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Article ; Online: L-type calcium channel antagonist isradipine age-dependently decreases plaque associated dystrophic neurites in 5XFAD mouse model.

Wickline, Jessica L / Smith, Sabrina / Shin, Riley / Odfalk, Kristian / Sanchez, Jesse / Javors, Martin / Ginsburg, Brett / Hopp, Sarah C

Neuropharmacology

2023 Volume 227, Page(s) 109454

Abstract: Epidemiological studies suggest that L-type calcium channel (LTCC) antagonists may reduce the incidence of age-associated neurodegenerative diseases including Alzheimer's disease (AD). However, the neuroprotective mechanism of LTCC antagonists is unknown. ...

Abstract	Epidemiological studies suggest that L-type calcium channel (LTCC) antagonists may reduce the incidence of age-associated neurodegenerative diseases including Alzheimer's disease (AD). However, the neuroprotective mechanism of LTCC antagonists is unknown. Amyloid-β (Aβ) pathology disrupts intracellular calcium signaling, which regulates lysosomes and microglial responses. Neurons near Aβ plaques develop dystrophic neurites, which are abnormal swellings that accumulate lysosomes. Further, microglia accumulate around Aβ plaques and secrete inflammatory cytokines. We hypothesized that antagonism of LTCCs with isradipine would reduce Aβ plaque-associated dystrophic neurites and inflammatory microglia in the 5XFAD mouse model by restoring normal intracellular calcium regulation. To test this hypothesis, we treated 6- and 9-month-old 5XFAD mice with isradipine and tested behavior, examined Aβ plaques, microglia, and dystrophic neurites. We found that isradipine treatment age-dependently reduces dystrophic neurites and leads to trending decreases in Aβ but does not modulate plaque associated microglia regardless of age. Our findings provide insight into how antagonizing LTCCs alters specific cell types in the Aβ plaque environment, providing valuable information for potential treatment targets in future AD studies.
MeSH term(s)	Mice ; Animals ; Amyloid beta-Protein Precursor/metabolism ; Neurites/metabolism ; Calcium Channel Blockers ; Calcium Channels, L-Type/metabolism ; Isradipine/metabolism ; Mice, Transgenic ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Microglia/metabolism ; Plaque, Amyloid/metabolism ; Disease Models, Animal
Chemical Substances	Amyloid beta-Protein Precursor ; Calcium Channel Blockers ; Calcium Channels, L-Type ; Isradipine (YO1UK1S598) ; Amyloid beta-Peptides
Language	English
Publishing date	2023-02-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2023.109454
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Article: Ground zero: a radiologist's perspective.

Javors, B R

Radiology

2001 Volume 221, Issue 3, Page(s) 581–582

MeSH term(s)	Disaster Planning ; Hospital Administration ; Hospitals ; Humans ; Interinstitutional Relations ; New York City ; Radiology Department, Hospital/organization & administration ; Terrorism ; Wounds and Injuries/therapy
Language	English
Publishing date	2001-12
Publishing country	United States
Document type	Editorial
ZDB-ID	80324-8
ISSN	1527-1315 ; 0033-8419
ISSN (online)	1527-1315
ISSN	0033-8419
DOI	10.1148/radiol.2213011618
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Article: Tortuosity of the splenic artery.

Javors, B R

Abdominal imaging

1999 Volume 24, Issue 3, Page(s) 313–314

MeSH term(s)	Adult ; Humans ; Splenic Artery/anatomy & histology ; Splenic Artery/embryology
Language	English
Publishing date	1999-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	1144553-1
ISSN	1432-0509 ; 0942-8925
ISSN (online)	1432-0509
ISSN	0942-8925
DOI	10.1007/s002619900504
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Article: Gas lock obstruction of the colon, or bursting the bubble.

Javors, B R

AJR. American journal of roentgenology

1999 Volume 172, Issue 6, Page(s) 1691

MeSH term(s)	Colon/physiopathology ; Colonic Pseudo-Obstruction/physiopathology ; Dilatation, Pathologic/physiopathology ; Gases ; Humans ; Posture/physiology
Chemical Substances	Gases
Language	English
Publishing date	1999-06
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	82076-3
ISSN	1546-3141 ; 0361-803X ; 0092-5381
ISSN (online)	1546-3141
ISSN	0361-803X ; 0092-5381
DOI	10.2214/ajr.172.6.10350318
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Article ; Online: San Antonio Nathan Shock Center: your one-stop shop for aging research.

Salmon, Adam B / Nelson, James F / Gelfond, Jonathan A L / Javors, Martin / Ginsburg, Brett / Lopez-Cruzan, Marisa / Galvan, Veronica / Fernandez, Elizabeth / Musi, Nicolas / Ikeno, Yuji / Hubbard, Gene / Lechleiter, James / Hornsby, Peter J / Strong, Randy

GeroScience

2021 Volume 43, Issue 5, Page(s) 2105–2118

Abstract: With evolving cores, enrichment and training programs, and supported research projects, the San Antonio (SA) Nathan Shock Center has for 26 years provided critical support to investigators locally, nationally, and abroad. With its existing and growing ... ...

Abstract	With evolving cores, enrichment and training programs, and supported research projects, the San Antonio (SA) Nathan Shock Center has for 26 years provided critical support to investigators locally, nationally, and abroad. With its existing and growing intellectual capital, the SA Nathan Shock Center provides to local and external investigators an enhanced platform to conduct horizontally integrated (lifespan, healthspan, pathology, pharmacology) transformative research in the biology of aging, and serves as a springboard for advanced educational and training activities in aging research. The SA Nathan Shock Center consists of six cores: Administrative/Program Enrichment Core, Research Development Core, Aging Animal Models and Longevity Assessment Core, Pathology Core, Analytical Pharmacology and Drug Evaluation Core, and Integrated Physiology of Aging Core. The overarching goal of the SA Nathan Shock Center is to advance knowledge in the basic biology of aging and to identify molecular and cellular mechanisms that will facilitate the development of pharmacologic interventions and other strategies to extend healthy lifespan. In pursuit of this goal, we provide an innovative "one-stop shop" venue to accelerate transformative research in the biology of aging through our integrated research cores. Moreover, we aim to foster and promote career development of early-stage investigators in aging biology through our research development programs, to serve as a resource and partner to investigators from other Shock Centers, and to disseminate scientific knowledge and enhanced awareness about aging research. Overall, the SA Nathan Shock Center aims to be a leader in research that advances our understanding of the biology of aging and development of approaches to improve longevity and healthy aging.
MeSH term(s)	Aging ; Animals ; Geroscience ; Healthy Aging ; Longevity
Language	English
Publishing date	2021-07-09
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2886586-8
ISSN	2509-2723 ; 2509-2715
ISSN (online)	2509-2723
ISSN	2509-2715
DOI	10.1007/s11357-021-00417-y
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Article ; Online: Differences in pituitary-adrenal reactivity in Black and White men with and without alcohol use disorder.

Price, Julianne L / Frazier, Ian R / Lewis, Ben / Walker, Robrina / Javors, Martin A / Nixon, Sara Jo / Adinoff, Bryon

Psychoneuroendocrinology

2018 Volume 100, Page(s) 180–189

Abstract: Background: Treatment-seeking men with alcohol use disorder (AUD) classically exhibit a blunted hypothalamic-pituitary-adrenal (HPA) axis response to pharmacologic and behavioral provocations during the early phases of abstinence from alcohol. ... ...

Abstract	Background: Treatment-seeking men with alcohol use disorder (AUD) classically exhibit a blunted hypothalamic-pituitary-adrenal (HPA) axis response to pharmacologic and behavioral provocations during the early phases of abstinence from alcohol. Independent of alcohol, a significant muting of HPA axis reactivity is also observed among racial minority (e.g. Black) individuals. The effect of AUD upon the altered HPA axis response of racial minority individuals has not been explored. The current work represents a secondary analysis of race and AUD status among a sample of men. Methods: Healthy male controls (17 White, 7 Black) and four-to six-week abstinent men with AUD (49 White, 13 Black) were administered a psychosocial stressor and two pharmacologic probes [ovine corticotropin releasing hormone (oCRH) and cosyntropin] to assess HPA axis reactivity. Plasma cortisol and adrenocorticotropin hormone (ACTH) were assessed at 10-20 min intervals prior to and following behavioral and pharmacological stimulation. Basal and net-integrated responses following provocations were analyzed to identify potential group differences. A measure of childhood adversity was also obtained to consider the implications of prior stressors upon HPA axis function. Results: A three-fold increase in oCRH-induced ACTH was seen in Black men relative to White men regardless of AUD status. Adversity exerted a dampening effect on this pituitary sensitivity within Black controls only. Adjusted for adversity, a significant blunting effect of AUD status on ACTH reactivity was identified within White participants following oCRH. No group differences were present following cosyntropin administration. In response to the psychosocial stressor, White, but not Black, men with AUD experienced the expected blunting of cortisol reactivity relative to White controls. Rather, Black men with AUD exhibited greater cortisol reactivity relative to White men with AUD. Conclusions: Differences in HPA axis reactivity associated with race were present in men with and without AUD. Explanatory biological mechanisms of the relationship between alcohol use and/or stress, in both healthy and unhealthy populations, may require a reassessment in different racial populations.
MeSH term(s)	Adrenocorticotropic Hormone/blood ; Adult ; African Americans/psychology ; African Americans/statistics & numerical data ; Alcoholism/ethnology ; Alcoholism/metabolism ; Alcoholism/physiopathology ; Case-Control Studies ; European Continental Ancestry Group/psychology ; European Continental Ancestry Group/statistics & numerical data ; Humans ; Hydrocortisone/blood ; Hypothalamo-Hypophyseal System/metabolism ; Hypothalamo-Hypophyseal System/physiopathology ; Male ; Middle Aged ; Pituitary-Adrenal System/physiopathology ; Young Adult
Chemical Substances	Adrenocorticotropic Hormone (9002-60-2) ; Hydrocortisone (WI4X0X7BPJ)
Language	English
Publishing date	2018-10-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	197636-9
ISSN	1873-3360 ; 0306-4530
ISSN (online)	1873-3360
ISSN	0306-4530
DOI	10.1016/j.psyneuen.2018.10.004
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Article ; Online: Author Correction: MTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation.

Nature cell biology

2021 Volume 23, Issue 5, Page(s) 564–565

Language	English
Publishing date	2021-04-06
Publishing country	England
Document type	Published Erratum
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/s41556-021-00655-4
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Article ; Online: Lifespan benefits for the combination of rapamycin plus acarbose and for captopril in genetically heterogeneous mice.

Strong, Randy / Miller, Richard A / Cheng, Catherine J / Nelson, James F / Gelfond, Jonathan / Allani, Shailaja Kesaraju / Diaz, Vivian / Dorigatti, Angela Olsen / Dorigatti, Jonathan / Fernandez, Elizabeth / Galecki, Andrzej / Ginsburg, Brett / Hamilton, Karyn L / Javors, Martin A / Kornfeld, Kerry / Kaeberlein, Matt / Kumar, Suja / Lombard, David B / Lopez-Cruzan, Marisa /

Miller, Benjamin F / Rabinovitch, Peter / Reifsnyder, Peter / Rosenthal, Nadia A / Bogue, Molly A / Salmon, Adam B / Suh, Yousin / Verdin, Eric / Weissbach, Herbert / Newman, John / Maccchiarini, Francesca / Harrison, David E

Aging cell

2022 Volume 21, Issue 12, Page(s) e13724

Abstract: ... of (R/S)-1,3-butanediol (BD), captopril (Capt), leucine (Leu), the Nrf2-activating botanical mixture ...

Abstract	Mice bred in 2017 and entered into the C2017 cohort were tested for possible lifespan benefits of (R/S)-1,3-butanediol (BD), captopril (Capt), leucine (Leu), the Nrf2-activating botanical mixture PB125, sulindac, syringaresinol, or the combination of rapamycin and acarbose started at 9 or 16 months of age (RaAc9, RaAc16). In male mice, the combination of Rapa and Aca started at 9 months and led to a longer lifespan than in either of the two prior cohorts of mice treated with Rapa only, suggesting that this drug combination was more potent than either of its components used alone. In females, lifespan in mice receiving both drugs was neither higher nor lower than that seen previously in Rapa only, perhaps reflecting the limited survival benefits seen in prior cohorts of females receiving Aca alone. Capt led to a significant, though small (4% or 5%), increase in female lifespan. Capt also showed some possible benefits in male mice, but the interpretation was complicated by the unusually low survival of controls at one of the three test sites. BD seemed to produce a small (2%) increase in females, but only if the analysis included data from the site with unusually short-lived controls. None of the other 4 tested agents led to any lifespan benefit. The C2017 ITP dataset shows that combinations of anti-aging drugs may have effects that surpass the benefits produced by either drug used alone, and that additional studies of captopril, over a wider range of doses, are likely to be rewarding.
MeSH term(s)	Mice ; Male ; Female ; Animals ; Acarbose/pharmacology ; Sirolimus/pharmacology ; Captopril/pharmacology ; Longevity ; Aging
Chemical Substances	Acarbose (T58MSI464G) ; Sirolimus (W36ZG6FT64) ; Captopril (9G64RSX1XD)
Language	English
Publishing date	2022-09-30
Publishing country	England
Document type	Journal Article
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13724
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Article: A new sign of ascites.

Javors, B R

AJR. American journal of roentgenology

1991 Volume 156, Issue 6, Page(s) 1325

MeSH term(s)	Ascites/diagnostic imaging ; Fluoroscopy ; Humans ; Male ; Methylcellulose ; Middle Aged
Chemical Substances	Methylcellulose (9004-67-5)
Language	English
Publishing date	1991-06
Publishing country	United States
Document type	Case Reports ; Letter
ZDB-ID	82076-3
ISSN	1546-3141 ; 0361-803X ; 0092-5381
ISSN (online)	1546-3141
ISSN	0361-803X ; 0092-5381
DOI	10.2214/ajr.156.6.2028902
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Article ; Online: Rapamycin-mediated mouse lifespan extension: Late-life dosage regimes with sex-specific effects.

Strong, Randy / Miller, Richard A / Bogue, Molly / Fernandez, Elizabeth / Javors, Martin A / Libert, Sergiy / Marinez, Paul Anthony / Murphy, Michael P / Musi, Nicolas / Nelson, James F / Petrascheck, Michael / Reifsnyder, Peter / Richardson, Arlan / Salmon, Adam B / Macchiarini, Francesca / Harrison, David E

Aging cell

2020 Volume 19, Issue 11, Page(s) e13269

Abstract: To see if variations in timing of rapamycin (Rapa), administered to middle aged mice starting at 20 months, would lead to different survival outcomes, we compared three dosing regimens. Initiation of Rapa at 42 ppm increased survival significantly in ... ...

Abstract	To see if variations in timing of rapamycin (Rapa), administered to middle aged mice starting at 20 months, would lead to different survival outcomes, we compared three dosing regimens. Initiation of Rapa at 42 ppm increased survival significantly in both male and female mice. Exposure to Rapa for a 3-month period led to significant longevity benefit in males only. Protocols in which each month of Rapa treatment was followed by a month without Rapa exposure were also effective in both sexes, though this approach was less effective than continuous exposure in female mice. Interpretation of these results is made more complicated by unanticipated variation in patterns of weight gain, prior to the initiation of the Rapa treatment, presumably due to the use of drug-free food from two different suppliers. The experimental design included tests of four other drugs, minocycline, β-guanidinopropionic acid, MitoQ, and 17-dimethylaminoethylamino-17-demethoxygeldanamycin (17-DMAG), but none of these led to a change in survival in either sex.
MeSH term(s)	Animals ; Antibiotics, Antineoplastic/pharmacology ; Antibiotics, Antineoplastic/therapeutic use ; Female ; Longevity/drug effects ; Male ; Mice ; Sex Factors ; Sirolimus/pharmacology ; Sirolimus/therapeutic use
Chemical Substances	Antibiotics, Antineoplastic ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2020-11-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13269
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