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  • 1
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    Online Resource
    Myocardial Cobalt Levels Are Elevated in the Setting of Total Hip Arthroplasty
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Journal of Bone and Joint Surgery Vol. 99, No. 22 ( 2017-11-15), p. e118-
    Details
    In: Journal of Bone and Joint Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 99, No. 22 ( 2017-11-15), p. e118-
    Abstract: Arthroplasty implants commonly contain elemental metal that may undergo wear-related release. Recently, cases of hip implant-associated myocardial injury have been reported. However, we are not aware of any previous study that has systematically measured myocardial metal levels or examined the relationship with total hip arthroplasty (THA). Methods: Archives of our institution were queried for autopsies of individuals who had undergone THA between 1990 and 2013. Myocardial tissue samples were analyzed for cobalt (Co) and chromium (Cr) levels with inductively coupled plasma mass spectroscopy. Seventy-five Co/Cr-on-polyethylene THA cases were included (mean age at time of death = 77.4 years; 49% women) as were 73 non-arthroplasty controls matched for age, sex, and history of hypertension and diabetes mellitus. Results: Significantly higher median myocardial concentrations of Co were observed in individuals with THA compared with controls (0.12 versus 0.06 μg/g, p 〈 0.0001). The median Co concentration was 69% higher in patients who had undergone THA revision (0.169 μg/g) than in those who underwent primary THA (0.100 μg/g; p = 0.004). In general, higher Co levels were observed in those with multiple replaced joints, although this finding only trended toward significance. Cardiomegaly, interstitial fibrosis, and decreased ejection fraction were observed more frequently in the postmortem samples of patients with implants than in those of controls (p = 0.0002, 0.044, and 0.0039, respectively). Conclusions: We believe this to be the first study to quantify metal levels in cardiac tissue in patients with and without joint replacement. The elevated Co levels, in concert with cardiomegaly and increased interstitial fibrosis found during autopsy, in the arthroplasty cohort are novel, important findings. Although Co levels were significantly elevated above those in controls, the majority were below those seen in clinical case reports of death from Co cardiotoxicity associated with metal-on-metal prostheses. Level of Evidence: Therapeutic Level III . See Instructions for Authors for a complete description of levels of evidence.
    Type of Medium: Online Resource
    ISSN: 0021-9355 , 1535-1386
    URL: Article
    DOI: 10.2106/JBJS.17.00159
    RVK:
    XA 52200.A
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
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  • 2
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    Eosinophilic myocarditis: Case report and brief review of the literature
    Elsevier BV ; 2023
    In:  Radiology Case Reports Vol. 18, No. 1 ( 2023-01), p. 306-311
    Details
    In: Radiology Case Reports, Elsevier BV, Vol. 18, No. 1 ( 2023-01), p. 306-311
    Type of Medium: Online Resource
    ISSN: 1930-0433
    URL: Article
    DOI: 10.1016/j.radcr.2022.10.036
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 2406300-9
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  • 3
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    Effects of central sodium on epithelial sodium channels in rat brain
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 299, No. 1 ( 2010-07), p. R222-R233
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 299, No. 1 ( 2010-07), p. R222-R233
    Abstract: We evaluated the effects of intracerebroventricular (icv) infusion of Na + -rich artificial cerebrospinal fluid (aCSF), with or without the mineralocorticoid receptor (MR) blocker spironolactone, on epithelial Na + channel (ENaC) subunits and regulators, such as MR, serum/glucocorticoid-inducible kinase 1, neural precursor cells expressed developmentally downregulated 4-like gene, 11β-hydroxylase, and aldosterone synthase, in brain regions of Wistar rats. The effects of icv infusion of the amiloride analog benzamil on brain tissue and CSF Na + concentration ([Na + ]) were also assessed. In the choroid plexus and ependyma of the anteroventral third ventricle, ENaC subunits are present in apical and basal membranes. Na + -rich aCSF increased β-ENaC mRNA and immunoreactivity in the choroid plexus and increased α- and β-ENaC immunoreactivities in the ependyma. Na + -rich aCSF increased α- and β-ENaC-gold-labeled particles in the microvilli of the choroid plexus and in basolateral membranes of the ependyma. Spironolactone only prevented the increase in β-ENaC immunoreactivity in the choroid plexus and ependyma. In the supraoptic nucleus, paraventricular nucleus, and subfornical organ, Na + -rich aCSF did not affect mRNA expression levels of the studied genes. Benzamil significantly increased CSF [Na + ] in the control, but not Na + -rich, aCSF group. In contrast, benzamil prevented the increase in hypothalamic tissue [Na + ] by Na + -rich aCSF. These results suggest that CSF Na + upregulates ENaC expression in the brain epithelia, but not in the neurons of hypothalamic nuclei. ENaC in the choroid plexus and ependyma appear to contribute to regulation of Na + homeostasis in the brain.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00834.2009
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 4
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    Abstract 3171: Expression of PKC iota in breast cancer
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 3171-3171
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 3171-3171
    Abstract: One in nine (11%) women is expected to develop breast cancer during their lifetime. Abnormal activation of the PI3K signaling cascade is common in breast cancer. The p110α catalytic subunit of PI3K is mutated in 20-40% of breast cancers. The two most common mutations are E545K in the helical domain and H1047R in the kinase domain; these mutations render PI3K constitutively active. PKC iota is a member of atypical class of PKC family serine/threonine kinases and a downstream effector in the PI3K signaling pathway. PKC iota has been implicated in carcinogenesis and oncogenic signaling in lung, colon and ovarian carcinomas but its role in breast cancer progression is unknown. Using immunohistochemistry (IHC), we have evaluated PKCι expression and localization in breast cancer tissue microarrays (TMA). Weak PKCι staining was detected in normal breast tissue. PKCι was over-expressed in subset of breast cancers with no staining in the surrounding stroma. Positive tumor staining was mainly cytoplasmic with nuclear staining in some cases. There was no significant correlation of positive PKCι staining with tumour type. PKCι overexpression was also seen in a subset of ductal carcinoma in situ samples. In vitro, we have also shown that PKCι is over-expressed and has higher levels of phosphorylation in a subset of breast cancer cell lines when compared to mammary epithelial cell lines. Stable cell lines expressing E545K or H1047R mutations were generated in the mammary myoepithelial cell line MCF-10A by retroviral transduction. Using Western blotting, we have shown that these mutations are sufficient to increase PKCι expression and activation. These results suggest a possible mechanism for the PKCι overexpression previously demonstrated by IHC. Two structurally independent PI3K inhibitors, Wortmannin and LY294-002, inhibited PKCι phosphorylation and activation in mutant PI3K expressing cells, confirming that the PKCι activation is PI3K-dependent. These inhibitors did not inhibit the low level of PKCι activation seen in MCF10A cells expressing wild-type PI3K control, suggesting that this activation occurs by a PI3K-independent mechanism. These results demonstrate that PKCι is overexpressed in some breast cancers, and that PI3KCA mutations may drive this overexpression. These results also indicate a potential role for PKCι in breast carcinogenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3171.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-3171
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 5
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    Clinical, biopsy, and mass spectrometry findings of renal gelsolin amyloidosis
    Elsevier BV ; 2017
    In:  Kidney International Vol. 91, No. 4 ( 2017-04), p. 964-971
    Details
    In: Kidney International, Elsevier BV, Vol. 91, No. 4 ( 2017-04), p. 964-971
    Type of Medium: Online Resource
    ISSN: 0085-2538
    URL: Article
    DOI: 10.1016/j.kint.2016.11.017
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
    detail.hit.zdb_id: 2007940-0
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  • 6
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    Effects of Central Sodium On Epithelial Sodium Channels (ENaC) Expression In Rat Brain
    Wiley ; 2008
    In:  The FASEB Journal Vol. 22, No. S1 ( 2008-03)
    Details
    In: The FASEB Journal, Wiley, Vol. 22, No. S1 ( 2008-03)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v22.S1
    DOI: 10.1096/fasebj.22.1_supplement.934.11
    Language: English
    Publisher: Wiley
    Publication Date: 2008
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 7
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    Abstract 1224: Repression of cancer cell senescence by PKCι
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 1224-1224
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 1224-1224
    Abstract: Senescence is an irreversible growth arrest phenotype adopted by cells that has a key role in protecting organisms from cancer. There is now considerable interest in therapeutic strategies that reactivate this process to control the growth of cancer cells. Protein kinase C iota (PKCι) is a member of the atypical protein kinase C family and an important downstream mediator in the phosphoinositide pathway. PKCι expression was found to be upregulated in a subset of breast cancers and breast cancer cell lines. Introduction of mutant, oncogenic PIK3CA, but not wild-type PIK3CA, into breast mammary epithelial cells increased both the expression and activation of PKCι. In breast cancer cell lines overexpressing PKCι, depletion of PKCι increased the number of senescent cells, as assessed by senescence-associated β-galactosidase, morphology and bromodeoxyuridine incorporation. This phenomenon was not restricted to breast cancer cells, as it was also seen in glioblastoma cells. Senescence induction did not require p53, p16 or Arf and was not associated with activation of the DNA damage response. Depletion of PKCι had no effect on senescence in normal mammary epithelial cell lines. We conclude that PKCι is overexpressed in a subset of cancers where it functions to suppress premature senescence. This function appears to be restricted to cancer cells and inhibition of PKCι may therefore be an effective way to selectively activate premature senescence in cancer cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1224. doi:10.1158/1538-7445.AM2011-1224
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-1224
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
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    SARS-CoV-2 Delta variant induces enhanced pathology and inflammatory responses in K18-hACE2 mice
    Public Library of Science (PLoS) ; 2022
    In:  PLOS ONE Vol. 17, No. 8 ( 2022-8-29), p. e0273430-
    Details
    In: PLOS ONE, Public Library of Science (PLoS), Vol. 17, No. 8 ( 2022-8-29), p. e0273430-
    Abstract: The COVID-19 pandemic has been fueled by SARS-CoV-2 novel variants of concern (VOC) that have increased transmissibility, receptor binding affinity, and other properties that enhance disease. The goal of this study is to characterize unique pathogenesis of the Delta VOC strain in the K18-hACE2-mouse challenge model. Challenge studies suggested that the lethal dose of Delta was higher than Alpha or Beta strains. To characterize the differences in the Delta strain’s pathogenesis, a time-course experiment was performed to evaluate the overall host response to Alpha or Delta variant challenge. qRT-PCR analysis of Alpha- or Delta-challenged mice revealed no significant difference between viral RNA burden in the lung, nasal wash or brain. However, histopathological analysis revealed high lung tissue inflammation and cell infiltration following Delta- but not Alpha-challenge at day 6. Additionally, pro-inflammatory cytokines were highest at day 6 in Delta-challenged mice suggesting enhanced pneumonia. Total RNA-sequencing analysis of lungs comparing challenged to no challenge mice revealed that Alpha-challenged mice have more total genes differentially activated. Conversely, Delta-challenged mice have a higher magnitude of differential gene expression. Delta-challenged mice have increased interferon-dependent gene expression and IFN-γ production compared to Alpha. Analysis of TCR clonotypes suggested that Delta challenged mice have increased T-cell infiltration compared to Alpha challenged. Our data suggest that Delta has evolved to engage interferon responses in a manner that may enhance pathogenesis. The in vivo and in silico observations of this study underscore the need to conduct experiments with VOC strains to best model COVID-19 when evaluating therapeutics and vaccines.
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
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    DOI: 10.1371/journal.pone.0273430
    DOI: 10.1371/journal.pone.0273430.g001
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    DOI: 10.1371/journal.pone.0273430.s006
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2022
    detail.hit.zdb_id: 2267670-3
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  • 9
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    The central role of the brain in salt-sensitive hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2006
    In:  Current Opinion in Cardiology Vol. 21, No. 4 ( 2006-07), p. 295-304
    Details
    In: Current Opinion in Cardiology, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 4 ( 2006-07), p. 295-304
    Type of Medium: Online Resource
    ISSN: 0268-4705
    URL: Article
    DOI: 10.1097/01.hco.0000231398.64362.94
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2006
    detail.hit.zdb_id: 2026894-4
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  • 10
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    Distribution of epithelial sodium channels and mineralocorticoid receptors in cardiovascular regulatory centers in rat brain
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 289, No. 6 ( 2005-12), p. R1787-R1797
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 289, No. 6 ( 2005-12), p. R1787-R1797
    Abstract: Epithelial sodium channels (ENaC) are important for regulating sodium transport across epithelia. Functional studies indicate that neural mechanisms acting through mineralocorticoid receptors (MR) and sodium channels (presumably ENaC) are crucial to the development of sympathoexcitation and hypertension in experimental models of salt-sensitive hypertension. However, expression and localization of the ENaC in cardiovascular regulatory centers of the brain have not yet been studied. RT-PCR and immunohistochemistry were performed to study ENaC and MR expression at the mRNA and protein levels, respectively. Both mRNA and protein for α-, β-, and γ-ENaC subunits and MR were found to be expressed in the rat brain. All three ENaC subunits and MR were present in the supraoptic nucleus, magnocellular paraventricular nucleus, hippocampus, choroid plexus, ependyma, and brain blood vessels, suggesting the presence of multimeric channels and possible regulation by mineralocorticoids. In most cortical areas, thalamus, amygdala, and suprachiasmatic nucleus, notable expression of γ-ENaC was undetectable, whereas α- and β-ENaC were abundantly expressed pointing to the possibility of a heterogeneous population of channels. The findings suggest that stoichiometrically different populations of ENaC may be present in both epithelial and neural components in the brain, which may contribute to regulation of cerebrospinal fluid and interstitial Na + concentration as well as neuronal excitation.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00063.2005
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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