Unraveling phytoremediation mechanisms of the common reed (Phragmites australis) suspension cells towards ciprofloxacin: Xenobiotic transformation and metabolic reprogramming.

Phytoremediation is an effective solution to treat pollution with antibiotic compounds in aquatic environments; however, the underlying mechanisms for plants to cope with antibiotic pollutants are obscure. Here we used cell suspension culture to investigate the distribution and transformation of ciprofloxacin (CIP) in common reed (Phragmites australis) plants, as well as the accompanying phenotypic and metabolic responses of plants. By means of radioactive isotope labelling, we found that in total 68 % of CIP was transformed via intracellular Phase I transformation (reduction and methylation), Phase Ⅱ conjugation (glycosylation), and Phase Ⅲ compartmentalization (cell-bound residue formation mainly in cell walls, 23 %). The reduction and glycosylation products were secreted by the cells. To mitigate stress induced by CIP and its transformation products, the cells activated the defense system by up-regulating both intra- and extra-cellular antioxidant metabolites (e.g., catechin, l-cystine, and dehydroascorbic acid), anti-C/N metabolism disorder metabolites (e.g., succinic acid), secreting signaling (e.g., nicotinic acid), and anti-stress (e.g., allantoin) metabolites. Notably, the metabolic reprogramming could be involved in the CIP transformation process (e.g., glycosylation). Our findings reveal the strategy of wetland plants to cope with the stress from CIP by transforming the xenobiotic compound and reprogramming metabolism, and provide novel insights into the fate of antibiotics and plant defense mechanisms during phytoremediation.

Genetic prediction of antihyperglycemic drug targets and risk of epilepsy: a mendelian randomisation study.

A connection between diabetes and an increased risk of epilepsy has been suggested by observational studies. Animal studies have also shown that antihyperglycemic drugs can improve seizures. However, it is unclear whether antihyperglycemic drugs have a causal role in epilepsy in humans. To investigate this potential causal relationship, a Mendelian randomisation study was conducted using International League Against Epilepsy data as the discovery set and FinnGen data as the replication set. It was discovered that three antidiabetic drug target genes, ETFDH, CYP21A2 and CYP2D6, were involved in the occurrence of epilepsy. In particular, ETFDH was identified as a target gene in both the discovery set (inverse variance weighting [IVW], odds ratio [OR] = 1.018, 95% confidence interval [CI], 1.004-1.033, p = 0.009) and replication set (IVW, OR = 1.074, 95% CI, 1.034-1.114, p = 0.00016), and CYP21A2 was identified in the discovery set (IVW, OR = 1.029, 95% CI, 1.005-1.053, p = 0.016) and replication set (IVW, OR = 1.057, 95% CI, 1.001-1.116, p = 0.045) as having a causal association with an increased risk of epilepsy. Conversely, the CYP2D6 gene was found to be a protective factor for epilepsy in both the discovery set (IVW, OR = 0.0984, 95% CI, 0.969-0.998, p = 0.025) and replication set (IVW, OR = 0.977, 95% CI, 0.955-1.000, p = 0.046). A search of DrugBank revealed that metformin, an anti-glucose drug, is an inhibitor of the ETFDH gene and may have a potential therapeutic effect on epilepsy.

Integrated Macrogenomics and Metabolomics Explore Alterations and Correlation between Gut Microbiota and Serum Metabolites in Adult Epileptic Patients: A Pilot Study.

Epilepsy (EP) is a complex brain disorder showing a lot of unknows reasons. Recent studies showed that gut microbiota can influence epilepsy via the brain-gut axis. Nevertheless, the mechanism by which gut microbiota affects adult epilepsy still remains unclear. In this study, fecal and serum samples were obtained from patients with epilepsy and normal controls. Using an integrated analysis, sequencing was performed by macrogenomics and high-throughput targeted metabolomics with various bioinformatics approaches. The macrogenomic sequencing revealed significant changes in microbial structure in patients suffering from epilepsy. For example, at the phylum level, the relative abundance of Actinobacteria, Bacteroidetes and Proteobacteria showed an increase in the patients with epilepsy, whereas that of Firmicutes decreased. In addition, the patients with epilepsy had significantly differential metabolite profiles compared to normal controls, and five clusters with 21 metabolites, mainly containing the upregulation of some fatty acids and downregulation of some amino acids. Tryptophan (AUC = 91.81, p < 0.0001), kynurenine (AUC = 79.09, p < 0.01) and 7Z,10Z,13Z,16Z-Docosatetraenoic acid (AUC = 80.95, p < 0.01) may be used as potential diagnostic markers for epilepsy. Differential serum metabolites have effects on tryptophan metabolism, iron death and other pathways. Furthermore, a multiomic joint analysis observed a statistically significant correlation between the differential flora and the differential serum metabolites. In our findings, a macrogenomic analysis revealed the presence of dysregulated intestinal flora species and function in adult epileptic patients. Deeper metabolomic analyses revealed differences in serum metabolites between patients with epilepsy and healthy populations. Meanwhile, the multiomic combination showed connection between the gut microbes and circulating metabolites in the EP patients, which may be potential therapeutic targets.

Causal relationship among obesity and body fat distribution and epilepsy subtypes.

Objective: The observational studies indicate an association between obesity and epilepsy, but it is unclear whether such an association responds to causality. The objective of this study was to determine the causal relationship between obesity and fat distribution and epilepsy subtypes based on waist circumference, hip circumference (HP), waist-hip ratio (WHR), and body mass index (BMI). Methods: A two-sample Mendelian randomization study was conducted separately for the four indicators of obesity and epilepsy and its seven subtypes, with reverse Mendelian randomization and multivariate Mendelian randomization for significant outcomes. Results: A two-sample Mendelian randomized analysis informed us that waist circumference was a risk factor for juvenile myoclonic epilepsy (beta = 0.0299, P = 4.60 × 10-3). The increase in hip circumference increased the risk of juvenile myoclonic epilepsy and epilepsy, with effect values of 0.0283 (P = 2.01 × 10-3) and 0.0928 (P = 1.40 × 10-2), respectively. Furthermore, children with a higher BMI exhibit a higher risk of epilepsy (beta = 0.0148 P = 1.05 × 10-3). The reverse Mendelian randomization study revealed that childhood absence epilepsy increased its BMI (beta = 0.8980, P = 7.52 × 10-7), and juvenile myoclonic epilepsy increased its waist circumference (beta = 0.7322, P = 3.26 × 10-2). Multivariate Mendelian randomization revealed that an increase in hip circumference and waist-hip ratio increased the risk of juvenile myoclonic epilepsy, with an effect value of 0.1051 (P = 9.75 × 10-4) and 0.1430 (P = 3.99 × 10-3), respectively, while an increase in BMI and waist circumference instead decreased their risk, with effect values of -0.0951 (P = 3.14 × 10-2) and-0.0541 (P = 1.71 × 10-2). In contrast, multivariate Mendelian randomization for childhood absence epilepsy and epilepsy did not identify any independent risk factors. Significance: Our findings provide novel evidence in favor of obesity as a risk factor for epilepsy and waist circumference as a risk factor for juvenile myoclonic epilepsy. Increased hip circumference confers an elevated risk of juvenile myoclonic epilepsy and epilepsy (all documented cases), and a high BMI increases the risk of childhood absence epilepsy. With this, new insights are provided into the energy metabolism of epilepsy, which supports further nutritional interventions and the search for new therapeutic targets.

Underlying Role of Rumination-Mediated Attachment Style Plays in PTSD after TIA and Stroke.

Objective: Attachment and rumination were examined as the intermediary variables on post-traumatic stress disorder and medication compliance in stroke or TIA patients. Methods: A total of 300 participants with stroke or TIA from the Second Hospital of Hebei Province were selected. Patients accomplished NIHSS, ABCD2, ECR, RSQ, and RRS on admission. After 3 months, the PCL-C and MMAS were collected. Results: In the stroke or TIA patients, the incident of PTSD was 7.7%; PTSD scores were significantly associated with attachment anxiety (r = 0.225, p < 0.01), symptom rumination (r = 0.197, p < 0.01), and obsessive thinking (r = 0.187, p < 0.01). After the Sobel test analysis and verification by the Baron and Kenny's stepwise approach we found that ruminant mediated the relationship between attachment anxiety and PTSD; obsessive thinking mediated the relationship between attachment anxiety and PTSD. Conclusions: The relationship between attachment anxiety and PTSD was positively predicted by rumination and obsessive thinking. Adult attachment style, rumination, and PTSD scores may not predict medication compliance.

Evolution of Oncology and Palliative Nursing in Meeting the Changing Landscape of Cancer Care.

Nursing is a vital health profession. In almost all clinical and hospital settings, nurses offer primary palliative care. Nurses are recognized for their strong philosophy of care for a wide spectrum of disorders. No matter the sickness, condition, or clinical situation, palliative care is considered essential in nursing practice. Palliative care nursing is the provision of palliative care services to cancer patients and their families, regardless of whether cancer can be cured or not. A large body of evidence shows that early palliative care nursing integration improves the quality of life and survival of cancer patients. Due to the intricacy of cancer, the landscape of cancer care is shifting. Cancer is a life-threatening disease with a high mortality rate. Oncology nurses' skills and experience are vital in providing specialized patient care and fulfilling the needs of patients and their families. The current study examines the shifting environment of palliative care nursing in oncology. However, new palliative care nursing approaches are required to adapt to the evolving cancer scenario.

[Environmental risks of antibiotics in soil and the related bioremediation technologies].

Antibiotics are widely used and prevalently distributed in the environment. The issue of antibiotic resistance genes has posed a huge threat to the global public health. Soil is an important sink of antibiotics in the environment. Antibiotic exposure may introduce adverse effects on soil organisms, and bring indirect but potential risks to human health. Therefore, it is urgent to take actions to remediate antibiotics-contaminated soil. This review summarized effects of antibiotics on phenotype growth of plants, physiological characteristics and community structure of animals, composition and structure of microbial communities, and transmission of antibiotic resistance genes among organisms in soil. Additionally, the potential and prospects of employing antibiotic-resistant soil plants, animals, microorganisms, and their combinations to treat antibiotics-contaminated soil were illustrated. Last but not least, the unaddressed issues in this area were proposed, which may provide insights into relevant research directions in the future.

Loss of profilin 2 contributes to enhanced epithelial-mesenchymal transition and metastasis of colorectal cancer.

Profilin 2 (PFN2) functions as an actin cytoskeleton regulator and serves an important role in cell motility. However, a role for PFN2 in the progression of colorectal cancer (CRC), particularly in metastasis, has yet to be clarified. The aim of the present study was to investigate whether PFN2 served specific roles in the progression of human CRC. The results demonstrated that PFN2 was differentially expressed in CRC tissues and cell lines by reverse transcription-quantitative polymerase chain reaction and western blotting. PFN2 expression was also negatively associated with the degree of tumor metastasis. Low PFN2 expression in CRC cells was related with enhanced epithelial-mesenchymal transition (EMT) and, in turn, may increase migratory capabilities. Overexpression of PFN2 in CRC cell lines with a low level of endogenous PFN2 inhibited the EMT process, as well as the associated migration; in addition, myosin light chain (MLC) phosphorylation was upregulated. Inhibition of MLC phosphorylation attenuated the inhibition of EMT and cell migratory abilities induced by PFN2 overexpression in CRC cell lines, the results suggested that PFN2 may suppress cancer EMT and the subsequent metastasis by regulating cytoskeletal reorganization. These results demonstrated that PFN2 may serve a suppressive role in the metastasis of CRC and therefore may provide a new potential target for cancer therapeutics.