Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult mallard ducks were fed a diet containing 50 ppm DDT for 6 months. Eggs laid during this period were collected and eggshell weight, thickness, and calcium were determined. Chronic ingestion of DDT resulted in production of eggshells that were significantly thinner and lighter than those of controls. Total calcium of thinned eggshells was also reduced; however, calcium per gram of eggshell was not altered, indicating that other eggshell constituents were not incorporated as well. Calcium adenosine triphosphatase activity in the microsomal fraction of eggshell gland epithelium was assayed in control and DDT-fed ducks. Enzyme activity in DDT-fed ducks was reduced to 65% of control values. Since Ca-ATPase has been shown to be associated with calcium transport, enzyme inhibition may be responsible for decreased eggshell weight and thickness. Electron microscopic evaluation of microsomal fractions showed elements of the plasma membrane, including cilia and microvilli, as well as rough and smooth endoplasmic reticulum. Inhibition of calcium transport at the plasma membrane of mucosal epithelium is proposed as a possible mechanism of DDT-induced eggshell thinning.
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PMID:Effects of DDT on eggshell quality and calcium adenosine triphosphatase. 14 96

1. Low levels of insuling stimulate transendothelial fluid transport from preswollen stroma to aqueous in rabbit corneal preparations. The rate of stromal thinning at the end of the first hour averages 30% faster with insulin, 3.5 x 10(-22) M (4.8 micromicron/ml.), than that of the paired control. This concentration is about the physiological level in rabbit aqueous. 2. The stimulation with insulin is transient. Rates of thinning average higher but not significantly different from control rates by the second hour. 3. High levels of insulin between 3.5 x 10(-9) M (480 micromicron/ml.) and 2.0 x 10(-6) M (2.75 X 10(5) micromicron/ml.) inhibit fluid transport. The inhibition at the low end of this range of concentrations becomes more pronounced with longer perfusion times but appears not to exceed ca. 50% of the control rate. 4. Ouabain also induces a biphasic effect on fluid transport which is characteristically different from that with insulin. The maximal stimulation observed at all times occurred with a fixed concentration of 10(-10) M. The stimulation is not transient but increases throughout the duration of the perfusion; the average rate is elevated 50% above the control rate by the third hour. 5. The transition from a stimulatory to an inhibitory effect occurs consistently at ca. 10(-8) M with ouabain, while a similar transition with insulin occurs at ca. 10(-9) M and appears to shift towards slightly higher concentrations during a 3 hr perfusion period. 6. Inhibition of fluid transport with ouabain, 3 x 10(-7) M, is increased from ca. 50% after 1 hr to more than 70% at the end of the third hour of perfusion. 7. The combined presence of stimulatory concentrations of ouabain and insulin affects tromal thinning in a manner resembling the effect of ouabain alone more than that of insulin; additive effects could not be discriminated. Progressively raising the concentration of insulin to a level (10(-8) M) that alone inhibits stromal thinning, ultimately abolishes the stimulatory effect of ouabain. Based on other evidence and current models of drug/hormone-membrane interaction, these results can be interpreted to indicate a concentration-dependent interaction between receptor complexes of ouabain and insulin with (Na+ + K+)-ATPase.
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PMID:Biphasic effects of insulin and ouabain on fluid transport across rabbit corneal endothelium. 63 30

Patients with medically intractable temporal lobe epilepsy (TLE) undergo medial temporal lobectomy with hippocampectomy for one of two reasons. (1) A lesion (tumor or arteriovenous malformation) adjacent to, but not invasive of, the hippocampus, results in the removal of the lesion and adjacent hippocampus in order to ensure a tumor-free margin. This group will be referred to as tumor-related TLE (TTLE) patients. (2) The operation is performed when depth electrode recordings and other evaluative techniques point to the hippocampus as the focus of seizure initiation. This group will be referred to as cryptogenic TLE (CTLE) patients. Analysis of the hippocampi of these two groups of patients reveals that the TTLE hippocampus is quite similar to that of autopsy subjects in its chemical neuroanatomy. However, the dentate gyrus of the CTLE patients shows considerable morphological and cytochemical reorganization. This reorganization is characterized by a number of features. (1) There is a loss of granule cells which occurs either as a patchy loss and/or a thinning of the granule cell layer. (2) Remaining granule cells which contain dynorphin appear to produce recurrent collaterals into the inner molecular layer of the dentate gyrus. (3) In the subgranular region of the hilus (the polymorphic layer) there is a selective loss of interneurons immunoreactive for somatostatin, neuropeptide Y and substance P. (4) There appears to be an increase in fibers immunoreactive for somatostatin and neuropeptide Y which extend throughout the dentate molecular layer. Somatostatin fibers being less numerous than neuropeptide Y fibers (5). The distributions of a number of neurotransmitter receptors also show striking reorganization in the dentate gyrus of the CTLE hippocampus. (6) Second messenger systems protein kinase C and adenylate cyclase, and Na+, K(+)-ATPase activity, as determined by ouabain binding, is increased in the molecular layer of CTLE. This remodeling of the CTLE hippocampus may hold the key to the mechanisms of hyperexcitability of the granule cells in the hippocampus of this group, and consequently the generation of seizures. The removal of the hippocampus in CTLE patients results in good control of seizures, whereas removal of hippocampi that do not show such reorganization, in a group of patients classified as atypical CTLE patients, results in inadequate seizure control. These findings suggest a complex series of processes in converting the properly regulated granule cells into hyperexcitable ones.
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PMID:Neurotransmitters and their receptors in human temporal lobe epilepsy. 136 31

We have studied the pathological changes of the ciliary body in Royal College of Surgeons (RCS) rats with an inherited retinal degeneration. Morphometric analyses were performed on sectioned ciliary bodies by a computerized morphometry system. Age-matched non-pigmented Sprague-Dawley (SD) rats were used as the control animals. The ciliary body of 26-day-old RCS dystrophic rats showed normal structure. However, the length and height of the pars plicata of the ciliary body became shorter and the area became smaller with increased age. Significant decreases in the values of these three parameters were observed between 26-day-old and 3-month-old RCS dystrophic rats. These parameters also showed significant differences when values of 3-month-old RCS dystrophic rats were compared to those of 3-month-old control SD rats. The same trends were observed in the ciliary body measurements in RCS dystrophic rats up to 1 year of age. Scanning electron microscopic examination demonstrated the progressive thinning of the pars plicata of the ciliary body with age in the RCS dystrophic rats. The total volume of the ciliary process of 6-month-old RCS dystrophic rats appeared to be one-half that of 26-day-old RCS dystrophic rats. Transmission electron microscopy revealed progressive cellular degenerative changes in the non-pigmented and pigmented ciliary epithelium of the RCS dystrophic rats. It was apparent that the pigmented ciliary epithelium had more severe degenerative changes than the non-pigmented ciliary epithelium. Immunostaining for Na+ + K+ ATPase of the ciliary epithelium was found to be less in the RCS dystrophic rats than in age-matched controls. This result suggests a possible dysfunction of ion transport in the ciliary body of the RCS dystrophic rats, which may account for their increased incidence of cataract formation. Although the mechanisms for the ciliary body degeneration in RCS dystrophic rats remain speculative, these findings add a new area of interest in this model of inherited retinal dystrophy.
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PMID:Ciliary body degeneration in the Royal College of Surgeons dystrophic rat. 164 4

Fetuses of streptozotocin-induced diabetic rats exhibited delayed lung maturation and a 40% reduction in the steady-state level of lung Na+,K(+)-ATPase alpha 1 subunit mRNA and Na+,K(+)-ATPase activity at 21 d of gestation. In in situ hybridization experiments the signal specific for Na(+)-pump alpha 1 subunit message was strongest above columnar epithelial cells of air-conducting structures. Strong labeling was also present above cuboidal cells lining the forming alveoli, but not above mesenchymal cells. Immunocytochemical localization of the protein paralleled the distribution of the mRNA. Mesenchymal cells were more abundant in fetal lungs of diabetic mothers, and thus the decreased overall levels of Na+,K(+)-ATPase may result from the observed morphological pulmonary immaturity. One day after birth there was no apparent difference in lung morphology at the light microscopic level, in the localization or the steady-state level of Na+,K(+)-ATPase alpha 1 isoform mRNA, or in enzyme activity. Na+,K(+)-ATPase has a likely role in the active phase of fluid absorption in the airways of newborns before the onset of breathing. Decreased fluid clearance and lack of thinning of the lung's connective tissue may contribute to the increased risk for respiratory distress in infants of diabetic mothers.
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PMID:Effects of maternal diabetes on fetal rat lung ion transport. Contribution of alveolar and bronchiolar epithelial cells to Na+,K(+)-ATPase expression. 184 38

Intracoronary administration of anticardiac cytotoxic serum increased the sarcolemma passive permeability for Ca2+ ions and reduced the activity of Na+-Ca2+ and Na+,K+-ATPase exchange in dogs. Electronic microscopy revealed thinning of glycocalix, destabilizing of the sarcolemma phospholipid bilayer, and development of intracellular oedema. Disturbances of the sarcolemma structure and function seem to be able to cause the development of cardiac insufficiency of immune origin.
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PMID:[Disordered ion-transport processes in the cardiomyocyte membranes in the immune action on the heart]. 245 77

The influence of soft contact lenses (SCL) with low (37%, L) and high (65%, H) water content on rabbit corneas was investigated. The lenses were worn continuously for 1, 2, 4, 7, 10, 14, 21 or 28 days. The changes in corneal transparency, hydration and enzyme activities were studied. A slight change in corneal transparency due to higher hydration caused by a decreased activity of Na+-K+-dependent adenosine triphosphatase (Na+-K+-ATPase) in the corneal endothelium is followed by a decrease in the activity of gamma-glutamyl transferase (GGT). Slight morphological disturbances appear within 4 days in animals wearing SCL (L). SCL (H) produce similar changes one week later. Subsequently, the corneal epithelium becomes thinner and changes in the size of corneal endothelial cells are obvious. Disturbances of enzyme activities in cells of all corneal layers are present. In the epithelium highly increased activities of acid glycosidases, acid phosphatase, and dipeptidyl peptidase I and II, in keratocytes decreased activities of alkaline phosphatase and GGT, and in the endothelium decreased activity of Na+-K+-ATPase and GGT were found. These changes are more severe after SCL (L). In this case, inflammatory cells displaying high activities of lysosomal hydrolases appear in the anterior part of the stroma during the 3rd and 4th weeks and local degradation of glycosaminoglycans and proteins takes place. In contrast, after SCL (H) a remarkable thinning of the corneas was observed during extended wear, accompanied by decreased stainability of stromal glycosaminoglycans and highly decreased enzyme activities in keratocytes. The histochemical methods proved very useful in the assessment of lesions caused by a continuous wear of SCL.
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PMID:Disturbances in the rabbit cornea after short-term and long-term wear of hydrogel contact lenses. Usefulness of histochemical methods. 289 48

Thinning of the egg shell is produced by p-p'-DDT and DDE in several species of birds. A study was made of the effect of DDE administered in vitro and in vivo on the Ca2+ binding and Ca2+-Mg2+-activated ATPase of a homogenate of the egg shell gland of ducks (Anas platyrhynchos var.). The concentration of Ca2+ was 1 X 10(-4) M and that of MgATP 1 X 10(-3) M. In vitro, DDE in concentrations of 2-16 micrograms/ml of incubation medium inhibited the Ca2+-Mg2+-activated ATPase in a concentration-dependent manner, whereas Mg2+-activated ATPase was not affected by these concentrations. The Ca2+ binding by the homogenate was reduced by DDE in the same concentrations. The sodium azide sensitive Ca2+ binding was most sensitive. In vivo, DDE administered in a concentration of 40 mg/kg dry weight of the food for 45 days reduced the egg shell index by 18% in comparison to controls. After 45 days of treatment the DDE concentrations in the egg shell gland mucosa was 1.20 +/- 0.16 micrograms/g of wet weight, while no DDE was detected in the controls. The Ca2+-Mg2+-activated ATPase was reduced by 32%, whereas the Mg2+-ATPase was not changed. The Ca2+ binding by the homogenate was reduced by 29%, the sodium azide sensitive part being most vulnerable, DDE increased the total Ca content of the egg shell gland mucosa by 44%. Since Ca is transported against a concentration gradient between blood plasma, and the lumen of the shell gland, it is suggested that DDE, by inhibiting the Ca2+-Mg2+-activated ATPase, decreased the Ca translocation over the egg shell gland mucosa.
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PMID:Effect of p-p'-DDE administered in vivo and in vitro on Ca2+ binding and Ca2+-Mg2+-ATPase activity in egg shell gland mucose of ducks. 612 33

The pesticide p-p'-DDT and its persistent metabolite p-p'-DDE cause thinning of the eggshells in several species of birds. In earlier investigations on ducks this thinning was found to be associated with a reduction of the ATP-dependent Ca2+ binding to a homogenate of the shell gland mucosal cells by DDE. The activity of a Ca2+-Mg2+-activated ATPase in the homogenate was also decreased on administration of DDE in vivo. We have therefore investigated the in vitro effects of some other chlorinated hydrocarbon pesticides of ecotoxicological interest on the ATP-dependent Ca2+ binding and the Ca2+-Mg2+-activated ATPase activity in a homogenate of the eggshell gland mucosa of the hen and determined the molar concentrations that produced 50% inhibition (=IC50). Several of the investigated compounds, namely toxaphene, chlordane, p-p'-DDD, o-p'-DDE, p-p'-DDT, methoxychlor and PCB (Arochlor 1242), had a similar IC50 to inhibit the Ca2+ binding as p-p'-DDE. Lindane, p-p'-DDA and biphenyl had an IC50 3.3-4 times higher and that of 2.4 D was 13.5 times higher than that of p-p'-DDE. When the IC50 of some of the compounds (p-p'-DDE, PCB, toxaphene, Lindane) was determined that decreased the Ca2+-Mg2+-activated ATPase of the homogenate it was found to be only 18 to 29 per cent of that needed to inhibit the Ca2+ binding by the homogenate. It is therefore probable that some other effect than inhibition of this enzyme is also involved in the Ca2+-binding process and affected by the compounds.
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PMID:The inhibitory effect of some chlorinated hydrocarbon pesticides on the ATP-dependent Ca2+ binding of the particulate fraction of the eggshell gland mucosa cells. 613 49

We have investigated the effect of ultraviolet-B (UVB) irradiation on the density of epidermal ATPase-positive Langerhans cells, and the modulation of this effect by indomethacin (IND). Depilated backs of albino guinea pigs were exposed to varying doses of UVB (10-550 mJ/cm2). Skin biopsies were taken serially. There was an UVB dose-dependent decrease in the density of dendritic epidermal Langerhans cells, as identified by their membrane ATPase activity. This was accompanied by thinning and shortening, or disappearance of dendritic processes. Such changes were followed by a gradual recovery of the cell density to preirradiation level by day 21. Despite the high doses of UVB given, the maximal decrease in the density of ATPase-positive cells was only 58%. Topical application of IND, a prostaglandin-synthetase inhibitor, after irradiation resulted in a decrease of the erythema; however, the decrease in the density of ATPase-positive cells was still observed. In contrast, guinea pigs that received IND topically prior to irradiation showed a decrease erythemal response, but failed to show any decrease in the density of ATPase-positive cells. Administration of IND orally for 3 days prior to UVB exposure did not prevent the decrease in the cell density. The protective effect of topical IND, applied prior to irradiation, may be explained by its in vitro absorbance at both the UVB and UVA ranges. Topical application of IND 20 min prior to exposure to UVB in 2 human subjects resulted in an increase in the minimal erythema dose, giving a sun protection factor of 1.6, which is comparable to that produced by an equimolar concentration of para-aminobenzoic acid solution. The sun-protective property of IND, together with its activity as a prostaglandin synthetase inhibitor, indicate that it potentially could be a useful sunscreen agent. Its clinical safety and efficacy, however, remain to be determined.
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PMID:Effect of indomethacin on alteration of ATPase-positive Langerhans cell density and cutaneous sunburn reaction induced by ultraviolet-B radiation. 622 48


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