Adverse events reporting of XPO1 inhibitor - selinexor: a real-word analysis from FAERS database.

As the world's first oral nuclear export inhibitor, selinexor is increasingly being used in clinical applications for malignant tumors. However, there is no extensive exploration on selinexor's adverse events (ADEs), necessitating a real-word assessment of its clinical medication safety. FAERS data (July 2019-June 2023) were searched for selinexor ADE reports across all indications. Use the system organ class (SOC) and preferred terms (PT) from the medical dictionary for regulatory activities (MedDRA) to describe, categorize, and statistic ADEs. Disproportionality analysis was employed through calculation of reporting odds ratio (ROR) and proportional reporting ratio (PRR). Based on total of 4392 selinexor related ADE reports as the primary suspect (PS), of which 2595 instances were severe outcomes. The predominant ADEs included gastrointestinal disorders, myelosuppression symptoms, and various nonspecific manifestations. 124 signals associated with selinexor ADE were detected, and 10 of these top 15 signals were not included into the instructions. Our study provides real-world evidence regarding the drug safety of selinexor, which is crucial for clinicians to safeguard patients' health.

Mitochondria transplantation alleviates cardiomyocytes apoptosis through inhibiting AMPKα-mTOR mediated excessive autophagy.

The disruption of mitochondria homeostasis can impair the contractile function of cardiomyocytes, leading to cardiac dysfunction and an increased risk of heart failure. This study introduces a pioneering therapeutic strategy employing mitochondria derived from human umbilical cord mesenchymal stem cells (hu-MSC) (MSC-Mito) for heart failure treatment. Initially, we isolated MSC-Mito, confirming their functionality. Subsequently, we monitored the process of single mitochondria transplantation into recipient cells and observed a time-dependent uptake of mitochondria in vivo. Evidence of human-specific mitochondrial DNA (mtDNA) in murine cardiomyocytes was observed after MSC-Mito transplantation. Employing a doxorubicin (DOX)-induced heart failure model, we demonstrated that MSC-Mito transplantation could safeguard cardiac function and avert cardiomyocyte apoptosis, indicating metabolic compatibility between hu-MSC-derived mitochondria and recipient mitochondria. Finally, through RNA sequencing and validation experiments, we discovered that MSC-Mito transplantation potentially exerted cardioprotection by reinstating ATP production and curtailing AMPKα-mTOR-mediated excessive autophagy.

Carbon tax-driven technological innovation may accelerate the directional recovery of waste cooking oil into bio-jet fuel: An evolutionary game approach.

Biofuel production from waste cooking oil (WCO) offers an alternative to fossil fuels, especially for high-value bio-jet fuel. However, this industry is hindered by informal recyclers who covertly divert large amounts of WCO to illegal gutter oil production. Investigating the dynamic evolution of stakeholder behavior will help explore solutions. Thus, this study presents a tripartite evolutionary game model that includes the government, formal recyclers, and informal recyclers, aims to redesign the government intervention strategy to promote the directional flow of WCO from restaurant trash cans to bio-jet fuel production. We find that the evolutionary game model exists eight possible evolutionary stability strategies (ESSs), and the choice of each ESS depends mainly on the trade-off between costs and revenues for each stakeholder. The numerical study results reveal that formal recyclers are driven to carry out technological innovation by government support, profiting from bio-aviation kerosene products, and income from carbon emission reduction. These factors also have an indirect impact on the transformation of informal recyclers. Therefore, the government should provide adequate support for technological innovation to formal recyclers and increase their profitability of products to enable them to actively implement innovative strategies. This can be achieved by expanding the sales channels of bio-jet fuel products, implementing patent protection measures, and improving the carbon reduction trading mechanism. Furthermore, the government's high tax rate on formal recyclers and the significant profits earned by informal recyclers through illegal gutter oil production may dissuade them from transitioning their businesses. Above findings are in line with the actual issues of WCO recycling and provide a new dynamic decision-making method for enterprises and government managers.

The design, synthesis and bioactivity evaluation of novel androgen receptor degraders based on hydrophobic tagging.

Prostate Cancer (PCa) easily progress to metastatic Castration-Resistant Prostate Cancer (mCRPC) that remains a significant cause of cancer-related death. Androgen receptor (AR)-dependent transcription is a major driver of prostate tumor cell proliferation. Proteolysis-targeting chimaera (PROTAC) technology based on Hydrophobic Tagging (HyT) represents an intriguing strategy to regulate the function of therapeutically androgen receptor proteins. In the present study, we have designed, synthesized, and evaluated a series of PROTAC-HyT AR degraders using AR antagonists, RU59063, which were connected with adamantane-based hydrophobic moieties by different alkyl chains. Compound D-4-6 exhibited significant AR protein degradation activity, with a degradation rate of 57 % at 5 µM and nearly 90 % at 20 µM in 24 h, and inhibited the proliferation of LNCaP cells significantly with an IC50 value of 4.77 ± 0.26 µM in a time-concentration-dependent manner. In conclusion, the present study lays the foundation for the development of a completely new class of therapeutic agents for the treatment of mCRPC, and further design and synthesis of AR-targeting degraders are currently in progress for better degradation rate.

Polyvinylpyrrolidone-Coated Cubic Hollow Nanocages of PdPt3 and PdIr3 as Highly Efficient Self-Cascade Uricase/Peroxidase Mimics.

Uricase-catalyzed uric acid (UA) degradation has been applied for hyperuricemia therapy, but this medication is limited by H2O2 accumulation, which can cause oxidative stress of cells, resulting in many other health issues. Herein, we report a robust cubic hollow nanocage (HNC) system based on polyvinylpyrrolidone-coated PdPt3 and PdIr3 to serve as highly efficient self-cascade uricase/peroxidase mimics to achieve the desired dual catalysis for both UA degradation and H2O2 elimination. These HNCs have hollow cubic shape with average wall thickness of 1.5 nm, providing desired synergy to enhance catalyst's activity and stability. Density functional theory calculations suggest the PdIr3 HNC surface tend to promote OH*/O* desorption for better peroxidase-like catalysis, while the PdPt3 HNC surface accelerates the UA oxidation by facilitating O2-to-H2O2 conversion. The dual catalysis power demonstrated by these HNCs in cell studies suggests their great potential as a new type of nanozyme for treating hyperuricemia.

Enhancing photodynamic immunotherapy by reprograming the immunosuppressive tumor microenvironment with hypoxia relief.

Tumor hypoxia impairs the generation of reactive oxygen species and the induction of immunogenic cell death (ICD) for photodynamic therapy (PDT), thus impeding its efficacy and the subsequent immunotherapy. In addition, hypoxia plays a critical role in forming immunosuppressive tumor microenvironments (TME) by regulating the infiltration of immunosuppressive tumor-associated macrophages (TAMs) and the expression of programmed death ligand 1 (PD-L1). To simultaneously tackle these issues, a MnO2-containing albumin nanoplatform co-delivering IR780, NLG919, and a paclitaxel (PTX) dimer is designed to boost photodynamic immunotherapy. The MnO2-catalyzed oxygen supply bolsters the efficacy of PDT and PTX-mediated chemotherapy, collectively amplifying the induction of ICD and the expansion of tumor-specific cytotoxic T lymphocytes (CTLs). More importantly, hypoxia releif reshapes the immunosuppressive TME via down-regulating the intratumoral infiltration of M2-type TAMs and the PD-L1 expression of tumor cells to enhance the infiltration and efficacy of CTLs in combination with immune checkpoint blockade (ICB) by NLG919, consequently eradicating primary tumors and almost completely preventing tumor relapse and metastasis. This study sets an example of enhanced immunotherapy for breast cancers through dual ICD induction and simultaneous immunosuppression modulation via both hypoxia relief and ICB, providing a strategy for the treatment of other hypoxic and immunosuppressive cancers.

Human umbilical cord mesenchymal stem cells protect against ferroptosis in acute liver failure through the IGF1-hepcidin-FPN1 axis and inhibiting iron loading.

Acute liver failure (ALF) is a significant global issue with elevated morbidity and mortality rates. There is an urgent and pressing need for secure and effective treatments. Ferroptosis, a novel iron-dependent regulation of cell death, plays a significant role in multiple pathological processes associated with liver diseases, including ALF. Several studies have demonstrated that mesenchymal stem cells (MSCs) have promising therapeutic potential in the treatment of ALF. This study aims to investigate the positive effects of MSCs against ferroptosis in an ALF model and explore the underlying molecular mechanisms of their therapeutic function. Our results show that intravenously injected MSCs protect against ferroptosis in ALF mouse models. MSCs decrease iron deposition in the liver of ALF mice by downregulating hepcidin level and upregulating FPN1 level. MSCs labelled with Dil are mainly observed in the hepatic sinusoid and exhibit colocalization with the macrophage marker CD11b fluorescence. ELISA demonstrates a high level of IGF1 in the CCL 4+MSC group. Suppressing the IGF1 effect by the PPP blocks the therapeutic effect of MSCs against ferroptosis in ALF mice. Furthermore, disruption of IGF1 function results in iron deposition in the liver tissue due to impaired inhibitory effects of MSCs on hepcidin level. Our findings suggest that MSCs alleviate ferroptosis induced by disorders of iron metabolism in ALF mice by elevating IGF1 level. Moreover, MSCs are identified as a promising cell source for ferroptosis treatment in ALF mice.

[Construction of A Nomogram Prediction Model for PD-L1 Expression 
in Non-small Cell Lung Cancer Based on 18F-FDG PET/CT Metabolic Parameters].

BACKGROUND: In recent years, immunotherapy represented by programmed cell death 1 (PD-1)/programmed cell death ligand 1 (PD-L1) immunosuppressants has greatly changed the status of non-small cell lung cancer (NSCLC) treatment. PD-L1 has become an important biomarker for screening NSCLC immunotherapy beneficiaries, but how to easily and accurately detect whether PD-L1 is expressed in NSCLC patients is a difficult problem for clinicians. The aim of this study was to construct a Nomogram prediction model of PD-L1 expression in NSCLC patients based on 18F-fluorodeoxy glucose (18F-FDG) positron emission tomography/conputed tomography (PET/CT) metabolic parameters and to evaluate its predictive value. METHODS: Retrospective collection of 18F-FDG PET/CT metabolic parameters, clinicopathological information and PD-L1 test results of 155 NSCLC patients from Inner Mongolia People's Hospital between September 2016 and July 2021. The patients were divided into the training group (n=117) and the internal validation group (n=38), and another 51 cases of NSCLC patients in our hospital between August 2021 and July 2022 were collected as the external validation group according to the same criteria. Then all of them were categorized according to the results of PD-L1 assay into PD-L1+ group and PD-L1- group. The metabolic parameters and clinicopathological information of patients in the training group were analyzed by univariate and binary Logistic regression, and a Nomogram prediction model was constructed based on the screened independent influencing factors. The effect of the model was evaluated by receiver operating characteristic (ROC) curve, calibration curve and decision curve analysis (DCA) in both the training group and the internal and external validation groups. RESULTS: Binary Logistic regression analysis showed that metabolic tumor volume (MTV), gender and tumor diameter were independent influences on PD-L1 expression. Then a Nomogram prediction model was constructed based on the above independent influences. The ROC curve for the model in the training group shows an area under the curve (AUC) of 0.769 (95%CI: 0.683-0.856) with an optimal cutoff value of 0.538. The AUC was 0.775 (95%CI: 0.614-0.936) in the internal validation group and 0.752 (95%CI: 0.612-0.893) in the external validation group. The calibration curves were tested by the Hosmer-Lemeshow test and showed that the training group (χ2=0.040, P=0.979), the internal validation group (χ2=2.605, P=0.271), and the external validation group (χ2=0.396, P=0.820) were well calibrated. The DCA curves show that the model provides clinical benefit to patients over a wide range of thresholds (training group: 0.00-0.72, internal validation group: 0.00-0.87, external validation group: 0.00-0.66). CONCLUSIONS: The Nomogram prediction model constructed on the basis of 18F-FDG PET/CT metabolic parameters has greater application value in predicting PD-L1 expression in NSCLC patients.

Multi-omics analysis reveals interferon-stimulated gene OAS1 as a prognostic and immunological biomarker in pan-cancer.

Introduction: OAS1(2'-5'-oligoadenylate synthetase 1) is a member of the Interferon-Stimulated Genes which plays an important role in the antiviral process. In recent years, the role of OAS1 in tumors has attracted attention, and it was found to be associated with prognosis in several tumors. However, the mechanism by which OAS1 affects tumors is unclear and pan-cancer study of OAS1 is necessary to better understand its implication in cancers. Methods: The expression, prognostic value, genetic alteration, alternative splicing events of OAS1 in pan-cancers were analyzed using TCGA, GTEx, HPA, GEPIA and OncoSplicing databases. OAS1 associated immune cell infiltration was evaluated using the ESTIMATE, xCell, CIBERSORT and QUANTISEQ algorithm. Single cell transcriptome data download using TISH database. Finally, the roles of the OAS1 on apoptosis, migration and invasion were investigated in two pancreatic cancer cells. Results: Our results revealed significant differences in OAS1 expression among various tumors, which had prognostic implications. In addition, we investigated the impact of OAS1 on genomic stability, methylation status, and other factors across different types of cancer, and the effects of these factors on prognosis. Notably, our study also demonstrated that OAS1 overexpression can contribute to CTL dysfunction and macrophage M2 polarization. In addition, cell experiments showed that the knockdown of OAS1 could reduce the invasive ability and increased the apoptosis rate of PAAD cells. Discussion: These results confirmed that OAS1 could be a prognostic biomarker and therapeutic target for its potential role in CTL dysfunction and macrophage M2 polarization.

Recent Advances of Tumor Microenvironment-Responsive Nanomedicines-Energized Combined Phototherapy of Cancers.

Photodynamic therapy (PDT) has emerged as a powerful tumor treatment tool due to its advantages including minimal invasiveness, high selectivity and thus dampened side effects. On the other side, the efficacy of PDT is severely frustrated by the limited oxygen level in tumors, thus promoting its combination with other therapies, particularly photothermal therapy (PTT) for bolstered tumor treatment outcomes. Meanwhile, nanomedicines that could respond to various stimuli in the tumor microenvironment (TME) provide tremendous benefits for combined phototherapy with efficient hypoxia relief, tailorable drug release and activation, improved cellular uptake and intratumoral penetration of nanocarriers, etc. In this review, we will introduce the merits of combining PTT with PDT, summarize the recent important progress of combined phototherapies and their combinations with the dominant tumor treatment regimen, chemotherapy based on smart nanomedicines sensitive to various TME stimuli with a focus on their sophisticated designs, and discuss the challenges and future developments of nanomedicine-mediated combined phototherapies.

A mitochondrial EglN1-AMPKα axis drives breast cancer progression by enhancing metabolic adaptation to hypoxic stress.

Mitochondria play essential roles in cancer cell adaptation to hypoxia, but the underlying mechanisms remain elusive. Through mitochondrial proteomic profiling, we here find that the prolyl hydroxylase EglN1 (PHD2) accumulates on mitochondria under hypoxia. EglN1 substrate-binding region in the ß2ß3 loop is responsible for its mitochondrial translocation and contributes to breast tumor growth. Furthermore, we identify AMP-activated protein kinase alpha (AMPKα) as an EglN1 substrate on mitochondria. The EglN1-AMPKα interaction is essential for their mutual mitochondrial translocation. After EglN1 prolyl-hydroxylates AMPKα under normoxia, they rapidly dissociate following prolyl-hydroxylation, leading to their immediate release from mitochondria. In contrast, hypoxia results in constant EglN1-AMPKα interaction and their accumulation on mitochondria, leading to the formation of a Ca2+ /calmodulin-dependent protein kinase 2 (CaMKK2)-EglN1-AMPKα complex to activate AMPKα phosphorylation, ensuring metabolic homeostasis and breast tumor growth. Our findings identify EglN1 as an oxygen-sensitive metabolic checkpoint signaling hypoxic stress to mitochondria through its ß2ß3 loop region, suggesting a potential therapeutic target for breast cancer.

A cleaved METTL3 potentiates the METTL3-WTAP interaction and breast cancer progression.

N6-methyladenosine (m6A) methylation of RNA by the methyltransferase complex (MTC), with core components including METTL3-METTL14 heterodimers and Wilms' tumor 1-associated protein (WTAP), contributes to breast tumorigenesis, but the underlying regulatory mechanisms remain elusive. Here, we identify a novel cleaved form METTL3a (residues 239-580 of METTL3). We find that METTL3a is required for the METTL3-WTAP interaction, RNA m6A deposition, as well as cancer cell proliferation. Mechanistically, we find that METTL3a is essential for the METTL3-METTL3 interaction, which is a prerequisite step for recruitment of WTAP in MTC. Analysis of m6A sequencing data shows that depletion of METTL3a globally disrupts m6A deposition, and METTL3a mediates mammalian target of rapamycin (mTOR) activation via m6A-mediated suppression of TMEM127 expression. Moreover, we find that METTL3 cleavage is mediated by proteasome in an mTOR-dependent manner, revealing positive regulatory feedback between METTL3a and mTOR signaling. Our findings reveal METTL3a as an important component of MTC, and suggest the METTL3a-mTOR axis as a potential therapeutic target for breast cancer.

Controllable hypoxia-activated chemotherapy as a dual enhancer for synergistic cancer photodynamic immunotherapy.

The efficacy of photodynamic therapy (PDT) is severely limited by the hypoxic tumor microenvironment (TME), while the performance of PDT-aroused antitumor immunity is frustrated by the immunosuppressive TME and deficient immunogenic cell death (ICD) induction. To simultaneously tackle these pivotal problems, we herein create an albumin-based nanoplatform co-delivering IR780, NLG919 dimer and a hypoxia-activated prodrug tirapazamine (TPZ) as the dual enhancer for synergistic cancer therapy. Under NIR irradiation, IR780 generates 1O2 for PDT, which simultaneously cleaves the ROS-sensitive linker for triggered TPZ release, and activates its chemotherapy via exacerbated tumor hypoxia. Meanwhile, firstly found by us, TPZ-mediated chemotherapy boosts PDT-induced tumor ICD to evoke stronger antitumor immunity including the development of tumor-specific cytotoxic T lymphocytes (CTLs). Eventually, enriched intratumoral GSH triggers the activation of NLG919 to mitigate the immunosuppressive TME via specific indoleamine 2,3-dioxygenase 1 (IDO-1) inhibition, consequently promoting the intratumoral infiltration of CTLs and the killing of both primary and distant tumors, while the resultant memory T cells allows nearly 100% suppression of tumor recurrence and metastasis. This nanoplatform sets up an example for dully enhanced photodynamic immunotherapy of breast cancer via hypoxia-activated chemotherapy, and paves a solid way for the treatment of other hypoxic and immunosuppressive malignant tumors.

Nivalenol disrupts mitochondria functions during porcine oocyte meiotic maturation.

Oocyte maturation is important for fertility in mammals, since the quality of oocytes directly affects fertilization, embryo attachment and survival. Nivalenol is widely present in nature as a common toxin that contaminates grain and feed, and it has been reported to cause acute toxicity, immunotoxicity, reproductive toxicity and carcinogenic effects. In this study, we explored the impact of nivalenol on the porcine oocyte maturation and its possible mechanisms. The extrusion of the first polar body was significantly inhibited after incubating oocytes with nivalenol. Meanwhile, nivalenol exposure led to the abnormal distribution of mitochondria, aberrant calcium concentration and the reduction of membrane potential caused a significant decrease in the capacity of mitochondria to generate ATP. In addition, nivalenol induced oxidative stress, and the level of ROS was significantly increased in the nivalenol-treated group, which was confirmed by the perturbation of oxidative stress-related genes. We found that nivalenol-treated oocytes showed positive Annexin-V and γH2A.X signals, indicating the occurrence of apoptosis and DNA damage. In all, our data suggest that nivalenol disrupted porcine oocyte maturation through its effects on mitochondria-related oxidative stress, apoptosis and DNA damage.

Long-term survival with anlotinib as a front-line treatment in an elderly NSCLC patient: A case report.

Background: Half of the population of non-small cell lung cancer (NSCLC) patients are older than 70 years and have limited therapeutic options due to poor tolerance and being excluded in most clinical trials. Anlotinib hydrochloride, a novel oral multi-target tyrosine kinase inhibitor, has been approved for the standard third-line treatment for NSCLC in China. Herein we report an elderly NSCLC patient without any driver gene mutations who was undergoing anlotinib as a front-line treatment and who achieved long-term survival. Case summary: The 77-year-old male patient was admitted to the hospital for chest tightness after engaging in physical activity for a week. The patient has been diagnosed with stage IIIB driver gene-negative squamous cell lung carcinoma. After that, he was treated with anlotinib for 2 years and 10 months from the first diagnosis until the last disease progression. Briefly, anlotinib combined with platinum-based chemotherapy was performed as the first-line therapy over six cycles. After 6 more cycles of anlotinib monotherapy maintenance, disease progression occurred. Then, anlotinib combined with tegafur was administered as a salvage treatment, and the disease was controlled again. After 29 cycles of anlotinib combined with tegafur regimens, the disease progressed finally. The patient achieved a total of 34 months of progression-free survival after anlotinib was used as the front-line treatment. He is still alive with a good performance status now (performance status score: 1). Conclusion: This patient achieved long-term survival using anlotinib as a front-line regimen combined with chemotherapy.

Reactive oxygen species-powered cancer immunotherapy: Current status and challenges.

Reactive oxygen species (ROS) are crucial signaling molecules that can arouse immune system. In recent decades, ROS has emerged as a unique therapeutic strategy for malignant tumors as (i) it can not only directly reduce tumor burden but also trigger immune responses by inducing immunogenic cell death (ICD); and (ii) it can be facilely generated and modulated by radiotherapy, photodynamic therapy, sonodynamic therapy and chemodynamic therapy. The anti-tumor immune responses are, however, mostly downplayed by the immunosuppressive signals and dysfunction of effector immune cells within the tumor microenvironment (TME). The past years have seen fierce developments of various strategies to power ROS-based cancer immunotherapy by e.g. combining with immune checkpoints inhibitors, tumor vaccines, and/or immunoadjuvants, which have shown to potently inhibit primary tumors, metastatic tumors, and tumor relapse with limited immune-related adverse events (irAEs). In this review, we introduce the concept of ROS-powered cancer immunotherapy, highlight the innovative strategies to boost ROS-based cancer immunotherapy, and discuss the challenges in terms of clinical translation and future perspectives.

High-Efficiency and Stable Long-Persistent Luminescence from Undoped Cesium Cadmium Chlorine Crystals Induced by Intrinsic Point Defects.

Application of long-persistent luminescence (LPL) materials in many technological fields is in the spotlight. However, the exploration of undoped persistent luminescent materials with high emission efficiency, robust stability, and long persistent duration remains challenging. Here, inorganic cesium cadmium chlorine (CsCdCl3 ) is developed, featuring remarkable LPL characteristics at room temperature, which is synthesized by a facile hydrothermal method. Excited by ultraviolet light, the CsCdCl3 crystals exhibit an intense yellow emission with a large photoluminescence quantum yield of ≈90%. Different from the reported systems with lanthanides or transition metals doping, the CsCdCl3 crystals without dopants perform yellow LPL with a long duration of 6000 s. Joint experiment-theory characterizations reveal the intrinsic point defects of CsCdCl3 act as the trap centers of excited electrons and the carrier de-trapping process from such trap sites to localized emission centers contributes to the LPL. Encouraged by the attractive fluorescence and persistent luminescence as well as good stability of CsCdCl3 against environment oxygen/moisture (75%), heat (100 °C for 10 h), and ultraviolet light irradiation, an effective dual-mode information storage-reading application is demonstrated. The results open up a new frontier for exploring LPL materials without dopants and provide an opportunity for advanced information storage compatible for practical applications.

Recent applications of phase-change materials in tumor therapy and theranostics.

Phase-change materials (PCMs) are a type of special material which can store and release a large amount of thermal energy without any significant temperature change. They are emerging in recent years as a promising functional material in tumor therapy and theranostics due to their accurate responses to the temperature variations, biocompatibility and low toxicity. In this review, we will introduce the main types of PCMs and their desirable physiochemical properties for biomedical applications, and highlight the recent progress of PCM's applications in the modulated release of antitumor drugs, with special attentions paid to various ways to initiate temperature-dependent phase change, the concomitant thermal therapy and its combination with or activation of other therapies, particularly unconventional therapies. We will also summarize PCM's recent applications in tumor theranostics, where both drugs and imaging probes are delivered by PCMs for controlled drug release and imaging-guided therapy. Finally, the future perspectives and potential limitations of harnessing PCMs in tumor therapy will be discussed.

Efficacy of non-invasive photodynamic therapy for female lower reproductive tract diseases associated with HPV infection: a comprehensive meta-analysis.

Photodynamic therapy (PDT) is a proposed non-invasive, highly effective, and fertility-preserving method for the treatment of lower reproductive tract diseases in women. We aim to evaluate the effect of PDT on complete remission, recurrence, and HPV clearance in diseases of the female lower reproductive tract associated with the human papillomavirus (HPV) infection in this meta-analysis. PubMed, EMBASE, Scopus, Cochrane Library, and China National Knowledge Infrastructure databases were searched to compare PDT with other treatments for complete remission, recurrence, and HPV clearance in women with lower genital tract disease. Fixed or random effect models were performed to assess the pooled effect size. Sensitivity analysis was performed to detect heterogeneity in the included studies. The Begg and Egger test assessed publication bias. There were 12 studies qualified for inclusion; compared to other treatments, PDT had a significant advantage in complete remission (OR=2.97, 95%CI, 2.18-4.04, I2=0, P<0. 001) and recurrence (OR, 0.21; 95%CI, 0.11-0.39; I2=34.9%, P<0. 001). Furthermore, PDT clears HPV quickly and lastingly compared to other therapies (OR, 2.65; 95% CI, 1.41-4.95; I2=71.0%, P=0.002). In addition, the heterogeneity test of sensitivity analysis suggested that the results were robust. Begg test (P=0.73) and Egger test (P=0.71) showed no publication bias. PDT treats diseases of the female lower reproductive tract associated with HPV infection: high complete remission, low recurrence, and rapid and lasting HPV clearance. The PDT seems to be a non-invasive, effective, and promising treatment of female lower reproductive tract diseases associated with HPV infection.

Prognostic Analysis of Skin Scar Loosening and Tissue-Expansive Autologous Skin Grafting in the Treatment of Skin Postburn Scars.

BACKGROUND: This study aims to observe and investigate the clinical value of scar loosening and tissue-expansive autologous skin grafting in the treatment of postburn scars and independent risk characteristics for surgery-related complications. METHODS: We retrospectively analyzed 94 cases with postburn scars, and all patients were treated with scar loosening and autologous skin grafting. Overall therapeutic effects were evaluated using the standard of cure and improvement of clinical diseases. Burn Specific Health Scale-brief was used to analyze patients' quality of life. The visual analog scale scores were used to analyze esthetic satisfaction. Surgery-related complications were recorded, and logistic regression model was used to analyze independent factors affecting surgery-related complications. RESULTS: As for overall efficacy evaluation, 50 cases were cured, 19 cases were markedly improved, 17 cases improved, and 8 cases were detected and tested, and the overall effective rate was 91.4%. The Burn Specific Health Scale-brief and visual analog scale score showed a trend of increasing gradually. It indicated that the patients were satisfied with the operation and their quality of life was improved. The logistic regression model showed that history of skin disease (OR=1.53 (1.08-2.16), P =0.02) and skin area (OR=2.50 (1.22-4.50), P <0.01) were significantly associated with surgery-related complications. CONCLUSIONS: Scar loosening and autologous skin grafting is a safe and effective treatment. The history of skin disease and skin area was the independent factors for surgery-related complications.