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by Lowell K. Handy Chalice, St Louis. 2000. 157 pp. $16.99. ISBN 0-8272-0815-4. HANDY OFFBRS A FRESH approach to the genre of short story in the Hebrew Bible and Apocrypha. [...]

Preaching and Worship by Thomas H. Troeger Preaching and its Partners. Chalice, St. Louis, 2003. 137 pp. $19.99. ISBN 0-8272-2978-X. PREACHING AND WORSHIP IS THE most recent book in the [...]

by James R. Nieman and Thomas G. Rogers Fortress, Minneapolis, 2001. 159 pp. $16.00. ISBN 0-8006-3234-5. THE NEED FOR A TEXT THAT addresses cross-cultural issues in homiletics prompted Nieman and [...]

by Pamela Ann Moeller. Chalice, St. Louis, 1998. 181 pp. $18.99. ISBN 0-8272-0813-8. Moeller defines worship as living in loving, dialogical relationship with God and neighbor. She views worship events [...]

Preaching the Women of the Bible by Lisa Wilson Davison Chalice, St. Louis, 2006. 138 pp. $16.99. ISBN 978-0-827229-90-7. LISA DAVISON STATES that the purpose of this book 'is an [...]

American libraries currently face a dramatic shift in how they are perceived, both by the public and by lawmakers. In order to preserve the traditional values observed by librarians, such as patron privacy and access to information, libraries must also preserve the traditional associations that have defined them. The value of libraries has been undermined by the threat of terrorism and the subsequent political pressure to find blame for the terrorist attacks. Librarians must choose whether or not to stick to the traditional library brand, or evolve and market libraries as something else. Without public support, definitions will not change easily. The American public still views the library as a place to read and find books, and this definition must prevail for libraries to retain their relevance in American life. [ABSTRACT FROM AUTHOR]

FKBP, a naturally occurring ubiquitous intracellular protein, has been proposed as a potential target for coronavirus replication. A non-immunosuppressive FKBP ligand, FK1706, was studied in vitro in a Vero cell model to assess potential activity alone and in combination with antivirals against SARS-CoV-2 replication. When combined with remdesivir, synergistic activity was seen (summary synergy score 24.7±9.56). FK1706 warrants in vivo testing as a potential new combination therapeutic for the treatment of COVID-19 infections.

Natural serine protease inhibitors (serpins) elicit sensing of a microbial cell intruder and activate an intrinsic cellular immune response in HIV and HCV infected cells. Here, we demonstrate in vitro inhibition of HSV with serpin antithrombin III (ATIII) early during infection pointing towards inhibition of an entry event. We also found reduction of mortality from 90% to 40% in an abrasion mice model demonstrating a strong reduction of infection in vivo . Our data also indicated that this treatment might be suitable for drug-resistant viruses since high inhibition of an acyclovir-resistant HSV-1 strain was found. Thus, an ATIII tropical treatment might be used for immunocompromised patients where prolonged treatment leads to drug resistant HSV-1 strains. Understanding how ATIII regulates HSV-1 infections may reveal new avenues for therapeutic interventions.

CMX157 is a lipid (1-0-hexadecyloxypropyl) conjugate of the acyclic nucleotide analog tenofovir (TFV) with activity against both wild-type and antiretroviral drug-resistant HIV strains, including multidrug nucleoside/nucleotide analog-resistant viruses. CMX157 was consistently >300-fold more active than tenofovir against multiple viruses in several different cell systems. CMX157 was active against all major subtypes of HIV-1 and HIV-2 in fresh human peripheral blood mononuclear cells (PBMCs) and against all HIV-1 strains evaluated in monocyte-derived macrophages, with 50% effective concentrations (EC(50)s) ranging between 0.20 and 7.2 nM. The lower CMX157 EC(50)s can be attributed to better cellular uptake of CMX157, resulting in higher intracellular levels of the active antiviral anabolite, TFV-diphosphate (TFV-PP), inside target cells. CMX157 produced >30-fold higher levels of TFV-PP in human PBMCs exposed to physiologically relevant concentrations of the compounds than did TFV. Unlike conventional prodrugs, including TFV disoproxil fumarate (Viread), CMX157 remains intact in plasma, facilitating uptake by target cells and decreasing relative systemic exposure to TFV. There was no detectable antagonism with CMX157 in combination with any marketed antiretroviral drug, and it possessed an excellent in vitro cytotoxicity profile. CMX157 is a promising clinical candidate to treat wild-type and antiretroviral drug-resistant HIV, including strains that fail to respond to all currently available nucleoside/nucleotide reverse transcriptase inhibitors.

Triciribine (TCN) is a tricyclic nucleoside that inhibits human immunodeficiency virus type 1 (HIV-1) replication by a unique mechanism not involving the inhibition of enzymes directly involved in viral replication. This activity requires the phosphorylation of TCN to its 5' monophosphate by intracellular adenosine kinase. New testing with a panel of HIV and simian immunodeficiency virus isolates, including low-passage-number clinical isolates and selected subgroups of HIV-1, multidrug resistant HIV-1, and HIV-2, has demonstrated that TCN has broad antiretroviral activity. It was active in cell lines chronically infected with HIV-1 in which the provirus was integrated into chromosomal DNA, thereby indicating that TCN inhibits a late process in virus replication. The selection of TCN-resistant HIV-1 isolates resulted in up to a 750-fold increase in the level of resistance to the drug. DNA sequence analysis of highly resistant isolate HIV-1(H10) found five point mutations in the HIV-1 gene nef, resulting in five different amino acid changes. DNA sequencing of the other TCN-resistant isolates identified at least one and up to three of the same mutations observed in isolate HIV-1(H10). Transfer of the mutations from TCN-resistant isolate HIV-1(H10) to wild-type virus and subsequent viral growth experiments with increasing concentrations of TCN demonstrated resistance to the drug. We conclude that TCN is a late-phase inhibitor of HIV-1 replication and that mutations in nef are necessary and sufficient for TCN resistance.