Alterations in phenotype and function of intestinal macrophages occur in inflammatory bowel disease (IBD) but it is unclear whether these changes result from the recruitment of circulating monocytes to the intestine or from proliferation of resident intestinal macrophages. We sought to demonstrate the arrival of blood monocytes, the precursors of macrophages, in IBD mucosa. Peripheral blood mononuclear cells were isolated from 23 patients with clinically active intestinal inflammation (13 Crohn's disease, eight ulcerative colitis, two infective colitis), then radiolabelled with 99mtechnetium (Tc)-stannous colloid (n = 13) or 111indium (In)-oxine (n = 10) before re-injection and abdominal scanning. Four patients had demonstrable intestinal monocyte uptake using [99mTc]-stannous colloid, while six [111In]-oxine-labelled monocyte scans were positive. Uptake sites correlated with actively inflamed regions. Patients demonstrating monocyte uptake had been treated with corticosteroids for a significantly (P < 0.02) shorter duration (median 3 vs 20 days) than those with negative scans. There was no significant difference between positive and negative scans for disease category, clinical or histological disease, activity, or radioisotope used. Biopsies of inflamed mucosa from two patients suffering ulcerative colitis who had positive scans showed a high proportion of CD14-positive macrophages, 4-9% of which contained autoradiographic grains. These results demonstrate that blood monocytes are recruited to the mucosa of actively inflamed bowel, and suggest that this process may be inhibited by corticosteroids. Moreover, the phenotype of the recently-arrived monocytes indicates their susceptibility to stimulation by lipopolysaccharide, and suggests a mechanism for the continuing inflammation in the bacterial product-rich milieu of IBD.

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Most of the pedicles of the lower lumbar spine and T12 are large enough to house the smallest commercially available screw. Understanding of the anatomy at the thoracolumbar junction is important, as the W of L1 is consistently smaller than T12.

Background: Recent clinical trials have shown mechanical thrombectomy (MT) to have clinical benefit for patients with acute ischemic stroke. The purpose of this study was to identify comorbid conditions that correlate with functional nonindependence in patients with acute ischemic stroke who underwent MT at a single comprehensive stroke center. Methods: Patients who had multiphase computed tomography angiography (MCTA) and subsequently underwent MT were included in this study. The modified Rankin Scale (mRS) scores at baseline (prestroke) and at 90 days were established by reviewing patients' histories and medical record documentation. Comorbid conditions were obtained from electronic medical records. Multivariate analysis was performed for body mass index, chronic hypertension, diabetes, hemoglobin A1c, peripheral artery disease, and hyperlipidemia to determine the impact of comorbidities on functional outcome. Age was analyzed using linear regression. Functional independence was defined as an mRS score of 0-2, and functional nonindependence was defined as an mRS score >2. Results: During the study period, 721 patients underwent MCTA, and 134 patients were included for MT. Patients with chronic hypertension and peripheral artery disease showed a statistically significant association with functional nonindependence at 90 days (P=0.005 and P=0.0125, respectively). Younger age at presentation was correlated with functional nonindependence using linear regression (P=0.0001). Conclusion: Hypertension, peripheral artery disease, and younger age at presentation are correlated with poor functional outcome in patients with acute ischemic stroke undergoing MT.

A family of mutants of Salmonella typhimurium with altered lipopolysaccharide (LPS) core chain lengths were assessed for sensitivity to freeze-thaw and other stresses. Deep rough strains with decreased chain length in the LPS core were more susceptible to novobiocin, polymyxin B, bacitracin, and sodium lauryl sulfate during growth, to ethylenediaminetetraacetic acid and sodium lauryl sulfate in resting suspension, and to slow and rapid freeze-thaw in water and saline, and these strains exhibited more outer membrane damage than the wild type or less rough strains. Variations in the LPS chain length did not dramatically affect the sensitivity of the strains to tetracycline, neomycin, or NaCl in growth conditions or the degree of freeze-thaw-induced cytoplasmic membrane damage. The deeper rough isogenic strains incorporated larger quantities of less-stable LPS and less protein into the outer membrane than did the wild type or less rough mutants, indicating that the mutations affected outer membrane synthesis or organization or both. Nikaido's model of the role of LPS and protein in determining the resistance of gram-negative bacteria to low-molecular-weight hydrophobic antibiotics is discussed in relation to the stress of freeze-thaw. The stress of freezing and thawing causes considerable damage to microbes, including loss of viability, membrane damage, deoxyribonucleic acid damage, ultrastructural changes, and loss of respiratory, active uptake, nutrient retention, and protein synthesis activities (3