13,457 research outputs found
The Complete Muhammad Ali
No full textIncluding material and photographs not included in most of the 100 other books about the champion, Ishmael Reed's The Complete Muhammad Ali is more than just a biography-it is a fascinating portrait of the 20th century and the beginning of the 21st. An honest, balanced portrayal of Ali, the book includes voices that have been omitted from other books. It charts Ali's evolution from Black Nationalism to a universalism, but does not discount the Nation of Islam and Black Nationalism's important influence on his intellectual development. Filipino American author Emil Guillermo speaks about how "The Thrilla' In Manila" brought the Philippines into the 20th century. Fans of Muhammad Ali, boxing fans, and those interested in modern African American history and the Nation of Islam will be fascinated by this biography by an accomplished American author.Intro -- DEDICATION -- INTRODUCTION -- The Curious History of an Icon -- CHAPTER 1 -- CHAPTER 2 -- CHAPTER 3 -- CHAPTER 4 -- CHAPTER 5 -- CHAPTER 6 -- CHAPTER 7 -- Did the Secret Government Fear a U.S. Muslim/Overseas Muslim Alliance? -- CHAPTER 8 -- CHAPTER 9 -- The Break Between the Prophet and his Disciple -- CHAPTER 10 -- CHAPTER 11 -- CHAPTER 12 -- The GOAT (Greatest Of All Time): Ali or Louis? -- CHAPTER 13 -- The Nation of Islam, the Mob, Showdowns in Canada and Sonny Liston -- CHAPTER 14 -- CHAPTER 15 -- The Taunts: Marketing or Racism? -- CHAPTER 16 -- CHAPTER 17 -- CHAPTER 18 -- CHAPTER 19 -- Boxing and the Brain -- CHAPTER 20 -- Ali's Feet -- CHAPTER 21 -- Mr. Dick -- CHAPTER 22 -- CHAPTER 23 -- The Opening Ceremonies, November 2005 -- CHAPTER 24 -- December 2005, Las Vegas -- CHAPTER 25 -- CHAPTER 26 -- June 16, 2004 -- CHAPTER 27 -- CHAPTER 28 -- CHAPTER 29 -- Aix-en-Provence -- CHAPTER 30 -- Ali as a Black Nationalist -- San Francisco, January 2004 Black Liberation Book Fair -- CHAPTER 31 -- January 31, 2004 -- CHAPTER 32 -- October 2005, Chicago -- CHAPTER 33 -- Why Ali remained with Elijah instead of following Malcolm -- CHAPTER 34 -- CHAPTER 35 -- February 4, 2006, Oakland, California -- CHAPTER 36 -- Like Zeus Descending from Mount Olympus -- CHAPTER 37 -- CHAPTER 38 -- Tuesday, February 28, 2006, New York -- CHAPTER 39 -- Bigger Than Boxing -- CHAPTER 40 -- Tribes Gallery, New York, April 2006 -- CHAPTER 41 -- June 2006, Louisville, Kentucky -- CHAPTER 42 -- CHAPTER 43 -- CHAPTER 45 -- Bad Company -- CHAPTER 46 -- Coxson, A Very Charming Rogue -- CHAPTER 47 -- Ali and the largest embezzlement scheme in Wells Fargo history -- CHAPTER 48 -- CHAPTER 49 -- "Lonnie is a stabilizing force."-Harry Belafonte -- October 29, 2006 -- CHAPTER 50 -- Abdul Rahman -- CHAPTER 51 -- CHAPTER 52 -- CHAPTER 53How Will Ali Be Remembered? New York, January 8, 2005 -- CHAPTER 54 -- CONCLUSION -- AFTERWORD -- Boxers' Rights? -- BIBLIOGRAPHY -- MUHAMMAD ALI -- ISLAM AND NATION OF ISLAM -- BOXING -- RELATED SUBJECTS -- ALSO AVAILABLE FROM BARAKA BOOKSIncluding material and photographs not included in most of the 100 other books about the champion, Ishmael Reed's The Complete Muhammad Ali is more than just a biography-it is a fascinating portrait of the 20th century and the beginning of the 21st. An honest, balanced portrayal of Ali, the book includes voices that have been omitted from other books. It charts Ali's evolution from Black Nationalism to a universalism, but does not discount the Nation of Islam and Black Nationalism's important influence on his intellectual development. Filipino American author Emil Guillermo speaks about how "The Thrilla' In Manila" brought the Philippines into the 20th century. Fans of Muhammad Ali, boxing fans, and those interested in modern African American history and the Nation of Islam will be fascinated by this biography by an accomplished American author.Description based on publisher supplied metadata and other sources.Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, YYYY. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries
Maktabat Al Muthanna Baghdad Feb-May 1962
No full textOn the same date, Ali Al-Mansouri issued an official financial statement confirming that the Al-Khanji Foundation owed a total of 11.375.أصدر علي المنصوري بيانًا ماليًا رسميًا بتاريخ 25 نيسان 1962 يُفيد بأن مؤسسة الخانجي مدينة بمبلغ إجمالي قدره 11,375
Syriac-Arabic Glosses of Isho bar Ali. Volume 2
No full textThese two volumes constitute the second part (nun-taw) of the Syriac-Arabic dictionary of the 10th cent. physician Isho bar Ali (the first half of the dictionary had been published in 1874 by G. Hoffmann). Each Syriac word is defined in Arabic, often with more than one Arabic equivalent; in addition, the author deals not just with individual Syriac words, but in some cases with phrases. Gottheil used 21 manuscripts (from Oxford, London, Paris, Berlin, Leiden, and Rome) for this edition, and he has supplied a thorough critical apparatus; the manuscripts are described in the introduction. While some manuscripts give the Arabic glosses in Syriac characters (i.e. Garshuni), Gottheil has presented them here in Arabic script. These two volumes will be of great interest to Syriac lexicographers and those who study interactions between Syriac and Arabic.Contains an English introduction by Richard J.H. Gotthei
Syriac-Arabic Glosses of Isho bar Ali. Volume 1
No full textThese two volumes constitute the second part (nun-taw) of the Syriac-Arabic dictionary of the 10th cent. physician Isho bar Ali (the first half of the dictionary had been published in 1874 by G. Hoffmann). Each Syriac word is defined in Arabic, often with more than one Arabic equivalent; in addition, the author deals not just with individual Syriac words, but in some cases with phrases. Gottheil used 21 manuscripts (from Oxford, London, Paris, Berlin, Leiden, and Rome) for this edition, and he has supplied a thorough critical apparatus; the manuscripts are described in the introduction. While some manuscripts give the Arabic glosses in Syriac characters (i.e. Garshuni), Gottheil has presented them here in Arabic script. These two volumes will be of great interest to Syriac lexicographers and those who study interactions between Syriac and Arabic.Contains an English introduction by Richard J.H. Gotthei
Activation of Estrogen Response Element-independent ERα signaling protects female mice from diet-induced obesity
No full text17β-estradiol (E2) regulates central and peripheral mechanisms that control energy and glucose homeostasis predominantly through estrogen receptor α (ERα) acting via receptor binding to estrogen response elements (ERE). ERα signaling is also involved in mediating the effects of E2 on diet-induced obesity (DIO), although the roles of ERE-dependent and -independent ERα signaling in ameliorating the effects of DIO remain largely unknown. We hypothesize that ERE-dependent ERα signaling is necessary to ameliorate the effects of DIO. We addressed this question using ERαKO (KO) and ERαKIKO (KIKO) female mice; the latter expressing an ERα that lacks a functional ERE binding domain. Females were ovariectomized, fed low-fat (LFD) or high-fat (HFD) diet, and orally dosed with vehicle or estradiol benzoate (EB, 300 μg/kg). After 9 weeks, body composition, glucose and insulin tolerance, peptide hormone and inflammatory cytokine levels, and hypothalamic arcuate nucleus and liver gene expression were assessed. EB reduced body weight and body fat in WT, regardless of diet, and in HFD-fed KIKO, in part by reducing energy intake and feeding efficiency. EB reduced fasting glucose levels in KIKO mice fed both diets but augmented glucose tolerance only in HFD-fed KIKO. Plasma insulin and IL-6 were elevated in KIKO and KO compared to WT on a LFD. Expression of arcuate neuropeptide and receptor genes and liver fatty acid biosynthesis genes was altered by HFD and by EB through ERE-dependent and -independent mechanisms. Therefore, ERE-independent signaling mechanisms in both the brain and peripheral organs mediate, in part, the effects of E2 during DIO.Peer reviewe
Regulation of gene expression by 17β-estradiol in the arcuate nucleus of the mouse through ERE-dependent and ERE-independent mechanisms
No full text17β-Estradiol (E2) modulates gene expression in the hypothalamic arcuate nucleus (ARC) to control homeostatic functions. In the ARC, estrogen receptor (ER) α is highly expressed and is an important contributor to E2's actions, controlling gene expression through estrogen response element (ERE)-dependent and -independent mechanisms. The objective of this study was to determine if known E2-regulated genes are regulated through these mechanisms. The selected genes have been shown to regulate homeostasis and have been separated into three subsections: channels, receptors, and neuropeptides. To determine if ERE-dependent or ERE-independent mechanisms regulate gene expression, two transgenic mouse models, an ERα knock-out (ERKO) and an ERα knock-in/knock-out (KIKO), which lacks a functional ERE binding domain, were used in addition to their wild-type littermates. Females of all genotypes were ovariectomized and injected with oil or estradiol benzoate (E2B). Our results suggest that E2B regulates multiple genes through these mechanisms. Of note, Cacna1g and Kcnmb1 channel expression was increased by E2B in WT females only, suggesting an ERE-dependent regulation. Furthermore, the NKB receptor, Tac3r, was suppressed by E2B in WT and KIKO females but not ERKO females, suggesting that ERα-dependent, ERE-independent signaling is necessary for Tac3r regulation. The adrenergic receptor Adra1b was suppressed by E2B in all genotypes indicating that ERα is not the primary receptor for E2B's actions. The neuropeptide Tac2 was suppressed by E2B through ERE-dependent mechanisms. These results indicate that E2B activates both ERα-dependent and independent signaling in the ARC through ERE-dependent and ERE-independent mechanisms to control gene expression.Peer reviewe
Estrogen response element-independent signaling partially restores post-ovariectomy body weight gain but is not sufficient for 17β-estradiol's control of energy homeostasis
No full textThe steroid 17β-estradiol (E2) modulates energy homeostasis by reducing feeding behavior and increasing energy expenditure primarily through estrogen receptor α (ERα)-mediated mechanisms. Intact ERαKO female mice develop obesity as adults exhibiting decreased energy expenditure and increased fat deposition. However, intact transgenic female mice expressing a DNA-binding-deficient ERα (KIKO) are not obese and have similar energy expenditure, activity and fat deposition as to wild type (WT) females, suggesting that non-estrogen response element (ERE)-mediated signaling is important in E2 regulation of energy homeostasis. Initial reports did not examine the effects of ovariectomy on energy homeostasis or E2's attenuation of post-ovariectomy body weight gain. Therefore, we sought to determine if low physiological doses of E2 (250 ng QOD) known to suppress post-ovariectomy body weight gain in WT females would suppress body weight gain in ovariectomized KIKO females. We observed that the post-ovariectomy increase in body weight was significantly greater in WT females than in KIKO females. Furthermore, E2 did not significantly attenuate the body weight gain in KIKO females as it did in WT females. E2 replacement suppressed food intake and fat accumulation while increasing nighttime oxygen consumption and activity only in WT females. E2 replacement also increased arcuate POMC gene expression in WT females only. These data suggest that in the intact female, ERE-independent mechanisms are sufficient to maintain normal energy homeostasis and to partially restore the normal response to ovariectomy. However, they are not sufficient for E2's suppression of post-ovariectomy body weight gain and its effects on metabolism and activity.Peer reviewe
The interaction of fasting, caloric restriction, and diet-induced obesity with 17β-estradiol on the expression of KNDy neuropeptides and their receptors in the female mouse
No full textArcuate neurons that coexpress kisspeptin (Kiss1), neurokinin B (Tac2), and dynorphin (Pdyn) mediate negative feedback of 17β-estradiol (E2) on the HPG axis. Previous studies report that fasting and caloric restriction reduce arcuate Kiss1 expression. The objective of this study was to determine the interactions of E2 with fasting, caloric restriction, and diet-induced obesity on KNDy gene and receptor expression. Ovariectomized female mice were separated into control and estradiol benzoate (E2B)-treated groups. E2B decreased Kiss1 and the tachykinin 2 receptor, Tac3r, in ARC tissue and Tac2 in Tac2 neurons. Diet-induced obesity decreased Kiss1 in oil-treated animals and the kisspeptin receptor, Kiss1r and Tac3r in the ARC of E2B-treated animals. Chronic caloric (30%) restriction reduced all three neuropeptides in oil-treated females and Kiss1r by E2B in CR animals. Taken together, our experiments suggest that steroidal environment and energy state negatively regulate KNDy gene expression in both ARC and Tac2 neurons.Peer reviewe
Linoleic acid causes greater weight gain than saturated fat without hypothalamic inflammation in the male mouse
No full textA significant change in the Western diet, concurrent with the obesity epidemic, was a substitution of saturated fatty acids with polyunsaturated, specifically linoleic acid (LA). Despite increasing investigation on type as well as amount of fat, it is unclear which fatty acids are most obesogenic. The objective of this study was to determine the obesogenic potency of LA vs. saturated fatty acids and the involvement of hypothalamic inflammation. Forty-eight mice were divided into four groups: low-fat or three high-fat diets (HFDs, 45% kcals from fat) with LA comprising 1%, 15% and 22.5% of kilocalories, the balance being saturated fatty acids. Over 12 weeks, bodyweight, body composition, food intake, calorimetry, and glycemia assays were performed. Arcuate nucleus and blood were collected for mRNA and protein analysis. All HFD-fed mice were heavier and less glucose tolerant than control. The diet with 22.5% LA caused greater bodyweight gain, decreased activity, and insulin resistance compared to control and 1% LA. All HFDs elevated leptin and decreased ghrelin in plasma. Neuropeptides gene expression was higher in 22.5% HFD. The inflammatory gene Ikk was suppressed in 1% and 22.5% LA. No consistent pattern of inflammatory gene expression was observed, with suppression and augmentation of genes by one or all of the HFDs relative to control. These data indicate that, in male mice, LA induces obesity and insulin resistance and reduces activity more than saturated fat, supporting the hypothesis that increased LA intake may be a contributor to the obesity epidemic.Peer reviewe
Differential gene regulation of GHSR signaling pathway in the arcuate nucleus and NPY neurons by fasting, diet-induced obesity, and 17β-estradiol
No full textGhrelin’s receptor, growth hormone secretagogue receptor (GHSR), is highly expressed in the arcuate nucleus (ARC) and in neuropeptide Y (NPY) neurons. Fasting, diet-induced obesity (DIO), and 17β-estradiol (E2) influence ARC Ghsr expression. It is unknown if these effects occur in NPY neurons. Therefore, we examined the expression of Npy, Agrp, and GHSR signaling pathway genes after fasting, DIO, and E2 replacement in ARC and pools of NPY neurons. In males, fasting increased ARC Ghsr and NPY Foxo1 but decreased NPY Ucp2. In males, DIO decreased ARC and NPY Ghsr and Cpt1c. In fed females, E2 increased Agrp, Ghsr, Cpt1c, and Foxo1 in ARC. In NPY pools, E2 decreased Foxo1 in fed females but increased Foxo1 in fasted females. DIO in females suppressed Agrp and augmented Cpt1c in NPY neurons. In summary, genes involved in GHSR signaling are differentially regulated between the ARC and NPY neurons in a sex-dependent manner.Peer reviewe
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