bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Ideal of Professionalism and the White Southern Baptist Ministry, 1870-1920
Authors: Harvey Paul 
Published: August 2007

In 1917, a Baptist minister in Henderson, North Carolina, wrote to a Southern Baptist Convention (SBC) worker of the frustrations pastors encountered in teaching their parishioners a “progressive” religious ethic appropriate for the age:Nearly all of us are driven by the force of circumstances to be a bit more conservative than it is in our hearts to be. I am frank to say to you that I have found it out of the question to move people in the mass at all, unless you go with a slowness that sometimes seems painful; and I have settled down to the conviction that it is better to lead people slowly than not at all.
Staking the Monster: A Politics of Remonstrance
Authors: Ingebretsen Edward J. 
Published: August 2007

Monster, you are an abomination. I love you.Marquis de Sade,JuliettePerversion is not an innate desire … but an identity and a category which is socially produced.Jeffrey Dollimore,Sexual DissidenceSome years ago I asked in an examination paper … “why were heretics persecuted in the thirteenth Century?” The question was very popular and the answer, with great confidence and near unanimity, “because there were so many of them.”R. I. Moore,The Formation of a Persecuting SocietyA social order reveals the limits of its imagination in two particular ways. The first is in the methods of fear by which it constructs the unspeakable (the “monstrous” or the “inhuman”) as symbolic center of social energy. The second is in the means, legal and extralegal, then used to repudiate and silence that energy.
Liberators for Colonial Anáhuac: A Rumination on North American Civil Religions
Authors: Walker Randi Jones 
Published: August 2007

Behold here the motives of that mysterious likeness which give merit to a comparison with Jesus in the work the Supreme Author confided to [Hidalgo]: to save the American people, the continent of Anáhuac!So spoke Padre Antonio Jose Martinez in 1832 in praise of Miguel Hidalgo on the tenth anniversary of the independence of the Republic of Mexico. That same year, Francis Gray extolled George Washington, the hero of another independence movement. Washington was the “Special instrument of divine providence for working out our political salvation, the cloud by day and pillar of fire by night which led us out of bondage.” Two new North American nations attempted to create a national identity and a useable mythology, side by side, if independent of each other. In this essay, I present a North American view of what could loosely be called civil religion.
Holy Martin: The Overlooked Canonization of Dr. Martin Luther King, Jr.
Authors: Hoffman Scott W. 
Published: August 2007

Martin Luther King, Jr., gazes serenely, almost expressionless, in a somber suit and tie before a backdrop of prison bars. Around his neck hangs a booking number, “7089.” Around his head is a brilliant golden halo. The picture is not a mug shot but an icon in the Byzantine tradition. It is, as its Greek inscription says, “Holy Martin.” St. Martin Luther King.This icon is a popular piece of merchandise for a mail-order Company in Vermont. Each January, just before King's birthday they receive a flood of Orders. This phenomenon is an enigma, the fountainhead for a flood of questions. How can a black Baptist minister become the subject of a popular icon? What in American society and culture fostered its creation? Who invokes this great civil rights leader as a saint? But the most basic question is, how can Martin Luther King be considered a saint in the first place? Was it simply because he was slain for the cause of civil rights? Others died for the cause, and there are no icons of them.
Calcitonin Gene-Related Peptide Expression in Sepsis: Postulation of Microbial Infection-Specific Response Elements within the Calcitonin I Gene Promoter
Authors: Domenech Vivian Suarez , Nylen Eric S. , White Jon C. , Snider Richard H. , Becker Kenneth L. , Landmann Regine , Müller Beat 
Published: August 2007

Background Recently, we reported an unexpected ubiquitous expression of calcitonin (CT)-mRNA in a hamster peritonitis model of sepsis. Using this animal model, we undertook a study to further investigate the pattern of expression of the calcitonin I ( CALC-I) gene and CT gene-related peptide (CGRP)-mRNA in sepsis. Methods Live Escherichia coli impregnated in agar pellets were implanted in the peritoneal cavities of hamsters. Twelve hours after sepsis induction, the septic and healthy control animals were sacrificed and tissues and peritoneal macrophages were collected. CGRP-mRNA content was evaluated by reverse transcription polymerase chain reaction (RT-PCR), quantitated by the Taq-Man technique, and compared with the mRNA expression of CT, tumor necrosis factor α (TNF-α), and interleukin-6 (IL-6). The 5′ untranslated regions of the mRNA and potential alternative splicing sites were identified by 5′ rapid amplification of cDNA ends. Results We found a tissue-wide, ubiquitous and uniform expression of CGRP-mRNA in all septic tissues examined. CGRP-mRNA was detectable by RT-PCR in various extraneuronal and extrathyroidal septic tissues, but not in healthy control tissues. As found for CT-mRNA in our earlier studies, CGRP-mRNA seemed to be more specifically up-regulated as compared with other classical cytokines (ie, IL-6 and TNF-α). Importantly, the 5′ untranslated sequence in control and septic thyroid was similar to the sequence obtained from septic spleen. Conclusions We postulate the presence of microbial infection-specific response elements in the CALC-I gene promotor, which, upon a specific stimulus, override the tissue-selective expression pattern. This new form of endocrine plasticity may be of importance in the response to systemic inflammation.
Fenamates Stimulate BKCa Channel Activity in the Human Osteoblast-Like MG-63 Cells
Authors: Wu Sheng-Nan , Jan Chung-Ren , Chiang Hung-Ting 
Published: August 2007

BackgroundThe fenamates, a family of nonsteroidal anti-inflammatory drugs that are derivatives of N-phenylanthranilic acid, are the inhibitors of cyclo-oxygenase. The ionic mechanism of actions of these compounds in osteoblasts is not well understood.MethodsThe effects of the fenamates on ionic currents were investigated in a human osteoblast-like cell line (MG-63) with the aid of the whole-cell and inside-out configurations of the patch-clamp technique.ResultsIn MG-63 cells, niflumic acid and meclofenamic acid increased K+outward currents ( IK). The niflumic acid-stimulated IKwas reversed by subsequent application of iberiotoxin or paxilline, yet not by that of glibenclamide or apamin. In the inside-out configuration, niflumic acid (30 μmol/L) added to the bath did not modify single-channel conductance but increased the activity of large-conductance Ca2+-activated K+(BKCa) channels. The EC50values for niflumic acid- and meclofenamic acid-induced channel activity were 22 and 24 μmol/L, respectively. Niflumic acid (30 μmol/L) and meclofenamic acid (30 μmol/L) shifted the activation curve of BKCachannels to less positive membrane potentials. Membrane stretch potentiated niflumic acid-stimulated channel activity. The rank order of potency for the activation of BKCachannels in these cells was niflumic acid = meclofenamic acid > tolfenamic acid > flufenamic acid > nimesulide. Evans blue and nordihydroguaiaretic acid increased channel activity; however, indomethacin, piroxicam, and NS-398 had no effect on it.ConclusionsThe fenamates can stimulate BKCachannel activity in a manner that seems to be independent of the action of these drugs on the prostaglandin pathway. The activation of the BKCachannel may hyperpolarize the osteoblast, thereby modulating osteoblastic function.
Prevention of Morphological Changes in Alginate Microcapsules for Islet Xenotransplantation
Authors: Hobbs Hasan A. , Kendall William F. , Darrabie Marcus , Opara Emmanuel C. 
Published: August 2007

Background Alginate microcapsule swelling, which occurs as a result of increased hydrophilicity owing to the Ca++ that remains after rapid chelation of the inner alginate core, is a problem in encapsulation. We have previously shown that exchange of the residual divalent Ca++ with the monovalent Na+ through the use of 6 mmol/L Na2SO4 decreases swelling in chelated alginate-polylysine-alginate microcapsules, and this process enhances their durability. The purpose of the present study was to examine the morphology of Na2SO4-treated microcapsules in long-term incubation with the use of serum-supplemented culture medium. Methods Spherical beads of purified alginate (3%) that were gelled with 1.1% CaCl2 were first coated with polylysine, and then with 0.24% alginate. After rapid chelation of the inner alginate core with 55 mmol/L sodium citrate, the capsules were either incubated for 30 minutes in 6 mmol/L Na2SO4 or left untreated (control). Each group of capsules was then placed in a flask containing Ham's culture medium supplemented with 20% porcine serum and incubated at 37°C. Results The diameters of Na2SO4-treated capsules only increased modestly from a mean±SD of 635±22.08 to 684.53±17.86 μm ( P <0.0001) by day 7, with no further increases thereafter. In contrast, control capsules showed a steady increase in their mean diameters, which changed from 639.55±21.44 to 735.48±108.85 μm ( P<0.0001) by day 66. In addition, whereas treated capsules remained spherical, control capsules showed progressive polymorphism. Conclusion We have developed a new method of making more durable and stable microcapsules that can be used for islet cell xenotransplantation.
Vascular Expression of Integrin-Associated Protein and Thrombospondin Increase after Mechanical Injury
Authors: Sajid Mansoor , Hu Zhaoyong , Guo Huiping , Li Husong , Stouffer George A. 
Published: August 2007

Background Integrin-associated protein (IAP) is a thrombospondin (TSP)-binding, Gi protein-coupled cell surface receptor. The vascular function of IAP has not been defined, and it is not known whether TSP and IAP are expressed at the same time in injured arteries. Methods Left brachial arteries of baboons were injured using balloon withdrawal technique. Arteries were harvested 1 week after injury, and immunohistochemistry and in situ hybridization were performed using standard techniques. Uninjured right brachial arteries served as a control. Proliferation studies were performed using cultured human aortic smooth muscle cells (SMC). Results We found significant IAP expression in the media and neointima 7 days after injury using BRIC-126, an immunoglobulin (Ig) G2b monoclonal antibody that recognizes IAP with high specificity. In contrast, IAP staining in the uninjured vessel was only observed in the endothelium. Concurrent with IAP expression, TSP mRNA and protein expression in the neointima and media was enhanced 1 week after injury. In cultured SMC, activation of IAP was sufficient to elicit a proliferative response. TSP-induced proliferation was inhibited by antibodies that block TSP binding to IAP and mimicked by 4N1K, a 10-amino acid peptide derived from the IAP binding site within the carboxyl terminus of TSP. Conclusions Vascular expression of IAP and TSP increased after mechanical injury and activation of IAP elicited a proliferative response in cultured SMC. These findings support the hypothesis that IAP participates in vascular healing responses.
Magnitude of Peroxisome Proliferator-Activated Receptor-γ Activation is Associated with Important and Seemingly opposite Biological Responses in Breast Cancer Cells
Authors: Clay Carl E. , Namen Andrew M. , Atsumi Gen-ichi , Trimboli Anthony J. , Fonteh Alfred N. , High Kevin P. , Chilton Floyd H. 
Published: August 2007

Background The nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ) has become a potential target for the prevention and treatment of breast cancer. However, recent in vitro and in vivo studies have raised the question of whether activation of PPARγ leads to the promotion or reduction of tumor formation. Studies using several cancer cell lines, animal models, and a variety of PPARγ agonists have shown discordant results, including changes in cellular proliferation, differentiation, and apoptosis of cancer cells and tumors. Methods We studied the effects of low-, moderate-, and high-dose treatment of the PPARγ ligands 15-deoxy-Δ12,14 prostaglandin J2 (15dPGJ2) and troglitazone (TGZ) on parameters of cell growth, differentiation, and apoptosis in the epithelial breast cancer cell line MDA-MB-231. Results The biologic effects of these compounds depend largely on ligand concentration and the degree of PPARγ activation. For example, low concentrations of 15dPGJ2 (<2.5 μM) and TGZ (<5 μM) increased cellular proliferation, but concentrations of 15dPGJ2 >10 μM and of TGZ at 100 μM blocked cell growth. TGZ (100 μM) slowed cell cycle progression, and 15dPGJ2 (10 μM) caused an S-phase arrest in the cell cycle and induced morphological characteristics consistent with apoptosis. Expression of CD36, a marker of differentiation in these cells, was induced by 2.5 μM 15dPGJ2 or 5 to 100 μM TGZ. However, higher concentrations of 15dPGJ2 did not alter CD36 expression. Transcriptional activation studies demonstrated that 15dPGJ2 is a more potent PPARγ ligand than TGZ. Regardless of the ligand used, though, low transcriptional activation correlated with an increased cellular proliferation, whereas higher levels of activation correlated with cell cycle arrest and apoptosis. Conclusions PPARγ activation induces several important and seemingly opposite changes in neoplastic cells, depending on the magnitude of PPARγ activation. These data may explain, at least in part, some of the discordant results previously reported.
Obesity is Associated with Impaired Ventricular Protein Kinase C-MAP Kinase Signaling and Altered ANP mRNA Expression in the Heart of Adult Zucker Rats
Authors: Morabito Dominique , Vallotton Michel B. , Lang Ursula 
Published: August 2007

Background In the obesity model of the Zucker rat, myocardial protein kinase C (PKC) activation by phorbol ester is impaired. The influence of obesity on myocardial cell signaling was investigated by studying the activation of PKC isozymes and MAP kinases (MAPK) p38 and p42/44 as well as the induction of ANP mRNA. Methods Isolated hearts obtained from 17-week-old lean and obese Zucker rats were perfused with 200 nM phorbol 12-myristate 13-acetate (PMA) at different time periods. Immunodetectable PKC isozymes, phosphorylated-MAPK, and ANP mRNA were determined by Western and Northern blots, respectively. Results PMA promoted a marked transient translocation of ventricular PKCα from the cytosol to the membranes within 10 minutes in lean rats, whereas it had a much weaker effect in obese rats. Moreover, PMA induced a significant activation of PKCΔ in lean but not in obese rat hearts. After PKC activation, increases in phosphorylation levels of myocardial p38 and p42 MAPK were approximately 3-fold higher in lean rats than in obese animals. Concerning the induction of ANP, PMA transiently tripled ANP mRNA within 60 minutes in lean but not in obese rats. Conclusions In the genetically obese Zucker rat, the myocardial signal transduction cascade PKC-MAPK-ANP mRNA seems to be markedly impaired. It can be speculated that this abnormal cardiac cell signaling in obese rats reflects an early phase in the cardiac pathogenesis accompanying obesity.
Basal and Post-Methionine Serum Homocysteine and Lipoprotein Abnormalities in Patients with Chronic Liver Disease
Authors: Ben-Ari Ziv , Tur-Kaspa Ran , Schafer Zehava , Baruch Yaacov , Sulkes Jacqueline , Atzmon Orna , Greenberg Avital , Levi Nurit , Fainaru Menahem 
Published: August 2007

Background Lipoprotein abnormalities are commonly found in chronic liver diseases (CLDs), particularly hypercholesterolemia in primary biliary cirrhosis (PBC). However, affected patients may not be at increased risk of coronary heart disease. Cirrhotic patients display impaired methionine clearance, and an increased level of homocysteine, a methionine metabolite, is an independent risk factor for coronary heart disease. Thus, we hypothesized that the low risk of coronary heart disease in patients with CLD may be related to low serum levels of homocysteine. The aim of this study was to test this hypothesis after methionine load and to describe the serum lipoprotein profile in patients with PBC and in patients with hepatocellular liver disease. Methods Fifteen female patients (mean age, 58.2±11.7 years) with PBC, 15 female patients (mean age, 54.5 ± 9.6 years) with other causes of CLD, and 15 healthy sex- and age-matched controls were given L-methionine (50 mg/kg of ideal body weight). Basal fasting serum homocysteine level and 2, 4, and 6 hours of post-methionine load were determined using high-performance liquid chromatography with a fluorometric detector. Levels of fasting serum cholesterol, triglycerides, high-density lipoprotein (HDL), low-density lipoprotein (LDL), lipoprotein (a) (Lp(a)), and apoprotein B were also determined. Results Results showed that mean basal and post-methionine load (6 hours) serum homocysteine levels were statistically significantly higher in the patients with PBC and with CLD than in the control group ( P=0.04) and that levels of serum cholesterol, LDL, HDL, and apoprotein B were significantly higher in the PBC patients than in the other two groups ( P≤0.05). There was no correlation between any of these parameters and the severity of liver disease. Serum HDL was significantly lower in the CLD group ( P≤0.05) and correlated with severity of liver disease. There was no significant difference in serum cholesterol, LDL, or apoprotein B between the CLD group and the controls. Serum triglyceride and Lp(a) levels were similar for all three groups. Conclusions In contrast to previous reports, the site of the methionine metabolic impairment was found to be below the homocysteine synthesis level. For most patients with CLD, factors other than serum homocysteine or Lp(a) are responsible for the reduction in the risk of coronary heart disease. Further studies with larger samples are needed.
Effect of Dexamethasone on TSH Secretion Induced by TRH in Human Obesity
Authors: Coiro Vittorio , Volpi Riccardo , Capretti Luigi , Speroni Guglielmina , Pilla Silvia , Cataldo Simona , Bianconcini Michele , Bazzani Emanuele , Chiodera Paolo 
Published: August 2007

Background The presence of an abnormally high thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) makes it difficult to distinguish some euthyroid obese subjects from subclinically hypothyroid obese patients. Here, we examine whether such distinction may be achieved after treatment with glucocorticoids, which inhibit TSH secretion at the hypothalamic-pituitary level. Methods TRH tests (200 μg as an intravenous bolus injection) were performed in 30 age- and weight-matched, obese, but otherwise healthy, men. All subjects were tested again with TRH after treatment with dexamethasone (dex) (2 mg/d in four divided doses orally for 3 days). Results In all subjects, total thyroxine and triiodothyronine concentrations were in the normal range. According to basal and TRH-stimulated serum thyrotropin (TSH) levels, subjects were divided into the following three groups: group I (n=10), euthyroid subjects; group II (n=10), euthyroid subjects with normal basal but abnormally elevated TSH responses to TRH; group III (n=10), subjects with elevated basal and TRH-induced TSH levels (subclinical hypothyroidism). Basal TSH levels were 1.8±0.4 mU/L in group I, 1.7±0.3 in group II, and 6.0±0.7 in group III. In both groups II and III, TRH-induced TSH increments were above the normal range (maximal increment>15 mU/L) and were significantly higher than in group I. After the second treatment with TRH, pretreatment with dex significantly decreased both basal TSH levels and peak TSH responses to TRH in all groups. However, a striking percentage decrease (>50%) in TRH-induced peak TSH responses was observed in euthyroid obese subjects of groups I and II, whereas hypothyroid subjects of group III showed only a slight decrement (<25%). Conclusions The sensitivity of the TSH secretory system to glucocorticoid inhibitory action is preserved in obese subjects with abnormally elevated TSH response to TRH, but not in subclinically hypothyroid obese patients. The TRH plus dex test might be useful in future studies to understand the mechanisms underlying alterations in TSH secretion in obesity.
Inhibition of L-Type Ca2+ Channel Current in Xenopus Oocytes by Amiodarone
Authors: Ding Shulan , Chen Fuhua , Klitzner Thomas S. , Wetzel Glenn T. 
Published: August 2007

Background Although amiodarone has been referred to as a class III antiarrhythmic agent, it also possesses electrophysiologic characteristics of the three other classes (classes I and IV and minor class II effects). Previous studies have demonstrated that amiodarone inhibits Ca2+ channel current in intact cardiac myocytes. However, it is not clear whether this response reflects a pure class IV effect (direct Ca2+ channel inhibition) or a class II effect (β-adrenergic receptor blockade) of amiodarone. Methods In the current study, the effects of amiodarone on Ca2+ current were studied in the absence of sympathetic regulation using a Xenopus oocyte expression system. The L-type Ca2+ channel α1C subunit was coexpressed with the α2Δ and β2a subunits in enzymatically digested Xenopus oocytes. Ca2+ currents were recorded using the cut-open oocyte preparation. Results We found that perfusion of 10 μM isoproterenol produced no significant change in peak Ca2+ current (from 223±33 to 210±29 nA, mean±SEM, n=5, P=not significant), indicating the absence of a functional stimulatory sympathetic signal pathway in these oocytes. After 10 minutes of exposure to 10 μM amiodarone, Ca2+ current amplitude was significantly decreased from 174±33 to 100±26 nA (n=8, P<0.01; control group: 220±33 to 212±29 nA, n=5, P=not significant). These effects were similar to those of 10 μM nifedipine (201±48 to 108±48 nA, n=6, P<0.05), a typical Ca2+ channel blocker. On the other hand, neither amiodarone nor nifedipine significantly altered the Ca2+ current activation or inactivation kinetics. Conclusions These results demonstrate that amiodarone inhibits Ca2+ current in the absence of a functional intrinsic β-adrenergic stimulatory system and, therefore, represents a true class IV effect.