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PubMed1998

Mechanism of atrial escape-capture bigeminy: second-degree sinoatrial exit and entrance block.

Two women with atrial escape-capture bigeminy were reported in whom sinus P waves and escape P waves alternated with each other. Their electrocardiographic findings showed that, during the bigeminal rhythm, 2:1 exit block of sinus impulses associated with entrance block of escape impulses occurred in the sinoatrial junction. Three phenomena are suggested to explain the observations. (1) Seeming bradycardia-dependent sinoatrial exit block may have occurred, probably as a result of phasic changes in vagal tone due to respiration, with decreased vagal tone depressing conductivity in the sinoatrial junction to a greater degree than automaticity in the sinus node. (2) In case 1, type II second-degree entrance block in the sinoatrial junction may have occurred, reflecting the presence of sinus parasystole with incomplete entrance block. (3) Sinus escape also may have occurred, especially in case 2. These phenomena have never been reported before.

Aged↗
PubMed1998

Successful ex utero intrapartum treatment (EXIT) procedure for congenital high airway obstruction syndrome (CHAOS) owing to laryngeal atresia.

Congenital high airway obstruction syndrome (CHAOS) caused by laryngeal atresia was diagnosed by prenatal ultrasound in a male fetus at 18-weeks-gestation. Findings included enlarged lungs, inverted diaphragms, dilated trachea distal to the obstruction, and ascites. At 35 weeks' gestation, a planned ex utero intrapartum treatment (EXIT) procedure was performed, allowing bronchoscopic evaluation of the airway and placement of a tracheostomy. The postnatal course was marked by gradual recovery of diaphragmatic function with corresponding weaning from conventional ventilation to positive airway pressure. The sustained improvement in diaphragmatic and pulmonary function after the EXIT procedure for laryngeal atresia is one of the first reported for this entity and provides encouragement for future attempts.

Adult↗
PubMed1993

Radionuclide constant pressure perfusion study on measurement of exit urine flow: experimental and preliminary clinical investigations.

To calculate exit urine flow from the renal pelvis to the bladder in hydronephrosis, a simple method, radionuclide constant pressure perfusion study, was used. The mathematical model proposed for calculation of the exit flow (F) was simple: F = (initial slope)/Do'/exp(-0.148d), where F is expressed as flow rate (ml. per minute) of infused radioactive solution into the bladder. The value of the initial slope is expressed as a count rate per minute of time-activity curve of the bladder. Do' is a count rate per ml. of infused radioactive solution, which was measured by a gamma camera in air, and d is depth (cm.) of the bladder from the body surface to the vesical mucosa. The number -0.148 indicates the effective linear attenuation coefficient of 99mtechnetium, which was determined by a phantom study. In the experimental studies calculated flow correlated well with real pump flow. In preliminary clinical studies in 16 patients (20 kidneys) who underwent nephrostomy, measurement of flow rate at steady intrapelvic pressure with no subtraction of intra-abdominal pressure in 12 of 14 nonobstructed cases demonstrated a pressure-dependent pattern in which flow increased linearly in response to the pressure increase. In 2 nonobstructed children radionuclide constant pressure perfusion study failed: 1 due to crying and 1 to unknown causes. In 2 cases of complete or equivocal obstruction by constant perfusion (Whitaker test) only minimal or no flow rate was found at the maximum intrapelvic pressure increase of 24 cm. water. The urine flow was observed only in the repeated study in 3 patients. These phenomena were assumed to be due to immature expertise in the new technique. This new technique can provide physiological measurement of the urine flow at variable levels of constant intrapelvic pressure in hydronephrotic patients, although the pressure-flow relationship for identifying partial obstruction from nonobstruction still remains to be clarified in further clinical studies.

Adolescent↗
PubMed1992

Laparoscopy for nonpalpable testes in childhood: is inguinal exploration also necessary when vas and vessels exit the inguinal ring?

Laparoscopy has proved to be a safe method for determining the status for nonpalpable testes. In a combined series 52 boys with 57 nonpalpable testes were evaluated laparoscopically. Of the 57 nonpalpable testes 26 were located above the internal inguinal ring (abdominal), 4 were found more distally, and blind-ending vas and vessels terminated in the abdomen in 3, and beyond the internal ring (vanished testes) in 24. Of 29 abdominal testes primary orchiopexy was performed in 15, 4 were removed, the vessels were transected (Fowler-Stephens) in 5, stage 1 of staged repairs was done in 2, distinct laparoscopic evidence of blind-ending vessels and vas obviated further surgery in 2, and testis was not identified either laparoscopically or by abdominal exploration. Finally, inguinal exploration in 28 children in whom vas and vessels were found to exit the internal ring resulted in localization of 4 testes that were brought into the scrotum. Removal of 23 testicular nubbins and their evaluation histologically resulted in identification of viable tubular structures in 3. We recommend inguinal exploration in all children who on laparoscopy are found to have vas and vessels exit the internal ring, and removal of testicular nubbins.

Blood Vessels↗
PubMed2000

Exit from G1 and S phase of the cell cycle is regulated by repressor complexes containing HDAC-Rb-hSWI/SNF and Rb-hSWI/SNF.

We present evidence that Rb forms a repressor containing histone deacetylase (HDAC) and the hSWI/SNF nucleosome remodeling complex, which inhibits transcription of genes for cyclins E and A and arrests cells in the G1 phase of the cell cycle. Phosphorylation of Rb by cyclin D/cdk4 disrupts association with HDAC, relieving repression of the cyclin E gene and G1 arrest. However, the Rb-hSWI/SNF complex persists and is sufficient to maintain repression of the cyclin A and cdc2 genes, inhibiting exit from S phase. HDAC-Rb-hSWI/SNF and Rb-hSWI/SNF then appear to maintain the order of cyclin E and A expression during the cell cycle, which in turn regulates exit from G1 and from S phase, respectively.

Binding Sites↗
PubMed1999

Exit from mitosis is triggered by Tem1-dependent release of the protein phosphatase Cdc14 from nucleolar RENT complex.

Exit from mitosis in budding yeast requires a group of essential proteins--including the GTPase Tem1 and the protein phosphatase Cdc14--that downregulate cyclin-dependent kinase activity. We identified a mutation, net1-1, that bypasses the lethality of tem1 delta. NET1 encodes a novel protein, and mass spectrometric analysis reveals that it is a key component of a multifunctional complex, denoted RENT (for regulator of nucleolar silencing and telophase), that also contains Cdc14 and the silencing regulator Sir2. From G1 through anaphase, RENT localizes to the nucleolus, and Cdc14 activity is inhibited by Net1. In late anaphase, Cdc14 dissociates from RENT, disperses throughout the cell in a Tem1-dependent manner, and ultimately triggers mitotic exit. Nucleolar sequestration may be a general mechanism for the regulation of diverse biological processes.

Cell Cycle Proteins↗
PubMed2000

Pachytene exit controlled by reversal of Mek1-dependent phosphorylation.

During yeast meiosis, a checkpoint prevents exit from pachytene in response to defects in meiotic recombination and chromosome synapsis. This pachytene checkpoint requires two meiotic chromosomal proteins, Red1 and Mek1; Mek1 is a kinase that phosphorylates Red1. In mutants that undergo checkpoint-mediated pachytene arrest, Mek1 is active and Red1 remains phosphorylated. Activation of Mek1 requires the initiation of meiotic recombination and certain DNA damage checkpoint proteins. Mek1 kinase activity and checkpoint-induced pachytene arrest are counteracted by protein phosphatase type 1 (Glc7). Glc7 coimmunoprecipitates with Red1, colocalizes with Red1 on chromosomes, and dephosphorylates Red1 in vitro. We speculate that phosphorylated Red1 prevents exit from pachytene and that completion of meiotic recombination triggers Glc7-dependent dephosphorylation of Red1.

Chromosomes↗
PubMed2001

Protein sorting upon exit from the endoplasmic reticulum.

It is currently thought that all secretory proteins travel together to the Golgi apparatus where they are sorted to different destinations. However, the specific requirements for transport of GPI-anchored proteins from the endoplasmic reticulum to the Golgi apparatus in yeast could be explained if protein sorting occurs earlier in the pathway. Using an in vitro assay that reconstitutes a single round of budding from the endoplasmic reticulum, we found that GPI-anchored proteins and other secretory proteins exit the endoplasmic reticulum in distinct vesicles. Therefore, GPI-anchored proteins are sorted from other proteins, in particular other plasma membrane proteins, at an early stage of the secretory pathway. These results have wide implications for the mechanism of protein exit from the endoplasmic reticulum.

Adenosine Triphosphatases↗
PubMed2002

The ribosomal exit tunnel functions as a discriminating gate.

Translation of SecM stalls unless its N-terminal part is "pulled" by the protein export machinery. Here we show that the sequence motif FXXXXWIXXXXGIRAGP that includes a specific arrest point (Pro) causes elongation arrest within the ribosome. Mutations that bypass the elongation arrest were isolated in 23S rRNA and L22 r protein. Such suppressor mutations occurred at a few specific residues of these components, which all face the narrowest constriction of the ribosomal exit tunnel. Thus, we suggest that this region of the exit tunnel interacts with nascent translation products and functions as a discriminating gate.

Amino Acid Motifs↗
PubMed2002

salvador Promotes both cell cycle exit and apoptosis in Drosophila and is mutated in human cancer cell lines.

The number of cells in an organism is determined by regulating both cell proliferation and cell death. Relatively few mechanisms have been identified that can modulate both of these processes. In a screen for Drosophila mutations that result in tissue overgrowth, we identified salvador (sav), a gene that promotes both cell cycle exit and cell death. Elevated Cyclin E and DIAP1 levels are found in mutant cells, resulting in delayed cell cycle exit and impaired apoptosis. Salvador contains two WW domains and binds to the Warts (or LATS) protein kinase. The human ortholog of salvador (hWW45) is mutated in three cancer cell lines. Thus, salvador restricts cell numbers in vivo by functioning as a dual regulator of cell proliferation and apoptosis.

Amino Acid Sequence↗
PubMedDate not supplied

Localization and regulation of Ca2+ entry and exit pathways in exocrine gland cells.

Studies of Ca2+ transport pathways in exocrine gland cells have been useful, chiefly because of the polarized nature of the secretory epithelial cells. In pancreatic acinar cells, for example, Ca2+ reloading of empty intracellular stores can occur solely via Ca2+ entry through the basal part of the plasma membrane. On the other hand, the principal site for intracellular Ca2+ release-with the highest concentration of inositol 1,4,5-trisphosphate (IP(3)) receptors-is in the apical secretory pole close to the apical plasma membrane. This apical part of the plasma membrane contains the highest density of Ca2+ pumps and is therefore the principal site for Ca2+ extrusion. On the basis of the known properties of Ca2+ entry and exit pathways in exocrine gland cells, the mechanisms controlling Ca2+ exit and entry are discussed in relation to recent direct information about Ca2+ transport into and out of the endoplasmic reticulum (ER) and the mitochondria in these cells.

Animals↗
PubMed1996

The exit of lymphocytes and RBCs from the peritoneal cavity of sheep.

The purpose of this study was to compare the exit rates and migration pathways of 51Cr-labeled lymphocytes from the peritoneal cavity into the blood with those of a non-motile cell population, 111In-RBCs, in order to determine whether lymphocytes actively migrate from the peritoneal cavity. Radiolabeled cells were infused into the peritoneal cavity and multiple samples of lymph draining from the peritoneal cavity and/or blood were obtained, then the animal was sacrificed and various tissues were harvested and assayed for radioactivity. The recovery of 51Cr-lymphocytes from the mesenteric nodes was not significantly different from that of nodes anatomically distant from the cavity, so it is unlikely that large numbers of lymphocytes migrate across the mesothelial lining of the cavity and into the mesenteric lymphatics. However, the caudal mediastinal node contained about 18-fold more 51Cr-lymphocytes and 473 times as many 111In-RBCs, confirming the importance of this node in the drainage of cells and fluid from the cavity. The hepatic node also appears to receive cells directly from the peritoneal cavity. We also calculated the recovery of labeled cells at the end of the experiment (T = 40 h), and found that the recovery of 51Cr-lymphocytes (3.87 +/- 1.29% ID) in the blood was much lower than that of 111In-RBCs (35.28 +/- 5.02% ID). This difference can be attributed mainly to the traffic of labeled lymphocytes out of the blood rather than the selective retention of lymphocytes within the peritoneal cavity. Cannulation of the caudal mediastinal efferent lymphatic and the thoracic duct, which drain the peritoneal cavity, revealed approximately a 3-fold higher cumulative recovery of 111In-RBCs than 51Cr-lymphocytes over 6 h. However, by 40 h the percentage of labeled RBCs and lymphocytes remaining in the cavity was not significantly different. While 51Cr-lymphocytes may leave the peritoneal cavity at a slower rate than 111In-RBCs, both cell populations appear to exit solely via lymphatic vessels.

Animals↗
PubMed2002

The ex utero intrapartum treatment (EXIT) procedure in fetal neck masses: a case report and review of the literature.

Large fetal neck masses can cause airway obstructions with potential fetal demise after delivery. The relationship of the neck mass to airway structures can be defined prenatally with ultrasound and magnetic resonance imaging (MRI). The ex utero intrapartum treatment (EXIT) procedure can be used to obtain a fetal airway while feto-maternal circulation is preserved to optimise fetal outcome. We present a case in which prenatally a large fetal neck mass was diagnosed on ultrasound and a successful EXIT procedure was performed. A review of the literature is given and the prenatal use of ultrasonography and MRI in case of fetal neck masses is discussed.

Adult↗
PubMed2004

The Groningen Orthopedic Exit Strategy (GOES): a home-based support program for total hip and knee arthroplasty patients after shortened hospital stay.

The number of total hip and knee arthroplasty patients in The Netherlands will increase progressively in the coming decades. A reaction to this trend is a shortening of hospital stays. This however should not result in uncertainty, lack of information and unnecessary medical consumption by patients at home. Based on insights from social cognitive theory, an exit strategy is described to support patients during their rehabilitation at home. It is our hypothesis that patients who participate in such a support program will be able to resume activities of daily living more quickly and effectively, and will reach higher levels of physical activity compared to patients who only follow the shortened program. To determine the effectiveness of the exit strategy, mediating variables (self-efficacy, social support and pain coping) and outcome variables (activities of daily living, physical activity behavior, health-related quality of life and gait analysis) will be measured.

Activities of Daily Living↗
PubMed1999

Exit jet particle velocity in the in vivo canine laryngeal model with variable nerve stimulation.

This study extends previous work on exit jet particle velocity in the in vivo canine model of phonation by measuring air particle velocity at multiple locations in the midline of the glottis and across multiple levels of recurrent laryngeal nerve (RLN) and superior laryngeal nerve (SLN) stimulation. In a second experiment, exit jet particle velocity was measured at midline and offmidline positions with constant levels of RLN and SLN stimulation. In this study, peak particle velocity was higher at the anterior commissure than at the posterior commissure in the midline of the glottis, and peak particle velocity was higher at the midline than at offmidline positions. In addition, increasing levels of RLN stimulation resulted in increasing peak particle velocity; however, increasing levels of SLN stimulation failed to produce a uniform effect on peak particle velocity.

Air↗
PubMed2001

The schedule of destruction of three mitotic cyclins can dictate the timing of events during exit from mitosis.

BACKGROUND: Degradation of the mitotic cyclins is a hallmark of the exit from mitosis. Induction of stable versions of each of the three mitotic cyclins of Drosophila, cyclins A, B, and B3, arrests mitosis with different phenotypes. We tested a recent proposal that the destruction of the different cyclins guides progress through mitosis. RESULTS: Real-time imaging revealed that arrest phenotypes differ because each stable cyclin affects specific mitotic events differently. Stable cyclin A prolonged or blocked chromosome disjunction, leading to metaphase arrest. Stable cyclin B allowed the transition to anaphase, but anaphase A chromosome movements were slowed, anaphase B spindle elongation did not occur, and the monooriented disjoined chromosomes began to oscillate between the spindle poles. Stable cyclin B3 prevented normal spindle maturation and blocked major mitotic exit events such as chromosome decondensation but nonetheless allowed chromosome disjunction, anaphase B, and formation of a cytokinetic furrow, which split the spindle. CONCLUSIONS: We conclude that degradation of distinct mitotic cyclins is required to transit specific steps of mitosis: cyclin A degradation facilitates chromosome disjunction, cyclin B destruction is required for anaphase B and cytokinesis and for directional stability of univalent chromosome movements, and cyclin B3 degradation is required for proper spindle reorganization and restoration of the interphase nucleus. We suggest that the schedule of degradation of cyclin A, cyclin B, and then cyclin B3 contributes to the temporal coordination of mitotic events.

Anaphase↗
PubMed2001

Order of function of the budding-yeast mitotic exit-network proteins Tem1, Cdc15, Mob1, Dbf2, and Cdc5.

The Dbf2 protein kinase functions as part of the mitotic-exit network (MEN), which controls the inactivation of the Cdc28-Clb2 kinase in late mitosis [1]. The MEN includes the Tem1 GTP binding protein; the kinases Cdc15 and Cdc5; Mob1, a protein of unknown function; and the phosphatase Cdc14 [2]. Here we have used Dbf2 kinase activity to investigate the regulation and order of function of the MEN. We find that Tem1 acts at the top of the pathway, upstream of Cdc15, which in turn functions upstream of Mob1 and Dbf2. The Cdc5 Polo-like kinase impinges at least twice on the MEN since it negatively regulates the network, probably upstream of Tem1, and is also required again for Dbf2 kinase activation. Furthermore, we find that regulation of Dbf2 kinase activity and actin ring formation at the bud neck are causally linked. In metaphase-arrested cells, the MEN inhibitor Bub2 restrains both Dbf2 kinase activity [3] and actin ring formation [4]. We find that the MEN proteins that are required for Dbf2 kinase activity are also required for actin ring formation. Thus, the MEN is crucial for the regulation of cytokinesis, as well as mitotic exit.

Fungal Proteins↗
PubMed2002

Mitotic exit: delaying the end without FEAR.

Activation of Cdc14 phosphatase, controlled by a signalling cascade known as the mitotic exit network, is the final switch that drives cells from mitosis into the next cell cycle. The recent discovery of a novel network that regulates early Cdc14 activation has revealed the unexpected existence of a two-step control of mitotic exit.

Anaphase↗