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Biomedical subjects

T Jensen

Publications and source records attributed to T Jensen.

At least 55 records · Page 3Linked to original sources
PubMed1998

[Clinical wound botulism in injecting drug addicts].

Wound botulism among drug abusers was first described in the USA in 1982. From 1988 to 1995, 46 laboratory confirmed cases were reported in California. The condition occurred for the first time in Norway in 1997 when three cases of suspected wound botulism among drug users who injected heroin subcutaneously or intramuscularly were reported. Two of these cases are presented here with neurophysiological findings and differential diagnosis.

Adult↗
PubMed1998

[Botulism after intake of half-fermented fish].

From 1975 to 1997, 21 cases of foodborn botulism have been reported in Norway. Half-fermented fish is the major cause. We describe one patient with botulism following intake of home-prepared half-fermented fish. Seven people had eaten fish from the same bucket, but only two developed symptoms. The fish was initially stored at 13 degrees C; this probably explains why toxin developed. Type E toxin in moderate concentrations was found in fish samples. The patient was treated with specific antitoxin and made a gradual recovery. He returned to work after eight months.

Adult↗
PubMed1998

[Combination therapy of rheumatoid arthritis].

The prevalence of rheumatoid arthritis (RA) is about 0.5-1%. The disease course is variable, but RA causes substantial morbidity and mortality. The effect of conventional therapy for RA, i.e. nonsteroidal antiinflammatory drugs (NSAID), glucocorticosteroids and Slow Acting Anti-Rheumatic Drugs (SAARD) including methotrexate, gold salts, anti-malarials, d-penicillamine and salazopyrine, is often suboptimal. Since the aim of treatment is a complete remission, combination therapy, i.e. treatment with two or more SAARDs, may be feasible since an additive/synergistic effect may be obtained. In this paper the literature about the effectiveness and toxicity of combination therapy is reviewed. Only a few randomized, clinically controlled trials have been published. None of them have documented that gold salts, d-penicillamine and azathioprine in combination with other SAARDs are better than monotherapy. However, recent trials have indicated that methotrexate in combination with salazopyrine and hydroxychloroquine or in combination with cyclosporine may cause a better therapeutic effect than methotrexate alone, without additional toxicity. Long term studies of the effect of combination therapy are not yet available.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

The vitamin D3 receptor and retinoid X receptors in psoriatic skin: the receptor levels correlate with the receptor binding to DNA.

It is unknown whether vitamin D3 analogues improve psoriasis by overcoming an intrinsic abnormality of the vitamin D3 signalling pathway in psoriatic skin. The effects of vitamin D3 are mediated through the vitamin D3 receptor (VDR). The VDR heterodimerizes with another transcriptional regulator, preferentially the retinoid X receptor (RXR). In the present study the levels of VDR and RXR in involved and uninvolved psoriatic skin were determined by immunoblotting, and the binding of the VDR-RXR complex to a vitamin D3 response element (VDRE) consisting of two hexanucleotides spaced by three nucleotides (DR-3) by the electrophoretic mobility shift assay. The levels of VDR were similar in involved and uninvolved skin. RXR alpha, but neither RXR beta nor RXR gamma, was detectable. The RXR alpha levels were slightly lower in involved psoriatic skin than in uninvolved psoriatic skin, but this difference was statistically insignificant. The binding of VDR-RXR to the DR-3 VDRE was similar in uninvolved and involved psoriatic skin. Furthermore, there was a strong linear correlation between the levels of both VDR and RXR alpha and their binding to DNA. In conclusion, the initial part of the vitamin D3 signalling pathway involving receptor levels and receptor binding to DNA is normal in involved psoriatic skin.

Carrier Proteins↗
PubMed1998

Aberrant expression of tissue-specific proteins in the thymus: a hypothesis for the development of central tolerance.

Herein we present the case for the existence of a thymic cortical epithelial cell that possesses an unusual gene transcription. It produces tissue-specific proteins that have their usual physiological functions outside the thymus and presents them, as well as household proteins, to the differentiating thymocytes. We suggest that this specialized cell enforces tolerance to most self-proteins by causing release of a signal for programmed cell death to thymocytes that express receptors for these self-antigens.

Animals↗
PubMed1998

Cervical human immunodeficiency virus type 1 shedding is associated with genital beta-chemokine secretion.

Forty human immunodeficiency virus type 1 (HIV-1)-infected women participated in a cross-sectional study of possible correlations between chemokine receptor (CCR5 and/or CCR2B) genotype, HIV-1 RNA and DNA load, and beta-chemokine levels (RANTES, MIP-1alpha, MIP-1beta) in blood and cervix. HIV-1 nucleic acid and beta-chemokines were found in all patient blood samples and in more than half of the cervical samples regardless of CCR5 or CCR2B genotype. High beta-chemokine concentrations were in general associated with high virus loads in blood and cervix. In the blood, the proviral DNA load was significantly correlated with the MIP-1alpha concentration, whereas the DNA load in cervix was significantly associated with the MIP-1beta concentration. The cervical viral RNA load was significantly associated with levels of all three chemokines. Thus, when HIV-1 shedding was highest in the genital tract, it was associated with other combinations of beta-chemokines than virus load in blood, suggesting that local immune reactions strongly influence virus load in the cervical compartment.

Cell Line↗
PubMed1998

Distinct determinants of human immunodeficiency virus type 1 RNA and DNA loads in vaginal and cervical secretions.

The relationship between human immunodeficiency virus type 1 (HIV-1) viral RNA and proviral DNA load in vagina and cervix and that found in the plasma and peripheral blood mononuclear cells (PBMC) was investigated in 28 HIV-1-infected women. Of the patients, 64% had > or = 1 HIV-1 RNA-positive genital sample, while 71% had > or = 1 DNA-positive sample. The higher the cervical HIV load, the more widespread was the virus in the genital tract. A strong correlation was found between viral RNA load in plasma and the genital tract, whereas the association between proviral DNA load in PBMC and the genital tract was less evident. Cervical HIV-1 DNA correlated with a viral RNA load > or = 50,000 copies/mL. Cervical HIV-1 RNA levels ranged from 10% to 100% of the plasma levels. Thus, a continuous transmission risk from untraumatized genital epithelium exists in the majority of HIV-1-infected women at all stages of infection.

Blood Transfusion↗
PubMed1998

Lake Vera revisited: parity and survival rates of Anopheles punctipennis at the site of a malaria outbreak in the Sierra Nevada foothills of California.

Parity and survival rates of Anopheles punctipennis were studied at the site of a 1952 outbreak of malaria in the Sierra Nevada foothills of California with the purpose of estimating blood feeding frequency and survivorship of such populations. Anopheles punctipennis was the dominant species in landing collections conducted for 20 consecutive nights in August and September 1990. The mean parity rate of An. punctipennis was 0.82. The gonotrophic cycle was estimated to last three days based on time series analysis of the number of nulliparous and parous mosquitoes collected each day. Survivorship was estimated to be 0.79 per gonotrophic cycle and 0.92 per day. Ovarian dilatation data indicated that some females had completed eight gonotrophic cycles prior to being collected and 45% of the females completed two or more cycles. The high prevalence of multiparous individuals, high parity rate, long survivorship and a short three-day gonotrophic cycle estimate indicates that this population is long lived and has a capacity to be an efficient vector of malaria.

Animals↗
PubMed1997

Heme from Alzheimer's brain inhibits muscarinic receptor binding via thiyl radical generation.

An endogenous inhibitor (< 3500 Da) of antagonist binding to the muscarinic acetylcholine receptor (mAChR) has been reported to be elevated 3-fold in Alzheimer's disease (AD) brain. This endogenous inhibitor was found to require the presence of reducing agents such as reduced glutathione (GSH) for optimal activity. In the presence of GSH, the inhibitor was shown to generate thiyl radicals which irreversibly inhibited the mAChR. We now report that the inhibitor contains free heme, a well-established source of oxidative stress capable of generating free radicals and causing neurotoxicity. While FeSO4, microperoxidase and hemin all inhibited antagonist binding to the mAChR, only hemin shared the inhibitor's requirement for GSH. Both the free radical scavengers Trolox and Mn2+, and the metal chelator, EDTA, blocked the activity of the endogenous AD inhibitor and of hemin. Heme oxygenase-1 (HO-1) markedly reduced the activity of both the endogenous AD inhibitor and hemin, indicating that the endogenous inhibitor contains heme. Mass spectrometric analysis confirmed the presence of free heme and heme fragments in fractions of the endogenous AD inhibitor. The antioxidants estrogen, vitamin E and vitamin C all protected the mAChR from irreversible inhibition by the endogenous inhibitor or hemin. These antioxidants may function to protect the integrity of the mAChR in vivo and may have therapeutic potential in AD where free heme could be a source of oxidative stress.

Alzheimer Disease↗
PubMed1997

T-cell recognition of tumor-associated carbohydrates: the nature of the glycan moiety plays a decisive role in determining glycopeptide immunogenicity.

Aberrant glycosylation is one of the most constant traits of the malignant cell phenotype. To study T-cell responses to tumor-associated glycans, the mouse hemoglobin-derived decapeptide Hb(67-76), which binds well to the MHC class II molecule E(k) and is nonimmunogenic in CBA/J mice, was either O- or N-glycosylated at its primary T-cell receptor contact residue, position 72, with different glycans attached to either threonine, serine, or asparagine. The carbohydrate moieties included tumor-associated mucins, i.e., the Tn and T antigens, mucin-related glycans, and mucin-unrelated glycans. The side chain of the amino acid in position 72 points away from the MHC binding site when the Hb(67-76) peptide is bound to E(k), so the assumption was that this was also the case for glycans attached to this position. The glycosylated Hb(67-76) peptide analogues were then studied for binding to E(k) and for immunogenicity in CBA/J mice. All 16 glycopeptides bound well to E(k), although those with the more complex carbohydrates bound more weakly than those with monosaccharides. Six of 12 O-glycosylated and 0 of 4 N-glycosylated glycopeptides were able to induce a T-cell proliferative response with a stimulation index above 3.0. Some glycopeptides were not immunogenic, suggesting that there may be holes in the T-cell repertoire due to a lack of T-cell receptor regions accommodating certain glycan structures. The four strongest immunogenic glycopeptides were all O-glycosylated, and interestingly, three of them carried the tumor-associated Tn or T antigen. On the other hand, the Hb(67-76) peptide analogue with the natural mucin Core2 structure attached did not elicit any T-cell response. T cells primed to a glycopeptide with a simple glycan structure such as Tn did not cross-respond significantly to other glycopeptides, indicating a high degree of carbohydrate specificity in T-cell recognition. T cells primed to a glycopeptide carrying the more complex T antigen showed a complicated pattern of cross-responses to glycopeptides with simpler glycan moieties. The fact that it is possible to raise MHC class II-restricted T-cell responses against tumor-associated carbohydrate structures opens new perspectives for the designing of cancer vaccines.

Animals↗
PubMed1997

Carbohydrate and peptide specificity of MHC class II-restricted T cell hybridomas raised against an O-glycosylated self peptide.

MHC class II E(k)-restricted, IL-2 secreting T cell hybridomas were raised against the synthetic glycopeptide Hb(67-76)-alpha-GalNAc, (T72(Tn)), in CBA/J mice (H-2(k)). The fine specificity of the hybridomas against the glycan moiety was investigated by testing their response against a panel of Hb(67-76)-derived glycopeptides, all with a glycan attached to serine or threonine at the position 72 in the peptide, but with different glycans. The hybridomas showed a high degree of specificity for the alpha-GalNAc moiety with few and faint cross-responses to the glycopeptides having other glycans attached even though some of these were structurally very similar to alpha-GalNAc. The fine specificity of the hybridomas for the peptide moiety was investigated by testing their responses to a panel of Hb(67-76)-alpha-GalNAc glycopeptides with alanine substitutions at all positions except at the two MHC binding anchor positions, I68 and K76, and the T72 to which the alpha-GalNAc was attached. Glycopeptides substituted with alanine at positions where the amino acid side chain pointed toward the TCR did not stimulate the hybridomas, whereas glycopeptides substituted with alanine at positions orientated down into the MHC binding groove stimulated many of the hybridomas. These results indicate that the glycan attached to the peptide as well as solvent-accessible parts of the peptide are recognized with a high degree of specificity by the T cells, whereas the parts of the peptide buried in the MHC binding site are less important or totally ignored by the T cells.

Animals↗
PubMed1997

Experimental infection/transmission of sculpins (Myoxocephalus scorpius) and cod (Gadus morhua) by sealworm (Pseudoterranova decipiens) larvae.

Five serial transmission experiments with sealworm larvae were carried out. Pseudoterranova decipiens third-stage larvae (L3) were transferred via a stomach tube from sculpin to cod, from cod to sculpin, from sculpin to sculpin, and from cod to cod. After a minimum of 37 days the recipient fish were killed and the numbers of surviving P. decipiens larvae were recorded. P. decipiens transferred to sculpins showed the greatest rate of survival.

Animals↗
PubMed1997

One-stage repair of truncus arteriosus, CAVC, and TAPVC.

An infant with truncus arteriosus, complete atrioventricular canal, and total anomalous pulmonary venous connection successfully underwent one-stage complete repair. Residual mitral valve regurgitation required reoperation after 12 days. The patient is doing well at 6 months' follow-up. Echocardiography demonstrates no residual defects, competent atrioventricular valves, and normal pulmonary pressure. This case illustrates the potential for successful one-stage repair even of associated complex heart defects involving venous, intracardiac, and arterial pathways.

Abnormalities, Multiple↗
PubMed1997

Early experience with the Norwood procedure.

The improved results of the Norwood procedure have recently stimulated its widespread adoption in many centres. Since 1993, 19 infants with hypoplastic left heart syndrome or similar conditions underwent a first-stage Norwood procedure. Circulatory arrest time was significantly reduced by using a modified repair of the aortic arch. The early mortality rate was 31.5% (n = 6). The addition of CO2 to the inspired gas mixture resulted in less early postoperative instability. Nine patients have subsequently undergone bidirectional cavopulmonary shunt and one fenestrated total cavopulmonary connection. Overall there have been five late deaths, two as result of failure of cavopulmonary operations. All the eight survivors are presently in good condition. One is awaiting bidirectional cavopulmonary shunt and the other seven total cavopulmonary connection. This early experience encourages the continued offering of the Norwood procedure to patients with hypoplastic left heart syndrome or its variants. Increasing experience with the perioperative care and a more careful evaluation before cavopulmonary operations may determine further improvement in the outcome.

Aorta, Thoracic↗
PubMed1997

Is the arterial switch operation still a challenge in small centers?

OBJECTIVE: In the last years, major changes as regards timing for operation, surgical technique, and perioperative care determined a great improvement in the arterial switch operation (ASO) allowing excellent mid-term results in a few leading centers. This stimulated the widespread adoption of ASO as procedure of choice for transposition of the great arteries (TGA), even in small institutions. We reviewed our early experience with ASO in an attempt to evaluate its safety in a small center. METHODS: Since April 1992, 39 consecutive patients underwent TGA repair by ASO in our department. There were 27 patients with simple TGA, 8 with TGA and VSD and 4 with Taussig-Bing heart and aortic coarctation. Median age and weight at operation were 7 days and 3.5 kg, respectively. Neonatal repair was performed in 34 patients. In accordance with the Planché coronary classification, type I was encountered in 21 patients, type II in 4 and type III in 14. Several modifications of the original technique were used, mainly regarding coronary relocation, pulmonary artery reconstruction and approaches for associated VSD closure and aortic arch repair. RESULTS: Early mortality was 2.6% (n = 1), the only operative death being related to unsatisfactory coronary relocation. Since modified ultrafiltration was adopted, mean ICU stay decreased from 5 +/- 4 days (n = 21) to 2 +/- 1 days (n = 17) (P < 0.05). Three patients required reoperation for residual ASD and/or VSD closure. There were no late deaths. After a mean follow-up of 26 +/- 15 months all survivors are thriving and are currently asymptomatic. CONCLUSIONS: Although this series is rather small, most of the major coronary anomalies and complex anatomic associations were encountered. This experience suggests that neonatal repair of TGA by ASO can be safely accomplished even in small centers. Modified ultrafiltration appears to improve the early outcome of neonates undergoing ASO.

Cause of Death↗
PubMed1997

Immunohistochemical quantification of heparan sulfate proteoglycan and collagen IV in skeletal muscle capillary basement membranes of patients with diabetic nephropathy.

In IDDM patients, an increased permeability of the glomerular capillaries has been associated with a general loss of negatively charged heparan sulfate proteoglycans (HSPGs) within basement membranes (BMs). In the present study, we used immunohistochemical staining to quantify heparan sulfate (HS), HSPG core protein, and collagen IV in capillary basement membranes of skeletal muscle biopsies taken from 9 healthy control subjects (C) and 20 IDDM patients: 7 with normal albumin excretion rate (<30 mg/24 h) (D0), 5 with incipient nephropathy (albumin excretion rate 30-300 mg/24 h) (D1), and 8 with clinical nephropathy (albumin excretion rate >300 mg/24 h) (D2). In the capillaries, staining was measured by a scanning and integrating microspectrophotometer. A significant difference in the absorbance of HS was found among the four subgroups (means +/- SD): 0.477 +/- 0.082 (C), 0.627 +/- 0.031 (D0), 0.542 +/- 0.098 (D1), and 0.371 +/- 0.118 (D2) (P = 0.006). Similarly, an overall significant difference in the absorbance of collagen IV was demonstrated (means +/- SD): 0.836 +/- 0.111 (C), 0.838 +/- 0.300 (D0), 0.970 +/- 0.173 (D1), and 0.512 +/- 0.248 (D2) (P = 0.02). No statistical difference in the absorbance of core protein was demonstrated among the groups. Within the diabetic groups, HS was inversely correlated to albuminuria (r = -0.76, P = 0.003) and albuminuria corrected for creatinine clearance (r = -0.69, P = 0.008). Because, in IDDM patients with albuminuria, alterations of the content of HS and collagen IV within the capillary BM have been demonstrated immunohistochemically, not only in the glomerular filtration barrier, but also in the skeletal muscle capillary BM, we suggest that these changes reflect universal quantitative or qualitative alterations within the capillary filtration barrier.

Adult↗
PubMed1997

Pathogenesis of diabetic vascular disease: evidence for the role of reduced heparan sulfate proteoglycan.

Insulin-dependent diabetic patients with increased urinary albumin excretion are characterized by elevated blood pressure and declining kidney function. In addition, such patients have a high risk of atherosclerotic vascular disease, proliferative retinopathy, and cardiomyopathy, suggesting that albuminuria is a marker of widespread vascular dysfunction. Increased transport of macromolecules across the vascular wall, elevated plasma levels of von Willebrand factor, and impaired fibrinolytic capacity have been demonstrated in albuminuric patients. The cause of this vascular vulnerability in susceptible patients is unknown, but increasing evidence has suggested that loss of the proteoglycan heparan sulfate in the vasculature may explain the widespread nature of the disease. Heparan sulfate is important for the glomerular endothelial cell and basement membrane charge densities, the anticoagulant properties of the vessel wall, and the growth regulation of intimal smooth muscle cells. Recent studies have shown that heparin increases the biosynthesis of heparan sulfate in endothelial cell cultures and prevents the characteristic glomerular basement membrane thickening when given to diabetic rats. Moreover, heparin has been shown to reduce albuminuria in patients with incipient diabetic nephropathy. Although increasing evidence supports the hypothesis that loss of heparan sulfate may play a pathophysiological role in the development of diabetic vascular complications, there are still many unresolved problems. What are the mechanisms of action of glycosaminoglycans at the molecular biology level, and how can we select compounds without anticoagulant activity suitable for long-term use in the prevention and treatment of late diabetic complications?

Albuminuria↗