A simple method of measurement for the determination of the sputum viscosity.
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Biomedical subjects
Publications and source records attributed to A Jensen.
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Meal from the brown seaweed Ascophyllum nodosum (L.) Le Jol. is mainly used as an animal feed supplement. Since moist weed often develops a marked mold growth and since little was known about the microflora of seaweed meal, a cultural procedure was developed to enumerate the populations of bacteria, yeasts, and molds of seaweed meals manufactured by different drying processes. The microflora could be supported by a variety of media varying in levels of nutrition and in the source and concentration of salts. Fresh weed contained less than 10(3) bacteria and less than 10(2) yeasts and molds per g (dry weight). The type and extent of microbial populations in seaweed meal appeared to be dependent upon the method of seaweed drying. Rotary drum-drying at temperatures decreasing from 800 to 80 C maintained or reduced the microbial populations to 10(3) organisms per g (dry weight). Although meals with high nutritional quality can be obtained with warm air- or rock-dried weed, these conditions can also permit bacterial and mold development. Extended rock-drying in variable weather conditions and prolonged storage of moist weed, both of which decrease the nutritional quality, also lead to high bacterial numbers and to a marked development of the halophilic brown mold Sporendonema minutum which attained populations of 10(8) viable spores per g of dried weed. A poultry diet containing 5% badly molded weed had no apparent toxic or growth-depressing effect when fed to chicks.
OBJECTIVE: There is increasing evidence from animal experiments that mild hypothermia induced during or after cerebral ischemia might protect the immature brain from neuronal cell damage. However, the exact interrelation between the postischemic time delay and the degree of mild hypothermia by which to achieve neuroprotective effects on ischemic insults of different severity has not yet been elucidated systematically. To determine optimal neuroprotection, we studied the interaction between these variables in a recently modified hippocampal slice model. METHODS: We investigated the recovery of energy metabolism and protein synthesis (PSR) in hippocampal slices from mature fetal guinea pigs after 20, 30, or 40 minutes of oxygen and glucose deprivation (OGD). Hypothermia of varying degrees was induced immediately or 2 or 4 hours after OGD and lasted for 12 hours. Prolonged inhibition of PSR after ischemia has been shown to be a sensitive marker of neuronal cell damage. RESULTS: Hypothermia initiated immediately after OGD significantly improved the recovery of energy metabolism and PSR. If there was a 2-hour delay in the onset of hypothermia, neuroprotection depended on the degree of hypothermia. Reduction of the incubation temperature to 31C diminished the disturbances of energy metabolism and PSR, whereas lowering the bath temperature to only 34C was not effective. Hypothermia induced 4 hours after OGD did not have any influence on the recovery of energy metabolism and PSR. CONCLUSION: We conclude that the effects of mild hypothermia on metabolic disturbances in hippocampal slices of mature fetal guinea pigs depended on the intervention delay and the degree of cooling. The shorter the postischemic intervention delay and the greater the degree of hypothermia, the better the neuroprotective effect seems to be.
The expression of beta 2-microglobulin, the invariable light chain of HLA class I molecules, of Kaposi's sarcoma from 11 AIDS patients and from 11 patients without known immunodeficiency was studied by immunohistochemistry using a polyclonal antibody to beta 2-microglobulin. The staining intensity of spindle cells in these lesions was scored in a semiquantitative system. We found that the spindle cells of Kaposi's sarcomas from AIDS patients showed significantly increased staining intensity for beta 2-microglobulin compared to those of Kaposi's sarcomas from non-AIDS patients. The results may indicate that Kaposi's sarcomas developing in immunocompromised individuals, such as AIDS patients, are not subject to immune selection by T cells eliminating HLA class I high-expressing tumor cells, while this may be the case in non-AIDS patients. Alternatively, the results may be caused by differences in the activity of cytokines, which upregulate the expression of HLA class I molecules on the cell surface.
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OBJECTIVE: The purpose of the present study was to determine whether endotoxins (lipopolysaccharides, LPS) affect the fetal cardiovascular system in a way likely to cause brain damage. METHODS: Thirteen fetal sheep were chronically instrumented at a mean gestational age of 107 +/- 1 days. After control measurements of organ blood flow (microsphere method), blood gases, and acid base balance were obtained, seven of 13 fetuses received LPS (53 +/- 3 microg/kg fetal weight) intravenously. Sixty minutes later, asphyxia was induced by occlusion of the maternal aorta for 2 minutes. Measurements of organ blood flows were made at -60, -1, +2, +4, +30, and +60 minutes. RESULTS: Unlike in the control group, after LPS infusion there was a significant decrease in arterial oxygen saturation (-46%; P <.001) and pH (P <.001). In LPS-treated fetuses the portion of combined ventricular output directed to the placenta decreased significantly (-76%; P <.001), whereas output to the fetal body (+60%; P <.001), heart (+167%; P <.05), and adrenals (+229%; P <.01) increased. Furthermore, during asphyxia circulatory centralization was impaired considerably in LPS-treated fetuses, and there was clear evidence of circulatory decentralization. This decentralization caused a severe decrease in cerebral oxygen delivery by 70%. Within 30 minutes after induction of asphyxia five of seven LPS-treated fetuses died, whereas all control fetuses recovered completely. CONCLUSIONS: Endotoxemia severely impaired fetal cardiovascular control during normoxia and asphyxia, resulting in a considerable decrease in cerebral oxygen delivery. These effects might have important effects in the development of fetal brain damage associated with intrauterine infection.
OBJECTIVE: Asphyxia is one of the main causes of perinatal brain damage that can result in psychomotor deficits during later development. Recently lubeluzole, a new glutamate antagonist, was shown to improve clinical outcome considerably without any safety concerns in adults who had acute ischemic stroke. However, our preliminary experiments showed transient alterations in heart rate as well as arterial hypertension after intravenous application of this compound in fetal sheep. The aim of the present study was to examine in detail whether lubeluzole affects circulatory responses to acute asphyxia in fetal sheep near term. METHODS: Eleven fetal sheep were chronically instrumented at a mean gestational age of 133 +/- 2 days (term is at 147 days). The fetuses in the study group (n = 6) received three bolus injections of lubeluzole at 30-minute intervals (3 x 0.11 mg/kg estimated body weight), and five controls received solvent. Organ blood flows and physiologic variables were measured before, during, and after arrest of uterine blood flow for 2 minutes (ie, at 0, 1, 2, 3, 4, and 30 minutes). RESULTS: Before asphyxia, distribution of combined ventricular output and physiologic variables in fetuses from the control group were in the normal range for chronically prepared fetal sheep near term. During acute asphyxia there was a redistribution of cardiac output toward the central organs accompanied by pronounced bradycardia and progressive increase in arterial blood pressure. There were nearly no differences between groups in the time course of physiologic and cardiovascular variables measured before, during, and after acute intrauterine asphyxia. CONCLUSION: Lubeluzole did not affect circulatory responses to acute asphyxia in fetal sheep near term.
UNLABELLED: Clinical and animal experiments suggest that fetal metabolic acidosis is influenced by placental transfer of lactate and bicarbonate. It was the aim of this study to answer the following questions: What kind of relationship does exist between fetal metabolic acidosis and maternal metabolic acidosis? Does fetal metabolic acidosis coincide with alterations of fetal heart rate and fetal oxygenation? Does the maternofetal difference of base deficit reflect fetal oxygen deprivation more accurately than the measurement of fetal base deficit alone? What is the maternofetal difference of base deficit in normoxia and mild hypoxia? In 100 pregnant women (gestational age greater than 37 weeks, fetal weight greater than 3 rd percentile) a fetomaternal blood analysis (FMBA) was performed during labour and immediately after delivery. The metabolic acidosis was measured as base deficit of extracellular fluid (BDECF). RESULTS: The fetal metabolic acidosis depends mainly on the buffer base concentration in the maternal blood. Moderate repetitive hypoxemia with no severe pathological FHR-alterations do not show a significant relationship to fetal metabolic acidosis. Moderate hypoxia (defined as the combination of oxygen saturation below 30%, periodical decelerations and basal fetal heart rate above 160 b/min) can be recognized most accurately by determining the maternofetal differences of BDECF. In fetal normoxia BDECF in the maternal blood is 4 mmol/l higher than in the fetal blood, in moderate hypoxia the maternofetal difference of BDECF is reduced to 1 mmol/l. These findings are in accordance with the results of Roversi et al. (1975). Conclusions for the intensive surveillance of the fetus during labour by fetal blood analysis: Within the range of pH 7.10-7.30 the maternal BDECF should be determined in addition to the fetal BDECF to calculate the maternal fetal difference of BDECF. If BDECF in the fetus exceeds the maternal BDECF, the risk of fetal hypoxia is increasing. In these cases, delivery should be performed as soon as possible avoiding additional hypoxic or mechanical birth injuries. The technical procedure of fetal maternal blood analysis is described and the difficulties of routine use are discussed.
Uterine blood flow decreases during uterine contractions. Under physiological conditions there is however an uterine hemodynamic buffer mechanism to guarantee a sufficient oxygen supply to the fetus even during uterine contractions. Heart rate decelerations occur therefore not during the period of cervical dilation but in the second stage of labor. In disorders of pregnancy uterine blood flow is primarily reduced and the slightest uterine contraction exhibits signs of fetal hypoxia, i.e. deceleration of fetal heart rate. Heart rate decelerations signify the possibility of the deterioration of the fetal acid base status. But the degree of fetal acidosis can be estimated only by fetal scalp blood sampling. A valuable tool to predict fetal hazard is to measure the transcutaneous PO2. Numerous hypoxic episodes decrease not only the arterial PO2 but also the skin blood flow which demonstrates a reduced peripheral circulation. This, however, is an indication of severe fetal stress in utero.
On the basis of our experience with prospective observation of immunofluorescence microscopy in 5775 biopsy specimens from 335 consecutively followed heart transplant cases, we describe the immunofluorescent method in detail and the potential artifacts and method of interpretation of the findings. A strategy for use of the method on the basis of the experience of the authors is proposed.