The role of sinking particles in the overwintering process of Vibrio parahaemolyticus in a marine environment

Abstract The behavioral pattern of Vibrio parahaemolytics during the winter season (December 1988 to March 1989) in the water column, sediment, plankton and sinking particles was determined in a eutrophic marine environment. A total of 15 environmental parameters and seven microbial characteristics were examined. This halophile was isolated sporadically from bottom water and plankton materials, whereas it was undetectable in the surface water and sediment samples. However, V. parahaemolyticus was isolated from the sinking particles continuously throughout the sampling period with highest counts during February 1989. Out of 195 strains identified, 10 Vibrio spp. and 3 Listonella spp. were observed of which V. alginolyticus was predominantly isolated irrespective of the samples tested. Simple correlation and multiple regression analyses show that the occurrence of V. parahaemolyticus is not governed by any single biotic or abiotic factor of the environment. Possibly, the cumulative effect of all these environmental parameters on the distribution of V. parahaemolyticus is conceivable.     

No or little production of singlet molecular oxygen in HOCl or HOClH2O2 a model system for myeloperoxidase/H2O2/Cl−

The HOCl in chlorine-water oxidizes DPF to cis-DBE in parallel to the HOCl concentration. The addition of H₂O₂ produces singlet molecular oxygen, and a bimol collision above pH 6.0, but not in the pH region 3.0 to 4.0. The DPF conversion to cis-DBE is initiated by a 1,2-position attack of OH^? and Cl⁺, followed by the HCl elimination. The oxidation potency of HOCl is much greater than the singlet molecular oxygen generated in chlorine-water/H₂O₂ solution, on the pH range 6.0 to 8.0 where both HOCl and OCl^? are present.     

Generation of electronic energy in the myoglobin-catalyzed oxidation of acetoacetate to methylglyoxal

The myoglobin- or peroxidase-catalyzed aerobic oxidation of acetoacetate to methylglyoxal produces a very weak emission. Light production, methylglyoxal formation, and O₂ uptake strictly correlate with each other. The excited species first formed appears to be triplet methylglyoxal. Formation of the latter species is supported by the increased light emission observed in the presence of very low concentrations of certain sensitizers which contain heavy atoms and have low-lying excited states. In an aprotic solvent the emitter is excited methylglyoxal. The results strongly support the inference that by catalyzing the reaction, myoglobin is damaged by a “photochemistry without light” effect. It is the consequence of the formation of excited methylglyoxal in a major process.     

Modulation of Mouse Anti-Trinitrophenyl Plaque-Forming Cell Affinity by Adjuvants or Lectins

The effects of several kinds of adjuvants or lectins, such as Corynebacterium parvum, dextran, poly AU, poly IC, dibutyryl cAMP, concanavalin A (Con A), phytohemagglutinin (PHA) and pokeweed mitogen (PWM) on anti-trinitrophenyl (TNP) direct plaque-forming cells (PFC) in the spleen of mice and the affinity of antibodies produced by these PFC were examined. The numbers of anti-TNP PFC in the spleens of mice which had been injected with C. parvum 7 days in advance were greater than those in controls after immunization with TNP-coupled heterologous erythrocytes, while the affinity of antibodies released by these PFC was not affected. On the contrary, simultaneous injection of dextran with TNP-erythrocytes did not increase the numbers of splenic anti-TNP PFC, but heightened the affinity of antibodies released by these PFC. Copolymers of nucleotides, poly AU and poly IC, were capable of enhancing splenic anti-TNP PFC responses, but showed almost no altering of PFC affinity. Dibutyryl cAMP did not have any effect on this system. Con A had potencies to both augment the number of anti-TNP PFC and heighten the PFC affinity, while PHA seemed to lack these potencies. Injection of PWM in the presence of antigen increased the number of anti-TNP PFC and heightened slightly the PFC affinity. These results indicate that the heightening of the affinity at the cellular level is regulated in ways different from the augmenting effects on the number of anti-TNP PFC by adjuvants or lectins. These results are discussed in the light of the mode of action of the substances used.     

Muscle D-glyceraldehyde-3-phosphate dehydrogenase from Caiman sp. II New data for enzyme characterization

Muscle GPDH from Caiman sp. was activated by dithioerythritol and 2-mercaptoethanol. Maximal activation was obtained with the reducing agent at 10mM final concentration. The binding of NAD to the apoenzyme occurs at four sites per tetramer, but ligand affinity seems to be heterogeneous. Incubation of the holo or the apoenzyme with NADH at 37 degrees C caused inactivation of the enzyme, with partial loss of SH-titrable groups. Incubation of the holo or the apoenzyme with G3P at 37 degrees C caused partial inactivation of the enzyme. The apoenzyme was demonstrated to be more stable than the respective holoenzyme, in the assay conditions used.     

Early Clinical Response after 2 Weeks of Sorafenib Therapy Predicts Outcomes and Anti-Tumor Response in Patients with Advanced Hepatocellular Carcinoma

Background & Aims

We evaluated the relationship between the early clinical response after 2 weeks of sorafenib therapy and the outcomes and anti-tumor response in patients with advanced hepatocellular carcinoma.

Methods

Fifty-seven patients who had intrahepatic hypervascular hepatocellular carcinoma and Child-Pugh (CP) class A disease at baseline were enrolled in this prospective, multicenter, observational, non-interventional study. As an early clinical response after 2 weeks of sorafenib therapy, changes in intra-tumor blood flow on contrast-enhanced computed tomography (CE-CT), alpha-fetoprotein (AFP) levels, and remnant liver function were investigated.

Results

After 2 weeks of sorafenib therapy, there were 26 patients (45.6%) without disappearance of arterial tumor enhancement on CE-CT, 15 patients (26.3%) with an AFP ratio of >1.2, and seven patients (12.3%) with two or more increments in the CP score. Multivariate analysis showed that the absence of disappearance of arterial tumor enhancement on CE-CT, AFP ratio of >1.2, and two or more increments in the CP score after 2 weeks of sorafenib therapy were significant and independent predictors of worse survival. Upon scoring these three variables as "poor prognostic factors", patients with poor prognostic score 4, 3 or 2 (n = 17) had significantly worse outcomes and a significantly higher progressive disease (PD) rate based on modified Response Evaluation Criteria in Solid Tumors at 6 weeks after sorafenib therapy than those with poor prognostic score 1 or 0 (n = 40) (median overall survival: 194 days vs. 378 days; p = 0.0010, PD rate: 70.6% vs. 20.0%; p = 0.0003, respectively).

Conclusions

Changes in intra-tumor blood flow on CE-CT, AFP levels, and remnant liver function after 2 weeks of sorafenib therapy may be useful for predicting the outcomes and anti-tumor response to sorafenib in patients with advanced hepatocellular carcinoma.