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An abstract of the article "Thermal index for bone for diagnostic scanners: actual ranges of ultrasound intensity measured in vitro" by K. Retz is presented.

Background: Early detection of bacteria and their antibiotic susceptibility patterns are critical to guide therapeutic decision-making for optimal care of septic patients. The current gold standard, blood culturing followed by subculture on agar plates for subsequent identification, is too slow leading to excessive use of broad-spectrum antibiotic with harmful consequences for the patient and, in the long run, the public health. The aim of the present study was to assess the performance of two commercial assays, QuickFISH® (OpGen) and Maldi Sepsityper™ (Bruker Daltonics) for early and accurate identification of microorganisms directly from positive blood cultures., Materials and Methods: During two substudies of positive blood cultures, the two commercial assays were assessed against the routine method used at the clinical microbiology laboratory, Unilabs AB, at Skaraborg Hospital, Sweden., Results: The Maldi Sepsityper™ assay enabled earlier microorganism identification. Using the cut-off for definite species identification according to the reference method (>2.0), sufficiently accurate species identification was achieved, but only among Gram-negative bacteria. The QuickFISH ® assay was time-saving and showed high concordance with the reference method, 94.8% (95% CI 88.4-98.3), when the causative agent was covered by the QuickFISH ® assay., Conclusions: The use of the commercial assays may shorten the time to identification of causative agents in bloodstream infections and can be a good complement to the current clinical routine diagnostics. Nevertheless, the performance of the commercial assays is considerably affected by the characteristics of the causative agents.

Rats were trained to detect intraperitoneal (IP) administration of cocaine, 10.0 mg/kg, using a two-lever choice discrimination procedure. Following training, cocaine was generalized to the cocaine training stimulus in a dose-dependent manner. Subsequently, bilateral cannulae were implanted in the lateral ventricles in ten animals, and intracerebroventricular (ICV) administration of cocaine was also generalized to the IP training dose in a dose-dependent manner with maximum generalization occurring with 80 micrograms cocaine. After baseline testing, training was halted and cocaine, 20 mg/kg/8-hr, was injected chronically in all rats for 6 days, and then the dose-effect curve for generalization of cocaine was redetermined. Chronic administration of cocaine significantly shifted the dose-effect curve three-fold to the right for both IP and ICV routes of administration. These data suggest that the stimulus properties of cocaine administered centrally are generalized in rats trained by peripheral administration and supports the hypothesis of central mediation of the cocaine stimulus. Also, the comparable shift of the cocaine dose-effect curve following chronic cocaine administration suggests that a central pharmacodynamic mechanism mediates tolerance to the discriminative stimulus properties of cocaine.

The NZB/BlNJ (NZB) mice are an autoimmune-prone strain, known to develop brain-reactive antibodies in serum at much earlier chronological ages than normal mice. Measurement of locomotor activity in 8-10 month old C57BL/6 (C57) mice following the administration of either oxotremorine or physostigmine, revealed a biphasic response consisting of inhibition at small doses, but increased motor activity at large doses. In contrast, age-matched NZB mice exhibited little inhibition at the smaller doses, but had much greater increases in activity after the larger doses. Similarly, when compared to C57 mice, NZB mice were less sensitive to oxotremorine-induced salivation, diarrhea and visible tremors. Moreover, oxotremorine-induced hypothermia occurred at smaller doses in C57 mice than in NZB mice and was of a greater magnitude. Thus, at an age when NZB mice possess high levels of brain-reactive antibodies, and exhibit impairment in tests of learning/memory, these mice also show diminished responses in several tests of cholinomimetic-induced behavior and physiological alterations.

Intrastriatal injection of either kainic acid (0.35 micrograms) or ibotenic acid (7.0 micrograms) in the mouse causes a profound and selective degeneration of striatal neurons accompanied by a secondary astrocytic response. The kainate injection (0.35 micrograms) resulted in significant decrements in the striatal levels of phosphocreatine and ATP by 30 min. a progressive reduction in adenosine phosphates between 30 min and 48 h, and a decrease in energy charge; whereas lactate levels increased by 44% at 2 h, glucose levels fell by 56%. Two hours after intrastriatal injection of ibotenic acid (7.0 micrograms) similar alternations in striatal high-energy phosphates and glucose disposition were found. Prior decortication protected against the neurotoxic effects of kainate in the mouse striatum and prevented the alterations in high-energy phosphates at 2 h although lactate levels increased by 212%. These findings in vivo are consistent with the hypothesis that the neurotoxic effects of acidic excitatory amino acids involve a profound activation of energy consumption by affected neurons.

Separate age groups of C57BL/6 and autoimmune New Zealand Black (NZB) mice were compared for diazepam-induced ataxia and barbiturate-induced loss of righting reflex. Between 1 and 3 months of age, both strains showed a similar age-related decrease in ED50 for diazepam-induced ataxia. However, between 3 and 12 months the decrease in ED50 was markedly greater in NZB mice. In contrast, age-related increases in the durations of loss of righting reflex following hexobarbital or barbital were similar in both strains. The results suggest that NZB mice show relatively accelerated age-related increases in sensitivity to benzodiazepine, but not to barbiturates.

The effects of acidic excitatory amino acids and 60 mM K+ on 45Ca uptake by synaptosomes prepared from rat striatum were examined. Both glutamic acid and 60 mM K+ significantly stimulated the uptake of 45Ca and these effects were antagonized by 30 mM Mg2+ and 0.5 mM La3+ but not by 5 microM tetrodotoxin. Neither kainic acid nor N-methyl-D,L-aspartic acid significantly affected the uptake of 45Ca. The results suggest that glutamate may activate a presynaptic receptor that is directly linked to calcium channels.

Acquisition and 48-h retention of a step-up active avoidance response were studied in separate age groups of C57BL/6NNia mice (aged 1.5, 3.5, 6, 12, or 26 months) and five strains of genetically autoimmune mice differing in life span. The C57BL/6NNia mice showed no change in ability to acquire the avoidance response between 1.5 and 3.5 months, but showed a steady decline in that ability thereafter. Mouse strains with early-onset autoimmune disorder (NZB/B1NJ, MRL/MpJ-lpr, and BXSB/MpJ) showed declines in acquisition capability between 1.5 and 3.5 months of age, whereas mouse strains with mild, late-onset autoimmune disorder (MRL/MpJ- + and NZBWF1/J) showed stable or improved acquisition during that period. Both the C57BL/6NNia and NZB/B1NJ mice showed age-dependent declines in 48-h retention performance by 12 months of age. These findings suggested that while 48-h retention performance deficits were most related to chronological age, avoidance acquisition deficits were related to development of autoimmunity.

Exposure to L-glutamate (10 mM) or 60 mM K+ for 1 min significantly stimulated the uptake of 45Ca2+ in slices from mouse striatum. Glutamate-induced stimulation was antagonized by 30 mM Mg2+ and by 5 or 10 mM L-glutamic acid diethyl ester, but not by 5 microM tetrodotoxin. Under these 1-min incubation conditions, neither kainate nor N-methyl-D,L-aspartate significantly affected the uptake of 45Ca2+ ion. By contrast, following preincubation for 10 min, glutamate and the conformationally restricted analogues, ibotenate, quisqualate, and kainate significantly inhibited the 60 mM K+-induced stimulation of the uptake of 45Ca2+. These effects of glutamate and kainate were not significantly affected by the presence of 1 mM Ca2+ in the preincubation medium. These results suggest that glutamate may activate a receptor directly linked to Ca2+ channels, whereas kainate may indirectly modulate the intracellular disposition of Ca2+.

The effects of several schedules of multiple morphine pellet implantation on body weight and dependence development in rats were studied. One schedule designated 6/7 (total number of pellets implanted per total number of treatment days), consisting of 1 pellet on day 0, 2 pellets on day 2 and 3 pellets on day 4 and a total treatment period of 7 days, produced high levels of dependence without affecting either body weight or rates of protein synthesis in whole brain or liver. The components of this schedule, 1/2 (one pellet on day 0 and a total treatment period of 2 days), 3/4 (one pellet on day 0 and two pellets on day 2 and a total treatment period of 4 days) and 6/7 (see above), produced a linear increase in the degree of dependence as measured by loss of body weight following naloxone-precipitated withdrawal. Hence, they were used to investigate the relationship between the degree of dependence and the rate of translation in vivo on free and membrane-bound polysomes in seven brain regions (cerebrum, cerebellum, mesencephalon, pons-medulla, striatum-septum, hippocampus-amygdala and thalamus-hypothalamus) following a 6 min pulse with a pool expansion dose of [3H]leucine. The rate of translation on free and membrane-bound polysomes was unaffected except on the bound polysomes of the pons-medulla and striatum-septum, where increased rates of translation were found to be closely correlated with degrees of dependence, measured as loss of body weight. Concomitant administration of naltrexone prevented both the stimulation of protein synthesis and the development of dependence, whereas administration of naltrexone alone did not affect translation rates in either polysome compartment of any region. Thus, it is concluded that the mechanisms underlying opiate dependence involve the stimulation of secretory protein synthesis in the pons-medulla and striatum-septum, presumably by the interaction between morphine and opiate receptors.

In 11-13 month C57BL/6Nnia mice, arecoline produced a dose-dependent decrease in motor activity at doses of 0.64-2.5 mg/kg, whereas at doses of 5.0-20.0 mg/kg arecoline produced a dose-dependent increase in motor activity. In marked contrast, age-matched NZB/B1NJ (New Zealand Black) mice failed to exhibit the first phase of the response, but showed a greater dose-dependent increase in motor activity following the doses of 10 and 20 mg/kg. Nicotine, 0.64-2.5 mg/kg, produced a dose-dependent decrease in motor activity in both strains. The effects of arecoline and nicotine were antagonized by scopolamine (2.5 mg/kg) and mecamylamine (1.0 mg/kg), respectively. These findings suggest that muscarinic neurotransmission may be altered in NZB/B1NJ mice, which produce brain-reactive autoantibodies, exhibit learning/memory dysfunctions, and also exhibit a loss of neurons staining positive for choline acetyltransferase.