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Biomedical subjects

F Jacobsen

Publications and source records attributed to F Jacobsen.

At least 37 records · Page 2Linked to original sources
PubMed1987

Nephroid metaplasia of the urinary tract. A survey of the literature, with the contribution of 5 new immunohistochemically studied cases, including one case examined by electron microscopy.

Nephroid metaplasia is an unusual lesion confined to the lamina propria of the lower urinary tract. It is defined by a characteristic histologic picture of tubular structures, formed by a single layer of cuboidal cells, surrounded by a thick basement membrane. Two main theories concerning the histogenesis of the condition have been proposed: embryonic origin, or metaplasia. Five cases of nephroid metaplasia were studied light-microscopically and by immunohistochemistry for the content of Tamm Horsfall's uromucoprotein. In addition, one case was examined by electron microscopy. The results were compared to current knowledge of the lesion obtained from a survey of the literature, with special reference to histogenesis. Morphologically, one case of nephroid metaplasia was associated with mesonephroid adenocarcinoma. It is concluded that nephroid metaplasia arises as a metaplastic lesion, nearly always in previously traumatized urothelial mucosa. The natural history of the typical nephroid metaplasia is benign, but a possible relationship to mesonephroid adenocarcinoma, representing the malignant counterpart of the lesion, is discussed in relation to the histological findings, suggesting a rare but possible malignant potential of nephroid metaplasia. The diverse nomenclature used for this histologic entity needs re-evaluation and should be changed to: nephroid metaplasia.

Adenocarcinoma↗
PubMed1987

Transurethral treatment of invasive tumours of the urinary bladder (T1, T2): recurrence and progression.

Forty-six newly diagnosed patients with T1 and T2 bladder tumours were treated with radical transurethral resection. During a six-month period more than 50% of the tumours recurred. Subsequently progression of tumours was seen within 24 months in 30 and 50% of the patients with T1 and T2 tumours, respectively. Prognosis with regard to the progression was significantly better in patients with Ta recurrence at first TUR control than in patients with invasive recurrent tumours.

Aged↗
PubMed1985

Flat intra-epithelial carcinoma in situ of the urinary bladder.

A follow-up investigation of 19 patients with carcinoma in situ per se of the urinary bladder (Tis) has been performed. Ten patients developed invasive cancer during a mean observation period of about 4 years. The natural history is unpredictable and therapeutic management of this potentially malignant neoplasm should be individualised. Early radical cystectomy is advocated in selected cases of Tis.

Aged↗
PubMed1985

Vascular graft infection: an analysis of sixty-two graft infections in 2411 consecutively implanted synthetic vascular grafts.

Among 2411 consecutive arterial reconstructions performed with synthetic prosthetic material in Denmark during a 4-year period, 62 patients (2.6%) developed graft infection. Graft infection occurred only when the groin had been incised. The incidence of infection and the spread of infection along the graft did not relate to the graft material used (Dacron velour, Dacron woven, polytetrafluoroethylene, and umbilical vein). Retrospective analysis disclosed predisposing or precipitating factors in 50 of the 62 cases; the most important seemed to be unsatisfactory surgical technique. Fifty-three percent of the graft infections occurred within 30 days. Gram-positive cocci were the most common pathogen. The 62 patients had been in the hospital for a mean of 90 days and had undergone an average of 1.4 operations for graft infections. Of the patients, 25.8% died and 30.6% underwent amputations. Vascular graft infection is still one of the major problems in vascular surgery; greater care should be taken to improve antiseptics, improve surgical technique, and establish a rational prophylactic antibiotic regimen. A prophylactic antibiotic regimen of a combination of cephalosporin and ampicillin is recommended.

Anti-Bacterial Agents↗
PubMed1983

Use of Trypanosoma equiperdum infected rabbits as a source of splenic mRNA; construction of cDNA clones and identification of a rabbit mu heavy chain clone.

Rabbits were infected by Trypanosoma equiperdum and the splenic mRNA was isolated. In vitro translation of this RNA and immunoprecipitation with anti-light chain, anti-heavy chain, anti-mu and anti-VH antibodies demonstrated that T. equiperdum infection elicits large quantities of splenic mRNA encoding mu and kappa chains. The mu and gamma heavy chains and the kappa light chains synthesized in the cell-free translation system were specifically immunoprecipitated by antisera to heavy chain VHa and light chain kappa b allotypes. In vitro labeling of spleen cells from trypanosome-infected animals demonstrated that the biosynthetically labeled IgM has a mu chain of higher molecular weight than the mu chain synthesized by in vitro translation, a difference that is largely abolished when cellular glycosylation is blocked with the antibiotic tunicamycin. Enrichment for heavy chain or light chain mRNA was achieved by fractionating mRNA from trypanosome-infected animals on a sucrose gradient. cDNA clones carrying mu heavy chain sequences were produced using a 'one tube' protocol and identified by cross species hybridization and hybridization selection. Infection of rabbits with T. equiperdum followed by sucrose gradient enrichment of splenic mRNA has provided sufficient quantities of mRNA encoding mu heavy chain suitable for cDNA cloning.

Animals↗
PubMed1983

Analyses of the splenic mRNA expressed by rabbits of different immunoglobulin kappa-light chain allotypes: conserved sequences in the 3' untranslated region and allotype-specific probes.

The allelism of the structural genes for the complex rabbit b allotypes of immunoglobulin kappa-light chains has been questioned because of observations of unexpected phenotypic expression of "latent" allotypes. We find that the coding sequences of the b4 and b5 "alleles" are only 80% homologous for the last 60 nucleotides but there is a high degree of homology (96%) in the 3' untranslated region (3'DT). The high conservation of 3' DT region sequences enabled us to detect kappa-light chain mRNAs from rabbits of different genetic types (b4, b5, b9 and bbas) on northern blots and dot blots. We can distinguish mRNA encoding b9 and b5 allotypes on dot blots with b5 fragment-probes of known sequence and detect mRNA produced by unstimulated cultured splenic lymphocytes. Analyses of mRNA from cultured cells manipulated to enhance mRNA synthesis and production of unexpected or "latent" b allotypes can now be conducted.

Animals↗
PubMed1982

The influence of prednisone on serum angiotensin-converting enzyme activity in patients with and without sarcoidosis.

The influence of prednisone on S-angiotensin-converting enzyme (SACE) activity was examined by serial measurements in 20 non-sarcoidosis patients and 8 sarcoidosis patients on prednisone, compared with 26 patients and healthy controls not under treatment. All but the sarcoidosis patients had SACE within normal limits (12.0-36.8 kU/l). In the three groups initial or pretreatment SACE levels (mean +/- SD) were 20.1 +/- 5.7, 66.9 +/- 27.4 and 26.4 +/- 4.1 kU/l, respectively. Non-sarcoidosis patients on prednisone had a lower pretreatment SACE than untreated control persons, presumably due to the different diseases represented in the groups. During the observation period SACE was rather stable in untreated patients and also in the treated group as a whole. But in 12 patients with SACE greater than 18.2 kU/l (mean of reference series minus 1 SD) a significantly decreasing SACE was observed after 1 week of treatment, whereas SACE was unchanged in patients with lower pretreatment levels, suggesting that in these patients prednisone could not decrease any further a level which was already low. In sarcoidosis the elevated SACE declined, reaching a normal level after 4 weeks on prednisone. In the assay ACE was markedly inhibited by SQ 14,255 (Captopril), moderately by methylprednisolone in concentrations exceeding those generally used clinically, while no inhibition was seen using acetylsalicylic acid.

Adolescent↗
PubMed1982

Increase of the in vitro complement-dependent cytotoxicity against autologous invasive human bladder tumor cells by neuraminidase treatment.

Complement-dependent cytotoxicity (CDC) was measured in a 51-Cr release assay against tumor cells from 13 non-invasive and 7 invasive transitional-cell tumors of the urinary bladder. CDC was compared between mechanically dispersed tumor cells and neuraminidase-treated tumor cells. Neuraminidase treatment of bladder tumor cells enhanced their susceptibility to complement-dependent cytolysis. There were no differences in CDC between autologous and allogenic sera. Mechanically dispersed tumor cells showed no significant differences in susceptibility when non-invasive and invasive tumor cells were compared, whereas significant differences in CDC were seen when neuraminidase-treated non-invasive and invasive tumor cells were used as targets. A C2 deficient serum showed significantly reduced cytotoxicity suggesting that the CDC reaction requires classical complement activation. A hypogammaglobulinemic serum showed stronger CDC compared to autologous and other allogenic sera and upon dilution of autologous sera and hypogammaglobulinemic serum CDC declined parallelly.

Adult↗
PubMed1981

Lymphocyte cytotoxicity against autologous bladder tumor cells in humans, investigated by use of a chromium-51 release assay.

A technique for isolation of a single cell suspension of viable tumor cells from bladder tumor biopsies is described. By application of the tumor cells as targets in a 51chromium release assay, the cytotoxicity of autologous lymphocytes was measured in 38 patients with transitional-cell tumors of the urinary bladder. The lymphocyte-medicated cytotoxicity was evaluated in relation to the histological grade and clinical stage of the bladder tumors. No significant correlations were found between the autologous cytotoxicity and the grade or stage of the bladder tumors.

Aged↗
PubMed1981

Cellular and humoral in vitro cytotoxicity against autologous bladder tumor cells in humans. Differences in autologous cytotoxicity against non-invasive and invasive transitional-cell tumors of the urinary bladder.

Lymphocyte-mediated cytotoxicity (LMC), antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) were measured in a 51Cr assay against autologous tumor cells from 7 patients with non-invasive and 9 patients with invasive transitional-cell tumors of the urinary bladder (TCC). Cytotoxicity against the invasive tumor cells were demonstrated in CDC. Heat-inactivation of sera lead to complete loss of cytotoxicity while addition of allogenic serum restored cytotoxicity. The cytotoxicity of allogenic sera from controls against invasive tumor targets showed no differences when compared with autologous sera. No or very weak cytotoxicity was found against non-invasive tumor targets in autologous or allogenic assays. LMC and ADCC showed weak or no reactivities. Intensive wash or trypsinization of effector cells did not affect the cytotoxicity in LMC. The results indicate the occurrence of complement-dependent antibodies directed against target cells from invasive tumors of the urinary bladder while no cytotoxic responses were detectable when the target cells originated from non-invasive tumors.

Adult↗
PubMed1981

In vitro cytotoxicity of lymphocyte subpopulations against autologous human bladder tumor cells.

The in vitro cytotoxicity of unfractionated blood lymphocytes and T and non-T lymphocytes respectively, was tested against autologous tumor cells from 21 patients with grade III-IV urothelial bladder carcinomas. Generally, little or no cytotoxicity was seen. However, some differences in autologous cytotoxicity between T and non-T lymphocytes were detectable. Four of 21 patients had cytotoxic non-T lymphocytes against autologous bladder tumor cells. The results indicate, that the effector cells are primarily non-T lymphocytes, and that cytotoxicity appears at lower levels of T lymphocytes in unfractionated lymphocyte preparations.

Adult↗
PubMed1981

Complement-dependent in vitro cytotoxicity against autologous invasive bladder tumor cells in humans. Evaluation of the possible role of naturally-occurring antibodies in complement-dependent cytotoxicity.

Complement-dependent serum-mediated cytotoxicity (CDC) was measured in a 51-chromium release assay against autologous tumor cells from 7 non-invasive and 9 invasive transitional-cell tumors of the urinary bladder. CDC was demonstrated against tumor cells from invasive tumors. Heat-inactivation of autologous sera lead to complete loss of cytotoxicity. There were no differences in CDC of autologous sera from patients and allogenic sera from controls. The cytotoxic response seems to be strongly dependent on the target cell. CDC was significantly reduced by use of an allogenic C 2 deficient serum. Direct immunofluorescence did not reveal any tumor cell associated immunoglobulins of IgG or IgM classes. Indirect immunofluorescence with autologous heat-inactivated sera demonstrated in most cases both IgG and IgM attachment to the tumor cells, but there were no obvious relations between indirect immunofluorescence and CDC. Absorption of allogenic sera to trypsin- or neuraminidase-treated erythrocytes did not affect CDC of these sera against invasive tumor targets. The results indicate a complement-dependent cytotoxicity against target cells from invasive bladder tumors. Complement seems to be activated through the classical pathway, but the possible role of naturally-occurring antibodies against invasive tumor targets is not clarified.

Aged↗
PubMed1980

Acute effects of insulin on plasma noradrenaline and the cardiovascular system.

It is now known that insulin has marked acute effects on plasma noradrenaline and the cardiovascular system. These effects of insulin are not due to hypoglycemia and occur without changes in plasma adrenaline. Intravenous injection of insulin in juvenile diabetics increased plasma noradrenaline and heart rate and decreased glomerular filtration rate, renal and peripheral blood flow, and plasma volume. Urinary excretion rates of beta-2-microglobulin and urinary volume decreased after insulin, whereas urinary albumin excretion increased. When blood glucose was maintained by glucose infusion after insulin, glomerular filtration rate and renal blood flow remained unaltered whereas plasma noradrenaline, heart rate, and urinary albumin excretion increased and beta-2-microglobulin excretion decreased. Decreases in glomerular filtration rate and renal blood flow after insulin are thus due to the fall in blood glucose. Rise in albumin excretion after insulin is probably of glomerular origin and not caused by the fall in blood glucose or by changes in renal hemodynamics. In patients with long-term diabetic nephropathy and albuminuria, insulin decreased albumin excretion (probably due to renal vasoconstriction) and plasma noradrenaline did not increase. In alloxan-diabetic rabbits the increase in heart rate after insulin was not abolished by autonomic blockade. In short-term streptozotocin-diabetic rats, muscle capillary endothelial cells showed a reduced number of free micropinocytotic vesicles. The number was nearly normalized 1 hr after intramuscular injection of insulin. The mechanism of action of insulin on plasma noradrenaline, heart rate, plasma volume, and urinary albumin excretion is not known. The rise in plasma noradrenaline after insulin may be compensatory to hypovolemia or to antagonizing effects of insulin on some actions of noradrenaline. The findings in streptozotocin-diabetic rats suggest that insulin may be essential for the normal function of capillary endothelial cells.

Adult↗
PubMed1979

Stimulation of heart rate by insulin: uninfluenced by beta-adrenergic receptor blockade in rabbits.

Intravenous injection of insulin increased heart rate approximately 20% in six alloxan-diabetic rabbits. Blood glucose concentrations after insulin did not decrease below the fasting level of non-diabetic animals and none of the rabbits had signs of hypoglycermia. Intravenous injection of saline or insulin solvent had no effect on heart rate. The stimulatory effect of insulin on heart rate was not influenced by autonomic nervous blockade by propranolol or by propranolol plus atropine.

Adrenergic beta-Antagonists↗