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A study examines the role of predictive models to observe the presence of bacillus stearothermophilus in foods. Military food items are considered for the study.

Selective σ2 ligands continue to be an active target for medications to attenuate the effects of psychostimulants. In the course of our studies to determine the optimal substituents in the σ2-selective phenyl piperazines analogues with reduced activity at other neurotransmitter systems, we discovered that 1-(3-chlorophenyl)-4-phenethylpiperazine actually had preferentially increased affinity for dopamine transporters (DAT), yielding a highly selective DAT ligand., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Glucoprivation is a strong signal for the initiation of gastrointestinal contractions. While this relationship between utilizable nutrient levels and gastric motility has been recognized for more than 100 years, the explanation of this phenomenon has remained incomplete. Using widely differing approaches, recent work has suggested that the hindbrain is responsible for this chemoreflex effect. Surprisingly, astrocytes may be the main glucodetector elements under hypoglycemic conditions. Our own work using in vitro live cell calcium imaging shows that astrocytes in the NST increase cytoplasmic calcium in a concentration dependent manner in reaction to reductions in glucose. This effect is reversed on restoration of normal glucose concentrations. In vivo single unit neurophysiological recordings show that brainstem neurons driving gastric motility are activated by glucoprivic stimuli. Studies in intact animals verify that both dorsal medullary and systemic glucoprivation significantly increases gastric motility. Astrocyte inactivation with fluorocitrate blocks the pro-motility effects of glucoprivation. Thus, it appears that intact astrocyte signaling may be essential to glucoregulatory control over gastric motility., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Previous studies from our laboratory illustrated the potential for stromal cell-derived factor one [CXCL12; also referred to as SDF-1] to act on its receptor [CXCR4] within the dorsal vagal complex [DVC] of the hindbrain to suppress gastric motility (Hermann et al., 2008). While CXCR4 receptors are essential for normal brain development, they also play a critical role in the proliferation of the HIV virus and initiation of metastatic cell growth in the brain. Anorexia, nausea, and failed autonomic regulation of gastrointestinal function are significant causes of morbidity and are contributory factors in the mortality associated with these disease states. The implication of our previous study was that CXCL12 caused gastric stasis by acting on gastric reflex circuit elements in the DVC. This hindbrain complex includes vagal afferent terminations in the solitary nucleus, neurons in the solitary nucleus (NST) and visceral efferent motorneurons in the dorsal motor nucleus (DMN) that are responsible for the regulation of digestive functions from the oral cavity to the transverse colon. In the current study, in vivo single-unit neurophysiological recordings from physiologically-identified NST and DMN components of the gastric accommodation reflex show that while injection of femtomole doses of CXCL12 onto NST or DMN neurons has no effect on their basal activity, CXCL12 amplifies the effect of gastric vagal mechanosensory input to activate the NST and, in turn, inhibit DMN motor activity., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Cholecystokinin (CCK) is a potent regulator of visceral functions as a consequence of its actions on vago-vagal reflex circuit elements. This paper addresses three current controversies regarding the role of CCK to control gastric function via vago-vagal reflexes. Specifically: (a) whether CNS vs. peripheral (vagal afferent) receptors are dominant, (b) whether the long (58) vs. short (8) isoform is more potent and (c) whether nutritional status impacts the gain or even the direction of vago-vagal reflexes. Our in vivo recordings of physiologically identified gastric vagal motor neurones (gastric-DMN) involved in the gastric accommodation reflex (GAR) show unequivocally that: (a) receptors in the coeliac-portal circulation are more sensitive in amplifying gastric vagal reflexes; (b) in the periphery, CCK8 is more potent than CCK58; and (c) the nutritional status has a marginal effect on gastric reflex control. While the GAR reflex is more sensitive in the fasted rat, CCK amplifies this sensitivity. Thus, our results are in stark contrast to recent reports which have suggested that vago-vagal reflexes are inverted by the metabolic status of the animal and that this inversion could be mediated by CCK within the CNS.

Eleven new cannabinoid esters, together with three known cannabinoid acids and Delta9-tetrahydrocannabinol ( Delta9-THC ), were isolated from a high-potency variety of Cannabis sativa. The structures were determined by extensive spectroscopic analyses to be beta-fenchyl Delta9-tetrahydrocannabinolate ( 1), epi-bornyl Delta9-tetrahydrocannabinolate ( 2), alpha-terpenyl Delta9-tetrahydrocannabinolate ( 3), 4-terpenyl Delta 9-tetrahydrocannabinolate ( 4), alpha-cadinyl Delta9-tetrahydrocannabinolate ( 5), gamma-eudesmyl Delta9-tetrahydrocannabinolate ( 6), gamma-eudesmyl cannabigerolate ( 7), 4-terpenyl cannabinolate ( 8), bornyl Delta9-tetrahydrocannabinolate ( 9), alpha-fenchyl Delta9-tetrahydrocannabinolate ( 10), alpha-cadinyl cannabigerolate ( 11), Delta9-tetrahydrocannabinol ( Delta9-THC ), Delta9-tetrahydrocannabinolic acid A ( Delta9-THCA ), cannabinolic acid A ( CBNA), and cannabigerolic acid ( CBGA). Compound 8 showed moderate antimicrobial activity against Candida albicans ATCC 90028 with an IC 50 value of 8.5 microg/mL. The isolated acids and the ester-containing fractions showed low affinity to the CB-1 receptor. [corrected]

Cocaine's toxicity can be mitigated by blocking its interaction with sigma-1 receptors. The involvement of sigma-2 receptors remains unclear. To investigate their potential role, we have designed compounds through a convergent synthesis utilizing a highly selective sigma-1 ligand and elements of a selective sigma-2 ligand. Among the synthesized compounds was produced a subnanomolar sigma-2 ligand with an 11-fold preference over sigma-1 receptors. These compounds may be useful in developing effective pharmacotherapies for cocaine toxicity.

Cholecystokinin (CCK) has been proposed to act in a vagally dependent manner to increase pancreatic exocrine secretion via actions exclusively at peripheral vagal afferent fibers. Recent evidence, however, suggests the CCK-8s may also affect brain stem structures directly. We used an in vivo preparation with the aims of 1) investigating whether the actions of intraduodenal casein perfusion to increase pancreatic protein secretion also involved direct actions of CCK at the level of the brain stem and, if so, 2) determining whether, in the absence of vagal afferent inputs, CCK-8s applied to the dorsal vagal complex (DVC) can also modulate pancreatic exocrine secretion (PES). Sprague-Dawley rats (250-400 g) were anesthetized and the common bile-pancreatic duct was cannulated to collect PES. Both vagal deafferentation and pretreatment with the CCK-A antagonist lorglumide on the floor of the fourth ventricle decreased the casein-induced increase in PES output. CCK-8s microinjection (450 pmol) in the DVC significantly increased PES; the increase was larger when CCK-8s was injected in the left side of the DVC. Protein secretion returned to baseline levels within 30 min. Microinjection of CCK-8s increased PES (although to a lower extent) also in rats that underwent complete vagal deafferentation. These data indicate that, as well as activating peripheral vagal afferents, CCK-8s increases pancreatic exocrine secretion via an action in the DVC. Our data suggest that the CCK-8s-induced increases in PES are due mainly to a paracrine effect of CCK; however, a relevant portion of the effects of CCK is due also to an effect of the peptide on brain stem vagal circuits.

We have previously reported that microinjections of endomorphin-2 (E-2; an endogenous mu-receptor agonist) into the medial subnucleus of the NTS (mNTS) elicit depressor and bradycardic responses via activation of ionotropic glutamate receptors located on secondary mNTS-neurons. Based on this report, it was hypothesized that activation of secondary mNTS neurons by E-2 may result in an exaggeration of baroreflex responses. In order to test this hypothesis, baroreflex responses were studied in adult, urethane-anesthetized, artificially ventilated, male Wistar rats before and after the microinjections of E-2 into the mNTS. Baroreceptors were stimulated by applying pressure increments (80-100 mm Hg) in the carotid sinus and by electrical stimulation (stimulus intensity: 0.5 V, frequencies 5, 10, and 25 pulses/s, pulse duration: 1 ms) of the aortic nerve for 30-s periods. Baroreceptor stimulation elicited depressor and bradycardic responses. Microinjections (100 nl) of E-2 (0.4 mmol/l) into the mNTS attenuated the baroreflex responses. Microinjections of naloxone (an opioid receptor antagonist) into the mNTS (0.5 mmol/l) did not alter baroreflex responses. Based on these results, it was concluded that activation of mu-opioid receptors in the mNTS attenuates baroreflex responses. Possible mechanisms for excitatory effects of E-2 in the mNTS resulting in depressor and bradycardic responses, on one hand, and inhibitory effects resulting in attenuation of baroreflex responses, on the other, are discussed.

Although several agonists and antagonists for different subtypes of metabotropic glutamate receptors (mGLURs) have become available in recent years, detailed information regarding their selectivity is not complete in the in vivo animal models. The purpose of the present investigation was to study the cardiovascular effects of microinjections of some of these mGLUR agonists and antagonists into the nucleus tractus solitarius (nTS). Microinjections (100 nl) of EC(50) concentrations of 3,5-DHPG (0.005 mM; mGLUR(1) agonist), APDC (17.3 mM; mGLUR(2/3) agonist), PPG (11.7 mM; mGLUR(8) agonist) and L-AP(4) (1 mM; mGLUR(4) agonist) into the nucleus tractus solitarius of urethane-anesthetized male Wistar rats elicited depressor and bradycardic responses which may be mediated by pre- and/or postsynaptic mechanisms. The blocking effect of mGLUR antagonists used here was not specific for any one type of glutamate receptors (GLURs). For example, AIDA (50 mM; mGLUR(1) antagonist) blocked the effects of EC(50) concentrations of 3,5-DHPG, and PPG. LY341495 (135 mM; mGLUR(2/3) antagonist) blocked all of the mGLURs and ionotropic GLURs. EGLU, APICA and MCCG (250 mM each; mGLUR(2/3) antagonists) blocked the effects of APDC, NMDA and AMPA. CPPG (80 mM) and MSOP (125 mM), mGLUR(4) antagonists, blocked the effects of 3,5-DHPG, PPG and L-AP(4.) D-AP7 (NMDA receptor antagonist) and NBQX (a non-NMDA receptor antagonist) did not alter the responses of any of the mGLUR agonists. The data presented may be useful in assessing the role of metabotropic and ionotropic GLURs in mediating different cardiovascular reflexes.

We study the performance of an adaptive optics (AO) system with four laser guide stars (LGSs) and a natural guide star (NGS). The residual cone effect with four LGSs is obtained by a numerical simulation. This method allows the adaptive optics system to be extended toward the visible part of the spectrum without tomographic reconstruction of three-dimensional atmospheric perturbations, resolving the cone effect in the visible. Diffraction-limited images are obtained with 17-arc ms precision in median atmospheric conditions at wavelengths longer than 600 nm. The gain achievable with such a system operated on an existing AO system is studied. For comparison, performance in terms of achievable Strehl ratio is also computed for a reasonable system composed of a 40 x 40 Shack-Hartmann wave-front sensor optimized for the I band. Typical errors of a NGS wave front are computed by use of analytical formulas. With the NGS errors and the cone effect, the Strehl ratio can reach 0.45 at 1.25 microm under good-seeing conditions with the Nasmyth Adaptive Optics System (NAOS; a 14 x 14 subpupil wave-front sensor) at the Very Large Telescope and 0.8 with a 40 x 40 Shack-Hartmann wave-front sensor.

Two monozygotic female twins with linear porokeratosis of Mibelli are described. One had only minimal lesions of the right elbow. The other had a linear lesion of the right arm following Blaschko's lines. Monozygotism was established using DNA fingerprinting. A single-gene defect of variable expressivity involving the clonal development of epidermal cutaneous cells according to the lines of cutaneous embryogenesis is suspected. Dithranol and carbon dioxide laser treatment are discussed.