Notes

The microbiota of high-moisture mozzarella cheese made with some other acidification approaches.
Age‑related cataract (ARC) is the leading cause of blindness worldwide. Oxidative DNA damage is a biochemical feature of ARC pathogenesis. The present study investigated the role of long non‑coding RNAs in the DNA repair of oxidative damage, partially the regulation of the DNA repair gene, 8‑oxoguanine DNA glycosylase (OGG1), in lens affected by ARC. The ogg1 mutant zebrafish model was constructed to verify the role of ogg1 in the lens. A high‑throughput lncRNA profiling was performed on human lens epithelial cells (LECs) following oxidative stress. The lncRNAs with the OGG1 target gene were analyzed for possible differentiated expression levels. The lens capsule samples of patients with ARC were collected to further verify the screening results. lncRNA was then overexpressed and knocked down in LECs to observe cell proliferation and apoptosis. The association between lncRNA, miRNA and the OGG1 mRNA 3'UTR were analyzed. The ogg1 mutant zebrafish developed more severe lens lesions following oxidative challenge. lncRNA NONHSAT143692.2 was distinctly expressed in various disease models. Selleckchem 3-TYP The knockdown of NONHSAT143692.2 downregulated the expression of OGG1 mRNA (P less then 0.001) and OGG1 protein (P less then 0.001), aggravated oxidative damage to LECs, increased apoptosis (P less then 0.001) and decreased cell proliferation (P less then 0.01). The overexpression of NONHSAT143692.2 reversed the above‑mentioned outcomes. miR‑4728‑5p was predicted to bind to NONHSAT143692.2 and OGG1 mRNA 3'UTR. The overexpression of miR‑4728‑5p downregulated the expression of NONHSAT143692.2 (P less then 0.001), OGG1 mRNA (P less then 0.001) and OGG1 protein (P less then 0.001). The knockdown of miR‑4728‑5p reversed the above‑mentioned outcomes. Overall, the findings of the present study demonstrate that the NONHSAT143692.2/miR‑4728‑5p/OGG1 axis may play an important role in the development of ARC. This novel concept may provide new insight into the molecular diagnosis and treatment of ARC.Axial spondyloarthritis (AxSpA) is a chronic rheumatic disease involving the axial skeleton. Recent evidence suggested that certain circular RNAs (circRNAs) have a crucial role in rheumatic diseases. However, the functions of circRNAs in AxSpA have remained largely elusive. The present study identified the utility of the circRNA Homo sapiens (hsa)_circ_0079787 as a potential biomarker for AxSpA. A total of 5 circRNAs (hsa_circ_0002715, hsa_circ_0001947, hsa_circ_0079787, hsa_circ_0000367 and hsa_circ_0035197) were determined in the peripheral blood of 46 patients with AxSpA, 46 patients with systemic lupus erythematosus (SLE) and 25 healthy controls (HC) by reverse transcription‑quantitative PCR analysis. The detailed clinical history of each patient was recorded and the correlations between these circRNAs and clinical characteristics were analyzed. Furthermore, receiver operating characteristic (ROC) curves were constructed to evaluate the diagnostic value of hsa_circ_0079787 and other factors for AxSpA. Of ombination of hsa_circ_0079787‑PLT‑MPV‑PCT may provide improved diagnostic accuracy for AxSpA. In addition, the levels of hsa_circ_0079787 in the peripheral blood were correlated with disease activity and severity of AxSpA.CD44 is widely expressed on the surface of most tissues and all hematopoietic cells, and regulates many genes associated with cell adhesion, migration, proliferation, differentiation, and survival. CD44 has also been studied as a therapeutic target in several cancers. Previously, an anti‑CD44 monoclonal antibody (mAb), C44Mab‑5 (IgG1, kappa) was established by immunizing mice with CD44‑overexpressing Chinese hamster ovary (CHO)-K1 cells. C44Mab‑5 recognized all CD44 isoforms, and showed high sensitivity for flow cytometry and immunohistochemical analysis in oral cancers. However, as the IgG1 subclass of C44Mab‑5 lacks antibody‑dependent cellular cytotoxicity (ADCC) and complement‑dependent cytotoxicity (CDC), the antitumor activity of C44Mab‑5 could not be determined. In the present study, we converted the mouse IgG1 subclass antibody C44Mab‑5 into an IgG2a subclass antibody, 5‑mG2a, and further produced a defucosylated version, 5‑mG2a‑f, using FUT8‑deficient ExpiCHO‑S (BINDS‑09) cells. Defucosylation of 5‑mG2a‑f was confirmed using fucose‑binding lectins, such as AAL and PhoSL. The dissociation constants (KD) for 5‑mG2a‑f against SAS and HSC‑2 oral cancer cells were determined through flow cytometry to be 2.8x10‑10 M and 2.6x10‑9 M, respectively, indicating that 5‑mG2a‑f possesses extremely high binding affinity. Furthermore, immunohistochemical staining using 5‑mG2a‑f specifically stained the membranes of oral cancer cells. In vitro analysis demonstrated that 5‑mG2a‑f showed moderate ADCC and CDC activities against SAS and HSC‑2 oral cancer cells. In vivo analysis revealed that 5‑mG2a‑f significantly reduced tumor development in SAS and HSC‑2 xenografts in comparison to control mouse IgG, even after injection seven days post‑tumor inoculation. Collectively, these results suggest that treatment with 5‑mG2a‑f may represent a useful therapy for patients with CD44‑expressing oral cancers.T‑2 toxin is a type A trichothecene mycotoxin. In order to reduce the side effects of T‑2 toxin and increase the tumor targeting ability, a pH‑sensitive liposome of T‑2 toxin (LP‑pHS‑T2) was prepared and characterized in the present study. The cytotoxicity of LP‑pHS‑T2 on A549, Hep‑G2, MKN‑45, K562 and L929 cell lines was tested by 3‑(4,5‑dimethylthiazolyl‑2)‑2,5‑diphenyltetrazolium bromide assay, with T‑2 toxin as the control. The apoptotic and migratory effects of LP‑pHS‑T2 on Hep‑G2 cells were investigated. The preparation process of LP‑pHS‑T2 involved the following parameters Dipalmitoyl phosphatidylcholine dioleoylphosphatidylethanolamine, 12; total phospholipid concentration, 20 mg/ml; phospholipidcholesterol, 31; 4‑(2‑hydroxyethyl)‑1‑piperazineethanesulfonic acid buffer (pH 7.4), 10 ml; druglipid ratio, 21; followed by ultrasound for 10 min and extrusion. The encapsulation efficiency reached 95±2.43%. The average particle size of LP‑pHS‑T2 after extrusion was 100 nm; transmission electron microscopy showed that the shape of LP‑pHS‑T2 was round or oval and of uniform size. The release profile demonstrated a two‑phase downward trend, with fast leakage of T‑2 toxin in the first 6 h (~20% released), followed by sustained release up to 48 h (~46% released). From 48‑72 h, the leakage rate increased (~76% released), until reaching a minimum at 72 h. When LP‑pHS‑T2 was immersed in 0.2 mol/l disodium phosphate‑sodium dihydrogen phosphate buffers (pH 6.5), the release speed was significantly increased and the release rate reached 91.2%, demonstrating strong pH sensitivity. Overall, antitumor tests showed that LP‑pHS‑T2 could promote the apoptosis and inhibit the migration of Hep‑G2 cells. The present study provided a new approach for the development of T‑2 toxin‑based anti‑cancer drugs.Endometriosis (EMS) is a common disease in women aged 25‑45 years, and pain is the main clinical symptom. The primary clinical treatment is surgical excision and drug therapy targeting the ectopic lesions, but these have not been very effective. Botulinum neurotoxin serotype A (BTX‑A) has been reported to be useful in the treatment of pain in a variety of diseases. Based on this, the aim of the present study was to explore the therapeutic effect and mechanism of BTX‑A on EMS. A model of nerve injury induced by oxygen glucose deprivation (OGD) was constructed in PC12 cells and EMS mice. Model cells and mice were treated with different concentrations of BTX‑A to observe the changes in pain behavior, to detect cell viability and the secretion of norepinephrine (NE) and methionine enkephalin (M‑EK) in cells and the spinal cord, and to evaluate the expression of apoptosis‑related molecules in spinal cord nerves. The results revealed that BTX‑A significantly reduced the amount of writhing in model mice, enhanced the activity of PC12 OGD cells, increased the secretion of NE and M‑EK in model cells and the spinal cord of mice, and decreased the apoptosis of neural cells in the spinal cord of the model mice. Therefore, it was hypothesized that BTX‑A may alleviate the pain induced by EMS by increasing the secretion of analgesic substances and promoting the repair of nerve injury. The present study provided a theoretical basis for the treatment of pain induced by EMS.The present study was performed to investigate the protective effects of tannic acid (TA) on liver injury induced by arsenic trioxide (ATO) and to elucidate the mechanism involved as related to the Kelch‑like ECH‑associated protein 1 (Keap1)‑nuclear factor erythroid 2‑related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway. Adult rats were intraperitoneally injected with TA, while ATO was administered 1 h later. On the 11th day, the rats were euthanized to determine any liver histological changes, liver function, and the activities of antioxidant, antiapoptosis and proinflammatory cytokines in the liver. Furthermore, the protein expression levels of nuclear Nrf2, total Nrf2, Keap1, Heme oxygenase‑1 (HO‑1), NADPH quinine oxidoreductase‑1 (NQO1), and γ‑glutamylcysteine synthetase (γ‑GCS) were determined using western blot analysis. The results showed that TA treatment ameliorated ATO‑induced liver histological changes and decreased the ATO‑induced increased alanine aminotransferase (ALT) and aspartate transaminase (AST) serum levels. Activities of the antioxidant enzymes significantly were increased, while the levels of malondialdehyde (MDA) and reactive oxygen species (ROS) were attenuated following TA treatment. In addition, TA treatment inhibited ATO‑induced liver apoptosis and inflammatory responses, increased Bcl‑2 protein expression level and reduced the levels of Bax, caspase‑3, interleukin (IL)‑1β, IL‑6 and tumor necrosis factor (TNF)‑α. Furthermore, TA treatment increased the protein expression levels of Nrf2 and Keap1, HO‑1, NQO1 and γ‑GCS. The results demonstrated that TA has a protective effect on ATO‑treated hepatic toxicity and that its underlying mechanism could be due to TA activation of the Keap1‑Nrf2/ARE signaling pathway, to reduce oxidative stress, apoptosis and inflammation in ATO‑intoxicated rats.Accumulation of non‑specific structural chromosomal aberrations (CAs) and telomere shortening contribute to genome instability, which constitutes as one of the hallmarks of cancer. CAs arise due to direct DNA damage or telomere shortening. CAs in peripheral blood lymphocytes (PBL), which are considered to be markers of exposure, have been previously reported to serve a role in the pathophysiology and progression of cancer through mechanisms that are poorly understood. In addition, the prognostic relevance of telomere length (TL) in patients with cancer remains to be elucidated. In the present study, CAs and TL in PBL isolated from patients with newly diagnosed cancer (151 breast, 96 colorectal, 90 lung) and 335 cancer‑free control individuals were investigated. These results were then correlated with clinicopathological factors and follow‑up data. The accumulation of CAs in PBL was observed with increased susceptibility to breast and lung cancer (P less then 0.0001), while individuals with longer TL were found to be at a higher risk of breast cancer (P less then 0.
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