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Background: Extracranial carotid atherosclerosis has been variably associated with dementia. Prior studies have focused on the association of carotid intima media thickness or carotid stenosis; however, there is evidence that carotid plaque may contribute to dementia, perhaps via microembolic phenomena., Objectives: We sought to evaluate the role of carotid plaque in contributing to cognitive impairment by performing a systematic review and meta-analysis to summarize the association between extracranial carotid plaque and cognitive dysfunction and dementia., Methods: We performed a comprehensive literature search evaluating the association of extracranial carotid plaque with cognition. We included studies measuring carotid plaque on ultrasound, computed tomography, or MR and also evaluated cognition through neuropsychological testing. Meta-analyses with assessment of study heterogeneity and publication bias were performed. Results were presented in a forest plot and summarized using a random-effects model., Results: After screening 1,674 studies, we included 40 for systematic review and 16 and 7 studies for two meta-analyses with a total of 19,029 and 27,325 patients, respectively. We found a positive relationship between the presence of extracranial carotid plaque and cognitive dysfunction with a pooled random-effects odds ratio (OR) of 1.83 (95% CI, 1.50, 2.24) and a pooled random-effects hazard ratio (HR) of 1.47 (95% CI, 1.15, 1.89), respectively. A sensitivity analysis of only longitudinal studies found a persistent positive association. Measures of heterogeneity showed moderate heterogeneity in each meta-analysis, respectively (I-squared statistic = 57% and 70%)., Conclusion: The presence of extracranial carotid plaque is significantly associated with cognitive dysfunction and dementia in both cross-sectional and longitudinal analyses. After further confirmation, our results support carotid plaque being a potentially modifiable risk factor in the development of dementia., (© 2022 S. Karger AG, Basel.)

Objective: Thoracic outlet syndrome classically results from constrictions in 1 or more of 3 specific anatomical locations: the interscalene triangle, costoclavicular space, and coracopectoral tunnel. Magnetic resonance and computed tomographic imaging studies suggest that, of the 3 potential locations for constriction, the costoclavicular space is the most susceptible to compression. This study of human cadavers aims to expand on the descriptive anatomy of the interscalene triangle and associated costoclavicular space., Methods: The interscalene angle, interscalene triangle base, and costoclavicular space were measured on 120 sides of embalmed human cadavers. Linear distances and angles were measured using a caliper and protractor, respectively. The data were analyzed by calculating the mean, range, and standard deviation., Results: The range for the interscalene base was 0 to 21.0 mm with a mean of 10.7 mm. For the interscalene angle, the range was 4° to 22° with a mean of 11.3°. Measurements for the costoclavicular space ranged from 6 to 30.9 mm with a mean of 13.5 mm., Conclusions: No significant differences were observed between left and right interscalene triangles or costoclavicular spaces; furthermore, there were no differences between the sexes concerning these 2 locations., (Copyright © 2012 National University of Health Sciences. Published by Mosby, Inc. All rights reserved.)

During the 3rd wk of postnatal life in the rat, dramatic maturational changes occur in the structure and function of the small intestine, enabling the animal to make the transition from milk to solid food. To investigate the role of GH in the regulation of this complex process, we studied postnatal intestinal maturation in the spontaneous dwarf rat, a strain of Sprague-Dawley rats with an autosomal recessive mutation in the GH gene resulting in complete but isolated GH deficiency. GH-deficient and GH-normal littermates were studied at d 7 and 14 (suckling) and d 23 (postweaned). The body weight of GH-deficient animals was inhibited by 60% at each age. Longitudinal growth of the small intestine was not inhibited, suggesting that longitudinal small bowel growth is independent of GH regulation. Mucosal cell mass was significantly lower in GH deficiency at all ages studied, and digestive hydrolase capacity per cm of intestine was significantly lower in GH-deficient postweaned animals. However, epithelial cell mass increased markedly in association with weaning and the maturation of lactase, sucrase, and aminooligopeptidase proceeded normally in GH deficiency. These data suggest that, although GH is not required for normal postnatal intestinal maturation, the mucosal epithelial hypoplasia found in GH-deficient animals suggests that GH or GH-dependent factors act as an intestinal mucosal growth factor whose function is to promote the homeostatic or steady-state regulation of mucosal epithelial growth.

Nine children receiving carnitine-free total parenteral nutrition for 7.2 +/- 2.6 years since birth were prospectively studied for 3 years. Plasma values of total and free carnitine were 50% lower than those of age-matched healthy control subjects (p less than 0.02) but did not decrease further during the 3-year period. No significant abnormalities in free fatty acids, triglycerides, or cholesterol were found. The mean levels of alanine and aspartate aminotransferases and of alkaline phosphatase were slightly increased (p less than 0.02) at the initiation of the study but remained in the same range 3 years later. The low plasma carnitine values appeared to be without clinical consequence after 10 years of carnitine-free total parenteral nutrition.

Renal function was assessed in 13 children at a mean (+/- SD) age of 9 +/- 4.9 years who had been receiving total parenteral nutrition for 7.9 +/- 4.1 years. All children had normal blood pressure, urinary sediment, and serum creatinine concentrations (58.3 +/- 1.0 mumol/L). Glomerular filtration rate was measured by plasma clearance of diethylenetriaminepentaacetic acid labeled with indium 111. All 13 children had decreased glomerular filtration rate (65.5 +/- 11.9 ml/min per 1.73 m2; range 49.5 to 83.7). Creatinine clearance was 69.1 +/- 10.9 ml/min per 1.73 m2. No tubular damage, as assessed by beta 2-microglobulinuria, was detectable. Renal ultrasonography showed normal architecture with no evidence of nephrocalcinosis in all subjects. The kidney size was normal in seven children; six had reduced (less than -1 SD) size. No relationship was seen between the true glomerular filtration rate and diagnosis, number of episodes of infections, or antibiotics used. The duration of total parenteral nutrition was inversely correlated with the true glomerular filtration rate (r = -0.66, p less than 0.01). The decrease in glomerular filtration rate was not related to the underlying disease or to the nephrotoxic drugs used; the mechanism was not identified. We conclude that long-term total parenteral nutrition is associated with a decrease in glomerular filtration rate.

The impact of overnight intravenous lipid emulsion (ILE) infusion on upper gastrointestinal tract physiology was assessed in 10 healthy volunteers. No changes in lower esophageal sphincter pressure (before infusion: 28 +/- 4 mm Hg; after infusion 20.5 +/- 3; p:NS), plasma concentrations of gastrointestinal hormones (gastrin: preprandial before/after lipids: 14 +/- 2.1/13 +/- 1.4 pM; postprandial before/after lipids: 28 +/- 2.7/30 +/- 3.4 pM, CCK: preprandial before/after lipids: 69 +/- 10/64 +/- 10 pM; postprandial before/after lipids: 96 +/- 11/95 +/- 12 pM; neurotensin: levels less than 6 pM in all samples; somatostatin levels undetectable in all samples) nor on pathologic gastroesophageal reflux episodes (% of time of pH less than 4, before/after lipids: 0.6 +/- 0.4/0.15 +/- 0.09), were found (p = NS). In contrast, technetium gastric emptying studies showed a significant delay when comparing pre- and post-lipid infusion values (37 +/- 4/54 +/- 4%) (p greater than 0.005). The mechanism of this effect remains unexplained.

Two different soy oil emulsions (Intralipid and Soyacal) were studied over a 2-week period in a random crossover study to determine if there were clinical or biochemical differences between the two preparations when used in patients requiring total parenteral nutrition (TPN). Each fat emulsion was infused randomly over 1 week and then switched to the other. Eighteen adult patients requiring a minimum of 14 days TPN were studied. None of the 26 metabolic parameters evaluated was statistically different between the two groups. Analysis of nutritional status, irrespective of lipid infused, showed that the patients who received 56 kcal/kg/day with 37% of the nonprotein calories from lipids (1.8 +/- 0.7 g/kcal/day) were in positive nitrogen balance on 80 of the 101 days studied. No adverse effects could be observed from either lipid emulsion during the short period of TPN used in this study. Both lipid emulsions were efficacious as a caloric source, and no clinical complications or biochemical abnormalities were found from either preparation.

Nutrition status was evaluated in 19 children aged 4 to 65 months who received total parenteral nutrition as their only source of nutrition (nine patients, group 1) or who ingested 30% to 70% of their total energy requirements orally and received the remainder intravenously (10 patients, group 2). All patients had received parenteral nutrition for 31.8 +/- 9.8 SD and 33.1 +/- 17.1 months, respectively. All patients in group 1 and four in group 2 had short bowel syndrome; five in group 2 had pseudo-obstruction syndrome. The children in group 1 had normal height, weight, midarm circumference (MAC), midarm muscle circumference (MAMC), and triceps skinfold thickness (TSF). In group 2 patients, height, MAC, and TSF, were significantly below normal, and their weight, MAMC, and TSF, were lower than in group 1. Hemoglobin, total lymphocyte count, and serum albumin concentration were below normal in group 1; serum total protein concentration was low in both groups. Serum bilirubin concentration was higher in group 1; serum glutamic pyruvic transaminase activity was elevated in both groups. These data indicate that children receiving long-term total parenteral nutrition can obtain and maintain normal height, weight, and other anthropometric measurements of nutritional status. Group 1 patients had better nutritional status than those in group 2, perhaps because of differences in the underlying medical disorders between the two groups, or possibly because of a propensity to underestimate the amount of parenteral nutrition needed by patients who ingest some nutrients.

The trace elements iron (Fe), copper (Cu), zinc (Zn), selenium (Se), chromium (Cr), manganese (Mn), nickel (Ni), rubidium (Rb), and bromine (Br) were determined in serum from 18 children, ages 4 to 65 months, who received long-term total parenteral nutrition (TPN). Nine patients (group 1) received TPN as their only source of nutrition; the other nine (group 2) ingested 30% to 70% of their total calorie requirement and received the remainder intravenously. The reference group consisted of 19 healthy children of similar age and sex distribution. Groups 1 and 2 had received parenteral nutrition for 28.4 +/- 13.7 (SD) and 23.1 +/- 17.1 (SD) months, respectively. All patients in group 1 and four in group 2 had short bowel syndrome; four in group 2 had pseudo-obstruction syndrome. Patients in group 1 had normal serum levels of Fe, Cu, and Mn, but increased levels of Zn; they had decreased serum concentrations of Se, Cr, Ni, Rb, and Br. Patients in group 2 had decreased serum levels of Mn, Cr, Ni, Rb, and Br. Those trace elements not supplemented in TPN solutions (Se, Cr, Mn, Ni, Rb, and Br) were lower in the children receiving TPN than in the control children, indicating inadequate intake of these trace elements from food and TPN solutions. However, no obvious clinical signs or symptoms of trace element deficiencies were observed.

Selenium levels were low in four children receiving long-term total parenteral nutrition (TPN) who developed erythrocyte macrocytosis (3/4), loss of pigmentation of hair and skin (2/4), elevated transaminase and creatine kinase activities (2/4), and profound muscle weakness (1/4). Initial mean selenium levels in serum and hair were 38 +/- 11 (SEM) ng/mL and 0.34 +/- 0.13 micrograms/g, respectively. Mean serum vitamin B12, folate, and vitamin E levels were normal. Intravenous supplementation with selenium was begun daily at 2 micrograms/kg/day. After 3 to 6 months, serum selenium levels rose almost threefold to 81 +/- 22 ng/mL. During this same time, erythrocyte mean corpuscular volume fell from 115 +/- 8 fL to 88 +/- 7 fL in the three children with macrocytosis. After 6 to 12 months of supplementation, hair selenium content had increased threefold to 1.02 +/- 0.19 micrograms/g. The two children with decreased pigmentation became darker skinned and their hair color changed from blonde to dark brown; a third child's hair, which had been blonde, also became darker. Transaminase and creatine kinase activities returned to near normal in those affected and, in the one child with severe myopathy, muscle weakness improved. Erythrocyte macrocytosis and loss of skin and hair pigmentation are previously undescribed manifestations of selenium deficiency. We recommend routine supplementation of TPN solution with selenium to avoid the clinical and biochemical syndrome of selenium deficiency in patients receiving long-term TPN.