Field-Programmable Gate Array-Based Implementation of Zero-Trust Stream Data Encryption for Enabling 6G-Narrowband Internet of Things Massive Device Access.

With the advent of 6G Narrowband IoT (NB-IoT) technology, IoT security faces inevitable challenges due to the application requirements of Massive Machine-Type Communications (mMTCs). In response, a 6G base station (gNB) and User Equipment (UE) necessitate increased capacities to handle a larger number of connections while maintaining reasonable performance during operations. To address this developmental trend and overcome associated technological hurdles, this paper proposes a hardware-accelerated and software co-designed mechanism to support streaming data transmissions and secure zero-trust inter-endpoint communications. The proposed implementations aim to offload processing efforts from micro-processors and enhance global system operation performance by hardware and software co-design in endpoint communications. Experimental results demonstrate that the proposed secure mechanism based on the use of non-repeating keys and implemented in FPGA, can save 85.61%, 99.71%, and 95.68% of the micro-processor's processing time in key block generations, non-repeating checks, and data block transfers, respectively.

Leukocyte-poor platelet-rich plasma and leukocyte-rich platelet-rich plasma promote myoblast proliferation through the upregulation of cyclin A, cdk1, and cdk2.

Muscle injuries are common among athletes and often treated with platelet-rich plasma (PRP). However, whether the leukocyte concentration affects the efficacy of PRP in treating muscle injuries remains unclear. This study investigated the effects of leukocyte-poor platelet-rich plasma (LP-PRP) and leukocyte-rich platelet-rich plasma (LR-PRP) on myoblast proliferation and the molecular mechanisms underlying these effects. Myoblasts were treated with 0.5% LP-PRP, 0.5% LR-PRP, 1% LP-PRP, or 1% LR-PRP for 24 h. The gene expression of the LP-PRP- and LR-PRP-treated myoblasts was determined using RNA sequencing analysis. Cell proliferation was evaluated using an bromodeoxyuridine (BrdU) assay, and cell cycle progression was assessed through flow cytometry. The expression of cyclin A, cyclin-dependent kinase 1 (cdk1), and cdk2 was examined using Western blotting. The expression of myoblast determination protein 1 (MyoD1) was examined through Western blotting and immunofluorescence staining. The LP-PRP and LR-PRP both promoted the proliferation of myoblasts and increased differential gene expression of myoblasts. Moreover, the LP-PRP and LR-PRP substantially upregulated the expression of cyclin A, cdk1, and cdk2. MyoD1 expression was induced in the LP-PRP and LR-PRP-treated myoblasts. Our results corroborate the finding that LP-PRP and LR-PRP have similar positive effects on myoblast proliferation and MyoD1 expression.

Lidocaine inhibits migration of tenocytes by downregulating focal adhesion kinase and paxillin phosphorylation.

Lidocaine is the most frequently applied local infiltration anesthetic agent for treating tendinopathies. However, studies have discovered lidocaine to negatively affect tendon healing. In the current study, the molecular mechanisms and effects of lidocaine on tenocyte migration were evaluated. We treated tenocytes intrinsic to the Achilles tendons of Sprague-Dawley rats with lidocaine. The migration ability of cells was analyzed using electric cell-substrate impedance sensing (ECIS) and scratch wound assay. We then used a microscope to evaluate the cell spread. We assessed filamentous actin (F-actin) cytoskeleton formation through immunofluorescence staining. In addition, we used Western blot analysis to analyze the expression of phospho-focal adhesion kinase (FAK), FAK, phospho-paxillin, paxillin, and F-actin. We discovered that lidocaine had an inhibitory effect on the migration of tenocytes in the scratch wound assay and on the ECIS chip. Lidocaine treatment suppressed cell spreading and changed the cell morphology and F-actin distribution. Lidocaine reduced F-actin formation in the tenocyte during cell spreading; furthermore, it inhibited phospho-FAK, F-actin, and phospho-paxillin expression in the tenocytes. Our study revealed that lidocaine inhibits the spread and migration of tenocytes. The molecular mechanism potentially underlying this effect is downregulation of F-actin, phospho-FAK, and phospho-paxillin expression when cells are treated with lidocaine.

On-site Ultrasound Screens out Asymptomatic Knee Lesions in Elite Adolescent Male Basketball Players.

Basketball is a popular sport worldwide with a high injury risk. In this study, we conducted survey composed of clinical symptom reporting scale, physical examination and meticulous portable musculoskeletal ultrasound to 19 elite male high school basketball players and 15 regular male high school students. Our study showed the incidence of ultrasonographic findings of any lesion, suprapatellar effusion and proximal patellar tendinopathy is significantly higher in player group, and the incidence of asymptomatic ultrasonographic lesion is also higher in player group. Screening for asymptomatic lesions bares clinical relevance and plays a role in prevention of symptom development. With the concise and easy-to-perform ultrasonography protocol we performed and being interpreted by sports team physician, the protocol can offer precise diagnosis of common injury and screening for asymptomatic lesion potentially progressive.

Anticipative QoS Control: A Self-Reconfigurable On-Chip Communication.

A self-reconfigurable Network-on-Chip (NoC) architecture that supports anticipative Quality of Service (QoS) control with penetrative switch ability is proposed to enhance the performance of bidirectional-channel NoC communication while supporting prioritized packet transmission services. The anticipative QoS control not only allows each communication channel to be dynamically self-configured to transmit flits in either direction for a better channel utilization of on-chip hardware resources, but also enhances the latency performance for QoS services. The proposed anticipative control is based on penetratingly observing channel direction requests of routers that is two hops away from the current one. The added ability enables a router to allocate high-priority packets to a dedicated virtual channel and then rapidly bypass it to the next destination router. The provided flexibility of packet switch promises better channel bandwidth utilization, lower packet delivery latency, and furthermore guarantees the high-priority packets being served with a better QoS. Accordingly, in this paper, an enhanced NoC architecture supporting the hybrid anticipative QoS, penetrative switch, and bidirectional-channel control, namely Anticipative QoS Bidirectional-channel NoC (AQ-BiNoC) is presented. Tested with cycle-accurate synthetic traffic patterns, significant performance enhancement has been observed when the proposed AQ-BiNoC architecture is compared against conventional NoC designs.

Lidocaine Inhibited Tendon Cell Proliferation and Extracellular Matrix Production by Down Regulation of Cyclin A, CDK2, Type I and Type III Collagen Expression.

Lidocaine injection is a common treatment for tendon injuries. However, the evidence suggests that lidocaine is toxic to tendon cells. This study investigated the effects of lidocaine on cultured tendon cells, focusing on the molecular mechanisms underlying cell proliferation and extracellular matrix (ECM) production. Tendon cells cultured from rat Achilles tendons were treated with 0.5, 1.0, or 1.5 mg/mL lidocaine for 24 h. Cell proliferation was evaluated by Cell Counting Kit 8 (CCK-8) assay and bromodeoxyuridine (BrdU) assay. Cell apoptosis was assessed by Annexin V and propidium iodide (PI) stain. Cell cycle progression and cell mitosis were assessed through flow cytometry and immunofluorescence staining, respectively. The expression of cyclin E, cyclin A, cyclin-dependent kinase 2 (CDK2), p21, p27, p53, matrix metalloproteinases-2 (MMP-2), matrix metalloproteinases-9 (MMP-9), type I collagen, and type III collagen were examined through Western blotting, and the enzymatic activity of MMP-9 was determined through gelatin zymography. Lidocaine reduced cell proliferation and reduced G1/S transition and cell mitosis. Lidocaine did not have a significant negative effect on cell apoptosis. Lidocaine significantly inhibited cyclin A and CDK2 expression but promoted p21, p27, and p53 expression. Furthermore, the expression of MMP-2 and MMP-9 increased, whereas that of type I and type III collagen decreased. Lidocaine also increased the enzymatic activity of MMP-9. Our findings support the premise that lidocaine inhibits tendon cell proliferation by changing the expression of cell-cycle-related proteins and reduces ECM production by altering levels of MMPs and collagens.

Simvastatin Downregulates Cofilin and Stathmin to Inhibit Skeletal Muscle Cells Migration.

Statins are the most effective therapeutic agents for reducing cholesterol synthesis. Given their widespread use, many adverse effects from statins have been reported; of these, musculoskeletal complications occurred in 15% of patients after receiving statins for 6 months, and simvastatin was the most commonly administered statin among these cases. This study investigated the negative effects of simvastatin on skeletal muscle cells. We performed RNA sequencing analysis to determine gene expression in simvastatin-treated cells. Cell proliferation and migration were examined through cell cycle analysis and the transwell filter migration assay, respectively. Cytoskeleton rearrangement was examined through F-actin and tubulin staining. Western blot analysis was performed to determine the expression of cell cycle-regulated and cytoskeleton-related proteins. Transfection of small interfering RNAs (siRNAs) was performed to validate the role of cofilin and stathmin in the simvastatin-mediated inhibition of cell migration. The results revealed that simvastatin inhibited the proliferation and migration of skeletal muscle cells and affected the rearrangement of F-actin and tubulin. Simvastatin reduced the expression of cofilin and stathmin. The knockdown of both cofilin and stathmin by specific siRNA synergistically impaired cell migration. In conclusion, our results indicated that simvastatin inhibited skeletal muscle cell migration by reducing the expressions of cofilin and stathmin.

Automatic Key Update Mechanism for Lightweight M2M Communication and Enhancement of IoT Security: A Case Study of CoAP Using Libcoap Library.

The ecosystem for an Internet of Things (IoT) generally comprises endpoint clients, network devices, and cloud servers. Thus, data transfers within the network present multiple security concerns. The recent boom in IoT applications has accelerated the need for a network infrastructure that provides timely and safe information exchange services. A shortcoming of many existing networks is the use of static key authentication. To enable the use of automatic key update mechanisms in IoT devices and enhance security in lightweight machine-to-machine (M2M) communications, we propose a key update mechanism, namely, double OTP (D-OTP), which combines both one-time password (OTP) and one-time pad to achieve an IoT ecosystem with theoretically unbreakable security. The proposed D-OTP was implemented into the Constrained Application Protocol (CoAP) through the commonly used libcoap library. The experimental results revealed that an additional 8.93% latency overhead was required to obtain an unbreakable guarantee of data transfers in 100 CoAP communication sessions.

Use of Platelet-Rich Plasma Plus Suramin, an Antifibrotic Agent, to Improve Muscle Healing After Injuries.

BACKGROUND: The increasing use of platelet-rich plasma (PRP) to treat muscle injuries raises concerns because transforming growth factor-beta (TGF-ß) in PRP may promote fibrosis in the injured muscle and thus impair muscle regeneration. PURPOSE: To investigate whether suramin (a TGF-ß inhibitor) can reduce muscle fibrosis to improve healing of the injured muscle after PRP treatment and identify the underlying molecular mechanism. STUDY DESIGN: Controlled laboratory study. METHODS: Myoblasts isolated from the gastrocnemius muscle of Sprague Dawley rats were treated with PRP or PRP plus suramin. MTT assays were performed to evaluate cell viability. The expression of fibrosis-associated proteins (such as type I collagen and fibronectin), Smad2, and phosphorylated Smad2 was determined using Western blot analysis and immunofluorescent staining. An anti-TGF-ß antibody was employed to verify the role of TGF-ß in fibronectin expression. Gastrocnemius muscles were injured through a partial transverse incision and then treated using PRP or PRP plus suramin. Hematoxylin and eosin staining was conducted to evaluate the healing process 7 days after the injury. Immunofluorescent staining was performed to evaluate fibronectin expression. Muscle contractile properties-fast-twitch and tetanic strength-were evaluated through electric stimulation. RESULTS: PRP plus 25 µg/mL of suramin promoted myoblast proliferation. PRP induced fibronectin expression in myoblasts, but suramin reduced this upregulation. The anti-TGF-ß antibody also reduced the upregulation of fibronectin expression in the presence of PRP. The upregulation of phosphorylated Smad2 by PRP was reduced by either the anti-TGF-ß antibody or suramin. In the animal study, no significant difference was discovered in muscle healing between the PRP versus PRP plus suramin groups. However, the PRP plus suramin group had reduced fibronectin expression at the injury site. Fast-twitch strength and tetanic strength were significantly higher in the injured muscle treated using PRP or PRP plus suramin. CONCLUSION: Simultaneous PRP and suramin use reduced fibrosis in the injured muscle and promoted healing without negatively affecting the muscle's contractile properties. The underlying molecular mechanism may be associated with the phosphorylated Smad2 pathway. CLINICAL RELEVANCE: Simultaneous PRP and suramin use may reduce muscle fibrosis without compromising muscle contractile properties and thus improve muscle healing.

Platelet-Rich Plasma Releasate Promotes Early Healing in Tendon After Acute Injury.

BACKGROUND: Acute tendon injury can limit motion and thereby inhibit tendon healing. Positive results have been found after the use of platelet-rich plasma (PRP) to treat tendon injury; however, the early effects of PRP on tendon regeneration are not known. PURPOSE/HYPOTHESIS: The purpose of this study was to evaluate the effects of PRP releasate (PRPr) on the early stages of tendon healing in a rat partial tenotomy model. It was hypothesized that PRPr can promote early healing of an Achilles tendon in rats. STUDY DESIGN: Controlled laboratory study. METHODS: PRP was prepared by a 2-step method of manual platelet concentration from 10 rats. PRPr was isolated from the clotted preparation after activation by thrombin and was applied to an Achilles tendon on 1 side of 30 rats on the second day after partial tenotomy, with normal saline used as the control on the other side. Achilles tendon samples were harvested 5 and 10 days after tenotomy. At each time point, 15 Achilles tendon samples were obtained, of which 5 samples were evaluated by Masson trichrome staining, apoptosis, and cell proliferation, while the other 10 samples were tested for tensile strength using a material testing machine. RESULTS: Compared with saline-treated control tendons, the PRPr-treated tendons showed increased collagen synthesis near the cut edge and fewer apoptotic cells (P = .01). An immunohistochemical analysis revealed more Ki-67-positive cells but fewer cluster of differentiation (CD) 68+ (ED1+) macrophages in PRPr tendons compared with saline-treated tendons (P < .01). Tendons treated with PRPr also showed higher ultimate tensile strength than those treated with saline (P = .03). CONCLUSION: PRPr treatment promotes tissue recovery in the early phase of tendon healing by stimulating tendon cell proliferation and collagen production while inhibiting cell apoptosis and CD68+ (ED1+) macrophage infiltration. CLINICAL RELEVANCE: These findings suggest that with PRPr treatment, higher loads can be applied to the healing tendon at an earlier time, which can help the patient resume activity earlier.

Alda-1, an activator of ALDH2, ameliorates Achilles tendinopathy in cellular and mouse models.

Achilles tendinopathy has a high re-injury rate and poor prognosis. Development of effective therapy for Achilles tendinopathy is important. Excessive accumulation of ROS and resulting oxidative stress are believed to cause tendinopathy. Overproduction of hydrogen peroxide (H2O2), the most common ROS, could lead to the tendinopathy by causing oxidative damage, activation of endoplasmic reticulum (ER) stress and apoptotic death of tenocytes. Activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2) is expected to alleviate oxidative stress and ER stress. Alda-1 is a selective and potent activator of ALDH2. In this study, we examined the cytoprotective benefit of Alda-1, an activator of ALDH2, on H2O2-induced Achilles tendinopathy in cellular and mouse models. We prepared cellular and mouse models of Achilles tendinopathy by treating cultured Achilles tenocytes and Achilles tendons with oxidative stressor H2O2. Subsequently, we studied the protective benefit of Alda-1 on H2O2-induced Achilles tendinopathy. Alda-1 pretreatment attenuated H2O2-induced cell death of cultured Achilles tenocytes. Treatment of Alda-1 prevented H2O2-induced oxidative stress and depolarization of mitochondrial membrane potential in tenocytes. Application of Alda-1 attenuated H2O2-triggered mitochondria- and ER stress-mediated apoptotic cascades in cultured tenocytes. Alda-1 treatment ameliorated the severity of H2O2-induced Achilles tendinopathy in vivo by preventing H2O2-induced pathological histological features of Achilles tendons, apoptotic death of Achilles tenocytes and upregulated expression of inflammatory cytokines IL-1ß and TNF-α. Our results provide the evidence that ALDH2 activator Alda-1 ameliorates H2O2-induced Achilles tendinopathy. Alda-1 could be used for preventing and treating Achilles tendinopathy.

Ibuprofen inhibited migration of skeletal muscle cells in association with downregulation of p130cas and CrkII expressions.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used to treat sports-related muscle injuries. However, NSAIDs were recently shown to impede the muscle healing process after acute injury. Migration of skeletal muscle cells is a crucial step during the muscle healing process. The present study was performed to investigate the effect and molecular mechanisms of action of ibuprofen, a commonly used NSAID, on the migration of skeletal muscle cells. METHODS: Skeletal muscle cells isolated from the gastrocnemius muscle of Sprague-Dawley rats were treated with ibuprofen. MTT assay (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) was used to evaluate cell viability, and cell apoptosis was evaluated by TUNEL assay, after ibuprofen treatment. Skeletal muscle cell migration and spreading were evaluated using the transwell filter migration assay and F-actin staining, respectively. The protein expression of p130cas and CrkII, which are cell migration facilitating genes, was determined by western blot analysis. The overexpression of p130cas of muscle cells was achieved by p130cas vector transfection. RESULTS: The results demonstrated that ibuprofen did not have a significant negative effect on cell viability and apoptosis. Ibuprofen inhibited the migration and spreading of skeletal muscle cells in a dose-dependent manner. Ibuprofen also dose-dependently decreased the protein expression of p130cas and CrkII. Furthermore, overexpression of p130cas resulted in the promotion of cell migration and spreading and counteracted ibuprofen-mediated inhibition. CONCLUSION: This study suggested that ibuprofen exerts a potentially adverse effect on the migration of skeletal muscle cells by downregulating protein expression of p130cas and CrkII. These results indicate a possible mechanism underlying the possible negative effect of NSAIDs on muscle regeneration.

Deformation of coracoacromial ligament during overhead movement as an early indicator of subacromial impingement in elite adolescent badminton players.

Objectives: Deformation of the coracoacromial ligament during overhead movement has been linked to shoulder pathologies such as impingement and rotator cuff tear. We, therefore, explored this relationship in a group of elite adolescent badminton players.Method: We performed bilateral shoulder physical and ultrasonographic examination in 35 adolescent asymptomatic badminton players, 13 players with unilateral shoulder pain, and 15 non-athletes of similar age. Coracoacromial ligament deformation, defined as the maximal vertical distance between the ligament apex to a line connecting the acromion and coracoid process, was measured during shoulder abduction and internal rotation and compared within and between groups. Other ultrasonographic measurements and the incidence of shoulder pathologies were also evaluated.Result: Among badminton athletes who reported dominant shoulder pain, coracoacromial ligament deformation was significantly larger in their dominant shoulder than in their non-dominant shoulder (3.5 and 2.0 mm, respectively; p = 0.013); this difference was not present in other groups. Regardless of the presence or absence of pain, athletes displayed more coracoacromial ligament deformation and increased supraspinatus tendon thickness in their dominant shoulder than did the control group. Abnormal ultrasound findings were noted in all groups; however, the incidence was not significantly different.Conclusion: Increased coracoacromial ligament deformation during overhead movement is associated with shoulder pain in elite adolescent badminton players. Our findings may help clinicians identify athletes at risk of subacromial impingement syndrome.

Autologous Blood-Derived Products Compared With Corticosteroids for Treatment of Plantar Fasciopathy: A Systematic Review and Meta-Analysis.

OBJECTIVE: This review article evaluated the efficacy of autologous blood-derived products, including whole blood and platelet-rich plasma, in reducing pain and improving function compared with corticosteroids for plantar fasciopathy patients. DESIGN: Literature comparing autologous blood-derived product and corticosteroids for the treatment of plantar fasciopathy was systematically reviewed. Twelve randomized controlled trials and four quasi-experimental studies were included. The visual analog scale pain score and American Orthopedic Foot and Ankle Society hindfoot score were evaluated at 1.5, 3, and 6 mos' follow-up. Subgroup analyses were performed concerning platelet-rich plasma preparation techniques, injection regiments, and study designs. RESULTS: Corticosteroids were found to reduce pain more effectively than whole blood at 1.5 and 3 mos, but the effect disappeared at 6 mos. Platelet-rich plasma reduced pain more effectively at 6 mos' postinjection than corticosteroids. However, there was no significant difference in the American Orthopedic Foot and Ankle Society score between platelet-rich plasma and corticosteroids injections at any time point. In the subgroup analyses, pain was significantly reduced at 6 mos by self-prepared platelet-rich plasma, one-step separation platelet-rich plasma, platelet-rich plasma of more than 3 ml, and platelet-rich plasma without local analgesics. CONCLUSIONS: The results of this meta-analysis suggest that platelet-rich plasma may provide a long-term effect in relieving pain in plantar fasciopathy patients. TO CLAIM CME CREDITS: Complete the self-assessment activity and evaluation online at http://www.physiatry.org/JournalCME CME OBJECTIVES: Upon completion of this article, the reader should be able to: (1) Compare the efficacy of whole blood (WB), platelet-rich plasma (PRP), and corticosteroid (CS) in short-term pain reduction in patients with plantar fasciopathy (PF); (2) Compare the efficacy of WB, PRP, and CS in long-term pain reduction in patients with PF; (3) Identify the potential complication of corticosteroid injection for plantar fasciopathy; and (4) Identify the components of whole blood that might influence the growth factors in healing process. LEVEL: Advanced ACCREDITATION: The Association of Academic Physiatrists is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.The Association of Academic Physiatrists designates this Journal-based CME activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Platelet-Rich Plasma Releasate Promotes Regeneration and Decreases Inflammation and Apoptosis of Injured Skeletal Muscle.

BACKGROUND: Platelet-rich plasma (PRP) contains various cytokines and growth factors that may be beneficial to the healing process of injured muscle. Based on the authors' previous study, PRP releasate can promote proliferation and migration of skeletal muscle cells in vitro, so animal studies are performed to support the use of PRP to treat muscle injury in vivo. PURPOSE: To investigate the effect of PRP releasate on regeneration of injured muscle, as well as its effect on inflammatory reaction and cell apoptosis, in the early stages of the muscle-healing process. STUDY DESIGN: Controlled laboratory study. METHODS: The gastrocnemius muscles of Sprague-Dawley rats were injured by partial transverse incision and then treated with PRP releasate. Hematoxylin and eosin stain was used to evaluate the healing process of injured muscle at 2, 5, and 10 days after injury. TUNEL assay was used to evaluate the cell apoptosis of injured muscle after PRP releasate treatment. Immunohistochemistry was used to stain the CD68-positive cells during the healing process. Muscle contractile properties, including fast-twitch and tetanic strength, were evaluated by electric stimulation. RESULTS: The results revealed that PRP releasate treatment could enhance the muscle-healing process and decrease CD68-positive cells and apoptotic cells. Furthermore, the tetanic strength was significantly higher in injured muscle treated with PRP releasate. CONCLUSION: In conclusion, PRP releasate could enhance the healing process of injured muscle and decrease inflammatory cell infiltration as well as cell apoptosis. CLINICAL RELEVANCE: PRP promotes skeletal muscle healing in association with decreasing inflammation and apoptosis of injured skeletal muscle. These findings provide in vivo evidence to support the use of PRP to treat muscle injury.

Rhythmic Neck Muscle Spasms and Upper Limb Muscle Myoclonic Jerks as an Unusual Initial Presentation of Posttraumatic Cervicothoracic Syringomyelia: A Case Report.

Posttraumatic syringomyelia with an initial presentation of involuntary movement is rare. We describe a 25-year-old patient who sustained complete traumatic spinal cord injury at the thoracic level and presented with rhythmic neck muscle spasms and upper limb muscle myoclonic jerks 1 month after trauma. Magnetic resonance imaging revealed syrinx formation between C3 and T1. Lumbar-peritoneal shunt and decompression were performed. The symptoms completely disappeared after surgery. This report highlights that rhythmic neck muscle spasms and upper limb muscle myoclonic jerks can be the initial and only manifestations of syringomyelia. LEVEL OF EVIDENCE: V.

Comparative Effectiveness of Nonoperative Treatments for Chronic Calcific Tendinitis of the Shoulder: A Systematic Review and Network Meta-Analysis of Randomized Controlled Trials.

OBJECTIVE: To investigate the effectiveness of various nonoperative treatments for chronic calcific tendinitis of the shoulder, a systematic review and network meta-analysis of randomized trials was performed to evaluate changes in pain reduction, functional improvements in patients with calcific tendinitis, and the ratio of complete resolution of calcific deposition. DATA SOURCES: Studies were comprehensively searched, without language restrictions, on PubMed, Embase, Cochrane Controlled Trials Register, the Cochrane, and other databases. The reference lists of articles and reviews were cross-checked for possible studies. STUDY SELECTION: Randomized controlled trials from before August 2016 were included. Study selection was conducted by 2 reviewers independently. DATA EXTRACTION: The quality of studies was assessed and data extracted by 2 independent reviewers. Disagreements were settled by consulting a third reviewer to reach a consensus. DATA SYNTHESIS: Fourteen studies with 1105 participants were included in the network meta-analysis that used a random-effect model to investigate the mean difference of pooled effect sizes of the visual analog scale, Constant-Murley score, and the ratio of complete resolution of calcific deposition on native radiographs. CONCLUSIONS: The present network meta-analysis demonstrates that ultrasound-guided needling (UGN), radial extracorporeal shockwave therapy (RSW), and high-energy focused extracorporeal shockwave therapy (H-FSW) alleviate pain and achieve complete resolution of calcium deposition. Compared with low-energy focused extracorporeal shockwave therapy, transcutaneous electrical nerve stimulation, and ultrasound therapy, H-FSW is the best therapy for providing functional recovery. Physicians should consider UGN, RSW, and H-FSW as alternative effective therapies for chronic calcific tendinitis of the shoulder when initial conservative treatment fails.

Platelet rich plasma promotes skeletal muscle cell migration in association with up-regulation of FAK, paxillin, and F-Actin formation.

Platelet rich plasma (PRP) contains various cytokines and growth factors which may be beneficial to the healing process of injured muscle. The aim of this study was to investigate the effect and molecular mechanism of PRP on migration of skeletal muscle cells. Skeletal muscle cells intrinsic to Sprague-Dawley rats were treated with PRP. The cell migration was evaluated by transwell filter migration assay and electric cell-substrate impedance sensing. The spreading of cells was evaluated microscopically. The formation of filamentous actin (F-actin) cytoskeleton was assessed by immunofluorescence staining. The protein expressions of paxillin and focal adhesion kinase (FAK) were assessed by Western blot analysis. Transfection of paxillin small-interfering RNA (siRNAs) to muscle cells was performed to validate the role of paxillin in PRP-mediated promotion of cell migration. Dose-dependently PRP promotes migration of and spreading and muscle cells. Protein expressions of paxillin and FAK were up-regulated dose-dependently. F-actin formation was also enhanced by PRP treatment. Furthermore, the knockdown of paxillin expression impaired the effect of PRP to promote cell migration. It was concluded that PRP promoting migration of muscle cells is associated with up-regulation of proteins expression of paxillin and FAK as well as increasing F-actin formation. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:2506-2512, 2017.

Platelet rich plasma releasate promotes proliferation of skeletal muscle cells in association with upregulation of PCNA, cyclins and cyclin dependent kinases.

Platelet rich plasma (PRP) contains various cytokines and growth factors which may be beneficial to the healing process of injured muscle. The purpose of this study is to investigate the effect and molecular mechanism of PRP releasate on proliferation of skeletal muscle cells. Skeletal muscle cells intrinsic to Sprague-Dawley rats were treated with PRP releasate. Cell proliferation was evaluated by 3-[4,5-Dimethylthiazol- 2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay and immunocytochemistry with Ki-67 stain. Flow cytometric analysis was used to evaluate the cell cycle progression. Western blot analysis was used to evaluate the protein expressions of PCNA, cyclin E1, cyclin A2, cyclin B1, cyclin dependent kinase (cdk)1 and cdk2. The results revealed that PRP releasate enhanced proliferation of skeletal muscle cells by shifting cells from G1 phase to S phase and G2/M phases. Ki-67 stain revealed the increase of proliferative capability after PRP releasate treatment. Protein expressions including cyclin A2, cyclin B1, cdk1, cdk2 and PCNA were up-regulated by PRP releasate in a dose-dependent manner. It was concluded that PRP releasate promoted proliferation of skeletal muscle cells in association with the up-regulated protein expressions of PCNA, cyclin A2, cyclin B1, cdk1 and cdk2.