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C A Erickson

Publications and source records attributed to C A Erickson.

At least 37 records · Page 2Linked to original sources
PubMed1996

Using dipyridamole-thallium imaging to reduce cardiac risk in aortic reconstruction.

UNLABELLED: Cardiac morbidity and mortality remain the major operative risk following aortic reconstruction (AR) performed for aneurysmal and occlusive disease. We reviewed the preoperative cardiac evaluation and outcome in 209 patients who had AR between 1987 and 1992. Dipyridamole-thallium stress test (DTST) was performed in 147 (70.3%) patients. Fifty-six of these patients had a normal DTST and only 1 (1.8%) had a perioperative myocardial infarction (MI). Forty-six patients had a fixed defect on their DTST and 3 (6.5%) had perioperative MI. Forty-five patients had reversible defects on their DTST and 2 (4.4%) had perioperative MI with 1 cardiac death. Following DTST, 29 coronary catheterizations were performed. Ten catheterizations were normal or had minimal one-vessel coronary artery disease with an associated postoperative death in 1 patient due to cardiac dysrhythmia. Nineteen patients had abnormal coronary angiography, 1 of whom had a perioperative myocardial infarction and 5 of whom underwent coronary artery revascularization (CABG) (3) or percutaneous transluminal angioplasty (2) prior to AR without subsequent cardiac events. Forty-three (20.6%) had either no cardiac symptoms (40) or prior CABG (3) precluding invasive cardiac evaluation. There was one fatal perioperative myocardial infarction (2.3%), resulting in a cardiac mortality of 2.3% in this group. The remaining 19 patients who did not have a DTST (9.1%) had coronary angiography based on evidence of significant cardiac disease resulting in one CABG and one percutaneous transluminal angioplasty. There was one (5.3%) perioperative myocardial infarction in this group and no cardiac deaths. Thirty-day mortality was 3.8%, perioperative MI rate was 3.8%, and perioperative cardiac mortality was 1.0%. During the follow-up period (median, 18 months; range, 1-89), there were 19 deaths (10%) and the 5-year cumulative survival was 76%. CONCLUSION: Selective use of DTST can direct further evaluation, intervention, and subsequent perioperative care. This algorithm has enabled us to perform AR even in patients with defined perfusion abnormalities with acceptable morbidity. The true sensitivity, specificity, and predictive value of DTST can only be determined by a prospective trial.

Adult↗
PubMed1996

Contribution of single-unit spike waveform changes to temperature-induced alterations in hippocampal population spikes.

Brain temperature changes accompany exploratory behavior and profoundly affect field potential amplitudes recorded in hippocampus. The waveform alterations in fascia dentata include a reduction in population spike area, which might be explained by fewer granule cells firing in response to a given stimulus or by an alteration in the size or shape of the individual action potentials. This study was designed to assess these alternate possibilities. In experiment 1, changes in the shape and firing rates of single cells recorded in the fascia dentata of awake rats were compared with changes in the population spike before and after a bout of activity. Single-unit amplitudes were significantly reduced following exploration, and there was a small (< 3%) change in unit spike-width. These changes, however, were insufficient to account, in a linear fashion, for the entire decline in the population spike. In experiment 2, radiant heat was used to manipulate brain temperature in anesthetized rats. As in the first experiment, the magnitude of change in the extracellular units was much smaller than the change in population spike amplitude. The spontaneous firing rates of the cells were also modified by brain temperature changes. In experiment 3, the polysynaptic, contralateral commissural response (which covaries with changes in the ipsilateral population spike at a fixed temperature) was measured as a function of either exploratory behavior or radiant heat. The relationship between the ipsilateral population spike and corresponding polysynaptic commissural response was altered following exploration and passive warming in a manner consistent with a reduction in net granule cell output, reduced transmission efficacy through the polysynaptic circuit, or a combination of these. Taken together these data suggest that at least two factors contribute to temperature-dependent changes in the perforant path-evoked population spikes recorded in the fascia dentata: changes in the size of individual action potentials and alterations in discharge of action potentials in response to a given stimulus.

Action Potentials↗
PubMed1996

Ongoing vascular laboratory surveillance is essential to maximize long-term in situ saphenous vein bypass patency.

PURPOSE: The purpose of this study was to assess the contribution of ongoing graft surveillance to maximize long-term patency of lower limb in situ saphenous vein bypasses. METHODS: From January 1981 to October 1994, 556 autogenous grafts were constructed in 499 patients. The distal anastomosis was at the popliteal level in 207 (37%) and the tibial level in 349 (63%). All patients were enrolled in a prospective surveillance protocol to identify lesions that compromise graft patency and were evaluated at 1 day, 1 week, 6 weeks, and 3 months. Surveillance studies were then obtained every 3 months for the first 2 postoperative years and every 6 months thereafter. RESULTS: Four-hundred-fifty abnormalities were detected in 236 grafts. The median interval from the initial procedure to detection of an abnormality was 12 months (range 0 to 113 months) and varied with the location of the defect. Later in the life of the graft, progression of atherosclerotic disease manifested as inflow obstruction at a median of 15 months, and outflow disease threatened the graft at a median of 29 months (r = 0.0003). Of the 450 surveillance abnormalities, 294 (65%) occurred within the first 2 years after operation, and 156 (35%) developed more than 2 years after operation. Of the 236 grafts that developed surveillance abnormalities, 50 (21%) developed the initial defect more than 2 years after the initial bypass procedure. Eleven percent of grafts remaining free of abnormality after 2 years went on to fail. Sixty-seven interventions were performed on 62 extremities after 24 months, with 30 involving previously unrevised grafts. CONCLUSIONS: Because lesions amenable to revision continue to develop years after vein bypass construction, perpetual surveillance is required to ensure optimal rates of graft patency.

Analysis of Variance↗
PubMed1996

The dorsal neural tube organizes the dermamyotome and induces axial myocytes in the avian embryo.

Somites, like all axial structures, display dorsoventral polarity. The dorsal portion of the somite forms the dermamyotome, which gives rise to the dermis and axial musculature, whereas the ventromedial somite disperses to generate the sclerotome, which later comprises the vertebrae and intervertebral discs. Although the neural tube and notochord are known to regulate some aspects of this dorsoventral pattern, the precise tissues that initially specify the dermamyotome, and later the myotome from it, have been controversial. Indeed, dorsal and ventral neural tube, notochord, ectoderm and neural crest cells have all been proposed to influence dermamyotome formation or to regulate myocyte differentiation. In this report we describe a series of experimental manipulations in the chick embryo to show that dermamyotome formation is regulated by interactions with the dorsal neural tube. First, we demonstrate that when a neural tube is rotated 180 degrees around its dorsoventral axis, a secondary dermamyotome is induced from what would normally have developed as sclerotome. Second, if we ablate the dorsal neural tube, dermamyotomes are absent in the majority of embryos. Third, if we graft pieces of dorsal neural tube into a ventral position between the notochord and ventral somite, a dermamyotome develops from the sclerotome that is proximate to the graft, and myocytes differentiate. In addition, we also show that myogenesis can be regulated by the dorsal neural tube because when pieces of dorsal neural tube and unsegmented paraxial mesoderm are combined in tissue culture, myocytes differentiate, whereas mesoderm cultures alone do not produce myocytes autonomously. In all of the experimental perturbations in vivo, the dorsal neural tube induced dorsal structures from the mesoderm in the presence of notochord and floorplate, which have been reported previously to induce sclerotome. Thus, we have demonstrated that in the context of the embryonic environment, a dorsalizing signal from the dorsal neural tube can compete with the diffusible ventralizing signal from the notochord. In contrast to dorsal neural tube, pieces of ventral neural tube, dorsal ectoderm or neural crest cells, all of which have been postulated to control dermamyotome formation or to induce myogenesis, either fail to do so or provoke only minimal inductive responses in any of our assays. However, complicating the issue, we find consistent with previous studies that following ablation of the entire neural tube, dermamyotome formation still proceeds adjacent to the dorsal ectoderm. Together these results suggest that, although dorsal ectoderm may be less potent than the dorsal neural tube in inducing dermamyotome, it does nonetheless possess some dermamyotomal-inducing activity. Based on our data and that of others, we propose a model for somite dorsoventral patterning in which competing diffusible signals from the dorsal neural tube and from the notochord/floorplate specify dermamyotome and sclerotome, respectively. In our model, the positioning of the dermamyotome dorsally is due to the absence or reduced levels of the notochord-derived ventralizing signals, as well as to the presence of dominant dorsalizing signals. These dorsal signals are possibly localized and amplified by binding to the basal lamina of the ectoderm, where they can signal the underlying somite, and may also be produced by the ectoderm as well.

Animals↗
PubMed1995

Healing of venous ulcers in an ambulatory care program: the roles of chronic venous insufficiency and patient compliance.

PURPOSE: A nurse-managed/physician-supervised treatment program for venous ulceration was evaluated to determine the influence of venous hemodynamics, comorbidities, patient behavior, and ulcer characteristics on time to healing and time to recurrence. METHODS: The clinical course and long-term follow-up of 71 patients with 99 venous ulcers diagnosed between November 1981 and August 1994 were analyzed by a retrospective review of clinic records. Demographic data, severity of venous insufficiency, ulcer characteristics, and patient compliance were studied. Outcome variables were time to complete ulcer healing and time to first recurrence. RESULTS: Ninety-one percent of the ulcers healed completely at a median 3.4 months. There were 52 (57%) recurrences at a median 10.4 months. Ulcers on limbs with a venous refill time of 10 seconds or less demonstrated a significantly longer time to complete healing (p < or = 0.03); however, no effect on time to recurrence was observed. Patients who were in strict compliance with the treatment regimen (n = 32) had significantly faster healing (p < or = 0.02) and fewer recurrences (p < or = 0.004) compared with patients who were less compliant (n = 67). CONCLUSIONS: Most venous ulcers can be expected to heal when patients are enrolled in a nurse-managed/physician-supervised ambulatory ulcer clinic. Photoplethysmography-derived venous refill time of 10 seconds or less predicted delayed healing. Strict compliance with the treatment protocol significantly decreased the time to healing and prolonged the time to recurrence.

Adult↗
PubMed1995

Changes in the fibronectin-specific integrin expression pattern modify the migratory behavior of sarcoma S180 cells in vitro and in the embryonic environment.

The molecules that mediate cell-matrix recognition, such as fibronectins (FN) and integrins, modulate cell behavior. We have previously demonstrated that FN and the beta 1-integrins are used during neural crest cell (NCC) migration in vitro as well as in vivo, and that the FN cell-binding domains I and II exhibit functional specificity in controlling either NCC attachment, spreading, or motility in vitro. In the present study, we have analyzed the effect of changes in the integrin expression patterns on migratory cell behavior in vivo. We have generated, after stable transfection, S180 cells expressing different levels of alpha 4 beta 1 or alpha 5 beta 1 integrins, two integrins that recognize distinct FN cell-binding domains. Murine S180 cells were chosen because they behave similarly to NCC after they are grafted into the NCC embryonic pathways in the chicken embryo. Thus, they provide a model system with which to investigate the mechanisms controlling in vitro and in vivo migratory cell behavior. We have observed that either the overexpression of alpha 5 beta 1 integrin or the induction of alpha 4 beta 1 expression in transfected S180 cells enhances their motility on FN in vitro. These genetically modified S180 cells also exhibit different migratory properties when grafted into the early trunk NCC migratory pathways. We observe that alpha 5 and low alpha 4 expressors migrate in both the ventral and dorsolateral paths simultaneously, in contrast to the parental S180 cells or the host NCC, which are delayed by 24 h in their invasion of the dorsolateral path. Moreover, the alpha 4 expressors exhibit different migratory properties according to their level of alpha 4 expression at the cell surface. Cells of the low alpha 4 expressor line invade both the ventral and dorsolateral pathways. In contrast, the high expressors remain as an aggregate at the graft site, possibly the result of alpha 4 beta 1-dependent homotypic aggregation. Thus, changes in the repertoire of FN-specific integrins enable the S180 cells to exploit different pathways in the embryo and regulate the speed with which they disperse in vivo and in culture. Our studies correlate well with known changes in integrin expression during neural crest morphogenesis and strongly suggest that neural crest cells that migrate into the dorsolateral path, i.e., melanoblasts, do so only after they have upregulated the expression of FN receptors.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Avian neural crest cells can migrate in the dorsolateral path only if they are specified as melanocytes.

Neural crest cells are conventionally believed to migrate arbitrarily into various pathways and to differentiate according to the environmental cues that they encounter. We present data consistent with the notion that melanocytes are directed, by virtue of their phenotype, into the dorsolateral path, whereas other neural crest derivatives are excluded. In the avian embryo, trunk neural crest cells that migrate ventrally differentiate largely into neurons and glial cells of the peripheral nervous system. Neural crest cells that migrate into the dorsolateral path become melanocytes, the pigment cells of the skin. Neural crest cells destined for the dorsolateral path are delayed in their migration until at least 24 hours after migration commences ventrally. Previous studies have suggested that invasion into the dorsolateral path is dependent upon a change in the migratory environment. A complementary possibility is that as neural crest cells differentiate into melanocytes they acquire the ability to take this pathway. When quail neural crest cells that have been grown in culture for 12 hours are labeled with Fluoro-gold and then grafted into the early migratory pathway at the thoracic level, they migrate only ventrally and are coincident with the host neural crest. When fully differentiated melanocytes (96 hours old) are back-grafted under identical conditions, however, they enter the dorsolateral path and invade the ectoderm at least one day prior to the host neural crest. Likewise, neural crest cells that have been cultured for at least 20 hours and are enriched in melanoblasts immediately migrate in the dorsolateral path, in addition to the ventral path, when back-grafted into the thoracic level. A population of neural crest cells depleted of melanoblasts--crest cells derived from the branchial arches--are not able to invade the dorsolateral path, suggesting that only pigment cells or their precursors are able to take this migratory route. These results suggest that as neural crest cells differentiate into melanocytes they can exploit the dorsolateral path immediately. Even when 12-hour crest cells are grafted into stage 19-21 embryos at an axial level where host crest are invading the dorsolateral path, these young neural crest cells do not migrate dorsolaterally. Conversely, melanoblasts or melanocytes grafted under the same circumstances are found in the ectoderm. These latter results suggest that during normal development neural crest cells must be specified, if not already beginning to differentiate, as melanocytes in order to take this path.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Neural crest cells prefer the myotome's basal lamina over the sclerotome as a substratum.

Anterior sclerotome is presumed to be the only somitic tissue that guides neural crest cells as they migrate ventrally. In contrast, we report here that crest cells prefer the myotome's basal lamina over the sclerotome as a substratum. This conclusion stems from four observations. First, crest cells migrating between the neural tube and somite invade lumbar and thoracic somites only after the myotome has formed a basal lamina, as though they use this basal lamina to penetrate the somite. Second, crest cells alter their trajectories dramatically when they contact this basal lamina. They abruptly turn laterally and align closely with the myotome's basal surface. Third, crest cells invade sclerotome only when they fail to contact this basal lamina. For instance, the lateral half of each myotome is initially devoid of basal lamina. When the first crest cells reach the lateral myotome, they depart from the myotome's basal surface and penetrate lateral sclerotome. Only later, when a higher population density prevents some cells from contacting the basal lamina, do crest cells penetrate medial sclerotome. Conversely, crest cells that migrate between somites do not have access to myotome and fail to turn laterally. Fourth, when we prevent myotome development by surgically removing its precursor (the dermamyotome), crest cells fail to turn laterally within the somite. Instead, they move directly ventrally and colonize medial sclerotome. The preference for myotomal basal lamina implies that anterior sclerotome is a suboptimal environment for neural crest migration. The myotome's basal lamina may facilitate rapid migration through the somite before impediments to ventral migration develop.

Animals↗
PubMed1994

Glycoconjugates mark a transient barrier to neural crest migration in the chicken embryo.

We report that two molecular markers correlate with a transient inhibition of neural crest cell entry into the dorsolateral path between the ectoderm and the somite in the avian embryo. During the period when neural crest cells are excluded from the dorsolateral path, both peanut agglutinin lectin (PNA)-binding activity and chondroitin-6-sulfate (C6S) immunoreactivity are expressed within this path. Both markers decline as neural crest cells enter. Moreover, both markers are absent after an experimental manipulation that accelerates neural crest entry into this path. Specifically, dermamyotome deletions abolish expression of both markers and allow neural crest cells to enter the dorsolateral path precociously. After partial deletions, dermatome remnants remain. These remnants retain PNA and C6S labeling and impede migration locally. Local glycoconjugate expression thus correlates directly with avoidance responses. Since both PNA-binding activity and C6S expression also typify inhibitory somitic tissues, molecules indicated by these markers (or co-regulated molecules) are likely to inhibit both neural crest and axon advance.

Animals↗
PubMed1993

Morphogenesis of the avian trunk neural crest: use of morphological techniques in elucidating the process.

Morphological data generated from light and electron microscopy form the basis of our understanding of avian morphogenesis. Because chicken embryos are readily and cheaply obtained and are easily accessible for experimental manipulation, morphogenetic processes have been studied extensively in this species. Such studies have allowed us to identify the cells involved during morphogenesis, observe the shape changes or cellular translocations that accompany a morphogenetic process, and determine the timing of these events. Elucidation of the molecular basis of morphogenesis has awaited the integration of several additional approaches. Among these are experimental embryology, which has allowed us to understand cellular behavior associated with morphogenesis; immunocytochemistry, which has identified the macromolecular cues that regulate cell movements and the environmental factors that control them; and molecular techniques, which will permit us eventually to clarify the genetic regulation of morphogenesis. Although current research in development is heavily biased towards molecular biology, morphological studies continue to frame the questions that are now being addressed using molecular techniques. This review focuses on the cells of the neural crest as a model system where questions of avian morphogenesis have been profitably addressed.

Animals↗
PubMed1993

Comparison of long-term enhancement and short-term exploratory modulation of perforant path synaptic transmission.

Long-term enhancement (LTE/LTP) is an artificially induced form of synaptic change that may underlie memory storage in the hippocampus; however, there is as yet no evidence that this process occurs naturally as a result of normal neural activity. In the dentate gyrus, synaptic change does occur in conjunction with an animal's recent history of exploratory behavior. This change, which persists for a short time (ca. 30 min) following cessation of exploration, has been called short-term exploratory modulation (STEM). This experiment examined the relationship between LTE and STEM by comparing the magnitude of STEM before and after induction of LTE in rats with chronically implanted stimulating electrodes in the perforant path and recording electrodes in the fascia dentata. The absolute magnitude of STEM was the same before and after LTE saturation, suggesting that the processes are independent of each other. Furthermore, quantitative and qualitative analyses of the types of changes seen in the evoked-potential waveforms reveal different types of alteration. LTE includes an increase in EPSP slope, whereas STEM reflects an increase in EPSP onset. These data suggest that it is unlikely that STEM and LTE reflect the same synaptic process, and are at least partly consistent with recent reports suggesting that STEM may be mediated by activity-dependent changes in brain temperature.

Animals↗
PubMed1993

The role of cell-cell and cell-matrix interactions in the morphogenesis of the neural crest.

The neural crest is an excellent model system with which to study the molecular controls of morphogenesis. Neural crest cells initiate their migration from the dorsal portion of the neural epithelium owing to an epithelial-mesenchymal transformation. They then followed stereotyped pathways for long distances before reaching their multiple destinations, and they cease migration in defined regions where they undergo terminal differentiation. Recent experimental evidence, which is summarized in this review, suggests that these various steps in neural crest morphogenesis are influenced by cell-cell and cell-matrix adhesions. Future studies employing genetic mutants and molecular techniques should provide more direct evidence for the role of cell-cell and cell-matrix interactions in neural crest morphogenesis.

Animals↗
PubMed1993

From the crest to the periphery: control of pigment cell migration and lineage segregation.

Pigment cells are one of many cell types derived from the neural crest. This review focuses on the mechanisms that control the timing and pathways of migration of pigment cells into the epidermis and determinants that control the differentiation of pigment cells. Several factors may control the timing and pattern of pigment cell migration in the dorsolateral space including the loss of inhibitory molecules in the pathway, the appearance of chemotactic molecules emanating from the dispersing dermatome, and the differentiation of pigment cells, which may be the only neural crest derivative capable of utilizing the substratum found in the dorsolateral path. Control of pigment cell differentiation remains controversial. A working model presented in this review suggests that multipotent neural crest cells that disperse ventrally upon separation from the neural tube preserve neurogenic ability and lose melanogenic ability, whereas those cells that are arrested at the entrance to the dorsolateral path lose neurogenic ability so that the population becomes primarily melanogenic. During the time that the latter population is arrested in migration it is speculated that the neural crest cells are exposed to an environment comprised of specific extracellular matrix molecules and/or growth factors that enhance pigment cell differentiation.

Animals↗
PubMed1993

Thresholds for synaptic activation of transcription factors in hippocampus: correlation with long-term enhancement.

Recent studies suggest a role for rapid induction of transcription factors in stimulus-induced neuronal plasticity in the mammalian brain. Synaptic activation of transcription factors has been analyzed in the hippocampus using the long-term potentiation or enhancement (LTP/LTE) paradigm. Using this approach, several studies have identified transcription factors that are induced in hippocampal granule cells by NMDA receptor-dependent mechanisms; however, the link between long-term plasticity and activation of these genes has been called into question by reports suggesting that the thresholds for LTE and gene activation differ. To address this issue, we have used a chronic in vivo recording technique to monitor mRNA responses of several transcription factor genes to two different patterns of LTE-inducing electrical stimulation of entorhinal cortical afferents to hippocampus. One pattern consisted of 10 repetitions of a 20 or 25 msec train of pulses at 400 Hz (80 or 100 pulses total). This "10-train" pattern has been used in previous studies of LTE and produces robust synaptic enhancement lasting at least 3 d (Barnes, 1979). The other stimulation pattern consisted of 50 repetitions of a 20 msec train delivered at 400 Hz (400 pulses total), which is similar to parameters used in other studies reporting induction of c-fos in association with LTE (Dragunow et al., 1989; Jeffery et al., 1990; Abraham et al., 1992). Our results indicate that expression of zif268, monitored by in situ hybridization and immunostaining, is strongly induced by the 10-train stimulus pattern to levels similar to those induced by seizure activity. JunB mRNA levels are also modestly increased by the 10-train stimulus pattern; however, increases in JunB immunostaining were not detected. Neither c-fos nor c-jun mRNA were detectably induced by this stimulus. In contrast, the 50-train stimulus pattern resulted in a robust induction of c-fos and c-jun mRNA, in addition to zif268 and junB. Transcription factor responses to either stimulus pattern were blocked by the noncompetitive NMDA receptor antagonist MK-801. Identical transcription factor responses were observed in adult (6-12-month-old) and aged (23-26-month-old) rats, suggesting that synaptic mechanisms involved in these responses are preserved in aged animals. Analysis of LTE following either the 10- or 50-train stimulus patterns revealed identical magnitudes of initial induction and decay kinetics (approximately 3 d) and indicates that the 10-train stimulus pattern is sufficient to produce maximal synaptic enhancement.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1992

Descriptive and experimental analysis of the dispersion of neural crest cells along the dorsolateral path and their entry into ectoderm in the chick embryo.

We have characterized the dispersion of neural crest cells along the dorsolateral path in the trunk of the chicken embryo and experimentally investigated the control of neural crest cell entry into this path. The distribution of putative neural crest cells was analyzed in plastic sections of embryos that had been incubated for 24 hr in HNK-1 antibody, a procedure that we show successfully labels neural crest cells in the dorsolateral path and ectoderm. In accord with earlier observations, crest cells delay entering the dorsolateral path until a day or more after their counterparts have colonized the ventral path. However, once crest cells enter, they disperse rapidly through the path dorsal to the somite but still delay migrating dorsal to the intersegmental space. During dispersion, crest cells invade the ectoderm at sites associated with local disruptions in the basal lamina which may be caused by crest cells. Finally, deleting the dermamyotome releases an inhibition of neural crest cell migration: crest cells enter the dorsolateral path precociously. We speculate that the epithelial dermatome may transiently produce inhibitory substances and that emerging dermis may provide a long-distance, stimulatory cue.

Animals↗
PubMed1991

Prognostic significance of carcinoembryonic antigen in colorectal carcinoma. Serum levels before and after resection and before recurrence.

The use of carcinoembryonic antigen was evaluated in 425 patients with a mean follow-up of 48 months. The preoperative and postoperative carcinoembryonic antigen levels were predictive of recurrence and survival independent of the tumor stage. In a multivariate regression analysis of age, location, tumor stage, and preoperative and postoperative carcinoembryonic antigen levels, the latter three factors were significant prognostic variables with respect to the adjusted survival. Recurrent disease was found in 42% of patients, excluding patients with stage IV disease. The carcinoembryonic antigen level at recurrence was greater than 5 ng/mL in 79% of the patients and in 89% of the intra-abdominal recurrences. Carcinoembryonic antigen level at recurrence was not predictive of postrecurrence survival except in the subgroup of locoregional disease. The life span in patients with liver and lung metastases was not influenced by carcinoembryonic antigen level at recurrence. Preoperative and postoperative carcinoembryonic antigen levels can indicate a poorer prognostic group of patients with colorectal cancer who may benefit from adjuvant treatment. The carcinoembryonic antigen at recurrence can be used effectively to diagnose intra-abdominal recurrences and project survival after development of local/regional disease.

Aged↗
PubMed1991

Changes in mesenchymal cell-shape, matrix collagen and tenascin accompany bud formation in the early chick lung.

In the chick, lung branches arise as buds from the center of the pre-existing mesobronchial tube. Budding is known to be controlled by the mesenchyme. We have investigated mesenchymal properties in budding vs non-budding regions of the early chick lung, including sources of mesenchyme, cell shapes and densities, morphology and composition of the basement membrane, and distribution of the ECM components collagen, fibronectin and tenascin. We found that at points of outgrowth--the buds and the distal tip of the mesobronchus-mesenchymal cells adjacent to the lung epithelium are flattened, and the basement membrane is markedly thinned. In these basement membranes collagen is largely absent and tenascin redistributed into amorphous clumps. Of these characteristics only the cell-shape change, which results in the flattened mesenchymal cells at the bud tips, is correlated with initiation of the bud. We suggest that the cell-shape change leads to localized loss of collagen, which promotes emergence of buds, and that tenascin, which is found in the mesenchyme only in the budding region, promotes outgrowth and elongation of the bud.

Animals↗