Differential Expression of KIF18B in Gastric Cancer and Its Role in Chemotherapy Sensitivity.

Gastric cancer (GC) is a main cause of cancer death in the world, and improving the chemotherapy sensitivity can enhance the chemotherapy efficacy of GC. The study objective is to explore the differential KIF18B expression in GC and its effect on GC chemotherapy sensitivity. The KIF18B expression in GC tissues and adjacent normal tissues was analyzed by real-time quantitative polymerase chain reaction. The relationship between differential KIF18B expression and different clinicopathological features was detected. It was found that KIF18B was highly expressed in GC tissues, and KIF18B expression was differential in patients with different clinicopathological features. The upregulation of KIF18B has a positive correlation with the poor therapeutic effect and high KIF18 was associated with lower 3-year overall survival and disease-free survival. The KIF18B-downregulated NCI-N87 cells were constructed and tested by cell counting kit-8 assay and colony formation. Cell migration and invasion were detected by Transwell assay. The xenograft tumor model was established to observe the effect of KIF18B on the efficacy of chemotherapy. The upregulation of KIF18B reduced the chemotherapy sensitivity of GC cells and enhanced their proliferation, migration, and invasion. Silencing KIF18B inhibited tumor growth and promoted chemotherapy efficacy in vivo. In summary, KIF18B inhibitor may have a potential function for improving the efficacy of chemotherapy in GC.

Identification of novel antioxidant collagen peptides for preventing and treating H2 O2 -induced oxidative stress in HepG2 cells through in vitro and in silico approaches.

BACKGROUND: Nowadays, the prevalence of oxidative stress-related chronic diseases is increasing. The identification of novel antioxidant collagen peptides to counteract oxidative stress for individuals' health has gained significant attention. RESULTS: In this study, collagen peptides with antioxidant activities were separated and identified by ion chromatography, reversed-phase high-performance liquid chromatography and liquid chromatography-tandem mass spectrometry. The identified antioxidant collagen peptides were further screened by molecular docking for Keap1-targeted peptide inhibitors and their theoretical interaction mechanisms were investigated. Four novel antioxidant collagen peptides, GPAGPIGPVG, GPAGPpGPIG, ISGPpGPpGPA and IDGRPGPIGPA, with high binding affinity to Keap1 were selected. Molecular docking results demonstrated that the putative antioxidant mechanism of the four antioxidant collagen peptides contributed to their blockage of Keap1-Nrf2 interactions. The results of antioxidant activity of the four antioxidant collagen peptides proved that IDGRPGPIGPA exerted a high scavenging capacity for DPPH and ABTS free radicals, while GPAGPpGPIG improved the resistance of cells to hydrogen peroxide-induced oxidative damage by promoting the activation of intracellular antioxidant enzymes and the production of reduced glutathione in human hepatoma (HepG2) cells. CONCLUSION: The antioxidant collagen peptides (GPAGPIGPVG, GPAGPpGPIG, ISGPpGPpGPA and IDGRPGPIGPA) will be developed as novel functional food for human health in the near future. © 2023 Society of Chemical Industry.

Exosomes from adipose-derived mesenchymal stem cells improve liver fibrosis by regulating the miR-20a-5p/TGFBR2 axis to affect the p38 MAPK/NF-κB pathway.

OBJECTIVE: Human adipose-derived mesenchymal stem cell exosomes (ADSC-Exos) are active constituents for treating liver fibrosis. This paper attempted to preliminarily explain the functional mechanism of ADSC-Exos in liver fibrosis through the p38 MAPK/NF-κB pathway. METHODS: The cell models of hepatic fibrosis were established by inducing LX-2 cells with TGF-ß1. Mouse models of liver fibrosis were established by treating mice with CCl4. The in vivo and in vitro models of liver fibrosis were treated with ADSC-Exos. ADSCs were identified by flow cytometry/Alizarin red/oil red O/alcian blue staining. ADSC-Exos were identified by transmission electron microscopy, nanoparticle tracking analysis, and Western blot. LX-2 cell proliferation/viability were evaluated by MTT/BrdU assays. Exosomes were tracked in vivo and body weight changes in mice were monitored. Hepatic pathological changes were observed by HE/Masson staining. α-SMA/collagen I levels in liver tissues were assessed by immunohistochemistry. HA/PIIINP concentrations were measured using the magnetic particle chemiluminescence method. Liver function was assessed using an automatic analyzer. miR-20a-5p level was measured by RT-qPCR. The mRNA levels of fibrosis markers were determined by RT-qPCR, and their protein levels and levels of MAPK/NF-κB pathway-related proteins, as well as TGFBR2 protein level were measured by Western blot. The P65 nuclear expression in mouse liver tissues was quantified by immunofluorescence. RESULTS: ADSC-Exos suppressed TGF-ß1-induced LX-2 cell proliferation and fibrosis and reduced mRNA and protein levels of fibrosis markers in vitro. ADSC-Exos ameliorated liver fibrosis by inhibiting the p38 MAPK/NF-κB pathway activation. ADSC-Exos inhibited activation of the p38 MAPK/NF-κB pathway via regulating the miR-20a-5p/TGFBR2 axis. The in vivo experiment asserted that ADSC-Exos were mainly distributed in the liver, and ADSC-Exos relieved liver fibrosis in mice, which was evidenced by alleviating decreased body weight, reducing collagen and enhancing liver function, and repressed the activation of the p38 MAPK/NF-κB pathway via the miR-20a-5p/TGFBR2 axis. CONCLUSION: ADSC-Exos attenuated liver fibrosis by suppressing the activation of the p38 MAPK/NF-κB pathway via the miR-20a-5p/TGFBR2 axis.

Serum basic fibroblast growth factor and interleukin-1ß predict the effect of first-line chemotherapy in patients with advanced gastric cancer.

BACKGROUND: The incidence and mortality rates of gastric cancer in China are the second-highest in the world, and most patients with gastric cancer lose their chance of surgery by the time of their diagnosis. AIM: To explore the predictive potential of serum basic fibroblast growth factor and interleukin-1ß levels for the effect of first-line chemotherapy in patients with advanced gastric cancer. METHODS: From the gastric cancer patients admitted to our hospital from May 2019 to April 2023, 84 patients were selected and randomly and equally assigned to the experimental or control group. The FLOT group received the FLOT chemotherapy regimen (composed of oxaliplatin + calcium folinate + fluorouracil + paclitaxel), while the SOX group received the SOX chemotherapy regimen (composed of oxaliplatin + tiga capsules). The clinical efficacy, tumor marker levels, adverse reactions, and survival rates of the two groups were compared 7 days after the end of the relevant treatments. RESULTS: The target effective rate of the FLOT group was 54.76%, which was much higher than that of the SOX group (33.33%; P < 0.05). After treatment, both the groups demonstrated lower levels of cancer antigen (CEA), carbohydrate antigen 199 (CA199), and peptide tissue antigen (TPS). For several patients before treatment (P < 0.05). Third and fourth grades. In terms of adverse reactions, the level of white blood cells in both the groups was lower. Moreover, the incidence of hand-foot skin reactions in these two study groups was lower (P < 0.05), while those of peripheral neuritis, vomiting, diarrhea, and abnormal liver function were significant (P < 0.05). No statistically significant difference was noted between the two groups (P < 0.05). The 1-year survival rate was higher in the FLOT group (P < 0.05). CONCLUSION: The FLOT regimen was effective in reducing the serum CEA, CA199, and TPS levels as well as in improving the 1-year survival rate of patients with good tolerability, making it worthy of clinical promotion and application.

Radioprotective efficacy of Astilbin in mitigating radiation-induced lung injury through inhibition of p53 acetylation.

Radiation-induced lung injury (RILI) is a common side effect in thoracic tumor patients undergoing radiotherapy. At present, there is no ideal radio-protective agent which is widely used in RILI treatment. Astilbin (AST), a bioactive flavonoid, exhibits various biological effects, including anti-inflammatory, antioxidant, and anti-fibrotic activities, which partly result from reducing oxidative stress and inflammation in various pathogenic conditions. However, the protective efficacy of AST to ameliorate RILI has not been reported. In this study, we employed network pharmacology, RNA sequencing, and experimental evaluation to reveal the effects and pharmacological mechanism of AST to treat RILI in vivo and in vitro. We observed that AST reduced radiation-induced apoptosis, DNA damage, inflammatory reactions, and the reactive oxygen species (ROS) level in human normal lung epithelial cells BEAS-2B. Further study showed that AST treatment significantly ameliorated RILI by reducing the radiation-induced pathology changes and inflammatory reaction of lung tissue in C57BL/6J mice. Mechanistically, the expression of epithelial-mesenchymal transition (EMT) markers and radiation-triggered acetylation of the p53 protein were alleviated by AST treatment. Furthermore, AST alleviated the acetylation of p53 after intervention of Trichostatin A (TSA). Our data indicate that AST can alleviate RILI by inhibiting inflammatory reactions and the EMT process through decreasing the expression of p53 acetylation. In conclusion, our study suggests that AST has great potential to be a new protective and therapeutic compound for RILI.

Comparison of toxic effects of 5 macrofungi against Drosophila melanogaster.

Traditional chemical pesticides pose potential threats to human health, the environment, and food safety, and there is an urgent need to develop botanical pesticides that are easily degradable, renewable, and environmentally compatible. This research serves to detect the lethal impacts of Amanita pantherina(DC.:Fr) Schrmm.(Agaricales, Amanitaceae, Amanita), Amanita virgineoides Bas (Agaricales, Amanitaceae, Amanita), Coprinus comatus (O.F.Müll.) Pers. (Agaricales, Psathyrellaceae, Coprinus), Pycnoporus cinnabarinus(Jacq.:Fr) Karst (Polyporales, Polyporaceae, Polyporus) and Phallus rubicundus (Bosc) Fr. (Phallales, Phallaceae, Phallus) on Drosophila melanogaster(Diptera, Drosophilidae, Drosophila), including their effects on lifespan, fecundity, offspring growth and developmental characteristics, antioxidant enzyme activity, peroxide content, and the gene transcription associated with signaling pathways and lifespan of D. melanogaster. The results demonstrated that they all produced lethal effects on D. melanogaster. Female flies were more sensitive to the addition of macrofungi to their diet and have a shorter survival time than male flies. The toxic activity of A. pantherina-supplemented diet was the strongest, so that the D. melanogaster in this group had no offspring. The macrofungal-supplemented diets were able to significantly reduce the activity of antioxidant enzymes, accumulate peroxidation products, up-regulatd the transcription of genes related to signaling pathways, inhibit the expression of longevity genes, reduce the lifespan and fertility of D. melanogaster. Consequently, we hypothetically suggest that medicinal C. comatus, P. cinnabarinus and P. rubicundus hold the potential to be developed into an environmentally friendly biopesticide for fly killing.

Neurofilament Light Protein Predicts Disease Progression in Idiopathic REM Sleep Behavior Disorder.

BACKGROUND: Idiopathic rapid eye movement sleep behavior disorder (iRBD) is increasingly recognized as a manifestation preceding the α-synucleinopathies like Parkinson's disease (PD). Neurofilament light chain (NfL) have been reported to be higher in synucleinopathies as a sign of neurodegeneration. OBJECTIVE: To evaluate whether plasma NfL is valuable in reflecting cognitive and motor status in iRBD and PD with a premorbid history of RBD (PDRBD), and predicting disease progression in iRBD. METHODS: Thirty-one patients with iRBD, 30 with PDRBD, and 18 healthy controls were included in the cross-sectional and prospective study. Another cohort from the Parkinson's Progression Markers Initiative (PPMI) dataset was enrolled for verification analysis. All patients received evaluations of cognitive, motor, and autonomic function by a battery of clinical tests at baseline and follow-up. Blood NfL was measured by the Quanterix Simoa HD-1. RESULTS: In our cohort, 26 patients with iRBD completed the follow-up evaluations, among whom eight (30.8%) patients displayed phenoconversion. Baseline plasma NfL cutoff value of 22.93 pg/mL performed best in distinguishing the iRBD converters from non-converters (sensitivity: 75.0%, specificity: 83.3%, area under the curve: 0.84). Cognitive and motor function were significantly correlated with NfL levels in PDRBD (correlation coefficients: -0.379, 0.399; respectively). Higher baseline NfL levels in iRBD were significantly associated with higher risks for cognitive, motor, autonomic function progression, and phenoconversion at follow-up (hazard ratios: 1.069, 1.065, 1.170, 1.065; respectively). The findings were supported by the PPMI dataset. CONCLUSION: Plasma NfL is valuable in reflecting disease severity of PDRBD and predicting disease progression and phenoconversion in iRBD.

Effect of different head-high lateral extubation on adverse reactions in the peri-extubation period of pediatric OSAS surgery under general anesthesia.

BACKGROUND: Children with OSAS are prone to various airway complications during tracheal extubation after tonsillectomy and adenoidectomy due to oropharyngeal secretions and oozing blood. However, few studies have examined the effect of position on airway complications after tracheal extubation in children with OSAS. The aim of this study was to investigate the appropriate position for extubation in children with OASA. METHODS: A total of 459 children aged 3-14 years with OSAS who underwent tonsillectomy and adenoidectomy were recruited for this study. All children were treated with the same surgical approach and standard anesthesia methods of induction of anesthesia, tracheal intubation and maintenance of anesthesia. At the end of surgery, the children were delivered to the post anesthesia care unit and randomly divided into three groups: Group A: Head-high 0° in lateral position; Group B: Head-high 15° in lateral position; Group C: Head-high 30° in lateral position. The main outcomes of this study were the pulse oxygen saturation (SpO2) and the Sedation-Agitation Scale (SAS) scores of the children after extubation, the outflow of oral-nasal secretions and the respiratory complications. Secondary outcomes were blood pressure, heart rate, end-respiratory carbon dioxide, respiratory rate, and post-operative awakening time of the children in three groups. RESULTS: Data from a total of 423 children were statistically analyzed, 141 in Group A, 142 in Group B, and 140 in Group C. The main results showed a significant decrease in choking response after extubation in Group B (46.5%) and Group C (40.7%) compared to Group A (60.3%) (P < 0.05). The SAS score for postoperative agitation was higher in Group A (4.6 [Formula: see text] 0.9) than in Group B (4.4 [Formula: see text] 0.7) and Group C (4.3 [Formula: see text] 0.6) (P < 0.05). Also the SpO2 after extubation was higher in Group B (97.2%) and Group C (97.1%) than in Group A (95.8%) (P < 0.05). In contrast, there was no difference in the occurrence of respiratory complication and postoperative agitation in children between Group B and Group C (all P > 0.05). In addition, there was no difference in the amount of oral-nasal secretions among the children in the three groups (all P > 0.05). CONCLUSION: The head-high 15° lateral position and head-high 30° lateral position can reduce the incidence of airway complications and agitation and provide safe and comfortable extubation conditions for children during the peri-extubation period after tonsillectomy and adenoidectomy, which has certain clinical guidance value. TRIAL REGISTRATION: Registration Number: NO.ChiCTR2200055835(20,01,2022) https://www.chictr.org.cn.

Gelatin-based anticancer drug delivery nanosystems: A mini review.

Drug delivery nanosystems (DDnS) is widely developed recently. Gelatin is a high-potential biomaterial originated from natural resources for anticancer DDnS, which can effectively improve the utilization of anticancer drugs and reduce side effects. The hydrophilic, amphoteric behavior and sol-gel transition of gelatin can be used to fulfill various requirements of anticancer DDnS. Additionally, the high number of multifunctional groups on the surface of gelatin provides the possibility of crosslinking and further modifications. In this review, we focus on the properties of gelatin and briefly elaborate the correlation between the properties and anticancer DDnS. Furthermore, we discuss the applications of gelatin-based DDnS in various cancer treatments. Overall, we have summarized the excellent properties of gelatin and correlated with DDnS to provide a manual for the design of gelatin-based materials for DDnS.

RAC3 Inhibition Induces Autophagy to Impair Metastasis in Bladder Cancer Cells via the PI3K/AKT/mTOR Pathway.

Background: Bladder cancer (BCa) is one of the most frequent malignant tumors globally, with a significant morbidity and mortality rate. Gene expression dysregulation has been proven to play a critical role in tumorigenesis. Ras-related C3 botulinum toxin substrate3 (RAC3), which is overexpressed in several malignancies and promotes tumor progression, has been identified as an oncogene. However, RAC3 has important but not fully understood biological functions in cancer. Our research aims to reveal the new functions and potential mechanisms of RAC3 involved in BCa progression. Methods: We explored the expression level of RAC3 and its relationship with prognosis by publicly accessible BCa datasets, while the correlation of RAC3 expression with clinicopathological variables of patients was analyzed. In vitro and in vivo proliferation, migration, autophagy, and other phenotypic changes were examined by constructing knockdown(KD)/overexpression(OE) RAC3 cells and their association with PI3K/AKT/mTOR pathway was explored by adding autophagy-related compounds. Results: Compared with non-tumor samples, RAC3 was highly expressed in BCa and negatively correlated with prognosis. KD/OE RAC3 inhibited/promoted the proliferation and migration of BCa cells. Knockdown RAC3 caused cell cycle arrest and decreased adhesion without affecting apoptosis. Inhibition of RAC3 activates PI3K/AKT/mTOR mediated autophagy and inhibits proliferation and migration of BCa cells in vivo and in vitro. Autophagy inhibitor 3MA can partially rescue the metastasis and proliferation inhibition effect caused by RAC3 inhibition. Inhibit/activate mTOR enhanced/impaired autophagy, resulting in shRAC3-mediated migration defect exacerbated/rescued. Conclusion: RAC3 is highly expressed in BCa. It is associated with advanced clinicopathological variables and poor prognosis. Knockdown RAC3 exerts an antitumor effect by enhancing PI3K/AKT/mTOR mediated autophagy. Targeting RAC3 and autophagy simultaneously is a potential therapeutic strategy for inhibiting BCa progression and prolonging survival.

Loss of EMP1 promotes the metastasis of human bladder cancer cells by promoting migration and conferring resistance to ferroptosis through activation of PPAR gamma signaling.

Metastasis, in which cancer cells detach from the original site and colonise other organs, is the primary cause of death induced by bladder cancer (BCa). Epithelial Membrane Protein 1 (EMP1) is dysregulated in many human cancers, and its clinical significance and biological function in diseases, including BCa, are largely unclear. Here, we demonstrated that EMP1 was downregulated in BCa cells. The deficiency of EMP1 promotes migration and confers resistance to ferroptosis/oxidative stress in BCa cells, favouring tumour cell metastasis. Mechanistically, we demonstrated that EMP1 deficiency enhanced tumour metastasis by increasing PPARG expression and promoting its activation, leading to upregulation of pFAK(Y397) and SLC7A11, which promoted cell migration and anti-ferroptotic cell death respectively. Moreover, we found EMP1-deficient sensitized cells to PPARG's ligand, which effect are metastatic phenotype promoted and could be mitigated by FABP4 knockdown. In conclusion, our study, for the first time, reveals that EMP1 deficiency promotes BCa cell migration and confers resistance to ferroptosis/oxidative stress, thus promoting metastasis of BCa via PPARG. These results revealed a novel role of EMP1-mediated PPARG in bladder cancer metastasis.

Predicting Nomogram for Severe Oral Mucositis in Patients with Nasopharyngeal Carcinoma during Intensity-Modulated Radiation Therapy: A Retrospective Cohort Study.

BACKGROUND: Oral mucositis is an acute adverse reaction with high incidence during radiotherapy. Severe oral mucositis can seriously affect patients' quality of life and compliance with radiotherapy. The aim of this study was to identify the risk factors for severe oral mucositis and to develop a nomogram for predicting severe oral mucositis in patients with nasopharyngeal carcinoma. METHODS: One hundred and ninety patients with nasopharyngeal carcinoma were retrospectively screened in this study. Least absolute shrinkage and selection operator regression and multivariate logistic regression analyses were performed to identify the best predictors of severe oral mucositis. A nomogram was constructed based on the factors. Finally, the discriminative ability of the nomogram was evaluated. RESULTS: Four independent factors predicting severe oral mucositis were identified: age, N stage, the cycle of induction chemotherapy, and dose-volumetric parameter V40 (%) of oral cavity. The area under the receiver of operating characteristic curve of the nomogram was 0.759 (95% confidence interval: 0.691-0.827). CONCLUSIONS: A predictive nomogram for severe oral mucositis was established and validated in this study. The nomogram provides a reliable and practical model for clinically predicting the probability of severe oral mucositis in patients with nasopharyngeal carcinoma before intensity-modulated radiation therapy.

Attenuated expression of SNF5 facilitates progression of bladder cancer via STAT3 activation.

BACKGROUND: SWI/SNF, a well-known ATP-dependent chromatin-remodeling complex, plays an essential role in several biological processes. SNF5, the core subunit of the SWI/SNF remodeling complex, inactivated in 95% of malignant rhabdoid tumors (MRT), highlighting its significance in tumorigenesis. However, the role of SNF5 in bladder cancer (BC) remains unknown. In this study, we aimed to investigate the function and potential clinical applicability of SNF5 in BC. METHODS: Data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO) and Cancer Cell Line Encyclopedia (CCLE) databases were used to evaluate the clinical significance of SNF5 in BC. We performed Gene Set Enrichment Analysis (GSEA) and functional assays to investigate the role of SNF5 in BC. Genomics of Drug Sensitivity in Cancer (GDSC) and drug-susceptibility tests were performed to identify the potential value of SNF5 in the treatment of BC. RESULTS: Low SNF5 expression conferred a poor prognosis and was significantly associated with the N-stage in BC. ROC curves indicated that SNF5 could distinguish BC from the normal tissues. In vitro and in vivo functional assays demonstrated that attenuated SNF5 expression could promote cell proliferation and enhance migration by STAT3 activation. We imputed that low SNF5 expression could confer greater resistance against conventional first-line drugs, including cisplatin and gemcitabine in BC. GDSC and drug-resistance assays suggested that low SNF5 expression renders T24 and 5637 cells high sensitivity to EGFR inhibitor gefitinib, and combination of EZH2 inhibitor GSK126 and cisplatin. CONCLUSIONS: To the best of our knowledge, the present study, for the first time, showed that low SNF5 expression could promote cell proliferation and migration by activating STAT3 and confer poor prognosis in BC. Importantly, SNF5 expression may be a promising candidate for identifying BC patients who could benefit from EGFR-targeted chemotherapy or cisplatin in combination with EZH2 inhibitor treatment regimens.

Effect of Deliberate Hypotension on Regional Cerebral Oxygen Saturation During Functional Endoscopic Sinus Surgery: A Randomized Controlled Trial.

Background: Deliberate hypotension can reduce bleeding and improve visualization of the surgical field during functional endoscopic sinus surgery (FESS). However, hypotension may cause brain hypoperfusion and subsequent ischemic injuries, such as delayed awakening, stroke, postoperative delirium, and postoperative cognitive dysfunction. Near-infrared spectroscopy (NIRS) can be used to monitor real-time regional cerebral oxygen saturation (rSO2) levels to estimate brain perfusion. The present study aimed to evaluate the change in rSO2 induced by deliberate hypotension during FESS, and assess the impact of deliberate hypotension on the surgical process. Material and Methods: A randomized controlled trial was registered with the Chinese clinical trial registry (ChiCTR2000039846). A total of 40 patients were enrolled and randomly divided into the control and intervention groups, and finally, 39 patients were analyzed. Deliberate hypotension was induced in the intervention group using nicardipine and esmolol, whereas the control group received general anesthesia without deliberate hypotension. We recorded mean arterial pressure (MAP), saturation of pulse oximetry (SpO2), rSO2, and heart rate (HR) before induction of anesthesia (T0), immediately after induction of anesthesia (T1), at the beginning of the operation (corresponding with the establishment of deliberate hypotension) (T2), 10 min (T3) and 20 min (T4) after the operation began, at the end of the operation (corresponding with the end of deliberate hypotension) (T5), and 5 min (T6) and 15 min (T7) after the operation. The partial pressure of end-tidal carbon dioxide (PetCO2) was recorded at T1, T2, T3, T4, T5, and T6. The duration of surgery, intraoperative blood loss, tracheal extubation time, and the number of patients that experienced cerebral desaturation events (CDEs) were recorded. The surgical field was estimated postoperation based on the Fromme score. Results: A 30% decrease from the baseline MAP resulted in a decrease of intraoperative bleeding, improvement in the quality of the surgical field, and the shortening of the duration of surgery during FESS in the intervention group compared with the control group. In addition, rSO2 was reduced and no CDEs were experienced in the intervention group. Linear regression analysis demonstrated a correlation between the decline in rSO2 and that in MAP. Conclusions: A decrease in MAP to a certain level will cause a decrease of rSO2 in patients undergoing FESS under general anesthesia. Based on our findings, we recommend that the deliberate hypotensive target indicated by MAP be reduced by 30%, while PetCO2 is maintained at 35-40 mmHg and HR is maintained at about 60 beats per minute during FESS.

Establishment of a risk assessment system for peptic ulcer recurrence and its value in individualized intervention.

OBJECTIVE: To investigate the establishment of a risk assessment system for peptic ulcer (PU) recurrence and implement an individualized intervention for PU patients with a moderate to high recurrence risk to reduce the recurrence of PU in patients with a moderate to high recurrence risk. METHODS: The factors for PU recurrence were collected through consulting the literature, and a risk prediction model for PU recurrence was established using the univariate binary and multivariate multinomial Logistic stepwise regression analysis. According to the model, a total of 235 PU patients were divided into patients with high, moderate and low recurrence risks. A total of 71 PU patients with moderate to high recurrence risks were selected as the study subjects, and further divided into the control group (n=35) and the experimental group (n=36). The control group was not treated with intervention, while the experimental group was treated with individualized intervention. The PU recurrence, adverse emotions and changes of pain degree were assessed in the two groups at 3, 6, 9 and 12 months after intervention. RESULTS: The univariate and multivariate Logistic regression analysis showed that drinking alcohol, smoking, chronic diseases, oral NSAIDS and depression were associated with the recurrence of PU. Individualized intervention improved the recurrence rate, anxiety, depression, pain degree and quality of life of patients with moderate to high PU recurrence risk. CONCLUSION: Drinking alcohol, smoking, chronic diseases, oral NSAIDS and depression were associated with the recurrence of PU. Individualized intervention can improve the quality of prognosis and the recurrence risk of PU in patients, which has positive clinical significance.

Assessing brain iron and volume of subcortical nuclei in idiopathic rapid eye movement sleep behavior disorder.

STUDY OBJECTIVES: The relationship of iron with cognitive and motor impairment in idiopathic rapid eye movement sleep behavior disorder (iRBD) remains unknown. METHODS: Twenty-nine (29) patients and 28 healthy controls (HCs) underwent susceptibility weighted imaging and susceptibility mapping. These images were used to evaluate the nigrosome-1 (N1) sign in the substantia nigra (SN), global and regional high-iron (RII) content, and volume of subcortical nuclei. RESULTS: The number of iRBD patients with N1 loss (12) was significantly higher than HCs (2) (p = 0.005). Compared with HCs, the iRBD patients had reduced volume of the right caudate nucleus (RCN) (p < 0.05, false discovery rate [FDR] correction) but no significant changes in global and RII iron of the subcortical nuclei (all p > 0.05, FDR correction). Multiple regression analysis revealed that: for cognitive function, the RII iron of the RCN was significantly correlated with visuospatial function and the global iron of the right dentate nucleus (RDN) was correlated with memory function; for motor function, the RII iron of the left DN (LDN) and global iron of the left CN correlated with the Alternate-Tap test (left, average), the global iron of the LDN correlated with the Alternate-Tap test (right), and the global iron of the left GP correlated with the 3-m Timed Up and Go test (all p < 0.05, FDR correction). CONCLUSIONS: Our exploratory analysis found that iRBD patients had a higher incidence of N1 loss and reduced RCN volume after FDR correction. Cognitive and motor impairment were associated with iron deposition in several cerebral nuclei after FDR correction.

Small Proline-Rich Protein 2B Facilitates Gastric Adenocarcinoma Proliferation via MDM2-p53/p21 Signaling Pathway.

BACKGROUND: The small proline-rich protein 2B (SPRR2B) was firstly reported as a member of the cross-linked envelope protein in keratinocytes. The effect of SPRR2B in gastric adenocarcinoma (GC) remains unclear. This study initially explored the clinical significance of SPRR2B in GC patients as well as its role in tumor progression. METHODS: Immunohistochemistry was performed to characterize the expression of SPRR2B in GC tissues and adjacent tissues. The relationship between SPRR2B expression and clinicopathological features of GC patients was analyzed by Chi-square test. Kaplan-Meier method and Cox regression analyses were utilized to identify the prognostic factors of GC. Overexpression and knockdown assays were conducted to investigate possible signaling pathways downstream of SPRR2B. Flow cytometry assays were performed to evaluate cell cycle and apoptosis. Xenograft experiments were performed to validate tumor-related role of SPRR2B in vivo. RESULTS: Both mRNA and protein levels of SPRR2B in cancerous tissue were significantly higher than those in non-cancerous tissues. Meanwhile, SPRR2B expression was significantly associated with tumor size and tumor stage. Survival analysis revealed SPRR2B as one of the independent prognosis factors for overall survival of GC patients. Cellular and xenografts data implicated that silencing SPRR2B blocked the cell cycle of GC cells perhaps through MDM2-p53/p21-CDK1 pathway, while overexpressing SPRR2B exhibited opposite effects. CONCLUSION: Our data suggest that SPRR2B may serve as a novel prognostic marker in GC, which functions at least partially by MDM2-p53/p21-CDK1 signaling pathway.

Analysis of mRNA expression differences in bladder cancer metastasis based on TCGA datasets.

OBJECTIVE: To investigate the metastatic mechanism of muscle invasive bladder cancer (MIBC), which accounts for approximately 30% of all bladder cancer cases, and is a considerable medical problem with high metastatic and mortality rates. METHODS: The mRNA levels of patients with metastatic MIBC and nonmetastatic MIBC from The Cancer Genome Atlas dataset were compared. An integrated bioinformatics analysis was performed of the differentially expressed genes (DEGs), and analyses of Gene Ontology, Kyoto Encyclopaedia of Genes and Genomes pathway, protein-protein interaction, and survival were performed to investigate differences between metastatic and nonmetastatic MIBC. RESULTS: Data from 264 patients were included (131 with, and 133 without, metastasis). A total of 385 significantly DEGs were identified, including 209 upregulated genes and 176 downregulated genes. Based on results using the STRING database and the MCODE plugin of Cytoscape software, two clusters were obtained. Moreover, two genes were identified that may be valuable for prognostic analysis: Keratin 38, type I (KRT38) and Histone cluster 1, H3f (HIST1H3F). CONCLUSION: The KRT38 and HIST1H3F genes may be important in metastasis of MIBC.

Antioxidant cuttlefish collagen hydrolysate against ethyl carbamate-induced oxidative damage.

Ethyl carbamate (EC) has been associated with the generation of reactive oxygen species (ROS) and depletion of glutathione (GSH), leading to a decline in cell viability. In this study, we found that the cuttlefish collagen hydrolysate (CCH) exhibited high antioxidant activity in scavenging hydroxyl radicals (IC50 = 0.697 mg mL-1), which was also effective in combating EC-induced oxidative damage in liver hepatocellular carcinoma HepG2 cells. The expression of genes related to oxidative stress response could be regulated by CCH to mitigate EC-induced oxidative stress. Pathway analysis confirmed that the protective ability of CCH could be related to ferroptosis and glutathione metabolism. Therefore, CCH could reduce the decline in cell viability by alleviating GSH depletion, and prevent EC-induced oxidative damage. Moreover, protective effect of CCH could be realized by upregulating the heme oxygenase-1 to achieve the preventation of cell sensitization. Considering these effects, CCH has potential for use in food to prevent oxidative stress.