ContributionsMagdy Selim --organized the trial hypotheses, designed the trial, provided guidance about the data analysis and interpretation and presentation of the data, and drafted most of the sections of the manuscript. Lydia Foster --involved in the statistical analysis and data interpretation, and Contributed to the development and revisions to the manuscript. Claudia Moy --involved in the oversight of the trial conduct and progress Guohua Xi --organized the trial hypotheses, and provided critical revisions to the manuscript. MH, MJ, VS, and WC contributed to recruitment and randomization of trial participants, and provided critical revisions to the manuscript. LM and SG were involved in the design of the trial and provided critical revisions to the manuscript. Casey Norton --provided volumetric measurements of imaging data. Yuko Palesch --involved in the design of the study, statistical analysis and data interpretation, and provided critical revisions to the manuscript. Sharon yeatts --involved in the design of the study, statistical analysis and data interpretation, and contributed to the development and revisions to the manuscript. The idef investigators (see appendix) --contributed to the identification and, when eligible, randomization of trial participants. DECLARATION OF INTERESTSThis was an investigator-initiated study, funded by the NINDS (U01 NS074425). Deferoxamine Mesylate is a generic drug, and there was no commercial or industrial support for the trial. None of the authors has any competing interests related to the submitted work. MS reports grants from the NIH/NINDS (i-DEF) and the American Heart Association (outside the submitted work), and personal fees for serving on the advisory board of CSL Behring (outside the submitted work) during the conduct of the trial. SDY reports grant support from the NINDS, personal fees from Genentech and other fees from CR Bard Inc. (outside the submitted work) during the conduct of the study. SG, LDF, YP, and GX report grants from the NIH/NINDS. MDH reports personal fees from Merck, nonfinancial support from Hoffmann-La Roche Canada Ltd, grants from Covidien (Medtronic), grants from Boehringer-Ingleheim, grants from Stryker Inc., grants from Medtronic LLC, grants from NoNO Inc., (outside the submitted work); In addition, MDH has a patent Systems and Methods for Assisting in Decision-Making and Triaging for Acute Stroke Patients pending to US Patent office Number: 62/086,077 and owns stock in Calgary Scientific Incorporated, a company that focuses on medical imaging software, is a director of the Canadian Federation of Neurological Sciences, a not-for-profit group and has received grant support from Alberta Innovates Health Solutions, CIHR, Heart & Stroke Foundation of Canada, and NINDS. LM, VS, WC, MJ, CM, and CN have nothing to disclose.
The objective of this study was to examine the pathophysiology of ischemic stroke with cancer. Methods: We conducted a prospective cross-sectional study from 2016 to 2020 at 2 hospitals. We enrolled 3 groups of 50 adult participants each. The main group included patients with active solid tumor cancer and acute ischemic stroke. The control groups included patients with acute ischemic stroke only or active cancer only. The patients with stroke-only and patients with cancer-only were matched to the patients with cancer-plus-stroke by age, sex, and cancer type, if applicable. The outcomes were prespecified hematological biomarkers and transcranial Doppler microemboli detection. Hematological biomarkers included markers of coagulation (D-dimer and thrombin-antithrombin), platelet function (P-selectin), and endothelial integrity (thrombomodulin, soluble intercellular adhesion molecule-1 [sICAM-1], and soluble vascular cell adhesion molecule-1 [sVCAM-1]). Hematological biomarkers were compared between groups using the Kruskal-Wallis and Wilcoxon Rank-Sum tests. In multivariable linear regression models, we adjusted for race, number of stroke risk factors, smoking, stroke severity, and antithrombotic use. Transcranial Doppler microemboli presence was compared between groups using chi-square tests.Results: Levels of all study biomarkers were different between groups. In univariate between-group comparisons, patients with cancer-plus-stroke had higher levels of D-dimer, sICAM-1, sVCAM-1, and thrombomodulin than both control groups; higher levels of thrombin-antithrombin than patients with cancer-only; and higher levels of P-selectin than patients with stroke-only. Findings were similar in multivariable analyses. Transcranial Doppler microemboli were detected in 32% of patients with cancer-plus-stroke, 16% of patients with stroke-only, and 6% of patients with canceronly (p = 0.005). Interpretation: Patients with cancer-related stroke have higher markers of coagulation, platelet, and endothelial dysfunction, and more circulating microemboli, than matched controls.
The clinical courses of 92 patients who had bacteremia due to Bacteroidaceae were reviewed. The overall mortality rate was 21% (19 patients). There was no significant difference between mortality rates when patients were grouped by anticipated clinical course of underlying disease (nonfatal, ultimately fatal, and rapidly fatal) and when they were grouped by type of antibacterial therapy (appropriate, including clindamycin, chloramphenicol, lincomycin, and carbenicillin; or inappropriate, signifying no antibiotic treatment or treatment with antibiotics other than the four listed above). However, there was a correlation between recovery of the patient and portal of entry of the infectious agent; patients whose source of infection was the gastrointestinal tract had a mortality rate of 29% (17 of 58 patients), whereas there were no deaths among the 26 women whose presumed source of bacteremia was the genital tract. Increasing age appeared to be an important factor as well; 17 of 19 deaths occurred in patients who were older than 40 years. There was no significant difference between the mortality rate of patients who were treated with clindamycin (15%, eight of 52 patients) and that of patients who were treated with chloramphenicol (44%, four of nine).
A prospective study was performed to evaluate four culture methods for the diagnosis of bacterial peritonitis in patients on continuous ambulatory peritoneal dialysis. Peritonitis was present in 44 of 85 patient admissions (52%). The overall sensitivity of the culture methods in detecting peritonitis was 66%. The sensitivities of the individual methods were as follows: bag culture method, 61%; blood culture broth method, 51%; filter method, 54%; and plate method, 39%. Our broad definition of peritonitis resulted in lower sensitivities. A combination of the bag and blood culture broth methods detected all positive cultures.
Background and Purpose— Comorbid cancer is common in patients with acute ischemic stroke (AIS). As blood mRNA profiles can distinguish AIS mechanisms, we hypothesized that cancer-related AIS would have a distinctive gene expression profile. Methods— We evaluated 4 groups of 10 subjects prospectively enrolled at 3 centers from 2009 to 2018. This included the group of interest with active solid tumor cancer and AIS and 3 control groups with active cancer only, AIS only, or vascular risk factors only. Subjects in the AIS-only and cancer-only groups were matched to subjects in the cancer-stroke group by age, sex, and cancer type (if applicable). Subjects in the vascular risk factor group were matched to subjects in the cancer-stroke and stroke-only groups by age, sex, and vascular risk factors. Blood was drawn 72 to 120 hours after stroke. Total RNA was processed using 3′ mRNA sequencing. ANOVA and Fisher least significant difference contrast methods were used to estimate differential gene expression between groups. Results— In the cancer-stroke group, 50% of strokes were cryptogenic. All groups had differentially expressed genes that could distinguish among them. Comparing the cancer-stroke group to the stroke-only group and after accounting for cancer-only genes, 438 genes were differentially expressed, including upregulation of multiple genes/pathways implicated in autophagy signaling, immunity/inflammation, and gene regulation, including IL (interleukin)-1, interferon, relaxin, mammalian target of rapamycin signaling, SQSTMI1 (sequestosome-1), and CREB1 (cAMP response element binding protein-1). Conclusions— This study provides evidence for a distinctive molecular signature in blood mRNA expression profiles of patients with cancer-related AIS. Future studies should evaluate whether blood mRNA can predict detection of occult cancer in patients with AIS. Clinical Trial Registration— URL: https://clinicaltrials.gov . Unique identifier: NCT02604667.
The efficacy and safety of amikacin were evaluated in 42 patients with infections presumed to be due to gram-negative rods. The dosage of 7.5 mg of amikacin/kg every 12 hr was administered intramuscularly to 32 patients and intravenously to seven patients; three patients with renal impairment were given a modified regimen. The duration of treatment was three to 51 days (mean, 9.6 days). Of 19 patients with acute pyelonephritis, five had positive blood culture results. Ten patients had chronic urinary infection, and isolates of Pseudomonas aeruginosa from four of these patients acquired resistance to amikacin during therapy. Of seven patients with gram-negative bacteremia from sources other than the urinary tract, four showed satisfactory and three had less than optimal responses to therapy with amikacin. Two patients with chronic osteomyelitis or soft tissue infection improved but subsequently relapsed. Two patients with acute febrile illness, in whom the etiologic agent was unidentified, recovered. Serial audiograms revealed no change in 26 of 27 patients; one had a significant deterioration in hearing. A transient rise in the level of serum creatinine was noted in three patients. Serial tests of liver function revealed no abnormalities.
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