Sponge aggregation factor and sponge hemagglutinin: possible relationships between two different molecules.
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Biomedical subjects
Publications and source records attributed to P Vaith.
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From the cell membranes of the sponge Geodia cydonium a component was isolated and purified which inhibits the aggregation factor isolated from the same source; the component was termed anti-aggregation receptor. This molecule was characterized as a glycoprotein (54% neutral carbohydrate) and its molecular weight is in the range of 180,000 One biological site of the anti-aggregation receptor was determined to be D-galactose. Indirect evidence presented seems to indicate that this molecule is present in an active form in aggregation-deficient cells and absent in aggregation-susceptible cells.
Human serum glycoproteins can be classified into those containing N-acetyl-D-galactosamine and into those lacking this hexosamine. The N-acetyl-D-galactosamine-containing serum glycoproteins have alkali-labile chains containing this hexosamine linked O-glycosidically to hydroxy amino acids. These alkali-labile chains can be demonstrated in neuraminic acid free serum glycoproteins by gas liquid chromatography and by using precipitating lectins from invertebrates and plants. They are represented by two chains, one containing only N-acetyl-D-galactosamine, the other with D-galactose linked (1--3) beta-glycosidically to this hexosamine forming a disaccharide. Serologically these two chains, which usually occur together on one molecule, can be characterized by their reaction with lectins from Helix pomatia (anti-A like) and from Agaricus bisporus and Arachis hypogaea (anti-TF specificity).
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Apolipoprotein C-III1 and apolipoprotein C-III2 each contain one oligosaccharide side chain, bound O-glycosidically to threonine in position 74 of the amino acid sequence. The studies reported in this paper characterize these alkali labile oligosaccharides, thereby demonstrating the complete structure of apolipoprotein C-III. Monosaccharide analysis revealed the following sugar composition: D-galactose/N-acetyl-D-galactosamine/sialic acid 1 : 1 : 1 and 1 : 1 : 2 for apolipoprotein C-III1 and apolipoprotein C-III2, respectively. Treatment of desialylated apolipoproteins with alkaline borohydride released the reduced disaccharide beta-D-galactosyl-(1 leads to 3)-N-acetyl-D-galactosaminitol, which was detected by gas-liquid chromatography. Further studies employing periodate oxidation and Smith degradation indicated that the structure of the trisaccharide from apolipoprotein C-III1 was alpha-N-acetylneuraminyl-(2 leads to 3)-beta-D-galactosyl-(1 leads to 3)-N-acetyl-D-galactosaminitol. The tetrasaccharide structure from apolipoprotein C-III2 is made up of this trisaccharide plus one sialic acid residue linked to C6 of N-acetyl-D-galactosaminitol, as was shown by the assessment of chromogens formed upon alkaline degradation.
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In the haemolymph of the Tridacnid bivalve clams anti-galactans occur which do not have only glycosubstance precipitating and cell agglutinating properties, but also show mitogenic activity with respect to the blast transformation of human peripheral lymphocytes. This new property can be inhibited in a specific way by galactans and is destroyed by the degradation of the mitogenic lectin into subunits by polymer bound pronase. Quite a number of invertebrate haemolymph samples and snail albumin gland extracts, containing agglutinin activity, proved to have no mitogenic potency. The only exception was found in an extract of the snail albumin gland of Ampullaria canaliculata which contained a strong mitogen of the lectin type.
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PATIENTS: Five patients (mean age 81.6 years) developed bilateral blindness and 3 additional patients suffered cerebral strokes (mean age 58 years) due to temporal arteritis. Bilateral blindness and strokes occurred despite corticosteroid treatment. RESULTS: In all patients with temporal arteritis, the diagnosis was made too late. Patients with bilateral blindness were referred to the Eye Hospital when one eye had already become blind. The delay between the first symptoms and blindness in one eye was (average) 7 weeks. The interval between blindness of the first and second eyes was (average) 5 days in 3 patients, and simultaneous blindness in both eyes occurred in 2 patients. The other eye also became blind despite mega-doses of prednisone in 3 patients. Three additional patients already showed neurological signs and symptoms at the beginning of the temporal headache. All 3 patients developed strokes after some weeks or months. The wrong diagnosis was made in the first examination(s) by the physician with patients having prodromal signs or symptoms, but who also showed signs of other vascular diseases (diabetes mellitus, hypertension or occlusion of the internal carotid artery) which masked the inflammatory disease of temporal arteritis. CONCLUSIONS: Early diagnosis is essential to prevent severe complications. In patients with a cerebral stroke the early neurological deficits are warning signs which means that one must observe the patient regularly at short intervals. After the diagnosis has been settled, treatment of the patients for several months with a high dosage of corticosteroids is mandatory.
In a twenty-nine year old female patient with progressive systemic sclerosis (scleroderma) (PSS) and an impressing involvement of the intestine (disturbance of the oesophageal motility, pseudo-obstruction, malabsorption) a spontaneous, asymptomatic pneumoperitoneum is observed. Perforation or pneumatosis cystoides intestinalis (PCI) could not be proved. The possible pathogenesis, course, prognosis and therapy of this rare complication are discussed.
We report on a case of Pfeifer-Weber-Christian panniculitis (PWCP) in a 40 year old woman. PWCP is a rare inflammatory disorder of the subcutaneous fatty tissue. It is characterized by painful relapsing, subcutaneous nodules occurring preferentially at the upper arm, thigh and trunk regions. The disease is often accompanied by recurrent temperatures and constitutional symptoms. The clinical course of our patient had already lasted for four years when we saw her for the first time. Besides local panniculitis of the arms and the trunk she suffered from recurrent temperatures. Antibiotics and/or antiinflammatory therapy failed to control the disease. Laboratory tests and chest X-ray did not reveal noteworthy pathological results. PWCP was proven histologically and distinguished from other soft tissue disorders. The findings are discussed in the context of previous reports. The etiopathology of PWCP remains unclear and a specific therapy still awaits introduction.