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Showing 1 to 12 of 14 entries
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Clostridial abomasitis in calves: case report and review of the literature.

Anaerobe

Glenn Songer J, Miskimins DW.
PMID: 16701586
Anaerobe. 2005 Oct;11(5):290-4. doi: 10.1016/j.anaerobe.2004.12.004. Epub 2005 Apr 25.

Infections by Clostridium perfringens type A are perhaps the most common causes of clostridial hemorrhagic enteritis in neonatal ruminants. Affected calves exhibit tympany, hemorrhagic abomasitis, and abomasal ulceration. Gram-positive bacilli are often found on affected mucosa and in submucosa....

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Glenn Songer J, Miskimins DW. Clostridial abomasitis in calves: case report and review of the literature. Anaerobe. 2005;11(5):290-4doi: 10.1016/j.anaerobe.2004.12.004.
Glenn Songer, J., & Miskimins, D. W. (2005). Clostridial abomasitis in calves: case report and review of the literature. Anaerobe, 11(5), 290-4. https://doi.org/10.1016/j.anaerobe.2004.12.004
Glenn Songer, J, and Miskimins, Dale W. "Clostridial abomasitis in calves: case report and review of the literature." Anaerobe vol. 11,5 (2005): 290-4. doi: https://doi.org/10.1016/j.anaerobe.2004.12.004
Glenn Songer J, Miskimins DW. Clostridial abomasitis in calves: case report and review of the literature. Anaerobe. 2005 Oct;11(5):290-4. doi: 10.1016/j.anaerobe.2004.12.004. Epub 2005 Apr 25. PMID: 16701586; PMCID: PMC7111123.
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Metformin and phenethyl isothiocyanate combined treatment in vitro is cytotoxic to ovarian cancer cultures.

Journal of ovarian research

Chan DK, Miskimins WK.
PMID: 22781119
J Ovarian Res. 2012 Jul 10;5(1):19. doi: 10.1186/1757-2215-5-19.

BACKGROUND: High mortality rates in ovarian cancer are largely a result of resistance to currently used chemotherapies. Expanding therapies with a variety of drugs has the potential to reduce this high mortality rate. Metformin and phenethyl isothiocyanate (PEITC) are...

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Chan DK, Miskimins WK. Metformin and phenethyl isothiocyanate combined treatment in vitro is cytotoxic to ovarian cancer cultures. J Ovarian Res. 2012;5(1):19doi: 10.1186/1757-2215-5-19.
Chan, D. K., & Miskimins, W. K. (2012). Metformin and phenethyl isothiocyanate combined treatment in vitro is cytotoxic to ovarian cancer cultures. Journal of ovarian research, 5(1), 19. https://doi.org/10.1186/1757-2215-5-19
Chan, Daniel K, and Miskimins, W Keith. "Metformin and phenethyl isothiocyanate combined treatment in vitro is cytotoxic to ovarian cancer cultures." Journal of ovarian research vol. 5,1 (2012): 19. doi: https://doi.org/10.1186/1757-2215-5-19
Chan DK, Miskimins WK. Metformin and phenethyl isothiocyanate combined treatment in vitro is cytotoxic to ovarian cancer cultures. J Ovarian Res. 2012 Jul 10;5(1):19. doi: 10.1186/1757-2215-5-19. PMID: 22781119; PMCID: PMC3439343.
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Genome divergence and increased virulence of outbreak associated .

Gut pathogens

Antony L, Behr M, Sockett D, Miskimins D, Aulik N, Christopher-Hennings J, Nelson E, Allard MW, Scaria J.
PMID: 30603048
Gut Pathog. 2018 Dec 24;10:53. doi: 10.1186/s13099-018-0279-0. eCollection 2018.

No abstract available.

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Antony L, Behr M, Sockett D, et al. Genome divergence and increased virulence of outbreak associated . Gut Pathog. 2018;10:53doi: 10.1186/s13099-018-0279-0.
Antony, L., Behr, M., Sockett, D., Miskimins, D., Aulik, N., Christopher-Hennings, J., Nelson, E., Allard, M. W., & Scaria, J. (2018). Genome divergence and increased virulence of outbreak associated . Gut pathogens, 1053. https://doi.org/10.1186/s13099-018-0279-0
Antony, Linto, et al. "Genome divergence and increased virulence of outbreak associated ." Gut pathogens vol. 10 (2018): 53. doi: https://doi.org/10.1186/s13099-018-0279-0
Antony L, Behr M, Sockett D, Miskimins D, Aulik N, Christopher-Hennings J, Nelson E, Allard MW, Scaria J. Genome divergence and increased virulence of outbreak associated . Gut Pathog. 2018 Dec 24;10:53. doi: 10.1186/s13099-018-0279-0. eCollection 2018. PMID: 30603048; PMCID: PMC6304783.
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β.

Oncogenesis

Lucido CT, Callejas-Valera JL, Colbert PL, Vermeer DW, Miskimins WK, Spanos WC, Vermeer PD.
PMID: 30297705
Oncogenesis. 2018 Oct 08;7(10):81. doi: 10.1038/s41389-018-0090-2.

The incidence of human papillomavirus-associated head and neck squamous cell carcinoma (HPV[ + ] HNSCC) is rapidly increasing. Although clinical management of primary HPV( + ) HNSCC is relatively successful, disease progression, including recurrence and metastasis, is often fatal....

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Lucido CT, Callejas-Valera JL, Colbert PL, et al. β. Oncogenesis. 2018;7(10):81doi: 10.1038/s41389-018-0090-2.
Lucido, C. T., Callejas-Valera, J. L., Colbert, P. L., Vermeer, D. W., Miskimins, W. K., Spanos, W. C., & Vermeer, P. D. (2018). β. Oncogenesis, 7(10), 81. https://doi.org/10.1038/s41389-018-0090-2
Lucido, Christopher T, et al. "β." Oncogenesis vol. 7,10 (2018): 81. doi: https://doi.org/10.1038/s41389-018-0090-2
Lucido CT, Callejas-Valera JL, Colbert PL, Vermeer DW, Miskimins WK, Spanos WC, Vermeer PD. β. Oncogenesis. 2018 Oct 08;7(10):81. doi: 10.1038/s41389-018-0090-2. PMID: 30297705; PMCID: PMC6175933.
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Lactate induces PD-L1 in HRAS.

Oncotarget

Verma AK, Messerli SM, Miskimins WK.
PMID: 32391119
Oncotarget. 2020 Apr 28;11(17):1493-1504. doi: 10.18632/oncotarget.27348. eCollection 2020 Apr 28.

Intratumoral lactate production negatively correlates with survival and tumor clearance in the setting of human papillomavirus positive oropharyngeal squamous cell carcinoma (HPV-positive OPSCC). Robust anti-tumor immune activity is required for tumor clearance in human patients and animal models of...

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Verma AK, Messerli SM, Miskimins WK. Lactate induces PD-L1 in HRAS. Oncotarget. 2020;11(17):1493-1504doi: 10.18632/oncotarget.27348.
Verma, A. K., Messerli, S. M., & Miskimins, W. K. (2020). Lactate induces PD-L1 in HRAS. Oncotarget, 11(17), 1493-1504. https://doi.org/10.18632/oncotarget.27348
Verma, Alexander K, et al. "Lactate induces PD-L1 in HRAS." Oncotarget vol. 11,17 (2020): 1493-1504. doi: https://doi.org/10.18632/oncotarget.27348
Verma AK, Messerli SM, Miskimins WK. Lactate induces PD-L1 in HRAS. Oncotarget. 2020 Apr 28;11(17):1493-1504. doi: 10.18632/oncotarget.27348. eCollection 2020 Apr 28. PMID: 32391119; PMCID: PMC7197448.
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Erratum to "Inhibition of cancer migration and invasion by knocking down delta-5-desaturase in COX-2 overexpressed cancer cells" [Redox Biol. 11 (2017) 653-662].

Redox biology

Yang X, Xu Y, Wang T, Shu D, Guo P, Miskimins K, Qian SY.
PMID: 28410935
Redox Biol. 2017 Aug;12:1062. doi: 10.1016/j.redox.2017.03.021. Epub 2017 Apr 12.

No abstract available.

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Yang X, Xu Y, Wang T, et al. Erratum to "Inhibition of cancer migration and invasion by knocking down delta-5-desaturase in COX-2 overexpressed cancer cells" [Redox Biol. 11 (2017) 653-662]. Redox Biol. 2017;12:1062doi: 10.1016/j.redox.2017.03.021.
Yang, X., Xu, Y., Wang, T., Shu, D., Guo, P., Miskimins, K., & Qian, S. Y. (2017). Erratum to "Inhibition of cancer migration and invasion by knocking down delta-5-desaturase in COX-2 overexpressed cancer cells" [Redox Biol. 11 (2017) 653-662]. Redox biology, 121062. https://doi.org/10.1016/j.redox.2017.03.021
Yang, Xiaoyu, et al. "Erratum to "Inhibition of cancer migration and invasion by knocking down delta-5-desaturase in COX-2 overexpressed cancer cells" [Redox Biol. 11 (2017) 653-662]." Redox biology vol. 12 (2017): 1062. doi: https://doi.org/10.1016/j.redox.2017.03.021
Yang X, Xu Y, Wang T, Shu D, Guo P, Miskimins K, Qian SY. Erratum to "Inhibition of cancer migration and invasion by knocking down delta-5-desaturase in COX-2 overexpressed cancer cells" [Redox Biol. 11 (2017) 653-662]. Redox Biol. 2017 Aug;12:1062. doi: 10.1016/j.redox.2017.03.021. Epub 2017 Apr 12. PMID: 28410935; PMCID: PMC5975204.
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Propranolol Promotes Glucose Dependence and Synergizes with Dichloroacetate for Anti-Cancer Activity in HNSCC.

Cancers

Lucido CT, Miskimins WK, Vermeer PD.
PMID: 30513596
Cancers (Basel). 2018 Nov 30;10(12). doi: 10.3390/cancers10120476.

Tumor cell metabolism differs from that of normal cells, conferring tumors with metabolic advantages but affording opportunities for therapeutic intervention. Accordingly, metabolism-targeting therapies have shown promise. However, drugs targeting singular metabolic pathways display limited efficacy, in part due to...

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Lucido CT, Miskimins WK, Vermeer PD. Propranolol Promotes Glucose Dependence and Synergizes with Dichloroacetate for Anti-Cancer Activity in HNSCC. Cancers (Basel). 2018;10(12)doi: 10.3390/cancers10120476.
Lucido, C. T., Miskimins, W. K., & Vermeer, P. D. (2018). Propranolol Promotes Glucose Dependence and Synergizes with Dichloroacetate for Anti-Cancer Activity in HNSCC. Cancers, 10(12), . https://doi.org/10.3390/cancers10120476
Lucido, Christopher T, et al. "Propranolol Promotes Glucose Dependence and Synergizes with Dichloroacetate for Anti-Cancer Activity in HNSCC." Cancers vol. 10,12 (2018). doi: https://doi.org/10.3390/cancers10120476
Lucido CT, Miskimins WK, Vermeer PD. Propranolol Promotes Glucose Dependence and Synergizes with Dichloroacetate for Anti-Cancer Activity in HNSCC. Cancers (Basel). 2018 Nov 30;10(12). doi: 10.3390/cancers10120476. PMID: 30513596; PMCID: PMC6316475.
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The major transcription initiation site of the p27Kip1 gene is conserved in human and mouse and produces a long 5'-UTR.

BMC molecular biology

Coleman J, Hawkinson M, Miskimins R, Miskimins WK.
PMID: 11696240
BMC Mol Biol. 2001;2:12. doi: 10.1186/1471-2199-2-12. Epub 2001 Oct 11.

BACKGROUND: The cyclin-dependent kinase inhibitor p27Kip1 is essential for proper control of cell cycle progression. The levels of p27Kip1 are regulated by several mechanisms including transcriptional and translational controls. In order to delineate the molecular details of these regulatory...

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Coleman J, Hawkinson M, Miskimins R, et al. The major transcription initiation site of the p27Kip1 gene is conserved in human and mouse and produces a long 5'-UTR. BMC Mol Biol. 2001;2:12doi: 10.1186/1471-2199-2-12.
Coleman, J., Hawkinson, M., Miskimins, R., & Miskimins, W. K. (2001). The major transcription initiation site of the p27Kip1 gene is conserved in human and mouse and produces a long 5'-UTR. BMC molecular biology, 212. https://doi.org/10.1186/1471-2199-2-12
Coleman, J, et al. "The major transcription initiation site of the p27Kip1 gene is conserved in human and mouse and produces a long 5'-UTR." BMC molecular biology vol. 2 (2001): 12. doi: https://doi.org/10.1186/1471-2199-2-12
Coleman J, Hawkinson M, Miskimins R, Miskimins WK. The major transcription initiation site of the p27Kip1 gene is conserved in human and mouse and produces a long 5'-UTR. BMC Mol Biol. 2001;2:12. doi: 10.1186/1471-2199-2-12. Epub 2001 Oct 11. PMID: 11696240; PMCID: PMC59625.
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Expression of constitutively active 4EBP-1 enhances p27Kip1 expression and inhibits proliferation of MCF7 breast cancer cells.

Cancer cell international

Jiang H, Coleman J, Miskimins R, Miskimins WK.
PMID: 12633504
Cancer Cell Int. 2003 Feb 18;3(1):2. doi: 10.1186/1475-2867-3-2.

BACKGROUND: Eukaryotic initiation factor 4E (eIF4E) is essential for cap-dependent initiation of translation. Cell proliferation is associated with increased activity of eIF4E and elevated expression of eIF4E leads to tumorigenic transformation. Many tumors express very high levels of eIF4E...

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Jiang H, Coleman J, Miskimins R, et al. Expression of constitutively active 4EBP-1 enhances p27Kip1 expression and inhibits proliferation of MCF7 breast cancer cells. Cancer Cell Int. 2003;3(1):2doi: 10.1186/1475-2867-3-2.
Jiang, H., Coleman, J., Miskimins, R., & Miskimins, W. K. (2003). Expression of constitutively active 4EBP-1 enhances p27Kip1 expression and inhibits proliferation of MCF7 breast cancer cells. Cancer cell international, 3(1), 2. https://doi.org/10.1186/1475-2867-3-2
Jiang, Hong, et al. "Expression of constitutively active 4EBP-1 enhances p27Kip1 expression and inhibits proliferation of MCF7 breast cancer cells." Cancer cell international vol. 3,1 (2003): 2. doi: https://doi.org/10.1186/1475-2867-3-2
Jiang H, Coleman J, Miskimins R, Miskimins WK. Expression of constitutively active 4EBP-1 enhances p27Kip1 expression and inhibits proliferation of MCF7 breast cancer cells. Cancer Cell Int. 2003 Feb 18;3(1):2. doi: 10.1186/1475-2867-3-2. PMID: 12633504; PMCID: PMC151675.
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Use of Antimetastatic SOD3-Mimetic Albumin as a Primer in Triple Negative Breast Cancer.

Journal of oncology

Messerli SM, Schaefer AM, Zhuang Y, Soltys BJ, Keime N, Jin J, Ma L, Hsia CJC, Miskimins WK.
PMID: 30941174
J Oncol. 2019 Feb 28;2019:3253696. doi: 10.1155/2019/3253696. eCollection 2019.

Of the deaths attributed to cancer, 90% are due to metastasis. Treatments that prevent or cure metastasis remain elusive. Low expression of extracellular superoxide dismutase (EcSOD or SOD3) has been associated with poor outcomes and increased metastatic potential in...

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Messerli SM, Schaefer AM, Zhuang Y, et al. Use of Antimetastatic SOD3-Mimetic Albumin as a Primer in Triple Negative Breast Cancer. J Oncol. 2019;2019:3253696doi: 10.1155/2019/3253696.
Messerli, S. M., Schaefer, A. M., Zhuang, Y., Soltys, B. J., Keime, N., Jin, J., Ma, L., Hsia, C. J. C., & Miskimins, W. K. (2019). Use of Antimetastatic SOD3-Mimetic Albumin as a Primer in Triple Negative Breast Cancer. Journal of oncology, 20193253696. https://doi.org/10.1155/2019/3253696
Messerli, Shanta M, et al. "Use of Antimetastatic SOD3-Mimetic Albumin as a Primer in Triple Negative Breast Cancer." Journal of oncology vol. 2019 (2019): 3253696. doi: https://doi.org/10.1155/2019/3253696
Messerli SM, Schaefer AM, Zhuang Y, Soltys BJ, Keime N, Jin J, Ma L, Hsia CJC, Miskimins WK. Use of Antimetastatic SOD3-Mimetic Albumin as a Primer in Triple Negative Breast Cancer. J Oncol. 2019 Feb 28;2019:3253696. doi: 10.1155/2019/3253696. eCollection 2019. PMID: 30941174; PMCID: PMC6420975.
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Self-concept and psychiatric symptomatology.

Journal of clinical psychology

Miskimins RW, Wilson LT, Braucht GN, Berry KL.
PMID: 5542462
J Clin Psychol. 1971 Apr;27(2):185-7. doi: 10.1002/1097-4679(197104)27:2<185::aid-jclp2270270207>3.0.co;2-u.

No abstract available.

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Miskimins RW, Wilson LT, Braucht GN, et al. Self-concept and psychiatric symptomatology. J Clin Psychol. 1971;27(2):185-7doi: 10.1002/1097-4679(197104)27:2<185::aid-jclp2270270207>3.0.co;2-u.
Miskimins, R. W., Wilson, L. T., Braucht, G. N., & Berry, K. L. (1971). Self-concept and psychiatric symptomatology. Journal of clinical psychology, 27(2), 185-7. https://doi.org/10.1002/1097-4679(197104)27:2<185::aid-jclp2270270207>3.0.co;2-u
Miskimins, R W, et al. "Self-concept and psychiatric symptomatology." Journal of clinical psychology vol. 27,2 (1971): 185-7. doi: https://doi.org/10.1002/1097-4679(197104)27:2<185::aid-jclp2270270207>3.0.co;2-u
Miskimins RW, Wilson LT, Braucht GN, Berry KL. Self-concept and psychiatric symptomatology. J Clin Psychol. 1971 Apr;27(2):185-7. doi: 10.1002/1097-4679(197104)27:2<185::aid-jclp2270270207>3.0.co;2-u. PMID: 5542462.
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Cell cycle arrest in Metformin treated breast cancer cells involves activation of AMPK, downregulation of cyclin D1, and requires p27Kip1 or p21Cip1.

Journal of molecular signaling

Zhuang Y, Miskimins WK.
PMID: 19046439
J Mol Signal. 2008 Dec 01;3:18. doi: 10.1186/1750-2187-3-18.

BACKGROUND: The antihyperglycemic drug metformin may have beneficial effects on the prevention and treatment of cancer. Metformin is known to activate AMP-activated protein kinase (AMPK). It has also been shown to inhibit cyclin D1 expression and proliferation of some...

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Zhuang Y, Miskimins WK. Cell cycle arrest in Metformin treated breast cancer cells involves activation of AMPK, downregulation of cyclin D1, and requires p27Kip1 or p21Cip1. J Mol Signal. 2008;3:18doi: 10.1186/1750-2187-3-18.
Zhuang, Y., & Miskimins, W. K. (2008). Cell cycle arrest in Metformin treated breast cancer cells involves activation of AMPK, downregulation of cyclin D1, and requires p27Kip1 or p21Cip1. Journal of molecular signaling, 318. https://doi.org/10.1186/1750-2187-3-18
Zhuang, Yongxian, and Miskimins, W Keith. "Cell cycle arrest in Metformin treated breast cancer cells involves activation of AMPK, downregulation of cyclin D1, and requires p27Kip1 or p21Cip1." Journal of molecular signaling vol. 3 (2008): 18. doi: https://doi.org/10.1186/1750-2187-3-18
Zhuang Y, Miskimins WK. Cell cycle arrest in Metformin treated breast cancer cells involves activation of AMPK, downregulation of cyclin D1, and requires p27Kip1 or p21Cip1. J Mol Signal. 2008 Dec 01;3:18. doi: 10.1186/1750-2187-3-18. PMID: 19046439; PMCID: PMC2613390.
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Showing 1 to 12 of 14 entries