Autophagy flux in bladder cancer: Cell death crosstalk, drug and nanotherapeutics.

Autophagy, a self-digestion mechanism, has emerged as a promising target in the realm of cancer therapy, particularly in bladder cancer (BCa), a urological malignancy characterized by dysregulated biological processes contributing to its progression. This highly conserved catabolic mechanism exhibits aberrant activation in pathological events, prominently featured in human cancers. The nuanced role of autophagy in cancer has been unveiled as a double-edged sword, capable of functioning as both a pro-survival and pro-death mechanism in a context-dependent manner. In BCa, dysregulation of autophagy intertwines with cell death mechanisms, wherein pro-survival autophagy impedes apoptosis and ferroptosis, while pro-death autophagy diminishes tumor cell survival. The impact of autophagy on BCa progression is multifaceted, influencing metastasis rates and engaging with the epithelial-mesenchymal transition (EMT) mechanism. Pharmacological modulation of autophagy emerges as a viable strategy to impede BCa progression and augment cell death. Notably, the introduction of nanoparticles for targeted autophagy regulation holds promise as an innovative approach in BCa suppression. This review underscores the intricate interplay of autophagy with cell death pathways and its therapeutic implications in the nuanced landscape of bladder cancer.

Effects of synchronous intermissive multi-ultrasound and esterification dual modification on functionalities of starch and its emulsion stabilization ability.

Dodecenylsuccinic anhydride (DDSA) has been widely used to obtain amphiphilic starches. In this study, we investigated the functionalities of synchronous intermissive multi-ultrasound-assisted esterified starch. Compared to native starch (NS), it was deduced that multi-ultrasound-modified starch (US), esterified starch (ES), and multi-ultrasound-assisted esterified starch (UES) exhibited increased viscosities but reduced gelatinization temperatures and thermal stabilities. The viscoelastic moduli, retrogradation behaviors and hydrophobicity of the ES and UES species significantly altered. Moreover, the results of structural characterization suggested that esterification reduced the molecular weight and structural order of starch, whereas the intermissive ultrasonication treatment did not aggravate the structural disruption of ES. Additionally, compared with NS and US, the emulsification abilities of the ES and UES specimens were improved, leading to the desirable effect of stabilizing astaxanthin. Overall, this study provides a method for preparing amphiphilic starch, which can be exploited as a potential emulsifier and emulsion stabilizer for bioactive compounds.

Immune modulatory roles of radioimmunotherapy: biological principles and clinical prospects.

Radiation therapy (RT) not only can directly kill tumor cells by causing DNA double-strand break, but also exerts anti-tumor effects through modulating local and systemic immune responses. The immunomodulatory effects of RT are generally considered as a double-edged sword. On the one hand, RT effectively enhances the immunogenicity of tumor cells, triggers type I interferon response, induces immunogenic cell death to activate immune cell function, increases the release of proinflammatory factors, and reshapes the tumor immune microenvironment, thereby positively promoting anti-tumor immune responses. On the other hand, RT stimulates tumor cells to express immunosuppressive cytokines, upregulates the function of inhibitory immune cells, leads to lymphocytopenia and depletion of immune effector cells, and thus negatively suppresses immune responses. Nonetheless, it is notable that RT has promising abscopal effects and may achieve potent synergistic effects, especially when combined with immunotherapy in the daily clinical practice. This systematic review will provide a comprehensive profile of the latest research progress with respect to the immunomodulatory effects of RT, as well as the abscopal effect of radioimmunotherapy combinations, from the perspective of biological basis and clinical practice.

RtNAC055 promotes drought tolerance via a stomatal closure pathway linked to methyl jasmonate/hydrogen peroxide signaling in Reaumuria trigyna.

The stomata regulate CO2 uptake and efficient water usage, thereby promoting drought stress tolerance. NAC proteins (NAM, ATAF1/2, and CUC2) participate in plant reactions following drought stress, but the molecular mechanisms underlying NAC-mediated regulation of stomatal movement are unclear. In this study, a novel NAC gene from Reaumuria trigyna, RtNAC055, was found to enhance drought tolerance via a stomatal closure pathway. It was regulated by RtMYC2 and integrated with jasmonic acid signaling and was predominantly expressed in stomata and root. The suppression of RtNAC055 could improve jasmonic acid and H2O2 production and increase the drought tolerance of transgenic R. trigyna callus. Ectopic expression of RtNAC055 in the Arabidopsis atnac055 mutant rescued its drought-sensitive phenotype by decreasing stomatal aperture. Under drought stress, overexpression of RtNAC055 in poplar promoted ROS (H2O2) accumulation in stomata, which accelerated stomatal closure and maintained a high photosynthetic rate. Drought upregulated the expression of PtRbohD/F, PtP5CS2, and PtDREB1.1, as well as antioxidant enzyme activities in heterologous expression poplars. RtNAC055 promoted H2O2 production in guard cells by directly binding to the promoter of RtRbohE, thus regulating stomatal closure. The stress-related genes RtDREB1.1/P5CS1 were directly regulated by RtNAC055. These results indicate that RtNAC055 regulates stomatal closure by maintaining the balance between the antioxidant system and H2O2 level, reducing the transpiration rate and water loss, and improving photosynthetic efficiency and drought resistance.

Functionality differences between esterified and pregelatinized esterified starches simultaneously prepared by octenyl succinic anhydride modification and its application in dough.

Octenyl succinic anhydride (OSA)-modified starches have gained widespread interest, but the modification can produce two starches with different states ignored. Herein, the two types of starches, esterified starch (ES) and pregelatinized esterified starch (PES), prepared by OSA modification were separated, and their structural and functional characteristics were comprehensively explored. Results showed that compared with native starch (NS), ES and PES exhibited high water-holding capacity, solubility, and swelling power and significantly decreased pasting temperature and thermal stability. Dynamic rheological tests illustrated that OSA modification changed the rheological behavior of starches. Fourier transform infrared spectroscopy confirmed that PES with higher degree of substitution showed more obvious ester carbonyl and carboxylate groups than ES. Laser confocal micro-Raman spectroscopy revealed that the short-range molecular order of ES, especially PES, decreased after modification. X-ray diffraction indicated that OSA modification disrupted the crystalline structure of starch, and that more amylose-lipid complex was formed in PES. Scanning electron microscopy showed that OSA modification eroded starchs surface and reduced its smoothness, and significantly disrupted PES integrity. ES and PES could be developed as food additives for retrogradation inhibition of dough. These results provide new insights into OSA modification and expand its functional application in foods.

miRNA-211-5p inhibition enhances the protective effect of hucMSC-derived exosome in Aß1-40 -induced SH-SY5Y cells by increasing NEP expression.

Exosomes derived from human umbilical cord mesenchymal stem cells (hucMSCs) could alleviate Alzheimer's disease (AD) defects. Additionally, engineered exosomes are more effective in treating diseases. In this study, we established an in vitro model of AD by treating SH-SY5Y cells with Aß1-40 . We observed that incubation with hucMSC-derived exosomes effectively protected SH-S5Y5 cells from Aß1-40 -induced damage. Since NEP plays a central role in suppressing AD development, we screened NEP-targeting miRNAs that are differentially expressed in control and AD patients. We identified miR-211-5p as a potent repressor of NEP expression. Exosomes purified from hucMSCs overexpressing miR-211-5p inhibitor exhibited significantly greater efficiency than control exosomes in mitigating the injury caused by Aß1-40 treatment. However, this enhanced protective effect was nullified by the knockdown of NEP. These observations demonstrate that inhibition of miR-211-5p has the potential to improve the efficacy of hucMSC-derived exosomes in AD treatment by increasing NEP expression.

Inflammatory response-based prognostication and personalized therapy decisions in clear cell renal cell cancer to aid precision oncology.

OBJECTIVE: The impact of inflammatory response on tumor development and therapeutic response is of significant importance in clear cell renal cell carcinoma (ccRCC). The customization of specialized prognostication approaches and the exploration of supplementary treatment options hold critical clinical implications in relation to the inflammatory response. METHODS: In the present study, unsupervised clustering was implemented on TCGA-KIRC tumors using transcriptome profiles of inflammatory response genes, which was then validated in two ccRCC datasets (E-MATB-1980 and ICGC) and two immunotherapy datasets (IMvigor210 and Liu et al.) via SubMap and NTP algorithms. Combining co-expression and LASSO analyses, inflammatory response-based scoring system was defined, which was evaluated in pan-cancer. RESULTS: Three reproducible inflammatory response subtypes (named IR1, IR2 and IR3) were determined and independently verified, each exhibiting distinct molecular, clinical, and immunological characteristics. Among these subtypes, IR2 had the best OS outcomes, followed by IR3 and IR1. In terms of anti-angiogenic agents, sunitinib may be appropriate for IR1 patients, while axitinib and pazopanib may be suitable for IR2 patients, and sorafenib for IR3 patients. Additionally, IR1 patients might benefit from anti-CTLA4 therapy. A scoring system called IRscore was defined for individual ccRCC patients. Patients with high IRscore presented a lower response rate to anti-PD-L1 therapy and worse prognostic outcomes. Pan-cancer analysis demonstrated the immunological features and prognostic relevance of the IRscore. CONCLUSION: Altogether, characterization of inflammatory response subtypes and IRscore provides a roadmap for patient risk stratification and personalized treatment decisions, not only in ccRCC, but also in pan-cancer.

A comparison of the burden of knee osteoarthritis attributable to high body mass index in China and globally from 1990 to 2019.

Background: Excess body mass index (BMI) plays a key role in the onset and progression of knee osteoarthritis (knee OA). However, the burden of knee OA attributable to high BMI at the global, Chinese, and regional levels have received far too little attention. The aim of this study is to provide evidence to support the design of policy by investigating long-term trends of years lived with disability (YLDs) for knee OA. Methods: To illustrate the trends of YLDs for knee OA attributable to high BMI and the temporal trends of the YLDs rate by age, period, and cohort, Joinpoint regression software and age-period-cohort (APC) were used to analyze the YLDs data of knee OA from the Global Burden of Disease (GBD) 2019. Results: In China, there were 549,963.5 YLDs for knee OA attributable to high BMI in 2019, which had increased by 460.7% since 1990. From 1990 to 2019, age-standardized disability-adjusted life year rate (ASDR) of knee OA attributable to high BMI trended upwards. The average annual percent change (AAPC) of knee OA attributable to high BMI in China and globe were 3.019, 1.419%, respectively. The longitudinal age curve of the APC model showed that the YLDs rates of knee OA due to high BMI increased with age, and YLDs rates were higher among females than males. The period rate ratios (RRs) of knee OA due to high BMI increased significantly. The cohort RRs of knee OA due to high BMI increased among those born between 1900 and 1970. The net drifts of knee OA attributable to high BMI in China and globe were above 1. Compared with global condition, the net drift values of knee OA attributable to high BMI in China was higher. Compared with females, males had higher net drift value. Countries with high socio-demographic index (SDI) have a much higher burden of knee OA caused by high BMI than countries with low SDI. Conclusion: In China, high BMI is a substantial cause of knee OA, the incidence of which has been increasing since 1990. In addition, women and the elderly are more vulnerable to knee OA caused by high BMI. The Chinese government must take the long-term impact of high BMI on knee OA into account and implement effective public health policies and resort to interventions to reduce the burden as soon as possible.

ANGPTL3 negatively regulates IL-1ß-induced NF-κB activation by inhibiting the IL1R1-associated signaling complex assembly.

Interleukin-1ß (IL-1ß)-induced signaling is one of the most important pathways in regulating inflammation and immunity. The assembly of the receptor complex, consisting of the ligand IL-1ß, the IL-1 receptor (IL-1R) type 1 (IL1R1), and the IL-1R accessory protein (IL1RAP), initiates this signaling. However, how the IL1R1-associated complex is regulated remains elusive. Angiopoietin like 3 (ANGPTL3), a key inhibitor of plasma triglyceride clearance, is mainly expressed in the liver and exists in both intracellular and extracellular secreted forms. Presently, ANGPTL3 has emerged as a highly promising drug target for hypertriglyceridemia and associated cardiovascular diseases. However, most studies have focused on the secreted form of ANGPTL3, while its intracellular role is still largely unknown. Here, we report that intracellular ANGPTL3 acts as a negative regulator of IL-1ß-triggered signaling. Overexpression of ANGPTL3 inhibited IL-1ß-induced NF-κB activation and the transcription of inflammatory genes in HepG2, THP1, and HEK293T cells, while knockdown or knockout of ANGPTL3 resulted in opposite effects. Mechanistically, ANGPTL3 interacted with IL1R1 and IL1RAP through its intracellular C-terminal fibrinogen-like domain (FLD) and disrupted the assembly of the IL1R1-associated complex. Taken together, our study reveals a novel role for ANGPTL3 in inflammation, whereby it inhibits the physiological interaction between IL1R1 and IL1RAP to maintain immune tolerance and homeostasis in the liver.

A positive feedback loop between ID3 and PPARγ via DNA damage repair regulates the efficacy of radiotherapy for rectal cancer.

OBJECTIVE: To study the effect of inhibitor of differentiation 3 (ID3) on radiotherapy in patients with rectal cancer and to explore its primary mechanism. METHODS: Cell proliferation and clonogenic assays were used to study the relationship between ID3 and radiosensitivity. Co-immunoprecipitation and immunofluorescence were performed to analyze the possible mechanism of ID3 in the radiosensitivity of colorectal cancer. At the same time, a xenograft tumor model of HCT116 cells in nude mice was established to study the effect of irradiation on the tumorigenesis of ID3 knockdown colorectal cancer cells in vivo. Immunohistochemistry was performed to analyze the relationship between ID3 expression and the efficacy of radiotherapy in 46 patients with rectal cancer. RESULTS: Proliferation and clonogenic assays revealed that the radiosensitivity of colorectal cancer cells decreased with ID3 depletion through p53-independent pathway. With the decrease in ID3 expression, MDC1 was downregulated. Furthermore, the expression of ID3, MDC1, and γH2AX increased and formed foci after irradiation. ID3 interacted with PPARγ and form a positive feedback loop to enhance the effect of ID3 on the radiosensitivity of colorectal cancer. Irradiation tests in nude mice also confirmed that HCT116 cells with ID3 knockdown were more affected by irradiation. Immunohistochemical study showed that rectal cancer patients with low expression of ID3 had better radiotherapy efficacy. CONCLUSIONS: ID3 and PPARγ influence the radiosensitivity of colorectal cancer cells by interacting with MDC1 to form a positive feedback loop that promotes DNA damage repair. Patients with low expression of ID3 who received neoadjuvant chemoradiotherapy can obtain a better curative effect.

Structural and physicochemical properties of the different ultrasound frequency modified Qingke protein.

There is a burgeoning demand for modified plant-based proteins with desirable physicochemical and functional properties. The cereal Qingke is a promising alternative protein source, but its use has been limited by its imperfect functional characteristics. To investigate the effect of ultrasound treatment on Qingke protein, we applied single- (40 kHz), dual- (28/40 kHz), and tri- (28/40/50 kHz) frequency ultrasound on the isolated protein and measured subsequent physicochemical and structural changes. The results showed that the physicochemical properties of proteins were modified following ultrasound treatment, and many of these changes significantly increased with increasing frequency. Compared with the native Qingke protein (control), the solubility, foaming activity, stability, and water or oil holding capacity of tri-frequency ultrasound modified Qingke protein increased by 43.54%, 20.83%, 20.51%, 28.9%, and 45.2%, respectively. Furthermore, ultrasound treatment altered the secondary and tertiary structures of the protein resulting in more exposed chromophoric groups and inner hydrophobic groups, as well as reduced ß-sheets and increasedrandom coils, relative to the control. Rheological and texture characterization indicated that the values of G' and G'', hardness, gumminess, and chewiness decreased after ultrasound treatment. This study could provide a theoretical basis for the application of multi-frequency ultrasonic technology for modification of Qingke protein to expand its potential use as an alternative protein source.

Time trends in the burden of stroke and subtypes attributable to PM2.5 in China from 1990 to 2019.

Background: Increasing studies have found that PM2.5 has large adverse effects on stroke mortality. We want to investigate the long-term trends in the mortality of stroke attributable to ambient particulate matter pollution and household air pollution to provide evidence facilitating the design of policy. Methods: The deaths data of stroke and its subtypes attributable to PM2.5 were obtained from the Global Burden of Disease (GBD) 2019, analyzed by Joinpoint regression software and the age-period-cohort (APC) method to assess the magnitude of the trends in mortality and the temporal trends in the mortality rate by age, period, and cohort. Results: From 1990 to 2019, the age-standardized mortality rate (ASMR) attributable to PM2.5 exposure trended downwards, but the trends of ambient particulate matter pollution and household air pollution were opposite. The trends varied among subtypes, the AAPC of intracerebral hemorrhage, ischemic stroke, and subarachnoid hemorrhage attributable to PM2.5 were 0.7, 2.5, and-3.3%, respectively. The longitudinal age curve of the APC model showed that the mortality rates due to PM2.5 exposure increased with age. The period RRs of ischemic stroke due to ambient particulate matter pollution increased significantly. The cohort RRs of ambient particulate matter pollution increased among those born from 1905 to 1990. The net drifts of all subtypes attributable to PM2.5 were below 0, but owing to the increase of ambient particulate matter pollution, the range of the decline was small. Males had higher net drift values, compared with females. Conclusions: Ambient particulate matter pollution has become the main type of PM2.5 leading to stroke in China. PM2.5 exposure is more harmful to ischemic stroke, males, and elderly. Chinese government should pay attention to the long-term impact of ambient air pollution on stroke and take effective public health policies and interventions.

Inhibitor of DNA binding 2 knockdown inhibits the growth and liver metastasis of colorectal cancer.

BACKGROUND: Liver metastasis of colorectal cancer (CRC) remains high mortality and the mechanism is still unknown. Here we investigated the effects of inhibitor of DNA binding 2 (Id2) on growth and liver metastasis of CRC. METHODS: qPCR and western blotting were used to demonstrate mRNA and protein expressions in Id2-knockdown HCT116 cells. Cell growth was observed by cell proliferation assay, colony formation assay and flow cytometry. Cell migration and invasion were observed with wound healing assay and transwell migration and invasion assay. The effects of Id2 knockdown on tumor growth and liver metastasis in vivo were evaluated respectively with subcutaneous tumor model and colorectal liver metastasis model by injecting HCT116 cells into the mesentery triangle of cecum in mice. RESULTS: Id2 overexpression was found in CRC cell lines. Id2 knockdown resulted in a reduction in the proliferation, colony formation, migration and invasion of HCT116 cells. The suppression of cell proliferation was accompanied by the cell cycle arrest in the G0/G1 phase with down-regulation of Cyclin D1, Cyclin E, p-Cdk2/3, Cdk6, p-p27 and up-regulation of p21 and p27. Id2 knockdown reversed epithelial-mesenchymal transition (EMT) through increasing E-Cadherin and inhibiting N-Cadherin, Vimentin, ß-catenin, Snail and Slug. Id2 was also found to inhibit CRC metastasis via MMP2, MMP9 and TIMP-1. Furthermore, Id2 knockdown suppressed CRC liver metastasis in vivo. CONCLUSION: Id2 promotes CRC growth through activation of the PI3K/AKT signaling pathway, and triggers EMT to enhance CRC migration and invasion.

Emerging roles of angiopoietin-like proteins in inflammation: Mechanisms and potential as pharmacological targets.

Angiopoietin-like proteins (ANGPTLs), a family of eight secreted glycoproteins termed ANGTPL1-8, are involved in angiogenesis, lipid metabolism, cancer progression, and inflammation. Their roles in regulating lipid metabolism have been intensively studied, as some ANGPTLs are promising pharmacological targets for hypertriglyceridemia and associated cardiovascular disease. Recently, the emerging roles of ANGPTLs in inflammation have attracted great attention. First, elevated levels of multiple circulating ANGPTLs in inflammatory diseases make them potential disease biomarkers. Second, multiple ANGPTLs regulate acute or chronic inflammation via various mechanisms, including triggering inflammatory signaling through their action as ligands for integrin or forming homo- /hetero-oligomers to regulate signal transduction via extra- or intracellular mechanisms. As dysregulation of the inflammatory response is a critical trigger in many diseases, understanding the roles of ANGPTLs in inflammation will aid in drug/therapy development. Here, we summarize the roles, mechanisms, and potential therapeutic values for ANGPTLs in inflammation and inflammatory diseases.

Impact of Pain and Psychosocial Factors on Frailty Among Older Adults With Physical Functional Limitations: A Cross-Sectional Study.

AIMS: The objective of this study was to determine the prevalence of frailty and pain among older adults with physical functional limitations in China. We also assessed the impact of pain and psychosocial determinants on frailty among this vulnerable population. DESIGN: This study was a cross-sectional study. SETTING AND PARTICIPANTS: Totally, 2,323 Chinese elders with physical functional limitation were enrolled. METHODS: Physical functioning was assessed by the Barthel Index, participants who reported "often troubled with pain" were further asked about the intensity of their pain using a 1-10 numeric rating scale, and frailty was assessed by the Assessment of frailty FRAIL scale. The impact of pain and psychosocial factors on frailty was assessed by multivariable binary logistic regression. RESULTS: The prevalence of frailty and pain were 30.9% and 46.1%, respectively. Compared with subjects who reported no pain, those who reported mild (odds ratio [OR] = 1.70, 95% confidence interval [CI] = 1.21-2.31), moderate (OR = 2.10, 95% CI = 1.53-2.82), or severe pain (OR = 2.31, 95% CI = 1.56-3.40) tended to be more vulnerable to frailty. Furthermore, compared with participants with positive psychosocial determinants, those with negative psychosocial determinants seemed more likely to be frail. CONCLUSIONS: These findings suggest that the incidence of pain, negative psychosocial status, and frailty were prevalent, and the presence of pain and negative psychosocial factors increased the risk of frailty among older adults with physical functional limitation.

Enablers and barriers to implementing care quality improvement program in nursing homes in China.

OBJECTIVE: To explore the perspectives of key stakeholders on necessary factors to implement care quality improvement program. METHODS: We conducted qualitative descriptive research in eight nursing homes in four major prefecture-level cities of Changsha, Xiangtan, Zhuzhou, and Yueyang. Data of 50 clinical nurses and 64 nurse assistants were included and analyzed. Ethical approval was given by the medical ethics committee of Chinese Clinical Trial Registry (No. ChiCTR-IOC-17013109, https://www.chictr.org.cn/index.aspx ). One-to-one interviews were used with the nursing managers, and separate focus group discussions were used with the clinical nurses and nurse assistants. All of the interviews were audio recorded and later transcribed verbatim. In addition, the first author documented the responses of every participant in the field notes during the interviews and focus groups. RESULTS: The participants' perspectives were characterized by two main themes: (1) enablers, with four subthemes of "organizational support", "the evidence-based practice ability", "proactivity", "nursing supervision and feedback;" and (2) barriers, with five sub-themes of "low educational background", "the limitations of self-role orientation", "resistance to change", "lack of job motivation", and "organizational constraints". CONCLUSION: These findings recognize factors at the organizational level, staff level and societal level that are necessary to implement effective mentoring. The results of this study can provide reference for nursing home in improving nursing management quality, formulating, implementing and revising training policies.

Coordination of nitrogen uptake and assimilation favours the growth and competitiveness of moso bamboo over native tree species in high-NH4+ environments.

Phenotypic plasticity and competitive strength are major mechanisms determining the success of invasive species and are influenced by abiotic factors. A rise in the ratio of ammonium (NH4+) to nitrate (NO3-) in soils is frequently associated with the invasion of bamboo into broad-leaved evergreen forests. However, the influence of soil nitrogen (N) chemistry on plant growth and interspecific competition in the context of invasion remains insufficiently studied. In the present work, differences in plasticity and interspecific competition between native tree species in broad-leaved evergreen forests and invasive bamboo in response to different N forms were investigated using seedlings grown in a controlled environment. We show that moso bamboo responded positively and strongly to increased soil NH4+/NO3- ratios, while the native tree species Sapium sebiferum, Camellia oleifera, and Machilus pauhoi responded negatively and exhibited limited plasticity. Native tree species growth was significantly inhibited in the presence of moso bamboo under high-NH4+ conditions, whereas native tree species were less affected by interspecific competition when NO3- was supplied as the sole N source. By contrast, moso bamboo growth was significantly inhibited, followed by seedling death, in both monoculture and in mixed culture with prolonged NO3- treatment. All species tested exhibited significantly higher rates of 15NH4+ than 15NO3- uptake, but the Michaelis constant (Km) for 15NH4+ uptake was lower in moso bamboo, indicating higher substrate affinity. Nitrate reductase (NR) and nitrite reductase (NiR) activities showed no inducible effects in moso bamboo compared to the induction response seen in the native tree species in response to NO3-. Activities of glutamine synthetase (GS), glutamate synthase (GOGAT), and glutamate dehydrogenase (GDH) significantly increased with NH4+ provision in roots of moso bamboo, contrasted by a less plastic response in the native tree species. Enhanced ammonification and reduced nitrification in soils is typically observed during bamboo invasion and appears to create a positive soil-plant feedback loop that, due to highly flexible and opportunistic NH4+-acquisition pathways, favours bamboo fitness and invasion into native forests when NH4+ is the dominant N form.

Multimodal imaging in the differential diagnosis of glioma recurrence from treatment-related effects: A protocol for systematic review and network meta-analysis.

BACKGROUND: Glioma is the most common malignant primary brain tumor and it will always recur. To date, various multimodal imaging including magnetic resonance imaging (MRI) and positron emission tomography computed tomography (PET/CT) was used to differentiate the diagnosis of true tumor recurrent (TuR) and treatment-related effects (TrE) in glioma patient but with no overall conclusion. In this study, SROC curve and Bayesian network meta-analysis will be used to conduct a comprehensive analysis of the results of different clinical reports, and assess the efficacy of multimodal imaging in difference TuR and TrE. METHODS: To find more comprehensive information about the application of multimodal imaging in glioma patients, we searched the EMBASE, Pubmed, and Cochrane Central Register of Controlled Trials for relevant clinical trials. We also reviewed their reference lists to avoid omissions. QUADAS-2, RevMan software, Stata, and R software will be used. RESULTS: This study will provide reliable evidence for the efficacy of multimodal imaging in the differential diagnosis of TuR and TrE in glioma patients. CONCLUSION: We will evaluate the effectiveness of different and rank each imaging method in glioma patients to provide a decision-making reference on which method to choose for clinicians. Protocol registration number: CRD42020217861.