This study was conducted to investigate the clinical utility of CEA, CA 19-9, and CA-50 in the diagnosis, monitoring, and prognosis of 62 gastric carcinoma patients having either adjuvant or palliative chemotherapy. Patients were divided in two groups: group A included patients treated on an adjuvant basis following a curative resection of gastric cancer, and group B included patients with residual disease post surgery or patients with inoperable tumor or generalized disease. Serum marker levels were measured in a prospective study just before the initiation of chemotherapy and before each course during chemotherapy. In group A, CEA was positive in 2/25 (8%) patients, CA 19-9 in 1/25 (4%), and CA-50 in 1/25 (4%). In group B the sensitivity of CEA was 48.6% (18/37 patients), of CA 19-9 64.9% (27/37 patients), and of CA-50 70.3% (26/37) patients. There was a significant correlation between the CA 19-9 and CA-50 levels in both groups. No correlation was found between the sensitivity or the absolute initial marker levels and the tumor's differentiation or extent of disease. In group A the only patient with initially elevated CA 19-9 and CA-50 values relapsed early while he was on adjuvant chemotherapy. It was also found that the rising final CA 19-9 and CA-50 values at the end of chemotherapy were correlated with an increased incidence of relapse, but not with the disease-free interval. In group B the initially low marker levels showed a trend to predict a favorable outcome of treatment. There was no statistically significant correlation between the marker titers before each course and response to chemotherapy. It is concluded that the comeasurement of CA 19-9 and CA-50, and to some degree of CEA, is justifiable for gastric cancer. The estimation of CA 19-9 and CA-50 may be useful for early detection of recurrence after curative surgery and adjuvant chemotherapy. In advanced or recurrent gastric cancer, the estimation of either CA 19-9 or CA-50 and CEA serum values may help in checking the prognosis, determining the efficacy of palliative treatment modalities, and recognizing recurrences.

A total of 76 patients with transitional cell carcinoma of the bladder were prospectively monitored with simultaneous serum value estimations of tumor polypeptide antigen (TPA), tumor-associated trypsin inhibitor (TATI), carcinoembryonic antigen (CEA), alpha-fetoprotein (AFP), beta-human chorionic gonadotropin (beta-HCG), prostatic specific antigen (PSA), squamous cell carcinoma antigen (SCC), and CA 19-9 in different stages and phases of their disease. In locally advanced disease positive values were noted for TATI in 22/28 patients (78.5%), for TPA in 17/28 (60.7%), for CA 19-9 in 10/28 (35.7%), for CEA 11/28 (39.2%), for beta-HCG in 3/28 (10.7%), for PSA in 6/28 (21.4%), for SCC in 6/28 (21.4%), and for AFP in 0/28. In metastatic disease elevated levels were observed for TATI in 43/48 patients (89.5%), for TPA in 41/48 (85.4%), for CA 19-9 in 19/48 (39.5%), for CEA in 20/48 (41.6%), for beta-HCG in 6/48 (12.5%), for PSA in 7/48 (14.5%), for SCC in 8/48 (16.6%), and for AFP in 1/48 (2.1%). In metastatic disease TATI and TPA values were significantly modified in patients with complete remission and TATI, TPA, and CA 19-9 in patients with partial remission and nonresponders. In T2-T4-N0M0 tumors, TPA, TATI, CA 19-9, and CEA were significantly increased in nonresponders. In patients with complete remission, a change in serum TATI, TPA, and CA 19-9 levels cannot be evidenced with the available numbers. The concurrent determination of TATI and TPA in T2-T4N0M0 tumors and TATI, TPA, and CA 19-9 in generalized disease could predict the response to chemotherapy. This study indicates that only the determination of TATI and TPA and in some degree the CA 19-9 is a potential tool for monitoring the efficacy of treatment.

BackgroundSleep disturbances are intertwined with the progression and pathophysiology of psychotic symptoms in schizophrenia. Reductions in sleep spindles, a major electrophysiological oscillation during non-rapid eye movement sleep, have been identified in patients with schizophrenia as a potential biomarker representing the impaired integrity of the thalamocortical network. Altered glutamatergic neurotransmission within this network via a hypofunction of the N-methyl-D-aspartate receptor (NMDAR) is one of the hypotheses at the heart of schizophrenia. This pathomechanism and the symptomatology are shared by anti-NMDAR encephalitis (NMDARE), where antibodies specific to the NMDAR induce a reduction of functional NMDAR. However, sleep spindle parameters have yet to be investigated in NMDARE and a comparison of these rare patients with young individuals with schizophrenia and healthy controls (HC) is lacking. This study aims to assess and compare sleep spindles across young patients affected by Childhood-Onset Schizophrenia (COS), Early-Onset Schizophrenia, (EOS), or NMDARE and HC. Further, the potential relationship between sleep spindle parameters in COS and EOS and the duration of the disease is examined.MethodsSleep EEG data of patients with COS (N = 17), EOS (N = 11), NMDARE (N = 8) aged 7–21 years old, and age- and sex-matched HC (N = 36) were assessed in 17 (COS, EOS) or 5 (NMDARE) electrodes. Sleep spindle parameters (sleep spindle density, maximum amplitude, and sigma power) were analyzed.ResultsCentral sleep spindle density, maximum amplitude, and sigma power were reduced when comparing all patients with psychosis to all HC. Between patient group comparisons showed no differences in central spindle density but lower central maximum amplitude and sigma power in patients with COS compared to patients with EOS or NMDARE. Assessing the topography of spindle density, it was significantly reduced over 15/17 electrodes in COS, 3/17 in EOS, and 0/5 in NMDARE compared to HC. In the pooled sample of COS and EOS, a longer duration of illness was associated with lower central sigma power.ConclusionsPatients with COS demonstrated more pronounced impairments of sleep spindles compared to patients with EOS and NMDARE. In this sample, there is no strong evidence that changes in NMDAR activity are related to spindle deficits.

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