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Biomedical subjects

B Engström

Publications and source records attributed to B Engström.

At least 73 records · Page 4Linked to original sources
PubMed1985

A technique for freeze-fracturing of the organ of Corti.

A modification of the conventional method of freeze-fracturing is described. By the use of polyvinyl-alcohol, a high viscous fluid, the organ of Corti is better stabilized in the specimen holder. This fluid also facilitates a clean fracture through the organ of Corti proper and in a high number of cases gives a large replica void of contaminating biological tissue and free of folds. Examples of results produced with this technique are demonstrated.

Freeze Fracturing↗
PubMed1984

Effects of chelating agents on oral uptake and renal deposition and excretion of cadmium.

The gastrointestinal absorption, transport, tissue deposition and excretion of cadmium was studied in adult male mice given a single oral LD50 dose of 109Cd-labeled CdCl2 alone or in combination with nitrilotriacetic acid (NTA), sodium tripolyphosphate (STPP) or ethylenediaminetetraacetic acid (EDTA). Blood, intestinal mucosa, liver and kidneys were analyzed for 109Cd at different times after exposure and the influence of the chelating agents on Cd binding to metallothionein and other tissue ligands was also studied. Acute toxicity was noted. Complex formation between Cd and EDTA was studied in solutions containing Cd:EDTA at 1:04 and 1:4 molar ratios. Adult male mice were exposed orally or by direct infusion into the stomach to either of the two solutions (containing an LD50 dose of Cd). Body retention and tissue deposition of Cd was recorded after 4 (direct infusion) or 21 days (oral exposure), and the mortality in different exposure groups observed. Adult male were also exposed to a low oral dose of 109Cd-labeled cadmium (0.5 mg/kg), followed by 18 months continuous administration of NTA, (500 ppm) STPP (500 ppm) or EDTA (50 ppm) in the drinking water or the chelating agent in combination with Cd (50 ppm), Cd alone (50 ppm) or deionized water. Whole-body retention of 109Cd, tissue deposition of 109Cd and total Cd and development of proteinuria were observed. When cadmium was given with an excess of EDTA, all Cd ions were bound in a 1:1 Cd-EDTA complex. Decreased acute toxicity was observed which was related to increased body elimination of cadmium. The Cd passes though the body still bound to EDTA and is excreted via the kidneys in this form. Similar results were found in mice exposed to Cd + NTA, while gavage of CD + STPP led to an initially decreased systemic uptake of Cd and thereafter to a prolongation of the biological half-time and thus a comparatively higher body retention of the metal. Cd may form a 2:1 complex with EDTA in the presence of excess cadmium. An increased retention and toxicity of cadmium was seen after direct infusion of this solution, while gavage resulted in a decreased toxicity. The effect of different chelating agents on acute cadmium toxicity and metabolism seemed to be due to changes in the stability of the administered chelate complexes, due to variation in pH and to the availability of metal binding ligands such as metallothionein in vivo. NTA, STPP and EDTA had no effect on the metabolism or toxicity of cadmium after long-term low dose oral exposure.

Absorption↗
PubMed1984

Fusion of stereocilia on inner hair cells in man and in the rabbit, rat and guinea pig.

The complexity of the problem of sensorineural hearing loss is illustrated by the well-known poor correlation between pure tone thresholds and loss of sensory cells in the organ of Corti and between pure tone thresholds and other auditory functions such as discrimination of speech and thresholds of the intra-aural muscle reflex (MER). The present work demonstrates that two types of inner ear pathology are present in several mammalian species, including man. Both types can be induced by noise. In addition to the earlier well-known loss of outer hair cells, it is shown that abnormal sensory hairs on inner hair cells are an important and frequent finding in acoustically damaged ears. Fusion and inclination of inner hair cell cilia were predominant in rabbits with moderate hearing loss and a rather common finding in rats and humans. In guinea pigs, damage to inner hair cell stereocilia was not common and was seen only in conjunction with considerable loss of outer hair cells. In summary, fusion of the stereocilia of inner hair cells was a common finding in several mammalian species.

Adult↗
PubMed1984

The effect of feeding diets containing avoparcin and monensin on the occurrence of Salmonella in caecum and liver in experimentally infected chickens.

In two experiments (Experiments A and B) chickens experimentally infected with S. infantis at 7 days of age and fed diets containing both avoparcin (10 ppm) and monensin (90 ppm) showed a higher frequency of Salmonella-positive livers and higher caecal counts of Salmonella 1 and 2 weeks after challenge than similarly infected chickens fed only avoparcin (10 ppm). The results may indicate a synergistic action between the two drugs on the ability of chickens to withstand Salmonella infections.

Animals↗
PubMed1983

Damage to sensory hairs of inner hair cells after exposure to noise in rabbits without outer hair cells.

We investigated if the noise-induced damage to the stereocilia of inner hair cells (IHCs) was dependent on the integrity of the outer hair cells (OHCs) in rabbit. Prior to the noise exposure a total loss of OHCs in the basal 1.5 to 2 turns was induced by administration of kanamycin (400 mg/kg for 10 days). This left the IHCs apparently normal as observed in the scanning electron microscope. These animals exhibited a 20-60 dB hearing loss before noise exposure. In spite of this pronounced hearing loss, the fusion and inclination of the IHC stereocilia were extensive in these noise-exposed ears. The stereocilia damage occurred at the same noise exposure and was as prominent or even more pronounced than has been noted in ears exposed to noise only. Under the assumption that kanamycin causes selective destruction of OHCs, the results can be interpreted as evidence that the OHCs facilitate the IHCs at low sound levels without being involved in the process which damages IHC stereocilia at high levels of noise.

Animals↗
PubMed1983

Ultrastructural studies of stereocilia in noise-exposed rabbits.

In rabbits with noise-induced, permanent hearing loss of more than 20 dB the stereocilia of the inner hair cells (IHCs) showed widespread signs of damage: fracturing, folding, fusion, and formation of giant hairs. Damage to the stereocilia on outer hair cells (OHCs) was much less pronounced in corresponding regions. On damaged OHCs the stereocilia were usually missing, except in the apical turn where fusion of stereocilia and formation of giant stereocilia occurred. On both IHCs and OHCs the 'neck' of the stereocilium appeared to be a site of fracture of the actin skeleton. On IHCs the actin cores of the former stereocilia were enclosed in a bulge of the apical cytoplasm to form a giant hair, with portions of the stereocilia projecting from the bulge. Inside the giant hairs profiles of the original stereocilia could be recognized, and these often retained their original circular form at least at the base of a giant hair. In the distal portion of the giant hair the actin filaments frequently formed a single thick bundle where the individual stereocilia could not be distinguished. Material had condensed between the surface membrane enclosing the former stereocilia and the actin cores. A thin kinocilium was often identified on IHCs. together with giant hairs possibly indicating a regenerative activation of the cell. It is suggested that fracture and fusion of stereocilia are due to different pathophysiological mechanisms, and that the actin of damaged cilia may undergo a slow reorganization and regeneration.

Actins↗
PubMed1983

Cochlear morphology in relation to loss of behavioural, electrophysiological, and middle ear reflex thresholds after exposure to noise.

Loss of auditory function was correlated with different pathological findings in the inner ear of the rabbit after 15 or 30 min exposure to high level broad band (2-7 kHz) noise. The ears from animals with post-exposure times ranging from 1 to 23 months were analysed by scanning electron microscopy (SEM). Complete cochleograms with quantification of loss of hair cells and damage to stereocilia were produced. Loss of function was defined by determining behavioural threshold, threshold of auditory brainstem response (ABR) to narrow-band stimuli and threshold of the middle ear muscle reflex (MER). A small scattered loss of OHCs and slight disarray of stereocilia were found in non-exposed ears of young animals, but fusion of IHC cilia was not observed. Normal auditory function was not found in any noise exposed animal with abnormal morphology. A loss of threshold sensitivity of up to about 30-40 dB was noted without loss of hair cells in the corresponding region of the cochlea. The mildest structural damage that correlated to a functional alteration consisted of damage to stereocilia of IHC. This correlated well to the MER threshold shift. In two animals a shift of MER threshold of about 20 dB was the only functional abnormality. In ears with more extensive IHC damage loss of OHCs was also found and these animals had primarily an increase in auditory threshold shift with only a small additional change in MER threshold. It is concluded that in the rabbit and with the methods used the IHC stereocilia are the structures most susceptible to damage by the noise used and that the degree of injury can be fairly well assessed by functional tests of a type that is used also routinely in the audiological clinic.

Animals↗
PubMed1983

Stereocilia of sensory cells in normal and hearing impaired ears. A morphological, physiological and behavioural study.

The aim of the present study was to investigate specific structural alterations in the cochlea of ears with sensory neural hearing loss and to determine the relation between structural damage and loss of auditory function. The results show that with the methods used in this study it is possible to obtain well preserved structures with consistent morphological characteristics. Examination and identification of small pathological alterations were thus possible. The stereocilia of the IHCs were found by scanning electron microscopy to be the structure most susceptible to damage by noise in the rabbit. The extent of IHC damage corresponded rather well with the frequency range for loss of auditory function, particularly threshold shift of the MER. The damage of the IHCs consisted of fusion, fracture and inclination of the stereocilia towards the OHCs. The OHC were frequently left unaltered even when the stereocilia of most IHCs exhibited pronounced alterations. In animals with a severe hearing loss and a postexposure time of more than two months, long "giant" cilia and often also a small thin kinocilium were found on the IHCs. IHC ciliary damage was found also in other species including man, but to a smaller extent than in the rabbit. The stereocilia of IHCs were also damaged by noise in ears of rabbits where the OHCs had been experimentally removed prior to the noise exposure. It was concluded that stereocilia damage is an important morphological alteration in ears with sensory neural hearing loss particularly with NIHL, and that cilia damage contributes to the observed loss of auditory function.

Animals↗
PubMed1982

Acoustic reflex after experimental lesions to inner and outer hair cells.

Chronic effects of noise or kanamycin on the acoustic intra-aural reflex in nonanesthetized rabbits were studied. The intra-aural reflex activity was simultaneously recorded in both ears upon alternate stimulation of the left and the right side. The inner ears were analyzed in scanning and transmission electronmicroscopy. Exposure to bandlimited high-level noise was found to induce extensive deformations in the sensory hairs of the inner hair cells without loss of outer hair cells. Kanamycin caused a degeneration of outer hair cells in the basal 1-2 turns without affecting the morphology of the inner hair cells. The morphological changes, as a function of the location on the basilar membrane, were compared to physiological changes, as a function of frequency. In the noise-exposed animals the threshold of the intra-aural reflex was found to be raised in a frequency range corresponding to the extent of abnormal sensory hairs of the inner hair cells. In the kanamycin-treated animals reflex changes correlated to the loss of outer hair cells. The observations were interpreted as indicating that both types of hair cells cooperate in the activation of the intra-aural reflex in rabbits.

Animals↗
PubMed1982

Mites living in hay: an important allergen source?

Fifty-two farmers and 21 non-farmers with symptoms related to hay contact were investigated. Skin prick tests (SPT) and RAST were performed with an extract made of barn dust (BDE) consisting of hay remnants. At microscopy, the barn dust was found to contain large amounts of dead mites, most of them identified as Lepidoglyphus destructor and Acarus siro. Twenty-one patients (9 farmers and 12 non-farmers) had positive RAST or BDE, with a good correlation to the case histories. Other allergies, especially to Dermatophagoides pteronyssinus, pollens, and animal danders were also common among patients. However, there was no correlation between positive SPT and RAST to BDE and any other allergen tested. This indicates that BDE contains distinct allergens, most likely of mite origin.

Allergens↗
PubMed1981

Lesions to cochlear inner hair cells induced by noise.

A total of 28 un-anesthetized rabbits of the small chinchilla strain were unilaterally exposed to noise (2-7 kHz, 135 dB SPL in the ear canal). After a follow-up time ranging from 15 minutes to 10 months, the ears were perfused with glutaraldehyde and prepared for analysis by secondary emission electron microscopy and transmission electron microscopy. The typical finding was a fusion and clumping of inner hair cell (IHC) sensory hairs. In two of the animals, no loss of outer hair cells (OHC) was observed; in several of the others, only a small local loss of OHC was observed in the 2 and 4 kHz regions in spite of extensive IHC abnormality. A frequency map of the rabbit cochlea was obtained by pure tone lesions to OHC. The extent of IHC abnormalities corresponds to the 1-16 kHz region. The findings may provide a basis for the study of the functional relationship between the IHC and OHC.

Animals↗
PubMed1981

Influence of chelating agents on toxicity and distribution of cadmium among proteins of mouse liver and kidney following oral or subcutaneous exposure.

Acute toxicity and organ distribution of cadmium was investigated in mice exposed to 1) single subcutaneous doses of 109Cd-labelled cadmium (3.2 mg (0.028 mmol)/kg b.wt.) alone or in combination with nitrilotriacetic acid, NTA (32 mg (0.167 mmol/kg b.wt.) or sodium tripolyphosphate, STPP (32 mg (0.087 mmol/kg b.wt.) and 2) single oral doses of cadmium (60 mg (0.53 mmol/kg b.wt.) alone or together with NTA (600 mg (3.14 mmol)/kg.b.wt.) or STPP (600 mg (1.63 mmol/kg b.wt.) Whole-body retention of radiolabelled cadmium as well as mortality was registered in all groups during 20-21 days. Five hours after exposure, 3-4 mice in each group were killed and cadmium distribution among proteins in liver and kidney studied by gel chromatography on a G-75 Sephadex column. Organ concentration of cadmium was also determined at sacrifice of all other mice after an observation time of 20-21 days. A markedly increased mortality was observed during the first 24 hours after subcutaneous exposure to Cd + NTA (70%) or Cd + STPP (40%) compared to Cd alone (0%). On the contrary, no mortality was seen after oral exposure to Cd + NTA (70%) or CD + STPP (while oral exposure to Cd alone or with NTA resulted in a mortality of about 45% during the same observation time. Five hours after subcutaneous exposure, liver cadmium concentrations were equal in all mice and bound mainly to a low molecular weight protein (probably metallothionein). In kidney, concentrations were about twice as high in mice given Cd + NTA or CD + STPP compared to mice given Cd alone. More cadmium was transferred to the kidneys in the presence of chelating agents. This was further supported by the decreased liver/kidney cadmium concentration ratio between 5 hours and 21 days. The increased mortality in mice given Cd + NTA or Cd + STPP may be due to an initially high accumulation of cadmium in liver, which may exceed the upper limit for metallothionein synthesis, whereby toxic damage of the hepatic cells and leakage of cadmium from the liver would occur. Five hours after oral exposure, cadmium retention in organs of mice given Cd + STPP was 4-6 times lower than in mice given Cd alone, while mice given Cd + NTA had slightly higher organ concentrations. The binding of more cadmium to metallothionein in liver of Cd + STPP-exposed mice 5 hours after exposure, may be due to the lower accumulation of cadmium in these mice compared to those given Cd alone or CD + NTA, where cadmium was bound mainly to high molecular proteins in the liver. After 20 days, mice given CD + STPP has slightly higher body and organ retention of cadmium compared to mice given Cd alone. This may be due to a binding of cadmium to metallothione in these mice which is known to prolong the retention time of cadmium in tissue.

Animals↗
PubMed1981

Specific prolactin binding in the rat adrenal gland: its characterization and hormonal regulation.

Rat adrenal prolactin receptors possess the same hormonal specificity as those in the prostate gland and liver, but are less stable during storage and after freezing. There is a gradual decrease in specific prolactin binding to the adrenal during sexual maturation in male rats; maximum binding capacity of 980 fmol/mg protein is at 25 days of age decreasing to approximately 100 fmol/mg protein at day 90. Prolactin receptors in the prostate are high at 25 days of age (700 fmol/mg protein), decrease sharply by day 30 (180 fmol/mg protein) and then gradually increase. Ovariectomy resulted in a significant rise in total prolactin binding in the adrenal gland, while the administration of oestradiol or testosterone reduced the binding, the reverse of changes in prolactin binding in the liver. Only oestrogen increased serum levels of prolactin in female rats. Ovine prolactin (500 micrograms) given to female rats resulted in a rapid increase over a period of 2-8 h total prolactin receptors in the adrenal, and these then decreased to normal levels, indicating a possible positive regulation of prolactin receptors by homologous hormone.

Adrenal Glands↗