1997 research outputs found
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Thrombolysis After Protamine Reversal of Heparin for Acute Ischemic Stroke After Cardiac Catheterization: Case Report and Literature Review
No full textBACKGROUND:
Patients with an acute ischemic stroke (AIS) following cardiac catheterization (CC) generally do not receive intravenous thrombolysis [intravenous tissue plasminogen activator (IV-tPA)] as it is contraindicated due to the coagulopathy related to the heparin used during the procedure. We report a case of AIS successfully treated with IV thrombolysis following protamine reversal of heparin effect. CASE REPORT:
An 87-year-old man with diabetes mellitus, hypertension, neurofibromatosis, and hyperlipidemia underwent elective transradial CC following an abnormal stress test. He had 2 drug-eluting stents for severe stenosis of mid-circumflex and right coronary arteries and received heparin 13,000 IU during procedure. He developed acute left hemiparesis with initial NIH stroke scale (NIHSS) of 4. Computed tomographic scan of the brain and computed tomographic angiogram of head and neck were unremarkable. Bedside activated clotting time was 181. Protamine 40 mg was administered and 30 minutes later, the activated clotting time level was normalized. IV-tPA was administered at 4 hours 25 minutes from his last known well. Within 15 minutes, his NIHSS was 0. Magnetic resonance imaging of brain showed no acute infarction 24 hours after stroke. CONCLUSIONS:
There are limited reports of protamine reversal of heparin before IV-tPA administration. To our knowledge, there are only 6 AIS cases including ours. Three cases received 0.6 mg/kg of tPA dose. All have favorable outcomes and no intracranial hemorrhage was reported. Protamine reversal of heparin for AIS after CC seems to be safe. Further studies are needed to confirm the therapeutic safety and efficacy of this strategy
Bringing Attention to Lesser-known Bone Remodeling Pathways
No full textOsteoporosis, a disease of low bone mass, places individuals at enhanced risk for fracture, disability, and death. In the USA, hospitalizations for osteoporotic fractures exceed those for heart attack, stroke, and breast cancer and, by 2025, the number of fractures due to osteoporosis is expected to rise to nearly three million in the USA alone. Pharmacological treatments for osteoporosis are aimed at stabilizing or increasing bone mass. However, there are significant drawbacks to current pharmacological options, particularly for long-term management of this chronic condition. Moreover, the drug development pipeline is relatively bereft of new strategies. Consequently, there is an urgent and unmet need for developing new strategies and targets for treating osteoporosis. Casual observation led us to hypothesize that much of the bone remodeling research literature focused on relatively few molecular pathways. This led us to perform bibliometric analyses to determine the relative popularity of bone remodeling pathways in publications and US National Institutes of Health funding of the last 10 years. In this review article, we discuss these findings and highlight several less-examined signaling pathways that may hold promise for future therapies
One Is in the Definition of All: The Renaissance Thomist Controversy Over a Rule for Names Said by Analogy
No full textIdentification of p38 MAPK as a Novel Therapeutic Target for Friedreich’s Ataxia
No full textFriedreich ataxia (FRDA) is an autosomal recessive neuro- and cardio-degenerative disorder caused by decreased expression of frataxin, a protein that localizes to mitochondria and is critical for iron-sulfur-cluster (ISC) assembly. There are no proven effective treatments for FRDA. We previously screened a random shRNA library and identified a synthetic shRNA (gFA11) that reverses the growth defect of FRDA cells in culture. We now report that gFA11 decreases cytokine secretion in primary FRDA fibroblasts and reverts other changes associated with cell senescence. The gene-expression profile induced by gFA11 is remarkably similar to the gene-expression profile induced by the p38 MAPK inhibitor SB203580. We found that p38 phosphorylation, indicating activation of the p38 pathway, is higher in FRDA cells than in normal control cells, and that siRNA knockdown of frataxin in normal fibroblasts also increases p38 phosphorylation. Treatment of FRDA cells with p38 inhibitors recapitulates the reversal of the slow-growth phenotype induced by clone gFA11. These data highlight the involvement of the p38 MAPK pathway in the pathogenesis of FRDA and the potential use of p38 inhibitors as a treatment for FRDA
On the Impact of Academic Performance by Semester: Student Mood & Academic Self-Efficacy
No full textThe Role of Retail Pharmacy in the Treatment of Mental Illness
Get PDFMental illness treatment in the United States has developed and changed drastically in the past century. Where in the early 1900s,one with a severe mental illness would be institutionalized, today, the same person could be treated with psychotherapy and medications.
Pharmacists are the modern bridge to aid those with mental illness to live on their own and contribute to society
Elucidating the Molecular Signatures Associated with Elevated Bone Formation Rate
Get PDFOsteoporosis is a disease of decreased bone density that occurs when bone resorption exceeds bone formation, thereby placing individuals at greater risk of fracture and disability. We previously reported that deletion of the Bmpr2 gene in embryonic skeletal progenitor cells causes substantially elevated bone density in young adulthood and reduced age-related decline in bone density, likely due to elevated bone formation rate. Thus, these mice may serve as a novel model in which to explore the mechanisms regulating bone formation in the aging skeleton. Here, we performed transcriptome profiling and identified a concise gene signature associated with elevated bone formation rate in Bmpr2 mutant mice, with 120 transcripts up-regulated and 131 transcripts down-regulated. Candidate-driven qRT-PCR provided secondary confirmation of this dataset. Notably, only 8 of these differentially-expressed transcripts have been previously implicated in bone physiology (Pak4, Rpl38, B2m, Fgf1, Nmu, Phospho1, Smpd3 and Inbe), thus representing potentially novel regulators of osteoblast function in the aging skeleton. Additionally, we sought to examine the cell communication events that are associated with elevated bone formation rate. Using protein samples from control and mutant mice, we took advantage of recent advancements in high-throughput phospho-profiling antibody arrays, which allow simultaneous detection of \u3e1,300 targets using very small quantities of protein. These results indicate that the phosphorylation status of at least 86 signaling effectors is differentially regulated in Bmpr2 mutant mice as compared to control littermates, including numerous proteins known to regulate osteoblast differentiation and/or activity. Collectively, our work highlights novel factors associated with elevated bone formation rate and may identify new opportunities for treating low bone density in humans
Writing In/For Strategic Instruction—and how it can make students better writers
Get PDFParticipants will create writing prompts in support of strategic instruction and brainstorm ways that strategic instruction can teach what students need in order to perform successfully on course writing assignments
Ultrasound-guided Great Saphenous Vein Access in Trauma Cases
No full textThe great saphenous vein (GSV) should be considered as a vascular access point in cases of difficult access such as in trauma patients or hypovolemic patients. The GSV has been proven to be a viable vessel for peripheral venous access, however its use in emergency departments (ED) is still limited nationally. Ultrasound guidance makes the GSV access procedure quick, easy, and accurate. Furthermore, with a handheld ultrasound machine, even first responders could be establishing access and providing life-saving fluids and medications in route to more substantial care