Howardraahauge0222
Our results show a possible regulatory target between neuroinflammation in the CNS and development of breast cancer, along with the reversal effect of quercetin on breast cancer progression.
Chronic stress may be an indicator of breast cancer and that quercetin could be an effective treatment for breast cancer patients with chronic stress.
Chronic stress may be an indicator of breast cancer and that quercetin could be an effective treatment for breast cancer patients with chronic stress.
At present, the primary treatment of esophageal cancer is surgery-based comprehensive treatment, including adjuvant therapy such as chemotherapy and/or radiotherapy. However, the role of adjuvant therapy for esophageal squamous cell carcinoma (ESCC) with pathologically node-negative (pN0) disease is controversial. This study aimed to evaluate the impact of postoperative adjuvant therapy on survival in patients with pN0 ESCC.
Patients with ESCC who underwent R0 esophagectomy in the Department of Thoracic Surgery of Sichuan Cancer Hospital from January 2008 to December 2013 were enrolled. Patients were divided into two groups a surgery alone (Group S) group or a surgery + adjuvant therapy (Group S + A) group. The primary outcomes were overall survival (OS) and disease-free survival (DFS), and every consecutive case was followed up until death or the last follow-up.
A total of 387 patients with ESCC patients who had pN0 were enrolled in the study. After propensity score matching (PSM), each group consistedCC who had pN0 disease. Fewer lymph node dissections and T3 stage tumors were independent risk factors for OS and DFS.
The oncogene, malignant T-cell-amplified sequence 1 (MCTS1), has been found to be highly expressed in a variety of cancer cell lines. It has been shown to be involved in cell cycle progression and to confer a growth advantage for lymphomas and breast cancer. Nevertheless, the role of MCTS1 in contributing to the development of oral cancer remains elusive.
We analyzed the gene expression profiles of MCTS1 in normal oral keratinocytes and cancerous cells. Cellular proliferation, invasion, and migration experiments were performed to detect the effect of MCTS1 on the biological evolution of oral cancer. The
results were verified by the
lymphatic metastasis test. The underlying mechanism of MCTS1 in promoting oral cancer invasion and metastasis correlated with the epithelial-mesenchymal transition (EMT) process as revealed by western blotting.
The results showed that MCTS1 was aberrantly expressed in oral cancer cells. MCTS1 overexpression significantly promoted tumor cell growth, proliferation, migration, and invasion. learn more MCTS1-mediated lymphatic metastasis was verified
using an intraplantar tumor model. Biomarkers associated with EMT progression were positively or negatively regulated upon knockdown or overexpression of MCTS1, respectively.
Higher MCTS1 expression in oral cancer may be connected with an unfavorable prognosis due to involvement of MCTS1. MCTS1 potentiates the growth and proliferation of oral cancer cells and subsequent metastasis by regulating cell cycle and modifying the EMT process.
Oral cancer; oncogene; malignant T-cell-amplified sequence 1 (MCTS1); metastasis; invasion.
Oral cancer; oncogene; malignant T-cell-amplified sequence 1 (MCTS1); metastasis; invasion.
To clarify the mechanism of notoginsenoside R1 in the treatment of septic acute lung injury (ALI) based on network pharmacological analysis, and to verify it in the model of septic ALI in rats.
Based on database searching, the related targets of notoginsenoside R1 and ALI were identified, and the component-disease-target network was constructed. The core targets were screened by protein-protein interaction (PPI), and the functional enrichment of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) was analyzed. The rat model of septic ALI was further established to investigate the pharmacological effects of notoginsenoside R1.
Notoginsenoside R1 possibly affected ALI through 150 targets, of which 36 were core targets. GO semantic similarity analysis showed that notoginsenoside R1 might play a role in regulating interleukin 17 (IL-17) signal pathway, tumor necrosis factor (TNF) signal pathway and other key links by regulating MAPK1, MAPK3, IL-1β and other targets. The results of pharmacological experiments showed that notoginsenoside R1 could significantly reduce the wetdry ratio of the lung in an animal model of ALI, improve the pathological injury of the lung, and reduce the content of IL-1β in serum and in bronchoalveolar lavage fluid (BALF) of experimental animals.
Notoginsenoside R1 can inhibit pulmonary edema, reduce inflammation, and improve lung lesions through multiple targets and pathways to achieve the pharmacological effects in the treatment of septic ALI.
Notoginsenoside R1 can inhibit pulmonary edema, reduce inflammation, and improve lung lesions through multiple targets and pathways to achieve the pharmacological effects in the treatment of septic ALI.
Abnormal lipid metabolism has been reported in patients with idiopathic pulmonary arterial hypertension (IPAH); however, the prognostic value of plasma free fatty acids (FFAs) for these patients is unclear. The present study aimed to determine whether FFA can play a role in predicting the survival of patients with IPAH.
A total of 69 blood samples from patients with IPAH were subjected to liquid chromatography-mass spectrometry (LC-MS). According to the classification criteria for pulmonary hypertension in the European Society of Cardiology (ESC) guidelines, patients were divided into low-risk, intermediate-risk, and high-risk groups. The FFA expression levels of patients in the three groups were compared, and the indicators with significant differences were selected. Cox regression analysis was performed to examine the associations between survival and different factors. Receiver operator characteristic (ROC) curves were used to assess the predictive effect of plasma lipids in assessing patients' risk offf value of 77.55, which had a sensitivity of 96.7% and a specificity of 62.5% for predicting survival. Kaplan-Meier curve analysis showed that a lower level of DHA predicted a poor outcome in patients with IPAH.
Our study suggested that FFA levels were correlated with disease severity. Lower levels of DHA predict poor survival in patients with IPAH.
Our study suggested that FFA levels were correlated with disease severity. Lower levels of DHA predict poor survival in patients with IPAH.
Fibroblast growth factor (FGF) 14 is a member of the FGF family that is mainly expressed in the central nervous system. FGF14 has a close association with the occurrence of neurodegenerative conditions; however, its significance in Alzheimer's disease (AD) has yet to be evaluated. Therefore, we sought to obtain a large amount of exogenous FGF14 protein and explore its effect in a cellular model of AD.
FGF14 protein was expressed in an
system using gene recombination technology. Purified protein was obtained through washing and renaturation of inclusion bodies combined with nickel column affinity chromatography. The AD model was established via Aβ25-35-induced injury in PC12 cells. Changes in the levels of lactate dehydrogenase and malondialdehyde were detected, and the neuroprotective effect of recombinant human FGF14 (rhFGF14) was evaluated through double-fluorescence staining and flow cytometry apoptosis detection. For further exploration of rhFGF14-mediated regulation of mitogen-activated protein kinase (MAPK) signaling, western blot was employed.
We successfully induced large amounts of insoluble rhFGF14. Following solubilization and refolding of the rhFGF14 from inclusion bodies, high purity rhFGF14 was purified by Nickel affinity column chromatography. The results showed that rhFGF14 alleviated Aβ25-3-induced PC12 cell injury by inhibiting the phosphorylation of p38, extracellular signal-regulated kinase 1/2, and c-Jun N-terminal kinase, thus suppressing the MAPK signaling pathway.
FGF14 performed a neuroprotective role in our
AD model via its inhibition of MAPK signaling, highlighting its potential as a therapeutic drug for neurodegenerative conditions.
FGF14 performed a neuroprotective role in our in vitro AD model via its inhibition of MAPK signaling, highlighting its potential as a therapeutic drug for neurodegenerative conditions.
Asthma is a heterogeneous disease with different phenotypes, endotypes and responses to treatment. Dust mite allergic asthma (DMAA) is the most common type in children. Compared with randomized control trials, a patient registry study (PRS) can reflect the real physical condition and clinical diagnosis more comprehensively.
Children who visited the asthma clinic of the Children's Hospital of Chongqing Medical University between August 2018 and August 2020, and met the inclusion criteria and also agreed to participate, were enrolled in the registry study. Clinical information, laboratory tests and peripheral blood samples were collected after informed consent was given by guardians.
To date, 208 children have been enrolled in the patient registry database of DMAA. They are mainly male, with >50% having a history of allergic rhinitis, cesarean section, positive family history and passive smoking. Eosinophils and total immunoglobulin E levels were all significantly higher than normal. According to results for the childhood asthma control test (c-ACT) and ratio of forced expiratory volume in 1 s to predicted value after inhaled corticosteroid treatment, the uncontrolled group had higher hemoglobin (Hb) levels than the control group. The group exhibiting abnormal pulmonary function was older, and had longer disease duration, higher fractional exhaled nitric oxide and Hb than the group in which pulmonary function was restored.
We have preliminarily established a registered study database of children with DMAA. By cluster analysis and using blood samples, we can further study the different pathophysiological mechanisms in order to provide more individualized and targeted treatments for all children.
We have preliminarily established a registered study database of children with DMAA. By cluster analysis and using blood samples, we can further study the different pathophysiological mechanisms in order to provide more individualized and targeted treatments for all children.
This study aimed to investigate the clinicopathological significance of sine oculis homeobox homolog 1 (SIX1) and eyes absent 1 (EYA1) in patients with chronic hepatitis B (CHB) and other liver diseases.
SIX1 and EYA1 levels were detected in human serum and liver tissues by enzyme linked immunosorbent assay (ELISA) and immunofluorescent staining method, respectively.
The serum SIX1 and EYA1 levels in 313 CHB patients were 7.24±0.11 and 25.21±0.51 ng/mL, respectively, and these values were significantly higher than those in 33 healthy controls (2.84±0.15 and 13.11±1.01 ng/mL, respectively; P<0.05). Serum SIX1 and EYA1 levels were also markedly increased in patients with numerous other liver diseases, including liver fibrosis, hepatocellular carcinoma, fatty liver disease, alcoholic liver disease, fulminant hepatic failure, autoimmune liver disease, and hepatitis C, compared to the healthy controls (P<0.05). Dynamic observation of these proteins over time in 35 selected CHB patients revealed that SIX1 and EYA1 serum levels increased over an interval.
