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PubMed1996

The stationary-phase-exit defect of cydC (surB) mutants is due to the lack of a functional terminal cytochrome oxidase.

The surB gene was identified as a gene product required for Escherichia coli cells to exit stationary phase at 37 degrees C under aerobic conditions. surB was shown to be the same as cydC, whose product is required for the proper assembly and activity of cytochrome d oxidase. Cytochrome d oxidase, encoded by the cydAB operon, is one of two alternate terminal cytochrome oxidases that function during aerobic electron transport in E. coli. Mutations inactivating the cydAB operon also cause a temperature-sensitive defect in exiting stationary phase, but the phenotype is not as severe as it is for surB mutants. In this study, we examined the phenotypes of surB1 delta(cydAB) double mutants and the ability of overexpression of cytochrome o oxidase to suppress the temperature-sensitive stationary-phase-exit defect of surB1 and delta(cydAB) mutants and analyzed spontaneous suppressors of surB1. Our results indicate that the severe temperature-sensitive defect in exiting stationary phase of surB1 mutants is due both to the absence of terminal cytochrome oxidase activity and to the presence of a defective cytochrome d oxidase. Membrane vesicles prepared from wild-type, surB1, and delta(cydAB) strains produced superoxide radicals at the same rate in vitro. Therefore, the aerobic growth defects of the surB1 and delta(cydAB) strains are not due to enhanced superoxide production resulting from the block in aerobic electron transport.

ATP-Binding Cassette Transporters↗
PubMed1996

Dephosphorylation of threonine 169 of Cdc28 is not required for exit from mitosis but may be necessary for start in Saccharomyces cerevisiae.

Entry into mitosis requires activation of cdc2 kinase brought on by its association with cyclin B, phosphorylation of the conserved threonine (Thr-167 in Schizosaccharomyces pombe) in the T loop, and dephosphorylation of the tyrosine residue at position 15. Exit from mitosis, on the other hand, is induced by inactivation of cdc2 activity via cyclin destruction. It has been suggested that in addition to cyclin degradation, dephosphorylation of Thr-167 may also be required for exit from the M phase. Here we show that Saccharomyces cerevisiae cells expressing cdc28-E169 (a CDC28 allele in which the equivalent threonine, Thr-169, has been replaced by glutamic acid) are able to degrade mitotic cyclin Clb2, inactivate the Cdc28/Clb2 kinase, and disassemble the anaphase spindles, suggesting that they exit mitosis normally. The cdc28-E169 allele is active with respect to its mitotic functions, since it complements the mitosis-defective cdc28-1N allele. Whereas replacement of Thr-169 with serine affects neither Start nor the mitotic activity of Cdc28, replacement with glutamic acid or alanine renders Cdc28 inactive for Start-related functions. Coimmunoprecipitation experiments show that although Cdc28-E169 associates with mitotic cyclin Clb2, it fails to associate with the G1 cyclin Cln2. Thus, an unmodified threonine at position 169 in Cdc28 is important for interaction with G1 cyclins. We propose that in S. cerevisiae, dephosphorylation of Thr-169 is not required for exit from mitosis but may be necessary for commitment to the subsequent division cycle.

Alleles↗
PubMed1998

Mutants of the yeast Yarrowia lipolytica defective in protein exit from the endoplasmic reticulum are also defective in peroxisome biogenesis.

Mutations in the SEC238 and SRP54 genes of the yeast Yarrowia lipolytica not only cause temperature-sensitive defects in the exit of the precursor form of alkaline extracellular protease and of other secretory proteins from the endoplasmic reticulum and in protein secretion but also lead to temperature-sensitive growth in oleic acid-containing medium, the metabolism of which requires the assembly of functionally intact peroxisomes. The sec238A and srp54KO mutations at the restrictive temperature significantly reduce the size and number of peroxisomes, affect the import of peroxisomal matrix and membrane proteins into the organelle, and significantly delay, but do not prevent, the exit of two peroxisomal membrane proteins, Pex2p and Pex16p, from the endoplasmic reticulum en route to the peroxisomal membrane. Mutations in the PEX1 and PEX6 genes, which encode members of the AAA family of N-ethylmaleimide-sensitive fusion protein-like ATPases, not only affect the exit of precursor forms of secretory proteins from the endoplasmic reticulum but also prevent the exit of the peroxisomal membrane proteins Pex2p and Pex16p from the endoplasmic reticulum and cause the accumulation of an extensive network of endoplasmic reticulum membranes. None of the peroxisomal matrix proteins tested associated with the endoplasmic reticulum in sec238A, srp54KO, pex1-1, and pex6KO mutant cells. Our data provide evidence that the endoplasmic reticulum is required for peroxisome biogenesis and suggest that in Y. lipolytica, the trafficking of some membrane proteins, but not matrix proteins, to the peroxisome occurs via the endoplasmic reticulum, results in their glycosylation within the lumen of the endoplasmic reticulum, does not involve transport through the Golgi, and requires the products encoded by the SEC238, SRP54, PEX1, and PEX6 genes.

ATPases Associated with Diverse Cellular Activitie↗
PubMed2005

Human LATS1 is a mitotic exit network kinase.

The kinase LATS/WARTS is a tumor suppressor protein conserved in evolution, but its function at the molecular level is not well understood. We report here that human LATS1 interacts with MOB1A, a protein whose homologue in budding yeast associates with kinases involved in mitotic exit. This suggested that LATS1 may be a component of the previously uncharacterized mitotic exit network in higher eukaryotes. Indeed, moderate overexpression of human LATS1 in cells exposed to microtubule poisons facilitated mitotic exit, and this activity required MOB1A. Reciprocally, small interfering RNA-mediated suppression of LATS1 or MOB1A prolonged telophase, but had no effect on the length of the earlier phases of mitosis. A role of LATS1 in mitotic exit may explain its previously described abilities to induce G2 arrest and promote cytokinesis.

Adaptor Proteins, Signal Transducing↗
PubMed1983

Contribution of variable entrance and exit block in protected foci to arrhythmogenesis in isolated ventricular tissues.

Automatic foci with membrane potentials in the range characterized by depolarization-induced automaticity exhibit entrance block. The present study demonstrates a role of variable entrance and exit block in arrhythmogenesis. We studied canine interventricular septa with the right bundle branch exposed, isolated false tendons and isolated feline papillary muscle using standard microelectrode techniques. Foci of automaticity were produced either by focal application of electric current or by exposure of the preparations to Tyrode's solution containing 1.5-2.0 mM KCl. Foci induced by mild depolarization exhibited entrance block with exit conduction and were subject to electrotonic modulation. With greater depolarization, varying degrees of exit block developed. Various rhythms, including Wenckebach periodicity, resulted. Delayed emergence of electrotonically accelerated activity led to closely coupled extrasystoles resembling reentrant activity. Exit conduction in some preparations was facilitated by enhanced normal pacemaker activity (membrane potentials -- 70 mV or greater) in tissue peripheral to the focus. Also, when there were two sites of automaticity separated by an area of depressed conduction, intermodulation between the two automatic regions generated complex arrhythmias. Shifts in maximum diastolic potential also changed conduction and led to changes in arrhythmic patterns. In some experiments, focal automaticity was terminated by single stimuli. We conclude that complex and variable behavior of automatic foci may result in activity with characteristics previously attributed to other arrhythmic mechanisms.

Animals↗
PubMed2003

Structural changes in silicon rubber peritoneal dialysis catheters in patients using mupirocin at the exit site.

Structural damage to polyurethane PD (peritoneal dialysis) catheters in patients using mupirocin ointment is widely appreciated, but damage to silicon rubber PD catheters is less well described. Ten catheters (6.6%) out of 152 were found to have structural alterations such as opacification, ballooning, thinning, and rupture. The duration of PD in these 10 patients ranged from 23 months to 80 months (mean duration 51.1 months). The frequency of mupirocin application varied from daily (2 cases) to 2-3 times per week (7 cases). In eight catheters opacification occurred at the exit site whereas one catheter showed opacification midway between the exit site and the titanium adaptor. One catheter showed opacification, ballooning, and thinning at the exit site ruptured in the form of two slit-like openings. In conclusion, various structural changes such as opacification, ballooning or thinning were seen in 6.6% of silicon rubber PD catheters in patients using mupirocin at the exit site. Although the mechanism remains elusive, mupirocin or the antiseptic solution alone or in combination may be contributory. We believe that this is an under-reported complication and encourage other health care givers to incorporate a search for such changes during clinic visits.

Adult↗
PubMed2002

Multiple telophase arrest bypassed (tab) mutants alleviate the essential requirement for Cdc15 in exit from mitosis in S. cerevisiae.

BACKGROUND: The Mitotic Exit Network (MEN) proteins - including the protein kinase Cdc15 and the protein phosphatase Cdc14 - are essential for exit from mitosis in Saccharomyces cerevisiae. To identify downstream targets of the MEN, we sought telophase arrest bypassed (tab) mutations that bypassed the essential requirement for CDC15. Previous studies identified net1(tab2-1) and CDC14(TAB6-1) as mutations in the RENT complex subunits Net1 and Cdc14, respectively, and revealed that the MEN acts by promoting release of Cdc14 from its nucleolar Net1 anchor during anaphase. However, the remaining tab mutants were not characterized. RESULTS: Fourteen out of fifteen tab mutants were mapped to three recessive (tab1-tab3) and three dominant (TAB5-TAB7) linkage groups. We show that net1(tab2-1) enables growth of tem1Delta, cdc15Delta, dbf2Delta dbf20Delta, and mob1Delta, but not cdc5Delta or cdc14Delta, arguing that whereas the essential task of the first four genes is to promote exit from mitosis, CDC5 possesses additional essential function(s). net1(tab2-1) but not CDC14(TAB6-1) resulted in a high rate of chromosome loss, indicating that Net1 promotes accurate chromosome segregation in addition to its multiple known roles. Finally, TAB1 was shown to be MTR10, a gene encoding nuclear transport receptor/adaptor. In some of the tab mutants including mtr10(tab1-1), defective nuclear export of the ribosomal protein Rpl11b was observed. Furthermore, the transport-defective -31 allele of the karyopherin SRP1, but not the transport competent -49 allele, exhibited a tab phenotype. CONCLUSIONS: Transport-defective mutations in two karyopherins can bypass cdc15Delta, suggesting that the function of the MEN is to promote mitotic exit by regulating nuclear transport.

Cell Cycle Proteins↗
PubMed1984

Anomalous exit of the C-6 nerve root via the C-6, C-7 foramen.

We report a case of the anomalous exit of the C-6 nerve root at the C-6, C-7 foramen. This caused intense radicular and cervical pain in a 25-year-old woman. At myelography, the 5th and 6th cervical roots appeared conjoined, and at operation the C-6 root and ganglion were found to turn acutely downward, lateral to the pedicle of C-6, and then to exit with the C-7 nerve root through the C-6, C-7 foramen. The ganglion of C-6 was placed nearly parallel to the dural sac and tethered at its origin on the dural sac and at the exit foramen with the C-7 root. The pedicle of C-6 was interposed between the dural sac and the ganglion of C-6. Cervical hemilaminectomy and resection of the pedicle of C-6 defined the anatomy and resulted in a clinical cure. The radiological features are described and contrasted with those of other anomalies. To our knowledge, this is the first report of such an anomalous course of exit of a cervical root.

Adult↗
PubMed2006

The puromycin-sensitive aminopeptidase PAM-1 is required for meiotic exit and anteroposterior polarity in the one-cell Caenorhabditis elegans embryo.

In the nematode Caenorhabditis elegans, sperm entry into the oocyte triggers the completion of meiosis and the establishment of the embryonic anteroposterior (AP) axis. How the early embryo makes the transition from a meiotic to a mitotic zygote and coordinates cell cycle changes with axis formation remains unclear. We have discovered roles for the C. elegans puromycin-sensitive aminopeptidase PAM-1 in both cell cycle progression and AP axis formation, further implicating proteolytic regulation in these processes. pam-1 mutant embryos exhibit a delay in exit from meiosis: thus, this peptidase is required for progression to mitotic interphase. In addition, the centrosomes associated with the sperm pronucleus fail to closely associate with the posterior cortex in pam-1 mutants, and the AP axis is not specified. The meiotic exit and polarity defects are separable, as inactivation of the B-type cyclin CYB-3 in pam-1 mutants rescues the meiotic exit delay but not the polarity defects. Thus PAM-1 may regulate CYB-3 during meiotic exit but presumably targets other protein(s) to regulate polarity. We also show that the pam-1 gene is expressed both maternally and paternally, providing additional evidence that sperm-donated gene products have important roles during early embryogenesis in C. elegans. The degradation of proteins through ubiquitin-mediated proteolysis has been previously shown to regulate the cell cycle and AP axis formation in the C. elegans zygote. Our analysis of PAM-1 requirements shows that a puromycin-sensitive aminopeptidase is also required for proteolytic regulation of the oocyte to embryo transition.

Amino Acid Sequence↗
PubMed2006

Exit from arsenite-induced mitotic arrest is p53 dependent.

BACKGROUND: Arsenic is both a human carcinogen and a chemotherapeutic agent, but the mechanism of neither arsenic-induced carcinogenesis nor tumor selective cytotoxicity is clear. Using a model cell line in which p53 expression is regulated exogenously in a tetracycline-off system (TR9-7 cells) , our laboratory has shown that arsenite disrupts mitosis and that p53-deficient cells [p53(-)], in contrast to p53-expressing cells [p53(+)], display greater sensitivity to arsenite-induced mitotic arrest and apoptosis. OBJECTIVE: Our goal was to examine the role p53 plays in protecting cells from arsenite-induced mitotic arrest. METHODS: p53(+) and p53(-) cells were synchronized in G2 phase using Hoechst 33342 and released from synchrony in the presence or absence of 5 microM sodium arsenite. RESULTS: Mitotic index analysis demonstrated that arsenite treatment delayed exit from G2 in p53(+) and p53(-) cells. Arsenite-treated p53(+) cells exited mitosis normally, whereas p53(-) cells exited mitosis with delayed kinetics. Microarray analysis performed on mRNAs of cells exposed to arsenite for 0 and 3 hr after release from G2 phase synchrony showed that arsenite induced inhibitor of DNA binding-1 (ID1) differentially in p53(+) and p53(-) cells. Immunoblotting confirmed that ID1 induction was more extensive and sustained in p53(+) cells. CONCLUSIONS: p53 promotes mitotic exit and leads to more extensive ID1 induction by arsenite. ID1 is a dominant negative inhibitor of transcription that represses cell cycle regulatory genes and is elevated in many tumors. ID1 may play a role in the survival of arsenite-treated p53(+) cells and contribute to arsenic carcinogenicity.

Apoptosis↗
PubMed1998

Wandering behavior and attempted exits among residents diagnosed with dementia-related illnesses: a qualitative approach.

Exiting attempts and wandering behavior among residents diagnosed with dementia-related illnesses were investigated. Residents were exposed to three test conditions: a mini-blind that concealed the view from the door, a cloth panel that concealed the panic bar of the door, and both the mini-blind and the cloth panel. During these test conditions, qualitative observations were conducted in addition to recording the attempted exits. The purpose of this paper is to present the qualitative findings in relationship to a model developed. The findings suggests that residents seemed to exit due to goal-orientation, exit-seeking behaviors, and attraction to the panic bar.

Aged↗
PubMed2005

Reflective liquid-crystal displays with asymmetric incident and exit angles.

The 2 x 2 matrix methods are extended to calculate the optical behaviors of reflective liquid-crystal displays with asymmetric incident and exit angles. Both the unfolding method and the backward-eigenwave method are employed to derive the 2 x 2 matrix representations. The simulation results for symmetric incident and exit angles from these two methods are identical and agree well with those obtained from the 4 x 4 matrix method when the air-panel surface reflections are neglected. Further, the derived 2 x 2 matrix methods are applied to the asymmetric cases with different incident and exit angles. The simulated results on the normally black vertical alignment and normally white mixed-mode twisted nematic reflective displays show reasonably good agreement with the reported experimental data. In addition, a rubbing effect related to contrast values is observed and analyzed in asymmetric reflective cases. We also find that this effect has a significant influence on the contrast ratios once the difference between the incident and exit angles becomes large.

Journal Article↗
PubMed2006

Smoking prevention and cessation intervention delivery by pediatric providers, as assessed with patient exit interviews.

OBJECTIVE: The goal was to evaluate the degree to which a smoking prevention and cessation intervention was delivered by providers to adolescents in the pediatric office setting. METHODS: Eight pediatric clinics in central Massachusetts were assigned randomly to either a special intervention (brief pediatric provider-delivered intervention plus peer counseling) or the usual care condition. Subjects (n = 2710) were adolescents 13 to 17 years of age, both smokers (smoked in the past 30 days) and nonsmokers/former smokers. The degree to which smoking prevention and treatment interventions were delivered by providers was assessed through patient exit interviews with adolescents after their clinic visits; interviews assessed the occurrence of 10 possible intervention steps. RESULTS: The percentage of providers engaging in the smoking interventions differed significantly between the special intervention and usual care conditions, according to adolescent reports in the patient exit interviews. For nonsmokers/former smokers, overall patient exit interview scores were 7.24 for the special intervention condition and 4.95 for the usual care condition. For current smokers, overall patient exit interview scores were 8.40 and 6.24 for the special intervention and usual care conditions, respectively. Intervention fidelity of special intervention providers was 72.2% and 84.0% for nonsmokers/former smokers and current smokers, respectively. CONCLUSIONS: Pediatric providers who receive training and reminders to deliver a brief smoking prevention and cessation intervention to adolescents in the context of routine pediatric primary care practice can do so feasibly and with a high degree of fidelity to the intervention protocol.

Adolescent↗
PubMed2005

Randomized, controlled trial of topical exit-site application of honey (Medihoney) versus mupirocin for the prevention of catheter-associated infections in hemodialysis patients.

The clinical usefulness of hemodialysis catheters is limited by increased infectious morbidity and mortality. Topical antiseptic agents, such as mupirocin, are effective at reducing this risk but have been reported to select for antibiotic-resistant strains. The aim of the present study was to determine the efficacy and the safety of exit-site application of a standardized antibacterial honey versus mupirocin in preventing catheter-associated infections. A randomized, controlled trial was performed comparing the effect of thrice-weekly exit-site application of Medihoney versus mupirocin on infection rates in patients who were receiving hemodialysis via tunneled, cuffed central venous catheters. A total of 101 patients were enrolled. The incidences of catheter-associated bacteremias in honey-treated (n = 51) and mupirocin-treated (n = 50) patients were comparable (0.97 versus 0.85 episodes per 1000 catheter-days, respectively; NS). On Cox proportional hazards model analysis, the use of honey was not significantly associated with bacteremia-free survival (unadjusted hazard ratio, 0.94; 95% confidence interval, 0.27 to 3.24; P = 0.92). No exit-site infections occurred. During the study period, 2% of staphylococcal isolates within the hospital were mupirocin resistant. Thrice-weekly application of standardized antibacterial honey to hemodialysis catheter exit sites was safe, cheap, and effective and resulted in a comparable rate of catheter-associated infection to that obtained with mupirocin (although the study was not adequately powered to assess therapeutic equivalence). The effectiveness of honey against antibiotic-resistant microorganisms and its low likelihood of selecting for further resistant strains suggest that this agent may represent a satisfactory alternative means of chemoprophylaxis in patients with central venous catheters.

Adult↗
PubMed1996

Nasal mupirocin prevents Staphylococcus aureus exit-site infection during peritoneal dialysis. Mupirocin Study Group.

A total of 1144 patients receiving continuous ambulatory peritoneal dialysis in nine European centers was screened for nasal carriage of Staphylococcus aureus. Two hundred sixty-seven subjects were defined as carriers of S. aureus by having had at least two positive swab results from samples taken on separate occasions, and were randomly allocated to treatment or control groups. Members of each group used a nasal ointment twice daily for 5 consecutive days every 4 wk. The treatment group used calcium mupirocin 2% (Bactroban nasal; SmithKline Beecham, Welwyn Garden City, United Kingdom) and the control group used placebo ointment. Patients were followed-up for a maximum period of 18 months. There were 134 individuals in the mupirocin group, and 133 individuals acted as control subjects. There were no differences in demographic data, cause of renal failure, type of catheter, system used, or method of exit-site care between the groups. Similarly, there were no differences in patient outcome or incidence of adverse events between both groups. Nasal carriage fell to 10% in those subjects who received active treatment and 48% in those who used the placebo ointment. There were 55 exit-site infections in 1236 patient-months in the control group and 33 in 1390 patient-months in the treatment group (not significant). S. aureus caused 14 episodes of exit-site infection in the mupirocin group and 44 in the control group (P = 0.006, mixed effects Poisson regression model). There were no differences in the rate of tunnel infection or peritonitis. There was no evidence of a progressive increase in resistance to mupirocin with time. Regular use of nasal mupirocin in continuous ambulatory peritoneal dialysis patients who are nasal carriers of S. aureus significantly reduces the rate of exit-site infections that occurs because of this organism.

Administration, Intranasal↗
PubMed2006

Budding yeast DNA damage adaptation mutants exhibit defects in mitotic exit.

In the presence of double strand breaks, DNA damage checkpoint halts cell cycle progression. However, cells ultimately escape the checkpoint arrest and reenter cell cycle in the presence of irreparable DNA damage. cdc5-ad was identified as a mutant that fails to adapt to the cell cycle arrest induced by DNA damage checkpoint. In budding yeast, Cdc5 protein kinase is a component of both MEN and FEAR pathways that are required for mitotic exit. It remains unclear whether the adaptation defect of cdc5-ad mutant cells is related to the function of Cdc5 in mitotic exit. Here we present evidence indicating that cdc5-ad mutant cells exhibit defects in mitotic exit. cdc5-ad mutant cells are sensitive to high dosage of Amn1, a negative regulator of MEN. It also shows synthetic growth defects with mutants in MEN pathway. Moreover, mutants in FEAR pathway exhibit defects in DNA damage adaptation. Thus, we conclude that the compromised mitotic exit pathway contributes to DNA damage adaptation defects in cdc5-ad mutant cells.

Adaptation, Physiological↗
PubMed1996

What managers can find out from exit interviews.

What are the best ways to find out not only why people leave the organization, but how to improve the environment and increase productivity or those that stay? Exit interviews can give you hints about what's going on that you can't get any other way. You can learn more about worker expectations, even if they were disappointed, from exit interviews than from a hiring interview. Exit interviews can also show when situations are worsening before that becomes clear through official channels. An exit interview may reveal a developing pattern of departures before the statistics are tabulated. Here are some guidelines for finding out what's really going on without wrecking the political climate and sending turnover to new levels.

Efficiency, Organizational↗
PubMed1998

[The effect of nasal and skin colonization on the development of exit site and peritoneal catheter tunnel infections in patients on peritoneal dialysis].

ESI remain a major problem in patients undergoing peritoneal dialysis and are frequently the reason for catheter removal. The treatment is often costly and not effective and the need for routine prophylactics has to be clarified. In this study 38 peritoneal dialysis patients (15 F & 23 M, age: 18-73) were analysed prospectively for ESI and TI in respect to skin (exit site and inguinal area) and nostrils colonisation. There were 14 diabetics and 24 non-diabetics. All had standard double-cuff Tenckhoff catheter and none presented with ESI prior to the study. No treatment was applied on the basis of positive culture only. In 27 patients swab were repeated after 6-11 months. Eight episodes of ESI and three TI were recorded. Following pathogens were cultured: S.aureus in 4 Klebsiella pneumoniae in 2, Corynebacterium sp. in 1, negative in 1 and with TI S.aureus in 3. Positive nasal cultures (S.aureus, Klebs.pn.) were observed in 5 patients subsequently developing ESI (p < 0.01) and in 2 with TI. In 2 cases exit site was also colonized by pathogens responsible for ESI (p = NS). Inguinal area was colonized by various pathogens in 7 patients, but only one of these developed ESI (p = NS) and no one TI. There was no difference between diabetic and non-diabetics neither in the frequency of ESI, TI nor in nasal carriage of pathogens. In the majority of patients nostrils and inguinal area were colonized by S.epidermidis. When the second culture was analyzed it appeared that significantly more patients had exit site colonized by S.epidermidis (2 and 11 patients in 2 consecutive cultures respectively (p < 0.01). In conclusion, it appears that nasal carriers of pathogens like S.aureus and Klebsiella pneumoniae are more prone to ESI. Inguinal area and exit site colonization does not seem to precede ESI or TI. We would suggest that nasal carriage status should be routinely identified in all patients entering peritoneal dialysis programme and the carriers properly treated.

Adult↗