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:6.3.4.6 (urease)
7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate radiologic findings of Helicobacter pylori (H. pylori) in the upper gastrointestinal (UGI) tract, we retrospectively reviewed consecutive records of 676 symptomatic adults with gastric biopsies (224 positive) and 150 symptomatic adults with rapid urease tests (57 positive). All the UGI series of patients with positive biopsies or urease tests for H. pylori were compared with the UGI series of patients with negative urease tests. UGI examinations were evaluated blindly by two gastrointestinal radiologists without knowledge of clinical findings, original radiologic interpretations, or test results. They agreed that 8 of 18 (44%) UGIs of patients with H. pylori had abnormally increased gastric folds in the fundus, body, or antrum as compared with none of 14 (0%) UGIs of patients without H. pylori (p < 0.01) (P.P.V. = 1.0). Interobserver agreement was good (kappa = 0.63). Endoscopy in the eight patients with radiographic evidence of enlarged gastric folds all demonstrated marked abnormalities such as prominent gastric folds, gastric erythema, erosions, or peptic ulcers. Our findings indicate that enlarged gastric folds on the UGI series of a symptomatic adult are very suggestive of H. pylori gastritis.
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PMID:Can the radiologist recognize Helicobacter pylori gastritis? 779 26

In a prospective case controlled study, we evaluated the adverse effects of long-term fluoride ingestion on the gastrointestinal tract. Ten patients with otosclerosis who were receiving sodium fluoride 30 mg/day for a period of 3-12 months, and 10 age- and sex-matched healthy volunteers were included. They were all evaluated clinically and subjected to a real time ultrasound examination, upper gastrointestinal endoscopy, and biopsies from the gastric antrum and duodenum. The biopsies were subjected to a rapid urease test as well as light and electron microscopic examinations. Ionic fluoride was estimated in the serum, urine, and drinking water using an ION 85 Ion Analyzer. Seven subjects (70%) ingesting fluoride had abdominal pain, vomiting, and nausea. Petechiae, erosions, and erythema were seen on endoscopy in all the subjects, but not in the controls. Histological examination of the gastric antral biopsy showed chronic atrophic gastritis in all the subjects but in only one (10%) healthy volunteer. Scanning electron microscopic examination showed "cracked-clay" appearance, scanty microvilli, surface abrasions, and desquamated epithelium in the subjects ingesting fluoride, but not in the controls. We conclude that long-term fluoride ingestion is associated with a high incidence of dyspeptic symptoms as well as histological and electron microscopic abnormalities.
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PMID:Toxic effects of chronic fluoride ingestion on the upper gastrointestinal tract. 803 13

In a prospective study, gastroscopy and biopsies from the gastric antrum and body were undertaken in 100 consecutive patients (67 women, 33 men; mean age 58.6 [11-90] years) with unknown Helicobacter pylori status. None had been on any bacteria-suppressing drugs. Main indications for gastroscopy were upper abdominal pain, dyspepsia, emesis and anaemia of unknown cause. The macroscopic criteria for the diagnosis of H. pylori gastritis were the presence of at least one of the following signs: (1) chronic antral erosions; (2) goose-pimple-like appearance of the antral mucosa; (3) spotty erythema in the antrum; (4) complex changes of the antral mucosa with both bizarre reddening and pale areas; and (5) increased areolar markings and diffuse or fine-spotty erythema in the mucosa of the body of the stomach. Four biopsies each from the antrum and body were examined with the urease quick-test, microscopically as smears, specific culture and histology as reference methods. 60 patients had H. pylori gastritis, recognized macroscopically in 59 (sensitivity 98.3%). A false-positive diagnosis was made in 10 of 40 H. pylori-negative patients (specificity 75%). The positive predictive value of macroscopic diagnosis was 85.5%, the negative predictive value 96.8%.
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PMID:[Is Helicobacter pylori gastritis a macroscopic diagnosis?]. 843 66

Ultraviolet B (UVB) irradiation of the skin causes immunosuppression which is relevant to the induction of skin cancer. The mechanism of this immunomodulation is unclear but various regulatory molecules have been implicated, including cis-urocanic acid (cis-UCA) and the cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin 10 (IL-10). Whether ultraviolet A (UVA) induces similar changes has not been investigated fully. We studied the effect of in vivo UVB and long-wave UVA (UVA1) exposure on the induction of TNF-alpha, IL-10 and cis-UCA in human skin. Volunteers were irradiated with three minimal erythema doses (MED) of UVB or UVA1. At different times after irradiation, suction blisters were raised from irradiated and from non-irradiated (control) skin. The TNF-alpha and IL-10 protein concentration, and the percentage of cis-UCA in the blister fluid, were then determined. UVB irradiation of human skin led to a rapid and significant increase in TNF-alpha concentration in suction-blister fluid, with maximal values 6 h after irradiation (n = 6, P < 0.05). In contrast, UVA1 irradiation led to a decrease in TNF-alpha concentration in the suction-blister fluid compared with non-irradiated skin, with the lowest values 6 h after irradiation (n = 6, P < 0.05). Both UVB and UVA1 exposure of the skin induced a slight increase in IL-10 concentration. However, the increase in IL-10 was only significant after UVB irradiation (UVB, n = 6, P < 0.05; UVA, n = 7, P < 0.1). As previously shown, both UVB and UVA1 result in the photo-isomerization of trans-UCA and an increased percentage of cis-UCA was found in the suction-blister fluid. Thus the results show differential effects of UVB and UVA1 irradiation on the induction of immunoregulatory molecules, which may help to explain the variation in immune responses after UVB and UVA1 exposure of human skin.
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PMID:Contrasting effects of ultraviolet A1 and ultraviolet B exposure on the induction of tumour necrosis factor-alpha in human skin. 960 63

UV-B irradiation (UVR) of the host, in both humans and animal models, induces dose-related acute and chronic changes in skin which include erythema and photoageing, and induction of cancer. It can also induce modulation of immune responses of the host to antigens presented following irradiation. Commercially-available, broad-spectrum, high SPF (15, 15 + ) sunscreens protect against most effects of UV irradiation. An exception is the effects of UVR on immune responsiveness, with varying degrees of protection having been reported. We examined a system of UV-induced systemic suppression of contact hypersensitivity (CHS) responses in BALB/c mice. A range of commercially-available, broad spectrum, high SPF (15 + ) sunscreens demonstrated at best partial protection against systemic immunosuppression, yet were able to protect against two hallmarks of acute UVR-induced damage: skin oedema and keratinocyte proliferation. Two major models have been identified for the induction of immunosuppression following UVR, one identifying trans-urocanic acid (trans-UCA; deaminated histidine, located in the stratum corneum) as the critical photoreceptor, the other featuring DNA. UVR of trans-UCA produces cis-UCA, which itself is immunomodulatory. There was some abrogation of trans to cis isomerisation of urocanic acid in UV-irradiated, sunscreen-protected mice. However, the majority of the immunomodulation seen in these mice was abrogated by pretreatment with a monoclonal antibody to cis-urocanic acid. It is possible to induce formation of cis-urocanic acid in BALB/c skin in the absence of immunosuppression, using lower doses of UV radiation, indicating that formation of cis-urocanic acid in the stratum corneum is not necessarily sufficient to induce immunosuppression in the UV-irradiated host. The mechanisms of induction of the immunomodulated state in the UV-irradiated host are potentially diverse and the subject of ongoing debate. Our studies maintain a role for cis-UCA, and form the basis for further studies on its involvement in immunomodulation by UVR in sunscreen-protected hosts.
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PMID:Photoprotection: sunscreens and the immunomodulatory effects of UV irradiation. 992 Apr 40

Exposure to ultraviolet (UV) radiation may induce erythema, DNA damage and suppression of immune responses. Melanin pigmentation offers protection against the first two of these effects, but immunosuppression seems to occur irrespective of the subject's pigmentation. Cis-urocanic acid (cis-UCA), produced by isomerization of trans-UCA in the stratum corneum on UV exposure, initiates some of the immunomodulatory effects of UV radiation. In the present study the relationship between skin pigmentation and UCA isomerization has been examined in 28 healthy individuals of skin types I-IV. Pigmentation is measured in five areas of not recently exposed back skin before irradiation with 0, 0.45, 0.9, 1.8 and 3.6 standard erythema dose (SED) of filtered broadband UV-B (1 SED = 10 mJ cm-2 at 298 nm). The concentration of UCA isomers is measured immediately after the irradiation. With 3.6 SED, the relative production of cis-UCA is close to the maximum obtainable, irrespective of skin type. A significant negative correlation is found between pigmentation and relative production of cis-UCA at 0.45 and 1.8 SED, and between pigmentation and absolute production of cis-UCA at 0.45 SED. At doses of 0.45 and 0.9 SED the relative and absolute production of cis-UCA are higher in the group with skin types I and II when compared with the group with skin types III and IV. The higher isomerization in the lightly pigmented subjects than in the more pigmented ones may indicate that people with fair skin are at a relatively higher risk of immunosuppression when exposed to low doses of UV radiation.
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PMID:Isomerization of urocanic acid after ultraviolet radiation is influenced by skin pigmentation. 1020 77

Commercial sunscreens may offer some protection from immunosuppression induced by ultraviolet (UV) radiation, but agreement concerning the degree of protection is lacking. Cis-urocanic acid, formed by the photoisomerization of transurocanic acid is considered an important mediator of the cutaneous immunomodulation resulting from exposure to UV radiation. We investigated the effect of sunscreens on the isomerization of urocanic acid in 17 human subjects. Two sunscreens containing chemical filters, sun protection factor (SPF) 4 and SPF 10, and a SPF 10 sunscreen with a physical filter were applied at a thickness of 2 mg/cm2. The effect of a thin layer (0.5 mg/cm2) of the chemical SPF 10 sunscreen was also evaluated, as the amount of sunscreen applied in practice may be considerably less than recommended. All areas were irradiated with a single UV dose of 3.6 SED (standard erythema doses). In irradiated unprotected skin the median net production of cis-urocanic acid was 52% (relative amount). In the sites treated with the chemical sunscreens, the production of cis-urocanic acid was 7.4% (SPF 4) and 3.5% (SPF 10), and isomerization was thus reduced more efficiently at a higher SPF (p<0.01). The physical sunscreen reduced the formation of cis-UCA to 15%, and was significantly less effective than both the chemical SPF 10 sunscreen (p<0.01) and the SPF 4 sunscreen (p<0.01). The production of cis-urocanic acid in the area treated with the thin layer of the chemical SPF 10 sunscreen was 22%. The protection against the production of cis-urocanic acid was therefore reduced significantly (p<0.01) when the sunscreen was applied in an amount lower than recommended.
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PMID:Sunscreen protection against cis-urocanic acid production in human skin. 1059 54

The effect of a null mutation for the metallothionein (MT)-I and -II isoforms in mice on the immunosuppressive action of ultraviolet B (UVB; 280-320 nm) radiation has been examined. Mice were exposed to a series of increasing daily UVB doses, each dose administered to the dorsum on 3 consecutive days. Erythema was assessed, and measured as its oedema component by the post-irradiation dorsal skinfold thickness, but there was no effect of the null mutation (MT-/-) observed after 3 x 3.4 kJ/m2 of UVB radiation. Immune function was assessed by the contact hypersensitivity (CHS) response, which was initiated by sensitization on unirradiated abdominal skin, and thus demonstrated the systemic effects of dorsal treatments. In comparison with the wild-type MT+/+ mouse, the MT-/- mouse was significantly more immunosuppressed by moderate daily UVB doses (1. 75-5.9 kJ/m2). When topically applied cis-urocanic acid (cis-UCA) replaced UVB radiation as the immunosuppressive agent, contact hypersensitivity in MT-/- mice was again markedly more suppressed than in MT+/+ mice, in a dose-responsive manner. The results infer that MT, which was shown immunohistochemically to be strongly induced in the epidermis of MT+/+ mice, but to be absent in MT-/- epidermis, has the potential to protect from photoimmunosuppression, and that the mechanism of action may be via the inactivation of the epidermal UVB-photoproduct, cis-UCA.
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PMID:Lack of metallothionein-I and -II exacerbates the immunosuppressive effect of ultraviolet B radiation and cis-urocanic acid in mice. 1092 64

Degranulating dermal mast cells in UV-B-irradiated skin have been implicated for many years in the mechanisms of irradiation erythema. There is now considerable evidence that dermal mast cells are important to the processes by which both UV-B radiation and cis-urocanic acid (cis-UCA) suppress immune responses to sensitizing antigens applied to non-irradiated/non-cis-UCA-exposed sites. Mast-cell-depleted mice are resistant to the immunosuppressive effects of UV-B radiation and cis-UCA for 'systemic' immunomodulation. However, these mice gain responsiveness if the dorsal skin is reconstituted six weeks prior to irradiation or cis-UCA administration at that site with cultured bone-marrow-derived mast cells from +/+ mice. The molecular triggers for initiating mast-cell degranulation are being actively sought. Evidence suggests that histamine, and not tumour necrosis factor alpha, is the major mast-cell product that signals altered immune responses to sensitizing antigens applied to non-irradiated, non-cis-UCA-exposed sites. Histamine may have multiple roles, but experiments with indomethacin administered to mice have shown that one process involves induction of prostanoid production.
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PMID:Mast cells in UV-B-induced immunosuppression. 1094 71

Terrestrial ultraviolet radiation (UVR) exposure, consisting of ultraviolet A (320-40 nm) and B (290-320 nm), results in the photoisomerizion of epidermal trans-urocanic acid (trans-UCA) to cis-urocanic acid (cis-UCA), a potential suppressor of local and systemic immune responses. This study examines urinary UCA isomers as biomarkers of UVA/B exposure. It presents results measuring both cis- and trans-UCA in human urine samples collected from a group of study subjects (skin types II/III) that underwent controlled UVA/B exposures similar to those administered in commercial suntanning parlors. The UCA isomers were purified from urine using C18 solid-phase extraction columns followed by high-performance liquid chromatography (HPLC) with UV absorbance (268 nm) detection. The UCA biomarker was expressed as the ratio of cis-UCA to trans-UCA (UCA ratio), or as cis-UCA concentration corrected for urine volume using creatinine (cis-UCA-Cr). The UCA ratio increased over baseline in the urine of individuals exposed to UVA/B. A single exposure to approximately 70 percent minimal erythema dose (MED) of UVR (95 % UVA/5 % UVB to approximately 90 % of skin area) produced a 4.75-fold increase in the UCA ratio (p< 0.001) relative to baseline. Repeated daily UV exposures of similar doses produced a minimal increase in UCA ratio above that of the single UV exposure. These findings indicate that UCA cis-trans ratio holds promise as a biomarker for recent solar UV exposure.
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PMID:The effect of clinical UVA/B exposures on urinary urocanic acid isomer levels in individuals with caucasian type (II/III) skin types. 1640 97


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