Comparison of the efficacy and safety of MAKO robot-assisted total knee arthroplasty versus conventional manual total knee arthroplasty in uncomplicated unilateral total knee arthroplasty a single-centre retrospective analysis.

PURPOSE: To compare the efficacy and safety of MAKO robot-assisted total knee arthroplasty (MA-TKA) with conventional manual total knee arthroplasty (CM-TKA) in patients with end-stage knee osteoarthritis (KOA) during the early postoperative period. METHOD: A retrospective analysis was conducted on 22 patients with KOA who underwent MA-TKA and 26 patients who underwent CM-TKA from April 2023 to July 2023. Hip-knee-ankle angle (HKA), lateral distal femoral angle (LDFA), medial proximal tibial angle (MPTA), American Knee Society Score (AKSS), Forgotten Joint Score-12 (FJS-12), visual analogue scale (VAS), and postoperative complications were recorded and compared between the two groups. RESULT: Both groups successfully completed the surgeries. In terms of radiographic parameters, postoperative one month LDFA and HKA in the MA-TKA group were significantly lower than those in the CM-TKA group (P < 0.05). At the one month follow-up, 19 patients (86.4%) in the MA-TKA group had an HKA less than 3°, compared to 20 patients (76.9%) in the CM-TKA group. Clinically, VAS scores at 24 h, 48 h, and 72 h postoperatively were lower in the MA-TKA group both at rest and during activity. At one month and three months postoperatively, AKSS Function Scores and FJS-12 scores in the MA-TKA group were significantly higher than those in the CM-TKA group (P < 0.05). Regarding postoperative complications, no complications occurred in the MA-TKA group, while one patient in the CM-TKA group experienced postoperative knee stiffness, which resolved after physical therapy, with no statistically significant difference (P > 0.05). CONCLUSION: Compared with conventional manual total knee arthroplasty, MAKO robot-assisted TKA demonstrates better short-term clinical efficacy, achieves better alignment planning, and maintains good safety.

Efficacy and safety of perioperative use of non-steroidal anti-inflammatory drugs for preemptive analgesia in lumbar spine surgery: a systematic review and meta-analysis.

OBJECTIVE: Lumbar spine disorders have become an increasingly common health problem in recent years. Modern clinical studies have shown that perioperative analgesia at certain doses can reduce postoperative pain by inhibiting the process of peripheral sensitization and central sensitization, which is also known as "preemptive analgesia," Non-steroidal anti-inflammatory drugs (NSAIDs) are a class of drugs that achieve antipyretic and analgesic effects by inhibiting cyclooxygenase (COX) and affecting the production of prostaglandins. Our meta-analysis aimed to assess the efficacy and safety of perioperative preemptive analgesia with non-steroidal anti-inflammatory drugs in patients with lumbar spine surgery. METHODS: We searched PubMed, ScienceDirect, the Cochrane Library, and the Web of Science for randomized controlled trials (RCTs) that met the inclusion criteria. A total of 12 clinical studies were included to assess the efficacy and safety of perioperative NSAIDs preemptive analgesia for lumbar spine surgery. RESULT: Twelve studies, including 845 patients, met the inclusion criteria. The results showed that perioperative receipt of NSAIDs for preemptive analgesia was effective and safe. Patient's postoperative morphine consumption (P < 0.05), visual analog scale (P < 0.05), and numerical rating scale (P < 0.05) were not statistically associated with postoperative complications (P > 0.05). CONCLUSION: Our findings suggest that NSAIDs are effective and safe for preemptive analgesia in the perioperative period of lumbar spine surgery and that more and better quality RCTs and more in-depth studies of pain mechanics are still needed.

[Neuroprotective effect and mechanism of cPLA2 inhibitor increases autophagic flux on spinal cord injury].

OBJECTIVE: To investigate the mechanism of cytosolic phospholipase A2(cPLA2) inhibitor to improve neurological function after spinal cord injury (SCI). METHODS: Thirty-six 3 months old female SD rats, with body mass (280±20) g, were divided into three groups (n=12):sham group, SCI group, and SCI+ arachidonyl trifluoromethyl ketone(AACOCF3) group. Balloon compression SCI model was established in all three groups. In the sham model group, the spinal cord compression model was created after the balloon was placed without pressure treatment, and the remaining two groups were pressurized with the balloon for 48 h. After successful modeling, rats in the SCI+AACOCF3 group were injected intraperitoneally with AACOCF3, a specific inhibitor of cPLA2. The remaining two groups of rats were injected intraperitoneally with saline. The animals were sacrificed in batches on 7 and 14 days after modeling, respectively. And the damaged spinal cord tissues were sampled for pathomorphological observation, to detect the expression of cPLA2 and various autophagic fluxPrelated molecules and test the recovery of motor function. RESULTS: Spinal cord histomorphometry examination showed that the spinal cord tissue in the sham group was structurally intact, with normal numbers and morphology of neurons and glial cells. In the SCI group, spinal cord tissue fractures with large and prominent spinal cord cavities were seen. In the SCI+AACOCF3 group, the spinal cord tissue was more intact than in the SCI group, with more fused spinal cord cavities, more surviving neurons, and less glial cell hyperplasia. Western blot showed that the sham group had the lowest protein expression of LC3-Ⅱ, Beclin 1, p62, and cPLA2 compared with the SCI and SCI+AACOCF3 groups (P<0.05) and the highest protein expression of LC3-Ⅰ (P<0.05). P62 and cPLA2 expression in the SCI group were higher than in the SCI+AACOCF3 group (P<0.05). Behavioral observations showed that the time corresponding to BBB exercise scores was significantly lower in both the SCI and SCI+AACOCF3 groups than in the sham group (P<0.05). Scores at 3, 7, and 14 days after pressurization were higher in the SCI+AACOCF3 group than in the SCI group (P<0.05). CONCLUSION: cPLA2 inhibitors can reduce neuronal damage secondary to SCI, promote neurological recovery and improve motor function by improving lysosomal membrane permeability and regulating autophagic flux.

Is coronal imbalance in degenerative lumbar scoliosis patients associated with the number of degenerated discs? A retrospective imaging cross-sectional study.

BACKGROUND: Degenerative lumbar scoliosis (DLS) is a common degenerative disease of the spine, that predominates in the elderly, and causes spinal deformities along with severe pain and reduced quality of life. The relationship between DLS and degenerated discs is now a new direction of research. Our study aimed to the relationship between the imaging parameters of coronal imbalance and the number of degenerated discs in patients with degenerative lumbar scoliosis and analyzed the segmental distribution of the degenerated discs in patients with DLS. METHODS: We performed a retrospective analysis of the imaging of 40 patients who met the inclusion criteria who attended our outpatient clinic between April 2021 and July 2021, measuring the intervertebral space height of the AV (high side and low side), Cobb angle, and AVT (Apical vertebral translation) from coronal X-ray. Degenerated discs were evaluated by the Pfirrmann score based on T2-weighted magnetic resonance images. We record the number of degenerated discs (Graded as Grade III, Grade IV or Grade V by the Pfirrmann score) and the segments in which they are located. Finally, we explore the relationship between the imaging parameters of coronal imbalance and the number of degenerated discs in patients with DLS. RESULT: Among the 40 patients with DLS in our study, all patients had degenerated discs in the lumbar spine, 95% of patients had degenerated discs(Pfirrmann score Grade III, Grade IV or Grade V) in 2 or more segments, with the L4-L5 segment being the most involved segment with the most degenerated discs, followed by the L3-L4 segment and the L5-S1 segment. There was no statistically significant relationship between the number of degenerated discs and the coronal imbalance in patients with DLS. CONCLUSION: Our results showed an association between DLS and degenerated discs, but there was no statistically significant relationship between imbalance in the coronal plane of the lumbar spine and the number of degenerated discs in patients with DLS. The distribution of degenerated disc segments in patients with DLS showed a higher likelihood of disc degeneration in 2 or more segments, and a higher frequency of disc degeneration in the inferior disc and in the adjacent segments of the AV.

STIM2 promotes the invasion and metastasis of breast cancer cells through the NFAT1/TGF-ß1 pathway.

A large amount of evidence indicates that the abnormal activation of multiple signal transduction pathways in cells is closely related to the occurrence and development of tumors. TGF-ß and NFAT1 signaling pathways can inhibit cell proliferation and promote apoptosis in the early stage of breast cancer, but with the increase of tumor malignancy, the two appear to promote tumor progression and deterioration. Therefore, the study of the relationship between STIM2 and NFAT1/TGF-ß1 is helpful for the discovery and treatment of breast cancer, which is of great significance for improving the survival rate of breast cancer patients. This article focuses on the effect of STIM2 molecules on breast cancer cell migration through the NFAT1/ TGF-ß1 pathway and discusses the regulatory mechanism of STIM2 affecting breast cancer cell migration. Experimental data shows that the positive rate of breast cancer NFAT1 is 54%, which is significantly lower than that of benign breast Tissue 85%; the positive expression rate of TGF-ß1 in benign breast tissue is 85%, and the positive expression rate in breast cancer tissue is 49%. The results show that STIM2 protein can promote the invasion and metastasis of breast cancer cells through the NFAT1 / TGF-ß1 pathway.

The effect of miR-138 on the proliferation and apoptosis of breast cancer cells through the NF-κB/VEGF signaling pathway.

The analyze the effect of miR-138 on the proliferation and apoptosis of breast cancer cells through the NF-κB/VEGF signaling pathway is the Objective of this experiment. For this aim, the endometrial stem breast cancer cell line MCF-7 was cultured in vitro, and the overexpression mimic miR-138 mimics and the inhibitor anti-miR-138 were transfected into the endometrial stem breast cancer cell line MCF-7, which was set to overexpress miR-138 group and interfere with miR-138, and set up negative control of overexpression and negative control of inhibitor. Observe the cell proliferation and apoptosis ability of each group, and the changes in tumor necrosis factor-α (TNF-α), interleukin 1ß, 6, 18 (IL-1ß, IL-6, IL-18) levels, and compare the Bax of each group, NF-κB, VEGF protein expression level. Results showed that the proliferation ability of the miR-138 overexpression group was significantly lower than that of the miR-138 overexpression control group (P<0.05); the proliferation ability of the miR-138 interference group was significantly higher than that of the miR-138 interference control group (P<0.05). The apoptosis rate, caspase-3 and caspase-9 expression levels of the miR-138 overexpression group were significantly higher than those of the miR-138 overexpression control group (P<0.05);  the apoptosis rate, caspase-3 and caspase-9 expression levels of the miR-138 interference group were significantly lower than those of the miR-138 interference control group (P<0.05). The expression levels of IL-1 ß, IL-6, IL-18 and TNF - α in the miR-138 overexpression group were significantly lower than those in the miR-138 overexpression control group (P < 0.05). The protein expression levels of Bax, NF-κB and VEGF in the miR-138 overexpression group were significantly lower than those in the miR-138 overexpression control group (P < 0.05); the protein expression levels of Bax, NF-κB and VEGF in the miR-138 interference group were significantly higher than those in the miR-138 interference control group (P <0.05). The proliferation ability of the miR-138 overexpression group was significantly lower than that of the miR-138 overexpression control group (P < 0.05); the proliferation ability of the miR-138 + NF-κB overexpression group was significantly higher than that of the miR-138 overexpression group (P<0.05). The apoptosis rate of the miR-138 + NF-κB overexpression group was significantly lower than that of the miR-138 overexpression group (P < 0.05). Then MiR-138 can significantly inhibit the proliferation of breast cancer cells, promote apoptosis, and regulate the expression of inflammatory factors in the cells. It is speculated that the related mechanism may be related to the negative regulation of the NF-κB/VEGF signaling pathway.