Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes a family in which eight individuals in three generations had mental retardation in association with a characteristic pattern of clinical problems and physical abnormalities including short stature, eczema, hernias, delayed puberty, dysmorphic facies and digital anomalies. The family history was consistent with a chromosomal rearrangement with transmission through balanced carriers. Routine ASG banding studies showed extra chromosomal material on a chromosome 16 but failed to demonstrate any differences between the affected individuals and the presumed carriers. However, subsequent studies utilizing trypsin banding and microspectrophotometry of individual chromosomes demonstrated that the affected individuals were partially trisomic for the distal band of the long arm of chromosome 5 and that 0.273 units of a chromosome 5 were translocated to chromosome 16. This definitive cytogenetic diagnosis permitted accurate prenatal diagnosis to be carried out on the fetus of a balanced carrier female. The application of these techniques to previously obscure familial dysmorphic syndromes is recommended.
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PMID:Partial trisomy for the distal long arm of chromosome 5 (region q34 leads to qter). A new clinically recognizable syndrome. 44 68

The levels of tryptase in the suction-blister fluid from patients with chronic urticaria, urticaria pigmentosa, cholinergic urticaria, urticarial dermographism, prurigo of unknown origin, eczema, psoriasis, atopic dermatitis, and from healthy controls were studied. The blister fluid from controls contained up to 15 micrograms/l of tryptase, whereas that from patients with active urticaria contained greater than 50 micrograms/l. This study demonstrates that patients with urticaria have mast cells that readily release tryptase in both the lesional and non-lesional areas of skin.
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PMID:Increased tryptase levels in suction-blister fluid from patients with urticaria. 187 96

Stomach extract of Atlantic herring Clupea harengus, Atlantic salmon Salmo salar, cod Gadus morhua, redfish Sebastes marinus, and plaice Pleuronectes platessa, degraded human epidermal keratin effectively in vitro. The keratin-degrading activity of all extracts showed a pH optimum around 3.3-3.4, and sheets of plantar callus were degraded with about the same efficacy as keratin. Pepstatin sensitivity, heat lability, and the acidic pH optimum demonstrated that the keratin-degrading activity was pepsin. The keratin-degrading activity of cod stomach extract had a temperature optimum of around 42 degrees C at optimal pH, and showed a similar pH dependency with collagen as with keratin as substrate. The keratin-degrading activity of pepsin I and pepsin II purified from cod showed a pH optimum of 3.7 and 3.1, respectively, similar to that obtained with hemoglobin as substrate. Pig pepsin showed a pH optimum of about 2 with keratin, hemoglobin, and collagen as substrates. The present investigation demonstrates that fish pepsin is effective in degrading human epidermal keratin in vitro, and in a contemporary study the same was shown with fish trypsin. This may suggest a possible mechanism for the development of irritative hand eczema caused by exposure to fish and acidified fish material.
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PMID:Degradation of human epidermal keratin by fish pepsin. 245 43

Cod Gadus morhua and bovine trypsin degraded human epidermal keratin with similar efficacies in vitro around optimal pH, which was at pH 8.4 for cod trypsin and at pH 9.5 for bovine trypsin. Extract of intestines of cod, Atlantic herring Clupea harengus, Atlantic salmon Salmo salar, and redfish Sebastes marinus degraded keratin with similar efficacies with pH optima between 8.5 and 9.5. Sheets of plantar callus were degraded with somewhat lower efficacy than keratin. The keratin-degrading activity of extract of cod intestines had a temperature optimum around 45 degrees C. Inhibition with benzamidine and 4-phenylbutylamine showed that trypsin amounted to more than 2/3 of the keratin-degrading activity in all extracts of fish intestines. Apart from cod intestines, which had the lowest chymotrypsin content, chymotrypsin made a smaller but significant contribution to the keratin-degrading activity. The present investigation demonstrates that fish trypsin and extract of fish intestines are effective in degrading human epidermal keratin in vitro, and in a recent investigation the same was shown with fish pepsin. This may suggest a possible mechanism for the development of irritative contact eczema caused by exposure to fish.
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PMID:Degradation of human epidermal keratin by cod trypsin and extracts of fish intestines. 246 41

The hormonal and immune status was investigated by a radioimmunoassay in 105 patients with dermatosis (55 female and 50 male patients aged 15 to 80): 51 suffered from eczema, 41--from psoriasis, and 13--from neurodermatitis. The results were compared with those of 32 controls. Serum concentrations of T3, T4, TSH, insulin, trypsin, C-peptide, cortisol, and IgE were investigated. Disorders of the hormonal and immune status were noted in the examinees with relation to sex, type of disease, season, time-period and extent of disease.
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PMID:[Radioimmunologic study of the hormonal and immune status in eczema, psoriasis and neurodermatitis]. 267 71

Several reports have shown the presence of T-helper lymphocytes with Th2 characteristics in the skin lesions of atopic dermatitis (AD). However, Th2 cells themselves require an exogenous pulse of IL-4 to initiate their differentiation and synthesis of IL-4. As mast cells have recently been shown to contain IL-4, this finding prompted us to investigate IL-4 in mast cells of AD lesions, to determine if they might provide the IL-4 pulse needed by the Th2 cells. In this study, we measured IL-4 immunoreactivity in mast cells of non-lesional and lesional skin sections from 20 patients with AD. Ten patients with nummular eczema (NE) without any atopic features or background, and five healthy subjects, served as the control groups. Mast cells were first identified using an enzyme--histochemical staining method for tryptase. Subsequently, the sections were photographed, the tryptase stain was removed, and IL-4 was demonstrated with a polyclonal antibody. The sections were photographed again, and the percentage of IL-4 positive mast cells was calculated. The percentage of mast cells exhibiting IL-4 immunoreactivity in the upper dermis in lesional vs. non-lesional skin was 66 +/- 18% vs. 37 +/- 18% in AD (P < 0.0001, paired t-test), but only 46 +/- 19% vs. 31 +/- 22% in NE. In the skin of healthy controls, only 23 +/- 25% of the mast cells were positive for IL-4. In addition, a significant difference was found between lesional skin of AD vs. NE patients (P < 0.008, unpaired t-test).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mast cells are one major source of interleukin-4 in atopic dermatitis. 791 8

The distribution of mast cells (MCs) containing tryptase (T) and chymase (C) was studied in the non-lesional and lesional skin of 26 patients with atopic dermatitis (AD) and 23 patients with non-atopic nummular eczema (NE), and in the skin of eight healthy controls. T and C activities were demonstrated enzymehistochemically using Z-Gly-Pro-Arg-MNA and Suc-Val-Pro-Phe-MNA as substrates, respectively. The T- and C-containing MCs were counted separately in the epidermis, in contact with the basement membrane, in the papillary dermis and in different dermal levels (0.2 mm each). Also, the C protein was determined immunohistochemically. T-positive MCs were similarly distributed in non-lesional and lesional skin of both AD and NE. The MC number was relatively high in the upper dermis (papillary dermis and levels I and II) of non-lesional and lesional skin of AD. In the upper dermis of non-lesional AD and NE skin and in normal skin, about 50% of T-positive MCs displayed C activity, whereas the percentage in lesional AD and NE skin was only about 30%. In this respect, the non-lesional and lesional samples differed significantly from each other in both dermatoses (in AD p = 0.003; in NE p = 0.002, Students' t-test). In all samples the MC number decreased in the deeper dermal levels, although numerous T-containing MCs were still counted in the deeper dermis (dermal levels IV-VII) of lesional AD and NE skin, differing significantly from the MC number in normal skin (In AD p = 0.005, In NE p = 0.041). In the deeper dermis, the percentage of MCs containing active C was about 70% in non-lesional and lesional AD and NE, and about 90% in normal healthy skin. However, in the upper dermis of non-lesional and lesional skin of both AD and NE, about 80% of all MCs contained the C protein, which differed significantly from the value of 100% in normal skin (p < 0.05). In conclusion, the increased number of T-positive MCs in the upper dermis of non-lesional and lesional AD contributes to promoting inflammation. C apparently loses its activity in the upper dermis of lesional AD and especially in NE. Thus, the enzyme partially lacks its capability to suppress inflammation, such as degradation of neuropeptides and proteins. The dysregulation of these proteinases exists already in non-lesional skin of AD and NE.
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PMID:Quantitative analysis of tryptase- and chymase-containing mast cells in atopic dermatitis and nummular eczema. 921 19

Among the cereals, wheat, rye, barley and oats, have been reported to cause protein contact dermatitis. However, in these cases neither the involvement of an immunological mechanism nor the role of specific protein(s) has been demonstrated. We present a case of protein contact dermatitis from corn. The patient presented with a Type I sensitization to corn, as shown by the presence of specific immunoglobulin (Ig)E and positivity to prick tests with both a flour suspension and the salt-soluble protein fraction of this cereal. The same corn preparations induced a strong urticarial reaction on scratch testing. This reaction was followed several days later by the appearance of erythema and then eczema at the site of application. When boiled, these preparations became inactive on both prick and scratch testing. Patch tests were negative in all cases. Immunoblotting performed with the patient's serum showed the presence of a unique IgE-binding protein band with a molecular weight of around 14 kDa, belonging to the salt-soluble corn protein fraction. Our results give the first clear evidence that cornflour can induce protein contact dermatitis. The IgE-binding 14-kDa protein has characteristics identical to those of the trypsin/alpha-amylase inhibitors from cereals.
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PMID:Contact urticaria and protein contact dermatitis from corn in a patient with serum IgE specific for a salt-soluble corn protein of low molecular weight. 1537 49

Human mast cells are well known to produce a serine protease, tryptase, which appears to play a pathogenic role in various skin inflammations. It was previously reported that a rat homologue of bikunin may inhibit tryptase activity. Various type of cells (i.e. keratinocytes) are able to produce this protein inhibitor, it still remains unclear if bikunin is present in dermal inflammatory milieu, in which mast cells, through secretion of tryptase, play an inflammatory role. Therefore, the purpose of the present study was to exploit expression and production of bikunin in dermis and dermal constituents. We first compared the dermal mast cells in psoriatic lesions with those in lesional skin of atopic dermatitis or of chronic eczema by use of immunoelectron microscopy and immunohistochemical analyses using antibodies to bikunin and tryptase. Then, we tested what kinds of cytokines may regulate the de novo synthesis of bikunin. To do so, RNA was extracted from a human mastocytic cell line, HMC-1, reverse-transcribed, and semiquantitative RT-PCR was performed using primers specific for bikunin. With immunoelectron microscopy, bikunin was found to localize on the cell membrane, while tryptase was in the secretary granules of the mast cells. In psoriatic lesions, around 70% of dermal mast cells were positive for both tryptase and bikunin, and the remaining was mostly positive for tryptase, but the expression of bikunin was under the detection limit of the experimental setting. This observation was seen in only psoriatic lesions, even in almost cured lesions, while in atopic dermatitis or chronic eczema only mast cells doubly positive for bikunin and tryptase were seen. In HMC-1, bikunin was constitutively expressed at an mRNA level, which was upregulated by stimulation with interleukine-4, but was suppressed by interferon-gamma. Bearing in mind the concept that in psoriasis local cytokine milieu is shifted toward a Th1 pattern (predominant secretion of interferon-gamma), tryptase-positive, bikunin-negative mast cells may be induced.
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PMID:The presence of tryptase-positive and bikunin-negative mast cells in psoriatic skin lesions. 1714 27

Rather than other drugs, propofol is more likely to be used for induction of anesthesia to cause an allergic reaction. Propofol is becoming the most common intravenous agent used for induction as well as maintenance of anaesthesia. Allergy to propofol is rarely reported. We present a case of 4-year-old boy presented for elective adenotonsillectomy with past medical history of eczema and multiple allergies to food. He developed what seems to be an allergic reaction to propofol. We concluded that anaesthetists should be alerted when using propofol in patients with history of atopy or several drug allergies. Current evidence suggests that egg allergic patients are not more likely to develop anaphylaxis when exposed to propofol. If reactions to drugs occurred, it is always advisable to ascertain the exact allergen in each individual case before deciding causality. Serum tryptase, skin prick, intradermal testing, or serologic testing should be done to confirm the diagnosis of an anaphylactic reaction.
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PMID:My patient is allergic to eggs, can i use propofol? A case report and review. 2118 62


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