Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a review of historical facets of research in cutaneous neurohistology. The silver stains, used for some 150 years, led to the discovery of the neurone theory and to contemporary comparative studies. The cholinesterase methods, used since 1950, are the most convenient for general studies of nerves. The fluorescence technique of Falck (1962) is valuable for the study of adrenergic fibers. The electron microscope techniques used since 1950 have allowed the comprehensive description of myelinated and unmyelinated nerve fibers and of corpuscles. The most important unsettled questions pertain to the physiology of cutaneous nerves and precise definitions of cutaneous sensibility.
J Invest Dermatol 1976 Jul
PMID:Cutaneous innervation. 5 52

Acetylcholinesterase (Ache) and pseudocholinesterase (BUche) activities were studied quantitatively in healthy skin by spectrophotometric methods and qualitatively by polyacrylamide gel electrophoresis. The results were compared to those obtained in plasma. The substrates used to reveal enzyme activities were acetylthiocholine (ATC) iodide and butyrylthiocholine (BTC) iodide, respectively. A linear relationship exists between the values of BUche and Ache activities in plasma and those in skin. Six isoenzymes of different electrophoretic mobility were observed in the skin. One of them, which is never found in plasma extracts, appears to be specific to the skin. On gradient gel electrophoresis, with both substrates (ATC and BTC), a single band of enzyme activity, corresponding to a molecular weight of 600,000 was observed. These results suggest that in the skin there is only one enzyme, most probably butyryl cholinesterase, which cleaves BTC somewhat faster than ATC. This methodology, when applied to the study of dermatoses in which abnormalities of cutaneous nerve terminals are suspected, should furnish precise functional pathophysiological details.
J Invest Dermatol 1979 Sep
PMID:Cholinesterases isoenzymes: a comparative study in the skin and plasma. 46 77

The frequency of the serum atypical pseudochloinesterase variant was significantly higher (p less than 0.005) in a group of 115 lepromatous leprosy patients than in a comparison group of 133 healthy individuals. This finding corroborates the results obtained in the group of patients from India, and supports the contention that the serum atypical pseudocholinesterase is one of the possible genetic factors involved in susceptibility to leprosy.
Int J Dermatol 1979 Dec
PMID:Serum atypical pseudocholinesterase and leprosy. 52 4

At the same temperature and with adequate circulation of blood or receptor solution beneath it the permeability of the stratum corneum of the rabbit ear to T2O or to 32P-TPP was the same in vivo as in vitro. When skin permeability was measured in vitro, the subcutaneous adipose tissue present in the full-thickness skin of the rat delayed the penetration of CR, a lipophilic substance with a low water solubility, and decreased the permeability constant by nearly 3x. The retardant solvent PEG 300 did not penetrate the stratum corneum; it formed a hydrogen-bonded complex with the cholinesterase inhibitor VX, thereby reducing the thermodynamic activity and penetration rate of this compound through the stratum corneum. The accelerant solvent DMSO removed protein components from the stratum corneum; electron microscope studies showed that the cells of stratum corneum so treated became separated from one another, and their contents became stainable in bulk with Pb++, indicating the creation of new diffusion pathways. When the temperature, clearance of penetrant from the lower surface of the stratum corneum and penetrant formulation were the same in vivo as in vitro, and the surface of the stratum corneum was saturated with the penetrant or its solution, the results of permeability measurements made in vivo were similar to those made in vitro.
Curr Probl Dermatol 1978
PMID:Factors affecting the permeability of skin. The relation between in vivo and in vitro observations. 75 61

S-(2-diisoproplaminoethyl) 0-ethyl methylphosphonothioate (VX), an anticholinesterase liquid of low volatility, was applied to the skin of 139 men at environmental temperatures of -18 degrees, 2 degrees, 18 degrees, or 46 degrees C. The skin was decontaminated after 3 hr and the men spent the next 21 hr at about 27 degrees C. The amount of VX penetrating the skin was estimated from the inhibition of red blood cell cholinesterase. The decimal fraction of the dose that penetrated in 3 hr ranged from 0.04 at -18 degrees C to 0.32 at 46 degrees C for the cheek and from 0.004 at +18 degrees C to 0.029 at 46 degrees C for the forearm. Further increase in cholinesterase inhibition after decontamination was evidence of a deposit of VX in the skin. The amount of VX remaining in the skin after decontamination was greater in the forearm and less in the cheek at higher temperatures.
J Invest Dermatol 1977 Jun
PMID:Environmental temperature and the percutaneous absorption of a cholinesterase inhibitor, VX. 86 76

Eccrine sweat collected from the human skin surface contains at least five different esterases. One of them is a cholinesterase. A non-specific carboxylesterase with the electrophoretic mobility of an alpha-globulin appears to be a serum protein. Besides this, there are two isoenzymes of human origin migrating with the same electrophoretic mobility as gamma-globulins. These two isoenzymes are immunologically identical with a non-specific carboxylesterase occurring in numerous organs and body fluids. Lipase activity could not be demonstrated.
Br J Dermatol 1976 Jul
PMID:Immunological demonstration of multiple esterases in human eccrine sweat. 95 42

Allergenic and photosensitizing effects of organophosphorus pesticides (OPP) have been detected, as well as their destructive effect on the skin cell ultrastructure, on the body metabolism and enzymic systems, and the inhibitory effect on cholinesterase activity. Pesticide-induced changes in polyunsaturated fatty acids (PUFA) are significant in the mechanism of dermatoses development. The complex of treatment-and-prophylaxis measures includes regular dermatologic check-ups and limitation of the number of subjects handling OPP. Subjects in whom premorbid shifts have been detected, should be followed up. The therapy and prevention of the dermatoses developing as a result of exposure to pesticides may be effectively carried out with antioxidants, amino acids, vitamins, etc.; diets with the optimal PUFA-tocopherol ratio are advisable. Overalls with multiple protective physicochemical characteristics, filtering respirators and such are recommended.
Vestn Dermatol Venerol 1989
PMID:[Measures for the combined therapy and prevention of dermatoses occurring in workers in contact with organophosphorus pesticides]. 253 Jul 19

Four patients with aquagenic pruritus (AP), one patient with polycythemia rubra vera, one patient with cold urticaria, and three normal control volunteers were studied to better understand the pathophysiology of water-induced itching. Punch biopsy specimens were taken before and after water contact; the specimens were immediately frozen, sectioned, and stained histochemically for acetylcholinesterase (AChE) activity. This was localized in the nerve fibers surrounding eccrine sweat glands and was quantified by microspectrophotometry. In AP and polycythemia rubra vera after water exposure a significantly increased AChE activity suggesting acetylcholine release was observed, whereas in the patient with cold urticaria and the controls, a significant decrease was noted. Two related patients with AP had an inherited abnormality of serum cholinesterase, which, however, had no obvious correlation with their particular disease. The proof of AChE activation might support the clinical diagnosis and indicate a hypothetical involvement of eccrine sweat glands in the pathogenesis of AP.
Arch Dermatol 1988 Jan
PMID:Aquagenic pruritus. Water-induced activation of acetylcholinesterase. 333 47

There is increasing evidence that neuropeptides may be involved in the pathogenesis of atopic dermatitis (AD). This study examines whether neuropeptide distribution in the skin of patients with AD differs from normal controls. The distribution and density of several neuropeptides were examined in lesional and non-lesional skin of AD patients (n = 5) and in normal controls (n = 4) using indirect immunofluorescence and image analysis. Cholinergic innervation was studied using cholinesterase histochemistry. Staining with the general neuronal marker protein gene product 9 x 5 showed a subepidermal network of nerves with fibres penetrating the epidermis, and nerves around blood vessels, sweat glands and hair follicles. Image analysis of nerves around sweat glands showed a significantly higher nerve density in non-lesional compared with both normal controls and lesional skin (P < 0.05); lesional compared with control skin showed no significant difference. In the epidermis the density of nerves was not significantly greater in non-lesional compared with lesional skin and controls. Calcitonin gene-related peptide immunoreactivity was similar in all subjects except in three of the AD patients, where more nerves appeared to penetrate the epidermis. Substance P immunoreactivity in the papillary dermis was seen in all AD patients but no controls. Vasoactive intestinal polypeptide and neuropeptide Y staining were similar in all groups. Acetylcholinesterase-positive nerves were found around sweat glands in all subjects, the staining being greatest in non-lesional and least in lesional skin. Occasional nerves were seen in the papillary dermis in lesional skin of two out of the four patients. We have demonstrated quantitative differences in nerve growth in clinically normal skin of AD patients, and altered cutaneous neuropeptide expression in these patients which may contribute to the pathogenesis of AD. The cause of atopic dermatitis (AD) has not been fully established but it is believed that there is a complex interaction between genetic susceptibility, precipitating environmental factors and disordered immune responsiveness. There is increasing evidence that neuropeptides may be involved in the pathogenesis of AD. Exacerbations of the disease can be provoked by stress, scratching and sweating which may be the result of neurogenic inflammation. One of the first features of an exacerbation is flushing of the affected skin and pruritus. Several neuropeptides that have been identified in human skin are potent inducers of vasodilation and may induce pruritus. Substance P (SP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) all cause vasodilation when injected intradermally, and SP and CGRP have been shown to be mediators of the weal and flare reaction. Spantide, a competitive antagonist of SP, has been shown to inhibit immediate and delayed-type hypersensitivity reactions. Part of these responses may be due to release of histamine and indeed elevated concentrations of histamine have been found in vivo in the skin and plasma of patients with AD. In this study the distribution and density of several neuropeptides were examined in lesional and nonlesional skin of AD patients and in normal controls using indirect immunofluorescence and image analysis. Cholinergic innervation was studied using cholinesterase histochemistry. Because many afferent fibres do not express CGRP or SP, the general neuronal marker protein gene product (PGP 9 x 5) was used to assess the overall nerve supply to the skin.
Clin Exp Dermatol 1995 Nov
PMID:Neuropeptides in the skin of patients with atopic dermatitis. 885 37

We report two cases of pressure ulcers in liver cirrhosis patients. In case 1, a 64-year-old Japanese woman had suffered from liver cirrhosis caused by hepatitis C virus and developed a pressure ulcer on her sacral and coccygeal area due to long-term bedrest. After she received a living donor liver transplantation from her child, the ulcer healed synchronizing with improvement of serum cholinesterase and bilirubin. Likewise, her systemic condition also got much better after the transplantation. In case 2, a 53-year-old Japanese man with hepatitis B virus cirrhosis and hepatocellular carcinoma developed a pressure ulcer on his sacral area. Although he received a living donor liver transplantation from his brother, his general status and pressure ulcer were fluctuating in conformity with the variance of serum bilirubin. However, at 5 weeks after the transplantation, the ulcer gradually started improving, entrained to serum bilirubin decrease. From these findings, the condition of the pressure ulcer in liver cirrhosis patients synchronized with serum bilirubin as well as systemic condition, suggesting a possible influence of bilirubin for wound healing.
J Dermatol 2007 Jun
PMID:Two cases of pressure ulcer healing after liver transplantation in cirrhosis patients. 1753 9


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