Lipids, as the basic component of cell membranes, play an important role in human health as well as brain function. The brain is highly enriched in lipids, and disruption of lipid homeostasis is related to neurologic disorders as well as neurodegenerative diseases such as Alzheimer’s disease (AD). Aging is associated with changes in lipid composition. Alterations of fatty acids at the level of lipid rafts and cerebral lipid peroxidation were found in the early stage of AD. Genetic and environmental factors such as apolipoprotein and lipid transporter carrying status and dietary lipid content are associated with AD. Insight into the connection between lipids and AD is crucial to unraveling the metabolic aspects of this puzzling disease. Recent advances in lipid analytical methodology have led us to gain an in-depth understanding on lipids. As a result, lipidomics have becoming a hot topic of investigation in AD, in order to find biomarkers for disease prediction, diagnosis, and prevention, with the ultimate goal of discovering novel therapeutics.
PurposeThe use of an intraoperative tourniquet for total knee arthroplasty (TKA) is a common practice. However, the effectiveness and safety are still questionable. A systematic review was conducted to examine that whether using a tourniquet in TKA was effective without increasing the risk of complications.MethodsA comprehensive literature search was done in PubMed Medicine, Embase, and other internet database. The review work and the following meta-analysis were processed to evaluate the role of tourniquet in TKA.ResultsEight randomized controlled trials and three high-quality prospective studies involving 634 knees and comparing TKA with and without the use of a tourniquet were included in this analysis. The results demonstrated that using a tourniquet could decrease the measured blood loss but could not decrease the calculated blood loss, which indicated actual blood loss. Patients managed with a tourniquet might have higher risks of thromboembolic complications. Using the tourniquet with late release after wound closure could shorten the operation time; whereas early release did not show this benefit.ConclusionsThe current evidence suggested that using tourniquet in TKA may save time but may not reduce the blood loss. Due to the higher risks of thromboembolic complications, we should use a tourniquet in TKA with caution.
This study introduces a sonographically assisted percutaneous technique for releasing trigger digits which provides direct visualization of the release and avoids the risks of incomplete release and injury to adjacent neurovascular structures associated with other percutaneous release techniques. The "safe zone" and an estimate of the size of the A1 pulley were determined in a separate cadaver study. We then used these landmarks in a prospective clinical study of 107 digits in 83 consecutive patients treated by this technique. During the follow-ups of between 9 and 15 months, we evaluated 104 digits in 80 patients. Pain was absent in 101 digits (97%) and considerably improved in the other three (3%). All mechanical problems had been resolved and none recurred during follow-up. This technique allows the surgeon to see and monitor, precisely, the percutaneous division of the A1 pulley without open surgery and, therefore, to avoid the inherent risks of percutaneous and open surgical release.
Objective. MicroRNA (miRNA) plays a role in autoimmune diseases. MiRNA-223 (miR-223) is upregulated in patients with rheumatoid arthritis (RA) and is involved in osteoclastogenesis, which contributes to erosive disease. The aim of this study was to test the feasibility of using lentiviral vectors expressing the miR-223 target sequence (miR-223T) to suppress miR-223 activity as a therapeutic strategy in a mouse model of collagen-induced arthritis (CIA).Methods. Levels of miR-223 in the synovial tissue of patients with RA or osteoarthritis (OA), as well as in the ankle joints of mice with CIA, were determined by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). Lentiviral vectors expressing miR-223T (LVmiR-223T) or luciferase short hairpin RNA (LVshLuc) as a control vector were injected intraperitoneally into mice with CIA. Treatment responses and disease-related bone mineral density were monitored. Levels of nuclear factor 1A (NF-1A), a direct target of miR-223, and macrophage colony-stimulating factor receptor (M-CSFR), which is critical for osteoclastogenesis, were measured by immunohistochemistry and quantitative RT-PCR. Osteoclasts were assessed by tartrate-resistant acid phosphatase staining.Results. MiR-223 expression was significantly higher in the synovium of RA patients and in the ankle joints of mice with CIA as compared to OA patients and normal mice. LVmiR-223T treatment reduced the arthritis score, histologic score, miR-223 expression, osteoclastogenesis, and bone erosion in mice with CIA. Down-regulation of miR-223 with concomitant increases in NF-1A levels and decreases in M-CSFR levels was detected in the synovium of LVmiR-223T-treated mice.Conclusion. This study is the first to demonstrate that lentivirus-mediated silencing of miR-223 can reduce disease severity of experimental arthritis. Furthermore, our results indicate that inhibition of miR-223 activity should be further explored as a therapeutic strategy in RA.
We sought to determine the possible neural conduction blockade of tramadol and whether there is evidence of localized neural toxicity with spinal somatosensory evoked potential (SSEP) measurements. Male Wistar rats were used. SSEP, elicited by supramaximally stimulating the hind paw and recorded from the thoracolumbar and the first and second lumbar interspinous ligaments, was monitored. SSEPs were obtained before drug application as the pretreatment baseline and measured every 15 min after treatment for 2 h and at 60-min intervals thereafter until SSEP returned to baseline or for another 4 h. Two small strips of Gelfoam (0.6 x 1.0 cm(2)) soaked with the drug were placed under and over the left sciatic nerve for a 30-min period. Gelfoam was prepared with tramadol hydrochloride (Tramal; the US trade name is Ultram) 5, 2.5, and 1.25 mg, diluted if needed with saline to a total volume of 100 microL (5%, 2.5%, and 1.25%, respectively). The control data were obtained from the right side limb with normal saline by following the same method. Spinal SSEPs were measured after 48 h to detect the late neural damage. The results showed that direct tramadol application on sciatic nerves dose-dependently reduced both the amplitude and conduction velocity of SSEPs when compared with the pretreatment baseline. All SSEPs returned to pretreatment baseline, and no significant changes of SSEP between bilateral limbs were noted at the 48-h measurements. No evidence of irreversible conduction blockade indicative of local neural toxicity was seen. Pretreatment with naloxone 1 mg/kg failed to block the changes of SSEP produced by 2.5% tramadol 100 microL. We conclude that tramadol exerts a local anesthetic-type effect on peripheral nerves.
The purpose of this study was to assess the value of using intraoperative sonography to assist percutaneous release of the A1 pulley in cadavers. By detailed sonographic examination and anatomical exploration, the authors determined the correlation of the actual A1 and A2 pulleys (and adjacent neurovascular bundles not visualized by sonography) to the clearly visualized flexor tendons and the metacarpophalangeal joint. The authors also evaluated their effectiveness as landmarks and the effectiveness of real-time sonographic monitoring during percutaneous release. Experiments were performed on 80 fingers and 20 thumbs in 10 cadavers. All digits were sonographically examined. The clearly delineated bony landmarks of the metacarpophalangeal joint were measured and marked. The A1 and A2 pulleys and the neurovascular bundles were surgically exposed, and their relation to the markers made during sonographic examination was measured. Using these parameters, sonographically assisted percutaneous release of the A1 pulley with a custom-made hook knife was performed on the contralateral side. The completeness of the A1 release and the potential risk of injuries to the A2, flexor tendon, and neurovascular bundles in each digit were examined. Results showed good correlation between the actual length of the A1 pulleys and the sonographically determined distance between the bony prominences of the metacarpophalangeal joint in all digits. Release was complete in 48 of the 50 digits (96 percent) and partial in two, with no injuries to neurovascular bundles. Sonography can clearly delineate the flexor tendon and underlying bony boundary of the metacarpophalangeal joint, which is useful in directing the percutaneous release of the A1 pulley. Sonography can also provide real-time intraoperative monitoring. The results using this new release technique were adequate. The method is safe and its clinical application should be encouraged.
CD4(+) T cells were activated during the onset of OA, but cartilage damage was more prominent at a later stage. CD4(+) T cells were involved in the pathogenesis of OA: they induced MIP-1γ expression and subsequent osteoclast formation.
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