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Biomedical subjects

C Mann

Publications and source records attributed to C Mann.

At least 91 records · Page 5Linked to original sources
PubMed1993

S. cerevisiae 26S protease mutants arrest cell division in G2/metaphase.

We isolated two mutants from the yeast Saccharomyces cerevisiae, cim3-1 and cim5-1, that arrest cell division in G2/metaphase at 37 degrees C. CIM3 (identical to SUG1; ref. 1) and CIM5 are similar to each other and are members of a family of putative ATPases that have been proposed to be 26S protease subunits. We show here that CIM5 is the functional yeast homologue of the human MSS1 protein and that homologues of CIM3 and CIM5 are present in a highly purified preparation of the Drosophila 26S protease. The short-lived ubiquitin-proline-beta-galactosidase fusion protein is stabilized in cim mutants, but Leu-beta-galactosidase is not. The CLB2 and CLB3 cyclins also accumulate in the cim mutants. Thus the 26S protease is required in vivo for the degradation of ubiquitinated substrates and for anaphase chromosome separation.

Adenosine Triphosphatases↗
PubMed1993

The SLT2 (MPK1) MAP kinase homolog is involved in polarized cell growth in Saccharomyces cerevisiae.

Bud emergence, spindle pole body duplication and DNA replication are all dependent on the activation of the CDC28 protein kinase at the Start point in the G1 phase of the cell cycle. Bud emergence requires polarization of the cytoskeleton and secretory vesicles to a specific site on the cell surface. Cdc28p activated by G1-cyclins triggers polarization of actin to the site of bud emergence and favors apical bud growth (Lew, D. J., and S. I. Reed. 1993. J. Cell Biol. 120:1305-1320). We isolated slt2-1 as a mutation that enhances the division defect of cdc28 mutants with defects at Start. Slt2p(Mpk1p) is a member of the MAP kinase family (Lee, K. S., K. Irie, Y. Gotoh, Y. Watanabe, H. Araki, E. Nishida, K. Matsumoto, and D. E. Levin. 1993. Mol. Cell. Biol. 13:3067-3075). We show that slt2 mutants exhibit phenotypes similar to those shown by mutants of the yeast actin cytoskeleton, including delocalization of chitin deposition and of actin cortical spots and the accumulation of secretory pathway membranes and vesicles. Furthermore, slt2::HIS3 act1-1 and slt2::HIS3 myo2-66 double mutants are inviable. We suggest that Slt2p functions downstream or in parallel with Cdc28p in promoting bud formation and apical growth.

Actins↗
PubMed1993

Peripheral nerve and muscle.

This review of the past year's literature on neurophysiology of muscles and peripheral nerves emphasizes areas with direct clinical interest. The subject is diversified but will be discussed under the following major headings: nerve conduction studies, electromyography, magnetic motor evoked potentials, quantitative sensory testing, assessment of peripheral pain fibers, and autonomic function assessment.

Autonomic Nervous System↗
PubMed1993

[Neurological pain].

Neurogenic pain is by definition linked to a lesion of the pain pathways at any level. There are many causes for the neurological pain which can be present in sympathetic disorders, in peripheral neuropathies and central nervous disorders too. In despite of these multiple aetiologies, the neurological pain is characterised by: demyelinisation at the anatomic lesion; a spontaneous firing described by the authors as related to three mechanisms, sensitivation, deafferentation and lost of inhibition; a common and specific clinical semiology very different indeed from the peripheral pain described as a surafferentation.

Humans↗
PubMed1992

Biochemical and genetic dissection of the Saccharomyces cerevisiae RNA polymerase C53 subunit through the analysis of a mitochondrially mis-sorted mutant construct.

RPC53 has previously been shown to encode an essential subunit required for tRNA gene transcription by RNA polymerase C in vivo (Mann, C., Micouin, J.-Y., Chiannilkulchai, N., Treich, I., Buhler, J.-M., and Sentenac, A. (1992) Mol. Cell. Biol. 12, in press). In this paper, we have determined that an unusual rho+ lethality associated with the rpc53::HIS3-1 disruption mutation is due to the inadvertent formation of a Pet56-C53 fusion protein. This fusion protein is missorted to mitochondria, thereby reducing the quantity of the C53 subunit available for RNA polymerase C assembly. We show that the carboxyl-terminal region of C53 contains the essential functional domain of the subunit and that a mutant RNA polymerase containing only this domain is thermolabile for its function in vivo and in vitro. The thermolability of the carboxyl-terminal C53 domain is suppressed by five different genes on multicopy plasmids, including RPC160, encoding the largest subunit of RNA polymerase C and SSD1/SRK1, which has been implicated in the activity of protein phosphatases.

Alleles↗
PubMed1992

Risk of major elective operation after myocardial revascularization.

Although an increased surgical risk of ischemic myocardial disease is widely accepted, amelioration of this risk after coronary artery bypass is poorly defined. We compared the outcomes of major elective general and peripheral vascular operations in 181 patients with prior coronary artery bypass grafting (CABG) with outcomes in an age-, gender-, and procedure-matched group without prior CABG (NOCABG). Despite the perception of a greater operative risk in the CABG patients (more CABG patients in American Society of Anesthesiologists [ASA] class III and fewer in ASA class I, p < 0.001), mortality (1.1% CABG versus 2.8% NOCABG) and morbidity (18.8% CABG versus 18.5% NOCABG) rates in the two groups were not significantly different. For patients who have undergone successful CABG, it appears that: (1) the risk of subsequent elective major general and vascular surgical operations is similar to that of an age-, gender-, and procedure-matched cohort, and (2) the mortality rate after elective operations is low.

Age Factors↗
PubMed1992

RPC53 encodes a subunit of Saccharomyces cerevisiae RNA polymerase C (III) whose inactivation leads to a predominantly G1 arrest.

RPC53 is shown to be an essential gene encoding the C53 subunit specifically associated with yeast RNA polymerase C (III). Temperature-sensitive rpc53 mutants were generated and showed a rapid inhibition of tRNA synthesis after transfer to the restrictive temperature. Unexpectedly, the rpc53 mutants preferentially arrested their cell division in the G1 phase as large, round, unbudded cells. The RPC53 DNA sequence is predicted to code for a hydrophilic M(r)-46,916 protein enriched in charged amino acid residues. The carboxy-terminal 136 amino acids of C53 are significantly similar (25% identical amino acid residues) to the same region of the human BN51 protein. The BN51 cDNA was originally isolated by its ability to complement a temperature-sensitive hamster cell mutant that undergoes a G1 cell division arrest, as is true for the rpc53 mutants.

Amino Acid Sequence↗
PubMed1991

Congestive cardiac manifestations from cerebrocranial arteriovenous shunts. Endovascular management in 30 children.

Since 1984 we have been involved in the management of 30 children who had cardiac manifestations secondary to cerebrocranial arteriovenous shunts. Aneurysm malformation of the vein of Galen was the most common vascular lesion observed (73% of cases). In 77% of the patients the cardiac symptoms were the main presenting complaint. Medical treatment and/or endovascular therapy were indicated, depending on the age of the patients and the severity of the cardiac manifestations. Following embolization, the cardiac symptoms resolved (73%) or improved (18%) in 1 or 2 sessions. Mortality in the embolized group was 9%, and transient nonneurologic morbidity occurred in one case. Overall mortality, including four patients rejected for embolization, was 20%. These results compare favorably with medical and/or surgical management, alone or combined. The technique, challenges, indications and contraindications of endovascular therapy are discussed. Embolization represents an effective adjunct treatment to control, improve or cure the congestive cardiac manifestations caused by cerebrocranial arteriovenous shunts.

Adolescent↗
PubMed1991

Fluoride mobilizes intracellular calcium and promotes Ca2+ influx in rat proximal tubules.

In the renal proximal tubule, external Ca2+ ([Ca2+]o) is required for parathyroid hormone to elevate cytosolic Ca2+ ([Ca2+]i). However, other hormones increase [Ca2+]i in the absence of [Ca2+]o. These differences may arise from a diversity of signal transduction pathways acting on external and internal Ca2+ pools. However, Ca2+ influx may be necessary to expedite and maintain the rise of [Ca2+]i for a period after the initial surge. In this study, F- was used to probe the roles of intracellular Ca2+ mobilization, Ca2+ influx, and phosphoinositide (PI) hydrolysis on the surge of [Ca2+]i in rat proximal tubules. In the presence of external Ca2+; 1-20 mM F- evoked incremental rises of [Ca2+]i in tubules loaded with aequorin. Whereas 10 mM F- increased [Ca2+]i in the absence of [Ca2+]o, the time constant for the [Ca2+]i surge was increased. These findings are consistent with a role of Ca2+ influx on the effect of F- on [Ca2+]i. Indeed, 10 mM F- also enhanced the uptake of 45Ca2+, and promoted Ca2+ influx in aequorin- and fura-2-loaded, Ca(2+)-deprived tubules. In tubules, F- also activated PI hydrolysis with a time course that paralleled Ca2+ mobilization. The effect of F- on [Ca2+]i was not altered when the 39-kDa pertussis toxin substrate was inactivated with the toxin. This G protein was most likely Gi, because prostaglandin E2, an activator of Gi in tubules, dissociated the pertussis toxin-sensitive protein. The results support the notion that activation of a signal-transduction complex, the F- substrate, causes Ca2+ influx, mobilizes internal Ca2+, and activates PI hydrolysis in rat proximal tubules.(ABSTRACT TRUNCATED AT 250 WORDS)

Aequorin↗
PubMed1991

Na(+)-Ca2+ exchange and Ca2+ depletion in rat proximal tubules.

The removal of external Ca2+ ([Ca2+]o) reduces cytosolic Ca2+ ([Ca2+]i) in rat proximal tubules. In this report the role of external Na+ ([Na+]o) on the changes of [Ca2+]i and Ca2+ efflux caused by withdrawal of [Ca2+]o is described in rat renal proximal tubules. In aequorin-loaded tubules [Ca2+]i decreased from 235 +/- 25 to 48 +/- 16 (n = 4, P = 0.017), and 45Ca2+ fractional efflux ratio (45Ca2+ FER) increased from 0.94 +/- 0.03 to 1.64 +/- 0.19 (n = 6, P = 0.021) when Ca2+ was withdrawn from the bathing media of Krebs buffer (KB). The fall of [Ca2+]i, as well as the activation of 45Ca2+ FER, was reversed when [Na+]o in Ca(2+)-free KB was lowered isosmotically from 150 to 15 mM. However, when tubules were superfused with only 5 mM [Na+]o before [Ca2+]o was removed, [Ca2+]i also declined, but 45Ca2+ FER did not increase. The Na(+)-Ca2+ exchange inhibitor dichlorobenzamil (DCB) added after [Ca2+]o was removed evoked responses similar to [Na+]o removal, although DCB also inhibited internal Ca2+ release. These results are congruous with stimulation of Na+ influx in exchange for [Ca2+]i in Ca(2+)-free KB. However, even though total tubular Na+ was higher in Ca(2+)-free KB after 10 min, the initial rate of 22Na+ influx was not different without or with [Ca2+]o.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1991

Access to computers for older adults: problems and solutions.

Activity that involves a personal computer is a valuable modality for the rehabilitation of older adults. The therapist without specialized training, however, may have difficulty integrating computer use with adults with chronic health problems that impede such use. The purpose of this paper was to describe positioning, visual access, and input problems that may interfere with computer access and to identify solutions for use by the occupational therapist. Through a review of occupational therapy and adaptive computer literature, resources for adaptive computer hardware, software, and positioning devices are identified. Examples of how computer activities can be integrated into existing nursing home, day-care, and home-care programs are provided. Recommendations are made for training for the occupational therapist with limited experience with personal computers and adaptive computer technology.

Aged↗
PubMed1990

Atrial natriuretic factor (ANF) is a potent bronchodilator in asthma.

The bronchodilating effects of atrial natriuretic factor (ANF) were compared to effects of salbutamol in a double-blind, placebo-controlled, crossover study in eight subjects with asthma and with airflow limitation. ANF was infused intravenously (0.1 microgram/kg/min during 30 minutes) and caused a short-lasting significant (p less than 0.012) bronchodilation in all patients similar in intensity to intravenous salbutamol (0.13 microgram/kg/min). The duration of the effect of the beta 2-agonist, however, was longer. No severe side effects were noted with ANF infusion. ANF may play a role in the modulation of the bronchial tone in humans, but its usefulness in the treatment of asthma remains to be determined.

Asthma↗
PubMed1990

[Anesthetic management for arteriographic evaluation and endovascular treatment in children with arteriovenous malformation of the vein of Galen].

In a series of 23 consecutive patients under 3 years old with VGAVM managed in Bicêtre from 1985 to 1990, 19 have been angiographically explored and 16/19 embolized (35 total procedures). Anaesthetic management must be adapted to the consequences of this disease: heart failure in newborns, intracranial hypertension in infants and the technical constraints of anaesthesiology in infants during neuroradiological explorations. Our results are satisfactory when compared to the classical bad prognosis of the disease: 90% of all the heart failures were ameliorated or cured; 10 infants are anatomically cured. The technical morbidity and mortality in embolized patients is nil. No perfusion breakthrough phenomena was observed in this series.

Anesthesia, General↗
PubMed1990

Use of suprathreshold test data to predict the results of quantitative testing in the nasal periphery.

We compared the results of suprathreshold testing of the nasal periphery with those of quantitative assessment of the same area. One eye each from 81 patients in four categories (normal [21 subjects], low-risk ocular hypertensive [20 subjects], high-risk ocular hypertensive [20 subjects] and early glaucoma [20 subjects]) was tested with the nasal suprathreshold points of the Octopus G1 program and the Sargon peripheral field-nasal (PFN) program. Simple algorithms were developed to generate from the nasal suprathreshold points of the G1 program two "qualitative indices", mean defect-qualitative (MD-Q) and loss variance-qualitative (LV-Q); these are analogous to the indices mean defect and loss variance respectively, which were calculated from the PFN program data. MD-Q and LV-Q were found to be well correlated with their quantitative counterparts. They provide a uniform method for interpreting the nasal suprathreshold points of the G1 program and help identify patients in whom further quantitative testing is likely to yield useful information.

Adult↗
PubMed1989

Molecular basis of lipid transfer protein deficiency in a family with increased high-density lipoproteins.

Plasma high density lipoproteins (HDL) are a negative risk factor for atherosclerosis. Increased HDL is sometimes clustered in families, but a genetic basis has never been clearly documented. The plasma cholesteryl ester transfer protein (CETP) catalyses the transfer of cholesteryl ester from HDL to other lipoproteins and therefore might influence HDL levels. Using monoclonal antibodies, we show that CETP is absent in two Japanese siblings who have markedly increased and enlarged HDL. Furthermore, they are homozygous for a point mutation in the 5'-splice donor site of intron 14 of the gene for CETP, a change that is incompatible with normal splicing of pre-messenger RNA. The results indicate that the family has an inherited deficiency of CETP due to a gene splicing defect, and illustrate the key role that CETP has in human HDL metabolism.

Adult↗
PubMed1989

Efficacy and safety of once-daily levobunolol for glaucoma therapy.

We studied the ocular hypotensive efficacy and safety of 0.5% levobunolol hydrochloride and 0.5% timolol maleate administered topically once daily for 3 months in 91 patients (46 in the levobunolol group and 45 in the timolol group) with primary or secondary open-angle glaucoma or ocular hypertension. In this randomized double-masked parallel clinical study, intraocular pressure (IOP) was successfully controlled in 78% of the patients who received levobunolol and 89% of those who received timolol. The overall mean decrease in IOP was 5.6 mm Hg (decrease of 23%) in the levobunolol group and 6.7 mm Hg (26%) in the timolol group, a nonsignificant difference. In both groups the overall mean IOP during treatment was significantly lower than the pretreatment value (p less than 0.001). For both treatment groups changes in heart rate and blood pressure were minimal. We conclude that both 0.5% levobunolol and 0.5% timolol administered once daily are effective and safe in lowering IOP in most patients with ocular hypertension or open-angle glaucoma.

Administration, Topical↗