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Preoperative assessment of the severity of pelvic adhesions in endometriosis remains challenging. Inflammation may drive adhesion formation, and the predictive value of the neutrophil percentage-to-albumin ratio (NPAR, the ratio multiplied by 10 for analysis), an emerging biomarker of systemic inflammation, in endometriosis pelvic adhesions has not been evaluated. In this study, we retrospectively analyzed the data of 246 patients with histologically confirmed ovarian endometriotic cysts and statistically analyzed NPAR. We evaluated the correlation between NPAR and pelvic adhesion severity in patients with endometriosis using logistic regression models and logistic fitted curves (to evaluate the dose-response relationships). Additionally, the predictive efficacy of NPAR for pelvic adhesion severity was assessed using a receiver operating characteristic (ROC) curve analysis. NPAR was positively correlated with the severity of pelvic adhesions, demonstrating statistically significant associations with moderate-to-severe pelvic adhesions in all models when utilized as a continuous variable, and the risk of moderate-to-severe pelvic adhesions increased by 82% for every 10-unit increase in NPAR (Odds Ratio, OR = 1.82); when used as a categorical variable, the risk of moderate-to-severe pelvic adhesions was remarkably increased in the highest tertile of NPAR. ROC curve analysis demonstrated that the area under the curve of the NPAR score was 0.717, which was superior to that of the CA125 (Area Under the Curve,AUC = 0.564). NPAR is an independent predictor of moderate to severe pelvic adhesions in patients with endometriosis and is superior to that of CA125. As an easily accessible blood-based biomarker, NPAR may be useful for preoperative risk stratification, guiding surgical planning and individualized treatment decisions.

Background Subarachnoid hemorrhage (SAH), a severe subtype of stroke, is characterized by notably high mortality and morbidity, largely due to the lack of effective therapeutic options. Although the neuroprotective potential of PPARg and Nrf2 has been recognized, investigative efforts into oroxin A (OA), remain limited in preclinical studies. Methods SAH was modeled in vivo through filament perforation in male C57BL/6 mice and in vitro by exposing HT22 cells to hemin to induce neuronal damage. Following the administration of OA, a series of methods were employed to assess neurological behaviors, brain water content, neuronal damage, cell ferroptosis, and the extent of neuroinflammation. Results The findings indicated that OA treatment markedly improved survival rates, enhanced neurological functions, mitigated neuronal death and brain edema, and attenuated the inflammatory response. These effects of OA were linked to the suppression of microglial activation. Moreover, OA administration was found to diminish ferroptosis in neuronal cells, a critical factor in early brain injury (EBI) following SAH. Further mechanistic investigations uncovered that OA facilitated the translocation of nuclear factor erythroid 2-related factor 2 (Nrf-2) from the cytoplasm to the nucleus, thereby activating the Nrf2/GPX4 pathway. Importantly, OA also upregulated the expression of FSP1, suggesting a significant and parallel protective effect against ferroptosis in EBI following SAH in synergy with GPX4. Conclusion In summary, this research indicated that the PPARg activator OA augmented the neurological results in rodent models and diminished neuronal death. This neuroprotection was achieved primarily by suppressing neuronal ferroptosis. The underlying mechanism was associated with the alleviation of cellular death through the Nrf2/GPX4 and FSP1/CoQ10 pathways.

PurposeForests play a critical role in terrestrial ecosystem carbon cycling and the mitigation of global climate change. Intensive forest management and global climate change have had negative impacts on the quality of forest soils via soil acidification, reduction of soil organic carbon content, deterioration of soil biological properties, and reduction of soil biodiversity. The role of biochar in improving soil properties and the mitigation of greenhouse gas (GHG) emissions has been extensively documented in agricultural soils, while the effect of biochar application on forest soils remains poorly understood. Here, we review and summarize the available literature on the effects of biochar on soil properties and GHG emissions in forest soils.Materials and methodsThis review focuses on (1) the effect of biochar application on soil physical, chemical, and microbial properties in forest ecosystems; (2) the effect of biochar application on soil GHG emissions in forest ecosystems; and (3) knowledge gaps concerning the effect of biochar application on biogeochemical and ecological processes in forest soils.Results and discussionBiochar application to forests generally increases soil porosity, soil moisture retention, and aggregate stability while reducing soil bulk density. In addition, it typically enhances soil chemical properties including pH, organic carbon stock, cation exchange capacity, and the concentration of available phosphorous and potassium. Further, biochar application alters microbial community structure in forest soils, while the increase of soil microbial biomass is only a short-term effect of biochar application. Biochar effects on GHG emissions have been shown to be variable as reflected in significantly decreasing soil N2O emissions, increasing soil CH4 uptake, and complex (negative, positive, or negligible) changes of soil CO2 emissions. Moreover, all of the aforementioned effects are biochar-, soil-, and plant-specific.ConclusionsThe application of biochars to forest soils generally results in the improvement of soil physical, chemical, and microbial properties while also mitigating soil GHG emissions. Therefore, we propose that the application of biochar in forest soils has considerable advantages, and this is especially true for plantation soils with low fertility.

Subarachnoid hemorrhage (SAH) is a very common cerebrovascular disease with high disability and death worldwide. The pathophysiological process and mechanisms involved in aneurysm rupture in SAH are quite complex and divided into early brain injury (EBI) and delayed brain injury (DBI). The initial mechanical insult results in brain tissue and vascular disruption with hemorrhages and neuronal necrosis, and subsequently, secondary injury is evoked, resulting in diffuse cerebral damage in the peri-core area. The molecular mechanisms of neuronal death following aneurysmal subarachnoid hemorrhage are complex and are not entirely understood. Regarding the pathogenesis of brain damage, multiple cell death pathways were stimulated. Particular attention should be devoted to necrosis, apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis. In the present review, we discuss the mechanism of neuronal death after SAH and its influence on brain injury after SAH.

The green microalga Chromochloris zofingiensis can accumulate significant amounts of valuable carotenoids, mainly natural astaxanthin, a product with applications in functional food, cosmetics, nutraceuticals, and with potential therapeutic value in cardiovascular and neurological diseases. To optimize the production of astaxanthin, it is essential to monitor the content of astaxanthin in algal cells during cultivation. The widely used HPLC (high-performance liquid chromatography) method for quantitative astaxanthin determination is time-consuming and laborious. In the present work, we present a method using flow cytometry (FCM) for in vivo determination of the astaxanthin content and the carotenoid-to-chlorophyll ratio (Car/Chl) in mixotrophic C. zofingiensis. The method is based on the assessment of fluorescent characteristics of cellular pigments. The mean fluorescence intensity (MFI) of living cells was determined by FCM to monitor pigment formation based on the correlation between MFI detected in particular channels (FL1: 533 ± 15 nm; FL2: 585 ± 20 nm; FL3: >670 nm) and pigment content in algal cells. Through correlation and regression analysis, a linear relationship was observed between MFI in FL2 (band-pass filter, emission at 585 nm in FCM) and astaxanthin content (in HPLC) and applied for predicting astaxanthin content. With similar procedures, the relationships between MFI in different channels and Car/Chl ratio in mixotrophic C. zofingiensis were also determined. Car/Chl ratios could be estimated by the ratios of MFI (FL1/FL3, FL2/FL3). FCM is thus a highly efficient and feasible method for rapid estimation of astaxanthin content in the green microalga C. zofingiensis. The rapid FCM method is complementary to the current HPLC method, especially for rapid evaluation and prediction of astaxanthin formation as it is required during the high-throughput culture in the laboratory and mass cultivation in industry.

Background Exosomal microRNAs (miRs) derived from mesenchymal stem cells (MSCs) have been shown to play roles in the pathophysiological processes of sepsis. Moreover, miR-27b is highly enriched in MSC-derived exosomes. Herein, we aimed to investigate the potential role and downstream molecular mechanism of exosomal miR-27b in sepsis. Methods Inflammation was induced in bone marrow-derived macrophages (BMDMs) by lipopolysaccharide (LPS), and mice were made septic by cecal ligation and puncture (CLP). The expression pattern of miR-27b in MSC-derived exosomes was characterized using RT-qPCR, and its downstream gene was predicted by in silico analysis. The binding affinity between miR-27b, Jumonji D3 (JMJD3), or nuclear factor κB (NF-κB) was characterized to identify the underlying mechanism. We induced miR-27b overexpression or downregulation, along with silencing of JMJD3 or NF-κB to examine their effects on sepsis. The production of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 was detected by ELISA. Results miR-27b was highly expressed in MSC-derived exosomes. Mechanistic investigations showed that miR-27b targeted JMJD3. miR-27b decreased expression of pro-inflammatory genes by inhibiting the recruitment of JMJD3 and NF-κB at gene promoter region. Through this, MSC-derived exosomal miR-27b diminished production of pro-inflammatory cytokines in LPS-treated BMDMs and septic mice, which could be rescued by upregulation of JMJD3 and NF-κB. Besides, in vitro findings were reproduced by in vivo findings. Conclusion These data demonstrated that exosomal miR-27b derived from MSCs inhibited the development of sepsis by downregulating JMJD3 and inactivating the NF-κB signaling pathway.

Spontaneous subarachnoid hemorrhage (SAH) is a common cerebrovascular disease with high mortality. There is much basic research had confirmed that the molecular mechanism of early brain injury (EBI) after SAH. Neuron's death and dysfunction are important reasons for the neurological dysfunction in patients with SAH. Ferroptosis is a nonapoptotic form of cell death, the classical characterize base on the iron-dependent accumulation of toxic lipid reactive oxygen species. Previously studies had indicated that this mechanism in regulated cell death events observed in many diseases included cancer, tumor resistance, Alzheimer’s disease, Parkinson's disease, stroke, and intracerebral hemorrhage, etc. And it also may play a very important role in early brain injury after SAH. Outstanding issues include the relationship between ferroptosis and other forms of cell death after SAH, the specific molecular mechanisms of EBI, how to activate or inhibit ferroptosis can be exploited to achieve desirable anti-EBI, and need to find a new molecular markers of ferroptosis that can be used to detect and study this process in vivo after SAH.

Subarachnoid hemorrhage (SAH) occurs most commonly after rupture of an aneurysm, resulting in high disability and mortality due to the absence of effective therapy. Its subsequent stage, early brain injury (EBI), promotes the sustainable development of injury in the brain and ultimately leads to poor prognosis. As a new antiepileptic drug, the effect of perampanel on EBI after SAH is unknown. Pyroptosis, a process of inflammatory programmed cell death, has been confirmed in most studies to play a substantial role in aggravating SAH-post EBI. Similarly, oxidative stress is closely involved in neuronal pyroptosis and the pathophysiological mechanism of SAH-post EBI, leading to a devastating outcome for SAH patients. Nonetheless, no studies have been conducted to determine whether perampanel reduces pyroptosis and oxidative stress in the context of SAH-induced EBI. Rat SAH model via endovascular perforation was constructed in this study, to assess the neuroprotective effect of perampanel on SAH-post EBI, and to clarify the possible molecular mechanism. By means of the neurological score, brain edema detection, FJB staining, immunofluorescence, WB, ELISA, and ROS assay, we found that perampanel can improve neuroscores and reduce brain edema and neuronal degeneration at 24 h after SAH; we also found that perampanel reduced oxidative stress, neuronal pyroptosis, and inhibition of the SIRT3-FOXO3α pathway at 24 h after SAH. When 3-TYP, an inhibitor of SIRT3, was administered, the effects of perampanel on the SIRT3-FOXO3a pathway, antioxidant stress, and neuronal pyroptosis were reversed. Taken together, our data indicate that perampanel attenuates oxidative stress and pyroptosis following subarachnoid hemorrhage via the SIRT3/FOXO3α pathway. This study highlights the application value of perampanel in subarachnoid hemorrhage and lays a foundation for clinical research and later transformation of perampanel in SAH.

Subarachnoid hemorrhage (SAH) is a severe type of stroke featuring exceptionally high rate of morbidity and mortality due to the lack of effective management. Ferroptosis can be defined as a novel iron-dependent programmed cell death in contrast to classical apoptosis and necrosis. Astragaloside IV (AS-IV) is an active ingredient extracted from Astragalus membranaceus with established therapeutic effect on CNS diseases. However, the exact role of ferroptosis in Astragaloside IV-mediated neuroprotection after SAH is yet to be demonstrated. In the present study, the SAH model of SD male rats with endovascular perforation was used to gauge the neuroprotective effect of AS-IV on SAH-induced early brain injury (EBI) and to clarify the potential molecular mechanism. We found that the induction of SAH reduced the levels of SLC7A11 and glutathione peroxidase 4 (GPX4) in the brain, exacerbated iron accumulation, enhanced lipid reactive oxygen species (ROS) level, and stimulated neuronal ferroptosis. However, the administration of AS-IV and the ferroptosis inhibitor Ferrostatin-1 (Fer-1) enhanced the antioxidant capacity after SAH and suppressed the accumulation of lipid peroxides. Meanwhile, AS-IV triggered Nrf2/HO-1 signaling pathway and alleviated ferroptosis due to the induction of SAH. The Nrf2 inhibitor ML385 blocked the beneficial effects of neuroprotection. These results consistently suggest that ferroptosis is profoundly implicated in facilitating EBI in SAH, and that AS-IV thwarts the process of ferroptosis in SAH by activating Nrf2/HO-1 pathway.

Tilianin is a commonly used pharmaceutical ingredient with various biological activities such as antioxidant, anti-inflammatory, and anticancer, which is able to exert antitumor effects by inhibiting tumor cell proliferation, inducing apoptosis and inhibiting angiogenesis. Studies have demonstrated to be particularly useful in a variety of cancers such as liver, lung and gastric cancers. Quantitative analysis of Tilianin can improve the quality control of related drugs and assist in guiding clinical application and disease treatment. However, there are limited studies on the quantitative analysis of Tilianin. High performance liquid chromatography (HPLC) and mass spectrometry (MS) are commonly used methods for the quantitative analysis of the components, but they often require complex pretreatment steps and specialized analytical capabilities, and are sample-destructive. The method based on Raman spectroscopy and deep learning is a widely used non-destructive analysis method. For this reason, this paper proposes a residual self-attention mechanism model based on Raman spectroscopy and deep learning for quantitative analysis of 6 concentrations of Tilianin. Six different concentrations of Tilianin-methanol solutions were prepared, and a total of 120 spectral samples were collected, which were pre-processed and inputted into our Raman Spectrum with Self-Attention Quantification Net (RSAQN) for analyzing and predicting. The structure of this model not only focuses on the deep and shallow features of the spectrum, but also the information between different channels, and the self-attention mechanism further extracts the features and outputs the predicted values of Tilianin concentration through the fully connected layer. In this paper, five sets of comparison models are set up, including two machine learning models (Random Forest, K-Nearest Neighbors, Artificial Neural Network) and two deep learning models (Convolutional Neural Network and Variational Autoencoder), and the results show that the model in this paper fits the best, obtaining an R 2 of 0.9144, as well as a small error.