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Institution

Southern Illinois University School of Medicine

EducationSpringfield, Illinois, United States
About: Southern Illinois University School of Medicine is a education organization based out in Springfield, Illinois, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 3747 authors who have published 5977 publications receiving 209115 citations. The organization is also known as: SIU School of Medicine.
Topics: Population, Cancer, Ototoxicity, Receptor, Health care


Papers
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Journal ArticleDOI
TL;DR: Progress is being made to elucidate the underlying mechanisms by which Rho GTPases activate the downstream signaling effectors, which are required for development of novel tumor therapeutic strategies targeting the R Ho GTPase signaling pathways to treat breast cancer.
Abstract: Small GTPase Rho signaling pathways regulate the growth, motility, invasion and metastasis of breast cancer cells. Aberrant Rho signaling, as results from alterations in the levels of Rho GTPase proteins, the status of activation, and the abundance of effector proteins, is found in breast cancers. Alterations of Rho signaling particularly impact the cytoskeleton, whose organization and reorganization underpin the motility of breast cancer cells during the invasive growth and metastasis of breast cancer. Progress is being made to elucidate the underlying mechanisms by which Rho GTPases activate the downstream signaling effectors. Further investigations are required for development of novel tumor therapeutic strategies targeting the Rho GTPase signaling pathways to treat breast cancer.

117 citations

Journal ArticleDOI
TL;DR: It is shown that the inferior colliculus was the most sensitive auditory center to the anticonvulsant action of 2-amino-7-phosphonoheptanoate and that imbalance between inhibitory and excitatory transmission within this brain structure may be crucial in the initiation of audiogenic seizures in the genetically epilepsy-prone rat.

117 citations

Journal ArticleDOI
TL;DR: Vascular function is abnormal in patients with Raynaud's phenomenon and Botox yielded a distinct improvement in perfusion and reduction in pain in patients failing conservative management, although its mechanism is unknown.
Abstract: Background:Treating patients with Raynaud's phenomenon who have chronic pain and ulcerations is extremely challenging. Unrelenting pain can lead to dysfunction and disuse, rendering the patient debilitated and/or chronically depressed. Pharmacologic vasodilators and surgical sympathectomies offer va

117 citations

Journal ArticleDOI
TL;DR: It is concluded that ginsenosides may release NO from endothelial cells, and enhance NO release from endotocyte cells elicited by other vasoactive substances and from perivascular nitrergic nerves in the corpus cavernosum.
Abstract: 1. Ginsenosides, the active ingredients extracted from Panax ginseng, have been shown to promote nitric oxide (NO) release in bovine aortic endothelial cells. Since the endothelial cells and the perivascular nerves in penile corpus cavernosum contain NO synthase and an NO-like substance has been shown to be released from these cells which relaxes corpus cavernosum, the possibility that ginsenosides may relax corpus cavernosum by releasing endogenous NO was examined. 2. With an in vitro tissue superfusion technique, ginsenosides (250, 500 and 750 micrograms ml-1) relaxed corpus cavernosum, concentration-dependently. 3. Using an in vitro tissue bath technique, acetylcholine (ACh)-induced relaxations were increased in the presence of ginsenosides (250 micrograms ml-1). 4. Ginsenosides at 100 micrograms ml-1 significantly enhanced the tetrodotoxin (TTX)-sensitive relaxation of corpus cavernosum elicited by transmural nerve stimulation. 5. The ginsenosides-induced, ACh-induced and ginsenosides-enhanced transmural nerve stimulation-elicited relaxations were significantly attenuated by NG-nitro-L-arginine (100 microM) and oxyhaemoglobin (oxyHb; 5-10 microM), and were enhanced by superoxide dismutase (SOD; 50 u ml-1). 6. The relaxations and their attenuation by NG-nitro-L-arginine and TTX were associated with increase and decrease in tissue cyclic GMP levels, respectively. 7. It is concluded that ginsenosides may release NO from endothelial cells, and enhance NO release from endothelial cells elicited by other vasoactive substances and from perivascular nitrergic nerves in the corpus cavernosum. These endothelial and neurogenic effects of ginsenosides in inducing relaxation of the corpus cavernosum may account for the aphrodisiac effect of Panax ginseng.

116 citations

Journal ArticleDOI
TL;DR: The results indicate that the absence of PRL reduces pituitary LH release, attenuates median eminence dopaminergic activity, and affects the growth of seminal vesicles and ventral prostate.
Abstract: Mice with a targeted disruption (knock-out) of the PRL gene (PRL-KO) were used to study the physiological role of PRL in the control of male neuroendocrine functions related to reproduction. Compared with normal males, PRL-KO mice had significant reductions in median eminence dopamine content, plasma LH levels, LH and FSH secretion in vitro (per mg pituitary), and weights of seminal vesicles and ventral prostate. PRL was not detectable in incubation medium with pituitaries from PRL-KO mice. No alterations were detected in PRL-KO mice in median eminence norepinephrine, plasma testosterone levels, or testosterone release (per mg testis) in vitro with or without LH. No differences were detected in PRL-KO vs. normal male mice in the interval from housing with normal female mice until conception, rate of pregnancy, or the number of live pups per litter. Pituitary weight in PRL-KO mice was increased (1.78 +/- 0.22 vs. 3.35 +/- 0.20 mg; P < 0.001), presumably due to reduced feedback inhibition and hypertrophy and/or hyperplasia of nonfunctional lactotrophs. These results indicate that the absence of PRL reduces pituitary LH release, attenuates median eminence dopaminergic activity, and affects the growth of seminal vesicles and ventral prostate. Although it was previously shown that PRL can repair the reproductive defect in male pituitary dwarf mice, our current results imply that the PRL deficiency alone is not sufficient to cause male infertility, although there are obvious alterations in reproductive neuroendocrine function in PRL-KO males.

116 citations


Authors

Showing all 3778 results

NameH-indexPapersCitations
Jatin P. Shah11972545680
Harold G. Koenig9967846742
Chawnshang Chang9753435629
Richard J. K. Taylor91154343893
Martin R. Farlow8238126820
David A. D'Alessio8027222955
Dirk R. Larson7927124067
Andrzej Bartke7851622865
Michael Brenner7656422010
Arnulf Stenzl7379123285
Wolfgang H. Dillmann7220017595
Michael Bonkowski6627913851
Jacob E. Friedman6519112485
Richard Salvi6544716289
Russell Noyes6322912790
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20237
202233
2021281
2020276
2019221
2018177