Effect of Garlic, Onion, and their Combination on the Quality and Sensory Characteristics of Irradiated Raw Ground Beef

Irradiated raw ground beef had lower a*- and b*-valuesthan nonirradiated ones regardless of garlic or onion treatment at 0 d. Irradiation increased TBARS values of control ground beef, but addition of 0.5% onion or 0.1% garlic + 0.5% onion reduced oxidative changes during storage. Addition of garlic or onion greatly increased the amounts of sulfur compounds, but the increase was greater with garlic. With irradiation, the profiles and amounts of Svolatiles in raw ground beef changed significantly. However,the intensity of irradiation aroma in irradiated raw ground beef with garlic or onion was similar to that of the nonirradiated control. This indicated that some of the sulfur compounds unique to garlic or onion interacted with common sulfur compounds detected in irradiated meat and masked or changed the odor characteristics of irradiated raw ground beef. It was concluded that \u3e 0.5% onion or \u3c 0.01% garlic would be needed to mask or prevent irradiation aromain irradiated raw ground beef

Resolution of Isolated Unilateral Hypoglossal Nerve Palsy Following Microvascular Decompression of the Intracranial Vertebral Artery

Isolated hypoglossal nerve paresis due to mechanical compression from a vascular lesion is very rare. We present a case of a 32-year-old man who presented with spontaneous abrupt-onset dysarthria, swallowing difficulty and left-sided tongue atrophy. Brain computed tomographic angiography and magnetic resonance imaging of the brainstem demonstrated an abnormal course of the left vertebral artery compressing the medulla oblongata at the exit zone of the hypoglossal rootlets that was relieved by microvascular decompression of the offending intracranial vertebral artery. This case supports the hypothesis that hypoglossal nerve palsy can be due to nerve stretching and compression by a pulsating normal vertebral artery. Microvascular decompression of the intracranial nerve and careful evaluation of the imaging studies can resolve unexpected isolated hypoglossal nerve palsy

Occupancy and Function of the −150 Sterol Regulatory Element and −65 E-Box in Nutritional Regulation of the Fatty Acid Synthase Gene in Living Animals

Upstream regulatory factor (USF) and sterol regulatory element binding protein (SREBP) play key roles in the transcriptional regulation of the fatty acid synthase (FAS) gene by feeding and insulin. Due to the dual binding specificity of SREBP, as well as the presence of multiple consensus sites for these transcription factors in the FAS promoter, their physiologically relevant functional binding sites have been controversial. Here, in order to determine the occupancy of the putative USF and SREBP binding sites, we examined their protein-DNA interactions in living animals by using formaldehyde cross-linking and immunoprecipitation of chromatin and tested the function of these elements by employing mice transgenic for a reporter gene driven by various 5′ deletions as well as site-specific mutations of the FAS promoter. We show that the −332 and −65 E-boxes are bound by USF in both fasted and refed mice, while the −150 SRE is bound by SREBP-1 only in refed mice. We also found that mutation of either the −150 SRE or the −65 E-box abolishes the feeding-induced activation of the FAS promoter in transgenic mice. Furthermore, in vivo occupancy of the FAS promoter by SREBP in the fed state can be prevented by mutation not only of the −150 SRE but, unexpectedly, of the −65 E-box as well. We conclude that the FAS promoter is activated during refeeding via the induced binding of SREBP to the −150 SRE and that USF binding to the −65 E-box is also required for SREBP binding and activation of the FAS promoter

Effect of Garlic, Onion, and their Combination on the Quality and Sensory Characteristics of Irradiated Raw Ground Beef

Irradiated raw ground beef had lower a*- and b*-valuesthan nonirradiated ones regardless of garlic or onion treatment at 0 d. Irradiation increased TBARS values of control ground beef, but addition of 0.5% onion or 0.1% garlic + 0.5% onion reduced oxidative changes during storage. Addition of garlic or onion greatly increased the amounts of sulfur compounds, but the increase was greater with garlic. With irradiation, the profiles and amounts of Svolatiles in raw ground beef changed significantly. However,the intensity of irradiation aroma in irradiated raw ground beef with garlic or onion was similar to that of the nonirradiated control. This indicated that some of the sulfur compounds unique to garlic or onion interacted with common sulfur compounds detected in irradiated meat and masked or changed the odor characteristics of irradiated raw ground beef. It was concluded that > 0.5% onion or < 0.01% garlic would be needed to mask or prevent irradiation aromain irradiated raw ground beef.</p

Inhibition of adipogenesis and development of glucose intolerance by soluble preadipocyte factor–1 (Pref-1)

Preadipocyte factor-1 (Pref-1) is a transmembrane protein highly expressed in preadipocytes. Pref-1 expression is, however, completely abolished in adipocytes. The extracellular domain of Pref-1 undergoes two proteolytic cleavage events that generate 50 and 25 kDa soluble products. To understand the function of Pref-1, we generated transgenic mice that express the full ectodomain corresponding to the large cleavage product of Pref-1 fused to human immunoglobulin-γ constant region. Mice expressing the Pref-1/hFc transgene in adipose tissue, driven by the adipocyte fatty acid–binding protein (aP2, also known as aFABP) promoter, showed a substantial decrease in total fat pad weight. Moreover, adipose tissue from transgenic mice showed reduced expression of adipocyte markers and adipocyte-secreted factors, including leptin and adiponectin, whereas the preadipocyte marker Pref-1 was increased. Pref-1 transgenic mice with a substantial, but not complete, loss of adipose tissue exhibited hypertriglyceridemia, impaired glucose tolerance, and decreased insulin sensitivity. Mice expressing the Pref-1/hFc transgene exclusively in liver under the control of the albumin promoter also showed a decrease in adipose mass and adipocyte marker expression, suggesting an endocrine mode of action of Pref-1. These findings demonstrate the inhibition of adipogenesis by Pref-1 in vivo and the resulting impairment of adipocyte function that leads to the development of metabolic abnormalities

Overexpression of Pref-1 in pancreatic islet β-cells in mice causes hyperinsulinemia with increased islet mass and insulin secretion

Preadipocyte factor-1 (Pref-1) is made as a transmembrane protein containing EGF-repeats at the extracellular domain that can be cleaved to generate a biologically active soluble form. Pref-1 is found in islet β-cells and its level has been reported to increase in neonatal rat islets upon growth hormone treatment. We found here that Pref-1 can promote growth of pancreatic tumor derived AR42J cells. To examine Pref-1 function in pancreatic islets in&nbsp;vivo, we generated transgenic mouse lines overexpressing the Pref-1/hFc in islet β-cells using rat insulin II promoter (RIP). These transgenic mice exhibit an increase in islet mass with higher proportion of larger islets in pancreas compared to wild-type littermates. This is in contrast to pancreas from Pref-1 null mice that show higher proportion of smaller islets. Insulin expression and insulin secretion from pancreatic islets from RIP-Pref-1/hFc transgenic mice are increased also. Thus, RIP-Pref-1/hFc transgenic mice show normal glucose levels but with higher plasma insulin levels in both fasting and fed conditions. These mice show improved glucose tolerance. Taken together, we conclude Pref-1 as a positive regulator of islet β-cells and insulin production

Mice Lacking Paternally Expressed Pref-1/Dlk1 Display Growth Retardation and Accelerated Adiposity

Preadipocyte factor 1 (Pref-1/Dlk1) inhibits in vitro adipocyte differentiation and has been recently reported to be a paternally expressed imprinted gene at human chromosome 14q32. Studies on human chromosome 14 deletions and maternal uniparental disomy (mUPD) 14 suggest that misexpression of a yet-to-be-identified imprinted gene or genes present on chromosome 14 causes congenital disorders. We generated Pref-1 knockout mice to assess the role of Pref-1 in growth and in vivo adipogenesis and to determine the contribution of Pref-1 in mUPD. Pref-1-null mice display growth retardation, obesity, blepharophimosis, skeletal malformation, and increased serum lipid metabolites. Furthermore, the phenotypes observed in Pref-1-null mice are present in heterozygotes that harbor a paternally inherited, but not in those with a maternally inherited pref-1-null allele. Our results demonstrate that Pref-1 is indeed paternally expressed and is important for normal development and for homeostasis of adipose tissue mass. We also suggest that Pref-1 is responsible for most of the symptoms observed in mouse mUPD12 and human mUPD14. Pref-1-null mice may be a model for obesity and other pathologies of human mUPD14