Br-to-Cl Transformation Guided the Formation of Polyhalogenated Dibenzo-p-dioxins/Dibenzofurans.

Polyhalogenated dibenzo-p-dioxins/dibenzofurans (PXDD/Fs) are commonly released into the environment as byproducts of combustion processes, accompanied by flue gases. Chlorinated (Cl) and brominated (Br) precursors play crucial roles in forming PXDD/Fs. However, the specific contributions of Cl-precursors and Br-precursors to PXDD/Fs formation have not been fully elucidated. Herein, we demonstrate that the formation of Br-precursors can increase the fraction of polychlorinated dibenzo-p-dioxins/dibenzofurans (PCDD/Fs) congeners substituted at specific positions, such as 1,2,3,4,6,7,8-HpCDD, OCDD, 2,3,4,7,8-PeCDF, and 2,3,4,6,7,8-HxCDF. This is attributed to the electrophilic chlorination reaction of the Br-precursors, which includes the Br-to-Cl transformation pathway, following the principle of regioselectivity. The observed formation of polybrominated/chlorinated dibenzo-p-dioxins/benzofurans (PBCDD/Fs) from 1,2-dibromobenzene (1,2-DiBBz) as a Br precursor provides direct evidence supporting the proposed Br-to-Cl transformation. Quantum chemical calculations are employed to discuss the principle of regioselectivity in the Br-to-Cl transformation, clarifying the priority of the position for electrophilic chlorination. Additionally, the concentration of PCDD/Fs formed from 1,2-DiBBz is 1.6 µg/kg, comparable to that of polybrominated dibenzo-p-dioxins/dibenzofurans (PBDD/Fs) (2.4 µg/kg), highlighting the potential of brominated organic pollutants as precursors for PCDD/Fs formation. This study provides three potential pathways for PCDD/Fs formation from Br-precursors, establishing a theoretical foundation for elucidating the formation mechanism of PXDD/Fs in the coexistence of Cl and Br.

The impact of neoadjuvant chemotherapy on the clinical efficacy and serum tumor marker levels in patients undergoing radical surgery for gastric cancer.

The objective of this article is to study the impact of neoadjuvant chemotherapy (NAC) on the clinical efficacy and serum tumor marker levels in patients undergoing radical surgery for gastric cancer (GC). Thirty patients who underwent routine radical surgery for GC in our hospital from January 2020 to June 2021 were included in the control group. Thirty patients who underwent radical surgery for GC after receiving NAC from July 2021 to December 2022 were included in the observation group. The treatment outcomes of the observation group were assessed and analyzed. The surgical indicators, tumor markers, Karnofsky Performance Status (KPS), and occurrence of adverse reactions were compared between the 2 groups. Comparisons were made between the 2 groups in terms of surgical duration, number of lymph node dissections, intraoperative blood loss, time to postoperative ambulation, length of hospital stay, and time to postoperative passage of flatus (P > .05). The observation group had a higher proportion of R0 resection at the surgical margin compared to the control group (P < .05). The serum tumor markers of the 2 groups were compared before treatment (P > .05). After treatment, the levels of serum carcinoembryonic antigen, alpha-fetoprotein, cancer antigen 125, and carbohydrate antigen 72-4 decreased in both groups, and the observation group showed a greater reduction in these tumor marker levels compared to the control group (P < .05). The KPS scores of the 2 groups were compared before treatment (P > .05). After treatment, the KPS scores increased in both groups, with the observation group showing a higher improvement compared to the control group (P < .05). The overall incidence of adverse reactions, including incision infection, pleural effusion, pulmonary infection, intestinal obstruction, and gastric emptying disorders, was lower in the observation group (6.67%) compared to the control group (26.67%) (P < .05). The combination of NAC with radical surgery for GC is safe and feasible. It can significantly increase the R0 resection rate, effectively improve the levels of serum tumor markers, enhance patient's quality of life, and result in fewer surgical adverse reactions.

Exploiting Propagation Delay in Underwater Acoustic Communication Networks via Deep Reinforcement Learning.

This article proposes a novel deep-reinforcement learning-based medium access control (DL-MAC) protocol for underwater acoustic networks (UANs) where one agent node employing the proposed DL-MAC protocol coexists with other nodes employing traditional protocols, such as time division multiple access (TDMA) or q -Aloha. The DL-MAC agent learns to exploit the large propagation delays inherent in underwater acoustic communications to improve system throughput by either a synchronous or an asynchronous transmission mode. In the sync-DL-MAC protocol, the agent action space is transmission or no transmission, while in the async-DL-MAC, the agent can also vary the start time in each transmission time slot to further exploit the spatiotemporal uncertainty of the UANs. The deep Q -learning algorithm is applied to both sync-DL-MAC and async-DL-MAC agents to learn the optimal policies. A theoretical analysis and computer simulations demonstrate the performance gain obtained by both DL-MAC protocols. The async-DL-MAC protocol outperforms the sync-DL-MAC protocol significantly in sum throughput and packet success rate by adjusting the transmission start time and reducing the length of time slot.

Serum homocysteine is a valuable marker for predicting aggravation of infection in intestinal obstruction patients.

The aim of this study was to investigate the expression of serum homocysteine (HCY), procalcitonin (PCT), and C-reactive protein (CRP) in abdominal infectious disease and analyze their relationship with the degree of abdominal infection. We conducted a retrospective study involving 157 patients with abdominal infections at Xuzhou Central Hospital between January 2016 and October 2019. The patients were composed of intestinal obstruction (73 cases), appendicitis (45 cases), perforation of the digestive tract (25 cases), and cholecystitis (14 cases). The HCY, PCT, and CRP levels of patients with abdominal infections were detected using enzyme-linked immunosorbent assay (ELISA), and correlation analysis between the HCY, PCT, and CRP levels and abdominal infection was performed using Pearson's correlation analysis. Compared with before treatment, the HCY, PCT, and CRP levels in the four groups decreased significantly after treatment. The levels in the patients in the intestinal obstruction group decreased more markedly than in those in the other groups. There were positive correlations among the HCY level, PCT, and CRP before treatment only in patients with intestinal obstruction (P < 0.001). The difference was statistically significant in the HCY level between the non-operation and the operation groups in patients with intestinal obstruction (P < 0.001). Serum HCY may be a valuable marker for predicting aggravation of infection in patients with intestinal obstruction.

A NEW DOSE DETERMINATION METHOD FOR HP(3) AND DP LENS FOR BETA REFERENCE RADIATION QUALITIES.

For the purpose of obtaining the smaller uncertainties for Hp(3) and Dp lens in 90Sr/90Y beta reference fields, a new dose determination method based on the Monte-Carlo simulation was proposed. The conversion coefficients from the absorbed dose in air, at the reference point of the extrapolation ionisation chamber, Dair, det to Hp(3; α) and the conversion factors from Dair, det to Dp lens(α) were calculated with EGSnrc, respectively, for the irradiation angles from 0° to 60°. Compared with the dose determination method in International Organization for Standardization (ISO) 6980 standard, the uncertainty reductions of 7.7-52.8% for Hp(3; α) and 7.9-55.0% for Dp lens(α) were achieved, respectively. In addition, for the conversion coefficients from the reference absorbed dose DR to Hp(3; α), the calculations were performed for more irradiation conditions, which are not included in the current ISO 6980 standard. For the calculations of the conversion factors from DR to Dp lens(α), the eye and head phantoms with Chinese characteristics were utilised, which makes the conversion factors more suitable for use in China.

TLR9 blockade inhibits activation of diabetogenic CD8+ T cells and delays autoimmune diabetes.

Diabetogenic CD8(+) T cells are primed in the pancreatic lymph nodes (PLNs) by dendritic cells (DCs) carrying islet cell Ags. TLR signaling modifies DC function. The goal of this study was to determine the effect of TLR9 signaling on diabetogenic CD8(+) T cell activation and the course of type 1 diabetes. We explored the effects of CpG oligonucleotide, TLR9 antagonists, and genetic TLR9 deficiency on the activation of diabetogenic CD8(+) T cells. NOD bone marrow-derived DCs pulsed with freeze-thawed insulinoma cells in the presence of TLR9 agonist CpG and CD40 agonist induced diabetogenic CD8(+) T cell activation. The addition of TLR9 antagonist oligodeoxynucleotide or chloroquine inhibited bone marrow-derived DCs activation and CD8(+) T cell priming in response to CpG. CpG alone or with CD40 agonist induced CTL activity that triggered diabetes development in 8.3-TCR transgenic NOD mice. Oligodeoxynucleotide treatment of 8.3-TCR transgenic NOD mice delayed spontaneous diabetes development. Chloroquine treatment delayed the spontaneous onset of diabetes in NOD mice, coincident with the decreased activation of PLN DCs. TLR9(-/-) NOD mice had delayed onset of diabetes compared with TLR9(-/+) NOD littermates. TLR9(-/-) NOD mice had lower levels of IFN-alpha in PLNs and decreased frequencies of plasmacytoid DCs and diabetogenic CD8(+) T cells compared with NOD mice. We propose that TLR9 activation contributes to the spontaneous onset of diabetes in NOD mice by increasing IFN-alpha and promoting diabetogenic CD8 T cell activation.

Calcium poisoning mechanism on the selective catalytic reduction of NOx by ammonia over the γ-Fe2O3 (001) surface.

γ-Fe2O3 has an excellent low-temperature selective catalytic reduction (SCR) deNOx performance, but its resistance to alkaline earth metal calcium (Ca) is poor. In particular, the detailed mechanism of Ca poisoning on the γ-Fe2O3 catalyst at the atomic level is not clear. Hence, the density functional theory method was used in this research to investigate the influence mechanism of Ca poisoning on the NH3-SCR over the γ-Fe2O3 catalyst surface. The findings reveal that NH3, NO, and O2 molecules can bind to the γ-Fe2O3 (001) surface to generate coordinated ammonia, monodentate nitroso, and adsorption oxygen species, respectively. The main active site is Fe1-top. For the γ-Fe2O3 with Ca poisoning, the Ca atom has a high adsorption energy on the surface of γ-Fe2O3 (001), which covers the catalyst surface and reduces the active sites. The presence of Ca atom decreases the adsorption performance of NH3, while slightly improving the NO and O2 adsorption. In particular, the Ca atom restrains the NH3 activation and NH2 formation, which is detrimental to the NH3-SCR process.

Phagocytosis of apoptotic cells by macrophages from NOD mice is reduced.

Macrophages limit inflammatory responses by clearing apoptotic cells. Deficiencies in apoptotic cell phagocytosis have been linked to autoimmunity. In this study, we determined the efficiency with which macrophages from diabetes-prone NOD and diabetes-resistant NOR, Idd5, Balb/c, and C57BL/6 mice phagocytose apoptotic thymocytes and NIT-1 insulinoma cells. Peritoneal and bone marrow-derived macrophages from NOD mice engulfed fewer apoptotic thymocytes than macrophages from Balb/c mice (P < 0.05). Peritoneal macrophages from NOR and Idd5 NOD congenic mice were more proficient at engulfment than their NOD counterparts. Annexin V blockade diminished apoptotic thymocyte clearance and heat-labile serum factors augmented clearance. Binding of apoptotic thymocytes to NOD macrophages was also reduced, suggesting that the deficiency in phagocytosis may be partly attributable to a recognition defect. Peritoneal macrophages from female Balb/c and NOD mice were equally efficient in the engulfment of microspheres, suggesting that the phagocytic deficiency observed in NOD mice was specific for apoptotic cells. In summary, we have demonstrated a deficiency in phagocytic function of macrophages from NOD mice. Normal and diabetes-prone neonatal rodents have a wave of beta-cell apoptosis coincident with the onset of target organ inflammation. A constitutive defect in the clearance of apoptotic beta-cells may be contributory to the initiation of autoimmunity.

A deficiency in the in vivo clearance of apoptotic cells is a feature of the NOD mouse.

Deficiencies in apoptotic cell clearance have been linked to autoimmunity. Here we examined the time-course of peritoneal macrophage phagocytosis of dying cells following the direct injection of apoptotic thymocytes into the peritoneum of NOD mice and BALB/c controls. Macrophages from NOD mice demonstrated a profound defect in the phagocytosis of apoptotic thymocytes as compared to control macrophages. Nonobese diabetic mice also demonstrated a decrease in the clearance of apoptotic cell loads following an apoptotic stimulus to thymocytes (dexamethasone) when compared to BALB/c or NOR controls. Further, NOD mice demonstrated an increase in apoptotic cell load following an apoptotic stimulus to keratinocytes (ultraviolet light, UVB) when compared to control strains. Animals deficient in macrophage phagocytosis of apoptotic debris often manifest an autoimmune phenotype characterized by the production of antinuclear autoantibodies (ANA). We determined whether increased apoptotic cell loads (through repeated exposure to UVB irradiation) could accelerate such autoimmune phenomena in young NOD mice. Following repeated UVB irradiation, NOD mice, but not BALB/c or NOR controls, developed ANA. We propose that abnormalities in apoptotic cell clearance by macrophages predispose NOD mice to autoimmunity.