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Soil saturated hydraulic conductivity (Ks) is a critical parameter for modeling water and solute transport in soils. Conventional laboratory measurements of Ks are labor-intensive, costly, and susceptible to measurement errors, underscoring the need for more reliable estimation techniques. This study systematically compares the performance of Ordinary Kriging (OK), Ordinary Co-Kriging (OCK), and Response Surface Methodology (RSM) for Ks estimation, thereby integrating geostatistical and statistical optimization frameworks. Soil samples were collected from 135 locations within the surface layer (0–30 cm), and Ks along with key soil physicochemical properties were determined. In the geostatistical domain, OK based on a spherical semivariogram (R 2  = 0.81; nugget/sill = 10.19%) yielded moderate predictive ability (R 2  = 0.70, RMSE = 3.62 mm day −1 , MAE = 10.02 mm day −1 ), whereas OCK employing an exponential cross-semivariogram (R 2  = 0.91; nugget/sill = 0.45%) substantially improved accuracy (R 2  = 0.85, RMSE = 3.21 mm day −1 , MAE = 9.43 mm day −1 ). By contrast, RSM achieved the highest predictive performance, with a quadratic model producing R 2  = 0.94 and Adeq Precision = 49.2. Optimization within the experimental range indicated a maximum Ks of 137.18 mm day −1 at 8.9% clay and 86% sand. Collectively, these findings demonstrate that while OK and OCK provide valuable insights into the spatial dependence of Ks, RSM offers superior predictive accuracy and practical applicability for optimizing soil hydraulic functions in water resources and agricultural management.

Lung cancer is the most commonly diagnosed cancer worldwide, and metastasis in lung cancer is the leading cause of cancer‐related deaths. Thus, understanding the mechanism of lung cancer metastasis will improve the diagnosis and treatment of lung cancer patients. Herein, we found that expression of cluster of differentiation 109 (CD109) was correlated with the invasive and metastatic capacities of lung adenocarcinoma cells. CD109 is upregulated in tumorous tissues, and CD109 overexpression was associated with tumor progression, distant metastasis, and a poor prognosis in patient with lung adenocarcinoma. Mechanistically, expression of CD109 regulates protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling via its association with the epidermal growth factor receptor (EGFR). Inhibition of CD109 decreases EGFR phosphorylation, diminishes EGF‐elicited activation of AKT/mTOR, and sensitizes tumor cells to an EGFR inhibitor. Taken together, our results show that CD109 is a potential diagnostic and therapeutic target in lung cancer patients. CD109 promotes lung cancer metastasis through promoting EGFR‐AKT‐mTOR signaling and CD109 is an independent prognostic marker for lung adenocarcinoma.

The Azure Kinect represents the latest generation of Microsoft Kinect depth cameras. Of interest in this article is the depth and spatial accuracy of the Azure Kinect and how it compares to its predecessor, the Kinect v2. In one experiment, the two sensors are used to capture a planar whiteboard at 15 locations in a grid pattern with laser scanner data serving as ground truth. A set of histograms reveals the temporal-based random depth error inherent in each Kinect. Additionally, a two-dimensional cone of accuracy illustrates the systematic spatial error. At distances greater than 2.5 m, we find the Azure Kinect to have improved accuracy in both spatial and temporal domains as compared to the Kinect v2, while for distances less than 2.5 m, the spatial and temporal accuracies were found to be comparable. In another experiment, we compare the distribution of random depth error between each Kinect sensor by capturing a flat wall across the field of view in horizontal and vertical directions. We find the Azure Kinect to have improved temporal accuracy over the Kinect v2 in the range of 2.5 to 3.5 m for measurements close to the optical axis. The results indicate that the Azure Kinect is a suitable substitute for Kinect v2 in 3D scanning applications.

This paper employs a firm-level collective bargaining dataset to investigate the effect of labor, as an important stakeholder of a firm, on debt contracting. I conjecture and provide evidence that firms with strong organized labor prefer bank loans to public bonds because, by communicating with banks privately, unionized firms can reduce the adverse selection costs while preserving the information asymmetry with organized labor. Furthermore, I show that organized labor influences the structure of syndicated loans. When firms with strong unions withhold public disclosures, but communicate privately with lead lenders, heightened information asymmetry between the lead lenders and the participant lenders induces the lead lenders to retain larger shares of the loans and form more concentrated syndicates. Overall, this study demonstrates that the proprietary costs of disclosure related to organized labor significantly influence firms' debt contracting decisions and outcomes.

Adverse drug reactions are a public health issue that draws widespread attention, especially for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) which have high mortality and lack of efficacious treatment. Though T-cell-mediated HLA-interacted immune response has been extensively studied, our understanding of the mechanism is far from satisfactory. This review summarizes infection (virus, bacterial, and mycoplasma infection), an environmental risk factor, as a trigger for SJS/TEN. The mutations or polymorphisms of drug metabolic enzymes, transporters, receptors, the immune system genes, and T-cell-mediated apoptosis signaling pathways that contribute to SJS/TEN are discussed and summarized. Epigenetics, metabolites, and mobilization of regulatory T cells and tolerogenic myeloid precursors are emerged directions to study SJS/TEN. Ex vivo lymphocyte transformation test has been exploited to aid in identifying the causative drugs. Critical questions on the pathogenesis of SJS/TEN underlying gene polymorphisms and T cell cytotoxicity remain: why some of the patients carrying the risky genes tolerate the drug and do not develop SJS/TEN? What makes the skin and mucous membrane so special to be targeted? Do they relate to skin/mucous expression of transporters? What is the common machinery underlying different HLA-B alleles associated with SJS/TEN and common metabolites?

The role of fibronectin (FN) in tumorigenesis and malignant progression has been highly controversial. Cancerous FN plays a tumor-suppressive role, whereas it is pro-metastatic and associated with poor prognosis. Interestingly, FN matrix deposited in the tumor microenvironments (TMEs) promotes tumor progression but is paradoxically related to a better prognosis. Here, we justify how FN impacts tumor transformation and subsequently metastatic progression. Next, we try to reconcile and rationalize the seemingly conflicting roles of FN in cancer and TMEs. Finally, we propose future perspectives for potential FN-based therapeutic strategies.

Oxaliplatin (OXA) is a third-generation platinum compound with clinical activity in multiple solid tumors. Due to the repetition of chemotherapy cycle, OXA-induced chronic neuropathy presenting as paresthesia and pain. This study explored the neuropathy of chemotherapy pain and investigated the analgesic effect of 2-bromopalmitate (2-BP) on the pain behavior of OXA-induced rats. The chemotherapy pain rat model was established by the five consecutive administration of OXA (intraperitoneal, 4 mg/kg). After the establishment of OXA-induced rats, the pain behavior test, inflammatory signal analysis and mitochondrial function measurement were conducted. OXA-induced rats exhibited mechanical allodynia and spinal inflammatory infiltration. Our fluorescence and western blot analysis revealed spinal astrocytes were activated in OXA rats with up-regulation of astrocytic markers. In addition, NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasome mediated inflammatory signal cascade was also activated. Inflammation was triggered by dysfunctional mitochondria which represented by increase in cyclooxygenase-2 (COX-2) level and manganese superoxide dismutase (Mn-SOD) activity. Intrathecally injection of 2-BP significantly attenuated dynamin-related protein 1 (Drp1) mediated mitochondrial fission, recovered mitochondrial function, suppressed NLRP3 inflammasome cascade, and consequently decreased mechanical pain sensitivity. For cell research, 2-BP treatment significantly reversed tumor necrosis factor-α (TNF-α) induced mitochondria membrane potential deficiency and high reactive oxygen species (ROS) level. These findings indicate 2-BP decreases spinal inflammation and relieves OXA-induced neuropathic pain via reducing Drp1-mediated mitochondrial dysfunction.

To evaluate the effectiveness and safety of S-ketamine for pain relief and analgesic consumption in surgical patients. Systematic review and meta-analysis of randomized controlled trials (RCTs). Perioperative setting. A total of 905 adult patients undergoing surgery using general anesthesia: 504 patients in the S-ketamine group and 401 patients in the placebo group. Intravenous S-ketamine as an adjuvant to general anesthesia compared with placebo. The primary outcomes were resting and movement pain scores (VAS/NRS 0–10) and morphine consumption within 4, 12, 24 and 48 h after surgery. The secondary outcomes included postoperative complications such as nausea, vomiting, and psychotomimetic adverse events. We used the guidelines of the Recommendation Assessment, Development, and Evaluation (GRADE) system to evaluate the level of certainty for the main results. A total of 12 studies were included. The types of surgery included abdominal surgery, thoracotomy, gynecologic surgery, arthroscopic anterior cruciate ligament repair, cardiac surgery, laparoscopic cholecystectomy, lumbar spinal fusion surgery, radical prostatectomy, and hemorrhoidectomy. There were significant improvements in resting pain scores at 4, 12 and 24 h with S-ketamine versus placebo [4 h: standardized mean difference (SMD) -1.11; 95% confidence interval (CI): −1.53, −0.68, p < 0.00001; GRADE = moderate; 12 h: SMD −0.88; 95%CI: −1.42, −0.34, p = 0.001; GRADE = moderate; 24 h: SMD -0.39; 95%CI: −0.73, −0.06, p = 0.02; GRADE = moderate]. The incidence of pain scores at 48 h showed no statistical difference between the two groups (SMD -0.27; 95%CI: −1.12, 0.58, p = 0.53, GRADE = moderate). The movement pain scores were not significantly different between the two groups at each time point (4 h: SMD −0.34; 95%CI: −0.73, 0.05, p = 0.09, GRADE = moderate; 12 h: SMD −0.42; 95%CI: −1.46, 0.63, p = 0.44, GRADE = low; 24 h: SMD −0.58; 95%CI: −1.25, 0.09, p = 0.09, GRADE = moderate; 48 h: SMD −0.49; 95%CI: −1.11, 0.14, p = 0.13, GRADE = low). At 4 and 12 h after surgery, the consumption of morphine was significantly reduced in the S-ketamine group (4 h: SMD −0.98; 95%CI: −1.37, −0.06, p < 0.00001, GRADE = moderate; 12 h: SMD −1.36; 95%CI: −2.26, −0.46, p = 0.003, GRADE = low). There were no significant differences in morphine use at 24 and 48 h between the two groups (24 h: SMD −0.70; 95%CI: −1.42, 0.02, p = 0.06, GRADE = low; 48 h: SMD −0.79; 95%CI: −2.26, 1.03, p = 0.39, GRADE = low). The risk for nausea [relative risk (RR) = 1.04; 95%CI: 0.83, 1.30, p = 0.73], vomiting (RR = 1.07; 95%CI: 0.84, 1.38, p = 0.57), and psychotomimetic adverse events (RR = 1.57; 95%CI: 0.82, 2.99, p = 0.17) showed no significant increase in the S-ketamine group. Intravenous S-ketamine as an adjunct to general anesthesia is effective for assisting analgesia and decreases the intensity of pain and opioid requirements in a short period of time after surgery, but it may increase the psychotomimetic adverse event rate. Overall, the level of certainty is moderate to low. •This is the only meta-analysis to assess S-ketamine for pain relief and lowering analgesic consumption in surgical patients.•Intravenous S-ketamine can reduce the dosage of opioids and postoperative pain score in a short period of time after surgery.•S-ketamine can be a good substitute for the use of racemic ketamine during the perioperative period.