Biomedical subjects

G Tallqvist

Publications and source records attributed to G Tallqvist.

At least 19 recordsLinked to original sources

PubMed1994

Replication errors in benign and malignant tumors from hereditary nonpolyposis colorectal cancer patients.

A replication error (RER) phenotype has been documented both in sporadic colorectal tumors and in tumors from patients with hereditary nonpolyposis colorectal cancer (HNPCC). In the current study 8 of 49 (16%) sporadic colorectal cancers (CRCs) and 25 of 29 (86%) CRCs from HNPCC patients were found to be RER+. All 9 (100%) CRCs from HNPCC patients with germline mutations of the mismatch repair gene MSH2 were found to be RER+, while 16 of 20 CRCs from HNPCC kindreds unlinked or not studied for linkage to MSH2 were RER+. Corresponding analysis in colorectal adenomas revealed that only 1 of 33 (3%) sporadic tumors but 8 of 14 (57%) HNPCC tumors were RER+. Moreover, RER was found in all 6 extracolonic cancers (endometrium, 2; kidney, 1; stomach, 1; duodenum, 1; and ovary, 1) derived from members of HNPCC families. These data suggest the involvement of mismatch repair deficiency in the premalignant stage of tumorigenesis in HNPCC cases, and suggest that mismatch repair genes (MSH2 or others) are defective in the germline of nearly all these patients.

Adenoma↗

PubMed1989

Mammography screening for breast cancer: first year results from Helsinki and surroundings.

11,789 women aged 50-59 years were invited for screening by the mammography screening centre of the Cancer Society of Finland in Helsinki. 9829 women (83.37%) attended and 3.85% of those were recalled for further studies. After complete examination seventy-one women (0.72%) were referred for surgical biopsy and breast cancer was histologically detected in 44 (0.45%) of those screened. The proportion of Stage I + TIS breast cancers detected was 75%, and of Stage II or more advanced, 25%. With modern mammography techniques and proper training of technicians and radiologists, with double reading of all the films, it is possible to minimise both the recall rate and the number of women who are referred for surgical biopsy, and still find cancers in their early stages.

Breast Neoplasms↗

PubMed1983

[Kidney biopsy].

Explore the source record for details and available documents.

Biopsy, Needle↗

PubMed1982

Effect of cyclosporin A on the in situ inflammatory response of rat renal allograft rejection.

The impact of cyclosporin A (CyA) on a normal kidney parenchyma and on the in situ inflammatory response of rejection was investigated in normal DA rats and after transplantation of DA renal allografts to Lewis recipients. In a normal, non-transplanted DA kidney more than 80 mg/kg/day of CyA induced light-microscopic changes in the distal tubular cells of the renal cortex and outer medulla. These changes were not accompanied by any visible inflammation and were directly proportional to the dose of the drug and to the duration of drug administration. Treatment of a transplant recipient with 40 mg/kg/day of CyA abolished or at least efficiently reduced the in situ inflammatory response of rejection both as analysed from tissue sections and as quantified from the recovery of inflammatory cells after enzymatic digestion. It also reduced efficiently not only the number of T and B blast cells of the inflammatory infiltrate but also the number of other inflammatory cells, such as in situ lymphocytes, monocytes, and macrophages, and abolished or at least reduced the generation of (T) killer cells in situ and in the recipient spleen. These effects were inversely proportional to the time elapsed between grafting and initiation of treatment: although a complete suppression of all three features was obtained if the drug treatment was initiated already on the day of transplantation, a significant reduction of these functions was still found if the treatment was initiated later when the blastogenic response was already underway.

Animals↗

PubMed1980

Survival in idiopathic glomerulonephritis.

Actuarial survival was studied in 285 adult patients with idiopathic glomerulonephritis (GN). Minimum follow-up was 7 years. 105 patients had minimal change GN (MC), 22 membranous GN (MGN), 20 acute GN (AGN), 11 mesangial sclerosis Gn (MSGN), 28 mesangiocapillary GN (MCGN), 8 crescentic GN (RPGN), 27 unclassifiable GN, 61 focal proliferative GN (FGN), and 3 focal segmental glomerular sclerosis and hyalinosis (FSGSH). Ten year survival was best in FGN (91%), and progressively poorer in MC (90%), AGN (85%), MSGN (83%), MGN (82%), MCGN (62%), unclassifiable GN (37%), and RPGN (16%). One of the three patients with FSGSH died during follow-up. At 10 years, survival differed significantly (p less than 0.01) from expected only in MCGN, RPGN and unclassifiable GN. Our results suggest that -- because survival was not significantly different from expected in most types of GN -- the current classification of GN is only a crude guide to prognosis. The nephrotic syndrome was found to worsen prognosis in MGN and MCGN.

Adolescent↗

PubMed1978

Nonprogressive, histologically mild membranous glomerulonephritis appearing in all evolutionary phases as histologically "early" membranous glomerulonephritis.

Seven adult patients with idiopathic nephrotic syndrome and with a glomerular histology considered normal but with ultrastructurally provable membranous glomerulonephritis (MNG) were studied. The glomerular lesions were found to represent all ultrastructural evolutionary phases (A,B, and C) of MGN. In patients with serial biopsies, the membranous lesion seemed to have passed through all of its evolutionary phases towards healing (C) without developing spikes or thickening of the glomerular basement membrane (GBM), i.e., the traditional light microscopic characteristics of MGN. This evolution was associated with a benign clinical course. The membranous lesions were associated with a vacuolization visible in obliquely or tangentially cut segments of the GBM in silver-stained paraffin sections. This alteration seemed to be created by irregularities of the argyrophilic lamina densa of the GBM and not by subepithelial deposits, as suggested previously. All seven patients had a remission of the nephrotic syndrome which appeared to be spontaneous and not drug-induced. The amount of proteinuria correlated with the ultrastructural phase of MGN and with the intensity of immunofluorescent staining. In one patient, the latter became negative.

Adrenal Cortex Hormones↗

PubMed1977

Two XX males in one family and additional observations bearing on the etiology of XX males.

Two XX males who were second cousins are reported. A genetic mechanism producing maleness is suggested. The putative factor had been transmitted solely through males, which excludes the possibility of a heritable X-Y interchange. Recent reports on fluorescent Y chromatin in Sertoli cells of XX males prompted investigations into the fluorescence patterns of testicular cells. Sertoli cells from three XX males displayed brightly fluorescent spots, but it was concluded that they did not represent Y chromosomes. Evidence for this conclusion was obtained from the study of testicular fluorescence in XX, XXY and XY males. No visually detectalbe cytogenetic evidence for an increase in length or altered banding pattern of one of the X chromosomes was found in three XX males. We conclude that an autosomal gene is the most likely explanation of the male differentiation in the two XX males presented here.

Adolescent↗

PubMed1976

Indentations of the glomerular basement membrane in renal diseases. A light and electron microscopic study on ultrathin serial sections.

Indentations of the glomerular basement membrane were observed by light microscopy in ultrathin Epon-embedded serial sections from the renal biopsies of patients who had membranous glomerulonephritis, minimal change glomerulonephrits, acute or resolving exudative glomerulonephritis and focal glomerulonephrits, interstitial nephritis, amyloidosis, rheumatoid arthritis, or ankylosing spondylitis. In patients with membranous glomerulonephritis, acute or resolving exudative glomerulonephritis, amyloidosis, or rheumatoid arthritis, the occurrence of indentations in the glomerular basement membrane differed significantly from that in controls. The presence of indentations did not correlate with proteinuria, hematuria, leukocyturia, arterial hypertension, or with the nephrotic syndrome or its treatment with steroids. Examination of alternate serial sections by light and be electron microscopy showed that the indentations that were light microscopically visible corresponded to craters on the epithelial surface of the glomerular basement membrane seen in the electron microscope. These craters contained protruding portions of the epithelial cells, extracellular electron-lucent material or electron-dense amorphous or striated membranous material. They were often surrounded by spikelike protrusions of the lamina densa. These indentations might represent solitary remnants of former subepithelial deposits.

Antigen-Antibody Complex↗

PubMed1975

Anicteric liver damage during nitrofurantoin medication.

Four patients are described in whom anicteric hepatitis appeared to be related to the use of nitrofurantoin. All the patients had increased serum transaminase levels, hypergammaglobulinaemia, and liver biopsies suggestive of chronic active hepatitis. Three patients showed cirrhotic features in the biopsy and two had circulating albumin-IgG-complexes ('tailing-albumin'). The serum transaminases became normal within weeks after withdrawal of the drug whereas the hypergammaglobulinaemia and the liver biopsy findings persisted essentially unchanged during two to six months of observation. One patient was re-challenged with nitrofurantoin, which resulted in recurrence of elevated serum transaminases after nine weeks medication.

Aged↗

PubMed1975

Studies of rectal mucosal catecholamines in ulcerative colitis.

Rectal mucosal biopsies from six patients suffering from ulcerative colitis were studied by estimating the catecholamine (CA) content and by fluorescence microscopy. Adrenergic nerve fibres were relatively scanty both in diseased and control patients. The adrenergic structures seem well preserved in the affected areas of the colon, although the nonspecific collagenous autofluorescence makes interpretation difficult. There was a significant rise in the noradrenaline (NA) content compared with the seven control patients (p smaller than 0.01). This may be a compensatory phenomenon to inhibit increased intestinal motility. The increased NA level may be due to the intense perivascular adrenergic plexus typical for ulcerative colitis. In both groups there were varying amounts of fluorescing enterochromaffin cells probably without relation to the diagnosis.

Adult↗

PubMed1974