Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:036187 (gut)
 73,132 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent information about the localization of sympathetic nerves and catecholamine-containing cells suggests sites of action not usually described in the neuroscience textbooks. In this study, we focused on the autonomic controls that affect ganglia, heart, gut, and chemoreceptors. As a result of some speculation derived mainly from histochemical observations and partially from physiologic data, we concluded that at the organ level the interplay between a nerve terminal-receptor serves as a local control. Additional controls may function at the ganglion level where catecholamine-containing chromaffin cells may serve as interneurons. We suggest that all peripheral catecholamine-containing elements which function in a modulatory role are not vital to the survival of the individual but rather serve as "fine tune" adjustment that do not involve the central nervous system.
J Invest Dermatol 1977 Jul
PMID:Controlling influences of the autonomic nervous system. 19 86

Malabsorption (M) is characterized by absorption defect of one or several nutriments in small bowel. Its clinical expression is rarely obvious and biological signs are: anaemia, low serum protein, albumin and lipid rates, low serum calcium, phosphorus and potassium level, and hypoprothrombinaemia. But only 4 simple and reliable tests are needed for diagnosis: i. e.: daily faecal fat amount measurement, daily faecal nitrogen excretion, the xylose test and the Schilling's test. This syndrome is related to many conditions which can be divided into 2 groups with and without intestinal abnormalities. The relationships between M and skin diseases belong to 4 types (J. Marks and S. Shuster): 1) M is responsible for the cutaneous signs, 2) M is caused by a skin disease, 3) both M and skin disease are the result of a same cause, 4) M and skin disease are associated in an indirect way. Only the two first types are dealt with in this report. Skin manifestations occur as a complication in 10 p. 100 to 20 p. 100 of cases of M. They are mostly polymorphous or non-specific, as they are related to multiple vitamin or essential amino acid deficiencies and heal with the treatment of M. The main conditions encountered are diffuse pigmentation, acquired ichthyosis, follicular keratosis, nail brittleness and hair loss. Mucous membrane lesions, purpura and eczematoid or psoriasis-like dermatitis have also been described. More uncommon are clubbing of fingers, finger print abnormalities, kwashiorkor or acrodermatitis enteropathica-like eruptions. The dermatogenic enteropathy, i. e. a M syndrome due to a skin disease, occurs as a result of widespread involvement of the body for instance in psoriasis or eczema; its clinical expression is rarely obvious, the histological record of gut biopsy usually normal and the results of biological tests often dissociated, but steatorrhoea is frequently found. The pathogenesis of the condition is still unknown but its importance is related to the extent of the skin disease and it only improves with the treatment of the latter. All these features and others are discussed in the report with a comprehensive review of the literature.
Ann Dermatol Venereol 1978 Dec
PMID:[Cutaneous manifestations of malabsorption diseases (author's transl)]. 38 Apr 45

In most cases the ano-cutaneous clinical symptoms correlated to diseases of the gastro-intestinal tract are not specific (erythema, itching, wounds or scarring). However in the following diseases occasional dermatological lesions may directly contribute to their diagnosis: in Crohn's disease, tuberculosis of bowel, chronic entamoebiasis and bilharziosis, the skin lesions of the anal area have the same histological structure as the gut lesions. Perianal fistulas and ulcers are frequent in Crohn's disease especially if there is a colonic and rectal spreading; they respond badly to steroid therapy and are often correlated with a worse prognosis. Perianal specific lesions occur often in oxyuriasis in children, in candidiasis of the digestive tract, in systemic aphthosis and in some malignancies. In other gastro-intestinal disturbances, the dermatological and features are less specific and can only be suggestive: iatrogenic and microbial diarrheas, side-effects of laxatives, proctological diseases. It has to be emphasized that pruritus ani is only induced by deeper lesions when they spread to the perianal skin. In proctological practice, contact dermatitis by sensitivity to anaesthetics or suppository balsams (Peruvian balsam), itching or burning atrophy by topical steroid abuse, non-diagnosed fungal (candidiasis), bacterial (erythrasma) or psoriatic intertrigos (flexural psoriasis) may sometimes explain the failure of therapy.
Ann Dermatol Venereol 1979 Jan
PMID:[Anal symptoms of gastro-intestinal diseases]. 48 13

Two unrelated infants had stiff skin and painful joint contractures in the first few months of life. Other features included gingival hyperplasia, small papules on the face and trunk, perianal nodules, and bloody diarrhea. Hyaline material was evident in the papillary dermis and gut mucosa in both patients. Ultrastructural examination revealed a distinctive fibrillogranular appearance. These infants have the same clinical, histologic, and ultrastructural features as four infants we reported previously with infantile systemic hyalinosis. One of the patients described here demonstrated some features that overlap with those of juvenile hyaline fibromatosis.
Pediatr Dermatol 1992 Sep
PMID:Clinical, histologic, and ultrastructural findings in two cases of infantile systemic hyalinosis. 148 75

Lymphocyte migration into the lymphoid organs and sites of inflammation is controlled by lymphocyte-endothelial cell interaction at sites where lymphocytes exit from the blood. Expression of Hermes-defined CD44 class of lymphocyte homing receptor and HECA-452 antigen specific for high-endothelium-mediating physiologic lymphocyte extravasation was studied in dermatitis herpetiformis, celiac disease, psoriasis, mycosis fungoides, lymphocytosis cutis, atopic dermatitis, and allergic contact dermatitis. Also, duodenal biopsies of patients suffering from dermatitis herpetiformis or celiac disease were studied for existence of these antigens. Infiltrating lymphocytes in the skin and in the duodenal area expressed homing receptor molecules when studied with monoclonal antibodies, Hermes-1 and Hermes-3, that recognize the CD44 class of molecules involved in lymphocyte binding to high endothelial venules in peripheral lymph nodes, mucosa-associated lymphatic tissues, and inflamed synovium. However, the HECA-452 antigen was not detected on the venules, neither in the skin nor in the duodenum. Even the venules possessing high endothelium morphologically were HECA-452 negative. These findings suggest the CD44 class of lymphocyte homing receptor(s) is also involved in lymphocyte homing to inflamed skin and the duodenal area of the gut. However, on the basis of HECA-452 staining, high endothelial venules in inflamed skin and duodenum are not antigenically identical with high endothelial venules in organized lymphoid tissues. This finding indirectly supports the idea that molecules and/or mechanisms mediating lymphocyte extravasation might be distinct in these organs.
J Invest Dermatol 1990 Jun
PMID:Lymphocyte migration into the skin: the role of lymphocyte homing receptor (CD44) and endothelial cell antigen (HECA-452). 169 39

Zinc deficiency in breast-fed infants is a rare disease caused by a low level of zinc in their mother's milk. Premature infants are more vulnerable to develop zinc deficiency than full-term infants because, despite their high zinc requirements, they have insufficient body stores of zinc and a poor capability to absorb zinc from the gut. The clinical aspect of zinc deficiency is acrodermatitis enteropathica, in which the severity is proportional to the zinc level. The patients respond well to oral zinc supplements.
Semin Dermatol 1991 Dec
PMID:Acquired zinc deficiency in breast-fed infants. 176 59

The epidermis of all strains of normal mice is populated by two distinct dendritic, bone marrow-derived cells: Langerhans cells and CD4-CD8- Thy-1+ dendritic epidermal T cells (DETC). The overwhelming majority of DETC are an unusually homogeneous population of thymic-dependent cells which express CD3-associated T-cell antigen receptors (TCRs) of the gamma/delta type, thereby distinguishing them from conventional CD4+CD8- or CD4-CD8+ T cells expressing CD3-associated alpha/beta TCR. Most DETC are ontogenetically primitive, derived from early fetal thymocytes with a preferential, but poorly understood tropism for the epidermis. Like the TCR on other populations of gamma/delta cells, which preferentially populate other epithelia such as in the gut and lung, the TCR on most DETC selectively utilize particular variable (V) gene segments (i.e., V gamma 3 and V delta 1 for DETC vs V gamma 5 and V delta 4 or V delta 6 for intestinal intraepithelial lymphocytes). However, unlike other gamma/delta populations whose TCR junctional regions exhibit marked heterogeneity, DETC junctional diversity is extremely limited. This lack of TCR heterogeneity among DETC suggests they recognize a narrow range of physiologic ligands (antigens) and that this recognition is restricted not by conventional polymorphic class-I or class-II MHC molecules, but rather by relatively nonpolymorphic self MHC-like molecules of the class Ib MHC type [e.g., Qa, TL, and CD1 (T6)]. Additional studies are required to clarify precisely what DETC recognize, their relevant biological functions, as well as their relationship(s) to the gamma/delta cells recently identified in human skin.
J Invest Dermatol 1990 Jun
PMID:TCR gamma/delta+ dendritic epidermal T cells as constituents of skin-associated lymphoid tissue. 197 73

Idiopathic hypereosinophilic syndrome (IHS) is reported in a 59-year-old farmer. Skin manifestations were represented by pruritic erythemato-squamous and papulonodular lesions, the heart was affected by endomyocardic fibrosis, and periodic intestinal colics denoted a possible gut involvement. A mild and transient beneficial effect was achieved by treatment with antihistamines, sodium-chromoglycate, steroids. Recent studies indicate that IHS hypereosinophilia is caused by interleukins 3 and 5, cytokines able to activate circulating eosinophils and to enhance the survival of these cells.
G Ital Dermatol Venereol 1990 Sep
PMID:[A case of idiopathic hypereosinophilic syndrome]. 207 52

The state of our understanding of the pathogenesis of DH relies on the integration of several key characteristics: (1) a high frequency of the HLA antigens HLA-B8, HLA-DR3, and HLA-DQw2, (2) an associated GSE, (3) the resolution of both the skin lesions and gut abnormalities in response to a gluten-free diet, and (4) the presence of granular deposits of IgA in normal and perilesional skin. The role of the HLA class II antigens expressed in patients with DH most likely relates to the afferent or initiating arm of the immune system. The association of the HLA-A1, -B8, -DR3, -DQw2 haplotype with Sjogren's syndrome, chronic hepatitis, Graves' disease, and other presumably immunologically mediated diseases, as well as the evidence that some normal HLA-B8, -DR3 individuals have an abnormal in vitro lymphocyte response to wheat protein and mitogens and have abnormal Fc-IgG receptor-mediated functions, suggests that this HLA haplotype or genes linked closely to it may confer a generalized state of immune susceptibility on its carrier, the exact phenotypic expression of which depends on other genetic or environmental determinants. It also is clear, from the association of DH with GSE and the ability to control the cutaneous manifestations of DH with a gluten-free diet, that the gut disease is a critical factor in the pathogenesis of DH. Several pathogenetic theories about the origin of the cutaneous IgA deposits in DH have been proposed, one of which states that the IgA is produced in the gut mucosa as a response to a dietary antigen or gut epithelial antigen and then cross-reacts with the skin of patients with DH. A second hypothesis is that the IgA produced in the gut binds to an antigen and is deposited in skin as an antigen-antibody complex. Finally, it could be that the gut mucosal abnormality simply allows an unknown antigen access to the central immune system where an IgA antibody is produced that binds to skin. The failure to detect circulating IgA anti-basement membrane zone antibodies in patients with DH suggests that either the structures to which the IgA binds are not present in normal skin without DH, that IgA cannot bind to these structures in vitro, or that the circulating IgA is too scant for detection with conventional methods. Finally, it must be considered that the IgA deposited in DH skin may bind as a result of non-antigen-antibody interactions that cannot be duplicated in vitro.(ABSTRACT TRUNCATED AT 400 WORDS)
Dermatol Clin 1990 Oct
PMID:Dermatitis herpetiformis. 224 67

Epidermotropic lymphocytes are an essential cellular component of the skin-associated lymphoid tissues (SALT). Dermal lymphocytic infiltrates are also characteristics of inflammatory dermatoses, such as psoriasis, and may be involved in the pathogenesis of the disease, although the mechanisms by which lymphocytes are recruited into these sites are not known. We have used an in vitro lymphocyte adherence assay to test the hypothesis that specialized endothelial cells are present in inflamed skin, and are capable of supporting lymphocyte adherence and promoting lymphocyte emigration. In this assay, we assessed the binding of lymphocytes overlaid onto frozen sections of normal and psoriatic skin. Peripheral blood mononuclear cells (PBMC) from patients, from healthy volunteers, and from rat thoracic duct bound specifically to dermal endothelia in psoriatic plaques, in steroid-resistant areas of plaques, but not in uninvolved skin or skin from healthy individuals. Analysis of the binding properties of lymphocyte subsets revealed preferential adherence by CD4+ T cells as compared with CD8+ T cells and to B cells. Interestingly, PBMC from patients undergoing ultraviolet light therapy failed to adhere to autologous skin or to lesion-containing skin sections from untreated patients. Additional studies indicate that the lymphocyte-endothelial interaction is an energy- and calcium-dependent process and involves surface glycoprotein and carbohydrate moieties, requirements similar to those found in specific lymphocyte interactions with high endothelial venules in lymph nodes during the homing process. Pretreatment of lymphocytes with antibodies directed against homing receptors mediating migration into lymph nodes and into gut-associated lymphoid tissues, however, did not interfere with lymphocyte adherence to psoriatic endothelium. In contrast, anti-lymphocyte function associated antigen (LFA)-1 antibody partially inhibited lymphocyte binding to chronic plaques. We conclude that a tissue-specific receptor/ligand interaction independent of LFA-1 directs lymphocyte emigration from the dermal microvasculature into the psoriatic dermis and that LFA-1 plays only an accessory role in the adhesion process.
J Invest Dermatol 1989 Aug
PMID:Lymphocyte recognition of psoriatic endothelium: evidence for a tissue-specific receptor/ligand interaction. 254 96


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