Book Reviews

A. K. Dickinson, P. J. Lee, and P. J. Rogers. Learning History. London: Heinemann Educational Books, Ltd., 1984. Pp. x, 230. Paper, $14.00; Donald W. Whisenhunt. A Student's Introduction to History. Boston: American Press, 1984. Pp. 31. Paper,$2.95. Review by Robert A. Calvert of Texas A&M University. Ronald J. Grele. Envelopes of Sound: The Art of Oral History. Chicago: Precendent Publishing, Inc. 1985. Second Edition. Pp. xii, 283. Cloth, $20.95. Review by Marsha Frey of Kansas State University. Reginald Horsman. The Diplomacy of the New Republic, 1776-1815. Arlington Heights, Illinois: Harlan Davidson., 1985. Pp. vii, 153. Paper,$7.95. Review by William Preston Vaughn of North Texas State University. Lynn Y. Weiner. From Working Girl to Working Mother: The Female Labor Force in the United States, 1820-1980. Chapel Hill and London: The University of North Carolina Press, 1985. Pp. xii, 187. Cloth, $17.95. Review by E. Dale Odom of North Texas State University. Mary Custis Lee de Butts, ed. Growing Up in the 1850s: The Journal of Agnes Lee. Chapel Hill and London: University of North Carolina Press, 1984. Pp. xx, 151. Cloth,$11.95. Review by Clarence L. Mohr of Tulane University. Raymond A. Mohl. The New City: Urban America in the Inudstrial Age, 1860-1920. Arlington Heights, Illinois: Harlan Davidson, Inc., 1985. Pp. 242. Paper, $8.95; Melvyn Dubofsky. Industrialism and the American Worker, 1865-1920 (Second Edition). Arlington Heights, Illinois: Harlan Davidson, Inc., 1985. Pp. 167. Paper,$8.95. Review by Richard L. Means of Mountain View College. David D. Lee. Sergeant York: An American Hero. Lexington, Kentucky: University Press of Kentucky, 1985. Pp. 162. Cloth, $18.00. Review by Richard Selcer of Mountain View College. Studs Terkel. "The Good War": An Oral History of World War Two. New York: Pantheon Books, 1984. Pp. xv, 589. Cloth,$19.95. Review by William Vance Trollinger of The School of the Ozarks. David W. Reinhard. The Republican Right Since 1945. Lexington: The University Press of Kentucky, 1983. Pp. ix, 294. Cloth, $25.00. Review by James C. Williams of Gavilan College. Christina Larner. Witchcraft and Religion: The Politics of Popular Belief. New York: Basil Blackwell, 1984. Pp. xi, 172. Cloth,$24.95. Review by K. Gird Romer of Kennesaw College. F. R. H. DuBoulay. Germany in the Later Middle Ages. New York: St. Martin's Press, Inc., 1984. Pp. xii, 260. Cloth, $30.00; Joseph Dahmus. Seven Decisive Battles of the Middle Ages. Chicago: Nelson Hall, 1984. Pp. viii, 244. Cloth,$23.95. Review by Robert H. Welborn of Clayton College. Gerald Fleming. Hitler and the Final Solution. With an Introduction by Saul Friedlaender. Berkeley: University of California Press, 1984 (German, 1982). Pp. xxxvi, 219. Cloth, $15.95; Sarah Gordon. Hitler, Germans, and the "Jewish Question." Princeton: Princeton University Press, 1984. Pp. xiv, 412. Cloth,$40.00; Limited Paper Edition, $14.50. Review by Thomas T. Lewis of Mount Senario College. Alan Cassels. Fascist Italy. Arlington Heights, Illinois: Harlan Davidson, Inc., 1985. Second Edition. Pp. x, 146. Paper,$8.95. Review by Lawrence S. Rines of Quincy Junior College; Additional response by Lawrence S. Rines of Quincy Junior College.   &nbsp

Dendritic Cell Immunoreceptor Regulates Chikungunya Virus Pathogenesis in Mice

Chikungunya virus (CHIKV) is a mosquito-borne alphavirus responsible for recent epidemic outbreaks of debilitating disease in humans. Alphaviruses are known to interact with members of the C-type lectin receptor family of pattern recognition proteins, and given that the dendritic cell immunoreceptor (DCIR) is known to act as a negative regulator of the host inflammatory response and has previously been associated with rheumatoid arthritis, we evaluated DCIR's role in response to CHIKV infection. Although we observed an increase in the proportion of dendritic cells at the site of CHIKV infection at 24 to 36 h postinfection, these cells showed decreased cell surface DCIR, suggestive of DCIR triggering and internalization. In vitro, bone marrow-derived dendritic cells from DCIR-deficient (DCIR−/−) mice exhibited altered cytokine expression following exposure to CHIKV. DCIR−/− mice exhibited more severe disease signs than wild-type C57BL6/J mice following CHIKV infection, including a more rapid and more severe onset of virus-induced edema and enhanced weight loss. Histological examination revealed that DCIR-deficient animals exhibited increased inflammation and damage in both the fascia of the inoculated foot and the ankle joint, and DCIR deficiency skewed the CHIKV-induced cytokine response at the site of infection at multiple times postinfection. Early differences in virus-induced disease between C57BL6/J and DCIR−/− mice were independent of viral replication, while extended viral replication correlated with enhanced foot swelling and tissue inflammation and damage in DCIR−/− compared to C57BL6/J mice at 6 to 7 days postinfection. These results suggest that DCIR plays a protective role in limiting the CHIKV-induced inflammatory response and subsequent tissue and joint damage

Reviving calm technology in the e-tourism context

Tourism industry practitioners should understand the controversial nature of the information and communication technology (ICT) proliferation to ensure the ICT solutions do not consume too much of their attention, thus jeopardizing consumer enjoyment of tourism services. The concept of calm technology or calm design serves this purpose. Calm design suggests that technology should quietly recede in the background and come into play with users when and if required, thus delivering and/or enhancing a desired experience. Although this concept is of relevance to e-tourism, until recently, it has never been considered within. This is where this paper contributes to knowledge as, for the first time, it introduces calm design into the e-tourism context and critically evaluates the determinants of its broader adoption within the tourism industry. It positions calm design within the e-tourism realm, discusses its implications for customer service management, supply chain management and destination management, and discloses opportunities for future research

Newly Developed Mg2+–Selective Fluorescent Probe Enables Visualization of Mg2+ Dynamics in Mitochondria

Mg2+ plays important roles in numerous cellular functions. Mitochondria take part in intracellular Mg2+ regulation and the Mg2+ concentration in mitochondria affects the synthesis of ATP. However, there are few methods to observe Mg2+ in mitochondria in intact cells. Here, we have developed a novel Mg2+–selective fluorescent probe, KMG-301, that is functional in mitochondria. This probe changes its fluorescence properties solely depending on the Mg2+ concentration in mitochondria under physiologically normal conditions. Simultaneous measurements using this probe together with a probe for cytosolic Mg2+, KMG-104, enabled us to compare the dynamics of Mg2+ in the cytosol and in mitochondria. With this method, carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP)–induced Mg2+ mobilization from mitochondria to the cytosol was visualized. Although a FCCP–induced decrease in the Mg2+ concentration in mitochondria and an increase in the cytosol were observed both in differentiated PC12 cells and in hippocampal neurons, the time-courses of concentration changes varied with cell type. Moreover, the relationship between mitochondrial Mg2+ and Parkinson's disease was analyzed in a cellular model of Parkinson's disease by using the 1-methyl-4-phenylpyridinium ion (MPP+). A gradual decrease in the Mg2+ concentration in mitochondria was observed in response to MPP+ in differentiated PC12 cells. These results indicate that KMG-301 is useful for investigating Mg2+ dynamics in mitochondria. All animal procedures to obtain neurons from Wistar rats were approved by the ethical committee of Keio University (permit number is 09106-(1))

Effect of sitagliptin on cardiovascular outcomes in type 2 diabetes

BACKGROUND: Data are lacking on the long-term effect on cardiovascular events of adding sitagliptin, a dipeptidyl peptidase 4 inhibitor, to usual care in patients with type 2 diabetes and cardiovascular disease. METHODS: In this randomized, double-blind study, we assigned 14,671 patients to add either sitagliptin or placebo to their existing therapy. Open-label use of antihyperglycemic therapy was encouraged as required, aimed at reaching individually appropriate glycemic targets in all patients. To determine whether sitagliptin was noninferior to placebo, we used a relative risk of 1.3 as the marginal upper boundary. The primary cardiovascular outcome was a composite of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for unstable angina. RESULTS: During a median follow-up of 3.0 years, there was a small difference in glycated hemoglobin levels (least-squares mean difference for sitagliptin vs. placebo, -0.29 percentage points; 95% confidence interval [CI], -0.32 to -0.27). Overall, the primary outcome occurred in 839 patients in the sitagliptin group (11.4%; 4.06 per 100 person-years) and 851 patients in the placebo group (11.6%; 4.17 per 100 person-years). Sitagliptin was noninferior to placebo for the primary composite cardiovascular outcome (hazard ratio, 0.98; 95% CI, 0.88 to 1.09; P<0.001). Rates of hospitalization for heart failure did not differ between the two groups (hazard ratio, 1.00; 95% CI, 0.83 to 1.20; P = 0.98). There were no significant between-group differences in rates of acute pancreatitis (P = 0.07) or pancreatic cancer (P = 0.32). CONCLUSIONS: Among patients with type 2 diabetes and established cardiovascular disease, adding sitagliptin to usual care did not appear to increase the risk of major adverse cardiovascular events, hospitalization for heart failure, or other adverse events

Ion channel clustering enhances weak electric field detection by neutrophils: apparent roles of SKF96365-sensitive cation channels and myeloperoxidase trafficking in cellular responses

We have tested Galvanovskis and Sandblom’s prediction that ion channel clustering enhances weak electric field detection by cells as well as how the elicited signals couple to metabolic alterations. Electric field application was timed to coincide with certain known intracellular chemical oscillators (phase-matched conditions). Polarized, but not spherical, neutrophils labeled with anti-K v 1.3, FL-DHP, and anti-TRP1, but not anti-T-type Ca 2+ channels, displayed clusters at the lamellipodium. Resonance energy transfer experiments showed that these channel pairs were in close proximity. Dose-field sensitivity studies of channel blockers suggested that K + and Ca 2+ channels participate in field detection, as judged by enhanced oscillatory NAD(P)H amplitudes. Further studies suggested that K + channel blockers act by reducing the neutrophil’s membrane potential. Mibefradil and SKF93635, which block T-type Ca 2+ channels and SOCs, respectively, affected field detection at appropriate doses. Microfluorometry and high-speed imaging of indo-1-labeled neutrophils was used to examine Ca 2+ signaling. Electric fields enhanced Ca 2+ spike amplitude and triggered formation of a second traveling Ca 2+ wave. Mibefradil blocked Ca 2+ spikes and waves. Although 10 μM SKF96365 mimicked mibefradil, 7 μM SKF96365 specifically inhibited electric field-induced Ca 2+ signals, suggesting that one SKF96365-senstive site is influenced by electric fields. Although cells remained morphologically polarized, ion channel clusters at the lamellipodium and electric field sensitivity were inhibited by methyl-β-cyclodextrin. As a result of phase-matched electric field application in the presence of ion channel clusters, myeloperoxidase (MPO) was found to traffic to the cell surface. As MPO participates in high amplitude metabolic oscillations, this suggests a link between the signaling apparatus and metabolic changes. Furthermore, electric field effects could be blocked by MPO inhibition or removal while certain electric field effects were mimicked by the addition of MPO to untreated cells. Therefore, channel clustering plays an important role in electric field detection and downstream responses of morphologically polarized neutrophils. In addition to providing new mechanistic insights concerning electric field interactions with cells, our work suggests novel methods to remotely manipulate physiological pathways.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46726/1/249_2005_Article_1.pd

Homologs of the Shigella IpaB and IpaC invasins are required for Salmonella typhimurium entry into cultured epithelial cells.

Entry into host cells is an essential feature in the pathogenicity of Salmonella spp. The inv locus of Salmonella typhimurium encodes several proteins which are components of a type III protein secretion system required for these organisms to gain access to host cells. We report here the identification of several proteins whose secretion into the culture supernatant of S. typhimurium is dependent on the function of the inv-encoded translocation apparatus. Nucleotide sequence analysis of the genes encoding two of these secreted proteins, SipB and SipC, indicated that they are homologous to the Shigella sp. invasins IpaB and IpaC, respectively. An additional gene was identified, sicA, which encodes a protein homologous to IpgC, a Shigella protein that serves as a molecular chaperone for the invasins IpaB and IpaC. Nonpolar mutations in sicA, sipB, and sipC rendered S. typhimurium unable to enter cultured epithelial cells, indicating that these genes are required for bacterial internalization

Differential Expression and Activation of p38 Mitogen-Activated Protein Kinase α, β, γ, and δ in Inflammatory Cell Lineages

AbstractFour p38 mitogen-activated protein kinases (p38α, β, γ, δ) have been described. To understand the role of p38 family members in inflammation, we determined their relative expression in cells that participate in the inflammatory process. Expression was measured at the level of mRNA by reverse-transcriptase PCR and protein by Western blot analysis. p38α was the dominant form of p38 in monocytes; expression of p38δ was low and p38β was undetected. In macrophages, p38α and p38δ were abundant, but p38β was undetected. p38α and p38δ were also expressed by neutrophils, CD4+ T cells, and endothelial cells. Again, p38β was not detected in neutrophils, although low amounts were present in CD4+ T cells. In contrast, p38β was abundant in endothelial cells. p38γ protein was not detected in any cell type, although p38γ mRNA was present in endothelial cells. Immunokinase assays showed a strong activation of p38α and a lesser activation of p38δ in LPS-stimulated macrophages. Abs specific for mono- and dual-phophorylated forms of p38 suggested that LPS induces dual phosphorylation of p38α, but primarily mono-phosphorylation of p38δ. IL-1β activated p38α and p38β in endothelial cells. However, p38α was the more activated form based on kinase assays and phosphorylation analysis. Expression and activation patterns of p38α in macrophages and endothelial cells suggest that p38α plays a major role in the inflammatory response. Additional studies will be needed to define the contribution of p38δ to macrophage, neutrophil, and T cell functions, and of p38β to signaling in endothelial cells and T cells.</jats:p