Surgical treatment of squamous cell carcinoma of the thoracic oesophagus.
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Carcinoma, Squamous Cell↗
Biomedical subjects
A Dabrowski
Publications and source records attributed to A Dabrowski.
Oesophageal surgical anatomy.
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Arteries↗
Oxidative stress as an early prognostic factor in acute pancreatitis (AP): its correlation with serum phospholipase A2 (PLA2) and plasma polymorphonuclear elastase (PMN-E) in different-severity forms of human AP.
The role of oxidative stress as an important pathogenetic factor in experimental AP is commonly accepted, but its role in human AP has still not been evaluated satisfactorily. In the present study we compared the parameters of oxidative stress to the level of PLA2 and PMN-E in patients with AP. The study was performed in 77 patients with mild (n = 31), moderate (n = 20), and severe (n = 26) AP (alcoholic and biliary) as assessed according to Ranson's and Balthazar's criteria. Serum and urine malondialdehyde (MDA) concentrations, as an index of oxidant-mediated lipid peroxidation, and sulfhydryl (SH) groups, a major nonenzymatic antioxidant, were measured along with serum PLA2 and plasma PMN-E at admission (day 0) and on days 2, 5, and 10 of the disease. The Serum MDA level in severe AP was elevated by 267% on day 0 and 230% after 10 days, in comparison to the control, by 104 and 105% in comparison to mild AP, and by 50 and 76% in comparison to moderate AP, respectively. This was accompanied by a decrease in serum SH groups by 23% on day 0 and 36% after 10 days, in comparison to the control, by 31 and 32% in comparison to mild AP, and by 20 and 11% (ns) in comparison to moderate AP, respectively. In all severity forms of AP, oxidative stress was proportionally accompanied by increased levels of PLA2 and plasma PMN-E. In conclusion, oxidative stress is an early phenomenon in patients with AP, and at the time of admission it is detectable in the serum and urine. The intensity of oxidative stress correlates with the severity of AP. Because of the significant correlation between MDA and PLA2 or PMN-E, we suppose that the parameters of oxidative stress may be useful as another early prognostic factor in human AP.
Acute Disease↗
Dispersion of QT interval in premature ventricular beats as a marker of susceptibility to arrhythmic events.
BACKGROUND: Clinical observations indicate that increased QT interval dispersion in sinus beats may portend malignant ventricular arrhythmias and sudden cardiac death. The purpose of this study was to test the hypothesis that measures of QT dispersion in ventricular premature beats (QTd-V) may be also useful in identifying patients at high risk of arrhythmic events. METHODS: In the group of 303 patients with ventricular premature beats on standard 12-lead ECG, the QTd-V was calculated as a difference between maximum and minimum QT interval in premature ventricular beats. During follow-up for 26 +/- 19 months the arrhythmic events (sustained ventricular tachycardia, ventricular fibrillation or sudden cardiac death) were noted in 42 patients. RESULTS: Patients with arrhythmic events had significantly (P < 0.005) greater values of QTd-V than those without arrhythmic events. Univariate predictors of arrhythmic events included QTd-V > or = 100 ms, left ventricular ejection fraction < 40%, QRS complex duration of ventricular premature beats > 150 ms, underlying heart disease and complete bundle branch block. Multivariate analysis using the Cox proportional hazard model showed that only QTd-V > or = 100 ms and ejection fraction < 40% were independent predictors of arrhythmic events. CONCLUSIONS: The results of this study indicate a significant relationship between QTd-V and the risk of arrhythmic events. The assessment of QTd-V may be useful for identifying patients with ventricular premature beats at high and low risk of subsequent arrhythmic events.
Aged↗
Low variability of cycle lengths in nonsustained ventricular tachycardia as an independent predictor of mortality after myocardial infarction.
In a group of 191 postinfarction patients, the low variability of cycle lengths in nonsustained ventricular tachycardia was associated with poor prognosis during follow-up. By use of Cox model analysis it was found that reduced ventricular rate variability was a powerful independent predictor of sudden death and all-cause mortality in this group of patients.
Analysis of Variance↗
Cholecystokinin and EGF activate a MAPK cascade by different mechanisms in rat pancreatic acinar cells.
The effects of activating the Gq protein-coupled cholecystokinin (CCK) receptor on different proteins/signaling molecules in the mitogen-activated protein kinase (MAPK) cascade in pancreatic acinar cells were analyzed and compared with the effects of activating the tyrosine kinase-coupled epidermal growth factor (EGF) receptor. Both EGF and CCK octapeptide rapidly increased the activity of the MAPKs [extracellular signal-regulated kinase (ERK) 1 and ERK2], reaching a maximum within 2.5 min when 3.9- and 8.5-fold increases, respectively, were observed. The EGF-induced increase of MAPK activity was transient, with only a slight elevation after 30 min, whereas CCK-stimulated MAPK remained at a high level of activation to 60 min. The protein kinase C inhibitor GF-109203X abolished the activation by phorbol ester and inhibited the effect of CCK by 78% but had no effect on EGF-activated MAPK activity. EGF and CCK activated both forms of MAPK kinase (MEK), with CCK having a much larger effect, activating MEK1 by 6-fold and MEK2 by 10-fold, whereas EGF activated both MEKs by only 2-fold. Immunoblotting revealed three different forms of Raf in pancreatic acinar cells. Of the total basal Raf kinase activity, 3.7% was Raf-A, 89.0% was Raf-B, and 7.3% was c-Raf-1. All three forms of Raf were stimulated to a greater extent by CCK than by EGF, which was especially evident for Raf-A and c-Raf-1. The effect of CCK in activating Rafs was at least partially mimicked by stimulation with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate. EGF significantly increased GTP-bound Ras by 183 and 164% at 2.5 and 10 min, respectively; CCK and TPA had no measurable effect. Our study suggests that CCK and EGF activate the MAPK cascade by distinct mechanisms in pancreatic acinar cells.
Animals↗
CCK activates p90rsk in rat pancreatic acini through protein kinase C.
The presence of the 90-kDa ribosomal S6 protein kinase (p90(rsk)) in isolated rat pancreatic acini was demonstrated by Western blotting and immunoprecipitation with anti-p90(rsk). Cholecystokinin (CCK) activated p90(rsk) activity in a time- and dose-dependent manner and increased its phosphorylation. The threshold concentration of CCK was 10 pM and the maximal effect was seen at 1 nM. An increase in p90(rsk) was observed 1 min after 1 nM CCK stimulation, reaching a maximum at 10 min, when p90(rsk) activity was increased 5.4-fold. Carbachol and bombesin, but not vasoactive intestinal peptide, also activated p90(rsk). CCK-induced activation of p90(rsk) appears to be mediated by protein kinase C (PKC), since 12-O-tetradecanoylphorbol-13-acetate increased p90(rsk) activity 5.3-fold. GF-109293X, a potent inhibitor of PKC, strongly inhibited CCK-evoked p90(rsk) activity. Treatment of acini with ionomycin or 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid had no effect, indicating that mobilization of intracellular Ca2+ by CCK is not important in p90(rsk) activation. Although there were some quantitative differences in the extent of inhibition, the specific inhibitors [rapamycin, wortmannin, mitogen-activated protein kinase (MAPK) kinase inhibitor PD98059, and GF-109293X] had parallel effects on p90(rsk) and p42(mapk) activities, consistent with a model in which p90(rsk) can be regulated in acini by MAPK.
Animals↗
Stimulation of both CCK-A and CCK-B receptors activates MAP kinases in AR42J and receptor-transfected CHO cells.
It was recently found that cholecystokinin (CCK) activates mitogen-activated protein kinases (MAPK) in isolated rat pancreatic acini. The present study evaluates whether one or both types of CCK receptors are capable of MAPK activation in pancreatic AR42J acinar cells as well as CHO cells transfected with CCK-A or CCK-B receptors. CCK significantly increased p44 MAPK and p42 MAPK activities in AR42J cells. Minimal, half-maximal, and maximal responses were observed at 30 and 500 pM and 10 nM, respectively, after CCK-8 stimulation and at 100 pM and 1.5 and 30 nM, respectively, after gastrin stimulation. Glycine-extended gastrin had no effect at 100 nM and a small but significant effect at 1 microM. The CCK-B receptor antagonist L365,260 almost totally blocked MAPK activation in AR42J cells after stimulation with gastrin and glycine-extended gastrin and substantially reduced the activation of both kinases by CCK-8, while the CCK-A receptor antagonist L364,718 was much less effective. The CCK-A-selective agonist A71376, however, was an effective stimulant of MAPK activity. In an alternative approach, stably transfected CHO cells bearing either CCK-A or CCK-B receptors were stimulated with CCK-8. Each receptor induced a time-dependent increase in activity of both MAPKs by five- to sixfold in CCK-A- and CCK-B-bearing cells. In conclusion, both CCK-A and CCK-B receptors activate MAPK in AR42J cells and in transfected CHO cells.
Animals↗
The role of the oesophageal branches of aorta for the blood supply to the oesophageal remnant.
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Adult↗
[Abdominal emergencies and Von Recklinghausen neurofibromatosis].
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Abdomen, Acute↗
[Carcinoid tumor in the retroperitoneal space].
Authors present a rare case of the pancreatic carcinoid. Diagnosis was based on clinical examination, ultrasonography, CT, and histopathological evaluation. The patient was operated on twice: (Whipple's procedure with the right hemicolectomy and then Roux-Y anastomosis). During follow-up the liver metastases appeared. The patient was treated with chemotherapy. She died 19 month after operation because of neoplastic dissemination.
Carcinoid Tumor↗
[Stomach and esophageal neoplasm. Changes over 16 years in clinical materials].
Increasing prevalence of adenocarcinoma of the esophagus and esophago-gastric junction has been reported. The aim of the study was to determine whether this phenomenon is reflected in the cohort of patients referred for surgery to our institution. Clinical and pathological records of patients with adenocarcinoma of the stomach (n = 433) or gastro-esophageal junction (n = 302), and squamous cell carcinoma of the esophagus (n = 266) were reviewed from 1981 to 1996. Yearly prevalence of carcinoma of the gastric cardia in comparison to carcinoma of (a more distal) stomach has not changed, ranging 19-46%. From 1981 to 1984 out of 58 gastric resections, 14 (24%) total gastrectomies were done, whereas from 1993 to 1996 total gastrectomies were performed in 104 out of 138 (75%) patients with gastric cancer (p < 0.001). In the first 4 years of the study period adenocarcinoma of the cardia and/or esophagus was found in 19% of all patients with esophageal and junctional tumors, while in the last 4 years,-in 30%. Resection rates for gastric and cardiac cancers have not changed significantly, 75-100% and 21-65% respectively. Resection rate for carcinoma of the esophagus increased from 50% (17/34) to 79% (53/67) (p = 0.006, test chi2). Increasing rate of total gastrectomies can be explained by a trend towards more proximal localisation of the primary gastric tumors and/or clinical application of Laurén classification for the choice of operative procedure. Higher resection rate for carcinoma of the esophagus is a result of increasing experience of the surgical team, improvement in preoperative staging, new palliative modalities, and application of preoperative chemo-/radiotherapy.
Carcinoma, Squamous Cell↗
[The effect of Nissen-Rossetti fundoplication on the motor function of swallowing in patients with reflux diseases].
This prospective study was undertaken to assess the motility of the middle and lower esophagus and LES resting pressure changes following the N-R fundoplication for GER. The study was carried out in 53 consecutive patients (37 women, 16 men, median age 49.1 +/- 6.2 years), operated due to antireflux mechanism insufficiency. Threefold solid state for manometry and double channel for pH metry catheters in the body of the esophagus were used before and after the operation (median follow up time was 18 months). The LES length and resting pressure were evaluated with Synectics On-line interface. The objective results obtained during 24-h pH metry and manometry were shown as median and standard deviation, with statistical significances determined using the SPSS/PC+ packet (p < 0.05 considered as significant). The individual patients' data were analyzed by Synectics software. 24-h pH metry confirmed that Nissen-Rossetti fundoplication efficaciously reduced pathological GER (significant decrease of DeMeester score from 105.6 +/- 12.2 to 5.2 +/- 3.4, p < 0.0002). Manometry proved the increase of the LES resting pressure from 7.6 +/- 3.2 to 18.2 +/- 4.2, p < 0.0005, and its total length from 3.1 +/- 0.8 to 4.2 +/- 1.0, p < 0.01. The improvement of the esophageal body peristalsis was found first of all in total period. Motility changes following N-R fundoplication during the reflux period were unsatisfactory. The frequency of peristalic contractions with higher amplitude and longer duration significantly increased after the operation in total period in all levels. The increase of the complete peristaltic contractions following N-R fundoplication was high significant from 22.15% to 60.21%, p < 0.0001. Although significant improvement of the efficacy of esophageal peristalis was observed, however it was still under 50% of normal level all the time (15.4% v. 41.7%, p < 0.002). The most impressive improvement of esophageal peristalis was noticed in the lower part of the esophagus. The increase of the complete peristaltic contractions during the reflux period was observed only in upright position. Least profitable changes in esophageal body motility were noticed during the reflux period in supine position. In comparison with the total period manometry results the efficacy of the esophageal perystalsis during the reflux period was defected before as well as after the operation, (11.2% v. 22.5%, p = NS).
Adult↗
[Prognostic significance of cellular immunity in surgical treatment of esophageal cancer].
The aim of the study was to investigate the influence of perioperative changes of the cellular immunity parameters on long-term survival following esophagectomy for carcinoma of the esophagus. In 39 patients several immunological parameters have been assessed before and 2 weeks after the operation: WBC, lymphocyte count, lymphocyte T% (E-rosette test), helper/suppressor lymphocyte T subpopulations (teophylline test), NBT test, and in vivo Multitest CMI (skin delayed hypersensitivity for recall antigens). Survival was analyzed using Kaplan-Meier method according to the stage (pTNM, UICC'92) and to the grade of perioperative cellular immunity (pCI) deterioration. Three groups of patients were identified with: 1) improvement or stabilization of pCI (n = 5); 2) deterioration of 1 or 2 pCI parameters (n = 21); and 3) deterioration of 3 or more pCI parameters (n = 13). Follow-up time ranged from 4 to 65 months. Eight patients died in hospital due to postoperative complications, 3 patients are alive (1 of them with Tis alive at 52 months of follow-up), and the remaining patients died during follow-up. Mean survival time of patients in stage II (n = 7), III (n = 17), and IV (n = 14) was 18, 17, and 6 months respectively (p = 0.017, log rank test). Mean survival time of patients in group 1, 2, and 3 was 21, 20, and 5 months respectively (p < 0.001, log rank test). On bivariate survival analysis encountering both factors, stage was found to be the only independent prognostic factor (p = 0.008, Cox regression model). Deterioration of the cellular immunity in the perioperative period is entirely related to the stage of the disease, which is the only independent prognostic factor in carcinoma of the esophagus.
Adenocarcinoma↗
[Retroperitoneal space carcinoid].
Authors present a rare case of the pancreatic carcinoid. Diagnosis was based on clinical examination, ultrasonography, CT, and histopathological evaluation. The patient was operated on twice: (Whipple's procedure with the right hemicolectomy and then Roux-Y anastomosis). During follow-up the liver metastases appeared. The patient was treated with chemotherapy. She died 10 month after operation because of neoplastic dissemination.
Anastomosis, Roux-en-Y↗
Serum and bronchoalveolar IgG against A60 and 38 kDa antigens in the diagnosis of tuberculosis.
SETTING: The ELISA test is generally accepted for serodiagnosis of tuberculosis. Its sensitivity and specificity depend on the antigen used and data are not always concordant. In some patients suspected of tuberculosis, sarcoidosis or lung cancer, bronchoalveolar lavage (BAL) is performed. BAL fluid (BALF) contains immunoglobulins--their source is transudation from the serum but local IgG synthesis of IgG is not excluded. OBJECTIVE: The comparison of BALF versus serum in the serodiagnosis of pulmonary tuberculosis, and its differentiation from sarcoidosis and lung cancer. DESIGN: The IgG against A60 and 38 kDa antigens in serum and BALF were measured using the commercially available IgG EIA kits. The study included 13 tuberculous patients, 8 patients with sarcoidosis, 10 patients with lung cancer and 9 healthy volunteers. RESULTS: In the serum studies the sensitivity of the assays did not exceed 40% and 60% in the estimation of IgG 38 kDa and IgG A60, respectively. The specificity of both assays was similar: 81% (IgG 38 kDa) and 69-75% (IgG A60). In BALF studies the sensitivity of the IgG 38 kDa assay was 50% and its specificity was 44%. The ranges of the IgG A60 concentrations in BALF were similar in all subject groups. CONCLUSION: In differentiation between tuberculosis, sarcoidosis and lung cancer, the measurement of IgG against A60 and 38 kDa antigens in serum is more useful than that in BALF.
Adult↗
[Iatrogenic esophageal injuries and their treatment].
In our Department 22 patients were treated due to esophagus perforations in the years 1990-1996. Most of them (16) occurred after endoscopic examinations: diagnostic-3, after strictures dilatation-10, endoscopic intubation-2, sclerotherapy-1, transesophageal cardioversion-1. There were 5 intraoperative perforations: 3-after cardiomyotomy, 2-after intubation. The following treatment was performed: oesophageal suture and drainage-5 patients, subtotal oesophagectomy with oesophagogastrostomy-3 patients, oesophagectomy with salivary fistula and oesophago-gastro or -colostomy in second operation--9 patients, perforation covered with gastric fundus--3, intubation--1 patient, conservative treatment--1 patient. Four (18%) patient died.
Dilatation↗
Cholecystokinin stimulates formation of shc-grb2 complex in rat pancreatic acinar cells through a protein kinase C-dependent mechanism.
Cholecystokinin (CCK) has recently been shown to activate the mitogen-activated protein kinase (MAPK) cascade (Ras-Raf-MAPK kinase-MAPK) in pancreatic acini. The mechanism by which the Gq protein-coupled CCK receptor activates Ras, however, is currently unknown. Growth factor receptors are known to activate Ras by means of adaptor proteins that bind to phosphotyrosine domains. We therefore compared the effects of CCK and epidermal growth factor (EGF) on Tyr phosphorylation of the adaptor proteins Shc and its association with Grb2 and the guanine nucleotide exchange factor SOS. Three major isoforms of Shc (p46, p52, p66) were detected in isolated rat pancreatic acini with p52 Shc being the predominant form. CCK and EGF increased tyrosyl phosphorylation of Shc (251 and 337% of control, respectively). CCK-stimulated tyrosyl phosphorylation of Shc as well as Shc-Grb2 complex formation was significant at 2.5 min, maximal at 5 min, and persisted for at least 30 min. Finally, SOS was found to be associated with Grb2 as assessed by probing of anti-Grb2 immunoprecipitates with anti-SOS. Since MAPK in pancreatic acini is activated via protein kinase C (PKC), we studied the effect of phorbol esters on Shc phosphorylation and found 12-O-tetradecanoylphorbol-13-acetate to be as potent as CCK. Furthermore, GF-109203X, a PKC inhibitor, abolished the effect of 12-O-tetradecanoylphorbol-13-acetate and also the effect of CCK but not the effect of EGF on Shc tyrosyl phosphorylation. CCK-induced tyrosyl phosphorylation of Shc was found to be phosphatidylinositol 3-kinase-independent, and CCK did not cause EGF receptor activation. These results suggest that formation of an Shc-Grb2-SOS complex via a PKC-dependent mechanism may provide the link between Gq protein-coupled CCK receptor stimulation and Ras activation in these cells.
3T3 Cells↗