Prevalence and genotype distribution of JC polyomavirus in urine from patients with hematological malignancies in Vietnam.

JC virus (JCV) causes progressive multifocal leukoencephalopathy in immunocompromised patients. The prevalence and genotype patterns of JCV vary between different geographical regions. This study was done to investigate the prevalence and genotype distribution of JCV in patients with hematological malignancies in Vietnam. A total of 48 urine samples were collected from patients with hematological malignancies. DNA was extracted and detection of JCV was by nested-polymerase chain reaction. Sequence analysis was obtained and a phylogenetic tree was constructed for genotyping of JCV. Twenty-seven (56.25%) urine samples tested positive for JCV. JCV genotype 7 was only observed in this study. Subtype analysis showed that JCV subtype 7A was the most commonly prevalent, followed by 7B1 and 7C1. Other subtypes were not detected in this population. There were no significant differences associated with age, gender, and biochemical parameters between patients with JCV and without JCV excretion in urine. The present study showed a high prevalence of JCV in the urine of patients with hematologic malignancies. The most common genotype found in this population was JCV subtype 7A.

Circadian integration of sleep-wake and feeding requires NPY receptor-expressing neurons in the mediobasal hypothalamus.

Sleep and feeding rhythms are highly coordinated across the circadian cycle, but the brain sites responsible for this coordination are unknown. We examined the role of neuropeptide Y (NPY) receptor-expressing neurons in the mediobasal hypothalamus (MBH) in this process by injecting the targeted toxin, NPY-saporin (NPY-SAP), into the arcuate nucleus (Arc). NPY-SAP-lesioned rats were initially hyperphagic, became obese, exhibited sustained disruption of circadian feeding patterns, and had abnormal circadian distribution of sleep-wake patterns. Total amounts of rapid eye movement sleep (REMS) and non-REMS (NREMS) were not altered by NPY-SAP lesions, but a peak amount of REMS was permanently displaced to the dark period, and circadian variation in NREMS was eliminated. The phase reversal of REMS to the dark period by the lesion suggests that REMS timing is independently linked to the function of MBH NPY receptor-expressing neurons and is not dependent on NREMS pattern, which was altered but not phase reversed by the lesion. Sleep-wake patterns were altered in controls by restricting feeding to the light period, but were not altered in NPY-SAP rats by restricting feeding to either the light or dark period, indicating that disturbed sleep-wake patterns in lesioned rats were not secondary to changes in food intake. Sleep abnormalities persisted even after hyperphagia abated during the static phase of the lesion. Results suggest that the MBH is required for the essential task of integrating sleep-wake and feeding rhythms, a function that allows animals to accommodate changeable patterns of food availability. NPY receptor-expressing neurons are key components of this integrative function.

Effects of USDA quality grade and cooking on water-soluble precursors of beef flavor.

The objective of the current study was to determine the effects of three USDA quality grades and cooking on the water-soluble flavor precursors of beef Longissimus lumborum. Raw and cooked steaks from beef strip loins of USDA Prime (PR; n = 8), Low-Choice (LC; n = 8), and Standard (ST; n = 8) were analyzed for extractable free amino acids, reducing sugars, and other nitrogenous organic compounds (NOCs). Overall, two-way quality grade × cooking interactions were found for the contents of most water-soluble precursors (Pquality grade × cooking < 0.05), which were greater in raw LC and ST and were changed more in ST and LC steaks by cooking. The magnitude of those changes suggested that cystine, a dimer of cysteine, glucose, and glucose 6-phosphate might play more important roles in beef flavor development than previously thought.

Effects of market type and time of purchase on oxidative status and descriptive off-odors and off-flavors of beef in Vietnam.

The objective of the current study was to determine the effects of market type (super market - SM, indoor market - IM, open market - OM) and sampling time (at the opening - T0 and 4 h after the opening - T4) on antioxidant capacity, lipid oxidation, and descriptive sensory attributes of beef in Vietnam. Values of FC and TEAC were greater in OM beef than IM and SM (P < 0.001) and FC value was also greater at T4 than T0 (P = 0.038). The beef from SM had 7% greater TBARS than IM and OM (P = 0.003). Livery odor was less intense in raw beef from OM when compared to SM and IM (P ≤ 0.047). Sour odor in raw beef, and livery flavor in cooked beef was increased from T0 to T4 (P ≤ 0.035). Principal component analysis of descriptive sensory attributes indicated that FC and TEAC could predict partial livery flavor in cooked beef, but not off-odors in raw beef.

Glioblastoma of the optic chiasm.

Primary malignant gliomas of the optic nerve and chiasm are rare, and are usually rapidly fatal in adults. We report a 48-year-old woman with a glioblastoma multiforme arising from the optic chiasm. Following radiotherapy, our patient survived nearly 14 months, which is the longest survival reported in patients with this diagnosis. There have only been four other reports of glioblastoma multiforme arising from the optic chiasm as distinct from secondary involvement of the chiasm, in the last 40 years.

Body fat of stock-type horses predicted by rump fat thickness and deuterium oxide dilution and validated by near-infrared spectroscopy of dissected tissues.

Body condition score and percent body fat (BF; %) of horses are positively correlated with reproductive efficiency and are indicative of metabolic issues. However, BF in horses may be poorly predicted because current procedures are either subjective or dependent on one anatomical location. Therefore, the objectives of the current study were to compare 2 methods of predicting BF using rump fat thickness (RFT) and deuterium oxide (DO) dilution with actual tissue fat analysis by near-infrared spectroscopy (NIRS) in stock-type horses and to identify the relationship between BF and BCS. Twenty-four stock-type horses were selected to be humanely euthanized based on 3 primary criteria: geriatric, crippled, and/or unsafe. Approximately 20 h before slaughter, horses were weighed and BCS assessed to be 1 ( = 1; 433 kg), 2 ( = 1; 415 kg), 3 ( = 1; 376 kg), 4 ( = 7; 468 ± 13 kg), 5 ( = 10; 455 ± 11 kg), and 6 ( = 4; 493 ± 12 kg) and RFT was measured using ultrasonography. Blood samples were collected immediately before and 4 h after DO infusion (0.12 g/kg BW). Deuterium oxide concentration of plasma was determined by gas isotope ratio mass spectrometry. Horses were housed in a dry lot overnight before being individually sedated (1.1 mg xylazine/kg BW) and anesthetized using a jugular venipuncture (2.2 mg ketamine/kg BW), and potassium chloride (KCl) solution was administered to cease cardiac function before exsanguination. After euthanasia, horse carcasses were processed and dissected and tissues were collected for NIRS analysis. Body fat predicted by DO dilution was correlated with BF measured by NIRS analysis on various weight bases ( = 0.76 to 0.81, < 0.001), whereas no correlation was observed for BF predicted by RFT. A paired -test indicated that both DO dilution and RFT overestimated BF by 2.48 to 3.26% ( < 0.001) and 5.81 to 6.59% ( < 0.001), respectively, compared with NIRS analysis. Body condition scores affected BF measured by NIRS analysis ( ≤ 0.038) and predicted by DO dilution ( < 0.001) and RFT ( = 0.042). The current study provided evidence that DO dilution was a better prediction method for BF than RFT and that BCS may serve as a BF predictor in stock-type horses.

Consumer palatability scores, sensory descriptive attributes, and volatile compounds of grilled beef steaks from three USDA Quality Grades.

Consumer palatability scores, sensory descriptive attributes, and volatile compounds were assessed for beef Longissimus lumborum steaks of USDA Prime, Low Choice, and Standard grades. Overall and flavor liking was greater (P<0.05) for Prime and Low Choice. Initial flavor impact and fat-like attributes were greater (P<0.05) among Prime and Low Choice. Prime had greater (P<0.05) brown/roasted, beef identity, overall sweetness, and umami. Cardboard was greater (P<0.05) in Standard. Volatile compounds representing flavor development pathways were varied with quality grade. Standard had greater (P<0.05) abundances of n-aldehydes. Phenylacetaldehyde was greater (P<0.05) in Prime and Low Choice. Both 2,3-butanedione and 3-hydroxy-2-butanone were greatest (P<0.05) in Prime. Overall liking was positively correlated with many descriptive attributes, 3-hydroxy-2-butanone, and phenylacetaldehyde, and negatively correlated with cardboard, green, and n-aldehydes. While the measured attributes and volatiles may not be causative of flavor, this data indicates potential for prediction of flavor through their measurement.

Assessment of volatile compounds, neutral and polar lipid fatty acids of four beef muscles from USDA Choice and Select graded carcasses and their relationships with consumer palatability scores and intramuscular fat content.

Fatty acids (FA) in neutral and polar lipids (NL and PL) and volatile compounds were determined in Gluteus medius (GM), Longissimus lumborum (LL), Serratus ventralis (SV), and Semimembranosus (SM) muscles from upper 2/3 USDA Choice and Select quality grades (QG). Concentrations of NL FA (mg/g) were influenced by intramuscular fat (IMF) content being greater in upper 2/3 Choice compared with Select. The SV contained greater concentrations of NL FA; meanwhile, the SM contained the lowest quantities of NL FA. Percentages (g/100g of total FA) of NL SFA and MUFA were increased in beef with greater IMF content. Concentrations and percentages of PL FA had muscle specific differences between QG. Volatile compounds were primarily affected by muscle. Increases in SFA and MUFA were related with consumer liking, regardless of lipid fraction. Overall the influence of QG on SFA and MUFA was muscle specific. Therefore, each muscle may require specific considerations when considering FA, volatile compounds, and ultimately consumer liking.

Zinc Methionine Supplementation Impacts Gene and Protein Expression in Calf-Fed Holstein Steers with Minimal Impact on Feedlot Performance.

Providing cattle a more bioavailable zinc (Zn) source prior to administering a beta adrenergic agonist (ßAA) may enhance the metabolic pool of primary nutrients that will influence the magnitude of the ßAA response. Calf-fed Holstein steers were supplemented with a Zn methionine supplement (ZnMet; ZINPRO(®); Zinpro Corporation, Eden Prairie, MN) for 115 ± 5 days prior to harvest along with zilpaterol hydrochloride (ZH; Zilmax(®); Merck Animal Health, Summit, NJ) for the last 20 days with a 3-day withdrawal to evaluate the effects on growth and carcass performance together with gene and protein expression of skeletal muscle, adipose tissue, and fatty acid composition of polar and neutral lipid depots. Steers (n = 1296; initial weight = 468.5 ± 0.5 kg) were sorted by weight, blocked by harvest date, and randomly assigned to pens (n = 12) and treatments: control (90 ppm Zn from ZnSO4) and ZnMet (Control plus 720 mg Zn from ZnMet/hd/d). There were no differences (P > 0.05) in growth performance or carcass characteristics. The ZnMet-fed cattle had reduced (P < 0.05) abundance of myosin heavy chain (MHC)-IIX, ß1-adrenergic receptor (ßAR), peroxisome proliferator-activated receptor gamma, and stearoyl-CoA desaturase mRNA in skeletal muscle tissue. The ZnMet cattle had greater (P < 0.05) abundance of MHC-II protein, increased MHC-IIA and IIX cross-sectional areas (P < 0.05), an increased percentage of MHC-I fibers (P < 0.05), and a decreased percentage of MHC-IIX fibers (P < 0.05). The combination of ZnMet and ZH had positive biological effects on musculoskeletal tissue; however, these molecular effects were not significant enough to impact overall feedlot and carcass performance.

Histochemical demonstration of hydrogen peroxide production by leukocytes in fixed-frozen tissue sections of inflammatory lesions.

The production of H2O2 by cells in cold paraformaldehyde-fixed frozen sections of inflammatory lesions was histochemically demonstrated by incubating them with diaminobenzidine (DAB) for 2 to 6 h. Catalase (150 micrograms/ml, about 1400 U/ml) inhibited the reaction, indicating that H2O2 was required to produce the chromogenic DAB product. Granulocytes (PMNs and eosinophils) were the main types of cells stained by the DAB reaction. Positive staining of macrophages was less frequent. The H2O2 was produced by metabolic enzymes that were still active after cell death and mild fixation. An atmosphere of 95 to 100% oxygen enhanced the specific DAB reaction, and an atmosphere of 100% nitrogen eliminated it. The DAB histochemical reaction to detect H2O2 requires the presence of peroxidases to produce the colored reaction product. Within our tissue sections, such peroxidases were evidently present in excess, because addition of low concentrations of H2O2 significantly increased the reaction product. Although some of the H2O2 produced by the granulocytes may have been derived from the dismutation of superoxide (O2-), the NADPH oxidase pathway for O2- formation did not seem to be involved: NADPH oxidase, a rather labile enzyme, should not be active after mild fixation, and diphenyleneiodonium (100 microM), an inhibitor of flavine-requiring NADPH oxidase, did not inhibit the reaction. Reactive nitrogen intermediates were also not involved, because NG-monomethyl-L-arginine and NG-nitro-L-arginine methyl ester, inhibitors of nitric oxide synthetase, did not appreciably inhibit the reaction. We conclude that stable, non-flavine-requiring oxidases, possibly cyclooxygenases or lipoxygenases, produced the H2O2 measured histochemically by our DAB reaction. These studies were made on tissue sections of acute dermal inflammatory lesions produced in rabbits by the topical application of 1% sulfur mustard [bis(2-chloroethyl) sulfide] in methylene chloride. Both intact PMNs and disintegrating PMNs in the base of the crust produced H2O2. Despite the production of H2O2 and the presence of peroxidase activity, no tissue damage was seen microscopically near the H2O2-producing cells, which indicates that the tissues are well protected by the antioxidants present in this self-limiting inflammatory reaction.

Effects of USDA beef quality grade and cooking on fatty acid composition of neutral and polar lipid fractions.

The effects of USDA beef quality grade (QG; Prime, Low Choice, and Standard; n=8) and cooking (RC) on fatty acid (FA) concentrations (mg/g dry matter) and percentages of neutral and polar lipid fractions (NL and PL, respectively)from strip steaks were explored. An increase in QG led to an accumulation of most FA, especially in the NL fraction (P < 0.001). Common effects on FA percentages were two-way interactions of either QG or RC with LF (P ≤ 0.019). Fatty acids were affected differently by QG and RC depending on their originating LF. Monounsaturated fatty acid (MUFA) and polyunsaturated fatty acid (PUFA) percentages of the PL were dependent on QG (P ≤ 0.014). Cooking and QG had minimal impact on FA percentages of the NL, however, greatly influenced PL MUFA and PUFA percentages (P b 0.001). There was evidence indicating that dry heat cookery affected not only PUFA, as generally thought, but also the MUFA of PL fraction.

Sensory evaluation of tender beef strip loin steaks of varying marbling levels and quality treatments.

The palatability of tender [Warner-Bratzler shear force values <33.34N (3.4kg)] beef strip loins of 10 different treatments [USDA Prime, High Choice (upper 1/3 Choice), Low Choice (lower 1/3 Choice), Select, Standard, Australian Wagyu, American Wagyu, Holstein Select, Holstein Top Choice (upper 2/3 Choice) and Grass-finished] was evaluated by consumers and a trained flavor panel. In general, tenderness, juiciness, flavor, and overall liking ratings as well as acceptability percentage for each trait, increased with increased fat levels. Moreover, overall liking was highly correlated (P<0.01) with flavor liking (r=0.96) as well as fat percentage (r=0.79). Beef flavor scores were positively associated (P<0.01) with fat-like (r=0.67) and umami (r=0.59) flavors. Fat level was the primary driver of beef flavor acceptability in all samples when no undesirable off-flavors were present.

Capsaicin-induced neuronal degeneration: silver impregnation of cell bodies, axons, and terminals in the central nervous system of the adult rat.

Capsaicin is a neurotoxic substance valued in neurobiological research because of its ability to selectively damage small unmyelinated primary sensory neurons. Previous work has indicated that systemic capsaicin administration causes permanent neuronal degeneration in neonatal rats, but evidence that capsaicin has a similar effect in adults is equivocal and incomplete. Therefore, we used silver impregnation, a method that labels degenerating neurons, to examine the central nervous system of adult rats after systemic capsaicin treatment. Adult rats were injected with a single intraperitoneal dose of capsaicin (50 or 90 mg/kg) or vehicle solution and killed 6, 12, 18, 24, 48, 96, or 240 hours later. Sections of brain and spinal cord were stained with the Carlsen-de Olmos cupric silver method. As reported previously, stained sections revealed degeneration in areas known to be innervated by small-diameter primary sensory fibers: the substantia gelatinosa of the spinal cord dorsal horn and spinal trigeminal nucleus, the solitary nucleus and tract, and the lateral borders of the area postrema. In addition, axon and terminal degeneration was observed in several discrete forebrain and hindbrain areas not previously associated with capsaicin-induced degeneration in either adult or neonatal rats: the inferior olive, the olivary pretectal nucleus, the interpeduncular nucleus, the suprachiasmatic nucleus, and the lateral septum/medial accumbens region. Furthermore, degenerating cell bodies were observed in the intrafascicular nucleus of the ventromedial midbrain tegmentum, in the supramammillary nucleus, and in the posterior hypothalamic area. Unilateral nodose ganglionectomy produced terminal staining on the denervated side very similar to that induced bilaterally by capsaicin. In addition, unilateral nodose ganglionectomy 1 month prior to capsaicin injection greatly attenuated staining in the ipsilateral nucleus of the solitary tract, confirming the hypothesis that capsaicin damages vagal sensory neurons innervating this nucleus. Capsaicin-induced damage in adult rats was long-lasting, since the second of two capsaicin treatments spaced 4.5 months apart produced no additional degeneration.

Prior optic nerve transection reduces capsaicin-induced degeneration in rat subcortical visual structures.

Capsaicin is a neurotoxin capable of causing degeneration in specific sites throughout the neuraxis, including the suprachiasmatic nucleus (SCh), the ventrolateral geniculate nucleus (VLG), the intergeniculate leaflet (IGL), and the olivary and medial pretectal nuclei (OPT and MPT). In this experiment, we tested the hypothesis that capsaicin-induced terminal degeneration in the SCh, VLG, IGL, OPT, and MPT results from destruction of retinal ganglion cells and their axonal projections to these sites. In the first experiment, silver stains were used to examine degeneration in the retina induced by systemic capsaicin treatment. Capsaicin caused degeneration of ganglion cells, bipolar cells, and nerve terminals in the retina, which could be observed between 2 and 24 hours after treatment. In the second experiment, 15-day-old rat pups were enucleated unilaterally. Five days or 2, 5, or 10 months later, they were injected systemically with capsaicin and killed 6 hours (pups) or 18 hours (adults) later for analysis with a cupric silver stain. In rats of all ages, prior monocular enucleation reduced or eliminated capsaicin-induced degeneration in the contralateral SCh, VLG, IGL, OPT, and MPT. In the third experiment, rat pups were treated systemically with capsaicin or vehicle solution at 12 days of age and given unilateral intravitreal injections of cholera toxin conjugated to horseradish peroxidase (CT-HRP) 3 days prior to sacrifice at 20 days of age. Transport of CT-HRP to the SCh, VLG, IGL, MPT, and OPT was attenuated but not abolished by capsaicin pretreatment. Results suggest that capsaicin causes degeneration in the SCh, VLG, IGL, MPT, and OPT by selective destruction of a subpopulation of retinal ganglion cells with axonal projections to these sites.

Age-related changes in capsaicin-induced degeneration in rat brain.

Previous results indicate that the pattern of capsaicin-induced degeneration in the rat central nervous system is age-related. Experiments utilizing capsaicin's selective neurodegenerative effects to study the function of central neural circuits will therefore require a detailed understanding of capsaicin's central neurotoxicity in rats of different ages. The goal of this experiment was to characterize the degeneration induced in the rat brain by systemic treatment with capsaicin at different ages (10, 15, 20, 25, 30 or 75 days, or 11 months), using a cupric silver stain to label degenerating neurons. Results revealed degenerating cell bodies in the ventromedial brainstem in capsaicin-treated rats of all age groups, though they were more numerous in adult rats than in pups. In addition, many areas contained capsaicin-induced nerve terminal degeneration both in rat pups and in adult rats. These areas were the substantia gelatinosa of the spinal cord dorsal horn; the solitary tract; the nucleus of the solitary tract, visceral portion; the area postrema; the trigeminal nerve and spinal trigeminal nucleus; the medial nucleus of the inferior olive; the rostral, dorsomedial and dorsolateral interpeduncular subnuclei and overlying interfascicular nucleus; the supramammillary area; the lateral septal nucleus; the bed nucleus of the stria terminalis, anterior medial portion; the optic nerve and tract; the suprachiasmatic nucleus, ventroposterolateral portion; the magnocellular subnucleus of the ventrolateral geniculate nucleus; the intergeniculate leaf; the medial pretectal nucleus and the olivary pretectal nucleus. In several, but not all of these areas, the apparent density of degenerating terminals was significantly less in adult rats than in pups. In other brain sites, capsaicin-induced degeneration was observed only in rats younger than 30 days of age. These areas were the lateral habenula, medial part; the sphenoid nucleus; and the stria medullaris. Still other brain sites lost their sensitivity to capsaicin sometime between 30 and 75 days of age. These areas were the bed nucleus of the stria terminalis, medial posteromedial part; the medial preoptic nucleus, central part; the septohypothalamic nucleus; the ventral reuniens area; and the ventromedial hypothalamic nucleus. Adult rats 75 days and 11 months of age did not differ detectably in their response to capsaicin. Thus, loss or attenuation of capsaicin sensitivity is not progressive throughout life. It does not occur in all capsaicin-sensitive sites. Where it does occur, loss of sensitivity occurs prior to adulthood and follows a distinct and reproducible time course that may differ for different sites.

Capsaicin-induced neuronal degeneration in the brain and retina of preweanling rats.

Capsaicin is a neurotoxin known for its ability to cause degeneration of small unmyelinated primary sensory neurons in both spinal and cranial nerves. Although lower motor neurons do not degenerate following capsaicin treatment, the extent to which capsaicin may damage neurons in the brain has not been thoroughly evaluated. This study examines the effects of systemic capsaicin (50-150 mg/kg) on the central nervous system of 10-day-old rats. Rat pups were injected with capsaicin or the injection vehicle and sacrificed 6 hours-10 days later. Brains, spinal cords, and retinas were stained with cupric silver to label degenerating neurons. As previously reported for capsaicin-treated rats, degenerating nerve terminals were present in areas receiving primary afferent input: the spinal cord dorsal horn, spinal trigeminal nucleus, nucleus of the solitary tract, and area postrema. However, degenerating terminals were also present in areas not known to receive primary sensory innervation: the inferior olivary nucleus, sphenoid nucleus, medial and olivary pretectal nuclei, interpeduncular nucleus, interfascicular nucleus, caudal linear, dorsal, median, and paramedian raphe nuclei, supramammillary area, lateral habenula, ventrolateral geniculate nucleus, ventral reuniens nucleus, ventromedial hypothalamic nucleus, lateral hypothalamic and preoptic areas, suprachiasmatic nucleus, septohypothalamic nucleus, bed nucleus of the stria terminalis, lateral septal nucleus, accumbens shell, olfactory bulb, and retina. Some areas where capsaicin caused degeneration in rat pups do not appear to be capsaicin-sensitive in adult rats. Results indicate that (1) capsaicin's neurotoxicity is not limited to primary sensory neurons and (2) developmental factors may alter the capsaicin sensitivity of some neuronal projections within the brain.

Immunotoxic destruction of distinct catecholamine subgroups produces selective impairment of glucoregulatory responses and neuronal activation.

The toxin-antibody complex anti-d(beta)h-saporin (DSAP) selectively destroys d(beta)h-containing catecholamine neurons. To test the role of specific catecholamine neurons in glucoregulatory feeding and adrenal medullary secretion, we injected DSAP, unconjugated saporin (SAP), or saline bilaterally into the paraventricular nucleus of the hypothalamus (PVH) or spinal cord (T2-T4) and subsequently tested rats for 2-deoxy-D-glucose (2DG)-induced feeding and blood glucose responses. Injections of DSAP into the PVH abolished 2DG-induced feeding, but not hyperglycemia. 2DG-induced Fos expression was profoundly reduced or abolished in the PVH, but not in the adrenal medulla. The PVH DSAP injections caused a nearly complete loss of tyrosine hydroxylase immunoreactive (TH-ir) neurons in the area of A1/C1 overlap and severe reduction of A2, C2, C3 (primarily the periventricular portion), and A6 cell groups. Spinal cord DSAP blocked 2DG-induced hyperglycemia but not feeding. 2DG-induced Fos-ir was abolished in the adrenal medulla but not in the PVH. Spinal cord DSAP caused a nearly complete loss of TH-ir in cell groups A5, A7, subcoeruleus, and retrofacial C1 and a partial destruction of C3 (primarily the ventral portion) and A6. Saline and SAP control injections did not cause deficits in 2DG-induced feeding, hyperglycemia, or Fos expression and did not damage catecholamine neurons. DSAP eliminated d(beta)h immunoreactivity but did not cause significant nonspecific damage at injection sites. The results demonstrate that hindbrain catecholamine neurons are essential components of the circuitry for glucoprivic control of feeding and adrenal medullary secretion and indicate that these responses are mediated by different subpopulations of catecholamine neurons.

Nodose ganglionectomy reduces angiotensin II receptor binding in the rat brainstem.

Angiotensin II (Ang II) receptor binding sites in the dorsomedial medulla of intact and unilaterally nodose ganglionectomized rats were identified and characterized using 125I-sarcosine,isoleucine Ang II. This radioligand bound saturably and with high affinity to rat brain homogenates and to sections of rat brainstem. Specific (1 microM angiotensin II displaceable) binding of 125I-sarcosine,isoleucine Ang II was displaced by angiotensin analogues with a potency order similar to that described for angiotensin II receptors. Unilateral nodose ganglionectomy caused a reduction in Ang II receptor binding in the medial solitary tract nucleus, dorsal motor nucleus of the vagus, and area postrema ipsilateral to the lesioned ganglion. This observation suggests that Ang II receptors in the dorsomedial medulla may be located on axon terminals of vagal afferents and cell bodies of vagal efferents.

Immunotoxic catecholamine lesions attenuate 2DG-induced increase of AGRP mRNA.

Injections of the immunotoxin, saporin conjugated to anti-dopamine-beta-hydroxylase (DSAP), into the hypothalamic paraventricular nucleus (PVH) selectively destroy norepinephrine (NE) and epinephrine (E) terminals in the medial hypothalamus and abolish glucoprivic feeding. We utilized PVH DSAP injections to examine the role of NE/E neurons in the previously reported 2-deoxy-D-glucose (2DG)-induced increases in mRNA levels for the orexigenic peptides, AGRP and NPY. Northern blot analysis revealed that DSAP lesions elevated basal but blocked 2DG-induced increases in AGRP mRNA levels. Changes in NPY mRNA were not detectable. AGRP neurons may contribute to circuitry activated by NE/E neurons for elicitation of glucoregulatory responses.

Tissue characterization and calcification potential of commercial bioprosthetic heart valves.

BACKGROUND: Tissue properties may contribute to intrinsic calcification of bioprosthetic heart valves. Phospholipids have been proposed as potential nucleation sites for calcification. Other tissue properties might also be important in calcification. METHODS: Commercial and control bioprosthetic valve tissues were characterized by shrinkage temperature, moisture content, free amine content, phospholipid content, and calcification level after 90-day rat subcutaneous implantation as described. RESULTS: Shrinkage temperature, moisture content, and free amine content were typical for glutaraldehyde-cross-linked tissues. Phospholipid and calcium levels varied considerably among valve types. There was a significant correlation between phospholipid levels and calcification (r = 0.63, p = 0.04). Sulzer Carbomedics Mitroflow and Toronto SPV valve tissues had significantly more calcification than other commercial bioprostheses in this study (p < 0.01). Carpentier-Edwards Duraflex, CE SAV, and CE PERIMOUNT valve tissues had significantly less calcification than Medtronic Mosaic in this animal model (p < 0.02). CONCLUSIONS: Processes that reduce phospholipid levels are associated with reduced calcification in the rat subcutaneous model. Significant differences in calcification level were found among commercially available valves. The clinical significance of these results is unknown.