Institution
Houston Methodist Hospital
Healthcare•Houston, Texas, United States•
About: Houston Methodist Hospital is a healthcare organization based out in Houston, Texas, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 9825 authors who have published 18872 publications receiving 779830 citations. The organization is also known as: The Methodist Hospital.
Topics: Population, Cancer, Medicine, Transplantation, Breast cancer
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TL;DR: It is concluded that a single FVC value obtained at an initial visit may serve as a clinically meaningful predictor of survival and disease progression in ALS.
Abstract: In a large cohort of 1034 patients with the diagnosis of definite or probable amyotrophic lateral sclerosis (ALS), the association of forced vital capacity (FVC) at baseline with (a) time to progression of 20 points in Appel ALS (AALS) score or (b) tracheostomy free survival was investigated. The median survival of ALS patients with baseline FVC 75% (p 75% (10.0 months, p<0.001). Moreover, FVC at first examination was identified as a significant predictor of survival and disease progression in both univariate and multivariate Cox regression models, after adjustment for age, sex, site of onset, diagnostic delay, riluzole therapy, and use of bilateral positive airway pressure and percutaneous endoscopic gastrostomy (p<0.001). We conclude that a single FVC value obtained at an initial visit may serve as a clinically meaningful predictor of survival and disease progression in ALS.
222 citations
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TL;DR: This review aims at classifying the different options to frontally align TKA implants, comparing their safety and efficacy with the one from MA TKAs, and answering the following questions: does alternative techniques to position TKA improve functional outcomes of TKA and is there any pathoanatomy not suitable for kinematic implantation of a TKA?
Abstract: In spite of improvements in implant designs and surgical precision, functional outcomes of mechanically aligned total knee arthroplasty (MA TKA) have plateaued. This suggests probable technical intrinsic limitations that few alternate more anatomical recently promoted surgical techniques are trying to solve. This review aims at (1) classifying the different options to frontally align TKA implants, (2) at comparing their safety and efficacy with the one from MA TKAs, therefore answering the following questions: does alternative techniques to position TKA improve functional outcomes of TKA (question 1)? Is there any pathoanatomy not suitable for kinematic implantation of a TKA (question 2)? A systematic review of the existing literature utilizing PubMed and Google Scholar search engines was performed in February 2017. Only studies published in peer-reviewed journals over the last ten years in either English or French were reviewed. We identified 569 reports, of which 13 met our eligibility criteria. Four alternative techniques to position a TKA are challenging the traditional MA technique: anatomic (AA), adjusted mechanical (aMA), kinematic (KA), and restricted kinematic (rKA) alignment techniques. Regarding osteoarthritic patients with slight to mid constitutional knee frontal deformity, the KA technique enables a faster recovery and generally generates higher functional TKA outcomes than the MA technique. Kinematic alignment for TKA is a new attractive technique for TKA at early to mid-term, but need longer follow-up in order to assess its true value. It is probable that some forms of pathoanatomy might affect longer-term clinical outcomes of KA TKA and make the rKA technique or additional surgical corrections (realignment osteotomy, retinacular ligament reconstruction etc.) relevant for this sub-group of patients. Longer follow-up is needed to define the best indication of each alternative surgical technique for TKA. Level I for question 1 (systematic review of Level I studies), level 4 for question 2.
222 citations
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TL;DR: The microsomal steroid-metabolizing enzyme activities may be grouped into three classes with regard to the mechanisms regulating their activity: (a) enzymes with a basal activity level regulated by nongonadal factors but reversibly inducible by androgens; (b) enzymes irreversibly "imprinted" or "programmed" by andosterone during the prepubertal period and reversibly stimulated by androgens postpubertally.
222 citations
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Mayo Clinic1, Houston Methodist Hospital2, Tufts University3, Medical College of Wisconsin4, Hennepin County Medical Center5, University of Michigan6, Emory University7, West Virginia University8, Ohio State University9, University of Puerto Rico10, University of Pennsylvania11, Henry Ford Health System12, Cleveland Clinic13, University of Cincinnati14, Yeshiva University15, University of Mississippi16, University of Rochester17
TL;DR: Insulin-like growth factor type I does not provide benefit for patients with amyotrophic lateral sclerosis and there was no difference between treatment groups in the primary or secondary outcome measures after the 2-year treatment period.
Abstract: We congratulate Sorenson et al.1 for their well-executed IGF-1 trial in patients with amyotrophic lateral sclerosis (ALS). While the title appropriately reflects the subcutaneous mode of IGF-1 delivery, the article fails to distinguish this critical limitation. What is the bioavailability in CSF and brain parenchyma in humans treated twice daily with 0.05 mg/kg IGF-1?
Animal studies indicate that subcutaneous delivery of ∼0.8 mg/kg IGF-1 results in a maximal CSF concentration of 3 ng/mL IGF-1 at 2 hours postinjection.2 This equates to 0.4 nM IGF-1 in CSF at peak. The Sorenson et al. trial dose was 16-fold lower, suggesting that the maximal CSF concentration in patients would be 0.025 nM. The Kd of the IGF-1 receptor is 0.15 nM.3 Therefore, at 0.025 nM, only 14% of high-affinity and less than 1% of low-affinity receptors will be occupied. Likewise, the concentration of IGF-1 in CSF overestimates the bioavailable concentration within the brain parenchyma.
IGF-1 injected into the lateral ventricle of rats exhibits a half-life of only 12 minutes in the CSF and penetrates …
222 citations
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TL;DR: The data suggest that AP-1 activation may represent one mechanism mediating hyperoxia-induced HO-1 gene transcription, which is associated with increased activator protein-1 (AP-1) binding activity and supershift of the AP- 1 complex by antibodies to c-Fos and c-Jun after hyperoxIA.
Abstract: Using hyperoxia as a model of oxidant-induced lung injury in the rat, we explored the regulation of heme oxygenase-1 (HO-1) expression in vivo and in vitro. We demonstrate marked increase of HO-1 messenger ribonucleic acid (mRNA) levels in rat lungs after hyperoxia. Increased HO-1 mRNA expression correlated with increased HO-1 protein and enzyme activity. Immunohistochemical studies of the rat lung after hyperoxia showed increased HO-1 expression in a variety of cell types, including the bronchoalveolar epithelium and interstitial and inflammatory cells. We then examined the regulation of HO-1 expression in vitro after hyperoxia and observed increased HO-1 gene expression in various cultured cells including epithelial cells, fibroblasts, macrophages, and smooth muscle cells. Increased HO-1 mRNA expression correlated with increased HO-1 protein in vitro, and resulted from increased gene transcription and not from increased mRNA stability. We show that transcriptional activation of the HO-1 gene by hyperoxi...
222 citations
Authors
Showing all 9852 results
Name | H-index | Papers | Citations |
---|---|---|---|
Hagop M. Kantarjian | 204 | 3708 | 210208 |
Robert M. Califf | 196 | 1561 | 167961 |
Eric J. Topol | 193 | 1373 | 151025 |
Nancy A. Jenkins | 155 | 741 | 101587 |
Neal G. Copeland | 154 | 726 | 100130 |
Joseph Jankovic | 153 | 1146 | 93840 |
Christopher P. Cannon | 151 | 1118 | 108906 |
Jan-Åke Gustafsson | 147 | 1058 | 98804 |
Peter B. Jones | 145 | 1857 | 94641 |
Stephen F. Badylak | 133 | 530 | 57083 |
Christie M. Ballantyne | 132 | 1012 | 77651 |
Jeremiah Stamler | 127 | 655 | 70751 |
Kamyar Kalantar-Zadeh | 118 | 1025 | 56187 |
Shahrokh F. Shariat | 118 | 1637 | 58900 |
Stephen Safe | 116 | 784 | 60588 |