Genome-wide identification and phylogenetic analysis of the tetraspanin gene family in lepidopteran insects and expression profiling analysis in Helicoverpa armigera.

The tetraspanin gene family encodes cell-surface proteins that span the membrane 4 times and play critical roles in a wide range of biological processes across numerous organisms. Recent findings highlight the involvement of a tetraspanin of the lepidopteran pest Helicoverpa armigera in resistance to Bacillus thuringiensis Cry insecticidal proteins, which are extensively used in transgenic crops. Thus, a better understanding of lepidopteran tetraspanins is urgently needed. In the current study, genome scanning in 10 lepidopteran species identified a total of 283 sequences encoding potential tetraspanins. Based on conserved cysteine patterns in the large extracellular loop and their phylogenetic relationships, these tetraspanins were classified into 8 subfamilies (TspA to TspH). Six ancestral introns were identified within lepidopteran tetraspanin genes. Tetraspanins in TspA, TspB, TspC, and TspD subfamilies exhibit highly similar gene organization, while tetraspanins in the remaining 4 subfamilies exhibited variation in intron loss and/or gain during evolution. Analysis of chromosomal distribution revealed a lepidopteran-specific cluster of 10 to 11 tetraspanins, likely formed by tandem duplication events. Selective pressure analysis indicated negative selection across all orthologous groups, with ω values ranging between 0.004 and 0.362. However, positive selection was identified at 18 sites within TspB5, TspC5, TspE3, and TspF10. Furthermore, spatiotemporal expression analysis of H. armigera tetraspanins demonstrated variable expression levels across different developmental stages and tissues, suggesting diverse functions of tetraspanin members in this globally important insect pest. Our findings establish a solid foundation for subsequent functional investigations of tetraspanins in lepidopteran species.

Neuronal Panx1 drives peripheral sensitization in experimental plantar inflammatory pain.

BACKGROUND: The channel-forming protein Pannexin1 (Panx1) has been implicated in both human studies and animal models of chronic pain, but the underlying mechanisms remain incompletely understood. METHODS: Wild-type (WT, n = 24), global Panx1 KO (n = 24), neuron-specific Panx1 KO (n = 20), and glia-specific Panx1 KO (n = 20) mice were used in this study at Albert Einstein College of Medicine. The von Frey test was used to quantify pain sensitivity in these mice following complete Freund's adjuvant (CFA) injection (7, 14, and 21 d). The qRT-PCR was employed to measure mRNA levels of Panx1, Panx2, Panx3, Cx43, Calhm1, and ß-catenin. Laser scanning confocal microscopy imaging, Sholl analysis, and electrophysiology were utilized to evaluate the impact of Panx1 on neuronal excitability and morphology in Neuro2a and dorsal root ganglion neurons (DRGNs) in which Panx1 expression or function was manipulated. Ethidium bromide (EtBr) dye uptake assay and calcium imaging were employed to investigate the role of Panx1 in adenosine triphosphate (ATP) sensitivity. ß-galactosidase (ß-gal) staining was applied to determine the relative cellular expression levels of Panx1 in trigeminal ganglia (TG) and DRG of transgenic mice. RESULTS: Global or neuron-specific Panx1 deletion markedly decreased pain thresholds after CFA stimuli (7, 14, and 21 d; P < 0.01 vs. WT group), indicating that Panx1 was positively correlated with pain sensitivity. In Neuro2a, global Panx1 deletion dramatically reduced neurite extension and inward currents compared to the WT group (P < 0.05), revealing that Panx1 enhanced neurogenesis and excitability. Similarly, global Panx1 deletion significantly suppressed Wnt/ß-catenin dependent DRG neurogenesis following 5 d of nerve growth factor (NGF) treatment (P < 0.01 vs. WT group). Moreover, Panx1 channels enhanced DRG neuron response to ATP after CFA injection (P < 0.01 vs. Panx1 KO group). Furthermore, ATP release increased Ca2+ responses in DRGNs and satellite glial cells surrounding them following 7 d of CFA treatment (P < 0.01 vs. Panx1 KO group), suggesting that Panx1 in glia also impacts exaggerated neuronal excitability. Interestingly, neuron-specific Panx1 deletion was found to markedly reduce differentiation in cultured DRGNs, as evidenced by stunted neurite outgrowth (P < 0.05 vs. Panx1 KO group; P < 0.01 vs. WT group or GFAP-Cre group), blunted activation of Wnt/ß-catenin signaling (P < 0.01 vs. WT, Panx1 KO and GFAP-Cre groups), and diminished cell excitability (P < 0.01 vs. GFAP-Cre group) and response to ATP stimulation (P < 0.01 vs. WT group). Analysis of ß-gal staining showed that cellular expression levels of Panx1 in neurons are significantly higher (2.5-fold increase) in the DRG than in the TG. CONCLUSIONS: The present study revealed that neuronal Panx1 is a prominent driver of peripheral sensitivity in the setting of inflammatory pain through cell-autonomous effects on neuronal excitability. This hyperexcitability dependence on neuronal Panx1 contrasts with inflammatory orofacial pain, where similar studies revealed a prominent role for glial Panx1. The apparent differences in Panx1 expression in neuronal and non-neuronal TG and DRG cells are likely responsible for the distinct impact of these cell types in the two pain models.

Choriocarcinoma That Had Transferred to the Right Inferior Pulmonary Vein and Left Atrium: A Case Report.

Here, we present a case of choriocarcinoma with metastasis only to the right inferior pulmonary vein and heart, which is unusual, as the skipping of lung metastasis is extremely rare. The 34-year-old patient presented with cough and hemoptysis. The diagnosis was challenging due to the absence of gynecological abnormalities and elevated ß-HCG levels, only revealing a cardiac mass upon imaging. While no abnormalities were found through gynecological ultrasound or gynecological examination, the serum human chorionic gonadotropin ß subunit (ß-HCG) level was abnormally raised. Echocardiography showed a left atrial myxoma with a size of approximately 6.3×1.81 cm. A left atrial mass resection was performed during cardiac surgery, where it was found that the left atrial mass had originated from the right inferior pulmonary vein. It was approximately 6×3×3 cm in size, with a flesh-red color and firm tissue. Postoperative pathology and immunohistochemistry indicated choriocarcinoma. The cardiac surgery unearthed a mass originating from the right inferior pulmonary vein. Its size and characteristics, along with the chemotherapy regimens that followed, are crucial details for understanding treatment approaches for such atypical cases. Highlight the patient's recovery post-treatment and the effectiveness of the chemotherapy regimen. This offers insights into the potential for successful treatment outcomes in atypical choriocarcinoma cases. The patient underwent chemotherapy regimens with etoposide, cisplatin (EP) ,etoposide, and methotrexate, and dactinomycin alternating with cyclophosphamide and vincristine (EMACO). A satisfactory result was achieved. This case enhances understanding of choriocarcinoma metastasis patterns. It underscores the need for a multidisciplinary approach in diagnosing and managing such rare presentations.

Grape seed proanthocyanins protect fluoride-induced hepatotoxicity via the Nrf2 signaling pathway in male rats.

Background: Fluoride is a necessary element for human health, but excessive fluoride intake is found toxic to the liver. Previous studies confirmed that Grape seed procyanidin extract (GSPE) protects against fluoride-induced hepatic injury. However, the mechanism underlying this protective effect remains obscure. To evaluate the protective effect of GSPE against fluoride-induced hepatic injury and explore the possible hepatoprotective role of the Nrf2 signaling pathway to find effective strategies for the treatment and prevention of fluoride-induced hepatotoxicity. This study aims to explore the mechanisms by which GSPE attenuates fluoride-induced hepatotoxicity through a rat drinking water poisoning model. Methods: Hepatic injury was determined by serum biochemical parameters, oxidative parameters, HE, and TUNEL analysis. The protein expression levels of apoptosis-related proteins like Bax, B-cell lymphoma-2 (Bcl-2), and Caspase-3 and the nuclear factor, erythroid 2 like 2 (Nrf2) were analyzed by Western blot. Resluts: Our results showed that GSPE administration reduced fluoride-induced elevated serum ALT and AST and enhanced the antioxidant capacity of the liver. In addition, GSPE mitigated fluoride-induced histopathological damage and reduced the liver cell apoptosis rate. Furthermore, GSPE significantly up-regulated the expression and nuclear translocation of the Nrf2 and decreased apoptosis-related proteins like Bax and caspase-3 in the hepatic. Conclusion: Taken together, GSPE exerts protective effects on the oxidative damage and apoptosis of fluoride-induced hepatic injury via the activation of the Nrf2 signaling pathway. This study provides a new perspective for the mechanism study and scientific prevention and treatment of liver injury induced by endemic fluorosis.

Effect of yeast extract on microbiologically influenced corrosion of X70 pipeline steel by Desulfovibrio bizertensis SY-1.

Microbiologically influenced corrosion (MIC) is a complicated process that happens ubiquitously and quietly in many fields. As a useful nutritional ingredient in microbial culture media, yeast extract (YE) is a routinely added in the MIC field. However, how the YE participated in MIC is not fully clarified. In the present work, the effect of YE on the growth of sulfate reducing prokaryotes (SRP) Desulfovibrio bizertensis SY-1 and corrosion behavior of X70 pipeline steel were studied. It was found that the weight loss of steel coupons in sterile media was doubled when YE was removed from culture media. However, in the SRP assays without YE the number of planktonic cells decreased, but the attachment of bacteria on steel surfaces was enhanced significantly. Besides, the corrosion rate of steel in SRP assays increased fourfold after removing YE from culture media. MIC was not determined for assays with planktonic SRP but only for biofilm assays. The results confirm the effect of YE on D. bizertensis SY-1 growth and also the inhibitory role of YE on MIC.

Accelerated deterioration corrosion of X70 steel by oxidation acid-producing process catalyzed by Acinetobacter soli in oil-water environment.

Deterioration corrosion occurs between the external surface of oil pipelines and aerobic oil-degrading microorganisms in oil fields. Microorganisms with aerobic oil pollution remediation capabilities may catalyze more serious anaerobic microbial corrosion due to the carbon source supply. In this study, Acinetobacter soli strains were isolated from oil-contaminated environments, and their role in the deterioration corrosion behavior of X70 steel in an oil-water environment was investigated using the EDS multipoint scanning method. The presence of oil controls the deposition of carbon and phosphorus and diffusion of oxygen, leading to significant adhesion attraction and initial growth inhibition of biofilm on the metal surface. A. soli facilitates oxygen transfer and iron ion dissolution, thereby accelerating the pitting corrosion of X70 steel. This corrosion of the X70 steel, in turn, further accelerates the microbial degradation of oil, inhibiting the appearance of calcareous scale in the later stage of corrosion. The corrosion of X70 steel is influenced by microbial degradation, and the specific corrosion behaviors are related to the activity of A. soli in the petroleum environment. This study sheds light on the corrosion mechanisms of X70 steel by A. soli at different stages, providing insights into the interactions between microorganisms, oil pollution, and metal corrosion in oil fields.

[Efficacy and Safety of Plerixafor Combined with G-CSF for Autologous Peripheral Blood Hematopoietic Stem Cell Mobilization in Lymphoma Patients].

OBJECTIVE: To investigate the efficacy and safety of plerixafor combined with granulocyte colony-stimulating factor (G-CSF) in mobilizing peripheral blood hematopoietic stem cells in patients with lymphoma. METHODS: The clinical data of lymphoma patients who received autologous hematopoietic stem cell mobilization using plerixafor combined with G-CSF from January 2019 to December 2021 were retrospectively analyzed. The patients received 3 kinds of mobilization regimens: front-line steady-state mobilization, preemptive intervention, and recuse mobilization. The acquisition success rate, excellent rate of collection, and incidence of treatment-related adverse reaction were counted. The influence of sex, age, disease remission status, bone marrow involvement at diagnosis, chemotherapy lines, number of chemotherapy, platelet count and number of CD34+ cells on the day before acquisition in peripheral blood on the collection results were analyzed to identify the risk factors associated with poor stem cell collection. RESULTS: A total of 43 patients with lymphoma were enrolled, including 7 cases who received front-line steady-state mobilization, 19 cases who received preemptive intervention, and 17 cases who received recuse mobilization. The overall acquisition success rate was 58.1% (25/43) after use of plerixafor combined with G-CSF, and acquisition success rate of front-line steady-state mobilization, preemptive intervention, and recuse mobilization was 100%, 57.9%(11/19), and 41.2%(7/17), respectively. The excellent rate of collection was 18.6%(8/43). A total of 15 patients experienced mild to moderate treatment-related adverse reactions. The number of CD34+ cells < 5 cells/µl in peripheral blood on the day before collection was an independent risk factor affecting stem cell collection. CONCLUSIONS: Plerixafor combined with G-CSF is a safe and effective mobilization regimen for patients with lymphoma. The number of CD34+ cells in peripheral blood on the day before collection is an predictable index for the evaluation of stem cell collection.

Cytotoxic phenyl polyketides from Hypericum curvisepalum N. Robson.

(±)-Hypecurvone A (1) and B (2), two new undescribed phenyl polyketides, along with seven known analogues (3-9) were isolated from the whole plant of Hypericum curvisepalum. Chiral separation of 1 and 2 yielded two pairs of enantiomers 1a/1b and 2a/2b, respectively. The structures of these compounds were elucidated by extensive spectroscopic analyses and ECD spectra simulations. All isolates exhibited moderate cytotoxicity against human hepatocellular carcinoma SMMC-7721 cells, and compound 3 also showed weak cytotoxicity toward MGC-803 cells. The cytotoxicity of these compounds was found to be related to enhanced mitochondria-mediated apoptosis and inhibition of the G2/M phase of the cell cycle.

Human Endogenous Retroviruses and Toll-Like Receptors.

Human endogenous retroviruses (HERVs) are estimated to comprise ∼8% of the entire human genome, but the vast majority of them remain transcriptionally silent in most normal tissues due to accumulated mutations. However, HERVs can be frequently activated and detected in various tissues under certain conditions. Nucleic acids or proteins produced by HERVs can bind to pattern recognition receptors of immune cells or other cells and initiate an innate immune response, which may be involved in some pathogenesis of diseases, especially cancer and autoimmune diseases. In this review, we collect studies of the interaction between HERV elements and Toll-like receptors and attempt to provide an overview of their role in the immunopathological mechanisms of inflammatory and autoimmune diseases.

Inadequate dosing of THPS treatment increases microbially influenced corrosion of pipeline steel by inducing biofilm growth of Desulfovibrio hontreensis SY-21.

Biocides are often used to mitigate the microbially influenced corrosion (MIC) of construction materials in many fields. To study the effect of inadequate dosing of non-oxidizing biocide tetrakis (hydroxymethyl) phosphonium sulfate (THPS) on corrosion of pipeline steel caused by microorganisms, a novel marine isolate Desulfovibrio hontreensis SY-21 was selected as a test microorganism. Weight loss rate determination, morphological analyses, and corrosion product analyses combined with electrochemical measurements were performed to investigate the influence of THPS on the MIC of X70 pipeline steel. The responses of sessile and planktonic cells of D. hontreensis to THPS were also studied. Results showed that D. hontreensis cells could significantly promote steel corrosion and induce local corrosion pits. With a THPS addition within the tolerance range of D. hontreensis for the biocide, MIC of the steel was further promoted by 65%. The growth of planktonic cells was inhibited by the biocide, but the number of biofilm cells was significantly increased. This study revealed that THPS concentrations within a specific range increased the corrosive effect of the presence of D. hontreensis by promoting the growth of sessile cells and biofilm formation. Therefore, the use of the biocide in practical applications needs to be properly considered and managed.

Synergistic effect of carbon starvation and exogenous redox mediators on corrosion of X70 pipeline steel induced by Desulfovibrio singaporenus.

In microbiologically influenced corrosion (MIC) induced by sulfate-reducing bacteria (SRB), the electrons released from iron were transferred via extracellular electron transfer (EET) to the inner cells. Electron mediators and carbon starvation have also been found to promote steel corrosion. This study aimed to investigate the synergistic effects of electron mediators and carbon starvation on MIC and their effect on biofilm catalytic activity. The results demonstrated that the weight losses of X70 steel were 0.68 and 1.03 mg/cm2 in 100% and 10% carbon source (CS) SRB solution, respectively. The addition of riboflavin and cytochrome c increased the corrosion rate by 1.76 and 1.87 times, respectively, in the 100% CS SRB medium compared to the medium without exogenous redox mediators. For the 10% CS SRB medium, the corrosion rate increased by 1.40 and 1.89 times, respectively, when riboflavin and cytochrome c were added. The addition of riboflavin and cytochrome c also enhanced the biocatalytic activity of the SRB biofilm in both the 100% and 10% CS SRB media.

Therapeutic potential of curcumin in diabetic retinopathy (Review).

Diabetic retinopathy (DR) is a type of retinal microangiopathy caused by diabetes mellitus. It has become the leading cause of blindness among working individuals worldwide. DR is becoming increasingly common among younger diabetic patients and there is a need for lifelong treatment. The pathogenic mechanisms of DR are influenced by a number of factors, such as hyperglycemia, hyperlipidemia, inflammatory response and oxidative stress, among others. Currently, the treatment methods for DR mainly include retinal photocoagulation, vitrectomy, or anti­vascular endothelial growth factor (VEGF) therapy. However, these methods have some disadvantages and limitations. Therefore, it is a matter of great interest and urgency to discover drugs that can target the pathogenesis of DR. Since ancient times, traditional Chinese medicine practitioners have accumulated extensive experiences in the use of Chinese herbal medicine for the prevention and treatment of diseases. In the theory of traditional Chinese medicine, curcumin has the effects of promoting blood circulation and relieving pain. A number of studies have also demonstrated that curcumin has multiple biological activities, including exerting anti­apoptotic, anti­inflammatory, antioxidant and antitumor properties. In recent years, studies have also confirmed that curcumin can prevent a variety of diabetic complications, including diabetic nephropathy (DN). However, the preventive and curative effects of curcumin on DR and its mechanisms of action have not yet been fully elucidated. The present review aimed to explore the therapeutic potential of curcumin in diabetes mellitus and DR.

Whole-genome sequencing to detect mutations associated with resistance to insecticides and Bt proteins in Spodoptera frugiperda.

The fall armyworm (FAW), Spodoptera frugiperda, is a major pest native to the Americas that has recently invaded the Old World. Point mutations in the target-site proteins acetylcholinesterase-1 (ace-1), voltage-gated sodium channel (VGSC) and ryanodine receptor (RyR) have been identified in S. frugiperda as major resistance mechanisms to organophosphate, pyrethroid and diamide insecticides respectively. Mutations in the adenosine triphosphate-binding cassette transporter C2 gene (ABCC2) have also been identified to confer resistance to Cry1F protein. In this study, we applied a whole-genome sequencing (WGS) approach to identify point mutations in the target-site genes in 150 FAW individuals collected from China, Malawi, Uganda and Brazil. This approach revealed three amino acid substitutions (A201S, G227A and F290V) of S. frugiperda ace-1, which are known to be associated with organophosphate resistance. The Brazilian population had all three ace-1 point mutations and the 227A allele (mean frequency = 0.54) was the most common. Populations from China, Malawi and Uganda harbored two of the three ace-1 point mutations (A201S and F290V) with the 290V allele (0.47-0.58) as the dominant allele. Point mutations in VGSC (T929I, L932F and L1014F) and RyR (I4790M and G4946E) were not detected in any of the 150 individuals. A novel 12-bp insertion mutation in exon 15 of the ABCC2 gene was identified in some of the Brazilian individuals but absent in the invasive populations. Our results not only demonstrate robustness of the WGS-based genomic approach for detection of resistance mutations, but also provide insights for improvement of resistance management tactics in S. frugiperda.

Analysis of risk factors for progressive fibrovascular proliferation in proliferative diabetic retinopathy.

PURPOSE: To investigate the risk factors associated with progressive fibrovascular proliferation (FVP) in proliferative diabetic retinopathy (PDR). METHODS: We retrospectively reviewed the clinical data of patients who underwent pars plana vitrectomy for PDR between August 2017 and October 2019 at our department of ophthalmology. The FVP was divided into five grades based on the coverage area of proliferative membrane. Then we compared the patients with different severities of FVP to analyze the risk factors for higher grade of FVP in PDR. RESULTS: Univariate analysis showed that positive urinary protein (p = 0.007), higher levels of serum blood urea nitrogen (BUN) (p < 0.001) and serum creatinine (p < 0.001), more severe stage of estimated glomerular filtration rate (p < 0.001), age < 45 years (p = 0.005), longer duration of diabetic retinopathy (p = 0.007), history of hypertension (p = 0.034) and smoking (p = 0.008) were related to FVP grade ≥ 3. Multivariate analysis showed that the level of BUN, age < 45 years and smoking were independent risk factors for FVP grade ≥ 3 in PDR patients. CONCLUSION: This study demonstrated that BUN (odds ratio [OR] = 1.318, 95% confidence interval [CI] = 1.150-1.511, p < 0.001), age ≤ 45 years (OR = 3.774, 95% CI = 1.762-8.082, p = 0.001) and smoking (OR = 2.111, 95% CI = 1.040-4.288, p = 0.039) were independent risk factors for progressive FVP in PDR among northeastern Chinese patients.

Microbiologically influenced corrosion of marine steels within the interaction between steel and biofilms: a brief view.

Marine is the harshest corrosive environment where almost all marine underwater equipment and facilities undergo corrosion caused by marine microorganisms. With the development of marine resources globally, the marine engineering and relevant infrastructures have increased exponentially. Microbiologically influenced corrosion (MIC) leads to severe safety accidents and great economic losses. The specific aggregation of corrosive microbial communities and their interactions with materials conform to a typical ecological adaptation mechanism. On the one hand, corrosive biofilms in the marine environment selectively colonize on a specific steel substrate by utilizing their complex community composition and various extracellular polymeric substances; on the other hand, the elemental composition and surface microstructure of different engineering steels affect the microbial community and corrosive process. MIC in the marine environment is a dynamic process evolving with the formation of corrosive biofilms and corrosion products. In this mini-review, the interactions between corrosive biofilm and steel substrates are explored and discussed, especially those conducted in situ in the marine environment. Herein, the important role of iron in the dynamic process of marine corrosion is highlighted.

miR­210­3p regulates cell growth and affects cisplatin sensitivity in human ovarian cancer cells via targeting E2F3.

The potential role of microRNA (miR)­210­3p in carcinogenesis and the cisplatin sensitivity of ovarian cancer were evaluated in the present study. The relative expression levels of miR­210­3p in cisplatin­sensitive SKOV­3 cells and cisplatin­resistant SKOV­3/DDP cells were determined using reverse transcription­quantitative polymerase chain reaction analysis. miR­210­3p mimics and inhibitors were transfected into SKOV­3/DDP cells. Cell Counting Kit­8, scratch and Transwell invasion assays and flow cytometry were conducted to evaluate the role of miR­210­3p in ovarian cancer cells. A luciferase reporter assay was used to verify the association between miR­210­3p and E2F transcription factor 3 (E2F3). Drug sensitivity was evaluated by treating the cells with cisplatin. The expression level of miR­210­3p was lower in SKOV­3/DDP cells than in SKOV­3 cells. Compared with the untransfected control, SKOV­3 cells transfected with miR­210­3p exhibited a significantly higher survival rate. The overexpression of miR­210­3p inhibited SKOV­3/DDP cell proliferation, migration and invasion, and promoted cell apoptosis. By contrast, the inhibition of miR­210­3p promoted cell migration and invasion. The luciferase reporter assay confirmed that E2F3 was a direct target gene of miR­210­3p. Cisplatin treatment resulted in a sharp decrease in the survival rate of SKOV­3/DDP cells transfected with the miR­210­3p mimics. The decrease in cell survival rate caused by the overexpression of miR­210­3p was rescued by the overexpression of E2F3 in SKOV­3/DDP cells. Taken together, these results suggest that miR­210­3p may act as a tumor suppressor in ovarian cancer cells and affect the sensitivity of cells to cisplatin by directly targeting E2F3. This indicates its potential use as a therapeutic target for improving drug resistance in ovarian cancer.

Antiapoptotic role of the cellular repressor of E1A-stimulated genes (CREG) in retinal photoreceptor cells in a rat model of light-induced retinal injury.

OBJECTIVE: Light injury-induced apoptosis of retinal photoreceptor cells can lead to vision loss. The mechanism underlying such injury remains unclear, and there are no effective therapies at present. The aim of this study was to examine the potential antiapoptotic role of the cellular repressor of E1A-stimulated genes (CREG) in retinal cells in a rat model of light-induced retinal damage. METHODS: CREG proteins were injected into the vitreous space of rats in which light retinal injury was induced. An equal volume of PBS was injected into the vitreous space of a control group. Retinas were collected for H&E staining and Western blotting analysis 1, 3, and 7 days later. Inhibitors or agonist for P38, JNK, and AKT were injected into the vitreous space to verify CREG function. RESULTS: In rats with light-induced retinal injury, the CREG treatment inhibited the expression of apoptosis-related proteins caspase-3, caspase-8, and caspase-9 and signaling proteins phosphorylated ERK (P-ERK), phosphorylated JNK (P-JNK), phosphorylated P38 (P-P38), and phosphorylated AKT (P-AKT). An inhibitor of PI3K-AKT and an agonists of P38 and JNK abrogated the inhibitory effect of CREG on caspase-3 expression. CONCLUSION: CREG protected retinal cells against apoptosis by inhibiting P38/MAPK and JNK/MAPK signaling pathways and activating the PI3K-AKT signaling pathway.

[Application of image guided technique in rhino-orbital related endoscopic surgery].

Objective:To review retrospectively six cases of rhino-orbital related endoscopic surgeries aided by Fusion electromagnetic system,to explore the indications and clinical value of image guided technique in endonasal endoscopic surgery.Method:Retrospective research methods were used.In this study,six cases of nasal endoscopic sinus surgery using Fusion electromagnetic system were analyzed,including 1 nasal penetrating foreign body,2 optic nerve decompressions,1 orbital apex hemangioma,1 sieve frontal sinus cyst,1 intraorbital mass biopsy.The preparation time of navigation system,the accuracy of intraoperative positioning and surgical coherence,intraoperative and postoperative complications of surgery were recorded.Result:The average preparation time was(8.13 ± 1.858)min.In the navigation,the sinus ostium,orbital cardboard,skull base,optic nerve,internal carotid artery and other important structures can be accurately located in all patients,while registrations had been accurate within 1 mm.Six patients were successfully operated by image guided technique.There was no intracranial or intraorbital complications due to intraoperation error.Conclusion:Image guided technique allows for a truely microinvasive and accurate rhino-orbital related endoscopic surgeries.It requires less preoperative preparation time,has high surgical navigation accuracy,improves the surgical coherence and safety,and reduces the surgical complicationgs.However,as an auxiliary tool,it can not replace the surgeon's anatomical knowledge,surgical training and clinical experience.

Interplay between long noncoding RNA ZEB1-AS1 and miR-101/ZEB1 axis regulates proliferation and migration of colorectal cancer cells.

Long noncoding RNAs (lncRNAs) are dysregulated in many diseases. MicroRNA-101 (miR-101) functions as a tumor suppressor by directly targeting ZEB1 in various cancers. However, the potential mechanism of lncRNA ZEB1-AS1 and miR-101/ZEB1 axis in CRC remains unknown. In this study, we further investigated the potential interplay between miR-101/ZEB1 axis and lncRNA ZEB1-AS1 in colorectal cancer (CRC). Results showed that ZEB1-AS1 was upregulated in CRC tissues and cells. MiR-101 was downregulated in CRC tissues and negatively correlated with ZEB1-AS1 and ZEB1 expression levels in CRC. Functional experiments showed that, consistent with ZEB1-AS1 depletion, miR-101 overexpression and ZEB1 depletion inhibited the proliferation and migration of CRC cells. Overexpression of miR-101 partially abolished the effects of ZEB1-AS1 on the proliferation and migration of these cells. Moreover, combined ZEB1-AS1 depletion and miR-101 overexpression significantly inhibited cell proliferation and migration of the CRC cells. Hence, ZEB1-AS1 functioned as a molecular sponge for miR-101 and relieved the inhibition of ZEB1 caused by miR-101. This study revealed a novel regulatory mechanism between ZEB1-AS1 and miR-101/ZEB1 axis. The interplay between ZEB1-AS1 and miR-101/ZEB1 axis contributed to the proliferation and migration of CRC cells, and targeting this interplay could be a promising strategy for CRC treatment.

microRNA-9 functions as a tumor suppressor in colorectal cancer by targeting CXCR4.

MicroRNAs (miRs) dysregulation has been proven to play a crucial role in the initiation and progression of colorectal cancer (CRC). miR-9 functions as a tumor suppressor in many cancer types, including CRC. However, the precise role of miR-9 and the underlying molecular mechanisms that miR-9 involves in CRC progression remain largely unknown. In this study, it was reported that miR-9 had lower expression in CRC tissue samples than in those matched adjacent non-tumor tissues. Deregulated miR-9 expression was inverse correlated with the TNM stage, lymph node metastasis, and prognosis of CRC patients. Ectopic miR-9 expression suppressed CRC cell proliferation, migration, and invasion. Dual-Luciferase Reporter Assay confirmed that C-X-C Motif Chemokine Receptor 4 (CXCR4) was a direct miR-9 target, and the effects of miR-9 were mimicked through CXCR4 depletion in vitro. CXCR4 rescue experiments further verified that CXCR4 is a functional target of miR-9. Animal xenograft assays also provided evidence that miR-9 functions as a tumor suppressor via targeting CXCR4 in vivo. Mechanistically, miR-9 overexpression or CXCR4 knockdown influenced cell proliferation and epithelial-mesenchymal transition (EMT). Results suggest that miR-9 acts as a tumor suppressor in CRC progression by regulating CXCR4.