结节病易误诊,据王洪武等~([1])收集国内18篇关于此病误诊的文献,误诊率高达63.2%,当然有误诊就会有误治,如孙永昌等~([2])报道26例结节病在影像学检查诊断的第一印象中拟诊结核5例,其中就有2例完成规范的抗结核治疗,为此应引起临床对本病诊治的重视。

Sarcoidosis

1. alpha(2)-Macroglobulin is known to bind and inhibit a number of serine proteinases. We show that it binds thiol and carboxyl proteinases, and there is now reason to believe that alpha(2)-macroglobulin can bind essentially all proteinases. 2. Radiochemically labelled trypsin, chymotrypsin, cathepsin B1 and papain are bound by alpha(2)-macroglobulin in an approximately equimolar ratio. Equimolar binding was confirmed for trypsin by activesite titration. 3. Pretreatment of alpha(2)-macroglobulin with a saturating amount of one proteinase prevented the subsequent binding of another. We conclude that each molecule of alpha(2)-macroglobulin is able to react with one molecule of proteinase only. 4. alpha(2)-Macroglobulin did not react with exopeptidases, non-proteolytic hydrolases or inactive forms of endopeptidases. 5. The literature on binding and inhibition of proteinases by alpha(2)-macroglobulin is reviewed, and from consideration of this and our own work several general characteristics of the interaction can be discerned. 6. A model is proposed for the molecular mechanism of the interaction of alpha(2)-macroglobulin with proteinases. It is suggested that the enzyme cleaves a peptide bond in a sensitive region of the macroglobulin, and that this results in a conformational change in the alpha(2)-macroglobulin molecule that traps the enzyme irreversibly. Access of substrates to the active site of the enzyme becomes sterically hindered, causing inhibition that is most pronounced with large substrate molecules. 7. The possible physiological importance of the unique binding characteristics of alpha(2)-macroglobulin is discussed.

/pdf/the-interaction-of-a2-macroglobulin-with-proteinases-nk4uc21aj1.pdf

The interaction of α2-macroglobulin with proteinases. Characteristics and specificity of the reaction, and a hypothesis concerning its molecular mechanism

Photoageing is the superposition of chronic ultraviolet (UV)-induced damage on intrinsic ageing and accounts for most age-associated changes in skin appearance. It is triggered by receptor-initiated signalling, mitochondrial damage, protein oxidation and telomere-based DNA damage responses. Photodamaged skin displays variable epidermal thickness, dermal elastosis, decreased/fragmented collagen, increased matrix-degrading metalloproteinases, inflammatory infiltrates and vessel ectasia. The development of cosmetically pleasing sunscreens that protect against both UVA and UVB irradiation as well as products such as tretinoin that antagonize the UV signalling pathways leading to photoageing are major steps forward in preventing and reversing photoageing. Improved understanding of the skin's innate UV protective mechanisms has also given rise to several novel treatment concepts that promise to revolutionize this field within the coming decade. Such advances should not only allow for the improved appearance of skin in middle age and beyond, but also greatly reduce the accompanying burden of skin cancer.

Photoageing: mechanism, prevention and therapy.

The basic mechanisms of sweat gland function and an updated review of some relatively common disorders of sweat secretion, are presented. Although sweat secretion and ductal absorption are basically biophysical and biologic cellular processes, a detailed description of the basic biophysical principles of membrane transport has been avoided to make the discussion more readable. The cited references will, however, help those readers primarily interested in the basic details of sweat gland function. Part I of this article includes a discussion of morphologic characteristics, central and peripheral nervous control of sweat secretion, neurotransmitters, intracellular mediators and stimulus secretion coupling, Na-K-Cl cotransport model for the ionic mechanism of sweat secretion, ingredients of sweat, ductal function, the pathogenesis of abnormal sweat gland function in cystic fibrosis, and the discovery of the apoeccrine sweat gland. Part II, to be published in the May issue of the Journal, reviews reports of all those major disorders of hyperhidrosis and hypohidrosis that have appeared in the literature during the past 10 years. It is hoped that this review will serve as a resource for clinicians who encounter puzzling disorders of sweating in their patients, as well as for investigators who wish to obtain a quick update on sweat gland function.

Biology of sweat glands and their disorders. I. Normal sweat gland function

Provided is an organic electroluminescence device having high luminous efficiency, high heat resistance and an extremely long lifetime. The organic electroluminescence device of the present invention includes an organic thin film layer composed of one or more layers containing at least a light emitting layer is interposed between a cathode and an anode. The light emitting layer includes a compound containing a condensed ring and a luminescent metal complex capable of emitting light having a red-based color. It is preferable that the compound containing a condensed ring includes a host material, while the luminescent metal complex capable of emitting light having a red-based color includes a phosphorescent dopant.

Organic Electroluminescent Device

Composition topique comportant des n-acétylaldosamines ou acides n-acétylaminés

A method for visibly reducing a facial wrinkle by topically applying to the wrinkle glucuronic acid or a topically effective salt thereof or glucuronolactone.

Method of treating wrinkles using glucuronic acid or glucuronolactone

A method for visibly reducing a facial wrinkle by topically applying to the wrinkle 2-phenyllactic acid or a topically effective salt thereof.

Method of treating wrinkles using 2-phenyllactic acid

Topical preparations containing α-hydroxy acids and closely related compounds were found to exert profound effects on epidermal keratinization in ichthyosis. Therapeutically efficacious compounds include citric acid, ethyl pyruvate, glycolic acid, glucuronic acid, 3-hydroxybutyric acid, 2-hydroxyisobutyric acid, lactic acid, malic acid, methyl pyruvate, pyruvic acid, tartaric acid, and tartronic acid. These materials appear to influence the process of keratinization per se, but do not seem to be keratolytic.

Control of keratinization with alpha-hydroxy acids and related compounds. I. Topical treatment of ichthyotic disorders.

Alpha-hydroxyacids in the treatment of signs of photoaging

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