Lanthanum chloride exerts therapeutic potential for chronic kidney disease by suppressing nanohydroxyapatite-induced mitophagy and mitochondria-mediated apoptosis.

OBJECTIVE: To investigate the protective effect of lanthanum chloride on kidney injury in chronic kidney disease and its mechanism. METHODS: 1. Patients with CKD stage 2-5 were selected to analyze the effect of lanthanum-containing preparations on CKD. 2. Sixty healthy male Wistar rats were randomly divided into control group, model group, lanthanum chloride groups (0.03 ng/kg, 0.1 ng/kg, 0.3 ng/kg, q.3d., i.v.), and lanthanum carbonate group (0.3 g/kg, q.d., p.o.). The model group was given 2 % adenine suspension (200 mg/kg, q.d., p.o.) for the first two weeks, followed by adenine (200 mg/kg, b.i.d., p.o.) for 2 weeks, and all animals were sacrificed after eight weeks of administration. 3. The serum and kidneys of rats in each group were collected to detect the oxidative stress indicators and the expressions of LC3B-Ⅱ/Ⅰ, p62, Bcl-2, Bax, Caspase-3 and Cleaved Caspase-3. 4. Human renal tubular epithelial cells (HK-2 cells) were divided into control group, model group, lanthanum chloride group, pyrophosphate (PPI) group, chloroquine (CQ) group, rapamycin group, doxorubicin (DOX) group and N-acetyl-L-cysteine (NAC) group. The mitochondrial status, mitophagy and apoptosis levels were detected. RESULTS: 1.Lanthanum-containing preparations can significantly reduce the biochemical indexes of kidney injury in patients with CKD. 2. In the model group, the glomerular and renal tubular edema, the mitochondria were short and round, and the expression of LC3B-Ⅱ/Ⅰ and Bax increased, while the expression of P62, Bcl-2 and Caspase-3 decreased, and there was a significant improvement in the administration group, especially the 0.1 ng/kg group and lanthanum carbonate group. 3. In the HK-2 cell model group, mitochondrial membrane potential decreased, morphology changed and the results were reversed by lanthanum chloride. CONCLUSION: Lanthanum chloride may alter the morphology of nano-hydroxyapatite, thereby inhibiting its induced mitophagy and mitochondria-mediated apoptosis, and ultimately improve CKD renal injury effectively.

Association between dietary copper, iron, zinc, selenium intake and osteopenia or osteoporosis in elderly hypertensive patients: a retrospective cohort study.

Aim: The study aimed to investigate the link between dietary copper, iron, zinc, selenium intake with osteopenia and osteoporosis in elderly hypertensive patients. Methods: The data of hypertensive patients were extracted from the National Health and Nutrition Examination Survey 2005-2010, 2013-2014, and 2017-2018. Data of dietary iron, zinc, copper and selenium intakes were obtained according to 24-h diet recall interviews. Osteopenia and osteoporosis were determined based on the bone mineral density. Weighted liner regression and weighted logistic regression were employed to assess the association between iron, zinc, copper, and selenium intakes with osteopenia and osteoporosis. All results were presented as ß, odds ratios (ORs), and 95% confidence intervals (CIs). Results: In total, 5,286 elderly hypertensive patients were included. Among them, 2,961 (56.02%) patients have osteopenia, and 566 (10.71%) have osteoporosis. After adjusting all covariates, dietary copper intake ≥the recommended daily allowance was positively correlated with bone mineral density on total femur (ß = 0.086, 95% CI: 0.021-0.152) and femoral neck (ß = 0.097, 95% CI: 0.016-0.178). Dietary zinc intake ≥the recommended daily allowance was also positively correlated with bone mineral density on total femur (ß = 0.092, 95% CI: 0.030-0.153) and femoral neck (ß = 0.122, 95% CI: 0.050-0.193). Dietary copper (O = 0.581, 95% CI: 0.394-0.858) and zinc (OR = 0.595, 95% CI: 0.429-0.827) intake ≥the recommended daily allowance levels were related to increased odds of osteoporosis in elderly with hypertension. Conclusion: Higher dietary copper and zinc intake was associated with lower odds of osteoporosis in the elderly hypertensive patients. Higher dietary intake included copper and zinc may be beneficial for the bone health in the elderly hypertensive patients.

SERS detection platform based on a nucleic acid aptamer-functionalized Au nano-dodecahedron array for efficient simultaneous testing of colorectal cancer-associated microRNAs.

A surface-enhanced Raman scattering (SERS) detection platform was constructed based on Au nano-dodecahedrons (AuNDs) functionalized with nucleic acid aptamer-specific binding and self-assembly techniques. SERS labels were prepared by modifying Raman signaling molecules and complementary aptamer chains and were bound on the aptamer-functionalized AuNDs array. Using this protocol, the limits of detection (LODs) of miR-21 and miR-18a in the serum were 6.8 pM and 7.6 pM, respectively, and the detection time was 5 min. Additionally, miR-21 and miR-18a were detected in the serum of a mouse model of colorectal cancer. The results of this protocol were consistent with quantitative real-time polymerase chain reaction (qRT-PCR). This method provides an efficient and rapid method for the simultaneous testing of miRNAs, which has great potential clinical value for the early detection of colorectal cancer (CRC).

Three new phenols and one new lignan from Clematis terniflora var. manshurica (Rupr.) Ohwi with their anti-inflammatory activity.

Three undescribed phenols, mandshusica C-E (1-3) and a new lignan, mandshusica F (5), along with six known compounds (4, 6-10) were isolated from the roots and rhizomes of Clematis terniflora var. manshurica (Rupr.) Ohwi. Their structures were elucidated by extensive spectroscopic analysis as well as NMR and ECD calculations. Moreover, the possible biosynthetic pathways of compounds 1-3 were also discussed. All compounds were evaluated for their anti-inflammatory activities in LPS-induced RAW 264.7 cells. Compounds 1, 3, 4 significantly reduced the levels of NO and TNF-α, while compounds 2 and 8 significantly inhibited NO production in LPS-induced RAW264.7 cells.

mir-150-5p inhibits the osteogenic differentiation of bone marrow-derived mesenchymal stem cells by targeting irisin to regulate the p38/MAPK signaling pathway.

PURPOSE: To study the effect of miR-150-5p on the osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs), and further explore the relationship between its regulatory mechanism and irisin. METHODS: We isolated mouse BMSCs, and induced osteogenic differentiation by osteogenic induction medium. Using qPCR to detect the expression of osteogenic differentiation-related genes, western blot to detect the expression of osteogenic differentiation-related proteins, and luciferase reporter system to verify that FNDC5 is the target of miR-150-5p. Irisin intraperitoneal injection to treat osteoporosis in mice constructed by subcutaneous injection of dexamethasone. RESULTS: Up-regulation of miR-150-5p inhibited the proliferation of BMSCs, and decreased the content of osteocalcin, ALP activity, calcium deposition, the expression of osteogenic differentiation genes (Runx2, OSX, OCN, OPN, ALP and BMP2) and protein (BMP2, OCN, and Runx2). And down-regulation of miR-150-5p plays the opposite role of up-regulation of miR-150-5p on osteogenic differentiation of BMSCs. Results of luciferase reporter gene assay showed that FNDC5 gene was the target gene of miR-150-5p, and miR-150-5p inhibited the expression of FNDC5 in mouse BMSCs. The expression of osteogenic differentiation genes and protein, the content of osteocalcin, ALP activity and calcium deposition in BMSCs co-overexpressed by miR-150-5p and FNDC5 was significantly higher than that of miR-150-5p overexpressed alone. In addition, the overexpression of FNDC5 reversed the blocked of p38/MAPK pathway by the overexpression of miR-150-5p in BMSCs. Irisin, a protein encoded by FNDC5 gene, improved symptoms in osteoporosis mice through intraperitoneal injection, while the inhibitor of p38/MAPK pathway weakened this function of irisin. CONCLUSION: miR-150-5p inhibits the osteogenic differentiation of BMSCs by targeting irisin to regulate the/p38/MAPK signaling pathway, and miR-150-5p/irisin/p38 pathway is a potential target for treating osteoporosis.

[Safe Utilization Effect of Passivator on Mild to Moderate Cadmium Contaminated Farmland].

In order to study the safe utilization of acid cadmium （Cd） contaminated soil， light and moderate Cd-contaminated farmland in Shangluo， Shaanxi Province was taken as the research object， and lime， biochar， and calcium magnesium phosphate fertilizer were applied. Through the wheat-maize rotation experiment， the safe utilization effect of different amounts of passivator on Cd-contaminated soil was explored， and the best ratio of passivator was selected. The results showed that： ① the soil quality could be improved to varying degrees by applying the passivator. ② After the application of amendments， the grain yield of wheat and maize increased to different degrees. ③ The lime 2 340 kg·hm-2 （C3） treatment had the best effect， which increased the soil pH of wheat and corn by 1.453 and 1.717 units， respectively， and reduced the available Cd content by 34.38% and 30.20%， respectively. ④ The application of biochar 1 800 kg·hm-2 （B2） treatment had the best effect on reducing the Cd contents in wheat roots， straws， and grains， which were significantly reduced by 53.60%， 38.86%， and 52.96%， respectively， compared with that in CK. The Cd content in wheat grains was reduced to 0.09 mg·kg-1， which was lower than the limit value of wheat Cd （0.1 mg·kg-1） specified in the "National food safety standard food pollutant limit" （GB 2762-2017）. The application of the biochar 1 260 kg·hm-2 （B1） treatment had the best comprehensive effect on reducing the Cd contents of maize roots， straws， and grains， which were significantly reduced by 43.74%， 53.20%， and 94.57%， respectively， compared with that in CK. The Cd content of maize grains was reduced to 0.001 9 mg·kg-1， which was far lower than the limit value of maize Cd （0.1 mg·kg-1） specified in the "National food safety standard food pollutant limit" （GB 2762-2017）. Therefore， under the conditions of the field experiment， considering the influence of various indexes， biochar had the best effect on farmland soil in the wheat-maize rotation area with mild to moderate Cd pollution.

Revolutionizing breast cancer treatment: Harnessing the related mechanisms and drugs for regulated cell death (Review).

Breast cancer arises from the malignant transformation of mammary epithelial cells under the influence of various carcinogenic factors, leading to a gradual increase in its prevalence. This disease has become the leading cause of mortality among female malignancies, posing a significant threat to the health of women. The timely identification of breast cancer remains challenging, often resulting in diagnosis at the advanced stages of the disease. Conventional therapeutic approaches, such as surgical excision, chemotherapy and radiotherapy, exhibit limited efficacy in controlling the progression and metastasis of the disease. Regulated cell death (RCD), a process essential for physiological tissue cell renewal, occurs within the body independently of external influences. In the context of cancer, research on RCD primarily focuses on cuproptosis, ferroptosis and pyroptosis. Mounting evidence suggests a marked association between these specific forms of RCD, and the onset and progression of breast cancer. For example, a cuproptosis vector can effectively bind copper ions to induce cuproptosis in breast cancer cells, thereby hindering their proliferation. Additionally, the expression of ferroptosis­related genes can enhance the sensitivity of breast cancer cells to chemotherapy. Likewise, pyroptosis­related proteins not only participate in pyroptosis, but also regulate the tumor microenvironment, ultimately leading to the death of breast cancer cells. The present review discusses the unique regulatory mechanisms of cuproptosis, ferroptosis and pyroptosis in breast cancer, and the mechanisms through which they are affected by conventional cancer drugs. Furthermore, it provides a comprehensive overview of the significance of these forms of RCD in modulating the efficacy of chemotherapy and highlights their shared characteristics. This knowledge may provide novel avenues for both clinical interventions and fundamental research in the context of breast cancer.

[Research progress on development and utilization of minor ginsenosides].

Minor ginsenosides are a class of processed saponins with minor natural content, high bioavailability, and outstanding bio-logical activity, which are usually obtained by biological or chemical transformation of prototype saponins directly extracted from Panax plants. In recent years, with the clarification of the biosynthetic pathway of saponins and the development of synthetic biology, it has become possible to use synthetic metabolic engineering methods with microorganisms as hosts to produce saponins. Minor ginsenosides have received widespread attention because of their remarkable biological activities in enhancing the immune function of the body and antitumor property. At present, most of the reviews on minor ginsenosides focus on transformation preparation, process optimization, and pharmacological activity, but there are some deficiencies in industrial analysis. This study summarized structural types, pharmacological activities, sources of acquisition, and transformation pathways of minor ginsenosides based on the relevant literature in China and abroad, proposed problems in the preparation of existing minor ginsenosides, and discussed the future research and utilization prospects, to provide a theoretical basis for improving the basic research of minor ginsenosides and promoting their industrialization.

Overexpression of MTFR1 promotes cancer progression and drug-resistance on cisplatin and is related to the immune microenvironment in lung adenocarcinoma.

OBJECTIVE: The roles of MTFR1 in the drug resistance of lung adenocarcinoma (LAC) to cisplatin remain unexplored. In this study, the expression, clinical values and mechanisms of MTFR1 were explored, and the relationship between MTFR1 expression and immune microenvironment was investigated in LAC using bioinformatics analysis, cell experiments, and meta-analysis. METHODS: MTFR1 expression and clinical values, and the relationship between MTFR1 expression and immunity were explored, through bioinformatics analysis. The effects of MTFR1 on the growth, migration and cisplatin sensitivity of LAC cells were identified using cell counting kit-8, wound healing and Transwell experiments. Additionally, the mechanisms of drug resistance of LAC cells involving MTFR1 were investigated using western blotting. RESULTS: MTFR1 was elevated in LAC tissues. MTFR1 overexpression was associated with sex, age, primary therapy outcome, smoking, T stage, unfavourable prognosis and diagnostic value and considered an independent risk factor for an unfavourable prognosis in patients with LAC. MTFR1 co-expressed genes involved in the cell cycle, oocyte meiosis, DNA replication and others. Moreover, interfering with MTFR1 expression inhibited the proliferation, migration and invasion of A549 and A549/DDP cells and promoted cell sensitivity to cisplatin, which was related to the inhibition of p-AKT, p-P38 and p-ERK protein expression. MTFR1 overexpression was associated with stromal, immune and estimate scores along with natural killer cells, pDC, iDC and others in LAC. CONCLUSIONS: MTFR1 overexpression was related to the unfavourable prognosis, diagnostic value and immunity in LAC. MTFR1 also participated in cell growth and migration and promoted the drug resistance of LAC cells to cisplatin via the p-AKT and p-ERK/P38 signalling pathways.

Prenatal diagnosis and treatment for fetal angiotensin converting enzyme deficiency.

OBJECTIVE: To elucidate an etiology in a case with persistent oligohydramnios by prenatal diagnosis and actively treat the case to achieve good prognosis. METHODS: We performed whole exome sequencing (WES) of DNA from the fetus and parents. Serial amnioinfusions were conducted until birth. Pressors were required to maintain normal blood pressure. The infant angiotensin-converting enzyme (ACE) activity, angiotensin II (Ang II, a downstream product of ACE), and compensatory enzymes (CEs) activities were measured. Compensatory enzyme activities in plasma from age-matched healthy controls were also detected. RESULTS: We identified a fetus with a severe ACE mutation prenatally. The infant was born prematurely without pulmonary dysplasia. Hypotension and anuria resolved spontaneously. He had almost no ACE activity, but his Ang II level and CE activity exceeded the upper limit of the normal range and the upper limit of the 95% confidence interval of controls, respectively. His renal function also largely recovered. CONCLUSION: Fetuses with ACE mutations can be diagnosed prenatally through WES. Serial amnioinfusion permits the continuation of pregnancy in fetal ACE deficiency. Compensatory enzymes for defective ACE appeared postnatally. Renal function may be spared by preterm delivery; furthermore, for postnatal vasopressor therapy to begin, improving renal perfusion pressure before nephrogenesis has been completed.

Two-year dermal carcinogenicity bioassay of triclosan in B6C3F1 mice.

Triclosan is a widely used antimicrobial agent in personal care products, household items, medical devices, and clinical settings. Due to its extensive use, there is potential for humans in all age groups to receive lifetime exposures to triclosan, yet data on the chronic dermal toxicity/carcinogenicity of triclosan are still lacking. We evaluated the toxicity/carcinogenicity of triclosan administered dermally to B6C3F1 mice for 104 weeks. Groups of 48 male and 48 female B6C3F1 mice received dermal applications of 0, 1.25, 2.7, 5.8, or 12.5 mg triclosan/kg body weight (bw)/day in 95% ethanol, 7 days/week for 104 weeks. Vehicle control animals received 95% ethanol only; untreated, naïve control mice did not receive any treatment. There were no significant differences in survival among the groups. The highest dose of triclosan significantly decreased the body weight of mice in both sexes, but the decrease was ≤ 9%. Minimal-to-mild epidermal hyperplasia, suppurative inflammation (males only), and ulceration (males only) were observed at the application site in the treated groups, with the highest incidence occurring in the 12.5 mg triclosan/kg bw/day group. No tumors were identified at the application site. Female mice had a positive trend in the incidence of pancreatic islet adenoma. In male mice, there were positive trends in the incidences of hepatocellular carcinoma and hepatocellular adenoma or carcinoma (combined), with the increase of carcinoma being significant in the 5.8 and 12.5 mg/kg/day groups and the increase in hepatocellular adenoma or carcinoma (combined) being significant in the 2.7, 5.8, and 12.5 mg/kg/day groups.

Development and Validation of Nomograms Based on Nutritional Risk Index for Predicting Extracapsular Extension and Seminal Vesicle Invasion in Patients Undergoing Radical Prostatectomy.

Background: The aim of the study was to investigate the predictive value of the nutritional risk index (NRI) for extracapsular extension (ECE) and seminal vesicle invasion (SVI) in prostate cancer (PCa) patients undergoing radical prostatectomy (RP), and further develop and validate predictive nomograms for ECE and SVI based on the NRI. Methods: We retrospectively analyzed 734 PCa patients who underwent RP between 2010 and 2020 in the Department of Urology at Peking University Third Hospital. The enrolled patients were randomly divided into a primary cohort (n = 489) and a validation cohort (n = 245) in a 2:1 manner. The baseline NRI of patients was calculated using serum albumin level and body mass index, and a malnutrition status was defined as NRI ≤ 98. Univariate and multivariate logistic regression analyses were conducted to identify predictors for ECE and SVI. Nomograms for predicting ECE and SVI were established based on the results of the multivariate logistic regression analysis. The performance of the nomograms was estimated using Harrell's concordance index (C-index), the area under curve (AUC) of receiver operating characteristic (ROC) curves and the calibration curves. Results: In the primary cohort, 70 (14.3%) patients with NRI ≤ 98 were classified as malnutrition, while the remaining 419 (85.7%) patients with NRI > 98 were considered to have normal nutrition. The nomograms for predicting ECE and SVI shared common factors including NRI, percentage of positive biopsy cores (PPC) and biopsy Gleason score, while prostate-specific antigen (PSA) levels and PSA density (PSAD) were only incorporated in ECE nomogram. The C-indexes of the nomograms for predicting ECE and SVI were 0.785 (95% confidence interval (CI): 0.745 - 0.826) and 0.852 (95% CI: 0.806 - 0.898), respectively. The calibration curves demonstrated excellent agreement between the predictions by the nomograms and the actual observations. The results remained reproducible when the nomograms were applied to the validation cohort. Conclusions: The NRI is significantly associated with ECE and SVI in PCa patients. The nomogram established based on the NRI in our study can provide individualized risk estimation for ECE and SVI in PCa patients, and may be valuable for clinicians in making well-informed decisions regarding treatment strategies and patient management.

Application of PVC pipes as an adjustable bilateral traction device in lower limb fractures.

OBJECTIVE: To introduce a new type of simple adjustable bilateral bidirectional polyvinyl chloride (PVC) tube traction device and discuss the value of using this device before surgery in patients with lower limb fractures. METHODS: To introduce the manufacturing process of an adjustable bilateral traction device made of PVC pipes. From August 2018 to November 2019, the data of 36 patients with lower limb fractures who were treated with this traction device were retrospectively analysed. The treatment outcomes were analysed, including length of both lower limbs, fracture reduction, lower limb mobility, visual analogue scale (VAS) score, incidence of complications, and patient satisfaction. RESULTS: All patients were able to move the affected limb immediately after using the device. The patient's pain was significantly reduced, they were able to turn over freely during bed rest, and the length of the affected limb was restored to that of the healthy limb. Thirty-four (94.5%) patients were satisfied with the reduction of the fracture end, 2 (5.5%) patients with tibiofibular fractures showed angular displacement of the fractured end and satisfactory reduction after the position of the bone traction needle was adjusted; 7 (19.5%) patients developed deep vein thrombosis of the affected lower limb during traction; there was no decubitus or vascular nerve injury, and the overall complication rate was 25% (9/36). All the patients and their families were satisfied with the results of this treatment. CONCLUSION: The aim of this study is to introduce a new type of traction device. It is advantageous in that it is light weight, low cost, easy to assemble, promotes immediate movement of the affected limb after assembly, improves patient comfort and can be used with a titanium steel needle for MRI examination under traction. In the clinical setting, it has been shown to be suitable for the temporary treatment of patients with lower leg fractures prior to surgery, particularly patients who, for various reasons, require nonsurgical treatment in the short term.

Semiquantitative magnetic resonance imaging parameters for differentiating parotid pleomorphic adenoma from Warthin tumor.

Background: Accurately distinguishing between pleomorphic adenoma (PA) and Warthin tumor (WT) is beneficial for their respective management. Preoperative magnetic resonance imaging (MRI) can provide valuable information due to its excellent soft tissue contrast. This study explored the value of semiquantitative contrast-enhanced MRI parameters in the differential diagnosis of PA and WT. Methods: Data from 106 patients, 62 with PA and 44 with WT (confirmed by histopathology) were retrospectively and consecutively analyzed. The tumor-to-spinal cord contrast ratios (TSc-CR) based on the mean, maximum, and minimum signal intensity (T1-mean TSc-CR, T1-max TSc-CR, and T1-min TSc-CR, respectively) in the early and delayed phases were calculated on contrast-enhanced T1-weighted images as semiquantitative parameters, and then compared between PA and WT. Receiver operating characteristic (ROC) curve analysis and areas under the curve (AUCs) were used to determine the performance of these parameters in the differential diagnosis of PA from WT. Results: Except T1-min TSc-CR in the early phase, all semiquantitative MRI parameters differed significantly between PA and WT (all P<0.05). T1-max TSc-CR showed higher sensitivity {70.45% [95% confidence interval (CI): 0.548-0.832]} and specificity [70.97% (95% CI: 0.581-0.818)] and had a higher AUC [0.707 (95% CI: 0.610-0.791)] in the early phase when using a cutoff value of 1.89. T1-max TSc-CR showed higher sensitivity [88.64% (95% CI: 0.754-0.962)], specificity [72.58% (95% CI: 0.598-0.831)], and AUC [0.854 (95% CI: 0.772-0.915)] in the delayed phase when using a cutoff value of 2.33. The sensitivity, specificity, and AUC were improved to 90.91% (95% CI: 0.783-0.975), 93.55% (95% CI: 0.843-0.982), and 0.960 (95% CI: 0.903-0.988), respectively, after combination of all semiquantitative parameters in the early and delayed phases. The two radiologists had excellent interobserver agreement on TSc-CRs [all interclass correlation coefficient (ICC) >0.75]. Conclusions: Semiquantitative parameters using TSc-CR are valuable in distinguishing PA from WT, and a combination of these parameters can improve the differential diagnostic efficiency.

Sulfasalazine inhibits esophageal cancer cell proliferation by mediating ferroptosis.

This study aimed to explore the potential mechanism by which sulfasalazine (SAS) inhibits esophageal cancer cell proliferation. A cell counting kit-8 (CCK-8) assay was used to detect the effect of SAS (0, 1, 2, and 4 mM) on the proliferation of TE-1 cells. Subsequently, TE-1 cells were divided into control group, SAS group, SAS + ferrostatin-1 (ferroptosis inhibitor) group, and SAS + Z-VAD (OH)-FMK (apoptosis inhibitor) group, and cell proliferation was measured using a CCK-8 assay. Real-time quantitative polymerase chain reaction and western blotting were used to determine the expression of solute carrier family member 7 11 (SLC7A11, also called xCT), glutathione peroxidase 4 (GPX4), and acyl-CoA synthase long-chain family member 4 (ACSL4) in TE-1 cells. Measurement of ferroptosis in TE-1 cells was achieved by flow cytometry. Compared with the control group (0 mM SAS), the proliferation of TE-1 cells was significantly inhibited by different concentrations of SAS for different time lengths, and 4 mM SAS treatment for 48 h could obtain the maximum inhibition rate (53.9%). In addition, SAS treatment caused a significant decrease in the mRNA and protein expression of xCT and GPX4, and a significant increase in ACSL4 expression in TE-1 cells treated with SAS. Flow cytometry results showed that the ferroptosis level was significantly increased after SAS treatment. However, the activation of ferroptosis by SAS was partially eliminated by treatment with ferrostatin-1 or Z-VAD (OH)-FMK. In conclusion, SAS inhibits the proliferation of esophageal carcinoma cells by activating the ferroptosis pathway.

[Immune-Related Pancreatitis Caused by Immune Checkpoint Inhibitor Nivolumab:Report of One Case].

In recent years,great progress has been achieved in the application of immune checkpoint inhibitors (ICI) in tumor immunotherapy.However,a variety of adverse reactions induced by ICI have been reported.Despite the high overall incidence of adverse reactions caused by ICI,some adverse reactions,such as immune-related pancreatitis,are rare in clinical practice.In this paper,a case of immune-related pancreatitis after treatment of advanced gastric cancer with nivolumab was identified.We analyzed the cause,treatment,incidence,and risk factors of the adverse reaction,aiming to improve the clinical diagnosis,treatment,and safe medication of rare adverse reactions associated with ICI.

Decreased APOC1 expression inhibited cancer progression and was associated with better prognosis and immune microenvironment in esophageal cancer.

Several studies have demonstrated the involvement of apolipoprotein C1 (APOC1) in multiple cancers. However, the role of APOC1 in esophageal cancer (ESCA) has not been elucidated. Hence, we examined the expression of APOC1 in ESCA tissues acquired from The Cancer Genome Atlas (TCGA) database and clinical samples from our hospital. An investigation of the association of APOC1 with the clinicopathological characteristics, prognosis, and diagnosis of ESCA was carried out on the basis of survival, receiver operating characteristics, and correlation analyses. Gene ontology, KEGG analysis, and protein-protein interaction network showed that co-expressed APOC1 genes were involved in the functions, mechanisms, and action network. The effects of APOC1 expression on ESCA cells were explored using CCK-8, migration and invasion assays. The relationship between APOC1 expression and ESCA immune-infiltrating cells and cell markers were examined using correlation analysis. We found that APOC1 was overexpressed in TCGA ESCA tissues and the same was validated in clinical ESCA tissues, with the area under the curve for APOC1 being 0.887. Overexpression of APOC1 was associated with short overall survival, disease-specific survival, progression-free interval, T stage, pathological stage, body mass index, and histological grade. Inhibition of APOC1 expression significantly reduced the proliferation, migration, and invasion of ESCA cells. Furthermore, APOC1 expression positively correlated with the ESTIMATE, immune, and stromal scores in ESCA. Overexpression of APOC1 correlated with the tumor purity, B cells, T helper cells, natural killer cells, cytotoxic cells, and other immune cells. Moreover, APOC1 was involved in ESCA progression via T cell receptor, B cell receptor, and other immune signaling pathways. Thus, APOC1 overexpression is expected to be a biomarker for dismal prognosis and diagnosis of ESCA. Inhibition of APOC1 expression significantly reduced the proliferation, migration, and invasion of ESCA cells. Overexpression of APOC1 was associated with the immune microenvironment in ESCA. Thus, APOC1 may be an efficient biomarker for proper prognosis and diagnosis of ESCA.