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Biomedical subjects

F Gudat

Publications and source records attributed to F Gudat.

At least 127 records · Page 7Linked to original sources

Ultrastructural alterations in hepatocytes and sinus endothelia in experimental non-A, non-B hepatitis in chimpanzees with and without immunoglobulin prophylaxis.

Three chimpanzees were inoculated with an infectious factor VIII preparation. Two of the chimpanzees received in addition a human immunoglobulin preparation as used for prophylaxis in humans. All three chimpanzees developed an acute limited non-A, non-B hepatitis as judged from light and electron microscopic markers after an incubation period of two weeks. The use of immunoglobulin did not prevent the infection. A prolonged incubation of 15 weeks, however, was observed in one animal when alanine aminotransferase (ALT) elevation was used as criterion of infection. In the electron microscope, non-A, non-B hepatitis was characterized by tubular structures, spongelike inclusions and attaching curved membranes, in the absence of nuclear viruslike particles. An additional finding were viruslike particles in crystalline arrays which were found in the cytoplasm of sinusoidal-lining endothelial cells and tubuloreticular complexes.

Animals↗

Characterization of a foamy virus isolated from Cercopithecus aethiops lymphoblastoid cells.

A virus derived from cells of a lymphoblastoid line originating from the lymph node of a healthy African green monkey was characterized as a typical member of the foamy virus subgroup of retroviridae by its morphological, physicochemical, biological and biochemical properties (reverse transcriptase activity). Besides the usual host range of foamy viruses, the isolated strain revealed a remarkable T-lymphotropism, distinguishing it from the prototypes of foamy viruses previously isolated from African green monkeys. Two foamy virus infections are demonstrated in human contacts of the African green monkey colony, with the animal harbouring the isolate.

Animals↗

Experimental non-A, non-B hepatitis in chimpanzees: light, electron and immune microscopical observations.

Two chimpanzees (Pan troglodytes) were inoculated and cross-challenged with a fibrinogen and factor VIII preparation, respectively. Successful non-A, non-B (NANB) infection was documented by biphasic elevations of aminotransferases (ALT), concomitant hepatitic reactions and typical electron microscopic alterations, the most consistent being dilatation of the endoplasmic reticulum, as well as tubular and sponge-like cytoplasmic inclusions in the absence of nuclear virus-like particles. An anti-nuclear (anti-DNA) antibody of the IgM class in one of the chimpanzees simulating an antiviral antibody is described.

Animals↗

Capillary sclerosis of the urinary tract and analgesic nephropathy.

Morphology, frequency and significance of capillary sclerosis (CS) in the ureter and electron microscopic findings in early papillary necrosis are described. CS of the urinary tract is characterized by a thickening of the basement membrane of capillaries lying just underneath the urothelium. The basement membrane changes can be demonstrated by PAS, Sudan stain and autofluorescence with equal reliability. By electron microscopy the thickened basement membranes exhibit a tree ring like pattern permeated by lipid vacuoles. CS is most often present in the renal pelvis and the ureter and only in particularly severe cases also in the urinary bladder. The most severe CS is found in the proximal and middle third of the ureter. In a prospective autopsy study CS was found in 3.5% of autopsies of adults and in 83% of clinically recognized phenacetin abusers. Since there is no association with other renal or metabolic diseases, CS can be considered as specific for phenacetin abuse. This finding is further substantiated by a significant correlation between the degree of severity of capillary sclerosis and the daily dose of phenacetin in grams. In about half of the patients with known analgesic abuse but without CS, possible causes for the lack of CS can be identified, of which the most important is regression of CS after stopping the abuse. Electron microscopic studies of early papillary necrosis show the same BM changes as in the ureter in peritubular capillaries, loops of Henle and similar BM alterations in the collecting ducts. The morphologic findings in the ureter and in the renal papilla suggest that CS in papillary necrosis are the consequence of a toxic damage of endothelial and in the kidney of endothelial and epithelial cells.

Adult↗

[Delta-antigen in hepatitis B].

Among 571 liver biopsies delta-Ag was found in 10 of 365 HBsAg positive patients (9 with CAH, 1 with CPH). Delta-Ag was demonstrated in nuclei and cytoplasm of liver cells in both cryostat and paraffin sections. Follow-up studies revealed persistence of delta-Ag for as long as 6 years and temporary appearance or loss of Dane particle-associated parameters without a change in the concomitant inflammation. These findings are compatible with the hypothesis that delta-Ag represents a defective viral agent which modulates, by superinfection, the typical viral expression patterns of HBV infection.

Hepatitis B↗

[Determination of hepatitis B E antigens, anti-hepatitis B E and Dane particles in the serum of hepatitis B S carriers and patients with chronic hepatitis B S antigen-positive hepatitis].

The correlation of HBeAg, anti-HBe, Dane particles and results of light microscopy of liver biopsies have been studied in 109 patients with chronic HBV infection and in 21 HBsAg carriers. The following conclusions may be drawn: 1. There is a good correlation between the presence of HBeAg and Dane particles. 2. Patients with both of these markers often have chronic active or lobular hepatitis. 3. The presence of anti-HBe points in 80% of these cases to a carriership or chronic persistent hepatitis. 4. 60% of patients without an HBe-marker and 20% of patients with anti-HBe exhibit presence of Dane particles.

Antibodies, Viral↗

Acute hepatitis non-A, non-B; are there any specific light microscopic features?

Coded examination of liver biopsies from a total of 24 patients with acute hepatitis non-A, non-B revealed two main histological trends: (a) acute viral hepatitis with confluent necrosis (sublobular and bridging) carrying a relatively good prognosis and taking a chronic course in only four out of 14 patients (29%); and (b) acute viral hepatitis with severe portal infiltration rich in lymphocytes and plasma cells, lymph follicles with germinal centers and bile duct lesions, as described by Poulsen & Christoffersen. The latter group showed a very high tendency to transition to chronic hepatitis (six out of seven patients, 86%) or a course characterized by one or multiple acute relapses (one out of seven patients, 14%). Bile duct lesions, if present in biopsies of patients with acute hepatitis, are of diagnostic and prognostic value. They point to the etiological possibility of a hepatitis non-A, non-B and, at the same time, they indicate a high likelihood of evolution to chronic liver disease.

Adult↗

An improved method for HBcAg demonstration in paraffin-embedded liver tissue.

Factors influencing the preservation of HBcAg in formalin-fixed, paraffin-embedded liver tissue have been analysed. Fixation time, choice of the embedding medium, deparaffinization and selection of anti-HBc proved to be critical variables. For optimal results, fixation in 4% buffered formalin for no longer than 24-48 h, the use of wax with a low melting point, a heating step prior to deparaffinization, and a search for anti-HBc specifically reactive for paraffinated HBcAg are recommended.

Fixatives↗

[Determination of leukemic B-lymphoma cells with the monoclonal antibody anti-Y 29/55].

The monoclonal antibody anti-Y 29/55 recognizes a group specific antigen on sessile human B-lymphocytes which do not belong to the recirculating lymphocyte pool. The occurrence of this antigen in malignant NHL, with or without leukemic state, and in other leukemias has been studied. The antigen was expressed on cells of various histologic B-cell types but not on leukemic cells of ALL, T-lymphoma, AML or CML. It is concluded that in malignant B-lymphoma, B-CLL and HCL, cells appearing in blood carry a marker characteristic of virgin or activated sessile B-lymphocytes. Anti-Y 29/55 permits differentiation of such cells from normal recirculating B-cells and other leukemic cells including ALL, AML and CML. In follow-up studies this antibody may be helpful in detecting early leukemic output. B-lymphocytic leukemia may reflect a disproportion between binding sites on the lymphatic reticulum and the neoplastic cells bearing this antigen, which might be involved in binding of B-lymphocytes to the supporting lymphatic reticulum.

Antibodies, Monoclonal↗

[The diagnostic value of T- and B-rosette formation and the unspecific acid esterase in the differential diagnosis of acute and chronic leukemia].

The diagnostic significance of acid non-specific alpha-naphthyl-acetate (ANAE) and of rosette formation of leukemic cells with sheep and mouse erythrocytes was studied in 8 patients with acute myeloic leukemia (AML), in 4 patients with acute lymphatic leukemia (ALL) and in 14 patients with chronic lymphatic leukemia (CLL). ANAE showed typical diffuse cytoplasmic activity in all cases of AML. The enzyme activity was granular in both of the lymphoid malignancies, T-ALL and B-CLL, allowing differentiation from AML but not between B- and T-leukemia cells. Rosette formation with mouse erythrocytes (ME) was diagnostic in all 14 cases of CLL and superior to labeling of surface immunoglobulin (8 of 14 cases positive). ME-rosette forming myeloblasts were detected in 2 of 4 evaluated cases of AML. Rosette formation with sheep erythrocytes (SE), including cytological evaluation of rosette-forming cells, was diagnostic in all cases of ALL (= T-ALL). In 6 of 9 patients with AML, however, rosette formation with SE was observed in a few cells, including myeloblasts with Auer rods. The occurrence of blasts in myeloic leukemia carrying lymphoid cell markers is discussed in the light of recent findings, according to which lymphoblastoid cells may arise in the course of myeloic leukemia requiring antileukemic treatment different from that of AML.

Animals↗

Shape changes induced by biologically active peptides and nerve growth factor in blood platelets of rabbits.

1 Nerve growth factor (NGF), substance P (SP) and thymopoietin all caused shape change reactions of rapid onset in rabbit platelets. NGF had the highest maximal effect, and SP the lowest EC50 (concentration causing half maximal shape change). The action of SP was reversible within 5 min, whereas that of NGF lasted for at least 1 h. A series of other peptides were inactive. 2 After preincubation of platelets with SP, a second application of SP no longer caused a shape change reaction, whereas the effect of NGF was not influenced. 3 An oxidized NGF-derivative without biological activity did not cause a shape change reaction, neither did epidermal growth factor. 4 Prostaglandin E1 (PGE1) and pretreatment of the platelets with 3% butanol, which counteract the shape changes caused by 5-hydroxytryptamine (5-HT) and adenosine 3',5'-diphosphate, also antagonized those induced by NGF and SP. Neither heparin nor methysergide, an antagonist of 5-HT-receptors, influenced the shape change induced by NGF or SP. The action of NGF was also antagonized by a specific antibody to NGF. 5 Thymopoietin, like the basic polypeptide polyornithine (mol. wt. 40,000) was not antagonized by PGE1 and butanol. Heparin, which counteracted the effect of polyornithine, did not influence that of thymopoietin. 6 In conclusion, different modes of action are involved in the shape change of blood platelets induced by polypeptides and proteins. SP and NGF may act by stimulating specific membrane receptors.

Animals↗

Acute viral hepatitis B with bridging necrosis: a follow-up study.

Forty patients with bridging necrosis (BN) on biopsies taken during the course of acute viral hepatitis B were included in a prospective study to assess the prognostic significance of this lesion. Of the 22 patients with complete clinical, biochemical and histological follow-up (histological follow-up 5-33 months), only two failed to eliminate HBs- and HBe-antigen in serum, a finding paralleled by transition to chronic active hepatitis and by the persistence of focal HBc- and HBs-antigen expression in liver tissue. Nineteen of 22 patients showed complete histological healing; one developed inactive cirrhosis. It is concluded that, in the setting of acute viral hepatitis B, the histological lesion of BN is of no particular prognostic significance, and that transition to chronic liver disease is much less frequent than has been assumed from previous studies of etiologically heterogeneous patient populations. Markers of poor prognosis are the failure of serological elimination of HBs- and HBe-antigen and the persistence of spotty expression of HBc- and HBs-antigen on immunofluorescence histology.

Acute Disease↗

Schönlein-Henoch glomerulonephritis. Characteristic ultrastructural changes in the glomerular basement membrane and localisation of osmiophilic deposits.

In glomerulonephritis accompanying the Schönlein-Henoch syndrome (SHS) a characteristic subepithelial basement membrane change is present in 85% of cases. The subepithelial change is a reaction to subepithelial deposits and consists of a garland or dome-like new formation of thin densa lamellae. This change is much more frequent in SHS than in IgA-nephritis or idiopathic glomerulonephritis or any other systemic disease. Furthermore, subepithelial deposits (50% of cases) are nearly as frequent as subendothelial deposits (65%) and more often present than formerly assumed.

Adolescent↗

Immunothrombocytopenia and IgA nephritis.

A 32 year old female patient demonstrates the rare combination of a typical IgA nephritis and familial immunothrombocytopenia. Although this association may be purely fortuitous, our observation adds a new facet to a spectrum of reports on (familial) "thromborenal syndromes". The pathogenesis of the IgA nephritis has not yet been clarified. However, since IgA deposits are found relatively frequently in the mesangium in a number of diverse underlying diseases, there might be common etiological factors. In view of this possibility more attention should be directed to the investigation of IgA associated diseases.

Adult↗