Long-term effects of chondrocyte death on rabbit articular cartilage in vivo

1976 ◽  
Vol 58 (4) ◽  
pp. 517-526 ◽  
Author(s):  
WH Simon ◽  
S Richardson ◽  
W Herman ◽  
JR Parsons ◽  
J Lane
Keyword(s):  
Articular Cartilage ◽  
Long Term Effects ◽  
Chondrocyte Death ◽  
Rabbit Articular Cartilage

scholarly journals Long-term effects of carbon containing engineered nanomaterials and asbestos in the lung: one year postexposure comparisons

2014 ◽  
Vol 306 (2) ◽  
pp. L170-L182 ◽  
Author(s):  
Anna A. Shvedova ◽  
Naveena Yanamala ◽  
Elena R. Kisin ◽  
Alexey V. Tkach ◽  
Ashley R. Murray ◽  
...  
Keyword(s):  
Lung Tumor ◽  
Inhalation Exposure ◽  
Geometric Feature ◽  
Width Ratio ◽  
Long Term Effects ◽  
Genotoxic Effects ◽  
Pulmonary Exposure ◽  
Pharyngeal Aspiration

The hallmark geometric feature of single-walled carbon nanotubes (SWCNT) and carbon nanofibers (CNF), high length to width ratio, makes them similar to a hazardous agent, asbestos. Very limited data are available concerning long-term effects of pulmonary exposure to SWCNT or CNF. Here, we compared inflammatory, fibrogenic, and genotoxic effects of CNF, SWCNT, or asbestos in mice 1 yr after pharyngeal aspiration. In addition, we compared pulmonary responses to SWCNT by bolus dosing through pharyngeal aspiration and inhalation 5 h/day for 4 days, to evaluate the effect of dose rate. The aspiration studies showed that these particles can be visualized in the lung at 1 yr postexposure, whereas some translocate to lymphatics. All these particles induced chronic bronchopneumonia and lymphadenitis, accompanied by pulmonary fibrosis. CNF and asbestos were found to promote the greatest degree of inflammation, followed by SWCNT, whereas SWCNT were the most fibrogenic of these three particles. Furthermore, SWCNT induced cytogenetic alterations seen as micronuclei formation and nuclear protrusions in vivo. Importantly, inhalation exposure to SWCNT showed significantly greater inflammatory, fibrotic, and genotoxic effects than bolus pharyngeal aspiration. Finally, SWCNT and CNF, but not asbestos exposures, increased the incidence of K-ras oncogene mutations in the lung. No increased lung tumor incidence occurred after 1 yr postexposure to SWCNT, CNF, and asbestos. Overall, our data suggest that long-term pulmonary toxicity of SWCNT, CNF, and asbestos is defined, not only by their chemical composition, but also by the specific surface area and type of exposure.

scholarly journals Metformin decreases hyaluronan synthesis by vascular smooth muscle cells

2019 ◽  
Vol 68 (2) ◽  
pp. 383-391 ◽  
Author(s):  
Annele Sainio ◽  
Piia Takabe ◽  
Sanna Oikari ◽  
Henriikka Salomäki-Myftari ◽  
Markku Koulu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Response To Treatment ◽  
Long Term Effects

Metformin is the first-line drug in the treatment of type 2 diabetes worldwide based on its effectiveness and cardiovascular safety. Currently metformin is increasingly used during pregnancy in women with gestational diabetes mellitus, even if the long-term effects of metformin on offspring are not exactly known. We have previously shown that high glucose concentration increases hyaluronan (HA) production of cultured human vascular smooth muscle cells (VSMC) via stimulating the expression of hyaluronan synthase 2 (HAS2). This offers a potential mechanism whereby hyperglycemia leads to vascular macroangiopathy. In this study, we examined whether gestational metformin use affects HA content in the aortic wall of mouse offspring in vivo. We also examined the effect of metformin on HA synthesis by cultured human VSMCs in vitro. We found that gestational metformin use significantly decreased HA content in the intima-media of mouse offspring aortas. In accordance with this, the synthesis of HA by VSMCs was also significantly decreased in response to treatment with metformin. This decrease in HA synthesis was shown to be due to the reduction of both the expression of HAS2 and the amount of HAS substrates, particularly UDP-N-acetylglucosamine. As shown here, gestational metformin use is capable to program reduced HA content in the vascular wall of the offspring strongly supporting the idea, that metformin possesses long-term vasculoprotective effects.

scholarly journals In Vivo Delivery of Recombinant Viruses to the Fetal Murine Cochlea: Transduction Characteristics and Long-Term Effects on Auditory Function

2006 ◽  
Vol 14 (3) ◽  
pp. 328-335 ◽  
Author(s):  
Jeffrey C. Bedrosian ◽  
Michael Anne Gratton ◽  
John V. Brigande ◽  
Waixing Tang ◽  
Jessica Landau ◽  
...  
Keyword(s):  
Auditory Function ◽  
Long Term Effects ◽  
Recombinant Viruses ◽  
In Vivo Delivery

scholarly journals In vivo effects of stromelysin on the composition and physical properties of rabbit articular cartilage in the presence and absence of a synthetic inhibitor

1995 ◽  
Vol 38 (11) ◽  
pp. 1678-1686 ◽  
Author(s):  
Lawrence J. Bonassar ◽  
Kimberly A. Jeffries ◽  
Eliot H. Frank ◽  
Vernon L. Moore ◽  
Michael W. Lark ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Physical Properties ◽  
Synthetic Inhibitor ◽  
Presence And Absence ◽  
In Vivo Effects ◽  
Rabbit Articular Cartilage

scholarly journals Melanopsin+RGCs Are fully Resistant to NMDA-Induced Excitotoxicity

2019 ◽  
Vol 20 (12) ◽  
pp. 3012 ◽  
Author(s):  
Beatriz Vidal-Villegas ◽  
Johnny Di Pierdomenico ◽  
Juan A Miralles de Imperial-Ollero ◽  
Arturo Ortín-Martínez ◽  
Francisco M Nadal-Nicolás ◽  
...  
Keyword(s):  
Intravitreal Injection ◽  
Ganglion Cells ◽  
Ex Vivo ◽  
Retinal Ganglion ◽  
Long Term Effects ◽  
Pou Domain ◽  
Short And Long Term ◽  
Sd Oct

We studied short- and long-term effects of intravitreal injection of N-methyl-d-aspartate (NMDA) on melanopsin-containing (m+) and non-melanopsin-containing (Brn3a+) retinal ganglion cells (RGCs). In adult SD-rats, the left eye received a single intravitreal injection of 5µL of 100nM NMDA. At 3 and 15 months, retinal thickness was measured in vivo using Spectral Domain-Optical Coherence Tomography (SD-OCT). Ex vivo analyses were done at 3, 7, or 14 days or 15 months after damage. Whole-mounted retinas were immunolabelled for brain-specific homeobox/POU domain protein 3A (Brn3a) and melanopsin (m), the total number of Brn3a+RGCs and m+RGCs were quantified, and their topography represented. In control retinas, the mean total numbers of Brn3a+RGCs and m+RGCs were 78,903 ± 3572 and 2358 ± 144 (mean ± SD; n = 10), respectively. In the NMDA injected retinas, Brn3a+RGCs numbers diminished to 49%, 28%, 24%, and 19%, at 3, 7, 14 days, and 15 months, respectively. There was no further loss between 7 days and 15 months. The number of immunoidentified m+RGCs decreased significantly at 3 days, recovered between 3 and 7 days, and were back to normal thereafter. OCT measurements revealed a significant thinning of the left retinas at 3 and 15 months. Intravitreal injections of NMDA induced within a week a rapid loss of 72% of Brn3a+RGCs, a transient downregulation of melanopsin expression (but not m+RGC death), and a thinning of the inner retinal layers.

Testicular oxytocin: effects of intratesticular oxytocin in the rat

1991 ◽  
Vol 130 (2) ◽  
pp. 231-NP ◽  
Author(s):  
H. D. Nicholson ◽  
S. E. F. Guldenaar ◽  
G. J. Boer ◽  
B. T. Pickering
Keyword(s):  
Leydig Cells ◽  
Light And Electron Microscopy ◽  
Male Rats ◽  
Plasma Testosterone ◽  
Epididymal Sperm ◽  
Long Term Effects ◽  
Sperm Counts ◽  
Term Administration

ABSTRACT The long-term effects of oxytocin administration on the testis were studied using intratesticular implants. Adult male rats had an Accurel device containing 20 μg oxytocin (releasing approximately 200 ng/day) implanted into the parenchyma of each testis; control animals received empty devices. The animals were killed at weekly intervals for 4 weeks. Some animals were perfused and the testes processed for light and electron microscopy. Blood was collected from the remaining animals for the measurement of testosterone, dihydrotestosterone, LH, FSH and oxytocin; epididymal sperm counts were measured and the testes were extracted and radioimmunoassayed for testosterone, dihydrotestosterone and oxytocin. Long-term administration of oxytocin resulted in a significant reduction in testicular and plasma testosterone levels throughout the 4-week period examined and, after 14 days of treatment, lipid droplets were seen in the Leydig cells of treated but not control animals. Concentrations of dihydrotestosterone in the plasma and testes of the oxytocin-treated animals, however, were significantly elevated after 7 and 14 days and at no time fell below control values. Plasma FSH levels were also lower in the oxytocin-treated animals. Intratesticular oxytocin treatment did not affect LH or oxytocin concentrations in the plasma, epididymal sperm counts or the number of Leydig cells in the testis. Empty Accurel devices had no effect on testicular morphology. This study provides the first evidence that oxytocin in vivo can modify steroidogenesis in the testis. Journal of Endocrinology (1991) 130, 231–238

Long-term effects of a high-dose methamphetamine regimen on subsequent methamphetamine-induced dopamine release in vivo

2001 ◽  
Vol 892 (1) ◽  
pp. 122-129 ◽  
Author(s):  
K.E. Sabol ◽  
J.T. Roach ◽  
S.L. Broom ◽  
C. Ferreira ◽  
M.M. Preau
Keyword(s):  
Dopamine Release ◽  
High Dose ◽  
Long Term Effects

Patellar Tendinopathy Alters the Distribution of Lower Extremity Net Joint Moments during Hopping

2010 ◽  
Vol 26 (3) ◽  
pp. 249-255 ◽  
Author(s):  
Richard B. Souza ◽  
Shruti Arya ◽  
Christine D. Pollard ◽  
George Salem ◽  
Kornelia Kulig
Keyword(s):  
Articular Cartilage ◽  
Lower Extremity ◽  
Sagittal Plane ◽  
Patellar Tendinopathy ◽  
Current Investigation ◽  
Long Term Effects ◽  
Joint Moments ◽  
Control Subjects ◽  
Plane Joint

The purpose of the current investigation was to test the hypothesis that subjects with patellar tendinopathy would demonstrate altered sagittal plane joint moment contributions during hopping tasks. Fourteen subjects (7 patellar tendinopathy, 7 controls) participated. Sagittal net joint moments of the lower extremity, total support moment, and joint contributions to the total support moment were calculated while subjects hopped continuously at a self-selected frequency and at 1.67 Hz. Significant differences were observed for contributions to the total support moment (p= .022). When averaged across hopping frequencies, subjects with patellar tendinopathy demonstrated greater hip contribution (p= .030) and lesser knee contribution (p= .006) compared with the control subjects. Shifting the workload away from the knee and toward the hip may result in a detrimental increase in hip demand and potentially harmful long-term effects on the articular cartilage of the hip.

scholarly journals BDNF-induced TrkB activation down-regulates the K+–Cl− cotransporter KCC2 and impairs neuronal Cl− extrusion

2002 ◽  
Vol 159 (5) ◽  
pp. 747-752 ◽  
Author(s):  
Claudio Rivera ◽  
Hong Li ◽  
Judith Thomas-Crusells ◽  
Hannele Lahtinen ◽  
Tero Viitanen ◽  
...  
Keyword(s):  
Hippocampal Slice ◽  
Neuronal Excitability ◽  
Epileptic Activity ◽  
Signaling Cascades ◽  
Gabaergic Inhibition ◽  
Long Term Effects ◽  
Mouse Hippocampus

Pathophysiological activity and various kinds of traumatic insults are known to have deleterious long-term effects on neuronal Cl− regulation, which can lead to a suppression of fast postsynaptic GABAergic responses. Brain-derived neurotrophic factor (BDNF) increases neuronal excitability through a conjunction of mechanisms that include regulation of the efficacy of GABAergic transmission. Here, we show that exposure of rat hippocampal slice cultures and acute slices to exogenous BDNF or neurotrophin-4 produces a TrkB-mediated fall in the neuron-specific K+–Cl− cotransporter KCC2 mRNA and protein, as well as a consequent impairment in neuronal Cl− extrusion capacity. After kindling-induced seizures in vivo, the expression of KCC2 is down-regulated in the mouse hippocampus with a spatiotemporal profile complementary to the up-regulation of TrkB and BDNF. The present data demonstrate a novel mechanism whereby BDNF/TrkB signaling suppresses chloride-dependent fast GABAergic inhibition, which most likely contributes to the well-known role of TrkB-activated signaling cascades in the induction and establishment of epileptic activity.

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