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Biomedical subjects

M Kowalska

Publications and source records attributed to M Kowalska.

At least 91 records · Page 5Linked to original sources
PubMedDate not supplied

Serum levels of carcinoembryonic antigen, gastrointestinal cancer-associated antigen and alphafetoprotein in staging and management of patients with advanced carcinoma of the stomach.

Serum levels of carcinoembryonic antigen (CEA), gastrointestinal cancer-associated antigen (GICA or CA 19-9), and alphafetoprotein (AFP) were concurrently determined in patients with carcinoma of the stomach: in 84 preoperatively, and in 67 serially postoperatively. Before surgery, serum CEA gave information about the tumor load analogous to serum GICA in 69% of the patients: true-positive in 25% and false-negative in 43%; less information in 18% and more in 14%. The sensitivity of the test tended to be better in the more advanced stages, and was higher for CEA with GICA than for CEA alone or GICA alone. During follow-up, serum CEA gave information about the presence or absence of active disease analogous to serum GICA in 78% of the patients: true-positive in 30%, true-negative in 36% and false-negative in 12%; less information in 9% and more in 13%. Neither test gave any false-positive indications. Sensitivity of the test rose from 67% for CEA alone and 60% for GICA alone to 81% for CEA with GICA. Serum AFP was elevated only preoperatively in 2% of patients. We conclude that joint application of CEA and GICA tests gave only slightly better preoperative sensitivity than CEA alone or GICA alone but proved fairly sensitive for postoperative follow-up of the patients. AFP was of little value for either purpose.

Antigens, Neoplasm↗
PubMedDate not supplied

Serum CA 15.3, CEA and ESR patterns in breast cancer.

Serum CA 15.3, CEA and ESR were longitudinally determined in 298 patients with breast cancer during postsurgical follow-up and/or therapy. Observation lasted until the death of the patient or at least for three years. With regards to longitudinal serum markers and ESR curves, four different patterns have been identified: pattern I: the markers and ESR stayed at normal levels; pattern II: the markers and ESR decreased from a peak level; pattern III: the markers and ESR fluctuated widely; pattern IV: the markers and ESR increased steadily. We have looked at over all survival (OS) and relapse-free survival ( RFS) versus longitudinal CA 15.3, CEA and ESR patterns. Univariate Cox regression analysis showed that OS and RFS were significantly associated with all four patterns.

Adult↗
PubMedDate not supplied

Haloperidol treatment selectively affects expression of Galpha(i)3 subunit mRNA in specific regions of the rat brain.

Relative abundance of GTP binding protein mRNA coding for subunits alpha(i)1, alpha(i)2 and alpha(i)3, and their changes induced with chronic blockade of D2 receptor by haloperidol were compared in the frontal cortex, striatum, hippocampus and cerebellar cortex of the rat using a specific method based on multiplex RT-PCR. Galpha(i) subtype 2 mRNA was the most abundant, followed by subtype 1 and subtype 3. The haloperidol treatment produced an area specific increase in Galpha(i)3 mRNA in the frontal cortex and a decrease of Galpha(i)3 in the striatum. After 8-day withdrawal period, haloperidol-induced,changes disappeared in the striatum but became accentuated in the frontal cortex. Changes in the relative expression of Galpha(i) subtypes may significantly influence long-lasting effects of chronic D2 receptor blockade.

Animals↗
PubMedDate not supplied

Adrenergic receptors' responsiveness after acute and chronic treatment with haloperidol in the presence of calcium channel blockade.

The effects of acute and chronic (14 days) treatment with haloperidol (0.5 mg/kg ip) given alone or 15 min after nifedipine (5 mg/kg ip) on responsiveness of the alpha1- and beta-adrenergic receptors was investigated ex vivo by measuring of the second messenger responses. The accumulation of inositol phosphate (IP) or cyclic AMP were measured in brain cortical slices challenged with noradrenaline or isoproterenol. The facilitatory effect of a single dose of haloperidol on IP accumulation (an increase by approximately 50%) was abolished by nifedipine pretreatment. After chronic treatment with haloperidol alone its facilitatory effect disappeared, but a treatment with haloperidol after nifedipine caused a significant increase in IP accumulation. No treatment affected the responses from beta-adrenoceptors. These data show that the action of chronically administered haloperidol may be changed by the concomitant calcium channel blockade that prevents development of adaptation to persistent presence of the drug.

Adrenergic alpha-Agonists↗