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Biomedical subjects

A Knapp

Publications and source records attributed to A Knapp.

At least 19 recordsLinked to original sources
PubMed1992

Hirudisins. Hirudin-derived thrombin inhibitors with disintegrin activity.

Recombinant hirudin variants have been designed which inhibit alpha-thrombin by the hirudin mechanism and which in addition exhibit disintegrin activity. These proteins, called "hirudisins," have been engineered by replacing the Ser-Asp-Gly-Glu sequence at the tip of hirudin's finger-like structure (residues 32-35) by Arg-Gly-Asp-Ser (RGDS) to yield hirudisin and Lys-Gly-Asp-Ser (KGDS) to obtain hirudisin-1. Comparison of thrombin inhibition activities showed that hirudisin is 2-fold more potent (K(i) = 160 +/- 70 fM) than hirudisin-1 (K(i) = 370 +/- 44 fM) and recombinant (r)-hirudin (K(i) = 270 +/- 50 fM). alpha-Thrombin-stimulated platelet aggregation was effectively inhibited by r-hirudin, hirudisin, and hirudisin-1 with IC50 of 5.7 to 6.8 nM. Unlike r-hirudin, hirudisin inhibits ADP-induced platelet aggregation (IC50 = 65 microM) 3- to 5-fold stronger than the linear GRGDS- and RGDS-peptide. Direct interaction of hirudisin with purified glycoprotein IIb-IIIa demonstrated that antiplatelet aggregation activity is due to the integrin-directed RGD motif. Disintegrin activity of hirudisin relative to that of reduced and carboxymethylated hirudisin suggests that the conformational strain favors binding to integrins. On the basis of these results, hirudisins appear to be interesting molecules for the design of potential antithrombotic agents with antithrombin as well as antiplatelet aggregation activities.

Adenosine Diphosphate↗
PubMed1990

Tryptophan metabolic studies in patients with presenile cataracts.

In 43 patients with presenile cataracts an oral tryptophan loading test with 5 g L-tryptophan was performed and the 24-hour urinary excretion of kynurenine and xanthurenic acid was determined. 5 cases showed pathological deviations and an excretion pattern of tryptophan metabolites via kynurenine, similar as in vitamin B6-dependent xanthurenic aciduria.

Adolescent↗
PubMed1990

[The HLA and protease inhibitor (Pi) system in erythropoietic (hepatic) protoporphyria. Family studies].

Relations between porphyrias (porphyria cutanea tarda, variegate porphyria) and HLA- or protease inhibitor (Pi-) system were repeatedly found or supposed. Corresponding investigations do not exist for erythropoietic protoporphyria (EP), for which an autosomal dominant mode of inheritance with highly varying expressiveness (additional genes?) is being discussed. Three families with five EP-patients were examined for possible relations between the manifestations of this disease (skin - and liver changes) and the above-mentioned genetic markers. It was remarkable that three of the patients had the HLA A 3, but nobody of the obvious gene-carriers of this disease without clinical manifestations. On the other hand, two ill couples of siblings were genetically different as to HLA A 3. One couple with liver morphological changes each were different as Pi M-carrier and Pi MS-carrier respectively. Thus, relations between the disease and the genetic markers examined could not be proved.

Erythrocytes↗
PubMed1989

[Studies of tryptophan metabolism in cancer of the urinary bladder].

In 100 patients suffering from urinary bladder cancer (pTA-4, Nx, M0-1, G0-3) we created an oral tryptophan load administering 5 g of L-type tryptophan. Thereafter the amount of both xanthurenic acid and kynurenin was determined quantitatively in the 24-hour urine. 16 patients revealed pathological test results and excretion pattern of tryptophan metabolites via kynurenin were similar to vitamin B6-dependent xanthurenic aciduria both in its homocygotic and heterocygotic pattern. It has not been possible to prove a direct correlation between xanthurenic aciduria and urinary bladder cancer. However, xanthurenic aciduria may be of significance as a risk factor in the etiopathogenesis of urinary bladder cancer.

Humans↗
PubMed1989

Nutrition and oral health in the elderly.

At every age, an adequate supply of nutrients is necessary to maintain optimal oral health. This article presents an overview of various factors that have an impact on the nutritional status of the elderly, current recommendations regarding nutrient requirements of this age group, as well as a discussion of nutrients that may be marginal in diet of elderly persons. Suggestions for assessing nutritional status in a dental practice are offered.

Aged↗
PubMed1988

Corneal amyloidosis associated with keratoconus.

Nodular, gray-white, central corneal opacities which extended from the subepithelial zone through the anterior four fifths of the stroma developed in a 50-year-old man with a longstanding history of hard contact lens wear for keratoconus. Results of histopathologic analysis of the corneal button obtained at the time of penetrating keratoplasty disclosed that the opacities were composed of amyloid. Corneal amyloidosis is rarely found in association with keratoconus. Although there were some similarities in the pattern of amyloid deposition to that seen in primary familial amyloidosis of the cornea, the authors believe that their patient is more likely to have had a secondary amyloidosis. Corneal amyloidosis should be considered in keratoconus patients with development of unusual forms of central corneal opacification.

Amyloidosis↗
PubMed1988

[Studies on tryptophan metabolism in calcium oxalate urolithiasis].

In 90 patients with calcium oxalate urolithiasis an oral tryptophan-loading test with 5 g L-tryptophan was performed and the 24-hour urinary excretion of xanthurenic acid and kynurenine was measured. In 10 cases pathological deviations and an excretion pattern of tryptophan metabolites via kynurenine similar as in the hereditary vitamin-B6-dependent xanthurenic aciduria in homozygous or heterozygous from were found. Correlations between the oxalate excretion and the tryptophan metabolism do not exist. A 2-year therapy with 60 mg vitamin B6 was favourable in patients with an excretion of more than 300 mumol XA after a tryptophan load.

Administration, Oral↗
PubMed1987

Serious corneal complications of glaucoma filtering surgery with postoperative 5-fluorouracil.

We studied four patients who, having received postoperative 5-fluorouracil after glaucoma filtering operations, developed serious corneal complications. All four patients had preexisting corneal abnormalities including keratoconjunctivitis sicca, exposure keratopathy, and bullous keratopathy. All of the patients developed epithelial defects in the postoperative period. The complications included bacterial corneal ulceration (two patients), sterile corneal ulceration and corneal perforation (one patient), and a keratinized corneal plaque with underlying sterile stromal infiltrate (one patient). The use of 5-fluorouracil, which is an antimetabolite with considerable corneal epithelial toxicity, after glaucoma filtering surgery frequently causes corneal epithelial defects that may lead to secondary complications. Patients receiving this drug should have their corneal status closely monitored. In patients with corneal epithelial disease, 5-fluorouracil should be used with caution.

Aged↗
PubMed1987

Mycobacterium avium-intracellulare corneal ulcer.

A healthy 28-year-old man developed a slowly progressive corneal ulcer 21 months after an episode of corneal trauma. Acid-fast bacilli were identified in corneal scrapings, and the causative organism was identified as Mycobacterium avium-intracellulare. Medical treatment with topical amikacin and oral rifampin was ineffective, and a therapeutic penetrating keratoplasty was necessary to cure the infection. To the best of our knowledge, this is only the second reported case of a corneal infection caused by a slow-growing nontuberculous mycobacterium (Runyon groups I, II, and III) and the first caused by M. avium-intracellulare. Slowly growing nontuberculous mycobacteria should be considered among those organisms that cause corneal infection, especially in cases characterized by a protracted course and lack of response to conventional antimicrobial therapy.

Adult↗