher intensity of exercise alone. Subjective breathlessness was rated with a visual analogue scale. 4. For a given ventilation, compared with exercise alone, breathlessness scores were similar during hypercapnia and were lower during hypoxia. 5. These results do not support the idea that during exercise, hypercapnia or hypoxia has a specific role in the genesis of the sensation of breathlessness. 6. The findings are consistent with the hypothesis that the degree of reflex ventilatory activation, however achieved, is an important determinant of the intensity of perceived breathlessness in healthy humans.
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The upper torso of a man was discovered under a highway sign next to tire tread marks leading from the highway and continuing beyond the sign. The victim's lower torso and automobile were also found along the same path 31 m (101 ft) and 41 m (133 ft) beyond the sign, respectively. The decedent was initially thought to be a disposed, homicide victim who had been dismembered by his assailant(s). Accident reconstruction revealed that the victim was the driver of the automobile and was transected by the highway sign stanchion as he protruded through the passenger side window of his moving vehicle. Based on the scene findings, autopsy, and psychological autopsy, the manner of death was classified as suicidal. The criteria used by medical examiners for vehicular suicide are also discussed.
The potassium-stimulated release of gamma-aminobutyric acid (GABA) from synaptosomes was determined in preparations from control rats and from rats treated with a convulsant agent [isonicotinic acid hydrazide (INH)] and an anticonvulsant agent (gabaculine). INH treatment brought about a significant decrease in Ca2+-dependent release of GABA with no effect on Ca2+-independent release, whereas gabaculine caused an increase in Ca2+-independent release with no effect on Ca2+-dependent release of GABA. Thus, the anticonvulsant action of gabaculine was not a simple reversal of the effects of INH on GABA release. The results indicate that there are at least two pools of GABA in nerve endings and support the hypothesis that exogenous GABA is taken up first into a pool that supplies GABA for Ca2+-independent release and then is transferred to a second pool (Ca2+-dependent releasable), where it mixes with newly synthesized GABA.
Total pulmonary resistance was measured from continuous records of flow and oesophageal pressure in five normal subjects on three separate days before and after inhalation of methacholine. The dose of methacholine produced, on average, a fivefold increase in airway resistance. Immediately after methacholine inhalation the subjects underwent a progressive exercise test on a cycle ergometer (day 1) or voluntary hyperventilation (day 2) or remained resting (day 3). On the first day during exercise pulmonary resistance fell rapidly to baseline levels within two to three minutes and remained there for the 10 minute duration of the exercise. On day 2 voluntary reproduction of the same level and pattern of ventilation as during exercise resulted in a similar fall of resistance. On the third day, when the subjects remained at rest, pulmonary resistance remained raised for 10 minutes. It is concluded that the bronchodilator effects of exercise can be explained by the increased ventilation rather than the exercise itself, but with much smaller tidal volumes than have previously been thought necessary to reduce drug induced bronchoconstriction.
The records of 100 consecutive patients undergoing transantral ligation of the internal maxillary artery (IMA) for epistaxis, including 15 patients who developed postoperative bleeding, were reviewed. Preoperative parameters predictive of surgical failure were advanced age, anemia, and a history of hypertension. The causes of postoperative epistaxis, as determined by surgical reexploration or angiography in 12 cases, included failure to identify the IMA in the pterygomaxillary space (6 cases), blood flow through partially closed clips on the IMA (2 cases), bleeding from posterior ethmoid arteries (2 cases), and revascularization of the nasal blood supply (2 cases). The incidence of surgical failure may be reduced by proper techniques of IMA identification and ligation.
Nine patients with chronic obstructive airways disease performed a 6 min self-paced walk (breathing air) on a treadmill and then identical (but operator-controlled) treadmill walks breathing either air or supplemental oxygen sufficient to just prevent arterial oxygen desaturation during the exercise. During the exercises, ventilation was recorded and patients recorded their sensation of breathlessness on a visual analogue scale (VAS) every 30 s. Breathing supplemental oxygen produced a small fall in mean exercise ventilation and a large and consistent reduction in mean exercise breathlessness. In seven patients the VAS scores were higher on air than with supplemental oxygen, at similar levels of ventilation. An analysis of covariance, to control for reduction in ventilation, showed a decrease in mean breathlessness when breathing supplemental oxygen, significant at the 8% level. The reduction in breathlessness produced by preventing exercise desaturation cannot be explained by the decrease in ventilation. This suggests that hypoxia may be a stimulus for breathlessness. The mechanism is unknown.
1. Six patients with chronic airflow limitation rebreathed CO2. Subsequently they voluntarily copied their stimulated breathing pattern while normocapnia was maintained. On a separate occasion four of these patients performed progressively increasing exercise and later copied these breathing patterns. 2. During all experiments flow, ventilation and pleural pressures were recorded. In addition, breathlessness was measured on a visual analogue scale every 30 s. 3. In these patients voluntary copying of either form of stimulated breathing resulted in diminished breathlessness and in some cases in complete abolition of the sensation, despite similar levels and patterns of ventilation in the two situations. 4. No systematic or consistent differences in the mechanics of breathing between stimulated and voluntarily copied breathing were found. 5. There was no correlation found between breathlessness score and any mechanical variable measured. 6. These results show that despite similarity in mechanics between stimulated and voluntary hyperventilation, the sensation of breathlessness is much diminished during the latter in these patients. This suggests that the sensation of breathlessness is more dependent upon the awareness of central processing than upon input from peripheral mechanoreceptors.
1. Nine normal subjects performed 6 min, constant-workload, exercise tests on a bicycle ergometer at either a 'high workload' or at a 'low workload'. During the first 'high workload' test their spontaneous breathing pattern was recorded on to magnetic tape. During one subsequent 'high workload' test and one 'low workload' test they voluntarily copied their recorded breathing pattern. During a second 'low workload' test they breathed spontaneously. Isocapnia was maintained by the operator throughout both the copying tests. During the exercise tests ventilation was recorded and subjects indicated the level of their sensation of breathlessness every 30 s. 2. Subjects felt markedly less breathless when a proportion of their ventilation was produced by voluntary effort than when the same total level of ventilation was produced entirely by the stimulus of exercise. Furthermore, voluntary isocapnic hyperventilation during exercise did not increase breathlessness above that normally associated with that level of exercise. 3. These results suggest that it is reflexly driven ventilation, and not simply the level of ventilation itself, which relates to the level of breathlessness during exercise.