6,794 research outputs found
Effects of the basic multicellular unit and lamellar thickness on osteonal fatigue life
No full textA remodeling cycle sets the size of the osteon and associated lamellae in the basic multicellular unit. Treatments and aging affect these micro-structural features. We previously demonstrated decreased fatigue life with an unexplained mechanism and decreased osteon size in cortical bone treated with high-dose bisphosphonate. Here, three finite element models were examined: type-1: a single osteon, as a homogeneous unit and with heterogeneous lamellae and interlamellae, type-2: a control, interstitial-only tissue and type-3: the osteon with cement line, set within the interstitial tissue. Models were loaded in simulated, sinusoidal bending fatigue. As osteon size was decreased, lamellar number and lamellar thickness were incrementally adjusted for each model. As hypothesized, lamellae within the larger type-1 models attained greater cycles to failure and the addition of an osteon to type-2 models (generating a type-3 model set) yielded increased fatigue life. However, as the osteon size was decreased, the potential for compressive damage nucleation was increased within the lamellae of the osteons versus the interstitium. Also, osteons with fewer, thicker lamellae displayed increased fatigue life. Osteonal microstructure plays a role in damage initiation location, especially when BMU size is smaller. Previous findings by us and others could partially be explained by this further understanding of increased probability for damage nucleation in smaller osteons.Peer reviewe
Chronic High Fructose Intake Reduces Serum 1,25(OH)<sub>2</sub>D<sub>3</sub>Levels in Calcium-Sufficient Rodents
No full textExcessive fructose consumption inhibits adaptive increases in intestinal Ca2+transport in lactating and weanling rats with increased Ca2+requirements by preventing the increase in serum levels of 1,25(OH)2D3. Here we tested the hypothesis that chronic fructose intake decreases 1,25(OH)2D3 levels independent of increases in Ca2+ requirements. Adult mice fed for five wk a high glucose-low Ca2+ diet displayed expected compensatory increases in intestinal and renal Ca2+ transporter expression and activity, in renal CYP27B1 (coding for 1α-hydroxylase) expression as well as in serum 1,25(OH)2D3 levels, compared with mice fed isocaloric glucose- or fructose-normal Ca2+ diets. Replacing glucose with fructose prevented these increases in Ca2+ transporter, CYP27B1, and 1,25(OH)2D3 levels induced by a low Ca2+ diet. In adult mice fed for three mo a normal Ca2+ diet, renal expression of CYP27B1 and of CYP24A1 (24-hydroxylase) decreased and increased, respectively, when the carbohydrate source was fructose instead of glucose or starch. Intestinal and renal Ca2+ transporter activity and expression did not vary with dietary carbohydrate. To determine the time course of fructose effects, a high fructose or glucose diet with normal Ca2+ levels was fed to adult rats for three mo. Serum levels of 1,25(OH)2 D3 decreased and of FGF23 increased significantly over time. Renal expression of CYP27B1 and serum levels of 1,25(OH)2D3 still decreased in fructose- compared to those in glucose-fed rats after three mo. Serum parathyroid hormone, Ca2+ and phosphate levels were normal and independent of dietary sugar as well as time of feeding. Thus, chronically high fructose intakes can decrease serum levels of 1,25(OH)2D3 in adult rodents experiencing no Ca2+ stress and fed sufficient levels of dietary Ca2+. This finding is highly significant because fructose constitutes a substantial portion of the average diet of Americans already deficient in vitamin D.Peer reviewe
Pannexin-1 and P2X7-Receptor Are Required for Apoptotic Osteocytes in Fatigued Bone to Trigger RANKL Production in Neighboring Bystander Osteocytes
No full textOsteocyte apoptosis is required to induce intracortical bone remodeling after microdamage in animal models, but how apoptotic osteocytes signal neighboring “bystander” cells to initiate the remodeling process is unknown. Apoptosis has been shown to open pannexin-1 (Panx1) channels to release adenosine diphosphate (ATP) as a “find me” signal for phagocytic cells. To address whether apoptotic osteocytes use this signaling mechanism, we adapted the rat ulnar fatigue-loading model to reproducibly introduce microdamage into mouse cortical bone and measured subsequent changes in osteocyte apoptosis, receptor activator of NF-kB ligand (RANKL) expression and osteoclastic bone resorption in wild-type (WT; C57Bl/6) mice and in mice genetically deficient in Panx1 (Panx1KO). Mouse ulnar loading produced linear microcracks comparable in number and location to the rat model. WT mice showed increased osteocyte apoptosis and RANKL expression at microdamage sites at 3 days after loading and increased intracortical remodeling and endocortical tunneling at day 14. With fatigue, Panx1KO mice exhibited levels of microdamage and osteocyte apoptosis identical to WT mice. However, they did not upregulate RANKL in bystander osteocytes or initiate resorption. Panx1 interacts with P2X7R in ATP release; thus, we examined P2X7R-deficient mice and WT mice treated with P2X7R antagonist Brilliant Blue G (BBG) to test the possible role of ATP as a find-me signal. P2X7RKO mice failed to upregulate RANKL in osteocytes or induce resorption despite normally elevated osteocyte apoptosis after fatigue loading. Similarly, treatment of fatigued C57Bl/6 mice with BBG mimicked behavior of both Panx1 KO and P2X7RKO mice; BBG had no effect on osteocyte apoptosis in fatigued bone but completely prevented increases in bystander osteocyte RANKL expression and attenuated activation of resorption by more than 50%. These results indicate that activation of Panx1 and P2X7R are required for apoptotic osteocytes in fatigued bone to trigger RANKL production in neighboring bystander osteocytes and implicate ATP as an essential signal mediating this process.Peer reviewe
sj-pdf-1-vdi-10.1177_10406387221105890 – Supplemental material for Salmonella enterica serovar Brandenburg abortions in dairy cattle
No full textSupplemental material, sj-pdf-1-vdi-10.1177_10406387221105890 for Salmonella enterica serovar Brandenburg abortions in dairy cattle by Christopher L. Siepker, Kent J. Schwartz, Tyler J. Feldhacker, Drew R. Magstadt, Orhan Sahin, Marcelo Almeida, Ganwu Li, Kristin P. Hayman and Patrick J. Gorden in Journal of Veterinary Diagnostic Investigation</p
Data for Thermodynamics of proton insertion across the perovskite-brownmillerite transition in La0.5Sr0.5CoO3-δ
No full textThe `protonation-of-lsco` zip includes the plots which appear in our manuscript, along with the data and scripts used to generate them. In addition to the structures, energies, and other data related to host, oxygen vacancy, and hydrogen interstitial structures of La0.5Sr0.5CoO3-δ (and SrCoO2.5), metadata (e.g., INCAR settings) related to the first-principle calculations is included in the data files. Each subfolder (`scripts`, `figures`, `dos_data`, and `data`) contains a detailed README.md file that provides additional information related to the files contained within.This repository exists to share the data and scripts used in the paper "Thermodynamics of proton insertion across the perovskite-brownmillerite transition in La0.5Sr0.5CoO3-δ" by Armand J. Lannerd, Nathan J. Szymanski, and Christopher J. Bartel. The files are contained in the folder `protonation-of-lsco` with additional detailed information presented in the `README.md` files of each subfolder (`scripts`, `figures`, `dos_data`, and `data`).This work was supported primarily by the National Science Foundation through the University of Minnesota MRSEC under Award Number DMR-2011401. This material is based upon work partially supported by the National Science Foundation Graduate Research Fellowship Program under Grant No. 2237827. Any opinions, findings, and conclusions or recommendations expressed in this material are those of the author(s) and do not necessarily reflect the views of the National Science Foundation. The authors acknowledge the Minnesota Supercomputing Institute (MSI) at the University of Minnesota for providing resources that contributed to the research results reported within this paper.Lannerd, Armand J; Szymanski, Nathan J; Bartel, Christopher J. (2026). Data for Thermodynamics of proton insertion across the perovskite-brownmillerite transition in La0.5Sr0.5CoO3-δ. Retrieved from the Data Repository for the University of Minnesota (DRUM), https://doi.org/10.13020/5etj-a120
Recommended from our members
Texas African American Millionaire Henry Miller Morgan’s Social Justice Crusade: Tyler Barber College Chain, 1933-1974
Full text linkThis thesis examines the social justice ideology of Henry Miller Morgan (also known as H.M. Morgan and Henry Morgan), the Texas African American millionaire and founder of a 1930s Texas African American barber school business. Tyler Barber College Chain was the first barber school in the nation for African Americans. It was founded in Tyler, Texas in 1933 during Jim Crow segregation after Texas passed a barber license law in 1929 that required all barbers to be trained and pass a state exam. Tyler Barber College Chain had locations all over the country during Jim Crow segregation and trained an estimated 80 percent of the nation’s African American barbers. Morgan was a barber, a businessman, and active with the Texas NAACP, the Democratic Progressive Voters League, his local Baptist church, and the National Negro Business League. When he died in Houston in 1961 at his hotel, Jet magazine reported that he was a millionaire
The effects of estrogen deficiency on cortical bone microporosity and mineralization
No full textRecent studies have demonstrated matrix-mineral alterations in bone tissue surrounding osteocytes in estrogen-deficient animals.While cortical bone porosity has been shown to be a contributor to the mechanical properties of bone tissue, little analysis has been done to investigate the effects of estrogen deficiency on bone's microporosities, including the vascular and osteocyte lacunar porosities. In this study we examined alterations in cortical bone microporosity, mineralization, and cancellous bone architecture due to estrogen deficiency in the ovariectomized rat model of postmenopausal osteoporosis. Twenty-week-old female Sprague–Dawley rats were subjected to either ovariectomy or sham surgery. Six weeks post-surgery tibiae were analyzed using high-resolution micro-CT, backscattered electron imaging, nanoindentation, and dynamic histomorphometry. Estrogen deficiency caused an increase in cortical bone vascular porosity, with enlarged vascular pores and little change in tissue mineral density in the proximal tibial metaphysis. Measurements of cancellous architecture corresponded to previous studies reporting a decrease in bone volume fraction, an increase in trabecular separation, and a decrease in trabecular number in the proximal tibia due to estrogen deficiency. Nanoindentation results showed no differences in matrix stiffness in osteocyte-rich areas of the proximal tibia of estrogen-deficient rats, and bone labeling and backscattered electron imaging showed no significant changes in mineralization around the vascular pores. The findings demonstrate local surface alterations of vascular pores due to estrogen deficiency. An increase in cortical vascular porosity may diminish bone strength as well as alter bone mechanotransduction via interstitial fluid flow, both of which could contribute to bone fragility during postmenopausal osteoporosis.Peer reviewe
sj-docx-2-dhj-10.1177_20552076241249925 - Supplemental material for Longitudinal clinical decision support for assessing decisions over time: State-of-the-art and future directions
No full textSupplemental material, sj-docx-2-dhj-10.1177_20552076241249925 for Longitudinal clinical decision support for assessing decisions over time: State-of-the-art and future directions by Tyler J Loftus, Jeremy A Balch, Jenna L Marquard, Jessica M Ray, Brian S Alper, Neeraj Ojha, Azra Bihorac, Genevieve Melton-Meaux, Gopal Khanna and Christopher J Tignanelli in DIGITAL HEALTH</p
sj-docx-1-dhj-10.1177_20552076241249925 - Supplemental material for Longitudinal clinical decision support for assessing decisions over time: State-of-the-art and future directions
No full textSupplemental material, sj-docx-1-dhj-10.1177_20552076241249925 for Longitudinal clinical decision support for assessing decisions over time: State-of-the-art and future directions by Tyler J Loftus, Jeremy A Balch, Jenna L Marquard, Jessica M Ray, Brian S Alper, Neeraj Ojha, Azra Bihorac, Genevieve Melton-Meaux, Gopal Khanna and Christopher J Tignanelli in DIGITAL HEALTH</p
Progressive hyperthermia elicits distinct responses in maximum and rapid torque production
Full text linkObjectivesTo investigate the effect of progressive whole-body hyperthermia on maximal, and rapid voluntary torque production, and their neuromuscular determinants.DesignRepeated measures, randomised.MethodsNine participants performed sets of neuromuscular assessments in HOT conditions (~50°C, ~35% relative humidity) at rectal temperatures (Tre) of 37, 38.5 and 39.5°C and in CON conditions (~22°C, ~5% relative humidity) at a Tre of ~37°C and pre-determined comparative time-points. Electrically evoked twitch (single impulse) and octet (8 impulses at 300 Hz) responses were measured at rest. Maximum voluntary torque (MVT), surface electromyography (EMG) normalised to maximal M-wave, and voluntary activation (VA) were measured during 3-5 s isometric maximal voluntary contractions. Rate of torque development (RTD) and normalised EMG were measured during rapid voluntary isometric contractions from rest.ResultsAll neuromuscular variables were unaffected by time in CON. In HOT, MVT, normalised EMG at MVT and VA were lower at 39.5°C compared to 37°C (p<0.05). Early- (0-50 ms) and middle- (50-100 ms) phase voluntary RTD were unaffected by increased Tre (p>0.05), despite lower normalised EMG at Tre 39.5°C (p<0.05) in rapid contractions. In contrast, late-phase (100-150 ms) voluntary RTD was lower at 38.5°C and 39.5°C compared to 37°C (p<0.05) in HOT. Evoked twitch and octet RTD increased with increased Tre (p<0.05). ConclusionsHyperthermia reduced late-phase voluntary RTD, likely due to reduced neural drive and the reduction in MVT. In contrast, early- and middle-phase voluntary RTD were unaffected by hyperthermia, likely due to the conflicting effects of reduced neural drive but faster intrinsic contractile properties.© 2021, Sports Medicine Australia. Published by Elsevier Ltd. The attached document (embargoed until 19/03/2023) is an author produced version of a paper published in JOURNAL OF SCIENCE AND MEDICINE IN SPORT uploaded in accordance with the publisher’s self-archiving policy. The final published version (version of record) is available online at the link. Some minor differences between this version and the final published version may remain. We suggest you refer to the final published version should you wish to cite from it.</p
- …
