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Biomedical subjects

M Behrens

Publications and source records attributed to M Behrens.

At least 37 records · Page 2Linked to original sources
PubMed1986

Ocular neuromyotonia. A clinical description of six patients.

We report the cases of six patients with ocular neuromyotonia, a disorder believed to result from episodic involuntary discharge of ocular motor nerves producing sustained and inappropriate contraction of their respective ocular muscles. Transient disturbances of ocular motility and diplopia result. Four patients had involvement of ocular muscles supplied by the third cranial nerve: one had presumed involvement of the superior oblique muscle, and one the lateral rectus muscle, suggesting abnormal discharge in the fourth and sixth cranial nerves, respectively. Four of six patients received prior radiation therapy for pituitary tumors, implying a possible pathogenic link. Three patients improved after treatment with membrane-stabilizing medication, suggesting that unstable membranes of injured ocular motor axons may generate spontaneous impulses, which produce involuntary sustained and inappropriate ocular muscle contraction.

Abducens Nerve↗
PubMed1984

Nystagmus in motor neuron disease: clinicopathological study of two cases.

Two patients with amyotrophic lateral sclerosis proved postmortem had nystagmus in addition to typical clinical signs of motor neuron disease. The first patient had gaze-evoked rotatory nystagmus that was followed by horizontal nystagmus in the primary position with supranuclear paresis of horizontal gaze and upgaze. The second patient had rotatory nystagmus that was evoked by lateral gaze, with normal range of eye movements. Nystagmus is so rare in motor neuron disease that these observations may imply another disease, but postmortem examination did not provide any other explanation. These two cases add to the increasing evidence that motor neuron disease comprises a heterogeneous group of disorders.

Abducens Nerve↗
PubMed1984

Bilateral central and centrocaecal scotomata due to mass lesions.

Unilateral central or centrocaecal scotoma may result from optic nerve compression. However, such defects bilaterally usually indicate non-compressive optic neuropathy of toxic or nutritional, hereditary, or demyelinating origin. Three cases are reported of patients who presented with somewhat atypical bilateral central or centrocaecal scotomata and were found to have suprasellar mass lesions demonstrated by CT scan and confirmed neurosurgically.

Adult↗
PubMed1982

Cytomegalovirus retinitis in a young homosexual male with acquired immunodeficiency.

A case is reported of histopathologically documented CMV retinitis. It is part of a recently appreciated syndrome in young homosexual men, in which cellular immune deficiency has been documented and in which CMV infection may play a role. This case demonstrates that CMV retinitis is not excluded by negative CMV serology or cultures.

Acquired Immunodeficiency Syndrome↗
PubMed1982

Hypopigmented iris spot. An early sign of tuberous sclerosis.

Hypopigmented skin spots, resembling the mountain ash leaf, may represent the earliest sign in tuberous sclerosis. We examined two patients with hypopigmented iris spots who suffered from this systemic disease. These iris spots may be analogous to the skin lesions, which have decreased amount of melanin in the melanosomes.

Adult↗
PubMed1981

Slowly alternating skew deviation: description of a pretectal syndrome in three patients.

Three patients who had slowly alternating skew deviation are described; each had elements of the Sylvian aqueduct syndrome. This combination of signs supports a pretectal location for lesions associated with alternating skew movements. Postmortem examination of a patient who died of chronic herpes simplex encephalitis showed extensive demyelination and periaqueductal spongiform degeneration; there was preservation of the oculomotor and trochlear nuclei, the medial longitudinal fasciculus, vestibular nuclei, and the interstitial nucleus of Cajal bilaterally. The slowly alternating dysconjugate vertical movements bear a resemblance to both see-saw nystagmus and the ocular tilt response.

Brain↗
PubMed1979

Acute posterior multifocal placoid pigment epitheliopathy associated with cerebral vasculitis and homonymous hemianopia.

An 18-year-old man developed acute posterior multifocal placoid pigment epitheliopathy and homonymous hemianopia. Cerebral angiography showed cerebral vasculitis probably with occipital infarction. To the best of our knowledge, this is the first reported case with such concomitant visual defects. Other published reports suggest that such cerebral vasculitis may not be unusual in acute posterior multifocal placoid pigment epitheliopathy.

Acute Disease↗
PubMed1978

Metabolism and cytotoxicity of 5-azacytidine in cultured Novikoff rat hepatoma and P388 mouse leukemia cells and their enhancement by preincubation with pyrazofurin.

5-Azacytidine transport into cells was measured in the absence of metabolism in adenosine triphosphate-depleted and uridine kinase-deficient Novikoff cells. Azacytidine is transported with about the same efficiency as uridine and cytidine by the facilitated nucleoside transport system of these cells. The phosphorylation of azacytidine in untreated, wild-type cells, however, is much more inhibited by uridine and cytidine than is its transport into the cell. This inhibition seems to be responsible for the specific protection of cells by these nucleosides from azacytidine toxicity. Azacytidine is incorporated by Novikoff and P388 cells into both RNA and DNA, and this incorporation seems to be responsible for its cytotoxicity; an inhibition of de novo pyrimidine nucleotide synthesis is not a major contributory factor. Incorporation of azacytidine into nucleic acids is relatively slow, but it is enhanced 3 to 4 times when cells are preincubated with pyrazofurin. Pyrazofurin inhibits de novo pyrimidine synthesis and thus causes a depletion of cellular pyrimidine nucleotides. Azacytidine is largely cytostatic for Novikoff and P388 cells, but a sequential treatment with pyrazofurin and azacytidine markedly increases the cytotoxicity over that observed with drug alone or when administered together with drug, even at higher concentrations. Increased cytotoxicity correlates with the increased incorporation of azacytidine into nucleic acids.

Amides↗
PubMed1977

Mechanism of action of inosine dialdehyde (NSC 118994) in the inhibition of proliferation of tumor cells in culture.

Inosine dialdehyde (INOX), the periodate oxidation product of inosine, inhibited the proliferation of various tumor cell lines in suspension culture in a concentration-dependent manner. A concentration of about 1 mM was required to completely inhibit the proliferation of Novikoff rat hepatoma and mouse L-cells, whereas about 0.1 mM completely inhibited the proliferation of L1210 and P388 mouse leukemia and Chinese hamster ovary cells. INOX inhibited in a similar time- and concentration-dependent manner the synthesis of protein, RNA, and DNA, as measured by the incorporation of labeled amino acid, uridine, and thymidine, into acid-insoluble material, without significantly affecting the incorporation of these precursors into the acid-soluble pool. Flow microfluorometric analyses showed that many of the INOX-treated cells became arrested in G2 + M. The results are consistent with the view that INOX affects multiple metabolic steps. The effects of INOX were quite different from those caused by typical inhibitors of ribonucleotide reductase, hydroxyurea, and 2,3-dihydro-1H-pyrazolo(2,3-a)imidazole, which very rapidly inhibited DNA synthesis and caused arrest of the cells in G1, with minimal effects on RNA and protein synthesis.

Aldehydes↗
PubMed1976

Inhibition of de novo pyrimidine nucleotide and DNA synthesis and growth of cultured Novikoff rat hepatoma cells and other cell lines by pyrazofurin (NSC 143095).

Pyrazofurin (PYF), a C-riboside, inhibited the replication of cultured Novikoff rat hepatoma cells, HeLa cells, and mouse L-cells at concentrations as low as 0.1 to 10 muM, but Novikoff cells were more sensitive than the cells of the other two cell lines. Inhibition of cell replication was completely prevented by the presence of 0.1 to 1 mM uridine in the medium, and partly by the presence of other pyrimidine, but not purine nucleosides. A 2- to 4-hr treatment of the cells with 10 muM PYF resulted in a 2-fold increase in the rate of incorporation of uridine into the acid-soluble pool and nucleic acids, while the rate of incorporation of adenosine into RNA was reduced about 85%. The incorporation of adenosine and deoxyuridine into DNA were reduced about 85 and 50%, respectively. The results are consistent with the view that PYF inhibits the de novo synthesis of pyrimidine nucleosides. The inhibition of cell replication seems to be due mainly to an inhibition of DNA rather than RNA synthesis, resulting from a rapid depletion of the pyrimidine deoxynucleotide pool, since addition of thymidine and deoxycytidine reversed the inhibition of DNA synthesis and cell replication by PYF. PYF must enter the cells to exert its toxicity since the toxicity of PYF was reduced 70 to 80% by the presence of 8 muM Persantin, a potent inhibitor of the facilitated and simple diffusion of various substrates, in the medium. If PYF is incorporated via normal nucleoside salvage pathways, its affinity for the nucleoside transport system(s) and kinases, must be low since, even at a concentration of 1 mM, it had only a slight effect on the initial rates of incorporation of various nucleosides into the nucleotide pool.

Adenosine↗