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Biomedical subjects

M Maus

Publications and source records attributed to M Maus.

At least 37 records · Page 2Linked to original sources
PubMed1998

Gore-Tex as an orbital implant material.

The use of Gore-Tex (W. L. Gore & Associates, Flagstaff, AZ, U.S.A.) spheres as orbital implants is investigated. The left eyes of six New Zealand white rabbits were enucleated and spherical implants made of modified Gore-Tex were implanted. After 6 weeks of follow-up, the implants were harvested. No rabbit developed a postoperative infection and no cases of exposure or extrusion were noted. Histopathologic study revealed varying degrees of acute and chronic inflammation surrounding each implant. There was also evidence of inflammatory infiltration and fibrovascular ingrowth into each implant to a maximum distance of 500 microns. This preliminary study demonstrates that the Gore-Tex implant is well tolerated in vivo, allows cellular ingrowth, and may have a role as a permanent implant.

Animals↗
PubMed1998

Thyroid-related ophthalmology.

The classic clinical triad of Graves' disease is hyperthyroidism, diffuse goiter, and exophthalmos. Caring for those undergoing the orbital changes of Graves' ophthalmopathy is often challenging, even as our understanding of the disease progresses. New therapeutic modalities for both Graves' disease and the associated orbitopathy have hastened rehabilitation and improved outcomes, although this disease continues to elude definitive cure.

Diagnosis, Differential↗
PubMed1996

Reduced glucose metabolism enhances the glutamate-evoked release of arachidonic acid from striatal neurons.

Glucose deprivation potentiates the glutamate receptor-evoked release of arachidonic acid from cultured mouse striatal neurons. In this study we investigated whether this potentiation would be modified by the end-products of glycolysis. These enhanced responses were completely reversed by the addition of increasing concentrations of either lactate or pyruvate. This reversal was not due to increased osmolarity as substituting sucrose for lactate or pyruvate did not mimic their effects. In contrast, in the presence of glucose, neither lactate nor pyruvate was effective. Furthermore, these monocarboxylic acids rescued neuronal respiration in the absence of glucose. Inhibiting glycolysis with iodoacetate in the presence of glucose reproduced the potentiated glutamate-evoked release of arachidonic acid observed following glucose deprivation and reduced neuronal respiration to the same extent as that observed in the absence of glucose. All of these effects were overcome by the addition of either lactate or pyruvate. The reversal of the potentiated glutamate-evoked release of arachidonic acid by lactate or pyruvate was inhibited by a specific inhibitor of monocarboxylic acid transport, alpha-cyano-4-hydroxycinnamic acid, suggesting that lactate and pyruvate act intracellularly. Therefore, we propose that the enhanced release of arachidonic acid evoked by glutamate during glucose deprivation results from reduced glycolysis and hence from a depletion of lactate or pyruvate.

Animals↗
PubMed1995

Oxygen free radicals enhance the nitric oxide-induced covalent NAD(+)-linkage to neuronal glyceraldehyde-3-phosphate dehydrogenase.

Nitric oxide (NO) induces a covalent modification of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) from various tissues. This phenomenon, which has previously been interpreted as an auto-ADP-ribosylation, is in fact a covalent binding of NAD+ to the enzyme. In the present study, we show that 3-morpholino-sydnonimine (SIN-1) is much more efficient than sodium nitroprusside (SNP) in stimulating the covalent labelling of GAPDH from cultured striatal neurones in the presence of [adenylate-32P]NAD+ (877 +/- 110 and 266 +/- 33% increase in NAD(+)-labelling induced by maximally effective concentrations of SIN-1 and SNP respectively). The difference in the efficacy of both NO-generating compounds could be due to the additional release of superoxide by SIN-1, since superoxide dismutase and the nitrone 5,5'-dimethyl pyrroline-1-oxide markedly inhibited the SIN-1-induced covalent binding of NAD+ to GAPDH. Catalase and selective scavengers of hydroxyl radicals, mannitol and dimethyl sulphoxide, did not alter the SIN-1-induced covalent modification of GAPDH, ruling out the involvement of hydroxyl radicals in this phenomenon. Supporting further a role of oxygen free radicals in the NAD+ linkage to GAPDH, pyrogallol, a superoxide generator, which alone was ineffective, potentiated the SNP-evoked response. The NAD+ linkage to neuronal GAPDH measured in the presence of NO and superoxide probably involves sulphydryl groups, since the radiolabelling of the protein was reversed by exposure to HgCl2 and prevented by pretreatment with the alkylating agent N-ethylmaleimide. Moreover, the NO-induced inhibition of GAPDH activity was enhanced by pyrogallol, which was ineffective alone. In conclusion, the present study indicates that superoxide anions potentiate NO-induced covalent NAD(+)-linkage to GAPDH and enzyme inactivation.

Animals↗
PubMed1995

Lasers in oculoplastic surgery.

Applications of laser-assisted surgery in oculoplastics are varied because the enormous scope of the specialty overlaps with ear, nose and throat, dermatology, plastic surgery, and ophthalmology, for example. All of these specialties have applications for lasers that in one fashion or another find their way into our armamentarium. In this article we present the last year's advances in laser applications in oculoplastics. By far, endonasal dacryocystorhinostomies are the most controversial and interest producing. Several articles address different approaches and conclusions. No final determination is available yet as to the effectiveness and ultimate success of this procedure. Dermatologic surgery for lesion removal and for cosmetic surgery also features in this year's review. The use of lasers for tattoo removal was reported in detail in a superb article. Overall there were no major breakthroughs in laser surgery, however, several well-thought-out articles have added to our understanding of this surgical modality.

Dacryocystorhinostomy↗
PubMed1994

Nicotine protects cultured striatal neurones against N-methyl-D-aspartate receptor-mediated neurotoxicity.

The role of cholinergic mechanisms in N-methyl-D-aspartate (NMDA)-mediated neuronal death was investigated using mouse striatal neurones in primary culture. A 30 min exposure of striatal neurones to increasing concentrations of NMDA resulted 24 h later in dramatic neuronal degeneration as assessed by MTT staining, crystal violet incorporation and determination of microtubule-associated protein 2. The NMDA-induced neurodegeneration was strongly inhibited by the co-application of two non-selective cholinergic agonists, acetylcholine or carbachol. This protective effect appears to be mediated by nicotinic receptors since it was insensitive to the muscarinic antagonist atropine but mimicked by nicotine, nornicotine and 1,1-dimethyl-4-phenyl-piperazinium. Moreover, the nicotine-evoked neuroprotection was inhibited by the central nicotinic antagonist hexamethonium. Therefore, this study suggests that cholinergic interneurones play an important role in neuronal survival in the striatum.

Acetylcholine↗
PubMed1994

Transcription of the rat dopamine-D2-receptor gene from two promoters.

Modulation of the expression of the D2-dopamine receptor gene is involved in several pathological and developmental circumstances. The gene and the corresponding promoter regions of the rat D2 receptor were isolated and partly characterized to study its regulation. The rat D2-receptor gene spans at least 50 kb, and possesses eight exons; its organization was compared to those of the other dopamine-receptor genes in a phylogenetic perspective. The gene contains two transcription-start sites: the major one is located about 320 bp upstream from the 3' end of the first exon, and a minor site is 70 bp further upstream. Transient-expression assays with fusion constructs comprising fragments of the D2-promoter region and the luciferase reporter gene confirmed the existence of two independent, TATA-lacking promoters. Both promoters separately induced transcription of the luciferase gene in C6 glioma, primary fibroblasts, GH3 and MMQ pituitary cell lines, among which only the MMQ cells normally express the D2 receptor. Transcription is enhanced by the reunion of the two promoters, and modified by the addition of upstream sequences. Thus the 1-kb promoter region analysed does not contain all the elements necessary to confer tissue-specific expression of the gene, but does carry some positive and negative regulatory elements, which remain to be characterized.

Animals↗
PubMed1993

Regulation of the quail tyrosine hydroxylase gene in neural crest cells by cAMP and beta-adrenergic ligands.

Expression of tyrosine hydroxylase (TH), the rate-limiting enzyme of catecholamine (CA) synthesis, was studied in quail neural crest (NC) cultures to investigate the role of environmental factors in the development of the adrenergic phenotype. First, the activity of the quail TH gene promoter was analyzed in immortalized quail NC cells by transient transfection assay. We found that chick embryo extract (CEE), which is known to trigger adrenergic differentiation of NC cells in vitro, strongly enhanced reporter gene transcription. A sequence of only 77 nucleotides, including a cAMP-responsive element, was sufficient to elicit this response. Implication of cAMP in the CEE effect was further supported by the fact that CEE produced a stimulation of adenylate cyclase activity that was sensitive to beta-adrenoreceptor antagonists. Moreover, stimulation of TH gene expression by CEE could be reduced by beta-adrenergic antagonists or CA-depleted extract. We have subsequently investigated the possibility that TH expression during differentiation of nontransformed NC cells could also be influenced by CA via the cAMP pathway. In dissociated cultures of 3-day-old quail sclerotomes and of 2-day-old quail trunk NC, differentiation of TH+ cells was induced in the presence of forskolin, an activator of adenylate cyclase, and modulated by beta-adrenoreceptor ligands. In particular, the adrenergic-promoting effect of 10% CEE on trunk NC cultures was inhibited by beta-adrenoreceptor antagonists or by eliminating CA from the extract. In conclusion, these data suggest that CA (through activation of beta-adrenergic receptors and cAMP production) can stimulate the initial expression of TH in cultured NC cells and enhance TH transcription in immortalized NC cells. This supports the notion that exogenous CA, which is present in the early embryo, may promote the differentiation of sympathoadrenal precursors in vivo by stimulating TH gene activity.

Adenylyl Cyclases↗
PubMed1993

D2-dopaminergic agonist quinpirole and 8-bromo-cAMP have opposite effects on Go alpha GTP-binding protein mRNA without changing D2 dopamine receptor mRNA levels in striatal neurones in primary culture.

Long-term coordinated regulations (during development or by agonists and second messenger molecules) of the expression of mRNAs encoding D2-dopamine (DA) receptors and D2 receptor-linked Go alpha proteins have been studied by Northern blot analysis in mouse embryonic striatal neurones in primary culture. During the course of the cell culture, the levels of both mRNAs increased, in conjunction with the maturation of the neurones. When the preparation was treated with the D2-DA agonist quinpirole (5-15 hrs, 10(-4) M), which decreases cAMP in these neurones, the levels of Go alpha mRNAs were enhanced whereas that of the D2 mRNA remained unchanged. Conversely, the Go alpha mRNAs, but not the D2 mRNA, decreased when the neurones were exposed to 8-bromo-cAMP (16 hrs, 10(-6) M). It is concluded that, in these experimental conditions where neurones have not yet established their connexions, the longterm regulation of the membrane transmission of D2-DA signal might implicate mainly the Go alpha encoding gene.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1992

Reversal of multidrug resistance by two novel indole derivatives.

Two new fused indoles were found to overcome multidrug resistance in P388/Adr cells in vitro. These agents potentiated the cytotoxicity of the antitumor drugs Adriamycin, vinblastine, and vincristine in multidrug-resistant cells with no effect on drug-sensitive parent P388 cells. They significantly increased the ATP-dependent accumulation of [3H]-vinblastine and inhibited efflux of the labeled drug from resistant cells. These compounds also inhibited photoaffinity labeling of P-glycoprotein by [3H]azidopine in P388/Adr cells and membranes isolated from these cells. In addition, the calcium antagonist activity of these compounds was very weak compared with that of verapamil. These data suggest that the compounds reported here may specifically overcome multidrug resistance without the serious hypotensive effects associated with calcium antagonists and that this activity may be independent of their ability to block calcium transport.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1992

High-level expression and purification of mature HIV-1 protease in Escherichia coli under control of the araBAD promoter.

A 1.3-kb segment of Escherichia coli DNA containing the regulatory gene, araC, and the promoter of the araBAD operon was amplified by the polymerase chain reaction (PCR) and cloned into pUC18, resulting in plasmid pKB130 that produced the alpha fragment of beta-galactosidase upon addition of L-arabinose (L-ara). A synthetic gene for human immunodeficiency virus (HIV)-1 preprotease was placed downstream of the ara-BAD promoter in pKB130 to create a translational fusion inducible by addition of L-ara. The fusion protein correctly autoprocessed in vivo to yield a mature 99-amino-acid HIV-1 protease, which was found predominantly in inclusion bodies. This material could be refolded to an active form, which was purified to homogeneity. A small fraction of the protease was expressed in vivo as a soluble active form, which allowed the monitoring of expression during fermentation by a rapid and simple whole cell assay employing an HIV-1 protease-specific fluorogenic substrate.

Amino Acid Sequence↗
PubMed1991

Treatment of intact striatal neurones with cholera toxin or 8-bromoadenosine 3',5'-(cyclic)phosphate decreases the ability of pertussis toxin to ADP-ribosylate the alpha-subunits of inhibitory and other guanine-nucleotide-binding regulatory proteins, Gi and Go. Evidence for two distinct mechanisms.

Using primary cultures of striatal neurones from the mouse embryo, we showed that treatment of intact cells with cholera toxin (5 micrograms/ml, 22 h) decreases the subsequent ADP-ribosylation of the alpha subunit of the guanine-nucleotide-binding regulatory protein Go (Go alpha) and the alpha subunit of the inhibitory guanine-nucleotide-binding regulatory protein (Gi alpha) of adenylate cyclase, which is catalyzed in vitro on neuronal membranes by pertussis toxin. The inhibitory effect of cholera toxin could not only be attributed to an increased production of cAMP in neurones. Treatment of cells with 0.1 microM 8-bromoadenosine 3',5'-(cyclic)phosphate (BrcAMP) for 16 h, or with 0.1 mM BrcAMP for 5 min, mimicked the effect of cholera toxin on the ADP-ribosylation of Go alpha and Gi alpha in vitro. However, the two agents seem to act through distinct mechanisms. The protein kinase inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpiperazine prevented the action of Br8cAMP but not that of cholera toxin. In addition, measurements of the pI of the Go alpha deduced from immunoblots of two-dimensional gels performed using a specific antibody directed against Go alpha suggest that treatment of neurones with cholera toxin induces ADP-ribosylation of Go alpha in intact cells, while BrcAMP does not.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Botulinum toxin therapy.

Botulinum toxin therapy has emerged as a treatment modality for a variety of spastic- or contracture-related muscle diseases. Its safety has been proven for long-term use in the treatment of benign essential blepharospasm, hemifacial spasm, and certain types of strabismus. Recent approval from the Federal Drug Administration should make botulinum toxin available for use in a greater number of patients.

Blepharospasm↗
PubMed1990

In vitro effects of 17 beta-oestradiol on the sensitivity of receptors coupled to adenylate cyclase on striatal neurons in primary culture.

Pretreatment of intact striatal neurons from the mouse embryo in primary culture with 17 beta-oestradiol (10(-9) M), 24 hours) enhanced the stimulation of adenylate cyclase activity induced by either dopamine (D1 receptors), isoproterenol, serotonin or 2-chloroadenosine (maximal effective concentrations) but suppressed inhibitory responses evoked by agonists of D2-dopaminergic or enkephalin (mu and delta) receptors. Binding studies indicated that some of these effects are (beta 1) or are not (D1 and D2) associated with changes in the number of receptors. Similar effects were partially seen with testosterone but not with 17 alpha-oestradiol, progesterone or dexamethasone and those induced by 17 beta-oestradiol were abolished when cells were exposed to inhibitors of mRNA transcription (alpha-amanitin) or protein synthesis (cycloheximide). Modifications in the properties of Gs or Go,i proteins were postulated because the number of adenylate cyclase catalytic subunits was not affected by 17 beta-oestradiol pretreatment. Results of ADP-ribosylation experiments with cholera toxin or pertussis toxin and of immunoblot experiments with anti-G alpha o and anti-G beta sera led us to suggest that 17 beta-oestradiol induces qualitative modifications in Go,i proteins leading to a stabilization of the associated form of the heterotrimer G alpha o,i beta gamma. In fact, pretreatment with pertussis toxin (which impairs G alpha o,i beta gamma dissociation) mimics the effects of 17 beta-oestradiol on responses of adenylate cyclase to stimulatory and inhibitory agonists.

Adenylyl Cyclases↗
PubMed1990

Choroidal detachment, flat anterior chamber, and hypotony as complications of neodymium: YAG laser cyclophotocoagulation.

Severe hypotony, flat anterior chamber, and serous choroidal detachment after transscleral neodymium: YAG laser cyclophotocoagulation (Nd:YAG-CPC) for three cases of intractable glaucoma are reported. The three patients had failed previous filtering surgery and were receiving maximal medical therapy. The types of glaucomas treated were two cases of primary open-angle and one chronic-angle closure. The complications were noted between 1 and 2 weeks from the time of treatment. One patient improved spontaneously after 1 week of observation. Another patient required drainage of the choroidal effusion and anterior chamber reformation. The last patient remains under observation with a low intraocular pressure (IOP) and a slowly resolving serous choroidal detachment. Though the incidence of shallow anterior chambers is three cases (0.5%) in this series of 750 Nd:YAG-CPCs, it represents a serious problem that had not been reported previously.

Aged↗