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Low protein

About: Low protein is a research topic. Over the lifetime, 8139 publications have been published within this topic receiving 213225 citations.


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Journal ArticleDOI
01 Aug 2008-RNA
TL;DR: Findings that at low protein:RNA ratios the RNA G quadruplex structure is slightly stabilized, whereas at high ratios is unfolded, suggest a mechanism by which the FMRP concentration variation in response to a neurotransmitter stimulation event could act as a regulatory switch for the protein function, from translation repressor to translation activator.
Abstract: Fragile X mental retardation syndrome, the most common form of inherited mental retardation, is caused by the absence of the fragile X mental retardation protein (FMRP). FMRP has been shown to use its arginine–glycine–glycine (RGG) box to bind to a subset of RNA targets that form a G quadruplex structure. We performed a detailed analysis of the interactions between the FMRP RGG box and the microtubule associated protein 1B (MAP1B) mRNA, a relevant in vivo FMRP target. We show that MAP1B RNA forms an intramolecular G quadruplex structure, which is bound with high affinity and specificity by the FMRP RGG box. We determined that hydrophobic interactions are important in the FMRP RGG box-MAP1B RNA association, with minor contributions from electrostatic interactions. Our findings that at low protein:RNA ratios the RNA G quadruplex structure is slightly stabilized, whereas at high ratios is unfolded, suggest a mechanism by which the FMRP concentration variation in response to a neurotransmitter stimulation event could act as a regulatory switch for the protein function, from translation repressor to translation activator.

75 citations

Journal ArticleDOI
TL;DR: Brown adipose tissue protein content and thermogenic capacity were greater than control values in sucrose-fed and protein-deficient animals, and the greatest levels of activity were seen in low protein-fed rats with a high fat intake.
Abstract: Voluntary intake of protein, fat and carbohydrate (CHO) was modified by feeding young rats either a control purified diet [% metabolizable energy (ME): protein 21, fat 7, CHO 72], a control diet plus sucrose solution (20%) to drink (final intakes 17, 6 and 77% ME as protein, fat and CHO, respectively) or a low protein diet substituted with either CHO (8, 7 and 85% ME as protein, fat and CHO, respectively) or fat (8, 20 and 72% ME as protein, fat and CHO, respectively). Total ME intakes corrected for body size were similar for all rats, but body weight, energy gain and net energetic efficiency were lower in both low protein-fed groups than in the control group. The acute thermogenic response (% rise in oxygen consumption) to a standard balanced-nutrient meal was higher (12%) in sucrose-supplemented and in low protein groups (15-16%) than in control rats (8%). Brown adipose tissue protein content and thermogenic capacity (assessed from purine nucleotide binding to isolated mitochondria) were greater than control values in sucrose-fed and protein-deficient animals, and the greatest levels of activity were seen in low protein-fed rats with a high fat intake. The results demonstrate that the changes in energy balance, thermogenesis and brown adipose tissue activity that result from protein deficiency cannot be ascribed to changes in the level of energy intake or to a specific increase in the amount or proportion of either CHO or fat. They suggest that the protein-to-energy ratio must be the primary influence on thermogenesis and brown fat activity in these animals.

75 citations

Journal ArticleDOI
24 Aug 1984-JAMA
TL;DR: Light et al 2 have shown that in a select group of patients, transudates and exudates can be separated in the laboratory by measuring the protein and lactate dehydrogenase.
Abstract: PLEURAL effusions are commonly seen in a variety of diseases. Based on the underlying pathophysiological abnormality, these effusions can be divided into transudates and exudates.1Transudative effusions develop when there is a change in systemic factors such as an increase in capillary hydrostatic pressure or a decrease in colloid osmotic pressure with no change in the pleural surface. Common causes of transudative effusions include congestive heart failure, chronic renal failure, and low protein states. Exudative effusions are caused by an altered permeability of the pleural vessels or by obstruction of lymphatics as is seen in neoplasms, infections, or other inflammatory processes. Physicians use a number of laboratory tests to determine which of these processes is occurring in a particular patient. Light et al2have shown that in a select group of patients, transudates and exudates can be separated in the laboratory by measuring the protein and lactate dehydrogenase

75 citations

Journal ArticleDOI
TL;DR: Permanency of the hydrophilic surfaces so generated was confirmed by surface contact angle experiments and total organic carbon leachables analysis of the aqueous contacting solutions, as determined by the Fluoraldehyde procedure.
Abstract: Low protein adsorbing polymer films have been prepared with which to fabricate intravenous containers, designed for compatibility with low concentrations of protein drugs. The material is economically manufactured utilizing physical melt blending of water-soluble surface-modifying polymers (PEO, PEOX, PVA, and PNVP) with a base polymer (EVA, PP, PETG, PMMA, SB, and nylon). Permanency of the hydrophilic surfaces so generated was confirmed by surface contact angle experiments and total organic carbon leachables analysis of the aqueous contacting solutions. Binding of IgG, albumin and insulin was studied. A sixfold reduction of protein adsorption was obtained by adding 5% PVA13K to EVA, for IgG at a bulk concentration of 2.5 ppm. Surface bound protein measured by micro-BCA colorimetry, agreed with the solution protein lost, as determined by the Fluoraldehyde procedure. Imaging of the protein exposed plastic surfaces by silver enhanced protein conjugated gold staining agreed with the quantitative assay determinations.

75 citations

Journal ArticleDOI
TL;DR: A systematic review of previously reported cases of sclerosing mesenteritis to determine the epidemiology, risk factors, methods of diagnosis, treatment patterns and outcomes for this disease is performed.
Abstract: Sclerosing mesenteritis includes a spectrum of inflammatory disorders involving the adipose tissue of the bowel mesentery. To perform a systematic review of previously reported cases of sclerosing mesenteritis (SM) to determine the epidemiology, risk factors, methods of diagnosis, treatment patterns and outcomes for this disease. Medline, PubMed, Google Scholar and Cochrane database were searched using keywords mesenteric panniculitis, retractile mesenteritis, mesenteric lipodystrophy and sclerosing mesenteritis. Data was collated into a single excel database, transferred into SPSS (Version 21.0) and analyzed. Patients diagnosed with SM were between ages of 3 and 88 with a mean age of 55 ± 19.2 years. SM was more common in Caucasians (n = 28, 60.8% of those reporting ethnicity) and men (n = 133, 69.3%) with a male to female ratio of 2.3:1. 28.6% (n = 55) of patients reported a prior abdominal surgery or abdominal trauma, 8.9% (n = 17) had a history of malignancy, and 5.7% (n = 11) of autoimmune disease. 85.4% (n = 164) underwent surgical abdominal exploration (open or laparoscopic); 41.7% (n = 80) had surgery with resection of the involved bowel and mesentery. 34.9% (n = 67) of patients received medical treatment with the majority of them receiving steroids (n = 56, 83.5%). Symptom duration of more than a month (66.7% vs 40.4%, p < 0.05), underlying autoimmune disorder (14.3% vs 4.0%, p < 0.05) or low protein (14.3% vs 4.0%, p < 0.05) at presentation were seen more frequently in those with poor treatment response whereas patients with tender abdomen (45.0% vs 19.0%, p < 0.05) or leukocytosis (20.5% vs 0.0%, p < 0.05) at presentation were likely to have good response to therapy. The most common complications included bowel obstruction/ileus/ischemia (n = 10, 23.8%) and obstructive uropathy/renal failure (n = 10, 23.8%). There were a total of 14 deaths, 12 (85.7%) of which were secondary to SM related complications. SM is a poorly understood chronic inflammatory disease. Our study is the first systematic review of the published cases of SM. Future work is required to better understand this disease and its optimal therapy.

75 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20227
2021298
2020300
2019278
2018308
2017306