Application of Cinnamomum burmannii Essential Oil in Promoting Wound Healing.

Skin wounds, leading to infections and death, have a huge negative impact on healthcare systems around the world. Antibacterial therapy and the suppression of excessive inflammation help wounds heal. To date, the application of wound dressings, biologics and biomaterials (hydrogels, epidermal growth factor, stem cells, etc.) is limited due to their difficult and expensive preparation process. Cinnamomum burmannii (Nees & T. Nees) Blume is an herb in traditional medicine, and its essential oil is rich in D-borneol, with antibacterial and anti-inflammatory effects. However, it is not clear whether Cinnamomum burmannii essential oil has the function of promoting wound healing. This study analyzed 32 main components and their relative contents of essential oil using GC-MS. Then, network pharmacology was used to predict the possible targets of this essential oil in wound healing. We first proved this essential oil's effects in vitro and in vivo. Cinnamomum burmannii essential oil could not only promote the proliferation and migration of skin stromal cells, but also promote M2-type polarization of macrophages while inhibiting the expression of pro-inflammatory cytokines. This study explored the possible mechanism by which Cinnamomum burmannii essential oil promotes wound healing, providing a cheap and effective strategy for promoting wound healing.

Dihydromyricetin confers cerebroprotection against subarachnoid hemorrhage via the Nrf2-dependent Prx2 signaling cascade.

BACKGROUND: Several clinical and experimental studies have shown that therapeutic strategies targeting oxidative damage are beneficial for subarachnoid hemorrhage (SAH). A brain-permeable flavonoid, dihydromyricetin (DHM), can modulate redox/oxidative stress and has cerebroprotective effects in several neurological disorders. The effects of DHM on post-SAH early brain injury (EBI) and the underlying mechanism have yet to be clarified. PURPOSE: This work investigated a potential role for DHM in SAH, together with the underlying mechanisms. METHODS: Cerebroprotection by DHM was studied using a SAH rat model and primary cortical neurons. Atorvastatin (Ato) was a positive control drug in this investigation. The effects of DHM on behavior after SAH were evaluated by performing the neurological rotarod and Morris water maze tests, as well as by examining its effects on brain morphology and on the molecular and functional phenotypes of primary cortical neurons using dichlorodihydrofluorescein diacetate (DCFH-DA), immunofluorescent staining, biochemical analysis, and Western blot. RESULTS: DHM was found to significantly reduce the amount of reactive oxygen species (ROS), suppress mitochondrial disruption, and increase intrinsic antioxidant enzymatic activity following SAH. DHM also significantly reduced neuronal apoptosis in SAH rats and improved short- and long-term neurological functions. DHM induced significant increases in peroxiredoxin 2 (Prx2) and nuclear factor erythroid 2-related factor 2 (Nrf2) expression, while decreasing phosphorylation of p38 and apoptotic signal-regulated kinase 1 (ASK1). In contrast, reduction of Prx2 expression using small interfering ribonucleic acid or by inhibiting Nrf2 with ML385 attenuated the neuroprotective effect of DHM against SAH. Moreover, DHM dose-dependently inhibited oxidative damage, decreased neuronal apoptosis, and increased the viability of primary cultured neurons in vitro. These positive effects were associated with Nrf2 activation and stimulation of Prx2 signaling, whereas ML385 attenuated the beneficial effects. CONCLUSION: These results reveal that DHM protects against SAH primarily by modulating the Prx2 signaling cascade through the Nrf2-dependent pathway. Hence, DHM could be a valuable therapeutic candidate for SAH treatment.

Integrated analysis reveals Atf3 promotes neuropathic pain via orchestrating JunB mediated release of inflammatory cytokines in DRG macrophage.

The dorsal root ganglion (DRG) is actively involved in the development of neuropathic pain (NP), serving as an intermediate station for pain signals from the peripheral nervous system to the central nervous system. The mechanism by which DRG is involved in NP regulation is not fully understood. The immune system plays a pivotal role in the physiological and pathological states of the human body. In recent years, the immune system has been thought to play an increasingly important role in the pathogenesis of NP. The immune system plays a key role in pain through specific immune cells and their immune-related genes (IRGs). However, the mechanism by which IRGs of DRG regulate NP action has not been fully elucidated. Here, we performed Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of IRGs in DRG bulk-RNA sequencing data from spared nerve injury (SNI) model mice and found that their IRGs were enriched in many pathways, especially in the immune response pathway. Subsequently, we analyzed single-cell RNA sequencing (scRNA-seq) data from DRGs extracted from the SNI model and identified eight cell populations. Among them, the highest IRG activity was presented in macrophages. Next, we analyzed the scRNA and bulk-sequencing data and deduced five common transcription factors (TFs) from differentially expressed genes (DEGs). The protein-protein interaction (PPI) network suggested that Atf3 and JunB are closely related. In vitro experiments, we verified that the protein and mRNA expressions of Atf3 and JunB were up-regulated in macrophages after lipopolysaccharide (LPS) stimulation. Moreover, the down-regulation of Atf3 reduced the release of inflammatory cytokines and decreased the protein and mRNA expression levels of JunB. The down-regulation of JunB also reduced the release of inflammatory cytokines. Furthermore, overexpression of JunB attenuated the effect of Atf3 down-regulation in reducing the release of inflammatory cytokines. Therefore, we speculated that Atf3 might promote NP through JunB-mediated release of inflammatory factors in DRG macrophages.

Identification and validation of biomarkers related to Th1 cell infiltration in neuropathic pain.

Neuropathic pain (NP) is a widespread chronic pain with a prevalence of 6.9-10% in the general population, severely affecting patients' physical and mental health. Accumulating evidence indicated that the immune environment is an essential factor causing NP. However, the mechanism is unclear. This study attempted to analyze NP-related immune infiltration patterns. We downloaded the expression profiles from the Gene Expression Omnibus (GEO) database. The novel method of single-sample gene set enrichment analysis (ssGSEA) algorithm and weighted gene co-expression network analysis (WGCNA) was applied to identify immune-related genes and verified in vitro and in vivo experiments. The spared nerve injury (SNI) group was closely related to type1 T helper cells (Th1 cells), and two key genes (Abca1 and Fyb) positively correlated with Th1 cell infiltration. At the single-cell level, Abca1 and Fyb were significantly expressed in macrophages. In addition, we verified that Abca1 could affect the function of macrophages. Finally, we hypothesized that Abca1 is involved in the infiltration of Th1 cells into dorsal root ganglion (DRG) tissues and induces NP via immunoinflammatory response. Hence, the present study aimed to elucidate the correlation between NP and neuroinflammation and identify a new therapeutic target for treating NP.

Comparison of revascularization and conservative treatment for hemorrhagic moyamoya disease in East Asian Countries: a single-center case series and a systematic review with meta-analysis.

Objective: The optimal treatment approach for hemorrhagic moyamoya disease (HMMD) remains a topic of debate, particularly regarding the comparative efficacy of revascularization versus conservative treatment. Our study, which included a single-center case series and a systematic review with meta-analysis, aimed to determine whether surgical revascularization is associated with a significant reduction in postoperative rebleeding, ischemic events, and mortality compared to conservative treatment among East Asian HMMD patients. Methods: We conducted a systematic literature review by searching PubMed, Google Scholar, Wanfang Med Online (WMO), and the China National Knowledge Infrastructure (CNKI). The outcomes of surgical revascularization and conservative treatment, including rebleeding, ischemic events and mortality, were compared. The authors' institutional series of 24 patients were also included and reviewed in the analysis. Results: A total of 19 East Asian studies involving 1,571 patients as well as our institution's retrospective study of 24 patients were included in the study. In the adult patients-only studies, those who underwent revascularization had significantly lower rates of rebleeding, ischemic events, and mortality compared to those who received conservative treatment (13.1% (46/352) vs. 32.4% (82/253), P < 0.00001; 4.0% (5/124) vs. 14.9% (18/121), P = 0.007; and 3.3% (5/153) vs. 12.6% (12/95), P = 0.01, respectively). In the adult/pediatric patients' studies, similar statistical results of rebleeding, ischemic events, and mortality have been obtained (70/588 (11.9%) vs. 103/402 (25.6%), P = 0.003 or <0.0001 in a random or fixed-effects model, respectively; 14/296 (4.7%) vs. 26/183 (14.2%), P = 0.001; and 4.6% (15/328) vs. 18.7% (23/123), P = 0.0001, respectively). Conclusion: The current single-center case series and systematic review with meta-analysis of studies demonstrated that surgical revascularization, including direct, indirect, and a combination of both, significantly reduces rebleeding, ischemic events, and mortality in HMMD patients in the East Asia region. More well-designed studies are warranted to further confirm these findings.

A systematic review of image-guided, surgical robot-assisted percutaneous puncture: Challenges and benefits.

Percutaneous puncture is a common medical procedure that involves accessing an internal organ or tissue through the skin. Image guidance and surgical robots have been increasingly used to assist with percutaneous procedures, but the challenges and benefits of these technologies have not been thoroughly explored. The aims of this systematic review are to furnish an overview of the challenges and benefits of image-guided, surgical robot-assisted percutaneous puncture and to provide evidence on this approach. We searched several electronic databases for studies on image-guided, surgical robot-assisted percutaneous punctures published between January 2018 and December 2022. The final analysis refers to 53 studies in total. The results of this review suggest that image guidance and surgical robots can improve the accuracy and precision of percutaneous procedures, decrease radiation exposure to patients and medical personnel and lower the risk of complications. However, there are many challenges related to the use of these technologies, such as the integration of the robot and operating room, immature robotic perception, and deviation of needle insertion. In conclusion, image-guided, surgical robot-assisted percutaneous puncture offers many potential benefits, but further research is needed to fully understand the challenges and optimize the utilization of these technologies in clinical practice.

High dietary lipid level promotes low salinity adaptation in the marine euryhaline crab (Scylla paramamosain).

The physiological processes involved in adaptation to osmotic pressure in euryhaline crustaceans are highly energy demanding, but the effects of dietary lipids (fat) on low salinity adaptations have not been well evaluated. In the present study, a total of 120 mud crabs (Scylla paramamosain, BW = 17.87 ± 1.49 g) were fed control and high-fat (HF) diets, at both medium salinity (23‰) and low salinity (4‰) for 6 wk, and each treatment had 3 replicates with each replicate containing 10 crabs. The results indicated that a HF diet significantly mitigated the reduction in survival rate, percent weight gain and feed efficiency induced by low salinity (P < 0.05). Low salinity lowered lipogenesis and activated lipolysis resulting in lipid depletion in the hepatopancreas of mud crabs (P < 0.05). Thus, HF diets enhanced the process of lipolysis to supply more energy. In the gills, low salinity and the HF diet increased the levels of mitochondrial biogenesis markers, the activity of mitochondrial complexes, and the expression levels of genes related to energy metabolism (P < 0.05). Consequently, the positive effects of the HF diet on energy metabolism in mud crabs at low salinity promoted osmotic pressure regulation. Specifically, significantly higher haemolymph osmotic pressure and inorganic ion content, as well as higher osmotic pressure regulatory enzyme activity in gills, and gene and protein expression levels of NaK-ATPase were observed in crabs fed the HF diet at low salinity (P < 0.05). In summary, high dietary lipid levels improved energy provision to facilitate mitochondrial biogenesis, which increased ATP provision for osmotic pressure regulation of mud crabs. This study also illustrates the importance of dietary lipid nutrition supplementation for low salinity adaptations in mud crabs.

AFM negatively regulates the infiltration of monocytes to mediate sepsis-associated acute kidney injury.

Background: Sepsis is organ dysfunction due to the host's deleterious response to infection, and the kidneys are one of the organs damaged in common sepsis. Sepsis-associated acute kidney injury (SA-AKI) increases the mortality in patients with sepsis. Although a substantial volume of research has improved the prevention and treatment of the disease, SA-SKI is still a significant clinical concern. Purpose: Aimed to use weighted gene co-expression network analysis (WGCNA) and immunoinfiltration analysis to study SA-AKI-related diagnostic markers and potential therapeutic targets. Methods: Immunoinfiltration analysis was performed on SA-AKI expression datasets from the Gene Expression Synthesis (GEO) database. A weighted gene co-expression network analysis (WGCNA) analysis was performed on immune invasion scores as trait data, and modules associated with immune cells of interest were identified as hub modules. Screening hub geneset in the hub module using protein-protein interaction (PPI) network analysis. The hub gene was identified as a target by intersecting with significantly different genes screened by differential expression analysis and validated using two external datasets. Finally, the correlation between the target gene, SA-AKI, and immune cells was verified experimentally. Results: Green modules associated with monocytes were identified using WGCNA and immune infiltration analysis. Differential expression analysis and PPI network analysis identified two hub genes (AFM and GSTA1). Further validation using additional AKI datasets GSE30718 and GSE44925 showed that AFM was significantly downregulated in AKI samples and correlated with the development of AKI. The correlation analysis of hub genes and immune cells showed that AFM was significantly associated with monocyte infiltration and hence, selected as a critical gene. In addition, Gene single-enrichment analysis (GSEA) and PPI analyses results showed that AFM was significantly related to the occurrence and development of SA-AKI. Conclusions: AFM is inversely correlated with the recruitment of monocytes and the release of various inflammatory factors in the kidneys of AKI. AFM can be a potential biomarker and therapeutic target for monocyte infiltration in sepsis-related AKI.

Public health implications of computer-aided diagnosis and treatment technologies in breast cancer care.

Breast cancer remains a significant public health issue, being a leading cause of cancer-related mortality among women globally. Timely diagnosis and efficient treatment are crucial for enhancing patient outcomes, reducing healthcare burdens and advancing community health. This systematic review, following the PRISMA guidelines, aims to comprehensively synthesize the recent advancements in computer-aided diagnosis and treatment for breast cancer. The study covers the latest developments in image analysis and processing, machine learning and deep learning algorithms, multimodal fusion techniques and radiation therapy planning and simulation. The results of the review suggest that machine learning, augmented and virtual reality and data mining are the three major research hotspots in breast cancer management. Moreover, this paper discusses the challenges and opportunities for future research in this field. The conclusion highlights the importance of computer-aided techniques in the management of breast cancer and summarizes the key findings of the review.

MAC mediates mammary duct epithelial cell injury in plasma cell mastitis and granulomatous mastitis.

Plasma cell mastitis (PCM) and granulomatous mastitis (GM) are common inflammatory nonbacterial mastitis (NBM). However, the pathogenesis of NBM is still unclear. METHODS: In this study, we statistically analyzed the pathological features of PCM and GM using pathological HE staining and tissue transmission electron microscopy. The levels of MAC (C5b-9n), P-selectin, E-selectin, and ICAM-1 were detected through IHC, WB, ELISA, and qPCR. The expression level and location of MAC were observed by tissue immunological electron microscopy. In addition, exosomes were isolated from tissues, identified using transmission electron microscopy, and the densities were detected by Nano-FCM. Finally, the expression intensity of MAC in exosomes was detected by flow cytometry and immunoelectron microscopy. RESULTS: The damage and apoptosis of mammary duct epithelial cells are the common pathological features of PCM and GM. MAC is primarily located in the cell membrane of mammary ductal epithelial cells and is significantly expressed in PCM and GM. The density of exosomes in PCM and GM tissues was elevated, and MAC was highly expressed in exosomes. In addition, the expression of P-selectin, E-selectin, and ICAM-1 in PCM and GM was significantly higher than in the normal group. CONCLUSION: We found severe damage of the mammary duct epithelial cells in PCM and GM tissues, which was verified by relevant pathological methods. Earlier studies demonstrated that MAC is highly expressed in PCM and GM tissues and exosomes seem to play a very important role in the understanding of MAC. Furthermore, MAC is involved in inflammatory infiltration and lesion of mammary duct epithelial cells upregulated by P-selectin, E-selectin, and ICAM-1. These findings provide new insights into PCM and GM molecular mechanisms.

Dietary cholesterol promotes growth and ecdysone signalling pathway by modulating cholesterol transport in swimming crabs (Portunus trituberculatus).

Cholesterol, as an indispensable nutrient, regulates molting and growth in crustacean. As crustaceans are unable to biosynthesize cholesterol de novo, it is central to understand how dietary cholesterol affects molting in crustaceans. An 8-week feeding trial was conducted to evaluate the effects of dietary cholesterol level (0.12%, 0.43%, 0.79%, 1.00%, 1.30% and 2.50%) on growth, cholesterol metabolism and expression of genes related to lipid and ecdysone metabolism in female swimming crabs (Portunus trituberculatus). A total of 192 crabs (1.41 ± 0.05 g) were randomly distributed into 192 aquaria. Each treatment had 4 replicates with each replicate containing 8 crabs. Crabs fed the 1.00% cholesterol diet showed best growth performance, and thus based on percent weight gain, the optimal dietary cholesterol requirement was calculated at 1.01%. Tissue cholesterol concentrations were positively correlated with dietary cholesterol level. The contents of functional fatty acids in hepatopancreas significantly increased as dietary cholesterol increased from 0.12% to 2.50% (P < 0.05). The expression levels of genes related to lipogenesis pathway, lipid catabolism and fatty acid oxidation were significantly down-regulated with increased dietary cholesterol level (P < 0.05). The highest expression levels of cholesterol transport genes, low-density lipoprotein receptor (ldlr) and low-density lipoprotein receptor-related protein 2 (lrp2) occurred in crabs fed the 1.30% cholesterol diet. Moreover, hormones related to molting such as crustacean hyperglycemic hormone (CHH), methyl farnesoate (MF), molt-inhibiting hormone (MIH), and ecdysone in hemolymph were significantly influenced by dietary cholesterol level (P < 0.05). The highest expression levels of ecdysone receptor (ecr) and chitinase 1 (chi1) in eyestalk and hepatopancreas were found in crabs fed the diet containing 1.00% cholesterol (P < 0.05). In conclusion, the optimal dietary level was beneficial to functional fatty acid accumulation, regulated lipid metabolism, promoted the ecdysone signalling pathway by improving the cholesterol transport, and improved the molting rate and growth of swimming crabs.

Identifying neuroimaging biomarkers for psychogenic erectile dysfunction by fusing multi-level brain information: A resting-state functional magnetic resonance imaging study.

BACKGROUND: Psychogenic erectile dysfunction (pED) patients who are under their 40s in China consist of a major component of erectile dysfunction. Existing neuroimaging studies have demonstrated that pED is a functional disorder with aberrant neural representations on the local level, the regional level, and the global level, respectively. Therefore, it is reasonable to incorporate brain information from all these levels simultaneously into consideration when identifying neuroimaging biomarkers for pED. However, no such endeavors have been made in previous studies to fully disclose the central mechanism of pED. METHOD: To incorporate multi-level brain features to fully explore the neural representation of pED, a novel machine learning framework was proposed in the current study. Specifically, we used amplitude of low-frequency fluctuation, regional homogeneity, and degree centrality as indices for local, regional, and global brain activity, respectively. A fully data-driven method, that is, support vector machine (SVM) with recursive feature elimination analyses, was used to investigate discriminative brain map between 48 pED patients and 39 healthy control subjects for resting state functional magnetic resonance imaging (rs-fMRI) data. RESULTS: By fusing multi-level brain features, our method led to a superb classification accuracy of 95.12% between two groups. Interestingly, the right anterior cingulate gyrus and the left precuneus showed abnormal representations at different levels simultaneously in pED patients, which also explicated highest discriminative power between groups. Moreover, the right insular, the left fusiform gyrus, the right inferior temporal gyrus, the right superior frontal gyrus, the right precentral gyrus, the bilateral parahippocampal gyrus, and the bilateral inferior frontal gyrus were discriminative for pED. Also, correlation analysis explicated that several core brain regions were associated with the clinical manifestations in pED patients. CONCLUSION: This is one of the first study investigating brain alterations on different levels simultaneously in pED patients. Our results suggested that pED involves multi-level aberrant brain representations in multi-dimensional neurobehavioral components, which closely interrelated with cognitive and psychosocial factors, that is, attention, appraisal, emotion, and sensorimotor. Our findings are likely to help foster new insights into the pathophysiological mechanisms of pED and the aberrant brain regions may serve as potential therapeutic targets for targeted therapy for brain.

Isoliquiritigenin mitigates oxidative damage after subarachnoid hemorrhage in vivo and in vitro by regulating Nrf2-dependent Signaling Pathway via Targeting of SIRT1.

BACKGROUND: Oxidative stress is a crucial factor leading to subarachnoid hemorrhage (SAH)-induced early brain injury (EBI). Isoliquiritigenin has been verified as a powerful anti-oxidant in a variety of diseases models and can activate sirtuin 1 and nuclear factor-erythroid 2-related factor 2 (Nrf2) pathways. However, the effects of isoliquiritigenin against EBI after SAH and the underlying mechanisms remain elusive. PURPOSE: The primary goal of this study is to verify the therapeutic effects of isoliquiritigenin on EBI after SAH and the possible molecular mechanisms. STUDY DESIGN: A prechiasmatic cistern SAH model in rats and a hemoglobin incubation SAH model in primary neurons were established. Isoliquiritigenin was administered after SAH induction. EX527 was employed to inhibit sirtuin 1 activation and ML385 was used to suppress Nrf2 signaling. METHODS: In our study, neurological scores, brain edema, biochemical estimation, western blotting, and histopathological study were performed to explore the therapeutic action of isoliquiritigenin against SAH. RESULTS: Our data revealed that isoliquiritigenin significantly mitigated oxidative damage after SAH as evidenced by decreased reactive oxygen species overproduction and enhanced intrinsic anti-oxidative system. Concomitant with the reduced oxidative insults, isoliquiritigenin improved neurological function and reduced neuronal death in the early period after SAH. Additionally, isoliquiritigenin administration significantly enhanced Nrf2 and sirtuin 1 expressions. Inhibition of Nrf2 by ML385 reversed the anti-oxidative and neuroprotective effects of isoliquiritigenin against SAH. Moreover, inhibiting sirtuin 1 by EX527 pretreatment suppressed isoliquiritigenin-induced Nrf2-dependent pathway and abated the cerebroprotective effects of isoliquiritigenin. In primary cortical neurons, isoliquiritigenin treatment also ameliorated oxidative insults and repressed neuronal degeneration. The beneficial aspects of isoliquiritigenin were attributed to the promotion of sirtuin 1 and Nrf2 signaling pathways and were counteracted by EX527. CONCLUSION: Our findings suggest that isoliquiritigenin exerts cerebroprotective effects against SAH-induced oxidative insults by modulating the Nrf2-mediated anti-oxidant signaling in part through sirtuin 1 activation. Isoliquiritigenin might be a new potential drug candidate for SAH.

Comprehensive Analysis of TRP Channel-Related Genes in Patients With Triple-Negative Breast Cancer for Guiding Prognostic Prediction.

Background: Triple-negative breast cancer (TNBC) is a special subtype of breast cancer. Transient Receptor Potential (TRP) channel superfamily has emerged as a novel and interesting target in a variety of tumors. However, the association of TRP channel-related genes with TNBC is still unclear. Methods: The The Cancer Genome Atlas (TCGA)-TNBC and GSE58812 datasets were downloaded from the public database. The differentially expressed TRP channel-related genes (DETGs) were screened by limma package, and mutations of the above genes were analyzed. Subsequently, new molecular subtypes in TNBC-based DETGs were explored by consensus clustering analysis. In addition, Lasso-Cox regression analysis was used to divide it into two robust risk subtypes: high-risk group and low-risk group. The accuracy and distinguishing ability of above models were verified by a variety of methods, including Kaplan-Meier survival analysis, ROC analysis, calibration curve, and PCA analysis. Meanwhile, CIBERSORT algorithm was used to excavate status of immune-infiltrating cells in TNBC tissues. Last, we explored the therapeutic effect of drugs and underlying mechanisms of risk subgroups by pRRophetic package and GSEA algorithm, respectively. Results: A total of 19 DETGs were identified in 115 TNBC and 113 normal samples from TCGA database. In addition, missense mutation and SNP were the most common variant classification. According to Lasso-Cox regression analysis, the risky formula performed best when nine genes were used: TRPM5, TRPV2, HTR2B, HRH1, P2RY2, MAP2K6, NTRK1, ADCY6, and PRKACB. Subsequently, Kaplan-Meier survival analysis, ROC analysis, calibration curve, and Principal Components Analysis (PCA) analysis showed an excellent accuracy for predicting OS using risky formula in each cohort (P < 0.05). Specifically, high-risk group had a shorter OS compared with low-risk group. In addition, T-cell CD4 memory activated and macrophages M1 were enriched in normal tissues, whereas Tregs were increased in tumor tissues. Note that the low-risk group was better therapeutic effect to docetaxel, doxorubicin, cisplatin, paclitaxel, and gemcitabine than the high-risk group (P < 0.05). Last, in vitro assays, Quantitative Real-time PCR (qRT-PCR) indicated that TRPM5 was significantly highly expressed in MDA-MB-231 and MDA-MB-468 cells compared with that in MCF-10A cells (P < 0.01). Conclusion: We identified a risky formula based on expression of TRP channel-related genes that can predict prognosis, therapeutic effect, and status of tumor microenvironment for patients with TNBC.

Decreased Expression of CIRP Induced by Therapeutic Hypothermia Correlates with Reduced Early Brain Injury after Subarachnoid Hemorrhage.

Early brain injury is considered to be a primary reason for the poor prognosis of patients suffering from subarachnoid hemorrhage (SAH). Due to its pro-inflammatory activity, cold-inducible RNA-binding protein (CIRP) has been implicated in the ischemic brain insult, but its possible interplay with hypothermia in SAH treatment remains to be evaluated. One-hundred and thirty-eight Sprague-Dawley rats (300-350 g males) were randomly allocated into the following groups: sham-operated (Sham); SAH; and SAH + hypothermia (SAH + H), each comprised of 46 animals. After treatments, the brain tissues of the three groups were randomly collected after 12 h, 1 d, 3 d, and 7 d, and the expression levels of the CIRP and mitochondrial apoptosis pathway-related proteins Bax, Bcl-2, caspase-9, caspase-3, and cytochrome c measured using Western blotting and real-time PCR. Brain damage was assessed by TUNEL and Nissl staining, the electron microscopy of brain tissue slices as well as functional rotarod tests. Expression of CIRP, Bax, caspase-9, caspase-3, and cytochrome c as well as reduced motor function incidence were higher in the SAH group, particularly during the first 3 d after SAH induction. Hypothermia blunted these SAH responses and apoptosis, thereby indicating reduced inflammatory signaling and less brain cell injury in the early period after SAH. Hypothermia treatment was found to effectively protect the brain tissue from early SAH injury in a rat model and its further evaluation as a therapeutic modality in SAH patients requires further study.

Clinical and radiological outcomes of combined modular prothesis and cortical strut for revision proximal femur in giant cell tumor of bone patients.

BACKGROUND: Femoral bone deficiency is a challenging problem in revision proximal femoral replacement. The purpose of this study is to evaluate the clinical and radiological outcomes of revision proximal femoral replacement as a salvage treatment for severe bone loss after oncologic proximal replacement surgery in patient with benign giant cell tumor of bone. METHODS: 16 patients (6 men and 10 women) were included in this retrospective study, with a mean age of 46.6 year at the time of revision surgery. All patients underwent revision proximal femoral replacement with the use of modular prosthesis and cortical strut allografts. The modified Harris Hip Score, Short Form 36, and musculoskeletal Tumor Society Score were used for patient evaluation. Regular follow-up was performed to evaluate the recurrence and metastases rate, limb function, and long-term complications of patients. RESULTS: The average follow-up was 46.3 months (range, 26-75 months), during which there was no local recurrence and metastases of patient. At the latest follow-up, the mean modified Harris Hip Score was 70.6 points, which was significantly improved compared with that of preoperative (p < 0.05). The final follow-up results of Short Form 36, Musculoskeletal Tumor Society Score, and limb-length discrepancy were also significantly improved compared to that of preoperative (p < 0.05). At the latest follow-up, the implanted femoral stems were all stable and all cortical strut allografts were also incorporated to their own bone. CONCLUSION: Using modular prosthesis and cortical strut allografts in revision, proximal femur replacement is an acceptable procedure for relatively young patient with severe proximal femoral bone loss after oncologic surgery with benign giant cell tumor of bone. More attentions should be paid to reduce the risk of complications in these complex reconstructions.