Site Of Arrest Research Articles

Foreign Bodies Causing Asphyxiation in Children: The Experience of the Buenos Aires Paediatric ORL Clinic

Inhalation or aspiration of a foreign body (FB) occurs relatively frequently in young children. The size, shape, type and site of arrest of the FB lead to variability in the clinical picture. The present study included data from 65 cases of FB inhalation presenting over 1 year at the Children's Hospital Gutierrez, Buenos Aires, Argentina, compared with information from four well-known published case series chosen as representative of other cultural and geographical backgrounds: the USA, Europe, North Africa (Egypt) and Asia (India). The mean age of children studied was 4.03 years. Injuries happened mainly at home (53 cases [81.54%]) and under adult supervision (59 cases [90.77%]). The most frequently inhaled FB was nuts, however, in contrast to previous reports, the majority of incidents involved inhalation of an inorganic, rather than an organic (food) FB. Complications included pneumonia (three cases), atelectasis (two cases) and pneumonitis (one case). No deaths were recorded. These data suggest that children play with objects inappropriate for their age, such as pins and nails, that adults may not be aware of the choking risks, and that more effort is required in educating caregivers about these risks.

Predictors for Good Cerebral Performance Among Adult Survivors of Out-of-Hospital Cardiac Arrest: Abe T, Yasuharu T, Ishimatsu S. Resuscitation 2009;80:431–6

This review of a prospectively obtained data registry of 9232 out-of-hospital cardiac arrest patients in Japan sought to identify predictors of good neurologic outcomes after out-of-hospital cardiac arrest. Of 9232 resuscitative attempts, 122 patients were found to have good cerebral performance (85/122 = 70%) or moderate cerebral disability (37/122 = 30%). The authors noted that those with good cerebral performance were more likely to have had a cardiac cause of arrest, receive bystander cardiopulmonary resuscitation at the site of arrest, have pupillary response upon arrival at the emergency department (ED), and have spontaneous respirations upon arrival at the ED.

Endothelial cell activation leads to neutrophil transmigration as supported by the sequential roles of ICAM-2, JAM-A, and PECAM-1

AbstractLeukocyte transmigration is mediated by endothelial cell (EC) junctional molecules, but the associated mechanisms remain unclear. Here we investigate how intercellular adhesion molecule-2 (ICAM-2), junctional adhesion molecule-A (JAM-A), and platelet endothelial cell adhesion molecule (PECAM-1) mediate neutrophil transmigration in a stimulus-dependent manner (eg, as induced by interleukin-1β [IL-1β] but not tumor necrosis factor-α [TNF-α]), and demonstrate their ability to act in sequence. Using a cell-transfer technique, transmigration responses of wild-type and TNF-α p55/p75 receptor-deficient leukocytes (TNFR−/−) through mouse cremasteric venules were quantified by fluorescence intravital microscopy. Whereas wild-type leukocytes showed a normal transmigration response to TNF-α in ICAM-2−/−, JAM-A−/−, and PECAM-1−/− recipient mice, TNFR−/− leukocytes exhibited a reduced transmigration response. Hence, when the ability of TNF-α to directly stimulate neutrophils is blocked, TNF-α–induced neutrophil transmigration is rendered dependent on ICAM-2, JAM-A, and PECAM-1, suggesting that the stimulus-dependent role of these molecules is governed by the target cell being activated. Furthermore, analysis of the site of arrest of neutrophils in inflamed tissues from ICAM-2−/−, JAM-A−/−, and PECAM-1−/− mice demonstrated that these molecules act sequentially to mediate transmigration. Collectively, the findings provide novel insights into the mechanisms of action of key molecules implicated in leukocyte transmigration.

Arthroscopically Assisted Central Physeal Bar Resection

Thirty-seven central physeal bars were removed with an arthroscopically assisted technique. Thirty children (32 cases) have been followed to maturity or physeal closure. There were 19 boys and 11 girls, aged 4-14 years (mean, 9.5 years). Site of arrest was distal femur (15), proximal tibia (9), distal tibia (6), and distal radius (2). Mean follow-up was 6.5 years (range, 2-12 years). Adequate longitudinal growth was realized in 21 patients (70%) just after bar resection. Five patients (17%) required osteotomy, lengthening, or epiphysiodesis in addition to bar resection. In 4 patients (13%), bar resection failed. Failures occurred in those patients whose source of growth arrest was infection (3) or degree of physeal trauma approached 50% (1 case). This is the first series that studies and documents the efficacy of the arthroscope in central physeal bar resection. It provides the best visualization with minimal morbidity. The technique is described, including a discussion of technical tips and pitfalls.

¿Están justificadas las dosis elevadas de adrenalina en la parada cardiorrespiratoria en niños?

To evaluate the impact on survival of intravenous or intraosseous high-dose epinephrine compared with standard doses in children with cardiorespiratory arrest. We performed a multicenter, prospective study. Cardiopulmonary resuscitation data from 283 children was collected following international guidelines (Utstein style) over 18 months. In a secondary analysis we studied survival in 92 children who were treated with intravenous or intraosseous epinephrine. One or more conventional doses of epinephrine (0.01 mg/kg) were administered in 12 patients and a first conventional dose followed by one or more high doses (0.1 mg/kg) were administered in 80 patients. The age and weight of children in the conventional-dose group were higher than those in the high-dose group (97.1 +/- 70.5 months vs 29.9 +/- 36.9 months, p = 0.03 and 24.7 +/- 20.8 kg vs 11.9 +/- 8.9 kg, p = 0.037, respectively). The number of doses administered in the conventional-dose group was lower than that in the high-dose group (4 +/- 4 vs 5.4 +/- 3.4, p = 0.01). No significant differences were observed between the two groups in type of arrest, site of arrest, initial electrocardiographic rhythm, response to resuscitation attempts with return of spontaneous circulation, total resuscitation time, neurological status at the end of the episode and survival to hospital discharge and at 1-year of follow-up. Although the present study has considerable limitations, the results suggest that high doses of epinephrine do not improve survival in cardiorespiratory arrest in children.

Direct visualization of nitric oxide release by liver cells after the arrest of metastatic tumor cells in the hepatic microvasculature 1

Background Our previous studies have shown that the injection of B16F1 melanoma cells into the mesenteric vein can induce the rapid local release of nitric oxide (NO) in the liver, causing apoptosis of the melanoma cells in the liver sinusoids and inhibiting the subsequent formation of hepatic metastases. In this study, we have investigated the distribution and cellular source of NO in this model. Materials and methods In situ liver perfusion was established in both wild-type (wt) and endothelial nitric oxide synthase knockout (eNOS KO) C57BL/6 mice. A specific fluorescent NO probe, 4,5-diaminofluorescein diacetate (DAF-2 DA) (5 μmol/L), was perfused into the portal venous system to label the liver tissue. Then, a MitoTracker Orange labeled B16F1 melanoma cell suspension (2 × 10 6 cells/ml) was injected through a portal vein catheter by a peristaltic pump. Images of the liver tissue were taken by confocal microscopy from a selected area to determine the cellular source of NO. For quantification, the fluorescence intensity of this area was measured over time by Fluoview software. Results Diaminotriazolofluorescein (DAF-2T) fluorescence (indicating NO generation) was detected in hepatic parenchymal cells located in the periportal region in both wt C57BL/6 and eNOS KO C57BL/6 mice and was intensified by increased flow rate in the portal venous system. The B16F1 cells arrested in the periportal sinusoids, corresponding to zone 1 of the hepatic acinus. DAF-2T fluorescence was expressed by both sinusoidal lining cells and hepatocytes at the site of tumor cell arrest. The fluorescence intensity of these cells increased ∼2-fold over a time of 500 s. In contrast, there was no increase in the fluorescence intensity of the sinusoidal lining cells and hepatocytes in mice perfused with buffer or in eNOS KO mice perfused with B16F1 cells. Conclusion This study demonstrates that NO is produced by hepatic parenchymal cells mainly located in the periportal zones and that the arrest of the B16F1 melanoma cells causes an eNOS-dependent local burst of NO by the sinusoidal lining cells and hepatocytes in the periportal areas.

Preoperative correlation of intraoperative cortical mapping with magnetic resonance imaging landmarks to predict localization of the Broca area

Broca identified the posterior third of the inferior frontal gyrus as a locus essential for the production of fluent speech. The authors have conducted this retrospective analysis in an attempt to find readily identifiable landmarks on magnetic resonance (MR) imaging that correspond to intraoperative cortical stimulation-induced speech arrest. These landmarks demonstrate novel structural-functional relationships that can be used preoperatively to predict the location of the Broca area. Using a neuronavigation system, sites where stimulation produced speech arrest (Broca area) were recorded in a consecutive series of patients undergoing awake tumor resections in the perisylvian territory of the dominant hemisphere. The authors reviewed 33 consecutive patients by projecting the MR imaging data sets and marking the site where the Broca area was identified. Sulcus topography was analyzed with respect to this site by scrolling into neighboring planes and classifying the frontal operculum into one of the four schemes of sulcus variability described by Ebeling, et al. The following categories of frontal opercula were found: 18 (69%) of 26 were Type I, eight (31%) of 26 were Type III, and seven cases eluded classification because of sulcal effacement. For patients with Type I anatomy, the Broca area was adjacent to, and distributed evenly around, the inferior precentral sulcus (IPS). Quantitatively, the site of speech arrest was located a mean of 2.4 +/- 0.25 cm from the anteroinferior aspect of the pars opercularis, where it abuts the subarachnoid space surrounding the apex of the pars triangularis. For all patients with Type III anatomy, the Broca area was adjacent to the accessory sulcus that lies immediately posterior to the IPS. In these patients the mean distance from the anterior inferior pars opercularis was 2.3 +/- 0.29 cm. The mean distance from the Broca area to the edge of the tumor for the 26 patients with clear sulcal anatomy was 1.29 +/- 0.12 cm. The results indicate a correlation between the structure of the frontal operculum as seen on MR imaging and the functional localization of speech arrest in the dominant hemisphere. Additionally, sulcal landmarks that can be used preoperatively to predict the location of the Broca area within the inferior frontal gyrus are described based on the patient population. This information will allow the surgeon to determine if an awake craniotomy is necessary to identify the Broca area when planning a surgical procedure near the dominant frontal operculum.

Arrest of B16 Melanoma Cells in the Mouse Pulmonary Microcirculation Induces Endothelial Nitric Oxide Synthase-Dependent Nitric Oxide Release that Is Cytotoxic to the Tumor Cells

Metastatic cancer cells seed the lung via blood vessels. Because endothelial cells generate nitric oxide (NO) in response to shear stress, we postulated that the arrest of cancer cells in the pulmonary microcirculation causes the release of NO in the lung. After intravenous injection of B16F1 melanoma cells, pulmonary NO increased sevenfold throughout 20 minutes and approached basal levels by 4 hours. NO induction was blocked by N(G)-nitro-L-arginine methyl ester (L-NAME) and was not observed in endothelial nitric oxide synthase (eNOS)-deficient mice. NO production, visualized ex vivo with the fluorescent NO probe diaminofluorescein diacetate, increased rapidly at the site of tumor cell arrest, and continued to increase throughout 20 minutes. Arrested tumor cells underwent apoptosis with apoptotic counts more than threefold over baseline at 8 and 48 hours. Neither the NO signals nor increased apoptosis were seen in eNOS knockout mice or mice pretreated with L-NAME. At 48 hours, 83% of the arrested cells had cleared from the lungs of wild-type mice but only approximately 55% of the cells cleared from eNOS-deficient or L-NAME pretreated mice. eNOS knockout and L-NAME-treated mice had twofold to fivefold more metastases than wild-type mice, measured by the number of surface nodules or by histomorphometry. We conclude that tumor cell arrest in the pulmonary microcirculation induces eNOS-dependent NO release by the endothelium adjacent to the arrested tumor cells and that NO is one factor that causes tumor cell apoptosis, clearance from the lung, and inhibition of metastasis.

Part 12: From Science to Survival

Part 12: From Science to Survival

Suppression of cell cycle progression by flavonoids: dependence on the aryl hydrocarbon receptor.

Some flavonoids are ligands of the aryl hydrocarbon receptor (AHR) and cause cell cycle arrest. The dependency of the cytostatic effects of five flavonoids (flavone, alpha-naphthoflavone, apigenin, 3'-methoxy-4'-nitroflavone and 2'-amino-3'-methoxyflavone) on a functional AHR was examined in AHR-containing rat hepatoma 5L cells and an AHR-deficient cell line (BP8) derived from the 5L line. The potent AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was cytostatic to the 5L line due to the induction of a G(1) arrest and dramatically elevated steady-state levels of CYP1A1 mRNA. TCDD affected neither the proliferation nor CYP1A1 mRNA contents of BP8 cells. With the exception of apigenin, the flavonoids under study induced G(1) arrest in both 5L and BP8 cells when used at concentrations at which they functioned as AHR agonists, but not antagonists. Apigenin-treated 5L and BP8 cultures primarily arrested in G(2)/M. The AHR-containing murine hepatoma cell line 1c1c7 arrested following exposure to AHR agonist concentrations of flavone and alpha-naphthoflavone, but not TCDD. Unlike the G(1) arrest observed in 5L cultures, the latter two flavonoids caused principally G(2)/M arrest in 1c1c7 cells. These studies demonstrate that the cytostatic activities of flavonoids do not require the AHR and the site of checkpoint arrest with a specific flavonoid can vary with cell type.

Localization and characterization of speech arrest during transcranial magnetic stimulation

Objective: To determine the anatomic and physiologic localization of speech arrest induced by repetitive transcranial magnetic stimulation (rTMS), and to examine the relationship of speech arrest to language function.Methods: Ten normal, right-handed volunteers were tested in a battery of language tasks during rTMS. Four underwent mapping of speech arrest on a 1 cm grid over the left frontal region. Compound motor action potentials from the right face and hand were mapped onto the same grid. Mean positions for speech arrest and muscle activation were identified in two subjects on 3-dimensional MRI.Results: All subjects had lateralized arrest of spontaneous speech and reading aloud during rTMS over the left posterior-inferior frontal region. Writing, comprehension, repetition, naming, oral praxis, and singing were relatively spared (P<.05). Stimulation on the right during singing abolished melody in two subjects, but minimally affected speech production. The area of speech arrest overlay the caudal portion of the left precentral gyrus, congruous with the region where stimulation produced movement of the right face.Conclusions: The site of magnetic speech arrest appears to be the facial motor cortex. Its characteristics differ from those of classic aphasias, and include a prominent dissociation among different types of speech output.

Forward and retrograde trafficking in mitotic animal cells. ER-Golgi transport arrest restricts protein export from the ER into COPII-coated structures.

Protein transport arrest occurs between the ER and Golgi stack of mitotic animal cells, but the location of this block is unknown. In this report we use the recycling intermediate compartment protein ERGIC 53/p58 and the plasma membrane protein CD8 to establish the site of transport arrest. Recycled ERGIC 53/p58 and newly synthesised CD8 accumulate in ER cisternae but not in COPII-coated export structures or more distal sites. During mitosis the tubulovesicular ER-related export sites were depleted of the COPII component Sec13p, as shown by immunoelectron microscopy, indicating that COPII budding structures are the target for mitotic inhibition. The extent of recycling of Golgi stack residents was also investigated. In this study we used oligosaccharide modifications on CD8 trapped in the ER of mitotic cells as a sensitive assay for recycling of Golgi stack enzymes. We find that modifications conferred by the Golgi stack-resident GalNac transferase do occur on newly synthesised CD8, but these modifications are entirely due to newly synthesised transferase rather than to enzyme recycled from the Golgi stack. Taken together our findings establish for the first time that the site of ER-Golgi transport arrest of mitotic cells is COPII budding structures, and they clearly speak against a role for recycling in partitioning of Golgi stack proteins via translocation to the ER.

Evidence for an early G1 ionic event necessary for cell cycle progression and survival in the MCF-7 human breast carcinoma cell line.

The mechanism of the G0/G1 arrest and inhibition of proliferation by quinidine, a potassium channel blocker, was investigated in a tissue culture cell line, MCF-7, derived from a human breast carcinoma. The earliest measurable effect of quinidine on the cell cycle was a decrease in the fraction of cells in S phase at 12 hr, followed by the accumulation of cells in G1/G0 phases at 30 hr. Arrest and release of the cell cycle established quinidine as a cell synchronization agent, with a site of arrest in early G1 preceding the lovastatin G1 arrest site by 5-6 hr. There was a close correspondence among the concentration-dependent arrest by quinidine in G1, depolarization of the membrane potential, and the inhibition of ATP-sensitive potassium currents, supporting a model in which hyperpolarization of the membrane potential and progression through G1 are functionally linked. Furthermore, the G1 arrest by quinidine was overcome by valinomycin, a potassium ionophore that hyperpolarized the membrane potential in the presence of quinidine. With sustained exposure of MCF-7 cells to quinidine, expression of the Ki67 antigen, a marker for cells in cycle, decreased, and apoptotic and necrotic cell death ensued. We conclude that MCF-7 cells that fail to progress through the quinidine-arrest site in G1 die.

Human Immunodeficiency Virus Seroprevalence Among Adults Treated for Out-of-Hospital Cardiac Arrest in Seattle, Washington, 1989–1993

Study objective: To estimate the potential risk of HIV exposure for those providing emergency care for out-of-hospital cardiac arrest in Seattle, Washington, by surveying the seroprevalence of HIV in the patient population. Methods: We surveyed the seroprevalence of HIV among 1,474 persons treated for out-of-hospital cardiac arrest by paramedics during the years 1989 through 1993. Blood specimens were obtained at the site of cardiac arrest, stripped of personal identifiers, and tested for HIV-1 and HIV-2 by enzyme immunoassay and Western blot. Results: Among the 1,011 men, 8 (.8%, 95 percent confidence interval .3% to 1.4%) were seropositive for HIV-1 during this 5-year period; all 8 were younger than age 55. No serologic evidence of HIV infection was detected among the 463 women. Conclusion: The seroprevalence of HIV in this population was relatively low. Risk of possible HIV transmission during paramedic treatment was remote. [Weinmann S, Siscovick DS, Raghunathan TE, Handsfield H, Copass M, Cobb LA: Human immunodeficiency virus seroprevalence among adults treated for out-of-patient cardiac arrest in Seattle, Washington, 1989–1993. Ann Emerg Med August 1998; 32:148-150.]

Echocardiographic observations during in hospital cardiopulmonary resuscitation.

To assess echocardiographic observations during in hospital cardiopulmonary resuscitation (CPR) and the utility of this information in the management of cardiac arrest. Echocardiographic system brought to the hospital site of cardiac arrest and applied to patients in conjunction with conventional CPR. Large community-hospital with portable echocardiographic system and an alerted cardiology team skilled in this technique. Mechanical asystole was initially observed in 18 (90%) of 20 cardiac arrest patients during CPR, including four patients with severe bradyarrhythmia as the arrest rhythm. The return of ventricular contractions in four of these 18 patients a short time after starting CPR prompted positive inotropic therapy. Ventricular wall motion was noted in two patients with severe bradyarrhythmia (pseudo-electromechanical dissociation) and the causes of cardiac arrest identified as massive pulmonary embolism and hypovolemia, respectively. A gel-like, coalescent echo contrast within the cardiac chambers was observed 20 to 30 mins after CPR in ten patients with unrelenting cardiac arrest and uniformly associated with an adverse outcome. Six patients survived resuscitation but only two patients survived to hospital discharge. An echocardiographic examination is feasible during CPR and may offer useful information in the management of the individual patients with cardiac arrest. It may depict the proximate cause of cardiac arrest, e.g., pulmonary embolism, cardiac tamponade, or hypovolemia, and signal the return of ventricular contractions in patients with initially absent mechanical activity. The appearance of intracardiac coalescent echo contrast in our patients with unrelenting cardiac arrest was associated with a failed outcome. The role of echocardiographic imaging in the setting of advanced cardiac life support requires further study.

Quality of mechanical, manual standard and active compression–decompression CPR on the arrest site and during transport in a manikin model

The quality of mechanical CPR (M-CPR) was compared with manual standard CPR (S-CPR) and active compression–decompression CPR (ACD-CPR) performed by paramedics on the site of a cardiac arrest and during manual and ambulance transport. Each technique was performed 12 times on manikins using teams from a group of 12 paramedic students with good clinical CPR experience using a random cross-over design. Except for some lost ventilations the CPR effort using the mechanical device adhered to the European Resuscitation Council guidelines, with an added time requirement of median 40 s for attaching the device compared with manual standard CPR. Throughout the study, in comparison with mechanical CPR the quality of CPR with either manual method was significantly worse. In particular, there were considerable individual variations during stretcher transport. With S-CPR and ACD-CPR the median compression times were 38 and 31%, significantly lower than the recommended 50%, and 46–98% of the decompression efforts with ACD-CPR were too weak, particularly during transport on the stairs. With both manual methods, there were no significant differences in the CPR effort between the site of the arrest and the ambulance transport. However, compression rates were reduced and became more erratic during stretcher transport to the ambulance. When walking horizontally, a median of 19% of S-CPR compressions and 84% of ACD-CPR compressions were to weak. On the stairs, 68% of S-CPR compressions and 100% of ACD-CPR compressions were too weak. In conclusion, when evaluated on a manikin, in comparison with manual standard and ACD-CPR, mechanical CPR adhered more closely to ERC guidelines. This was particularly true when performing CPR during transport on a stretcher.

Thiol-bearing compounds selectively inhibit protein kinase C-dependent oxidative events and proliferation in human T cells

The aminothiol cysteamine at 10 −5 to 10 −4 M concentrations inhibited both the proliferation of mitogenically stimulated human peripheral mononuclear cells and the phorbol myristate acetate-mediated oxidation of 2′,7′-dichlorofluorescin within these cells. Both 2′,7′-dichlorofluorescin oxidation and the proliferative response were maximally sensitive to cysteamine-induced inhibition during the first 2 h of mitogenic stimulation. This period of sensitivity indicates that cysteamine preferentially arrests cells transiting from G 0 to G 1 and is the first such demonstration, of an early cell cycle site of arrest for this compound. 2,3-Dimercapto-1-propane-sulfonic acid and WR 1065 were found to be more effective than cysteamine in attenuating T cell replication but not N-acetylcysteine. Aminothiols preferentially inhibited the intracellular oxidation of 2′,7′-dichlorofluorescin, rather than the activity of protein kinase C, which initiates the oxidation, indicating that oxidative events are one of a number of crucial and independent events required for the successful transition through G 0–G 1. Since aminothiols affect both lectin and PMA/ionomycin-directed proliferation, these aminothiol-sensitive events may serve to integrate and regulate common pathways in T cell activation.

Breeding System and Reproductive Success of Thryptomene calycina (Myrtaceae)

Thryptomene calycina (Lindl.) Stapf is a small bush with a long flowering period in winter. Hundreds of small flowers open at one time. Its breeding system is highly self-incompatible, with an index of Self-Incompatibility of 0 - 0.1. The site of arrest of self-incompatible tubes is near the micropyle. In wild populations the natural seed set varies between 9 and 13%. Pollination is not a factor limiting seed set in these flowers since every stigma examined from wild populations carried some germinated pollen grains. The low level of seed production is because most pollinations are probably ineffective selfs which occur when pollen exudes from pores in the anthers directly over the stigma; air currents and rain splashing probably accentuate the effect. Self-pollination is facilitated by the long period of stigma receptivity which occurs for 12 days commencing 2 days after anthesis. Each flower contains approximately 60 000 pollen grains that are viable for up to 15 days. The pollen-ovule ratio is high, up to 32 000. Most pollen is shed 3 days after anthesis, but this depends on temperature, relative humidity and probably the water potential of flowers. The flowers are visited by few flying insects during most of the flowering season. In warm weather near the end of flowering a wide range of insects visit the flowers. Although the visitors are mostly small flies these are ineffective pollinators. The main potential pollinators are medium sized flies and bees.

Outcome after prehospital resuscitation is influenced by site of cardiac arrest

Outcome after prehospital resuscitation is influenced by site of cardiac arrest

The rubella virus E1 glycoprotein is arrested in a novel post-ER, pre-Golgi compartment.

Evidence is accumulating that a distinct compartment(s) exists in the secretory pathway interposed between the rough ER (RER) and the Golgi stack. In this study we have defined a novel post-RER, pre-Golgi compartment where unassembled subunits of rubella virus (RV) E1 glycoprotein accumulate. When RV E1 is expressed in CHO cells in the absence of E2 glycoprotein, transport of E1 to the Golgi complex is arrested. The compartment in which E1 accumulates consists of a tubular network of smooth membranes which is in continuity with the RER but has distinctive properties from either the RER, Golgi, or previously characterized intermediate compartments. It lacks RER and Golgi membrane proteins and is not disrupted by agents which disrupt either the RER (thapsigargin, ionomycin) or Golgi (nocodazole and brefeldin A). However, luminal ER proteins bearing the KDEL signal have access to this compartment. Kinetically the site of E1 arrest lies distal to or at the site where palmitylation occurs and proximal to the low temperature 15 degrees C block. Taken together the findings suggest that the site of E1 arrest corresponds to, or is located close to the exit site from the ER. This compartment could be identified morphologically because it is highly amplified in cells overexpressing unassembled E1 subunits, but it may have its counterpart among the transitional elements of non-transfected cells. We conclude that the site of E1 arrest may represent a new compartment or a differentiated proximal moiety of the intermediate compartment.