Publications by authors named "Littlefield N"

Psychosocial rehabilitation and psychosocial disability research have been a longstanding topic in healthcare, demanding continuous exploration and analysis to enhance patient and clinical outcomes. As the prevalence of psychosocial disability research continues to attract scholarly attention, many scientific articles are being published in the literature. These publications offer profound insights into diagnostics, preventative measures, treatment strategies, and epidemiological factors.

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Objectives: Recently, deep learning medical image analysis in orthopedics has become highly active. However, progress has been restricted by the absence of large-scale and standardized ground-truth images. To the best of our knowledge, this study is the first to propose an innovative solution, namely a deep few-shot image augmentation pipeline, that addresses this challenge by synthetically generating knee radiographs for training downstream tasks, with a specific focus on knee osteoarthritis Kellgren-Lawrence (KL) grading.

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Hypertension is a leading risk factor in cardiovascular disease (CVD) with the highest national rates in southeastern and Appalachian counties. To reduce hypertension health disparities and CVD risk, the Kentucky Department for Public Health Heart Disease and Stroke Program (KHDSP) designed, implemented, and continuously evaluated the Cardiovascular Assessment Risk Reduction and Education Self-Measured Blood Pressure (CARE SMBP) program in rural and Appalachian Kentucky. Ten health care systems and two local health departments implemented CARE SMBP.

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Article Synopsis
  • This study looks at how AI can help doctors understand the bones in the hip and knee better for surgeries, but also checks for problems like unfairness in these AI systems.
  • The focus is on using regular X-rays instead of fancy scans because X-rays are easier to get and cheaper.
  • They found ways to fix biases related to things like gender, race, and age, and shared their work to help doctors make better decisions and promote fairness in healthcare.
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Purpose: Heart disease is the leading cause of death in the United States. HMG-CoA reductase inhibitors, or statins, are medications at the forefront of the battle against cardiovascular disease. Despite their effectiveness, patient compliance with statins has lagged because of medication cost and adverse effects, namely myopathy.

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Background: We examined aerobic and anaerobic exercise energy expenditure and excess post-exercise oxygen consumption (EPOC) between a 250 Watt, 1-minute bout of cycling and uphill treadmill running.

Methods: Fourteen active to well-trained subjects volunteered for the investigation (VO2 max: 57.0 +/- 12.

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Repair and replicative DNA synthesis were measured at different stages of the cell cycle in control and cadmium-treated Chinese hamster ovary (CHO-K1) cells. Cells were synchronized by counterflow centrifugal elutriation. Elutriation resulted in five repair and four replication subphases.

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The effect of cadmium ion (Cd) and ascorbic acid (Asc) on the induction of oxidative DNA damage and on the activities of antioxidant enzymes were investigated in human lymphoblastoid cells (AHH-1 TK+/-). Cd at low concentrations of 5-35 microM induced the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) and caused nuclear DNA strand breaks. The formation both of 8-OHdG and of DNA strand breaks was dose-dependent at the low Cd concentration; both parameters were linearly correlated with each other (R = 0.

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Nickel (Ni) and magnesium (Mg) exert separate and interacting effects on cells: Ni is toxic while Mg enhances the transformation response of transformed cells and protects from heavy metal-induced toxicity. Transformed rat liver epithelial cells were used in the soft agar (SA) assay to measure the effect of Ni and/or Mg on the expression of anchorage independence. Cells were exposed to +/- Ni and +/- Mg in a single passage of growth medium (GM) prior to assay in SA.

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The interactive effects of the anti-oxidant ascorbate (Asc) and the metals cadmium (Cd, as CdCl2) or nickel (Ni, as NiCl2) on the in vitro formation of breaks in double-stranded deoxyribonucleic acid (d/s DNA) were determined. Concentrations of 50 microM Cd or 200 microM Ni were dosed for 4 hours in factorial combinations with 500 microM Asc in RPMI 1640 medium (7 percent bovine serum) in which AHH-1 TK+/- cells (a spontaneously transformed human B lymphoblastoid cell line by Gentest Corp.) were replicating.

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Magnesium, an essential metal that is important in the normal functioning of DNA, has been shown to interact with some of the toxic heavy metals in respect to biochemical and molecular mechanisms and in altering the tumorigenic process. This study examined the influence of magnesium in combination with nickel and cadmium in respect to damage of the DNA molecule. The purpose of this study was to evaluate the influence of magnesium on the amelioration of the toxic metals nickel and cadmium in respect to sustaining DNA damage.

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The effects of magnesium (Mg) restriction on cell growth and the cell cycle were determined in transformed (TRL-8) and non-transformed (TRL-12-15) epithelial-like rat liver cells. Cells were cultured in RPMI 1640 medium in which the Mg concentration was reduced to 0.5, 0.

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Nickel (Ni), a carcinogenic and genotoxic metal, has been shown to enhance deglycosylation and hydroxylation of 2'-deoxyguanosine (dG) that has been caused by ascorbic acid and H2O2. There is evidence that Mg is a competitive antagonist of the toxicological effects of Ni. A factorial design was used to examine the interactive influence of Mg and Ni on the deglycosylation and hydroxylation of dG under a range of pH conditions in which ascorbate (Ascb) and H2O2 were added.

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Fischer 344 rats were given 10, 40, 600, 1200 or 2400 ppm sulphamethazine (SMZ) in the diet to determine the toxicity and potential carcinogenicity of SMZ. There were 225 rats of each sex in the control groups and 135 of each sex in each dose group. Animals were killed after 3, 12, 18 or 24 months of continuous dosing.

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A chronic feeding study was carried out in B6C3F1 mice with sulphamethazine (SMZ). The test substance was administered in the diet at dose levels of 0 (control), 300, 600, 1200, 2400 and 4800 ppm for 24 months. Mice were killed after 12, 18 and 24 months of continuous dosing.

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A chronic feeding study was carried out in the F1a generation of dosed Fischer 344 rats of both sexes with gentian violet (GV). The test substance was administered in the diet to 570 male and 570 female rats at dose levels of 0 (control), 100, 300 and 600 ppm for 24 months. Rats were killed and necropsied after 12, 18 and 24 months of continuous dosing.

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Fischer 344 rats (810 of each sex) were divided into treatment groups and fed diets containing 0, 10, 40, 600, 1200, or 2400 ppm sulfamethazine. Serum samples were analyzed for levels of thyroid-stimulating hormone (TSH), total thyroxine (T4), total triiodothyronine (T3), and T3 uptake after 12, 18, or 24 mo of continuous dosing. There were no statistically significant differences in T3 levels or percent T3 uptake for either sex after any of the exposure periods.

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Gentian violet is a dye belonging to a chemical class known as the di- and triaminophenylmethanes. Although it has been used for many years for the control of fungal and intestinal parasites, for various uses in veterinary medicine, and as an additive to the feed of chickens to inhibit propagation of mold and fungus, very few long-term toxicity data are available. A life span dosing study of gentian violet in the diet of 720 males and 720 females of B6C3F1 mice (C57BL/6 X C3H) at dose levels of 0, 100, 300, and 600 ppm was done to determine its toxicity and carcinogenicity.

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Male and female (840 each) BALB/cStCrlfC3Hf/Nctr mice were given 0, 7, 14, 28, 55, 110 and 220, and 0, 7, 19, 38, 75, 150 and 300 ppm, respectively, of 4-aminobiphenyl in their drinking water. Necropsies on killed animals were performed at 13, 26, 39, 52 and 96 weeks on dose. Dose-related neoplasms were angiosarcomas, bladder urothelial carcinomas and hepatocellular neoplasms.

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One element of the ED01 Study contained a group of animals that were dosed with 2-acetylaminofluorene for 9, 12, 15, 18, or 24 mo and then sacrificed at 18 or 24 mo. This provided data to compare the relative effects on carcinogenicity of dose rate versus total dose. The prevalence of liver and bladder tumors were used as the comparison.

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A lifespan exposure of mice to benzidine dihydrochloride was conducted for 33 m using both sexes of two populations of mice with the same gene pool. One population was the genetically homogeneous F1 hybrid produced by crossing BALB/cStCrlC3Hf/Nctr males with C57BL/6jfC3Hf/Nctr females. The second population consisted of genetically heterogenous monohybrid cross (MC) offspring produced by mating the F1 hybrids inter se.

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One hundred and forty four Fischer 344 rats and 144 B6C3F1 mice of both sexes were fed either a control diet or a diet containing 300, 600, 1200, 2400 or 3600 ppm sulfamethazine for 90 days. They were then necropsied and tissue specimens were evaluated for pathological changes by light and transmission electron microscopy. No gross or light microscopic lesions related to sulfamethazine administration were evident in the mice.

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Benzidine, recognized as a bladder carcinogen in man and as a liver carcinogen in experimental animals, is the chemical basis of as many as 200 commercial dyes. Physiological processes can metabolize these dyes to release benzidine, thereby creating a potential exposure hazard. To assess this hazard, both sexes of F1 hybrid (genetically homogeneous) and monohybrid (genetically heterogeneous) mice from a BALB/c male and C57BL/6 female cross were exposed for their respective lifespans to benzidine dihydrochloride in their drinking water at concentrations of 0, 30, 40, 60, 80, 120, and 160 ppm for males, and 0, 20, 30, 40, 60, 80, and 120 ppm for females.

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