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Biomedical subjects

G H Jansen

Publications and source records attributed to G H Jansen.

At least 55 records · Page 3Linked to original sources
PubMed1999

Fast fluid-attenuated inversion recovery (FLAIR) compared with T2-weighted spin-echo in the magnetic resonance diagnosis of mesial temporal sclerosis.

RATIONALE AND OBJECTIVES: The authors compare coronal fast fluid-attenuated inversion recovery (FLAIR) with coronal T2-weighted spin-echo (SE) magnetic resonance (MR) techniques in the diagnosis of mesial temporal sclerosis (MTS). METHODS: In this prospective study, the authors assessed MR scans of 30 patients with drug-resistant temporal lobe epilepsy (based on clinical symptomatology and electroencephalographic registrations) with MR features suggestive of MTS. MR scans of age-, sex-, and scanner-matched patients, referred for MR assessment of white matter disease, without a history of epilepsy and with no visible abnormalities on MR, were used as controls. In 16 patients the MR diagnosis was confirmed by histologic abnormalities consistent with MTS. Coronal T2 SE and FLAIR images of patients and controls were presented to two experienced radiologists in random order for independent blinded review. Hippocampal and associated extrahippocampal temporal lobe abnormalities were used for the diagnosis of MTS. RESULTS: The sensitivity of observer A was 97% for the T2 SE sequence and 100% for the FLAIR; the specificity of observer A for both techniques was 100%. The sensitivity of observer B was 53% for T2 SE and 83% for FLAIR; the specificity for observer B was 93% for the T2 SE and 100% for FLAIR. CONCLUSION: Coronal FLAIR images provide a similar or increased yield in the detection of MTS compared with T2-weighted SE images.

Diagnosis, Differential↗
PubMed1999

Early-onset but not late-onset endothelin-A-receptor blockade can modulate hypertension, cerebral edema, and proteinuria in stroke-prone hypertensive rats.

-The ability of endothelin receptor blockade to prevent and to treat established cerebral and renal injury was explored in salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP) with the endothelin receptor subtype-A antagonist A127722. SHRSP were subjected to 1% NaCl intake. The start of treatment with A127722 (35 and 70 mg. kg-1. d-1, respectively) was either synchronized with salt loading or initiated after the first observation of cerebral edema with T2-weighted magnetic resonance imaging. In untreated control animals median survival was 54 days (range, 32 to 80 days) after the start of salt loading. Early-onset A127722 treatment increased median survival to 233 days (range, 92 to 407 days; P<0.05 versus controls) with 35 mg/kg and to 124 days (range, 97 to 169 days; P<0.05 versus control) with 70 mg/kg. The development of cerebral edema was prevented, and systolic blood pressure and proteinuria were dose-dependently reduced. However, all rats in the 70-mg/kg treatment group developed hemorrhages in the basal ganglia shortly before death. Late-onset A127722 treatment failed to affect survival, systolic blood pressure, or proteinuria. Nevertheless, cerebral edema was reduced but not as well as in early-onset treatment. Development of hypertension, cerebral edema, and proteinuria was prevented in SHRSP when A127722 treatment was initiated at the start of salt-loading. However, A127722 treatment did not prolong survival in SHRSP with cerebral edema. This suggests that in SHRSP the endothelin A receptor participates actively in the development of increased blood pressure and initiation of organ damage but participates minimally in established malignant hypertension and progression of target-organ damage.

Animals↗
PubMed1998

Ultraviolet-B induced hyperplasia and squamous cell carcinomas in the cornea of XPA-deficient mice.

In Xeroderma Pigmentosum (XP) patients, due to a defective repair of UV-induced DNA damage, neoplastic changes occur in sunlight-exposed areas of the skin and eyes. There are seven complementation groups in XP (XP-A to XP-G). Recently, we have generated XPA-deficient mice (group-A XP) by gene targeting in embryonic stem cells. In order to evaluate UV-B sensitivity, XPA-deficient mice (n = 20), wild type (n = 7) and heterozygous mice (n = 13) were exposed to low daily doses of UV-B for 14 weeks at a cumulative dose of 22 kj m-2 (250-400 nm). For a period of 32 weeks, the mice were checked twice a week for the development of pathology. The UV-B treatment induced eye abnormalities in the XPA-deficient mice. Initially, photophobia was noticed, followed by a loss of transparency of the cornea, eventually affecting nearly all XPA-deficient mice (19 out of 20). In 12 out of 19 mice, the pathology progressed to give eye protrusion. Histology of these eyes showed hyperplasia and squamous cell carcinomas of the corneal epithelium. No eye-lesions were found in control (wild-type and heterozygous) mice that were exposed to the same UV-B dose. The corneal abnormalities found in the XPA-deficient mice appear to be similar to those found in human XP patients. These results confirm the role of the functional XPA gene in protecting the cornea from pathology by UV-B irradiation. In addition, they suggest that the XPA-deficient mouse is a suitable animal model for the study of XPA ocular disorders.

Animals↗
PubMed1998

Prognostic relevance of cell proliferation markers and DNA-ploidy in gliomas.

The prognostic significance of clinically, histologically and flow cytometrically derived parameters was assessed in 49 glioma patients. With flow cytometry, DNA-index, S-phase fraction (SPF), 5-bromo-2'-deoxyuridine (BrdUrd)-labelling index (LI), and potential doubling time (Tpot) were determined. After univariate analysis of clinical variables such as, age, seizures as initial symptom, and duration of first symptom were found to be significantly associated both with proliferation rate and with local progression free survival (LPFS). Cytomorphological features such as, the presence or absence of mitosis, necrosis, and endothelial proliferation, were separately analysed and appeared to be significantly associated with LPFS. With respect to the cell proliferation markers, we observed a longer LPFS to be associated with a low SPF, a low LI, and a short Tpot. We did not observe a significant association between DNA-ploidy and LPFS. After multivariate analysis both of high and of low grade tumours, we found that neither LI, SPF, nor age had additional prognostic significance for cells in mitoses. We also demonstrated, that necrosis and endothelial proliferation had no additional prognostic significance to that for cells in mitoses. In the subgroup of low grade gliomas, in contrast to high grade gliomas, we noted prognostic significance for LI. We concluded, that i) the presence or absence of cells in mitoses was the strongest single prognosticator in gliomas, ii) in low grade gliomas LI holds prognostic significance.

Brain Neoplasms↗
PubMed1998

Absence of characteristic features in two patients with inclusion body myositis.

According to recently published criteria a diagnosis of definite sporadic inclusion body myositis is made if the typical histopathological abnormalities (rimmed vacuoles and abnormal accumulations of proteins, in addition to mononuclear cell infiltrates) are present. The two women described here presented with myositis which was unresponsive to treatment. Patient 1 had features of non-progressive sporadic inclusion body myositis clinically, whereas patient 2 had a very slowly progressive limb girdle syndrome. The cryostat sections of the first biopsies did not show rimmed vacuoles, even in retrospect. Only a repeated biopsy, 12 years after presentation in one patient and 18 years after presentation in the other, disclosed the typical features of sporadic inclusion body myositis. The initial absence of abnormal fibres probably represents a real absence or scarcity rather then a sampling error due to a multifocal nature of the histological abnormalities. It is of importance for the clinician to realise that some patients with myositis unresponsive to treatment, even if both clinical and histological features do not suggest sporadic inclusion body myositis, may prove to have the disease on repeated histopathological examination.

Adult↗
PubMed1998

Proteinuria precedes cerebral edema in stroke-prone rats: a magnetic resonance imaging study.

BACKGROUND AND PURPOSE: Stroke-prone spontaneously hypertensive rats (SHRSP) subjected to high sodium intake develop severe hypertension, cerebral edema, and proteinuria, culminating in organ damage and early death. MRI, which can be applied serially, provides the unique opportunity to study temporal and quantitative relations between these changes and whether diminution of sodium intake can attenuate established cerebral edema. METHODS: SHRSP were subjected to 1% NaCl in drinking water. Cerebral MRI, proteinuria and systolic blood pressure (SBP) were measured serially. After detection of cerebral edema (T2-weighted MRI), 6 rats were killed for histology, to confirm the diagnosis of cerebral edema. The others were followed up for 7 more days while salt loading was continued (n = 10, group 1) or after sodium intake was normalized (n = 7, group 2). RESULTS: SHRSP invariably developed cerebral edema in 30 days (range, 8 to 54 days). At this point neurological signs were absent in 16 of 23 rats. SBP rose until 1 week before detection of cerebral edema, and then stabilized at approximately 265 mm Hg. Proteinuria invariably preceded cerebral edema, with a concentration exceeding 40 mg/d predicting development of cerebral edema in 9 days (range, 3 to 15 days). There was linear correlation (R=.62, P<.0001) between proteinuria and cerebral edema (pixels with an intensity above a defined threshold). Rats in group 1 showed an increase in cerebral edema (from 5.8+/-1.1% to 12.5+/-2.8%; P<.05), and proteinuria remained high (from 305+/-44 to 338+/-29 mg/d); and 2 died spontaneously. Rats in group 2 showed no significant change in edema (from 4.9+/-0.5% to 6.9+/-1.3%) but a marked fall in proteinuria (from 294+/-24 to 119+/-10 mg/d; P<.05), both significantly different from group 1 (P<.05); all survived. SBP remained unaltered in both groups. CONCLUSIONS: Our data establish MRI as a sensitive method for detection of cerebral edema, often prior to neurological signs, in SHRSP. Proteinuria predicts cerebral edema, and these two variables, both obtained noninvasively, are quantitatively related. Moreover, in SHRSP normalizing sodium intake after salt loading attenuates development of cerebral edema and reduces proteinuria.

Animals↗
PubMed1998

Enalapril prevents imminent and reduces manifest cerebral edema in stroke-prone hypertensive rats.

BACKGROUND AND PURPOSE: Stroke-prone spontaneously hypertensive rats (SHRSP), subjected to high NaCl intake, show severe hypertension, organ damage, and early death. Preventive treatment with an angiotensin-converting enzyme (ACE) inhibitor is known to reduce mortality. Previously we found that proteinuria always precedes cerebral edema in SHRSP. Hence, in this study ACE inhibition was started later, ie, directly after manifestation of either proteinuria or cerebral edema. METHODS: SHRSP were subjected to 1% NaCl intake. Group 1 served as a control. In group 2 early-onset treatment with the ACE inhibitor enalapril was initiated after proteinuria was >40 mg/d. In group 3 late-onset ACE inhibition was started after the first observation of cerebral edema with T2-weighted MRI. Cerebral edema was expressed as the percentage of pixels with an intensity above a defined threshold. RESULTS: In controls median survival was 54 days (range, 32 to 80 days) after start of salt loading. The terminal level of cerebral edema was 19.0+/-3.0%. Under early-onset enalapril, median survival increased to 320 days (range, 134 to 368 days; P<0.01 versus group 1). Cerebral edema was prevented in all but 1 rat. Systolic blood pressure was slightly and transiently reduced at day 14. Proteinuria was markedly reduced (52+/-7 versus 190+/-46 mg/d in group 1 at day 7; P<0.05). Under late-onset enalapril, median survival was 264 days (range, 154 to 319 days; P<0.01 versus group 1). Cerebral edema decreased to baseline levels (9.6+/-2.9 at day 0 to 3.4+/-0.5% at day 3; (P<0.05). Ultimately cerebral edema reoccurred in 6 of the 8 rats. SBP decreased slightly at day 7 only. Proteinuria decreased from 283+/-27 at day 0 to 116+/-22 mg/d at day 7 (P<0.05). Complete remission of the original locus of cerebral edema was confirmed histologically. CONCLUSIONS: In SHRSP with proteinuria, treatment with an ACE inhibitor both prevented the development of cerebral edema and reduced manifest cerebral edema and proteinuria. Survival was markedly prolonged. These findings support the use of ACE inhibition for treatment in hypertensive encephalopathy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Bilateral temporal lobe necrosis after radiotherapy: confounding SPECT results.

A patient with seizures and a contrast-enhancing temporal lesion after radiation therapy for a chondrosarcoma of the nasal septum is described. To differentiate between radiation necrosis and recurrent tumor, thallium-201 (201Tl) SPECT was used. 201Tl SPECT revealed high local accumulation suggesting tumor growth; however, pathologic examination demonstrated focal necrosis with reactive changes but without tumor. The 201Tl SPECT findings in this patient demonstrate a possible diagnostic pitfall in differentiating recurrent tumor from radiation necrosis.

Bone Neoplasms↗
PubMed1997

[Microscopic tumor embolisms in metastasized breast carcinoma].

In two patients, women of 54 and 46 years old, with metastatic carcinoma of the breast, multiple microscopic tumour emboli in the lungs were found at autopsy. Ante mortem, unexplained respiratory distress in the former and an atypical thrombotic thrombocytopenic purpura-like syndrome in the latter were the most characteristic clinical features. Pulmonary microscopic tumour embolism is a rare diagnosis but it may occur in all types of cancer. Clinically, thrombotic pulmonary emboli are difficult to distinguish from microscopic tumour embolism. Special attention is to be paid to typical findings on radionuclide perfusion lung scanning (multiple subsegmental perfusion defects at the periphery of the bronchopulmonary segments with a normal ventilation named "segmental contour pattern'). Microangiopathic haemolytic anaemia and consumption coagulopathy are associated disorders. Tumour-directed therapy is the treatment of choice.

Breast Neoplasms↗
PubMed1997

S-phase fraction, 5-bromo-2'-deoxy-uridine labelling index, duration of S-phase, potential doubling time, and DNA index in benign and malignant brain tumors.

Seventy-one histologically malignant brain tumors, 52 histologically benign brain tumors, and 14 cerebral metastases were characterized according to DNA content and proliferative capacity. DNA ploidy, DNA index (DI), S-phase fraction (SPF), 5-bromo-2'-deoxy-uridine (BrdUrd) labelling index (LI), duration of S-phase (Ts), and potential doubling time (Tpot) were assessed by flow cytometry (FCM). In histologically benign tumors, a high percentage of DNA diploid tumors and a low proliferative capacity in DNA diploid tumors were found. Histologically malignant tumors and cerebral metastases were both found to be characterized by a low percentage of DNA diploid tumors and a high proliferative capacity in DNA diploid tumors. The proliferative capacity of DNA aneuploid benign tumors and that of DNA aneuploid malignant tumors, however, appeared not to differ significantly. The number of DNA aneuploid tumors was small. Duration of S-phase was short (range 3.9-4.7 hr) and appeared not to differ between the three groups. From this, the observed differences in Tpot values should be accredited mainly to differences in LI. High-grade as well as low-grade gliomas both appeared to be characterized by malignant (FCM) features, i.e., 1) a high percentage DNA aneuploidy, 2) a high mean DI (for DI > 1), and 3) a high proliferative capacity.

Aneuploidy↗
PubMed1997

Arteriovenous malformation of the vein of Galen in three neonates: emphasis on associated early ischaemic brain damage.

UNLABELLED: Vein of Galen malformation is a rare intracranial disorder in newborns. In recent years the survival rate has improved due to improvement in endovascular treatment of this abnormality. We describe three neonates with a vein of Galen malformation for whom treatment was not attempted because of associated severe cerebral damage, of antenatal origin in two and of perinatal origin in the other. Autopsy was performed in two neonates. Periventricular leukomalacia was present in both cases, associated in one case with cortical infarction, gliosis and atrophy. CONCLUSION: We recommend careful evaluation of associated cerebral damage prior to attempted treatment of the vein of Galen malformation.

Atrophy↗
PubMed1997

Assessment of the preferred plane and sequence in the depiction of mesial temporal sclerosis using magnetic resonance imaging.

RATIONALE AND OBJECTIVES: Definition of optimal magnetic resonance (MR) scanning plane and conventional MR sequence for the detection of mesial temporal sclerosis (MTS). METHODS: Coronal and axial T2-weighted images and axial T2-weighted images parallel to the long axis of the hippocampus (APLAH) and coronal inversion recovery (IR) images were obtained in patients with medically intractable temporal lobe epilepsy in their phase 1 preoperative evaluation. Thirty-three consecutive MR scans were reviewed by a panel of three radiologists. Twenty-three patients had MR abnormalities consistent with MTS, and ten scans were normal. To assess the best single scanning technique, another group of three radiologists, who were masked to all patient data, individually assessed the different planes and sequences of the 33 studies presented separately in a random fashion. For each plane and sequence, the likelihood (L) ratio for the correct diagnosis was determined separately. RESULTS: For all planes considered separately, a likelihood ratio of 4.4 was optimal for the coronal T2-weighted images. The likelihood ratio of APLAH T2 was 2.2; of axial T2, 3.9; of coronal IR, indefinite because of 100% specificity. CONCLUSIONS: For the assessment of MTS, coronal T2-weighted images were considered the best single scanning technique.

Adolescent↗
PubMed1997

Antibodies against enteroviruses in intravenous Ig preparations: great variation in titres and poor correlation with the incidence of circulating serotypes.

Antibody titres in immunoglobulin preparations for intravenous use were tested against 24 different enterovirus serotypes and varied between 1:100 and 1:10,000 within a single batch. Differences up to 8-fold were found for homologous titres between two different batches that were prepared 6 years apart. The lowest titre obtained was 1:40. The observed differences within and between the two batches could not be explained by different incidence of serotypes of enteroviruses circulating at the time blood was collected. Differences in titres of up to 18-fold were observed when several strains of the same serotype were tested suggesting that intratypic variation influences antibody titres. It is concluded that immunoglobulin preparations contain antibodies against many enteroviruses, but that titres can be low and cannot be predicted from the incidence of any particular serotype circulating in the community. Because of intratypic variation, selection of a batch for specific treatment should be based on results obtained with the patient's own isolate, and not with a reference strain.

Antibodies, Viral↗
PubMed1996

Peripheral neuropathy in mice transgenic for a human MDR3 P-glycoprotein mini-gene.

We have generated mice transgenic for a human MDR3 mini-gene, under control of a hamster vimentin promoter. Expression of the MDR3 transgene was found in mesenchymal tissues, peripheral nerves, and the eye lens. These MDR3 transgenic mice have a slowed motor nerve conduction and dysmyelination of their peripheral nerves. An extensive dysmyelination in some transgenic strains results in a severe peripheral neuropathy with paresis of the hind legs. How expression of the MDR3 transgene causes these abnormalities is unknown. The MDR3 gene encodes a large glycosylated plasma membrane protein with multiple transmembrane spanning domains, which are involved in the translocation of the phospholipid phosphatidylcholine through the hepatocyte canalicular membrane. The ability of the MDR3 P-glycoprotein to alter phsopholipid distribution in the plasma membrane of Schwann cells may cause the damage. It is also possible, however, that the presence of a large glycoprotein in the cell membrane may be sufficient to severely disturb myelination of peripheral nerves.

ATP Binding Cassette Transporter, Subfamily B, Mem↗