With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

Platelets are reprogrammed by cancer via a process called education, which favors cancer development. The transcriptional profile of tumor-educated platelets (TEPs) is skewed and therefore practicable for cancer detection. This intercontinental, hospital-based, diagnostic study included 761 treatment-naïve inpatients with histologically confirmed adnexal masses and 167 healthy controls from nine medical centers (China, n = 3; Netherlands, n = 5; Poland, n = 1) between September 2016 and May 2019. The main outcomes were the performance of TEPs and their combination with CA125 in two Chinese (VC1 and VC2) and the European (VC3) validation cohorts collectively and independently. Exploratory outcome was the value of TEPs in public pan-cancer platelet transcriptome datasets. The AUCs for TEPs in the combined validation cohort, VC1, VC2, and VC3 were 0.918 (95% CI 0.889-0.948), 0.923 (0.855-0.990), 0.918 (0.872-0.963), and 0.887 (0.813-0.960), respectively. Combination of TEPs and CA125 demonstrated an AUC of 0.922 (0.889-0.955) in the combined validation cohort; 0.955 (0.912-0.997) in VC1; 0.939 (0.901-0.977) in VC2; 0.917 (0.824-1.000) in VC3. For subgroup analysis, TEPs exhibited an AUC of 0.858, 0.859, and 0.920 to detect early-stage, borderline, non-epithelial diseases and 0.899 to discriminate ovarian cancer from endometriosis. TEPs had robustness, compatibility, and universality for preoperative diagnosis of ovarian cancer since it withstood validations in populations of different ethnicities, heterogeneous histological subtypes, and early-stage ovarian cancer. However, these observations warrant prospective validations in a larger population before clinical utilities.
Humans ; Female ; Blood Platelets/pathology* ; Biomarkers, Tumor/genetics* ; Ovarian Neoplasms/pathology* ; China

MicroRNA-365 (miR-365) is upregulated in the ischemic brain and is involved in oxidative damage in the diabetic rat. However, it is unclear whether miR-365 regulates oxidative stress (OS)-mediated neuronal damage after ischemia. Here, we used a transient middle cerebral artery occlusion model in rats and the hydrogen peroxide-induced OS model in primary cultured neurons to assess the roles of miR-365 in neuronal damage. We found that miR-365 exacerbated ischemic brain injury and OS-induced neuronal damage and was associated with a reduced expression of OXR1 (Oxidation Resistance 1). In contrast, miR-365 antagomir alleviated both the brain injury and OXR1 reduction. Luciferase assays indicated that miR-365 inhibited OXR1 expression by directly targeting the 3'-untranslated region of Oxr1. Furthermore, knockdown of OXR1 abolished the neuroprotective and antioxidant effects of the miR-365 antagomir. Our results suggest that miR-365 upregulation increases oxidative injury by inhibiting OXR1 expression, while its downregulation protects neurons from oxidative death by enhancing OXR1-mediated antioxidant signals.

Whether and how garlic-derived -allylmercaptocysteine (SAMC) inhibits hepatocellular carcinoma (HCC) is largely unknown. In the current study, the role of low-density lipoprotein receptor (LDLR)-related protein 6 (LRP6) in HCC progression and the anti-HCC mechanism of SAMC was examined in clinical sample, cell model and xenograft/orthotopic mouse models. We demonstrated that SAMC inhibited cell proliferation and tumorigenesis, while induced apoptosis of human HCC cells without influencing normal hepatocytes. SAMC directly interacted with Wnt-pathway co-receptor LRP6 on the cell membrane. LRP6 was frequently over-expressed in the tumor tissue of human HCC patients (66.7% of 48 patients) and its over-expression only correlated with the over-expression of -catenin, but not with age, gender, tumor size, stage and metastasis. Deficiency or over-expression of LRP6 in hepatoma cells could partly mimic or counteract the anti-tumor properties of SAMC, respectively. administration of SAMC significantly suppressed the growth of Huh-7 xenograft/orthotopic HCC tumor without causing undesirable side effects. In addition, stable down-regulation of LRP6 in Huh-7 facilitated the anti-HCC effects of SAMC. In conclusion, LRP6 can be a potential therapeutic target of HCC. SAMC is a promising specific anti-tumor agent for treating HCC subtypes with Wnt activation at the hepatoma cell surface.

BACKGROUND: Preliminary studies have found that the oral intake of contraceptives reduces the rate of orthodontic tooth movement. This study mainy explores the effects of oral contraceptives on periodontium remodeling during orthodontic tooth movement in a female rat model. OBJECTIVE: To investigate the effects of combined oral contraceptives (COCs) on the expression levels of progesterone receptor and osteoprotegerin, as well as the number of osteoclasts in the periodontium during orthodontic tooth movement. METHODS: Eighty 3-month-old female Sprague-Dawley rats were randomly divided into two groups (n=40 per group), and COCs (marvelon, experimental group) or normal saline (control group) was then given by gavage. At 7 days after administration, the right maxillary first molars were moved mesially under a force of 50 g delivered by nickel-titanium coil springs, and 10 rats were killed on day 7, 14, 21 and 28 after loading, respectively. The expression levels of progesterone receptor and osteoprotegerin in the periodontium were detected by immunohistochemistry, and the number of activated osteoclasts was measured by tartrate-resistant acid phosphatase staining. RESULTS AND CONCLUSION: At 28 days after force loading, the expression level of progesterone receptor in the periodontium in the experimental group (0.307±0.03) was significantly higher than that in the control group (0.194±0.11), (P < 0.01). The number of osteoclasts in the maxillary first molars in the experimental group was significantly less than that in the control group at 7, 14, 21 and 28 days after force loading (P < 0.05). The average absorbance value of osteoprotegerin in the experimental group was significantly higher than that in the control group (P < 0.01). These results show that COCs are able to promote osteogenesis and slow bone absorption during periodontal reconstruction, indicating that the course of orthodontic treatment for female patients with a history of COCs intake may be extended.

Objective To observe the effects of Shuangdan Mingmu Capsules on the expressions of HIF-1α and NF-κB; To explore its possible mechanism of treatment. Methods SD rats were injected with STZ (50 mg/kg) into the tail vein to induce diabetes mellitus. After the DR model was confirmed by fundus fluorescein angiography, the rats were randomly divided into model group, Shuangdan Mingmu Capsules group and positive medicine group, and normal rats were set as control group. After the last administration, the blood glucose level and retinopathy in rats were measured. The protein and gene expression of HIF-1α and NF-κB in the retina were detected by Western blot and RT-PCR respectively. Results Compared with control group, the blood glucose in the model group was significantly increased; the retinal capillaries increased; the leakage of fluorescein was obvious; the protein and gene expressions of HIF-1α,NF-κB were significantly increased.After administration of Shuangdan Mingmu Capsules,the model rats decreased blood glucose; retinal microvascular volume decreased; fluorescein leakage area was significantly reduced; protein and gene expressions of HIF-1α and NF-κB were decreased. Conclusion Shuangdan Mingmu Capsules can effectively inhibit the neovascularization of DR rats and protect the retina, which may be related to the down-regulation of the expressions of HIF-1α and NF-κB.

PURPOSE: Conditional survival (CS) provides important information on survival for a period of time after diagnosis. Currently, information on CS patterns of patients with nasopharyngeal carcinoma (NPC) is lacking. We aimed to analyze survival rate over time and estimate CS for NPC patients using a national population-based registry. MATERIALS AND METHODS: Patients diagnosed with NPC between 1973 and 2007 with at least 5-year follow-up were identified from the Surveillance Epidemiology End Results registry. Traditional survival rates and crude CS estimateswere calculated using Kaplan-Meier analysis. Risk-adjusted survival curves were plotted from the proportional hazards model using the correct group prognosis method. RESULTS: For 7,713 patients analyzed, adjusted baseline 5-year overall survival improved significantly from 36.0% in patients diagnosed in 1973-1979, 41.7% in 1980-1989, 46.6% in 1990-1999, to 54.7% in 2000-2007 (p < 0.01). CS analysis demonstrated that for every additional year survived, adjusted probability of surviving the next 5 years increased from 66.7% (localized), 54.0% (regional), and 35.3% (distant) at the time of diagnosis, to 83.7% (localized), 75.0% (regional), and 62.2% (distant) for patients who had survived 5 years. Adjusted 5-year CS differed among age, sex, tumor histology, ethnicity, and stage subgroups initially, but converged with time. CONCLUSION: Treatment outcomes of NPC patients have greatly improved over the decades. Increases in CS become more prominent in patients with distant disease than in those with localized or regional disease as patients survive longer. CS provides more dynamic prognostic information for patients who have survived a period of time after diagnosis.
Diagnosis ; Epidemiology* ; Follow-Up Studies ; Humans ; Kaplan-Meier Estimate ; Methods ; Nasopharyngeal Neoplasms ; Prognosis ; Proportional Hazards Models ; SEER Program ; Survival Rate

Two previously undescribed steroidal compounds, 16, 23-epoxy-22, 26-epimino-cholest-22(N), 23, 25(26)-trien-3β-ol-3-O-β-D-glucopyranosyl-(1→2)-β-D-glucopyranosyl-(1→4)-β-D-galactopyranoside (1) and 26-O-β-D-glucopyranosyl-(25R)-5α-furost-20(22)-en-3β, 26-diol (2), together with 7 known ones including 26-O-β-D-glucopyranosyl-(25R)-5, 20(22)-dien-furost-3β, 26-diol (3), (25R)-5-en-spirost-3β-ol-O-β-D-glucopyranosyl-(1→4)-[α-L-rhmanopyranosyl-(1→2)]-β-D-galactopyranoside (4), funkioside D (5), aspidistrin (6), tigogenin-3-O-β-D-lucotrioside (7), desglucolanatigonin II (8), and degalactotigonin (9), were isolated from Solanum lyratum Thunb. Their cytotoxic activities were tested in two cancer cell lines by MTT method. One of the steroidal glycosides (6) showed significant cytotoxic activity against gastric cancer SGC7901 and liver cancer BEL-7402 cells.
Alkaloids ; chemistry ; isolation & purification ; toxicity ; Antineoplastic Agents ; chemistry ; isolation & purification ; toxicity ; Cell Line, Tumor ; Cell Survival ; drug effects ; Glycosides ; chemistry ; pharmacology ; toxicity ; Humans ; Inhibitory Concentration 50 ; Molecular Structure ; Phytosterols ; chemistry ; isolation & purification ; toxicity ; Plant Extracts ; chemistry ; toxicity ; Plants, Medicinal ; chemistry ; Solanum ; chemistry ; Sterols ; chemistry ; pharmacology ; toxicity