Effect of meat (beef, chicken, and bacon) on rat colon carcinogenesis.
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High intake of red meat or processed meat is associated with increased risk of colon cancer. In contrast, consumption of white meat (chicken) is not associated with risk and might even reduce the occurrence of colorectal cancer. We speculated that a diet containing beef or bacon would increase and a diet containing chicken would decrease colon carcinogenesis in rats. One hundred female Fischer 344 rats were given a single injection of azoxymethane (20 mg/kg i.p.), then randomized to 10 different AIN-76-based diets. Five diets were adjusted to 14% fat and 23% protein and five other diets to 28% fat and 40% protein. Fat and protein were supplied by 1) lard and casein, 2) olive oil and casein, 3) beef, 4) chicken with skin, and 5) bacon. Meat diets contained 30% or 60% freeze-dried fried meat. The diets were given ad libitum for 100 days, then colon tumor promotion was assessed by the multiplicity of aberrant crypt foci [number of crypts per aberrant crypt focus (ACF)]. The ACF multiplicity was nearly the same in all groups, except bacon-fed rats, with no effect of fat and protein level or source (p = 0.7 between 8 groups by analysis of variance). In contrast, compared with lard- and casein-fed controls, the ACF multiplicity was reduced by 12% in rats fed a diet with 30% bacon and by 20% in rats fed a diet with 60% bacon (p < 0.001). The water intake was higher in bacon-fed rats than in controls (p < 0.0001). The concentrations of iron and bile acids in fecal water and total fatty acids in feces changed with diet, but there was no correlation between these concentrations and the ACF multiplicity. Thus the hypothesis that colonic iron, bile acids, or total fatty acids can promote colon tumors is not supported by this study. The results suggest that, in rats, beef does not promote the growth of ACF and chicken does not protect against colon carcinogenesis. A bacon-based diet appears to protect against carcinogenesis, perhaps because bacon contains 5% NaCl and increased the rats' water intake. (+info)
Ruminally undegraded intake protein in sheep fed low-quality forage: effect on weight, growth, cell proliferation, and morphology of visceral organs.
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To determine the influence of increasing levels of supplemental ruminally undegraded intake protein (UIP) on visceral organ weights, growth, cell proliferation, and morphology, 20 mature ewes of mixed breeding were fed a 6.55% CP grass hay:straw mixture (40:60) and assigned to one of four supplemental treatments. Supplements were control (no supplement) and low, medium, and high levels of UIP. After 42 to 46 d on treatment, ewes were infused i.v. with 5-bromo-2-deoxy-uridine (BrdU, a thymidine analog used to provide an index of the rate of intestinal cell proliferation) and slaughtered 1 h later. Visceral organs were weighed, and subsamples were obtained to evaluate visceral DNA, RNA, and protein contents (frozen samples) as well as intestinal morphology (fixed samples). Final BW; eviscerated BW (EBW); total visceral weight; and liver fresh, dry, and dry fat-free weights were increased (P<.10) in protein-supplemented ewes compared with controls, but were not influenced by increasing levels of UIP. Tissue weights of duodenum, jejunum, ileum, cecum, and colon were not greatly influenced by treatment. There were no differences among treatments in intestinal DNA and protein concentrations and the ratios RNA:DNA and protein:DNA. Jejunal RNA concentration and content was increased (P<.10) in low compared with medium and high treatments. Jejunal RNA content also was decreased (P<.10) in high compared with the medium UIP treatment. Liver RNA and protein contents were increased (P<.10) with protein supplementation. In contrast, contents of RNA, DNA, and protein in duodenum, ileum, cecum, and colon were not influenced by treatment. In addition, neither the rate of intestinal proliferation (BrdU labeling) nor intestinal morphology (crypt depth, villus length, or villus width) were affected by treatment. These data indicate that the influence of protein supplementation on visceral growth involves primarily the liver and not the intestines. These data also indicate that visceral growth, except in jejunum, are not altered by differing levels of UIP supplementation. (+info)
BDNF is a target-derived survival factor for arterial baroreceptor and chemoafferent primary sensory neurons.
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Brain-derived neurotrophic factor (BDNF) supports survival of 50% of visceral afferent neurons in the nodose/petrosal sensory ganglion complex (NPG; Ernfors et al., 1994a; Jones et al., 1994; Conover et al., 1995; Liu et al., 1995; Erickson et al., 1996), including arterial chemoafferents that innervate the carotid body and are required for development of normal breathing (Erickson et al., 1996). However, the relationship between BDNF dependence of visceral afferents and the location and timing of BDNF expression in visceral tissues is unknown. The present study demonstrates that BDNF mRNA and protein are transiently expressed in NPG targets in the fetal cardiac outflow tract, including baroreceptor regions in the aortic arch, carotid sinus, and right subclavian artery, as well as in the carotid body. The period of BDNF expression corresponds to the onset of sensory innervation and to the time at which fetal NPG neurons are BDNF-dependent in vitro. Moreover, baroreceptor innervation is absent in newborn mice lacking BDNF. In addition to vascular targets, vascular afferents themselves express high levels of BDNF, both during and after the time they are BDNF-dependent. However, endogenous BDNF supports survival of fetal NPG neurons in vitro only under depolarizing conditions. Together, these data indicate two roles for BDNF during vascular afferent pathway development; initially, as a target-derived survival factor, and subsequently, as a signaling molecule produced by the afferents themselves. Furthermore, the fact that BDNF is required for survival of functionally distinct populations of vascular afferents demonstrates that trophic requirements of NPG neurons are not modality-specific but may instead be associated with innervation of particular organ systems. (+info)
A function of CBP as a transcriptional co-activator during Dpp signalling.
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CBP/p300 is a transcriptional co-activator that is recruited to enhancers by various DNA-binding proteins, including proteins whose activity is controlled by extracellular signals. Here, we report that Drosophila CBP loss-of-function mutants show specific defects which mimic those seen in mutants that lack the extracellular signal Dpp or its effector Mad. Furthermore, we find that CBP loss severely compromises the ability of Dpp target enhancers to respond to endogenous or exogenous Dpp. Finally, we show that CBP binds to the C-terminal domain of Mad. Our results provide evidence that CBP functions as a co-activator during Dpp signalling, and they suggest that Mad may recruit CBP to effect the transcriptional activation of Dpp-responsive genes during development. (+info)
Detection of human retrovirus 5 in patients with arthritis and systemic lupus erythematosus.
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OBJECTIVE: To examine whether human retrovirus 5 (HRV-5) infection is associated with autoimmune rheumatic disease. METHODS: DNA from patients with various disorders including inflammatory diseases and from normal subjects was tested by nested polymerase chain reaction (PCR) for HRV-5 proviral DNA. Positive results were confirmed by DNA sequencing. RESULTS: HRV-5 proviral DNA was detected in 53% of synovial samples from arthritic joints, in 12% of blood samples from patients with rheumatoid arthritis (RA), and in 16% of blood samples from patients with systemic lupus erythematosus. In contrast, it was not detectable by PCR of affected tissues from patients with several other autoimmune diseases and was found in only 1 of >200 tissue specimens obtained at autopsy from non-RA patients. Sequence analysis of the amplified viral segment showed genetic variation between samples with maintenance of the open reading frame, typical of a replicating infectious retrovirus. CONCLUSION: This is the first report of the frequent detection of HRV-5 in any disease. We propose that the possible involvement of HRV-5 in autoimmune and rheumatic disease should be investigated further. (+info)
RVLM and raphe differentially regulate sympathetic outflows to splanchnic and brown adipose tissue.
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To determine whether neurons in the rostral raphe pallidus (RPa) specifically control the sympathetic nerve activity to brown adipose tissue (BAT SNA), thereby regulating adipocyte metabolism and BAT thermogenesis, the responses in BAT SNA to disinhibition of RPa neurons and to disinhibition of neurons in the vasomotor region of the rostral ventrolateral medulla (RVLM) were compared with those in splanchnic (Spl) SNA, which primarily regulates visceral vasoconstriction. In urethan-chloralose-anesthetized ventilated rats, both acute hypothermia and microinjection of bicuculline into RPa produced significantly larger increases in BAT SNA (542 and 1,949% of control) than in Spl SNA (19 and 24% of control). The enhanced burst discharge in BAT SNA was not coherent with that in Spl SNA or with the arterial pressure (AP) at any frequency except the central respiratory frequency. Microinjections of bicuculline into RVLM evoked increases in Spl SNA (86% of control) and AP (32 mmHg), but reduced BAT SNA to low, normothermic levels. Microinjections of muscimol into RVLM reduced Spl SNA (-82% of control) and AP (-59 mmHg), but did not prevent the increase in BAT SNA after disinhibition of RPa neurons. These results indicate that the neural networks generating BAT SNA in response to disinhibition of RPa neurons are independent of those generating basal Spl SNA and support a model in which sympathetic outflow to tissues involved in thermoregulation and metabolism is regulated by central pathways, including neurons in RPa, that are distinct from those involved in the sympathetic control of the cardiovascular system. (+info)
Role of adipocytokines on the pathogenesis of atherosclerosis in visceral obesity.
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Obesity which is defined as accumulation of excess body fat, is a major cause of atherosclerotic vascular disease in industrial countries. Recent advances in the biology of adipose tissue have revealed that adipose tissue is not simply an energy storage organ but it also secretes a variety of molecules which affect the metabolism of the whole body. Through a systematic search of active genes in adipose tissue, we found that adipose tissue, especially visceral fat expressed numerous genes for secretory proteins (about 30% of total genes analyzed). Among them, plasminogen activator-1 (PAI-1), which is a regulator of the fibrinolytic system, was overexpressed in the visceral fat in an animal model of obesity. Plasma levels of PAI-1 were closely correlated with visceral fat adiposity. Thus, PAI-1 secreted from visceral fat may play some role in thrombotic vascular disease in visceral obesity. Adiponectin, a novel adipose-specific gene product, which has a matrix-like structure, is abundantly present in the bloodstream. Dysregulated secretion of adiponectin may be related to vascular disease in obesity. Biologically active molecules secreted from adipose tissue (adipocytokines) may have important roles in the development of atherosclerotic disease in obesity. (+info)
Effects of corn processing and dietary fiber source on feedlot performance, visceral organ weight, diet digestibility, and nitrogen metabolism in lambs.
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In Exp. 1, early-weaned Targhee and Polypay crossbred lambs (60 ewes and 66 rams; initial BW 24 +/- 1.0 kg) were used in a 2 x 3 factorial experiment to determine the effects of corn processing (whole shelled corn [WSC] or ground and pelleted corn [GC]) in combination with supplemental fiber (none [control]; soybean hulls, SBH [highly digestible]; or peanut hulls, PH [highly indigestible]) on DMI, ADG, feed efficiency, and visceral organ weight. For the total trial, WSC resulted in a 4% increase (P < .01) in ADG vs GC, and supplemental fiber resulted in increased (P < .01) DMI and ADG vs the control diet. Experiment 2 was conducted using 12 Targhee and Polypay crossbred wether lambs (initial BW 25 +/- 7 kg) to determine the effects of corn processing and fiber source in high-concentrate diets on diet digestibility and N retention using the same diets as in Exp. 1. Lambs fed WSC had greater (P < .001) apparent N digestion, true N digestion, and N retention (P < .01) than those fed GC. The apparent digestibilities of DM, OM, and NDF were greater (P < .001) for WSC than for GC diets. Peanut hulls resulted in decreased (P < .01) DM, OM, and NDF apparent digestibilities compared with the control and SBH diets. Starch digestion was not affected (P > .10) by diet. Whole corn resulted in improved DM, OM, NDF, and N digestibility compared with GC. Overall, both the SBH and PH diets resulted in greater DMI and ADG than the control diet, which lacked supplemental fiber. (+info)