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Biomedical subjects

W Arnold

Publications and source records attributed to W Arnold.

At least 433 records · Page 24Linked to original sources

Liver-cell-membrane autoantibody specific for inflammatory liver diseases.

With an immunofluorescence technique using rabbit hepatocytes isolated by a non-enzymatic method an autoantibody directed against liver-cell-membrance was identified. Sera from 361 patients with various liver diseases and 274 patients with primary non-hepatic diseases-many associated with non-organ-specific auto-antibodies-were examined. The antibody (LMA) was found in 27 out of 72 patients with hepatitis-B-surgace antigen (HBsAg)-negative chronic active hepatitis and in 17 out of 28 patients with HBsAg-negative non-alcoholic cirrhosis. Only two patients had LMA and HBsAg, and both had chronic active hepatitis. One patient with extrhepatic disease was found to have LMA, and this patient had biochemical evidence of liver disease. Hence there is a close correlation between the presence of LMA and HBsAg-negative chronic inflammatory liver diseases and its detection may help in diagnosis.

Adult↗

[Pathogenesis and clinical observations of papillomatous diseases of the skin and of the mucous membranes (author's transl)].

In the certain skin-warts, condylomata acuminata, oral-, laryngeal- and bronchial papillomas a morphologically identic virus is often seen. This virus belongs to the papova-virus-group and causes papillomas: Independant of their localization their clinical behaviour is very similar. Using cytophotometric methods we tried to find out if there are any signs which allow to reveal malignancy in continous reappearing papillomas.

Adult↗

[Methodical problems for evidence of the hepatitis-B-surface and hepatitis-B-core antigens in tissue (author's transl)].

Liver biopsy material of 22 in the serum HBsAg positive patients was tested with the fluorescent antibody technique for the localization of HBcAg and HBsAg in the liver tissue. Comparative studies were done with the following tissue preparation techniques: Cryostat technique, freeze drying, freeze substitution, cold ethanol paraffin embedding technique (SAINTE MARIE) and isolated liver cells. The investigations revealed the following results: 1. No HB-components could be detected with the cold ethanol paraffin embedding technique and freeze substitution. 2. Using the cryostat technique HBsAg could be demonstrated in 16/22 (cytoplasmatic localization) and HBcAg in 8/22 (nuclear localization). 3. With freeze drying HBsAg and HBcAg could be found in the same cases. The excellent tissue preparation allowed a correct localization of the HB-components to the cell structure. 4. In comparison to cryostat sections in isolated liver cells HBcAg could be demonstrated in 11/16 and HBcAg in 8/8 cases.

Fluorescent Antibody Technique↗

Localisation of e-antigen in nuclei of hepatocytes in HBsAg-positive liver diseases.

By the direct immunofluorescence technique 19 liver biopsies were examined for the presence of the e-antigen associated with the hepatitis B virus infection. With the use of double incubation and blocking experiments with FITC and Rhodamine labelled antisera against hepatitis B core antigen and e-antigen, evidence is presented that the e-antigen is localised in the nuclei of the hepatocytes. We conclude that the e-antigen and the core antigen are not identical, although they are often present simultaneously in the nucleus of the hepatocyte.

Cell Nucleus↗

HLA in different forms of chronic active hepatitis. A comparison between adult patients and children.

108 adult patients and 34 children with chronic active hepatitis (CAH) are divided in four groups on the basis of presence and absence of hepatitis B surface antigen (HBsAg) and autoantibodies (AutoAb). There are significant differences in the numeric distribution among the four groups and the sex distribution between adult patients and children, but no differences in the frequencies of the HLA antigens tested. An increased frequency of HLA-B8 (and HLA-A1) compared with normal controls and the other groups is only found in autoimmune types of CAH, characterized as HBsAg-negative, AutoAb-positive CAH. HBsAg-negative, AutoAb-negative forms of CAH are called cyptogenic CAH and these are most likely non-hepatitis B virus induced types of CAH. In these and hepatitis B virus induced forms of CAH no significant deviation of any HLA antigen tested could be found.

Adolescent↗

Inhibition of experimental metastatic spread by nonspecific stimulants.

It has been demonstrated by a syngeneic metastatic model of the XVII mouse that pretreatment of the animals with BCG and Freund's adjuvant brings about a significant inhibition of metastatic growth. This inhibition is further increased by combined pretreatment with nonspecific stimulants and additional specific immunisation of the animals against the given tumor.

Animals↗

e System and intrahepatocelullar HBcAG and HBsAG in HBsAG positive patients with liver diseases and healthy carriers.

Patients with hepatitis-B surface antigen positive liver diseases and healthy carriers were studied for the presence of e-antigen and anti-e as well as for intrahepatocellular HBsAG and hepatitis-B core antigen. The e-antigen was demonstrated in 9 out of 12 patients with chronic perisitent hepatitis, in 15 out of 39 patients with chronic active hepatitis, in 3 out of 40 patients with acute type B hepatitis, and in 2 out of 9 patients with a protracted course of type B hepatitis. No e-antigen was found in healthy HBsAG carriers nor in patients with complete recovery from type B hepatitis one year after onset of the disease. Anti-e was detected in 24 out of 61 healthy HBsAG carriers with a normal liver histology and in one patient with a mild form of a chronic persistent hepatitis. The presence of e-antigen in serum was highly associated with the presence of HBcAG in the nuclei of the liver cells. Twenty-seven out of 29 e-positive patients had HBcAG in the liver cell nuclei. In contrast, none of 20 patients with anti-e in serum had HBcAG in the liver cells.

Acute Disease↗

[Chronic mucous effusions of the middle ear and the influence on inner ear function (author's transl)].

Audiometric recordings of children suffering from chronic mucous effusion of the middle ear have revealed a statistically significant and permanent sensorineural hearing loss of high frequences. Attemps for mechanical or physical factors as explanation are not convincing. We believe that inner ear disturbances in chronic mucous effusion rise by direct intoxication of the basal turns of the cochlea caused by pathologic alterations of mucous membrane tissue. Certain substances like lysozymes or histamine are supposed to diffuse via round window membrane to the inner ear. On the other hand mucous effusion which fills the middle cavity prevents oxygen to diffuse from the middle ear to the inner ear. Maass et al. (1976) and Morgenstern (1977) clearly have shown that under physiological conditions oxygen tension in the perilymph of the basal cochlear turn partly depends on diffusion from the middle ear. The results of our clinical observations indicate that early diagnosis and prompt treatment is necessary to prevent permanent sensorineural hearing loss of high frequencies, especially in infants and children.

Audiometry↗

Stimulation of guanylate cyclase by sodium nitroprusside, nitroglycerin and nitric oxide in various tissue preparations and comparison to the effects of sodium azide and hydroxylamine.

Sodium nitroprusside, nitroglycerin, sodium azide and hydroxylamine increased guanylate cyclase activity in particulate and/or soluble preparations from various tissues. While sodium nitroprusside increased guanylate cyclase activity in most of the preparations examined, the effects of sodium azide, hydroxylamine and nitroglycerin were tissue specific. Nitroglycerin and hydroxylamine were also less potent. Neither the protein activator factor nor catalase which is required for sodium azide effects altered the stimulatory effect of sodium nitroprusside. In the presence of sodium azide, sodium nitroprusside or hydroxylamine, magnesium ion was as effective as manganese ion as a sole cation cofactor for guanylate cyclase. With soluble guanylate cyclase from rat liver and bovine tracheal smooth muscle the concentrations of sodium nitroprusside that gave half-maximal stimulation with Mn2+ were 0.1 mM and 0.01 mM, respectively. Effective concentrations were slightly less with Mg2+ as a sole cation cofactor. The ability of these agents to increase cyclic GMP levels in intact tissues is probably due to their effects on guanylate cyclase activity. While the precise mechanism of guanylate cyclase activation by these agents is not known, activation may be due to the formation of nitric oxide or another reactive material since nitric oxide also increased guanylate cyclase activity.

Animals↗

Simultaneous presence of HBsAg and anti-HBs in the serum of different subtypes (serological and immunofluorescent studies).

Serological and immunofluorescent studies were performed in 3 patients with the simultaneous presence of HBsAg and anti-HBs in the serum. Our investigations revealed the following results: HBsAg and anti-HBs in the serum were of different subtypes. HBsAg in the serum and in the liver had the same subtype. HBsAg in the liver did not react with the circulating anti-HBs in the patient's own serum. HBsAg-anti-HBs immune complexes could not be detected in the serum or in the liver tissue. These phenomena can most readily be explained by at least 2 contacts with hepatitis-B-viruses of different subtypes, one leading to immune tolerance and the other to an immune response. In a follow-up study there was no evidence for a short-term change in HBsAg subtype. Unexplained remains the cause why one contact with HBV did lead to immune tolerance and a second to an immune response.

Adult↗

[Sudden deafness as a consequence of rupture of a basilar artery aneurysm (author's transl)].

A sixty-eight year old female patient died from a subarachnoid hemorrhage three days after experiencing sudden hearing loss in her right ear. Autopsy showed that the cause of death was a large aneurism of the basilar artery. Temporal bone sections uncovered a massive infiltrate of erythrocytes about the nerves in the internal auditory canal. The blood cells had extended along the nerve bundles to enter Rosenthal's canal and the other fluid channels of the modiolus, and could be found within all perilymphatic spaces. The presence of hemosiderin within the inner ear correlates clinically with the onset of sudden deafness three days prior to demise, and is substantial evidence for the loss of hearing due to rupture of the basilar aneurism.

Acute Disease↗

Experiments on mechanisms of metastasation: dependence on reaction susceptibility in the host.

The present paper describes experiments on artificial hematogenous metastasation of chemically induced tumours in mice and rats. Total-body irradiation prior to tumour cell application greatly increased metastatic dissemination. The metastasation is significantly inhibited by pretreatment of the animals with a carcinogenic agent. Similarly, a significant inhibition of metastatic growth was observed in primary tumour animals after surgery.

Animals↗

[The characterization of clinically healthy hepatitis-b-surface-antigen (HBsAg)-carriers. Clinical, biochemical, histiological and immunological investigations in 129 case of a prospective study (author's transl)].

129 blood donors found to be HBsAg-positive on routine testing were studied for evidence of hepatic disease. Twelve had already lost the antigen from the serum when histologically examined. None of these has had clinical or histological evidence of inflammatory liver disease. Two of the 129 patients showed mild icteric hepatitis, cleared the antigen during the follow up and became anti-HBs positive. The remaining 115 patients who appeared clinically healthy and who had no history of previous icteric liver disease remained HBsAg positive during a mean follow up period of 17.3 +/- 3.0 months. Forty patients from these had a normal liver histology and 37 mild to distinct steatosis but no signs of inflammatory liver disease. 11 patients a mild nonspecific mesenchymal activity but no focal necrosis, 16 patients had mild infiltration in portal tracts and a few necrotic parenchymal cells with mesenchymal reaction, 6 patients had chronic persistent hepatitis, 4 chronic aggressive hepatitis, and 1 definite posthepatic cirrhosis.

Adolescent↗