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Journal articles on the topic 'Therapeutic ends'
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1
Close, Henry. "Book Review: Narrative Means to Therapeutic Ends." Journal of Pastoral Care 46, no. 1 (1992): 84. http://dx.doi.org/10.1177/002234099204600115.
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Akinyela, Makungu M. "Testimony of Hope: African Centered Praxis for Therapeutic Ends." Journal of Systemic Therapies 24, no. 1 (2005): 5–18. http://dx.doi.org/10.1521/jsyt.2005.24.1.5.
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Floh�, Leopold. "Superoxide dismutase for therapeutic use: Clinical experience, dead ends and hopes." Molecular and Cellular Biochemistry 84, no. 2 (1988): 123–31. http://dx.doi.org/10.1007/bf00421046.
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Aziz, Miriam, and Murray Earle. "Legalising Cannabis for Therapeutic Use: A Comparative Assessment." Medical Law International 3, no. 4 (1998): 273–85. http://dx.doi.org/10.1177/096853329800300402.
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Therapeutic use of cannabis as a palliative treatment for certain medical conditions has been hotly debated in Britain in recent months. The weight of public opinion is behind a reform of the law; reform would legalise the possession and use of cannabis for therapeutic ends. This paper will endorse that argument by concentrating on a central contradiction within the law: while the law meticulously categorises the drugs which it regulates and prohibits, it is unwilling divide users of particular drugs into recreational and therapeutic groupings. This paper argues that the traditional arguments against making such a change in the law are unable to hold water, particularly when viewed in comparison with developments in Germany. We will also propose that the medical practitioner fulfil an existing traditional function as gate keeper in order to ensure supply and quality are both kept to a certain minimum standard. This policy will serve the ends of patients for whom this treatment is effective and cheap and which is justified in the public interest.
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Relitti, Nicola, Akella P. Saraswati, Stefano Federico, et al. "Telomerase-based Cancer Therapeutics: A Review on their Clinical Trials." Current Topics in Medicinal Chemistry 20, no. 6 (2020): 433–57. http://dx.doi.org/10.2174/1568026620666200102104930.
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Telomeres are protective chromosomal ends that shield the chromosomes from DNA damage, exonucleolytic degradation, recombination, and end-to-end fusion. Telomerase is a ribonucleoprotein that adds TTAGGG tandem repeats to the telomeric ends. It has been observed that 85 to 90% of human tumors express high levels of telomerase, playing a crucial role in the development of cancers. Interestingly, the telomerase activity is generally absent in normal somatic cells. This selective telomerase expression has driven scientists to develop novel anti-cancer therapeutics with high specificity and potency. Several advancements have been made in this area, which is reflected by the enormous success of the anticancer agent Imetelstat. Since the discovery of Imetelstat, several research groups have contributed to enrich the therapeutic arsenal against cancer. Such contributions include the application of new classes of small molecules, peptides, and hTERT-based immunotherapeutic agents (p540, GV1001, GRNVAC1 or combinations of these such as Vx-001). Many of these therapeutic tools are under different stages of clinical trials and have shown promising outcomes. In this review, we highlight the current status of telomerase-based cancer therapeutics and the outcome of these investigations.
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Khalipaev, M. G., I. M. Azizov, and Z. M. Zukhrabova. "ETIOPATHOGENESIS, DIAGNOSIS AND THERAPEUTIC AND PREVENTIVE MEASURES OF POSTPARTUM CATARRHAL-PURULENT ENDOMETRITIS OF COWS." Scientific Notes Kazan Bauman State Academy of Veterinary Medicine 245, no. 1 (2021): 204–10. http://dx.doi.org/10.31588/2413-4201-1883-245-1-204-210.
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The article presents the results of studies on the etiopathogenesis, clinical signs of postpartum catarrhal-purulent endometritis in cows, pathomorphological and histostructural changes in the geni-tals at the beginning of the disease and the results of treatment with intrauterine use of non-antibiotic, foaming and iodine-containing liquid drug "Metrasil". We believe that the restoration of the body mucosa and uterine horns as a result of treatment is difficult and long-lasting and ends by 30-35 days after the start of therapy and ends simultane-ously with positive processes and in the macroscopic picture of the organ.
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Brorson, Kurt, and Audrey Y. Jia. "Therapeutic monoclonal antibodies and consistent ends: terminal heterogeneity, detection, and impact on quality." Current Opinion in Biotechnology 30 (December 2014): 140–46. http://dx.doi.org/10.1016/j.copbio.2014.06.012.
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Landreth, Gary. "The Immunology of Alzheimer’s Disease: Prospects Towards Harnessing Disease Mechanisms for Therapeutic Ends." Journal of Neuroimmune Pharmacology 2, no. 2 (2007): 131–33. http://dx.doi.org/10.1007/s11481-007-9067-1.
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Carrasco, Patricia, Iratxe Zuazo-Gaztelu, and Oriol Casanovas. "Sprouting strategies and dead ends in anti-angiogenic targeting of NETs." Journal of Molecular Endocrinology 59, no. 1 (2017): R77—R91. http://dx.doi.org/10.1530/jme-17-0029.
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Neuroendocrine tumors (NETs) are a heterogeneous group of neoplasms that arise from cells of the neuroendocrine system. NETs are characterized by being highly vascularized tumors that produce large amounts of proangiogenic factors. Due to their complexity and heterogeneity, progress in the development of successful therapeutic approaches has been limited. For instance, standard chemotherapy-based therapies have proven to be poorly selective for tumor cells and toxic for normal tissues. Considering the urge to develop an efficient therapy to treat NET patients, vascular targeting has been proposed as a new approach to block tumor growth. This review provides an update of the mechanisms regulating different components of vessels and their contribution to tumor progression in order to develop new therapeutic drugs. Following the description of classical anti-angiogenic therapies that target VEGF pathway, new angiogenic targets such as PDGFs, EGFs, FGFs and semaphorins are further explored. Based on recent research in the field, the combination of therapies that target multiple and different components of vessel formation would be the best approach to specifically target NETs and inhibit tumor growth.
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Rutten, Eric Andreas, and Christophe Badie. "Radiation Biomarkers: Silver Bullet, or Wild Goose Chase?" Journal of Personalized Medicine 11, no. 7 (2021): 603. http://dx.doi.org/10.3390/jpm11070603.
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Burroughs, Andrew, Daniel Hochhauser, and Tim Meyer. "Systemic treatment and liver transplantation for hepatocellular carcinoma: two ends of the therapeutic spectrum." Lancet Oncology 5, no. 7 (2004): 409–18. http://dx.doi.org/10.1016/s1470-2045(04)01508-6.
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Tsolekile, Ncediwe, Simphiwe Nelana, and Oluwatobi Samuel Oluwafemi. "Porphyrin as Diagnostic and Therapeutic Agent." Molecules 24, no. 14 (2019): 2669. http://dx.doi.org/10.3390/molecules24142669.
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The synthesis and application of porphyrins has seen a huge shift towards research in porphyrin bio-molecular based systems in the past decade. The preferential localization of porphyrins in tumors, as well as their ability to generate reactive singlet oxygen and low dark toxicities has resulted in their use in therapeutic applications such as photodynamic therapy. However, their inherent lack of bio-distribution due to water insolubility has shifted research into porphyrin-nanomaterial conjugated systems to address this challenge. This has broadened their bio-applications, viz. bio-sensors, fluorescence tracking, in vivo magnetic resonance imaging (MRI), and positron emission tomography (PET)/CT imaging to photo-immuno-therapy just to highlight a few. This paper reviews the unique theranostic role of porphyrins in disease diagnosis and therapy. The review highlights porphyrin conjugated systems and their applications. The review ends by bringing current challenges and future perspectives of porphyrin based conjugated systems and their respective applications into light.
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Barnaś, Edyta. "Pattern ethical communication in the therapeutic team." Health Promotion & Physical Activity 1, no. 1 (2016): 9–22. http://dx.doi.org/10.5604/01.3001.0010.7697.
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The time of dynamic development of the narrow medical specialties along with the progressive spread of technology in medicine, on the one hand contribute to the improvement of health care, on the other hand are often the reason for the rise in patients feel isolation as a result of fragmentary treatment of their problems. The counterweight to this state of affairs is to create a multidisciplinary therapeutic teams whose primary objective is to restore the welfare of bio-psycho-social and spiritual patient. An elementary part of the operation of the team is the process of communication at various levels. The aim of the article is to present the principles of proper communication with the patient, the whole ends in a proposition ethical standard of communication in the therapeutic team. This proposed model is by no means a ready-to-use algorithm showing what one should do and how he/she should act for it could become a routine. The author intended to present a general construct/ standard of communication, which may be “applied” for a “living” reality of dialogue in every situation.
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Giménez-Orenga, Karen, and Elisa Oltra. "Human Endogenous Retrovirus as Therapeutic Targets in Neurologic Disease." Pharmaceuticals 14, no. 6 (2021): 495. http://dx.doi.org/10.3390/ph14060495.
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Human endogenous retroviruses (HERVs) are ancient retroviral DNA sequences established into germline. They contain regulatory elements and encoded proteins few of which may provide benefits to hosts when co-opted as cellular genes. Their tight regulation is mainly achieved by epigenetic mechanisms, which can be altered by environmental factors, e.g., viral infections, leading to HERV activation. The aberrant expression of HERVs associates with neurological diseases, such as multiple sclerosis (MS) or amyotrophic lateral sclerosis (ALS), inflammatory processes and neurodegeneration. This review summarizes the recent advances on the epigenetic mechanisms controlling HERV expression and the pathogenic effects triggered by HERV de-repression. This article ends by describing new, promising therapies, targeting HERV elements, one of which, temelimab, has completed phase II trials with encouraging results in treating MS. The information gathered here may turn helpful in the design of new strategies to unveil epigenetic failures behind HERV-triggered diseases, opening new possibilities for druggable targets and/or for extending the use of temelimab to treat other associated diseases.
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Haoudi, Abdelali, and James M. Mason. "Reverse transcriptase can stabilize or destabilize the genome." Genome 43, no. 6 (2000): 949–56. http://dx.doi.org/10.1139/g00-067.
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Telomeres, the eukaryotic chromosome termini, are deoxyribonucleoprotein structures that distinguish natural chromosome ends from broken DNA. In most organisms, telomeres are extended by a reverse transcriptase (RT) with an integrated RNA template, telomerase; in Drosophila melanogaster, however, telomere-specific retrotransposons, HeT-A and TART, transpose specifically to chromosome ends. Whether telomeres are extended by a telomerase or by retrotransposons, an RT is a key component. RT has been studied extensively, both for its important role in converting RNA genomes to DNA, which has great evolutionary impact, and as a therapeutic target in human retroviral diseases. Here we discuss a few important aspects of RT usage during retrotransposition and telomere elongation.Key words: telomeres, telomerase, retrotransposons, reverse transcriptase.
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Callahan, Ann M. "Growing through Organizational Change." Families in Society: The Journal of Contemporary Social Services 90, no. 3 (2009): 329–31. http://dx.doi.org/10.1606/1044-3894.3898.
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This article describes the authors experience as an organizational change agent. The need to enhance client access to mental health care was the rallying cry for clinic transformation. The author describes how facility management, staff development, and therapeutic community were used to improve clinic functioning. The article ends with suggestions for how the reader might engage in organizational change.
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Corey, Robert M., and Dane H. Salazar. "Entrapment of the Superficial Peroneal Nerve Following a Distal Fibula Fracture." Foot & Ankle Specialist 10, no. 1 (2016): 69–71. http://dx.doi.org/10.1177/1938640016640887.
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Although peripheral nerve injury may result from fractures involving the long bones, bony entrapment of peripheral nerves is infrequently encountered. This report demonstrates a rare case of superficial peroneal nerve entrapment between 2 fracture ends of the distal fibula following a closed ankle fracture resulting from a supination-external rotation mechanism. Levels of Evidence: Therapeutic, Level IV: Case report
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Bär, Christian, and Maria A. Blasco. "Telomeres and telomerase as therapeutic targets to prevent and treat age-related diseases." F1000Research 5 (January 20, 2016): 89. http://dx.doi.org/10.12688/f1000research.7020.1.
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Telomeres, the protective ends of linear chromosomes, shorten throughout an individual’s lifetime. Telomere shortening is a hallmark of molecular aging and is associated with premature appearance of diseases associated with aging. Here, we discuss the role of telomere shortening as a direct cause for aging and age-related diseases. In particular, we draw attention to the fact that telomere length influences longevity. Furthermore, we discuss intrinsic and environmental factors that can impact on human telomere erosion. Finally, we highlight recent advances in telomerase-based therapeutic strategies for the treatment of diseases associated with extremely short telomeres owing to mutations in telomerase, as well as age-related diseases, and ultimately aging itself.
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Redmon, R. B. "How children can be respected as 'ends' yet still be used as subjects in non-therapeutic research." Journal of Medical Ethics 12, no. 2 (1986): 77–82. http://dx.doi.org/10.1136/jme.12.2.77.
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Ghiulai, Roxana, Oana Janina Roşca, Diana Simona Antal, et al. "Tetracyclic and Pentacyclic Triterpenes with High Therapeutic Efficiency in Wound Healing Approaches." Molecules 25, no. 23 (2020): 5557. http://dx.doi.org/10.3390/molecules25235557.
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Wounds are among the most common skin conditions, displaying a large etiological diversity and being characterized by different degrees of severity. Wound healing is a complex process that involves multiple steps such as inflammation, proliferation and maturation and ends with scar formation. Since ancient times, a widely used option for treating skin wounds are plant- based treatments which currently have become the subject of modern pharmaceutical formulations. Triterpenes with tetracyclic and pentacyclic structure are extensively studied for their implication in wound healing as well as to determine their molecular mechanisms of action. The current review aims to summarize the main results of in vitro, in vivo and clinical studies conducted on lupane, ursane, oleanane, dammarane, lanostane and cycloartane type triterpenes as potential wound healing treatments.
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Webb, C. J., G. Porter, M. G. Spencer, and G. R. J. Sissons. "Cavernous haemangioma of the nasal bones: an alternative management option." Journal of Laryngology & Otology 114, no. 4 (2000): 287–89. http://dx.doi.org/10.1258/0022215001905364.
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The authors present a case of bilateral cavernous haemangiomas affecting the posterior ends of both inferior turbinates of the nose. The condition was treated by angiographically controlled embolization. Review of the literature back to 1967 has revealed no other report of embolization being used specifically for this condition. All previous treatments have involved surgery; we describe an alternative therapeutic option.
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Rawlings, Barbara, and Rex Haigh. "Therapeutic communities and planned environments for serious offenders in English prisons." BJPsych Advances 23, no. 5 (2017): 338–46. http://dx.doi.org/10.1192/apt.bp.115.015636.
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SummarySeveral English prisons contain democratic therapeutic communities (TCs) for personality disordered offenders, and addiction TCs for serious substance misusers. This article describes how these are organised and comments on how they are specifically tailored and accredited for use in custodial settings. It also describes ‘psychologically informed planned environments’ (PIPEs), offender pathways for those with personality disorders and psychopathy which provide additional support for psychological treatment. It ends by explaining how ‘enabling environments’ are assessed, since these are now becoming widely adopted in prisons to reverse toxic environments – which affect staff, the prison and the outside world as well as the individual prisoner – and to counter negative learning found in custodial institutions.Learning Objectives• Understand the key components of treatment in democratic and addiction TCs• Understand how TCs can operate in a custodial environment• Appreciate the differences between a planned environment and a psychological treatment programme in a custodial environment
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Williams, Britton. "The R-RAP revisited: Current conceptualizations and applications." Drama Therapy Review 6, no. 2 (2020): 183–201. http://dx.doi.org/10.1386/dtr_00027_1.
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Existing research finds that how the client feels towards the therapist and the therapist towards the client will have a direct impact on the therapeutic relationship. Yet little has been written about how to understand and process the therapist‐client relationship in drama therapy. Therefore, the purpose of this article is to illustrate how a relational perspective and use of the Relational-Roles Assessment Protocol (R-RAP) may be implemented in the therapist’s embodied supervision and collaborative therapeutic processes. This article extends the existing R-RAP by providing how-to steps and case illustrations for applying the R-RAP to supervisory settings and in collaboration with clients. The article ends with emergent ideas and considerations for future applications.
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Lerner, Aaron, Patricia Jeremias, and Torsten Matthias. "Gut-thyroid axis and celiac disease." Endocrine Connections 6, no. 4 (2017): R52—R58. http://dx.doi.org/10.1530/ec-17-0021.
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Autoimmune thyroiditis has an increased prevalence in patients with celiac disease and vice versa. The objective of the current review is to highlight the epidemiological, clinical, serological, pathological, pathophysiological, hormonal, genetic and immunological factors shared between the two entities. They might represent the two ends of the gut-thyroid axis where the cross-talks’ pathways are still unravelled. New observations are reviewed, highlighting some gut-thyroid interrelated pathways that potentially might lead to new therapeutic strategies.
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Bender, N. "Gene therapy: a concept for the future in medical practice?" Hämostaseologie 24, no. 03 (2004): 173–78. http://dx.doi.org/10.1055/s-0037-1619633.
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SummaryGene therapy is a new therapeutic approach which is tested in numerous diseases connected with either non or only limited therapeutic effects. This paper aims at discussing the actual state of the clinical development of gene-therapy which targets an approval by either the FDA or EMEA. Basis of all the figures and tables presented is a BioMedNet/Medline search reviewing all titles found under the keywords gene therapy and/or clinical development. The review period begins in the year 1992 and ends in 2002. Publications identified were sorted into the following categories: therapeutic areas with gene therapy activities; indications and diseases with gene-therapy activities; vectors used in gene therapy and clinical studies using gene therapy. Only in some indications like breast cancer, colorectal cancer, HIV, and cystic fibrosis a variety of clinical studies had been published indicating a serious attempt to develop the indication for approval. But most developments are still in phase I/II. In all other therapeutic areas no systematic continuous approach was identified. Clinical activities in cardiovascular diseases and in peripheral vascular diseases increased during the preceding five years compared other therapeutic areas.
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Estep, Katrina N., Thomas J. Butler, Jun Ding, and Robert M. Brosh. "G4-Interacting DNA Helicases and Polymerases: Potential Therapeutic Targets." Current Medicinal Chemistry 26, no. 16 (2019): 2881–97. http://dx.doi.org/10.2174/0929867324666171116123345.
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Background:Guanine-rich DNA can fold into highly stable four-stranded DNA structures called G-quadruplexes (G4). In recent years, the G-quadruplex field has blossomed as new evidence strongly suggests that such alternately folded DNA structures are likely to exist in vivo. G4 DNA presents obstacles for the replication machinery, and both eukaryotic DNA helicases and polymerases have evolved to resolve and copy G4 DNA in vivo. In addition, G4-forming sequences are prevalent in gene promoters, suggesting that G4-resolving helicases act to modulate transcription.Methods:We have searched the PubMed database to compile an up-to-date and comprehensive assessment of the field’s current knowledge to provide an overview of the molecular interactions of Gquadruplexes with DNA helicases and polymerases implicated in their resolution.Results:Novel computational tools and alternative strategies have emerged to detect G4-forming sequences and assess their biological consequences. Specialized DNA helicases and polymerases catalytically act upon G4-forming sequences to maintain normal replication and genomic stability as well as appropriate gene regulation and cellular homeostasis. G4 helicases also resolve telomeric repeats to maintain chromosomal DNA ends. Bypass of many G4-forming sequences is achieved by the action of translesion DNS polymerases or the PrimPol DNA polymerase. While the collective work has supported a role of G4 in nuclear DNA metabolism, an emerging field centers on G4 abundance in the mitochondrial genome.Conclusion:Discovery of small molecules that specifically bind and modulate DNA helicases and polymerases or interact with the G4 DNA structure itself may be useful for the development of anticancer regimes.
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Cabral, Filipe, and Pedro Barata. "Losartan no tratamento das lesões musculares." Revista de Medicina Desportiva Informa 12, no. 2 (2021): 26–28. http://dx.doi.org/10.23911/losartan_musculo_2021_mar.
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Muscle injuries are very common in sports medicine. Frequently the muscle repair process ends in the formation of a fibrotic scar, that not only limits the complete functional recovery, but also increases the likelihood of injury recurrence. TGF-β1 is the main profibrogenic factor involved in this healing process. By blocking its activity, Losartan has proven it efficacy in reducing fibrosis and increasing regenerative and functional capacity post muscle injury. Therefore, its use should be considered as an alternative therapeutic for this kind of injuries.
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Murphy, Joseph F. "Trends in Cancer Immunotherapy." Clinical Medicine Insights: Oncology 4 (January 2010): CMO.S4795. http://dx.doi.org/10.4137/cmo.s4795.
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Modulation of the immune system for therapeutic ends has a long history, stretching back to Edward Jenner's use of cowpox to induce immunity to smallpox in 1796. Since then, immunotherapy, in the form of prophylactic and therapeutic vaccines, has enabled doctors to treat and prevent a variety of infectious diseases, including cholera, poliomyelitis, diphtheria, measles and mumps. Immunotherapy is now increasingly being applied to oncology. Cancer immunotherapy attempts to harness the power and specificity of the immune system for the treatment of malignancy. Although cancer cells are less immunogenic than pathogens, the immune system is capable of recognizing and eliminating tumor cells. However, tumors frequently interfere with the development and function of immune responses. Thus, the challenge for cancer immunotherapy is to apply advances in cellular and molecular immunology and develop strategies that effectively and safely augment antitumor responses.
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Yu, Chunxiao, Longfei Wang, R. Grant Rowe, et al. "A nanobody targeting the LIN28:let-7 interaction fragment of TUT4 blocks uridylation of let-7." Proceedings of the National Academy of Sciences 117, no. 9 (2020): 4653–63. http://dx.doi.org/10.1073/pnas.1919409117.
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The LIN28:pre-let-7:TUTase ternary complex regulates pluripotency and oncogenesis by controlling processing of the let-7 family of microRNAs. The complex oligouridylates the 3′ ends of pre-let-7 molecules, leading to their degradation via the DIS3L2 exonuclease. Previous studies suggest that components of this complex are potential therapeutic targets in malignancies that aberrantly express LIN28. In this study we developed a functional epitope selection approach to identify nanobody inhibitors of the LIN28:pre-let-7:TUT4 complex. We demonstrate that one of the identified nanobodies, Nb-S2A4, targets the 106-residue LIN28:let-7 interaction (LLI) fragment of TUT4. Nb-S2A4 can effectively inhibit oligouridylation and monouridylation of pre-let-7g in vitro. Expressing Nb-S2A4 allows maturation of the let-7 species in cells expressing LIN28, highlighting the therapeutic potential of targeting the LLI fragment.
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Straka, R. J., T. J. Hoon, R. L. Lalonde, J. A. Pieper, and M. B. Bottorff. "Liquid chromatography and fluorescence polarization immunoassay methods compared for measuring flecainide acetate in serum." Clinical Chemistry 33, no. 10 (1987): 1898–900. http://dx.doi.org/10.1093/clinchem/33.10.1898.
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Abstract We analyzed 99 patients' serum samples for concentrations of a new antiarrhythmic agent, flecainide acetate, by fluorescence polarization immunoassay (FPIA) and "high-performance" liquid chromatography (HPLC). Within-day and between-day coefficients of variation at concentrations in the low and high ends of the therapeutic range were less than 7% for HPLC and less than 9% for FPIA. There was no statistical difference in the mean (+/- SD) concentrations of the clinical serum samples measured by the two methods (607 +/- 334 micrograms/L by HPLC, 602 +/- 344 micrograms/L by FPIA), but results by each differed by a mean of 0.13%. FPIA and HPLC measurements correlated significantly (r = 0.98, P less than 0.05), and were linearly related (slope = 0.970, intercept = 13 micrograms/L) as assessed by orthogonal regression. Both assay methods produced similar concentration measurements and were sufficiently accurate and precise to be used in therapeutic drug monitoring.
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Millbrook, Alyssa. "Digital storymaking: Dramatherapy with young people online." Dramatherapy 40, no. 1 (2019): 28–40. http://dx.doi.org/10.1177/0263067218817296.
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The Internet has become thoroughly embedded into most aspects of modern life, and no one is more plugged-in than the youngest generations. With the aim of utilising the omnipresence of the digital space to therapeutic ends, this article examines the application of online storymaking interventions with adolescents. The young people discussed are quite isolated and high-need; they have self-excluded from mainstream school and are now pursuing education in an alternative online provision, where they also have access to therapy. Following an overview of the current literature on web-based therapies, this article offers two illustrative case studies in which a story-based dramatherapy intervention was delivered online. This will include an evaluation of the therapeutic work from the case studies using the BASIC Ph assessment method, as well as a broader discussion on the experience of working as a therapist online.
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Ruiz, Amanda. "Generation Lobotomy." Stance: an international undergraduate philosophy journal 2, no. 1 (2019): 9–17. http://dx.doi.org/10.33043/s.2.1.9-17.
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This paper primarily explores the ethical debate surrounding the use of memory erasure for therapeutic ends. It argues that procedures such as kinase inhibition therapy, which can entail memory erasure in the individual, incur a high cost in terms of the integrity of our individual identities, thus jeopardizing our claim to individual rights and accountability. Therefore, we should reserve such therapies for the extreme cases in which the procedures have the potential to actually restore a person’s autonomy. Furthermore, this paper goes on to explore which situations might fit this criterion, while still accounting for the cost of memory erasure in each instance.
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Fernandes, Stina George, Rebecca Dsouza, Gouri Pandya, et al. "Role of Telomeres and Telomeric Proteins in Human Malignancies and Their Therapeutic Potential." Cancers 12, no. 7 (2020): 1901. http://dx.doi.org/10.3390/cancers12071901.
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Telomeres are the ends of linear chromosomes comprised of repetitive nucleotide sequences in humans. Telomeres preserve chromosomal stability and genomic integrity. Telomere length shortens with every cell division in somatic cells, eventually resulting in replicative senescence once telomere length becomes critically short. Telomere shortening can be overcome by telomerase enzyme activity that is undetectable in somatic cells, while being active in germline cells, stem cells, and immune cells. Telomeres are bound by a shelterin complex that regulates telomere lengthening as well as protects them from being identified as DNA damage sites. Telomeres are transcribed by RNA polymerase II, and generate a long noncoding RNA called telomeric repeat-containing RNA (TERRA), which plays a key role in regulating subtelomeric gene expression. Replicative immortality and genome instability are hallmarks of cancer and to attain them cancer cells exploit telomere maintenance and telomere protection mechanisms. Thus, understanding the role of telomeres and their associated proteins in cancer initiation, progression and treatment is very important. The present review highlights the critical role of various telomeric components with recently established functions in cancer. Further, current strategies to target various telomeric components including human telomerase reverse transcriptase (hTERT) as a therapeutic approach in human malignancies are discussed.
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Peronne, Lauralie, Eric Denarier, Ankit Rai, et al. "Two Antagonistic Microtubule Targeting Drugs Act Synergistically to Kill Cancer Cells." Cancers 12, no. 8 (2020): 2196. http://dx.doi.org/10.3390/cancers12082196.
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Paclitaxel is a microtubule stabilizing agent and a successful drug for cancer chemotherapy inducing, however, adverse effects. To reduce the effective dose of paclitaxel, we searched for pharmaceutics which could potentiate its therapeutic effect. We screened a chemical library and selected Carba1, a carbazole, which exerts synergistic cytotoxic effects on tumor cells grown in vitro, when co-administrated with a low dose of paclitaxel. Carba1 targets the colchicine binding-site of tubulin and is a microtubule-destabilizing agent. Catastrophe induction by Carba1 promotes paclitaxel binding to microtubule ends, providing a mechanistic explanation of the observed synergy. The synergistic effect of Carba1 with paclitaxel on tumor cell viability was also observed in vivo in xenografted mice. Thus, a new mechanism favoring paclitaxel binding to dynamic microtubules can be transposed to in vivo mouse cancer treatments, paving the way for new therapeutic strategies combining low doses of microtubule targeting agents with opposite mechanisms of action.
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Dresser, Rebecca. "Alive and Well: The Research Imperative." Journal of Law, Medicine & Ethics 40, no. 4 (2012): 915–21. http://dx.doi.org/10.1111/j.1748-720x.2012.00720.x.
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The government-sponsored Tuskegee syphilis study had a huge impact on U.S. research ethics and policy. Study investigators regarded subjects as “mere means” to their research ends, which led to a variety of ethical violations. Investigators used deception so that subjects would see participation as therapeutic — researchers promoted the therapeutic misconception because this advanced study objectives. The research would produce important information, and this justified lying to research subjects.Today we see this sort of intentional deception as unjustified no matter how important a study might be. But what do we make of the claim that the syphilis study had value? As James Jones reported, its objectives were to test the prevailing views that syphilis affected blacks and whites differently, and that the disease was less harmful to blacks than whites. U.S. Public Health Service researchers and officials assumed the study had sufficient value to justify not only deceiving subjects, but also depriving them of safe and effective treatment.
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Mirkes, Renée. "Transhumanist Medicine: Can We Direct Its Power to the Service of Human Dignity?" Linacre Quarterly 86, no. 1 (2019): 115–26. http://dx.doi.org/10.1177/0024363919838134.
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The medicalization of transhumanist technologies demands our prompt and undivided attention. This article surveys the principal body/mind enhancement goals of transhumanist medicine and the means it would employ—genetic, robo, info-, and nanotechnologies—to accomplish those ends (Part One). Second, it engages Christian anthropological and natural law principles to evaluate the populist and essentialist concerns these therapeutic/enhancement interventions provoke (Part Two). And, third, it proposes formation of a Catholic medical think tank to appraise whether transhumanist biotechnologies can serve human dignity and, to the extent they can, to formulate wise clinical/administrative guidelines for their inclusion in US Catholic healthcare settings (Part Three). Nontechnical summary: This article explores the body/mind enhancement goals of transhumanist medicine, evaluates the biotechnological means to accomplish those therapeutic/enhancement goals, and suggests the formation of a Catholic medical think tank to formulate wise clinical/administrative guidelines for the inclusion of genetic, robo, info-, and nanotechnologies in US Catholic healthcare settings.
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Ramaswamy, Gomathi, Preetheekha Elangovan, Mammallan Arumugam, et al. "Traditional Therapeutic Approach for the Management of Non-Healing, Chronic Diabetic Ulcer – A Case Report." Journal of Evolution of Medical and Dental Sciences 10, no. 30 (2021): 2358–61. http://dx.doi.org/10.14260/jemds/2021/483.
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Diabetic ulcer is an outcome of the combined effect of diabetes related vascular disease and neuropathy. 1 People prone to diabetes mellitus across the world were estimated to be 131 million in 2000; it is expected to increase to 366 million by 2030. 2 According to several studies, about 25 - 50 % of diabetic patients receive instantaneous amputation at the first visit due to the infection. 3 Slight injury to glucose laden tissue will cause infection which is progressed by an ulcer and it tends to a state of non-healing which has been shown to precede amputation up to 85 % of cases. 4,5 Diabetic ulcer management in the contemporary science includes drainage of pus, debridement of dead tissue, local amputation of necrotic digits and antibiotics.6 Siddha system of medicine also has 64 unique categories of internal and external medicines including 32 in each. 7 Both these ends have their own strengths and limitations too. Though treating a non-healing diabetic ulcer is a very big challenge in the current scenario, an integrated approach will give a light on the path of successful management. P
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Yong, EL, Q. Wang, TG Tut, FJ Ghadessy, and SC Ng. "Male infertility and the androgen receptor: molecular, clinical and therapeutic aspects." Reproductive Medicine Review 6, no. 2 (1997): 113–31. http://dx.doi.org/10.1017/s0962279900001459.
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Idiopathic male infertility has previously been diagnosed imprecisely, and has been treated using regimes that are not based on a clear understanding of the underlying pathophysiology; however, this is gradually changing, and a more rational approach is being adopted. Testosterone and its metabolite, DHT, is allimportant for the maintenance of sperm production and this has led us to examine the AR for causes of male infertility. Some, but not all, androgen-binding studies have indicated that in a certain proportion of cases of male infertility, defective androgen binding occurs. The cloning of the AR gene allowed for a more rigorous examination of the molecular pathogenesis which turned out to be both subtle and heterogeneous. Genetic screening of a large group of men with defective spermatogenesis has indicated that up to 30% of infertile males could have variations in the androgenicity of their AR caused by polymorphisms in the length of the polyglutamine tract. Substitutions of the AR in the LBD and the DBD can also lead to reduced AR function and male infertility. In this regard, it is interesting to note that depressed spermatogenesis and prostate cancer represent opposite ends of the spectrum of AR action (Figure 6). Although empirical treatment of AR mutants in some cases has been shown to restore normal AR function and to improve spermatogenesis, a fully rational basis of treatment has to be based on an understanding of the crystallographic structure of the AR LBD. A full understanding could lead to the construction and the administration of ‘designer’ androgen analogues to treat male infertility caused by mutations of the AR gene.
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Tolmachov, Oleg, and Charles Coutelle. "Covalent attachment of multifunctional chimeric terminal proteins to 5′ DNA ends: A potential new strategy for assembly of synthetic therapeutic gene vectors." Medical Hypotheses 68, no. 2 (2007): 328–31. http://dx.doi.org/10.1016/j.mehy.2006.06.055.
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Palermo, Christine M., William C. Wimley, and Charles S. Hemenway. "Enhancing the Therapeutic Potential of an Anti-Leukemic Peptide." Blood 106, no. 11 (2005): 245. http://dx.doi.org/10.1182/blood.v106.11.245.245.
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Abstract Despite ongoing success in the treatment of childhood acute lymphoblastic leukemia (ALL), patients harboring translocations involving the genetic locus 11q23 continue to have a poor prognosis. The majority of 11q23 translocations result in the formation of a functional fusion protein consisting of the N-terminus of MLL fused to the C-terminal portion of one of more than 30 fusion partners. This translocation results in a functional chimeric protein critical for leukemogenesis. Recently, our lab has identified an interaction between two common MLL fusion partners, AF4 and AF9. Through a series of mapping experiments we identified a small region of human AF4 to be sufficient for its interaction with AF9. Based on these studies, a synthetic peptide (PFWT) that mimics the AF9 binding site on AF4 was developed. Treatment of leukemia cells that express the MLL-AF4 protein with PFWT results in apoptosis with no observable affects on CD34+ hematopoietic stem cells, suggesting the AF9-AF4 interaction is a promising chemotherapeutic target. To improve upon the therapeutic potential of PFWT, we developed a high-throughput enzyme-linked colorimetric assay to identify peptidomimetics that block the AF9-AF4 interaction. A combinatorial peptide library was synthesized in which each position of the 10-mer sequence was substituted with either the α- or corresponding β-amino acid. β-Amino acids which are similar to α-amino acids but contain an additional carbon in their backbone were chosen because of their resistance to proteases (210= 1024 possible unique sequences). To date, 30 of the peptides screened compare favorably with PFWT for disrupting the AF4-AF9 interaction. Sequencing of the peptides by MS/MS revealed substitutions at the N- and C-terminal ends are well tolerated. In addition, peptides can incorporate as many as three β-amino acids and still retain biological activity. These data are important for establishing a sequence with improved pharmacokinetic properties as compared to PFWT and serve as the first step in our design towards an optimal peptide sequence for drug development. They also validate the utility of a high-throughput assay system for drug screening. Future studies for the identified peptides include determining their biological half-lives, AF9 binding affinities, and ability to induce apoptosis in leukemia cells.
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Xie, Zhipeng, Hanqi Wei, Jiahui Meng, et al. "The Analogs of Temporin-GHa Exhibit a Broader Spectrum of Antimicrobial Activity and a Stronger Antibiofilm Potential against Staphylococcus aureus." Molecules 24, no. 22 (2019): 4173. http://dx.doi.org/10.3390/molecules24224173.
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The abuse of antibiotics has led to the emergence of multidrug-resistant bacteria, which is becoming a serious worldwide problem people have to face. In our previous study, temporin-GHa (GHa) cloned from Hylarana guentheri showed antimicrobial activity against Gram-positive bacteria. In order to improve its therapeutic potential, we used a template-based and a database-assisted design to obtain three derived peptides by replacing the histidine at both ends of GHa with lysine, which exhibited faster and stronger bactericidal activity and a broader spectrum than the parent peptide. GHaK and GHa4K targeted to the bacterial membrane to exert their antibacterial activities at a faster membrane damage rate. The derived peptides inhibited the initial adhesion and the formation of Staphylococcus aureus biofilms, and eradicated the mature biofilms, which indicated that the derived peptides effectively penetrated the biofilm and killed bacteria. The therapeutic index (TI) and cell selectivity index (CSI) of the derived peptides increased significantly, which means a broader therapeutic window of the derived peptides. The derived peptides with improved activity and cell selectivity have the potential to be the promising candidates for the treatment of S. aureus infections. Our research also provides new insights into the design and development of antimicrobial peptides.
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Ge, Jiaxin, and Xinjun Zhang. "The Emerging Roles of Circular RNAs in Colorectal Cancer." Research in Health Science 4, no. 2 (2019): p126. http://dx.doi.org/10.22158/rhs.v4n2p126.
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Colorectal cancer (CRC) is one of the most common malignant diseases and the forth common cause for death in the world. Circular RNAs (circRNAs) are a group of non-coding RNAs (ncRNAs), which have a covalent closed loop without 5’ and 3’ ends. Studies indicated that many circRNAs are differently expressed in CRC cells and tissues. Their different expression levels are significantly correlated with clinicopathological features and overall survival time of CRC patients. Additionally, they regulate CRC cell proliferation, apoptosis, invasion, and migration mainly by acting as competing endogenous RNAs (ceRNAs). In this review, we reviewed CRC-associated circRNAs, described their functions and mechanisms, discussed their potential as diagnostic or prognostic biomarkers and therapeutic targets of CRC.
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Ran, Qian, Feng Jin, Yang Xiang, et al. "CRIF1 as a potential target to improve the radiosensitivity of osteosarcoma." Proceedings of the National Academy of Sciences 116, no. 41 (2019): 20511–16. http://dx.doi.org/10.1073/pnas.1906578116.
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Resistance to ionizing radiation (IR), which is a conventional treatment for osteosarcoma that cannot be resected, undermines the efficacy of this therapy. However, the mechanism by which IR induces radioresistance in osteosarcoma is not defined. Here, we report that CR6-interacting factor-1 (CRIF1) is highly expressed in osteosarcoma and undergoes nuclear-cytoplasmic shuttling of cyclin-dependent kinase 2 (CDK2) after IR. Osteosarcoma cells lacking CRIF1 show increased sensitivity to IR, which is associated with delayed DNA damage repair, inactivated G1/S checkpoint, and mitochondrial dysfunction. CRIF1 interacts with the DNA damage checkpoint regulator CDK2, and CRIF1 and CDK2 colocalize in the nucleus after IR. Nuclear localization of CDK2 is associated with phosphorylation changes that promote DNA repair and activation of the G1/S checkpoint. CRIF1 knockdown synergized with IR in an in vivo osteosarcoma model, leading to tumor regression. Based on these findings, we identify CRIF1 as a potential therapeutic target in osteosarcoma that can increase the efficacy of radiotherapy. More broadly, our findings may provide insights into the mechanism for other types of radioresistant cancers and be exploited for therapeutic ends.
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Avis, Paul. "Are we Receiving ‘Receptive Ecumenism’?" Ecclesiology 8, no. 2 (2012): 223–34. http://dx.doi.org/10.1163/174553112x630471.
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‘Receptive Ecumenism’, though initially a movement of ecclesiological renewal within the Roman Catholic Church, holds considerable potential for all churches that are engaged in the ecumenical movement and for their closer unity. This article asks why Receptive Ecumenism is needed, given that the process of reception is inherent in ecumenism. It then examines the tension between rhetoric and reality in much ecumenical and ecclesiological discourse, and goes on to ask whether Receptive Ecumenism is a threat to the time-honoured agenda of the Faith and Order tradition in seeking visible unity through theological dialogue. The article touches on the therapeutic dimension of greater mutual receptivity between churches and ends by arguing that Receptive Ecumenism and traditional theological dialogue are mutually dependent.
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Pal, Sharmistha, Jakub P. Kaplan, Sylwia A. Stopka, et al. "DDRE-32. THERAPEUTIC TARGETING OF A NOVEL METABOLIC ADDICTION IN DIFFUSE MIDLINE GLIOMA." Neuro-Oncology Advances 3, Supplement_1 (2021): i13. http://dx.doi.org/10.1093/noajnl/vdab024.054.
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Abstract Diffuse midline glioma (DMG) is a uniformly fatal pediatric cancer that is in need of urgent “outside the box” therapeutic approaches. Recent studies show that tumor cells adapt to stresses created by oncogenic mutations and these oncogene-induced adaptations create vulnerabilities that can be exploited to therapeutic ends. To uncover these oncogene-induced vulnerabilities in DMGs we conducted a genome-wide CRIPSR knockout screen in three DMG lines. The top common DMG dependency pathway that we discovered is de novo pyrimidine biosynthesis. Under normal conditions pyrimidine nucleotide needs are met through the salvage pathway. However, in DMG tumorigenesis, pyrimidine nucleotide synthesis is rewired such that the cells become dependent on the de novo biosynthesis pathway. De novo pyrimidine synthesis is catalyzed by CAD, DHODH and UMPS; all three genes are identified as dependencies in our screen and have been validated using shRNA mediated gene knockdown. Interestingly, DMG cells did not exhibit a dependency on the de novo purine biosynthesis pathway. Using a small molecule inhibitor of DHODH, BAY2402234 [currently studied in phase I trial for myeloid malignancies (NCT03404726)], we have demonstrated and validated, (i) efficacy and specificity of de novo pyrimidine synthesis inhibition in vitro in DMG cells; (ii) de novo pyrimidine addiction is not attributable to cell proliferation; (iii) DHODH inhibition induces apoptosis by hindering replication and inciting DNA damage; (iv) DHODH and ATR inhibition act synergistically to induce DMG cell death; and (v) critical in vivo efficacy. The in vivo experiment documents that BAY2402234 crosses the blood-brain barrier, is present in the brain at therapeutically relevant concentrations, suppresses de novo pyrimidine biosynthesis in intracranial DMG tumors in mice, and prolongs survival of orthotopic DMG tumor bearing mice. Taken together, our studies have identified a novel metabolic vulnerability that can be translated for the treatment of DMG patients.
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Konikkat, Salini, Michelle R. Scribner, Rory Eutsey, N. Luisa Hiller, Vaughn S. Cooper, and Joel McManus. "Quantitative mapping of mRNA 3’ ends in Pseudomonas aeruginosa reveals a pervasive role for premature 3’ end formation in response to azithromycin." PLOS Genetics 17, no. 7 (2021): e1009634. http://dx.doi.org/10.1371/journal.pgen.1009634.
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Pseudomonas aeruginosa produces serious chronic infections in hospitalized patients and immunocompromised individuals, including patients with cystic fibrosis. The molecular mechanisms by which P. aeruginosa responds to antibiotics and other stresses to promote persistent infections may provide new avenues for therapeutic intervention. Azithromycin (AZM), an antibiotic frequently used in cystic fibrosis treatment, is thought to improve clinical outcomes through a number of mechanisms including impaired biofilm growth and quorum sensing (QS). The mechanisms underlying the transcriptional response to AZM remain unclear. Here, we interrogated the P. aeruginosa transcriptional response to AZM using a fast, cost-effective genome-wide approach to quantitate RNA 3’ ends (3pMap). We also identified hundreds of P. aeruginosa genes with high incidence of premature 3’ end formation indicative of riboregulation in their transcript leaders using 3pMap. AZM treatment of planktonic and biofilm cultures alters the expression of hundreds of genes, including those involved in QS, biofilm formation, and virulence. Strikingly, most genes downregulated by AZM in biofilms had increased levels of intragenic 3’ ends indicating premature transcription termination, transcriptional pausing, or accumulation of stable intermediates resulting from the action of nucleases. Reciprocally, AZM reduced premature intragenic 3’ end termini in many upregulated genes. Most notably, reduced termination accompanied robust induction of obgE, a GTPase involved in persister formation in P. aeruginosa. Our results support a model in which AZM-induced changes in 3’ end formation alter the expression of central regulators which in turn impairs the expression of QS, biofilm formation and stress response genes, while upregulating genes associated with persistence.
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CHARLTON, ED. "Apartheid Acting Out: Trauma, Confession and the Melancholy of Theatre in Yaël Farber's He Left Quietly." Theatre Research International 42, no. 1 (2017): 55–71. http://dx.doi.org/10.1017/s0307883317000062.
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In 1984, Duma Kumalo was sentenced to death under the apartheid law of common purpose. He was only spared by the transitional negotiations that led to South Africa's first democratic elections in 1994. However, his suffering did not end with his release. Nor did his appearance alongside many other victims of human rights abuse at the country's Truth and Reconciliation Commission provide any measure of therapeutic relief. Instead, he continued to confess, as part of his performance in Yaël Farber's He Left Quietly (2002), to a trauma so overwhelming as to undo, it seems, any such a claim to healing. It has now been ten years since Kumalo passed away and this article returns to Farber's play in order to examine the theatrical form this melancholy takes, the challenge it poses to confessional orthodoxy and the ethical ends towards which such a melancholy performance might potentially drive, even still.
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Ashton, Daniel, and Seth Giddings. "At work in the toybox." International Journal of Entrepreneurship and Innovation 19, no. 2 (2018): 81–89. http://dx.doi.org/10.1177/1465750318757157.
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Key companies and commentators on the new economy have identified play as a crucial aspect of entrepreneurship and commercial innovation. We will argue that play and place are inseparable in these discourses: from places such as Google’s headquaters (HQ) – the Googleplex, with its ball pits and slides – to schemes and practices such as LEGO Serious Play, children’s play and sites of play are taken as the model for, and wellspring of, imagination and creativity, modes and spaces of thinking and experimentation that can invigorate and innovate the adult worlds of cultural and technological production. Taking as case studies Google’s reimagining of cultural practices of play, and LEGO Serious Play’s deployment of playful experimentation for corporate/therapeutic ends, this article argues that to understand the possibilities of playful working places, it is necessary to question the generally uncritical assumptions about the character and potential of play itself that underpin these initiatives.
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Shen, Chia-Lin, Bo-Sheng Wu, Tse-Jen Lien, An-Hang Yang, and Chih-Yu Yang. "BK Polyomavirus Nephropathy in Kidney Transplantation: Balancing Rejection and Infection." Viruses 13, no. 3 (2021): 487. http://dx.doi.org/10.3390/v13030487.
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BK polyomavirus nephropathy (BKVN) and allograft rejection are two closely-associated diseases on opposite ends of the immune scale in kidney transplant recipients. The principle of balancing the immune system remains the mainstay of therapeutic strategy. While patient outcomes can be improved through screening, risk factors identification, and rapid reduction of immunosuppressants, a lack of standard curative therapy is the primary concern during clinical practice. Additionally, difficulty in pathological differential diagnosis and clinicopathology’s dissociation pose problems for a definite diagnosis. This article discusses the delicate evaluation needed to optimize immunosuppression and reviews recent advances in molecular diagnosis and immunological therapy for BKVN patients. New biomarkers for BKVN diagnosis are under development. For example, measurement of virus-specific T cell level may play a role in steering immunosuppressants. The development of cellular therapy may provide prevention, even a cure, for BKVN, a complex post-transplant complication.
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Haberichter, Jarod, Scott Roberts, Imran Abbasi, Phonphanh Dedthanou, Prajakta Pradhan, and Marie L. Nguyen. "The Telomerase Inhibitor MST-312 Interferes with Multiple Steps in the Herpes Simplex Virus Life Cycle." Journal of Virology 89, no. 19 (2015): 9804–16. http://dx.doi.org/10.1128/jvi.01006-15.
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ABSTRACTThe life cycle of herpes simplex virus (HSV) has the potential to be further manipulated to yield novel, more effective therapeutic treatments. Recent research has demonstrated that HSV-1 can increase telomerase activity and that expression of the catalytic component of telomerase, telomerase reverse transcriptase (TERT), alters sensitivity to HSV-dependent apoptosis. Telomerase is a cellular enzyme that synthesizes nucleotide repeats at the ends of chromosomes (telomeres), which prevents shortening of the 3′ ends of DNA with each cell division. Once telomeres reach a critical length, cells undergo senescence and apoptosis. Here, we used a cell-permeable, reversible inhibitor of the telomerase enzyme, MST-312, to investigate telomerase activity during HSV infection. Human mammary epithelial cells immortalized through TERT expression and human carcinoma HEp-2 cells were infected with the KOS1.1 strain of HSV-1 in the presence of MST-312. MST-312 treatment reduced the number of cells displaying a cytopathic effect and the accumulation of immediate early and late viral proteins. Moreover, the presence of 20 μM to 100 μM MST-312 during infection led to a 2.5- to 5.5-log10decrease in viral titers. MST-312 also inhibited the replication of HSV-2 and a recent clinical isolate of HSV-1. Additionally, we determined that MST-312 has the largest impact on viral events that take place prior to 5 h postinfection (hpi). Furthermore, MST-312 treatment inhibited virus replication, as measured by adsorption assays and quantification of genome replication. Together, these findings demonstrate that MST-312 interferes with the HSV life cycle. Further investigation into the mechanism for MST-312 is warranted and may provide novel targets for HSV therapies.IMPORTANCEHerpes simplex virus (HSV) infections can lead to cold sores, blindness, and brain damage. Identification of host factors that are important for the virus life cycle may provide novel targets for HSV antivirals. One such factor, telomerase, is the cellular enzyme that synthesizes DNA repeats at the ends of chromosomes during replication to prevent DNA shortening. In this study, we investigate role of telomerase in HSV infection. The data demonstrate that the telomerase inhibitor MST-312 suppressed HSV replication at multiple steps of viral infection.