RESUMEN
This study investigated whether adding Herba Houttuyniae to feed can improve intestinal function and prevent diseases for koi carp (Cyprinus carpio) infected with Aeromonas veronii. There was a total of 168 koi carp with an average body length of (9.43 ± 0.99) cm and an average body weight of (26.00 ± 11.40) g. The K group was the control group fed with basal feed, while the C group was fed with feed with a H. houttuyniae content of six per thousand. After 14 days of feeding, the fish were fasted for a day and then intraperitoneally injected with A. veronii for artificial infection, injection dose is 0.2 mL, and the concentration is 1 × 107 CFU/mL. Samples were collected from the two groups on days 0, 1, 2, and 4. The fold height, intestinal villus width, and muscle layer thickness in the gut of the koi carp were measured. In addition, on day 4, the activities of trypsin, α-amylase, and lipase in the gut were determined, and the intestinal flora of the carp in both groups was tested. The results showed that on the second and fourth days of sampling, the fold height and muscle layer thickness in the C group were significantly higher than those in the K group (P < 0.05). The villus width in the C group was slightly higher than that in the K group, but the difference was not significant (P > 0.05). Microscopic observation revealed that the intestinal structure of the carp in the C4 (day 4 in C group) group was more intact than that in the K4 (day 4 in K group) group. Moreover, the activities of trypsin, α-amylase, and lipase in the foregut and midgut in the C4 group were higher than those in the K4 group (P < 0.05). The activities of trypsin and α-amylase in the hindgut in the C4 group were higher than those in the K4 group (P < 0.05). Furthermore, beneficial bacteria, especially those in the genus Cetobacterium, were more abundant in the intestinal tract of the carp in the C4 group compared to the K group. In addition, comparisons and tests of IL-4 and IL-10 in the intestines of the fish in both groups demonstrated that the H. houttuyniae added to feed enhanced the immune function of the fish intestines after bacterial attack. In conclusion, for koi carp infected with A.veronii, adding H. houttuyniae to their feed not only improves the activity of digestive enzymes and the morphological structure of the intestine but also optimizes the beneficial intestinal microbiota, thereby protecting the intestinal tract.
Asunto(s)
Aeromonas veronii , Alimentación Animal , Carpas , Enfermedades de los Peces , Microbioma Gastrointestinal , Infecciones por Bacterias Gramnegativas , Intestinos , Animales , Carpas/microbiología , Enfermedades de los Peces/microbiología , Enfermedades de los Peces/inmunología , Infecciones por Bacterias Gramnegativas/veterinaria , Infecciones por Bacterias Gramnegativas/microbiología , Microbioma Gastrointestinal/efectos de los fármacos , Intestinos/microbiología , Alimentación Animal/análisis , Houttuynia , Lipasa/metabolismo , Dieta/veterinaria , alfa-Amilasas/metabolismoRESUMEN
Noncoding RNAs have been verified to regulate the infiltration of macrophages to accelerate tumor biological progression, however the regulation of macrophages by circular RNAs in hepatocellular carcinoma (HCC) remains unresolved. Using high-throughput RNA sequencing, we demonstrated that hsa_circ_0003410 was clearly upregulated in HCC. 5-Ethynyl-2'-deoxyuridine and transwell assays showed that hsa_circ_0003410 facilitated the proliferation and migration of HCC cells in vitro. We knocked down the expression of hsa_circ_0003410 in HepG2 cells and performed next-generation sequencing to determine possible target genes of hsa_circ_0003410. Kyoto Encyclopedia of Genes and Genomes analysis revealed that different genes were mainly enriched in immune-related pathways. Mechanistically, we identified CCL5 as the target gene of hsa_circ_0003410. RNA-FISH showed the co-expression of hsa_circ_0003410 and CCL5. Western blot and ELISA also verified that hsa_circ_0003410 could upregulate the expression of CCL5 protein. Flow cytometry and immunofluorescence assays indicated that CCL5 activated and recruited M2 macrophages and increased the ratio of M2/M1 macrophages to promote the progression of HCC. Animal experiments in vitro also confirmed our results. Taken together, our experiments revealed that noncoding RNAs play a critical role in the HCC microenvironment and can be considered as markers for the diagnosis and prognosis of HCC.
Asunto(s)
Carcinoma Hepatocelular/genética , Quimiocina CCL5/genética , Neoplasias Hepáticas/genética , MicroARNs/genética , ARN Circular/genética , Macrófagos Asociados a Tumores/inmunología , Animales , Carcinoma Hepatocelular/inmunología , Carcinoma Hepatocelular/patología , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular/genética , Quimiocina CCL5/inmunología , Regulación Neoplásica de la Expresión Génica , Humanos , Neoplasias Hepáticas/inmunología , Neoplasias Hepáticas/patología , Ratones , Microambiente Tumoral/inmunologíaRESUMEN
The fabrication processes of high-speed oxide-confined single-mode (SM)-vertical-cavity surface-emitting lasers (VCSELs) are complex, costly, and often held back by reliability and yield issues, which substantially set back the high-volume processing and mass commercialization of SM-VCSELs in datacom or other applications. In this article, we report the effects of Al2O3 passivation films deposited by atomic layer deposition (ALD) on the mesa sidewalls of high-speed 850-nm SM-VCSELs. The ALD-deposited film alleviates the trapping of carriers by sidewall defects and is an effective way to improve the performance of SM-VCSELs. The ALD-passivated SM-VCSELs showed statistically significant static performance improvements and reached a believed to be record-breaking SM-modulation bandwidth of 29.1 GHz. We also propose an improved microwave small-signal equivalent circuit model for SM-VCSELs that accounts for the losses attributed to the mesa sidewalls. These findings demonstrate that ALD passivation can mitigate processing-induced surface damage, enhance the performance of SM-VCSELs, and enable mass production of high-quality SM-VCSELs for mid- to long-reach optical interconnects.
RESUMEN
PURPOSE: Pancreatic cancer (PC) is a common malignant tumor of the digestive system, and its 5-year survival rate is only 4%. N6-methyladenosine (m6A) RNA methylation is the most common post-transcriptional modification and dynamically regulates cancer development, while its role in PC treatment remains unclear. MATERIALS AND METHODS: We treated PC cells with gemcitabine and quantified the overall m6A level with m6A methylation quantification. Real-time quantitative reverse transcription polymerase chain reaction and Western blot analyses were used to detect expression changes of m6A regulators. We verified the m6A modification on the target genes through m6A-immunoprecipitation (IP), and further in vivo experiments and immunofluorescence (IF) assays were applied to verify regulation of gemcitabine on Wilms' tumor 1-associated protein (WTAP) and MYC. RESULTS: Gemcitabine inhibited the proliferation and migration of PC cells and reduced the overall level of m6A modification. Additionally, the expression of the "writer" WTAP was significantly downregulated after gemcitabine treatment. We knocked down WTAP in cells and found target gene MYC expression was significantly downregulated, m6A-IP also confirmed the m6A modification on MYC. Our experiments showed that m6A-MYC may be recognized by the "reader" IGF2BP1. In vivo experiments revealed gemcitabine inhibited the tumorigenic ability of PC cells. IF analysis also showed that gemcitabine inhibited the expression of WTAP and MYC, which displayed a significant trend of co-expression. CONCLUSION: Our study confirmed that gemcitabine interferes with WTAP protein expression in PC, reduces m6A modification on MYC and RNA stability, thereby inhibiting the downstream pathway of MYC, and inhibits the progression of PC.
Asunto(s)
Gemcitabina , Neoplasias Pancreáticas , Humanos , Neoplasias Pancreáticas/tratamiento farmacológico , Neoplasias Pancreáticas/genética , Adenina , Adenosina/farmacología , Factores de Empalme de ARN , Proteínas de Ciclo CelularRESUMEN
Photocatalytic hydrogen peroxide (H2O2) synthesis from water and O2 is an economical, eco-friendly, and sustainable route for H2O2 production. However, single-component photocatalysts are subjected to limited light-harvesting range, fast carrier recombination, and weak redox power. To promote photogenerated carrier separation and enhance redox abilities, an organic/inorganic S-scheme photocatalyst is fabricated by in situ growing In2S3 nanosheets on a covalent organic framwork (COF) substrate for efficient H2O2 production in pure water. Interestingly, compared to unitary COF and In2S3, the COF/In2S3 S-scheme photocatalysts exhibit significantly larger light-harvesting range and stronger visible-light absorption. Partial density of state calculation, X-ray photoelectron spectroscopy, and femtosecond transient absorption spectroscopy reveal that the coordination between In2S3 and COF induces the formation of mid-gap hybrid energy levels, leading to smaller energy gaps and broadened absorption. Combining electron spin resonance spectroscopy, radical-trapping experiments, and isotope labeling experiments, three pathways for H2O2 formation are identified. Benefited from expanded light-absorption range, enhanced carrier separation, strong redox power, and multichannel H2O2 formation, the optimal composite shows an impressive H2O2-production rate of 5713.2 µmol g-1 h-1 in pure water. This work exemplifies an effective strategy to ameliorate COF-based photocatalysts by building S-scheme heterojunctions and provides molecular-level insights into their impact on energy level modulation.
RESUMEN
To explore the changes in nitrite nitrogen, ammoniacal nitrogen, nitrate nitrogen, phosphates, pH, dissolved oxygen, salinity, and water temperature over time and the correlations and mutual influences between these indexes in the traditional farming of largemouth bass, this study selected three ponds in Lizigu Farm in Baodi District of Tianjin, China as research objects. From May to October 2021, nutrient salts and other water quality indexes in the ponds were measured, and water samples were collected at different depths for repetition, Water is collected from the ponds using Plexiglas samplers and sent back to the lab for determination of water quality indexes using our national laboratory standards. According to the analysis of the measurement results, in traditional farming, nitrite nitrogen, ammoniacal nitrogen, nitrate nitrogen, phosphates, pH, dissolved oxygen, salinity, and water temperature in the ponds for largemouth bass all change significantly over time, with different changing trends and certain correlations with each other. In particular, nutrient salts indexes in ponds are influenced by other water quality indexes, human activities, and phytoplankton. During the breeding process, strengthening the dynamic monitoring of nutrient salts and other water quality indexes in the ponds and adjusting the nitrogen, phosphorus, and ammonia levels in the ponds artificially play an important role in preventing eutrophication in the water and promoting the green and sustainable production of pond ecosystems, in particular, allowing better quality growth of the largemouth bass, as well as ensuring the production and economic efficiency. This study provides a theoretical basis and data support for further optimization of traditional pond aquaculture in similar regions, in order to provide aquatic products with better quality and achieve higher economic benefits.
RESUMEN
Myocardial pathology segmentation (MyoPS) can be a prerequisite for the accurate diagnosis and treatment planning of myocardial infarction. However, achieving this segmentation is challenging, mainly due to the inadequate and indistinct information from an image. In this work, we develop an end-to-end deep neural network, referred to as MyoPS-Net, to flexibly combine five-sequence cardiac magnetic resonance (CMR) images for MyoPS. To extract precise and adequate information, we design an effective yet flexible architecture to extract and fuse cross-modal features. This architecture can tackle different numbers of CMR images and complex combinations of modalities, with output branches targeting specific pathologies. To impose anatomical knowledge on the segmentation results, we first propose a module to regularize myocardium consistency and localize the pathologies, and then introduce an inclusiveness loss to utilize relations between myocardial scars and edema. We evaluated the proposed MyoPS-Net on two datasets, i.e., a private one consisting of 50 paired multi-sequence CMR images and a public one from MICCAI2020 MyoPS Challenge. Experimental results showed that MyoPS-Net could achieve state-of-the-art performance in various scenarios. Note that in practical clinics, the subjects may not have full sequences, such as missing LGE CMR or mapping CMR scans. We therefore conducted extensive experiments to investigate the performance of the proposed method in dealing with such complex combinations of different CMR sequences. Results proved the superiority and generalizability of MyoPS-Net, and more importantly, indicated a practical clinical application. The code has been released via https://github.com/QJYBall/MyoPS-Net.
Asunto(s)
Corazón , Infarto del Miocardio , Humanos , Miocardio/patología , Imagen por Resonancia Magnética/métodos , Redes Neurales de la Computación , Procesamiento de Imagen Asistido por Computador/métodosRESUMEN
BACKGROUND: Pancreatic carcinoma (PC) is a highly lethal cancer with an increasing mortality rate, its five-year survival rate is only approximately 4%. N6-methyladenosine (m6A) modification is the most common posttranscriptional modification of RNA, it could affect tumor formation by regulating m6A modifications in the mRNA of key oncogenes or tumor suppressor genes. However, its role in PC remains unclear. METHODS: We combined bioinformatic analysis with in vitro and in vivo experiments to investigate the expression profile of methylation modulators and identify key m6A regulators in the progression of PC. Further study focused on exploring the target genes binding to the regulators through RIP and immunofluorescence staining experiment. RESULTS: TCGA and Gene Expression Omnibus (GEO) analyses revealed an overall increasing trend in the expression of m6A regulators in PC, and consensus clustering analysis of m6A modification showed that the expression of regulators was negatively correlated with the survival rate. LASSO-Cox regression analysis revealed that IGF2BP2, METTL3, ALKBH5 and KIAA1429 were associated with hazard ratios (HR), but only IGF2BP2 was sufficiently appropriate for the m6A survival prognosis model. The IHC and WB results verified high protein expression of IGF2BP2 in PC, and IGF2BP2 knockdown inhibited the proliferation and migration of PC cells. We predicted and verified B3GNT6 was observably regulated by IGF2BP2 via RIP assays. In addition, IF staining confirmed the co-expression of IGF2BP2 and B3GNT6. The tumor-promoting effect of IGF2BP2 and its co-expression with B3GNT6 were verified in an animal model. CONCLUSIONS: Elevated m6A levels promote PC progression. IGF2BP2 is a credible marker and modulates B3GNT6 mRNA stability, indicating that IGF2BP2 is a potential prognostic marker and therapeutic target in PC progression.
Asunto(s)
Neoplasias Pancreáticas , Animales , Metilación , ARN Mensajero/genética , Neoplasias Pancreáticas/genética , ARN , Neoplasias PancreáticasRESUMEN
Myocardial pathology segmentation (MyoPS) is critical for the risk stratification and treatment planning of myocardial infarction (MI). Multi-sequence cardiac magnetic resonance (MS-CMR) images can provide valuable information. For instance, balanced steady-state free precession cine sequences present clear anatomical boundaries, while late gadolinium enhancement and T2-weighted CMR sequences visualize myocardial scar and edema of MI, respectively. Existing methods usually fuse anatomical and pathological information from different CMR sequences for MyoPS, but assume that these images have been spatially aligned. However, MS-CMR images are usually unaligned due to the respiratory motions in clinical practices, which poses additional challenges for MyoPS. This work presents an automatic MyoPS framework for unaligned MS-CMR images. Specifically, we design a combined computing model for simultaneous image registration and information fusion, which aggregates multi-sequence features into a common space to extract anatomical structures (i.e., myocardium). Consequently, we can highlight the informative regions in the common space via the extracted myocardium to improve MyoPS performance, considering the spatial relationship between myocardial pathologies and myocardium. Experiments on a private MS-CMR dataset and a public dataset from the MYOPS2020 challenge show that our framework could achieve promising performance for fully automatic MyoPS.
Asunto(s)
Medios de Contraste , Infarto del Miocardio , Humanos , Imagen por Resonancia Cinemagnética/métodos , Gadolinio , Miocardio/patología , Infarto del Miocardio/diagnóstico por imagen , Imagen por Resonancia Magnética/métodos , Valor Predictivo de las PruebasRESUMEN
INTRODUCTION: Solid pseudopapillary tumor of the pancreas (SPTP) is a rarely diagnosed, low-malignancy pancreatic neoplasm, which mostly can be cured by surgery. AIM: To investigate the surgical effect and prognosis of SPTP. MATERIAL AND METHODS: The data of 39 patients diagnosed with SPTP and treated with surgery between 2013 and 2020 were analyzed retrospectively. The data included the clinical characteristics, surgical management, pathological findings and therapeutic outcome. RESULTS: The mean age of the patients was 34.0 ±12.1 years, and the female : male ratio was 32 : 7. Most of the patients were asymptomatic (48.7%). The mean diameter of the tumors was 4.81 ±2.36 cm. Operative procedures were conducted according to the location and size of the tumors. Laparoscopic surgery, especially laparoscopic distal pancreatectomy (LDP), provided a smaller incision, a shorter postoperative hospital stay and a shorter postoperative fasting time. There was no observed difference in the amount of blood loss or complication rate. The median follow-up was 24 months. One patient with 20% expression of Ki-67 developed liver metastasis after surgery. CONCLUSIONS: SPTP is a rare disease with low malignancy. Minimally invasive surgery, especially LDP, has been proven to be a feasible and safe treatment method for SPTP with early recovery. The prognosis of SPTP is favorable. Lifetime surveillance is necessary especially in patients with a high expression rate of Ki-67.
RESUMEN
BACKGROUND: Liver ischemia and reperfusion (I/R) is a common but severe clinical problem. Previous studies have revealed that the expression level of ß-arrestin2 affects serum deprivation (SD)-induced cell apoptosis and was involved in lipopolysaccharide (LPS) stimulated TLR4 signaling pathway. However, little is known about ß-arrestin2 in liver apoptosis and immune response induced by I/R. METHODS: A non-lethal model of segmental (70%) hepatic ischemia was utilized. Histology examination, cell apoptosis and cytokine levels were measured using H&E staining, TUNEL assay, and ELISA, respectively. Apoptosis-related protein and gene level of cytokines were respectively detected using Western blot and Real-time PCR. RESULTS: Our data showed that knockout (KO) of ß-arrestin2 gene significantly deteriorated the injury of liver caused by I/R according to liver histology, higher serum liver enzyme, and increased level of cell apoptosis. ß-arrestin2 KO could result in increased level of apoptosis related protein and decreased level of Akt phosphorylation. Furthermore, decreased levels of Bcl-2 and Bad phosphorylation, but increased level of Bax were found in ß-arrestin2 KO group. In addition, the levels of p-ERK1/2, p-p38MAPKs, and p-NF-κB in ß-arrestin2 KO group were significantly higher than that in WT group. CONCLUSIONS: ß-arrestin2 protected liver from I/R injury and this effect may be due to the regulating of Akt pathway, Bcl-2/Bax ratio, MAPKs and NF-κB pathway.
Asunto(s)
Inflamación/tratamiento farmacológico , Proteínas Proto-Oncogénicas c-akt/metabolismo , Daño por Reperfusión/tratamiento farmacológico , Receptor Toll-Like 4/metabolismo , Arrestina beta 2/uso terapéutico , Animales , Apoptosis , Humanos , Hepatopatías/tratamiento farmacológico , Hepatopatías/patología , Masculino , Ratones , Ratones Noqueados , Daño por Reperfusión/patología , Transducción de Señal , Arrestina beta 2/farmacologíaRESUMEN
High-throughput methods have been used to explore the mechanisms by which androgen-sensitive prostate cancer (ASPC) develops into castration-resistant prostate cancer (CRPC). However, it is difficult to interpret cryptic results by routine experimental methods. In this study, we performed systematic and integrative analysis to detect key miRNAs that contribute to CRPC development. From three DNA microarray datasets, we retrieved 11 outlier microRNAs (miRNAs) that had expression discrepancies between ASPC and CRPC using a specific algorithm. Two of the miRNAs (miR-125b and miR-124) have previously been shown to be related to CRPC. Seven out of the other nine miRNAs were confirmed by quantitative PCR (Q-PCR) analysis. MiR-210, miR-218, miR-346, miR-197, and miR-149 were found to be over-expressed, while miR-122, miR-145, and let-7b were under-expressed in CRPC cell lines. GO and KEGG pathway analyses revealed that miR-218, miR-197, miR-145, miR-122, and let-7b, along with their target genes, were found to be involved in the PI3K and AKT3 signaling network, which is known to contribute to CRPC development. We then chose five miRNAs to verify the accuracy of the analysis. The target genes of each miRNA were altered significantly upon transfection of specific miRNA mimics in the C4-2 CRPC cell line, which was consistent with our pathway analysis results. Finally, we hypothesized that miR-218, miR-145, miR-197, miR-149, miR-122, and let-7b may contribute to the development of CRPC through the influence of Ras, Rho proteins, and the SCF complex. Further investigation is needed to verify the functions of the identified novel pathways in CRPC development.