Correction NoticeErratum to: Successful use of early, repeat fecal microbiota transplantation for initial treatment of severe, refractory Clostridioides difficile colitis.
Successful use of early, repeat fecal microbiota transplantation for initial treatment of severe, refractory Clostridioides difficile colitis, Catherine M. Cappetto. Am J Health-Syst Pharm. 14 April 2021 (Case Report).
In the originally published version of this manuscript, the abstract included the following sentence: “A stool sample was collected and resulted positive via by both polymerase chain reaction and enzyme-linked immunosorbent assay for Clostridioides difficile.” This sentence has been corrected online to read: “A stool sample was collected and resulted positive for Clostridioides difficile by both polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA).”
Cappetto CM
American Journal of Health-system Pharmacy : AJHP
2021
2021-07-16
Journal Article
<table width="91" style="border-collapse:collapse;width:68pt;"><colgroup><col width="91" style="width:68pt;" /></colgroup><tbody><tr style="height:15pt;"><td width="91" height="20" class="xl18" style="width:68pt;height:15pt;"><a href="http://doi.org/10.1093/ajhp/zxab273">http://doi.org/10.1093/ajhp/zxab273</a></td>
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Characterization of vascular endothelial growth factor (VEGF) in the uterine cervix over pregnancy: effects of denervation and implications for cervical ripening.
Female; Animals; Immunohistochemistry; Pregnancy; Rats; Microcirculation; Phosphorylation; Down-Regulation; Enzyme-Linked Immunosorbent Assay; Reverse Transcriptase Polymerase Chain Reaction; Cervical Ripening/*metabolism; Cervix Uteri/blood supply/innervation/*metabolism; Denervation; Nitric Oxide Synthase Type III; Nitric Oxide Synthase/biosynthesis; Protein Isoforms/biosynthesis/metabolism; Protein-Serine-Threonine Kinases/biosynthesis; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins/biosynthesis; Vascular Endothelial Growth Factor A/biosynthesis/*metabolism; Vascular Endothelial Growth Factor Receptor-2/biosynthesis; Wistar; Animal/*metabolism
Bilateral neurectomy of the pelvic nerve (BLPN) that carries uterine cervix-related sensory nerves induces dystocia, and administration of its vasoactive neuropeptides induces changes in the cervical microvasculature, resembling those that occur in the ripening cervix. This study was designed to test the hypothesis that (a) the cervix of pregnant rats expresses vascular endothelial growth factor (VEGF) and components of the angiogenic signaling pathway [VEGF receptors (Flt-1, KDR), activity of protein kinase B, Akt (phosphorylated Akt), and endothelial nitric oxide synthase (eNOS)] and von Willebrand Factor (vWF) and that these molecules undergo changes with pregnancy, and (b) bilateral pelvic neurectomy (BLPN) alters levels of VEGF concentration in the cervix. Using RT-PCR and sequencing, two VEGF isoforms, 120 and 164, were identified in the rat cervix. VEGF, VEGF receptor-1 (Flt-1), eNOS, and vWF immunoreactivities (ir) were localized in the microvasculature of cervical stroma. Their protein levels increased during pregnancy but decreased to control levels by 2 days postpartum. VEGF receptor-2 (KDR)-ir was confined to the epithelium of the endocervix. BLPN downregulated levels of VEGF by a third. Therefore, the components of the angiogenic signaling pathway are expressed in the cervix and change over pregnancy. Furthermore, angiogenic and sensory neuronal factors may be important in regulating the dynamic microvasculature in the ripening cervix and may subsequently play a role in cervical ripening and the birth process.
Mowa C N; Jesmin S; Sakuma I; Usip S; Togashi H; Yoshioka M; Hattori Y; Papka R
The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
2004
2004-12
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1369/jhc.4A6455.2004" target="_blank" rel="noreferrer noopener">10.1369/jhc.4A6455.2004</a>
Endothelin-mediated in vivo pressor responses following TRPV1 activation.
*Blood Pressure/drug effects; *Vasoconstriction/drug effects; Adrenergic alpha-Agonists/administration & dosage; Analysis of Variance; Animal; Animals; Azepines/administration & dosage; Biphenyl Compounds/administration & dosage; Capsaicin/administration & dosage; Cells; Cultured; Diabetes Mellitus; Diabetic Angiopathies/genetics/*metabolism/physiopathology; Dipeptides/administration & dosage; Disease Models; Dose-Response Relationship; Drug; Endothelial Cells/metabolism; Endothelin A Receptor Antagonists; Endothelin A/metabolism; Endothelin B Receptor Antagonists; Endothelin B/metabolism; Endothelin-1/*metabolism; Enzyme-Linked Immunosorbent Assay; Femoral Artery/drug effects/*metabolism/physiopathology; Inbred C57BL; Indoles/administration & dosage; Infusions; Intravenous; Knockout; Male; Mice; Phenylephrine/administration & dosage; Receptor; TRPV Cation Channels/agonists/deficiency/genetics/*metabolism; Type 2/genetics/*metabolism/physiopathology; Vasoconstrictor Agents/administration & dosage
Transient receptor potential vanilliod 1 (TRPV1) channels have recently been postulated to play a role in the vascular complications/consequences associated with diabetes despite the fact that the mechanisms through which TRPV1 regulates vascular function are not fully known. Accordingly, our goal was to define the mechanisms by which TRPV1 channels modulate vascular function and contribute to vascular dysfunction in diabetes. We subjected mice lacking TRPV1 [TRPV1((-/-))], db/db, and control C57BLKS/J mice to in vivo infusion of the TRPV1 agonist capsaicin or the alpha-adrenergic agonist phenylephrine (PE) to examine the integrated circulatory actions of TRPV1. Capsaicin (1, 10, 20, and 100 mug/kg) dose dependently increased MAP in control mice (5.7 +/- 1.6, 11.7 +/- 2.1, 25.4 +/- 3.4, and 51.6 +/- 3.9%), which was attenuated in db/db mice (3.4 +/- 2.1, 3.9 +/- 2.1, 7.0 +/- 3.3, and 17.9 +/- 6.2%). TRPV1((-/-)) mice exhibited no changes in MAP in response to capsaicin, suggesting the actions of this agonist are specific to TRPV1 activation. Immunoblot analysis revealed decreased aortic TRPV1 protein expression in db/db compared with control mice. Capsaicin-induced responses were recorded following inhibition of endothelin A and B receptors (ET(A) /ET(B)). Inhibition of ET(A) receptors abolished the capsaicin-mediated increases in MAP. Combined antagonism of ET(A) and ET(B) receptors did not further inhibit the capsaicin response. Cultured endothelial cell exposure to capsaicin increased endothelin production as shown by an endothelin ELISA assay, which was attenuated by inhibition of TRPV1 or endothelin-converting enzyme. TRPV1 channels contribute to the regulation of vascular reactivity and MAP via production of endothelin and subsequent activation of vascular ET(A) receptors. Impairment of TRPV1 channel function may contribute to vascular dysfunction in diabetes.
Ohanyan Vahagn A; Guarini Giacinta; Thodeti Charles K; Talasila Phani K; Raman Priya; Haney Rebecca M; Meszaros J Gary; Damron Derek S; Bratz Ian N
American journal of physiology. Heart and circulatory physiology
2011
2011-09
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajpheart.00082.2011" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00082.2011</a>
Altered Neuroinflammation and Behavior after Traumatic Brain Injury in a Mouse Model of Alzheimer's Disease.
Alzheimer Disease/etiology/*metabolism/pathology; Alzheimer's disease; Amyloid beta-Peptides/*metabolism; Animal; Animal/physiology; Animals; Behavior; Blotting; Brain Injuries; Brain/*metabolism/pathology; Disease Models; Enzyme-Linked Immunosorbent Assay; Flow Cytometry; Humans; Immunohistochemistry; Inbred C57BL; Inflammation/*metabolism/pathology; macrophage; Mice; neuroinflammation; Transgenic; traumatic brain injury; Traumatic/complications/*metabolism/*pathology; Western
Traumatic brain injury (TBI) has acute and chronic sequelae, including an increased risk for the development of Alzheimer's disease (AD). TBI-associated neuroinflammation is characterized by activation of brain-resident microglia and infiltration of monocytes; however, recent studies have implicated beta-amyloid as a major manipulator of the inflammatory response. To examine neuroinflammation after TBI and development of AD-like features, these studies examined the effects of TBI in the presence and absence of beta-amyloid. The R1.40 mouse model of cerebral amyloidosis was used, with a focus on time points well before robust AD pathologies. Unexpectedly, in R1.40 mice, the acute neuroinflammatory response to TBI was strikingly muted, with reduced numbers of CNS myeloid cells acquiring a macrophage phenotype and decreased expression of inflammatory cytokines. At chronic time points, macrophage activation substantially declined in non-Tg TBI mice; however, it was relatively unchanged in R1.40 TBI mice. The persistent inflammatory response coincided with significant tissue loss between 3 and 120 days post-injury in R1.40 TBI mice, which was not observed in non-Tg TBI mice. Surprisingly, inflammatory cytokine expression was enhanced in R1.40 mice compared with non-Tg mice, regardless of injury group. Although R1.40 TBI mice demonstrated task-specific deficits in cognition, overall functional recovery was similar to non-Tg TBI mice. These findings suggest that accumulating beta-amyloid leads to an altered post-injury macrophage response at acute and chronic time points. Together, these studies emphasize the role of post-injury neuroinflammation in regulating long-term sequelae after TBI and also support recent studies implicating beta-amyloid as an immunomodulator.
Kokiko-Cochran Olga N; Ransohoff Lena; Veenstra Mike; Lee Sungho; Saber Maha; Sikora Matt; Teknipp Ryan; Xu Guixiang; Bemiller Shane M; Wilson Gina; Crish Samuel; Bhaskar Kiran; Lee Yu-Shang; Ransohoff Richard M; Lamb Bruce T
Journal of neurotrauma
2016
2016-04
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1089/neu.2015.3970" target="_blank" rel="noreferrer noopener">10.1089/neu.2015.3970</a>
A L.E.A.P.S. heteroconjugate vaccine containing a T cell epitope from HSV-1 glycoprotein D elicits Th1 responses and protection.
Amino Acid Sequence; Animals; CD4-Positive T-Lymphocytes/immunology; CD8-Positive T-Lymphocytes/immunology; Conjugate/immunology; Delayed/immunology; Enzyme-Linked Immunosorbent Assay; Epitopes/*immunology; Female; Herpes Simplex Virus Vaccines/*immunology; Herpes Simplex/pathology/prevention & control; Herpesvirus 1; Human/*immunology; Hypersensitivity; Inbred BALB C; Interferon-gamma/biosynthesis; Lymphocyte Count; Mice; Molecular Sequence Data; Peptides/immunology; Th1 Cells/*immunology; Vaccines; Viral Envelope Proteins/*immunology
The L.E.A.P.S. heteroconjugate vaccine antigen (JgD), composed of a T cell epitope from glycoprotein D (gD(8-23)) of herpes simplex virus (HSV) linked with a peptide sequence from beta-2-microglobulin (aa38-50), elicited protection against lethal intraperitoneal (IP) challenge and prevented disease signs in most, and limited disease progression, for the rest of BALB/c mice challenged in the epidermal abrasion-zosteriform spread mouse infection model. JgD elicited a Th1 response in vaccinated mice as indicated by delayed type hypersensitivity (DTH) responses to HSV antigen, and gD and virion specific antibodies with an IgG2a/IgG1 \textgreater1. Vaccination with the JgD peptide delayed the onset of disease signs, reduced severity of the disease and reduced mortality rates in mice with different MHC backgrounds as compared to their respective control mice. CD8 cells were demonstrated as important for initiation of the immune response to JgD and CD4 cells and interferon gamma (IFN-gamma) for delivering immune protection in BALB/c mice, as indicated in monoclonal antibody ablation studies. JgD, and other
Goel N; Rong Q; Zimmerman D; Rosenthal K S
Vaccine
2003
2003-10
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/s0264-410x(03)00429-8" target="_blank" rel="noreferrer noopener">10.1016/s0264-410x(03)00429-8</a>
miR-217 regulates ethanol-induced hepatic inflammation by disrupting sirtuin
Alcoholic/genetics/*metabolism; Animals; Chromatin Immunoprecipitation; Enzyme-Linked Immunosorbent Assay; Ethanol/toxicity; Fatty Liver/metabolism; Hepatitis; Immunoblotting; Inbred C57BL; Inflammation/genetics/*metabolism; Kupffer Cells/metabolism; Lipopolysaccharides/toxicity; Male; Mice; MicroRNAs/*metabolism; Nuclear Proteins/*metabolism; Phosphatidate Phosphatase/*metabolism; Real-Time Polymerase Chain Reaction; Signal Transduction/*physiology; Sirtuin 1/*metabolism; Transfection
Ethanol-mediated injury, combined with gut-derived lipopolysaccharide (LPS), provokes generation of proinflammatory cytokines in Kupffer cells, causing hepatic inflammation. Among the mediators of these effects, miR-217 aggravates ethanol-induced steatosis in hepatocytes. However, the role of miR-217 in ethanol-induced liver inflammation process is unknown. Here, we examined the role of miR-217 in the responses to ethanol, LPS, or a combination of ethanol and LPS in RAW 264.7 macrophages and in primary Kupffer cells. In macrophages, ethanol substantially exacerbated LPS-mediated induction of miR-217 and production of proinflammatory cytokines compared with LPS or ethanol alone. Consistently, ethanol administration to mice led to increases in miR-217 abundance and increased production of inflammatory cytokines in isolated primary Kupffer cells exposed to the combination of ethanol and LPS. miR-217 promoted combined ethanol and LPS-mediated inhibition of sirtuin 1 expression and activity in macrophages. Moreover, miR-217-mediated sirtuin 1 inhibition was accompanied by increased activities of two vital inflammatory regulators, NF-kappaB and the nuclear factor of activated T cells c4. Finally, adenovirus-mediated overexpression of miR-217 led to steatosis and inflammation in mice. These findings suggest that miR-217 is a pivotal regulator involved in ethanol-induced hepatic inflammation. Strategies to inhibit hepatic miR-217 could be a viable approach in attenuating alcoholic hepatitis.
Yin Huquan; Liang Xiaomei; Jogasuria Alvin; Davidson Nicholas O; You Min
The American journal of pathology
2015
2015-05
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.ajpath.2015.01.030" target="_blank" rel="noreferrer noopener">10.1016/j.ajpath.2015.01.030</a>
MicroRNA-9 promotion of interleukin-6 expression by inhibiting monocyte chemoattractant protein-induced protein 1 expression in interleukin-1beta-stimulated human chondrocytes.
Academic Medical Centers; Aged; Articular/drug effects/*metabolism; Cartilage; Cells; Chondrocytes – Physiology; Chondrocytes/drug effects/*metabolism; Cultured; Enzyme-Linked Immunosorbent Assay; Funding Source; Gene Knockdown Techniques; Hip/*genetics/metabolism; Human; Humans; Immunoblotting – Utilization; Immunoprecipitation; Interleukin-1beta/pharmacology; Interleukin-6/*genetics/metabolism; Interleukins – Physiology; Messenger/drug effects/*metabolism; MicroRNAs/drug effects/*genetics/metabolism; Middle Aged; Ohio; Osteoarthritis; Osteoarthritis – Complications; Osteoarthritis – Physiopathology; Reverse Transcriptase Polymerase Chain Reaction; Ribonucleases/drug effects/*genetics/metabolism; RNA; T-Tests; Transcription Factors/drug effects/*genetics/metabolism
OBJECTIVE: Enhanced expression of interleukin-6 (IL-6) plays an important role in the pathogenesis of osteoarthritis (OA). Monocyte chemoattractant protein-induced protein 1 (MCPIP-1) is a novel posttranscriptional regulator of IL-6 expression and is targeted by microRNA-9 (miR-9). We investigated the expression of MCPIP-1 in OA cartilage and explored whether targeting of MCPIP-1 by miR-9 contributes to enhanced IL-6 expression in OA. METHODS: Gene and protein expression in
Makki Mohammad S; Haseeb Abdul; Haqqi Tariq M
Arthritis & rheumatology (Hoboken, N.J.)
2015
2015-05
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1002/art.39173" target="_blank" rel="noreferrer noopener">10.1002/art.39173</a>