NK cell activity in treated prostate cancer patients as a probe for circulating tumor cells: hormone regulatory effects in vivo.

Natural killer (NK) cell activity was studied together with tumor marker serotests (PSA, PAP) and blood testosterone, estradiol, cortisol, and prolactin concentrations in treated prostate cancer patients. NK cell activity data were correlated with tumor stage (stage D0 + D1 versus stage D2) and showed statistically insignificant differences. Both tumor progression and stabilization of metastatic disease, triggered by the application of more appropriate therapy in progressive subjects, yielded low NK activity data. By contrast, normal NK activity was found during both partial remission of stage D2 tumor and stabilization of the same disease, after an initial period of tumor remission. Differences between NK activity data from the aforementioned two groups are statistically significant (P less than 0.01). In subjects examined, the application of NK activity assay to those with advanced disease reflected changes in the outcome of the treatment more closely than it did routine tumor marker assessment. The activity of NK cells seems unaffected by changes in basal blood estradiol, cortisol, testosterone, and prolactin concentrations that occur during therapy with pharmacological agents (estradiol, cyproterone acetate, diethylstilbestrol, and flutamide) and during surgical castration. The reported NK activity recordings in treated prostate cancer patients might be indicative of the presence of tumor cells in the circulation. If this holds true, the measurement of NK activity would appear to furnish urological oncology with a new tool for early, rapid recognition of progressive metastatic tumors.     

Intra-abdominal adhesion formation is initiated by phospholipase A2

The etiology of intra-abdominal adhesions is explained by hydrolysis of the peritoneal phospholipid layer caused by phospholipase A₂ activity. This view could unify the pre-existing hypotheses that intra-abdominal adhesions are due to ischemia or increased plasminogen activator activity. New therapeutic approaches are suggested.     

Biventricular Assist Using a Portable Driver in Combination with Implanted Devices: Preliminary Experience

Abstract: Left ventricular assist systems with portable drive units are increasingly used in the clinical setting. However, such systems usually are not suitable for right ventricular support, and therefore, in the case of biventricular heart failure, they must be combined with other support devices that require additional drive consoles. As a result, most of the benefits of the wearable drive units (early mobilization and outpatient care) are lost. This present study was performed to evaluate biventricular support with implanted assist devices and a portable DC/battery-powered driver (Thoratec TLC-II). Electronic control by nonvolatile RAM accessible via RS232 interface, internal backup emergency battery, and optional manual activation are additional features of this 6 kg biventricular drive unit. In 3 bovine experiments (body weight 70 ± 5 kg) partial cardiopulmonary bypass (CPB) was established, and two ventricular assist devices were implanted into a preperitoneal pocket on each side after connection to the right atrium and the pulmonary artery and to the left atrium and aorta, respectively.     

Iodine-123 labeled nor-β-CIT as a potential tracer for serotonin transporter imaging in the human brain with single-photon emission tomography

Iodine-123 labelled 2β-carbomethoxy-3β-(4-iodophenyl) (nor-β-CIT) is an analogue of β-CIT, which has high affinity to the serotonin transporter. Initial single-photon emission tomography (SPET) studies with [¹²³I]nor-β-CIT were performed in five healthy volunteers. In addition, its metabolism in plasma was investigated with gradient high performance liquid chromatography. [¹²³I]nor-β-CIT was prepared by a method which gave a specific radioactivity of more than 180 GBq/μmol. Unchanged [¹²³I]nor-β-CIT in plasma accounted for 43% and 19% of total radioactivity after 30 and 180 min, respectively. The dynamic SPET studies demonstrated a high and rapid uptake of radioactivity in the brain (6%/ID at 30 min). Highest accumulation was observed in the striatum, the mid-brain and the thalamus. The specific binding in the mid-brain was 33% higher compared with that of [¹²³I]β-CIT. The high radioactivity in the mid-brain is assumed to represent the accumulation of [¹²³I]nor-β-CIT in the serotonin transporter-rich regions, which indicates that [¹²³I]nor-β-CIT might be a potential tracer for visualization of serotonin transporter sites in the human brain with SPET. Received 23 May and in revised form 2 September 1997     

Results of Contracture Tests with Halothane, Caffeine, and Ryanodine Depend on Different Malignant Hyperthermia-associated Ryanodine Receptor Gene Mutations

Background: More than 20 mutations in the gene encoding for the ryanodine receptor (RYR1), a Ca2+ release channel of the skeletal muscle sarcoplasmic reticulum, have been found to be associated with malignant hyperthermia (MH). This study was designed to investigate the effects of different mutations in the RYR1 gene on contracture development in in vitro contracture tests (IVCT) with halothane, caffeine, and ryanodine.

Methods: Ninety-three MH-susceptible (MHS) patients, diagnosed by the standard IVCT with halothane and caffeine, were included in this prospective study. Surplus muscle specimens were used for an IVCT with 1 [mu]m ryanodine. The contracture course during the ryanodine IVCT was described by the attainment of different time points: onset time of contracture and times when contracture reached 2 mN or 10 mN. In addition, all patients were screened for mutations of the RYR1 gene.

Results: In 36 patients, four different mutations of the RYR1 gene (C487-T, G1021-A, C1840-T, G7300-A) were found. The IVCT threshold concentrations of halothane and caffeine were lower in patients with the C487-T mutation compared with patients without a detected mutation in the RYR1 gene. In the IVCT with ryanodine, contracture levels of 2 mN and 10 mN were reached earlier in muscle specimens from patients with C487-T, C1840-T, and G7300-A mutations compared with specimens from patients with the G1021-A mutation and patients without detected mutation in the RYR1 gene.