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Biomedical subjects

K Wessel

Publications and source records attributed to K Wessel.

At least 91 records · Page 5Linked to original sources
PubMed1990

[Drusen papilla with vision disorder and pathologic visual evoked potentials].

Six cases of optic nerve head drusen ophthalmoscopically are reported. Five of these had pathological latencies of the P 100 potentials on VEP examination. Only three of the patients had subjective visual complaints; all six, however, had variable visual field defects. Optic nerve head drusen are an important differential diagnosis, which can be readily established especially in those younger patients who need neurological and ophthalmological examination because of visual disturbances and pathological VEP responses.

Adult↗
PubMed1989

Prostaglandin E2 production is synergistically increased in cultured human glomerular mesangial cells by combinations of IL-1 and tumor necrosis factor-alpha 1.

Both IL-1 alpha and IL-1 beta and TNF-alpha induced a time- and dose-dependent release of authentic PGE2 from cultured human glomerular mesangial cells (HMC). This release became significant only after a 4- to 6-h lag phase, and was abolished by inhibition of protein synthesis, and was not related to cell proliferation. Combinations of IL-1 and TNF-alpha when added simultaneously to HMC resulted in a dose-dependent synergistic increase in PGE2 production. These stimulatory effects were specifically inhibited by anticytokine antibodies and the synergistic effect required the simultaneous presence of both IL-1 and TNF-alpha. Arachidonic acid (AA) release experiments and measurement of cyclooxygenase activity, revealed that while both were increased by IL-1 beta and TNF-alpha alone (IL-1 beta greater than TNF-alpha), combinations of IL-1 beta and TNF-alpha resulted in only additive increases in AA release and cyclooxygenase activity. Taken together, these data suggest that stimulation of PGE2 in HMC, by combinations of these cytokines, is not rate limited by AA release or cyclooxygenase activation, but may be related to the induction of the distal enzymes controlling specific PG synthesis.

Adult↗
PubMed1989

Cholera toxin modulates the T cell antigen receptor/CD3 complex but not the CD2 molecule and inhibits signaling via both receptor structures in the human T cell lymphoma Jurkat.

The human T cell lymphoma Jurkat can be activated by stimuli directed either against the T cell antigen receptor-CD3 antigen complex (TcR/CD3) or the CD2 molecule. Stimulation of cells via the TcR/CD3-complex or via the CD2 molecule increases inositol phosphates and cytoplasmic free calcium. Pretreatment of Jurkat cells with cholera toxin leads to a decrease of TcR/CD3 expression on the surface of the cells, while the expression of CD2 is unaffected. In contrast to this distinct effect on the receptor expression, signaling via both pathways is inhibited by cholera toxin. The most convincing explanation for the cholera toxin-mediated inhibition of signaling is that cholera toxin interrupts the signaling pathways at a point where both, stimulation via TcR/CD3 and via CD2, use the same route. The earliest common point of the two signaling pathways, at least in the Jurkat cell line, seems to be the CD3 complex because after its down-regulation (and functional inactivation) both pathways of activation are interrupted.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1989

Virus-transformed macrophage-like cell line as tool for eicosanoid research.

The ability of a virus-transformed murine macrophage like cell line HA 38 to produce different eicosanoid metabolites was examined. HA 38 cells release similar amounts of prostaglandins and leukotrienes as did murine peritoneal macrophages in response to both physiological and non-physiological stimuli. Enzyme systems known to be involved in the regulation of eicosanoid synthesis are expressed. HA 38 cells thus are a well defined macrophage model system and are well suited to study eicosanoid synthesis in macrophages and effects of drugs on the prostaglandin and leukotriene synthesis pathways.

Animals↗
PubMed1989

Significance of MRI-confirmed atrophy of the cranial spinal cord in Friedreich's ataxia.

The severity of Friedreich's ataxia was graded in ten patients by clinical examination and in five by use of posturography. These data were compared with neuroradiology findings. CT-confirmed infratentorial atrophy occured only in advanced cases of Friedreich's ataxia; the correlation with the clinical score was poor. On mid-sagittal MRI planes the diameters of fourth ventricle, brain stem at the level of the inferior olive and spinal cord at the levels of the foramen magnum and C3 were measured. Patients with Friedreich's ataxia had significant MRI-confirmed atrophy of the cranial spinal cord as compared with a normal, age-matched control group. This was also observed in patients with Friedreich's ataxia in the early stages. A reliable correlation between atrophy of the cranial spinal cord and the clinical score, however, could again not be found. MRI exploration of the cranial spinal cord may be recommended as an additional diagnostic marker in Friedreich's ataxia.

Adult↗
PubMed1989

Aluminium fluoride enhances phospholipase A2 activity and eicosanoid synthesis in macrophages.

Eicosanoid synthesis in macrophages is controlled by the availability of free arachidonic acid. Activation of the phospholipase A2 (PLA2) is an important mechanism leading to increased eicosanoid synthesis. In order to obtain further insight into the regulatory mechanisms of eicosanoid release, we incubated macrophages with the protein kinase C (PKC) activator dioctanoylglycerol (DiC8) or aluminium fluoride (AIF4-), a well-described activator of guanine nucleotide binding proteins (G-proteins). Arachidonic acid release, membrane-bound PLA2 activity and prostaglandin production in macrophages were enhanced by both substances in a time-dependent manner. Incubation with the phorbol ester TPA had no effect on the PLA2-activity. AIF4- elevated the cellular diacylglycerol content. The results suggest that activation of PLA2 and successive eicosanoid synthesis by AIF4- is mediated by direct activation of PLA2 by the AIF4(-)-induced generation of diacylglycerol.

Aluminum↗
PubMed1988

Biological properties of dihydro-leukotriene B4, an alternative leukotriene B4 metabolite.

Dihydro-leukotriene B4 (a 5,12-dihydroxy-eicosatrienoic acid) has been shown to be the primary metabolite of leukotriene B4 (LTB4) in a variety of cells other than human polymorphonuclear leukocytes (PMNLs). In this report we show that dihydro-LTB4 is significantly less active than LTB4 in different biological assay systems, i.e. leukocyte chemotaxis, chemokinesis, aggregation, adhesion to endothelium and superoxide anion production. This suggests that primary reduction constitutes a second so far unknown deactivation pathway for LTB4.

Cell Adhesion↗
PubMed1988

Cerebellar dysfunction in patients with bronchogenic carcinoma: clinical and posturographic findings.

Neurological examination and posturography showed cerebellar signs in 13 of 50 unselected patients with bronchogenic carcinoma not complicated by other diseases. The occurrence of cerebellar signs did not depend on the histological type of tumour or the extent of tumour spread. Most of the clinically affected patients had mild to pronounced cerebellar atrophy, revealed by CT. The correlation between the amount of CT-confirmed atrophy and the severity of clinical symptoms, however, was poor. Since other reasons for cerebellar dysfunction (e.g. chemotherapy, chronic alcoholism, metastases) were excluded, cerebellar signs were attributed to paraneoplastic cerebellar degeneration or to a consequence of severe neoplastic illness. The high incidence of cerebellar dysfunction in patients with bronchogenic carcinoma confirms the frequent histopathological finding of cortical cerebellar degeneration in malignant disease.

Aged↗
PubMed1988

Cerebellar dysfunction in patients with bronchogenic carcinoma: immunological investigations.

Sera from seven patients with bronchogenic carcinoma and cerebellar dysfunction were tested for anti-Purkinje cell antibodies (APCA) by indirect immunofluorescence and indirect immunoperoxidase reaction. Specific APCA as described in paraneoplastic cerebellar degeneration (PCD) were not detected in any of these patients or in control patients. The lack of APCA in patients with bronchogenic carcinoma and their presence in association with ovarian or breast cancer indicate that different pathogenetic mechanisms may play a role in PCD.

Aged↗
PubMed1988

Electrophysiological follow up of experimental allergic neuritis mediated by a permanent T cell line in rats.

Acute experimental allergic neuritis (EAN) was produced in Lewis rats by transfer of lymphocytes from a permanent T cell line specific for bovine P2 protein. In 3 groups of rats receiving 10(4), 10(5) and 10(6) total injected P2-specific lymphocytes, respectively, the time course of illness was followed by measuring several electrophysiological parameters including the H reflex or F wave and lumbospinal somatosensory evoked potentials (SEP). The severity and time course of both the electrophysiological and clinical (e.g., loss of weight and development of paresis) parameters of illness depended on the number of injected lymphocytes. Lower numbers of injected cells were correlated with a later onset and less severe symptoms as well as with an earlier and more complete recovery. According to clinical observation EAN mediated by lymphocytes is a monophasic illness. According to our electrophysiological measurements, however, the disease can be described by the following successive stages: (a) an early stage of hyperexcitability; (b) a stage of acute partial conduction block; (c) 14 days later a stage of maximal demyelination; and (d) a recovery phase. Although demyelination is the prominent feature of the disease, axonal degeneration also occurs to an extent directly related to the number of cells injected. Degeneration was not observed in rats from the group with the lowest number (10(4] of injected lymphocytes.

Animals↗
PubMed1988

Mitochondrial myopathies with necrotizing encephalopathy of the Leigh type.

Two patients with mitochondrial encephalomyopathy (MEP) serve to emphasize the variability of this group of diseases. Cerebral insults, mitochondrial cardiopathy, relapsing ileus, cerebral angioma, ataxia, and myoclonic seizures characterized the first case of an adult man with similar diseases in his family, interpreted as transitional form between mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and myoclonus epilepsy associated with ragged red fibers (MERRF). The second patient, a floppy infant with cardiomyopathy and myoclonism, statomotoric and mental retardation showed combined defects in mitochondrial respiratory chain at NADH-CoQ reductase and cytochrome c oxidase and a deficiency of carnitine. In both patients neuropathologically criteria of Leigh's syndrome could be demonstrated in the cerebral cortex, in case 2 also clinically. The classificatory problems of the relationships between KSS, MELAS, MERRF, Leigh's as well as Alpers' syndromes are discussed.

Adult↗
PubMed1988

[Mitochondrial encephalomyopathy: clinical aspects, CT morphology and neuropathology].

Basing on the example of two cases, the clinical and morphological variability of mitochondrial encephalomyopathies is demonstrated. Both patients were of short build, and the clinical signs and symptoms were dementia, ataxia, epilepsy and hardness of hearing, whereas signs of myopathy were very mild or absent. Computed tomography showed infratentorial pronounced atrophy of the brain and basal ganglia calcifications, in one case additionally ischemic infarctions, as can be seen in "mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes syndrome" (MELAS). A CT follow-up over 8 years with a progression of the abnormalities parallel to the progressive clinical course is demonstrated. Besides typical "ragged red fibres-myopathy" different abnormalities of mitochondria were seen by the electron microscope. One of the patients died; he had exceptional pathological-anatomical findings with mitochondrial cardiomyopathy, angioma and necrotising encephalopathy of Leigh's type. The two case reports show that in patients with such multisystemic neurological signs and CT-findings mitochondrial encephalomyopathy should be considered and a muscle biopsy should be performed.

Adult↗
PubMed1988

[Anesthesia for eye operations in mitochondrial encephalomyelopathy].

Mitochondrial encephalomyopathy involves a disturbance of the mitochondrial respiratory chain, as a result of which the blood lactate level is elevated. In stress situations a lactate acidosis can occur. The disease may be subdivided into three main syndromes: Kearns-Sayre syndrome (KKS), "myoclonus epilepsy with ragged red fibers syndrome" (MERRF), and "mitochondrial myopathy, encephalopathy, lactic acidosis and strokelike episodes syndrome" (MELAS). There are also several intermediate forms. Ophthalmological symptoms are frequent and occasionally have to be treated surgically. A 20-year-old male patient with a mixed form of these syndromes including elements of KSS and MERRF had to undergo cataract extraction. The authors decided to perform the operation under local anesthesia and sedation, with the anesthetist on standby. No problems arose. In all cases where mitochondrial encephalomyopathy is suspected the diagnosis should be confirmed by a muscle biopsy and the risk of cardiac arrest, respiratory insufficiency, and epileptic seizures ruled out prior to surgery. Local anesthesia with sedation appears to be the most favorable form of anesthesia provided the maximum dose is observed and a substance with a high convulsion threshold is chosen. Perioperative monitoring by an anesthetist and temporary provision of a cardiac pacemaker are necessary.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Myotonia congenita with familial spastic paraparesis].

An association of myotonia congenita and hereditary spastic paraplegia has not been reported up to now. We present three cases in one family, who suffer from this combination of syndromes. There are no hints for a pathophysiological connection between these diseases of different systems. A combination of autosomal dominant myotonia congenita and autosomal recessive spastic paraplegia is supposed. Under this hypothesis the risk for an association of the syndromes in the last generation of the reported family with two affected patients is 1/36. A coincidence of these two hereditary diseases seems to be possible.

Adult↗
PubMed1987

Pseudotumor cerebri: clinical and neuroradiological findings.

Pseudotumor cerebri (PTC) is a diagnosis per exclusionem applied to a condition of increased intracranial pressure in the absence of an intracranial infection, a space-occupying lesion, or hydrocephalus. Diagnostic criteria should include the evaluation of possibly disturbed cerebral venous outflow, which may result in similar clinical findings. Disturbed venous drainage should be separated from the syndrome of PTC because it represents a condition of well-defined origin and therapeutic regimen. Course and prognosis of PTC are not related to the increased intracranial pressure, the degree of papilledema, or to the duration of the disease. Functional cerebral disorders and EEG abnormalities are rare, indicating that brain tissue is not primarily affected. Correspondingly, computerized tomography (CT) scans with respect to the cerebrum are normal in about 90% of the cases; but enlarged optic nerve sheaths (46.7%) and empty sella (45.7%) are frequent findings on CT-scans. They most likely represent a direct consequence of long-term increased pressure within CSF spaces. This observation favors the assumption of disturbed CSF-pressure regulation either by increased production of CSF or its decreased rate of absorption. Brain edema (slit ventricles) as assessed by CT is a rare finding (11.4% of our cases). It may be a hint towards a different pathogenetic entity.

Adult↗