Efficacy and safety of ultrasound-guided pulsed radiofrequency in the treatment of the ophthalmic branch of postherpetic trigeminal neuralgia.

Objective: To investigate the efficacy and safety of ultrasound-guided pulsed radiofrequency (PRF) targeting the supraorbital nerve for treating the ophthalmic branch of postherpetic trigeminal neuralgia. Methods: A retrospective cohort study was conducted involving patients who presented at the Department of Pain, Affiliated Hospital of Southwest Medical University from January 2015 to January 2022. The patients were diagnosed with the first branch of postherpetic trigeminal neuralgia. In total, 63 patients were included based on the inclusion and exclusion criteria. The patients were divided into the following two groups based on the treatment method used: the nerve block (NB) group (n = 32) and the PRF + NB group (radiofrequency group, n = 31). The visual analog scale (VAS) score, Pittsburgh Sleep Quality Index (PSQI) score, and pregabalin dose were compared between the two groups before treatment, 1 week after the procedure, and 1, 3, and 6 months post-procedure, and the complications, such as local infection, local hematoma, and decreased visual acuity, were monitored post-treatment. Results: No significant difference was found in terms of pretreatment age, sex, course of disease, preoperative VAS score, preoperative PSQI score, and preoperative pregabalin dose between the two groups (P > 0.05). The postoperative VAS score, PSQI score, and pregabalin dose were significantly decreased in both groups. Furthermore, significant differences were found between the two groups at each preoperative and postoperative time point (P < 0.05). The VAS score was lower in the radiofrequency group than in the NB group at 1, 3, and 6 months, and the difference was statistically significant (P < 0.05). The PSQI score was lower in the radiofrequency group than in the NB group at 1 week, 1, 3, and 6 months post-procedure, and the difference was statistically significant (P < 0.05). The dose of pregabalin was lower in the radiofrequency group than in the NB group at 1 week, 1, 3, and 6 months post-procedure, and the difference was statistically significant at 3 and 6 months (P < 0.05). After 6 months of treatment, the excellent rate of VAS score in the radiofrequency group was 70.96%, and the overall effective rate was 90.32%, which was higher than that in the NB group. The difference in the efficacy was statistically significant (P < 0.05). Conclusion: PRF targeting the supraorbital nerve can effectively control the pain in the first branch of the trigeminal nerve after herpes, enhance sleep quality, and reduce the dose of pregabalin. Thus, this study shows that PRF is safe under ultrasound guidance and is worthy of clinical application.

TRIM28 Fosters Microglia Ferroptosis via Autophagy Modulation to Enhance Neuropathic Pain and Neuroinflammation.

This study explores the molecular underpinnings of neuropathic pain (NPP) and neuroinflammation, focusing on the role of TRIM28 in the regulation of autophagy and microglia ferroptosis. Leveraging transcriptomic data associated with NPP, we identified TRIM28 as a critical regulator of ferroptosis. Through comprehensive analysis, including Gene Ontology enrichment and protein-protein interaction network assessments, we unveiled GSK3B as a downstream target of TRIM28. Experimental validation confirmed the capacity of TRIM28 to suppress GSK3B expression and attenuate autophagic processes in microglia. We probed the consequences of autophagy and ferroptosis on microglia physiology, iron homeostasis, oxidative stress, and the release of proinflammatory cytokines. In a murine model, we validated the pivotal role of TRIM28 in NPP and neuroinflammation. Our analysis identified 20 ferroptosis regulatory factors associated with NPP, with TRIM28 emerging as a central orchestrator. Experimental evidence affirmed that TRIM28 governs microglial iron homeostasis and cell fate by downregulating GSK3B expression and modulating autophagy. Notably, autophagy was found to influence oxidative stress and proinflammatory cytokine release through the iron metabolism pathway, ultimately fueling neuroinflammation. In vivo experiments provided conclusive evidence of TRIM28-mediated pathways contributing to heightened pain sensitivity in neuroinflammatory states. The effect of TRIM28 on autophagy and microglia ferroptosis drives NPP and neuroinflammation. These findings offer promising avenues for identifying novel therapeutic targets to manage NPP and neuroinflammation.

Clinical Efficacy Evaluation of Ultrasound-Guided C2 Dorsal Root Nerve Pulsed Radiofrequency Combined with Stellate Ganglion Block in the Treatment of Cervicogenic Headache: A Retrospective Cohort Study.

Purpose: To explore the therapeutic effect of C2 dorsal root ganglion pulsed radiofrequency (PRF) combined with stellate ganglion block (SGB) in patients with cervicogenic headache (CEH). Patients and Methods: We retrospectively reviewed 90 patients diagnosed with CEH who were admitted to our hospital between May 2019 and May 2022. All patients were divided into three groups (n = 30 each) according to the actual treatment method used: ultrasound-guided SGB, ultrasound-guided C2 dorsal root ganglion PRF treatment, and ultrasound-guided C2 dorsal root ganglion PRF combined with SGB treatment. Patients' pain intensity, sleep, and mood changes were assessed by statistically analyzing their pain visual analog scale (VAS), Pittsburgh Sleep Quality Inventory (PSQI), and short-form McGill Pain Questionnaire affective item scores before and after treatment. Results: The post-treatment VAS, PSQI, and McGill scores were significantly decreased in all patients (P < 0.05), and all three scores in ultrasound-guided C2 dorsal root ganglion PRF combined with SGB were lower than those in ultrasound-guided SGB alone and ultrasound-guided C2 dorsal root ganglion PRF alone (P < 0.05). Conclusion: The use of ultrasound-guided C2 dorsal root ganglion PRF combined with SGB in patients with CHE is effective in alleviating pain and improving sleep, and deserves to be replicated in the clinic.

Mycotic Pseudoaneurysm of Thoracic Aortic Caused by Salmonella Paratyphi A: A Case Report.

Background: Mycotic pseudoaneurysm, also known as infectious pseudoaneurysm, is a severe disease with a high mortality rate. Although Salmonella infection is a common etiological factor for mycotic pseudoaneurysm, Salmonella paratyphi A infection causing mycotic pseudoaneurysm is extremely rare. Endovascular therapy has been described as a feasible treatment for mycotic pseudoaneurysm. Case Presentation: A 63-year-old female patient had a thoracic aortic pseudoaneurysm caused by Salmonella paratyphi A infection. The patient associated with diabetes had a fever, abdominal pain, and low back pain, who was successfully treated using endovascular stents treatment and antibiotics. Conclusion: Salmonella paratyphi A is a bloodstream infection bacterium with the ability to cause mycotic pseudoaneurysm. To treat mycotic pseudoaneurysms of the thoracic aorta, endovascular stent-graft treatment combined with antibiotics is an alternative treatment for patients who cannot tolerate open surgery.

High-throughput transcriptome sequencing reveals the critical role of long non-coding RNA Gm14376 in the occurrence of neuropathic pain.

Long noncoding RNAs (lncRNAs) have been suggested as important regulators in neuropathic pain. Our study aims to explore the possible molecular mechanism underlying the role of long non-coding RNA (lncRNA) Gm14376 in neuropathic pain in mice by high-throughput transcriptome sequencing. A mouse model of spared nerve injury (SNI) was constructed for mechanical, thermal and spontaneous pain testing. Transcriptomic changes in lncRNAs and mRNAs in the dorsal root ganglion (DRG) of SNI mice were analyzed using RNA-sequencing techniques in conjunction with public data analysis. AAV5 viral vector was constructed to assess the effect of Gm14376 on SNI-induced pain hypersensitivity and inflammatory response. Cis-target genes of Gm14376 were obtained and the functions of Gm14376 were analyzed by GO and KEGG pathway enrichment analyses. Results from bioinformatic analysis identified a conserved Gm14376, which was up-regulated in the DRG of SNI mice, specifically in response to nerve injury. Overexpression of Gm14376 in DRG induced neuropathic pain-like symptoms in mice. Furthermore, the functions of Gm14376 were related to the phosphatidylinositol 3-kinase (PI3K)/Akt pathway and fibroblast growth factor 3 (Fgf3) was identified as the cis-target gene of Gm14376. Gm14376 could directly up-regulate Fgf3 expression to activate the PI3K/Akt pathway, which alleviated pain hypersensitivity to mechanical and thermal stimuli and reduced the release of inflammatory factors in SNI mice. From our data, we conclude that SNI-induced up-regulation of Gm14376 expression in DRG activates the PI3K/Akt pathway through up-regulation of Fgf3 expression, thereby promoting the development of neuropathic pain in mice.

Postherpetic Trigeminal Neuralgia of the V2 Branch Treated with Electrodes Placed through the Foramen Ovale: A Case Report.

Varicella-zoster virus (VZV) is a deoxyribonucleic acid (DNA) virus that causes both primary and recurrent viral infections. Herpes zoster (HZ), also known as shingles, is a unique condition that is induced by VZV reactivation. Neuropathic pain, malaise, and sleep disruption are prodromal symptoms in such cases. Postherpetic trigeminal neuralgia is a neuropathic pain caused by VZV infection of the trigeminal ganglion or branches, which remains or reappears after herpes crusting. In this report, we present a case of post-herpetic trigeminal neuralgia of the V2 branch, exhibiting findings of unusual involvement of the trigeminal nerve. Notably, the patient was treated using electrodes placed through the foramen ovale.

AQP4 mitigates chronic neuropathic pain-induced cognitive impairment in mice.

Neuropathic pain is a risk factor for cognitive defects. The ubiquitous expression of AQP4 in astrocytes throughout the central nervous system is altered in the neurodegenerative disease. However, the exact role of AQP4 in cognitive impairment induced by chronic neuropathic pain remains unclear. In this study, we discovered that AQP4 protein and mRNA expression decreased time-dependently in the model of chronic neuropathic pain-induced cognitive disorder. AQP4 overexpression recovered mice from cognitive impairment. Furthermore, the concentration of Aß1-42 in the serum and hippocampus reduced in mice with AQP4 overexpression adeno-associated virus injection. In conclusion, AQP4 in astrocytes is important in mitigating cognitive impairment caused by chronic neuropathic pain.

Amelioration of central neurodegeneration by docosahexaenoic acid in trigeminal neuralgia rats through the regulation of central neuroinflammation.

Trigeminal neuralgia (TN) is a stubborn head and face neuropathic pain with complex pathogenesis. Patients with TN have a significantly increased risk of central neurodegeneration, which manifests as cognitive impairment and memory loss, but the specific mechanism underlying central nervous degeneration is still unclear. This study aimed to explore central neurodegeneration and its possible mechanism of action in TN rats based on changes in the brain fatty acid content and microglia-related neuroinflammation. Using a TN neuropathic pain model established by us, we found that TN rats have obvious cognitive impairment. Furthermore, changes in the brain fatty acid content were analyzed using gas chromatography-mass spectrometry (GC-MS). It was found that the docosahexaenoic acid (DHA) content in the central nervous system (CNS) of TN rats was significantly decreased compared to that in the CNS of Sham rats. An important component in maintaining brain cognition, DHA also plays a key role in regulating central neuroinflammation. Here, by continuous supplementation of DHA, the CNS DHA content was increased to a certain extent in TN rats. The cognitive impairment of TN rats was improved after restoring the central DHA level; this may be related to the improvement of neuroinflammation through the DHA-mediated regulation of microglial polarization. Overall, this study provides a theoretical basis for explaining the pathogenesis of central neurodegeneration in TN. It also suggests DHA as a target for protecting the CNS of patients with TN from damage.

Effect of lidocaine on expression of P2X7, p-p38 and IL-Iß in the thalamus of rats with trigeminal neuralgia.

We investigated whether lidocaine can increase the pain threshold of rats with trigeminal neuralgia by affecting the expression of P2X7, p-p38 and IL-Iß proteins in the thalamus. Thirty-three male Sprague-Dawley (SD) rats were randomly divided into three groups (n = 11): Sham group, Ion-CCI (infraorbital nerve chronic constriction injury) group and Ion-CCI+L group(Ion-CCI+lidocaine 10 mg/kg/day, i.p.). The mechanical pain threshold of rats was measured preoperatively and at 1, 3, 5, 7, 9, 11 and 14days after operation with the von Frey filament sensor tester. Fourteen days after operation, the rats were dissected to collect their whole brain, thalamus and trigeminal ganglion to detect IL-1ß, P2X7, p38, and p-p38 protein expression. The pain threshold of rats in Ion-CCI+L group was lower than that in Sham group (p < 0.01) and higher than that in Ion-CCI group (p < 0.01).ELISA showed that IL-1ß in the thalamus and trigeminal ganglion in Ion-CCI+L group were lower than those in ion-CCI group (p < 0.05) but higher than those in Sham group (p < 0.05). Western blot showed that the expression levels of P2X7 and p-p38 in the thalamus of rats in Ion-CCI+L group were lower than those in Ion-CCI group (p < 0.01) and higher than thaose in Sham group (p < 0.01),while the expression levels of IL-1ß in the thalamus in Ion-CCI+L group were lower than those in Ion-CCI group (p < 0.05) and higher than those in Sham group (p < 0.01). Immunofluorescence showed that p-p38 in the thalamus in Ion-CCI+L group was lower than that in Ion-CCI group (p < 0.05) and higher than that in Sham group (p < 0.05). Lidocaine can reduce the inflammatory response of the central nervous system and increase the pain threshold of trigeminal neuralgia rats by inhibiting p2x7-p38-IL-1ß signaling pathway.This pathway play an important role in the pathogenesis of trigeminal neuralgia, and it may be one of the targets for the treatment of trigeminal neuralgia.

Ischemic postconditioning reduces spinal cord ischemia-reperfusion injury through ATP-sensitive potassium channel.

STUDY DESIGN: Animal study. OBJECTIVES: Explore the neuroprotective effect of remote limb ischemic postconditioning (Post C) in spinal cord ischemic reperfusion injury (SCII) and related mechanisms. SETTING: Anesthesiology Laboratory of Southwest Medical University. METHODS: We established a rabbit SCII model and processed it with Post C. To evaluate the neural function, spinal cord tissue was taken 48 h later, normal neurons were evaluated by HE staining, and the expression of ATP-sensitive potassium channel (KATP) marker molecule Kir6.2 was detected by Western blot. Immunofluorescence detection of spinal cord Iba-1 expression, ELISA detection of M1 type microglia marker iNOS and M2 type microglia marker Arg, and Western blot detection of NF-κB and IL-1ß expression. Through these experiments, we will explore the protective effect of Post C in SCII, observe the changes in the protective effect after using KATP blockers, and verify that Post C can play a neuroprotective effect in SCII by activating KATP. RESULTS: We observed that Post C significantly improved exercise ability and the number of spinal motor neurons in the SCII model. Microglia are activated and expression of M1 microglia in the spinal cord was decreased, while M2 was increased. This neuroprotective effect was reversed by the nonspecific KATP inhibitor. CONCLUSION: Post C has a neuroprotective effect on SCII, and maybe a protective effect produced by activating KATP to regulate spinal microglia polarization and improve neuroinflammation.

NLRP3 Inflammasome Mediates Neurodegeneration in Rats with Chronic Neuropathic Pain.

ABSTRACT: Patients with chronic neuropathic pain (NP) have a significantly increased risk of central nervous degeneration. Trigeminal neuralgia (TN) is a typical NP, and this manifestation is more obvious. In addition to severe pain, patients with TN are often accompanied by cognitive dysfunction and have a higher risk of central nervous system degeneration, but the mechanism is not clear. The NOD-like receptor 3 (NLRP3) inflammasome assembles inside of microglia on activation, which plays an important role in neurodegeneration such as Alzheimer disease. MCC950 is a specific blocker of NLRP3 inflammasome, which can improve the performance of degenerative diseases. Although NLRP3 inflammasome assembles inside of microglia on activation has been shown to be essential for the development and progression of amyloid pathology, its whether it mediates the neurodegeneration caused by NP is currently unclear. By constructing a rat model of chronic TN, we found that as the course of the disease progresses, TN rats have obvious cognitive and memory deficit. In addition, Tau hyperphosphorylation and Aß expression increase in the cortex and hippocampus of the brain. At the same time, we found that NLRP3 expression increased significantly in model rats. Interestingly, NLRP3 specific blocker MCC950 can alleviate the neurodegeneration of trigeminal neuralgia rats to a certain extent. It is suggested that our NLRP3 inflammasome plays an important role in the neurodegeneration of trigeminal neuralgia rats. And it is related to the activation of central nervous system inflammation.

Activation of SK3 channel plays a pivotal role in modulation of trigeminal neuralgia.

Objective: To investigate whether small conductance Ca2+ activatedK+ channels; Trigeminal ganglion; Trigeminal neuralgia. (SK3) exists in normal rats' trigeminal ganglions (TG) and its effect on their pain thresholds.Methods: In total, 110 healthy adult male Sprague-Dawley (SD) rats were involved in this study. Ten rats were dissected to collect their liver tissues, TG and DRG. The rest of the rats were randomly assigned to either the experimental group or the control group. The animal model of trigeminal neuralgia (TN) was established by infraorbital nerve ligation. The expression of SK3 channels in their livers, TG and dorsal root ganglions (DRG) were detected. And different doses of SK3 channel activator and inhibitor were administered to the rats in both groups 15 days after the operation; meanwhile, their pain thresholds were also measured.Results: The expression of SK3 channel was found in TG. In the experimental group, the pain threshold was significantly decreased and there was a decreased level of SK3 than that in the control group at 15 days after operation. The administration of SK3 channel agonist (CyPPA) could significantly improve the pain threshold, while, the pain threshold decreased after administration of SK3 channel antagonist (Apamin).Conclusion: The SK3 channel may play a pivotal role in the pathogenesis of trigeminal neuralgia, and it may be one of the potential targets for the treatment of trigeminal neuralgia.

The complete chloroplast genome sequence of Populus szechuanica, a medicinal plant for child anesthesia application.

Populus szechuanica C.K. Schneid. is used for wind and sand fixation, farmland protection, soil and water conservation. And some varieties bud fat and inflorescence are available for medicinal use; poplar bark contains tannin and can be used as tanning material. It is also widely used in afforestation and greening in cities across China. In addition, the P. szechuanica also showed vital important application values on the child anesthesia, which could significantly reduce the occurrence of hypotension after anesthesia. The complete chloroplast genome sequence of P. szechuanica was characterized from Illumina pair-end sequencing. The chloroplast genome of P. szechuanica was 156,717 bp in length, containing a large single-copy region (LSC) of 84,900 bp, a small single-copy region (SSC) of 16,527 bp, and two inverted repeat (IR) regions of 27,645 bp. The overall GC content is 36.70%, while the corresponding values of the LSC, SSC, and IR regions are 34.5%, 30.7%, and 41.9%, respectively. The genome contains 131 complete genes, including 86 protein-coding genes (68 protein-coding gene species), 37 tRNA genes (29 tRNA species) and 8 rRNA genes (4 rRNA species). The Maximum Likelihood phylogenetic analysis showed that P. szechuanica and P. koreana clustered together as sisters to other Populus species.

Effects of Pulsed Radiofrequency with Different Temperature on Model Rats of Chronic Constriction Injury.

OBJECTIVES: The treatment for neuropathic pain is still a big challenge. Pulsed radiofrequency technique has been widely used to relieve neuropathic pain in recent years. The purpose of this study is to optimize the temperature for pulsed radiofrequency therapy. DESIGN: Animal, experimental study. METHODS: Seventy-five male SD rats were randomly divided into five groups: Sham operation group (Sham group), chronic constriction injury group (CCI group), PRF 42°C group (P42 group), PRF 50°C group (P50 group), and PRF 60°C group (P60 group). The hindpaw withdrawal threshold (HWT), paw thermal withdrawal latency (PTWL), sciatic nerve structure, and the concentration of spinal methionine enkephalin(M-ENK) were detected to identify which temperature is the best for PRF treatment. RESULTS: PRF at 42°C, 50°C and 60°C significantly alleviated the pain in CCI rats. The therapeutic effects of 50°C and 60°C were similar, and both were better than 42°C. In addition, PRF using 42°C, 50°C, and 60°C mediated nerve injury to sciatic nerve were grade 1, 1, and 2, respectively. The concentration of M-ENK in spinal cord increased accompanying with the increasing of the temperature of PRF. CONCLUSIONS: PRF using 50°C could induce less damage while achieving better improvement of mechanical and thermal pain threshold than 42°C and 60°C in CCI rats, which may be achieved by promoting the expression of M-ENK in spinal cord.

Spinophilin modulates pain through suppressing dendritic spine morphogenesis via negative control of Rac1-ERK signaling in rat spinal dorsal horn.

Both spinophilin (SPN, also known as neurabin 2) and Rac1 (a member of Rho GTPase family) are believed to play key roles in dendritic spine (DS) remodeling and spinal nociception. However, how SPN interacts with Rac1 in the above process is unknown. Here, we first demonstrated natural existence of SPN-protein phosphatase 1-Rac1 complex in the spinal dorsal horn (DH) neurons by both double immunofluorescent labeling and co-immunoprecipitation, then the effects of SPN over-expression and down-regulation on mechanical and thermal pain sensitivity, GTP-bound Rac1-ERK signaling activity, and spinal DS density were studied. Over-expression of SPN in spinal neurons by intra-DH pAAV-CMV-SPN-3FLAG could block both mechanical and thermal pain hypersensitivity induced by intraplantar bee venom injection, however it had no effect on the basal pain sensitivity. Over-expression of SPN also resulted in a significant decrease in GTP-Rac1-ERK activities, relative to naive and irrelevant control (pAAV-MCS). In sharp contrast, knockdown of SPN in spinal neurons by intra-DH pAAV-CAG-eGFP-U6-shRNA[SPN] produced both pain hypersensitivity and dramatic elevation of GTP-Rac1-ERK activities, relative to naive and irrelevant control (pAAV-shRNA [NC]). Moreover, knockdown of SPN resulted in increase in DS density while over-expression of it had no such effect. Collectively, SPN is likely to serve as a regulator of Rac1 signaling to suppress DS morphogenesis via negative control of GTP-bound Rac1-ERK activities at postsynaptic component in rat DH neurons wherein both mechanical and thermal pain sensitivity are controlled.

c-Abl-p38α signaling pathway mediates dopamine neuron loss in trigeminal neuralgia.

Trigeminal neuralgia is a common neuropathic pain in the head and face. The pathogenesis of trigeminal neuralgia is complex, and so far, the pathogenesis of trigeminal neuralgia involving peripheral and central nervous inflammation theory has not been explained clearly. The loss of dopamine neurons in striatum may play an important role in the development of trigeminal nerve, but the reason is not clear. C-Abl is a nonreceptor tyrosine kinase, which can be activated abnormally in the environment of neuroinflammation and cause neuron death. We found that in the rat model of infraorbital nerve ligation trigeminal neuralgia, the pain threshold decreased, the expression of c-Abl increased significantly, the downstream activation product p38 was also activated abnormally and the loss of dopamine neurons in striatum increased. When treated with imatinib mesylate (STI571), a specific c-Abl family kinase inhibitor, the p38 expression was decreased and the loss of dopaminergic neurons was reduced. The mechanical pain threshold of rats was also improved. In conclusion, c-abl-p38 signaling pathway may play an important role in the pathogenesis of trigeminal neuralgia, and it is one of the potential targets for the treatment of trigeminal neuralgia.

Comparison of analgesic efficacy of continuous transversus abdominis plane block with continuous epidural analgesia in patients undergoing abdominal surgery: a systematic review and meta-analysis.

BACKGROUND: A novel technique of continuous transversus abdominis plane block (TAPB) has been reported to be beneficial to patients undergoing abdominal surgery because it can significantly relieve postoperative pain. The aim of our study is to compare this novel technique with a traditional technique of continuous epidural analgesia (EA). METHODS: We conducted our meta-analysis in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Only randomized controlled trials (RCTs) that compared the efficacy of continuous TAPB and continuous EA to relieve postoperative pain were included. Patients were classified by nationality (Chinese, non-Chinese) for the subgroup analysis. RESULTS: Nine RCTs with 598 patients were included in our study. Pain levels measured by visual analog scale (VAS) scores at rest on postoperative day 1 were equivalent for continuous TAPB groups and continuous EA groups in non-Chinese and Chinese patients. The TAPB groups experienced a lower rate of hypotension, sensorimotor disorder, and nausea compared with the continuous EA group within 48 hours after surgery. CONCLUSION: Continuous TAPB and continuous EA are equally effective in relieving postoperative pain at rest 24 hours after surgery, but EA was associated with more side effects such as hypotension, nausea, and sensorimotor disorder.

Ozone Treatment Unveils the Veil of Candida parapsilosis Infection in the Knee Joint: A Case Report and Literature Review.

Candida infection is common, while Candida parapsilosis infection in the knee joint is rare. Local symptoms of Candida infections in the knee are atypical, rarely associated with systemic symptoms, and difficult to distinguish from other types of knee arthritis. We here report a special case of C. parapsilosis infections in the knee joint. A patient had previously undergone knee puncture in a private clinic for the treatment of osteoarthritis and developed a left knee joint infection with C. parapsilosis. However, the patient only showed more severe local knee symptoms, and there was no systemic manifestation associated with any Candida infection. Surprisingly, after receiving ozone lavage, the patient showed symptoms of a systemic infection such as fever and chills. There was no positive finding in the blood cultures. Finally, the synovial fluid cultures showed a C. parapsilosis infections. After antifungal treatment and another knee ozone therapy, the patient did not experience recurrence of the infections. It is suggested that in this special case, the strong sterilization with ozone caused the destruction of C. parapsilosis, leading to a transient systemic toxin reaction. In addition, we reviewed the 17 cases of C. parapsilosis infections that have been reported thus far.

Oleanolic acid inhibits mouse spinal cord injury through suppressing inflammation and apoptosis via the blockage of p38 and JNK MAPKs.

Spinal cord injury (SCI) is reported as a devastating disease, leading to tissue loss and neurologic dysfunction. However, there is no effective therapeutic strategy for SCI treatment. Oleanolic acid (OA), as a triterpenoid, has anti-oxidant, anti-inflammatory, and anti-apoptotic activities. However, its regulatory effects on SCI have little to be elucidated, as well as the underlying molecular mechanisms. In this study, we attempted to explore the role of OA in SCI progression. Behavior tests suggested that OA treatments markedly alleviated motor function in SCI mice. Evans blue contents up-regulated in spinal cords of SCI mice were significantly reduced by OA in a dose-dependent manner, demonstrating the improved blood-spinal cord barrier. Moreover, we found that OA treatments significantly reduced the apoptotic cell death in spinal cord samples of SCI mice through decreasing the expression of cleaved Caspase-3. In addition, pro-inflammatory response in SCI mice was significantly attenuated by OA treatments. Furthermore, SCI mice exhibited higher activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) signaling pathways, but these effects were clearly blocked in SCI mice with OA treatments, as evidenced by the down-regulated phosphorylation of p38, c-Jun-NH 2 terminal kinase (JNK), IκB kinase α (IKKα), inhibitor of nuclear factor κB-α (IκBα) and NF-κB. The protective effects of OA against SCI were confirmed in lipopolysaccharide (LPS)-stimulated mouse neurons mainly through the suppression of apoptosis and inflammatory response, which were tightly associated with the blockage of p38 and JNK activation. Together, our data demonstrated that OA treatments could dose-dependently ameliorate spinal cord damage through impeding p38- and JNK-regulated apoptosis and inflammation, and therefore OA might be served as an effective therapeutic agent for SCI treatment.