Objective:To compare the relative proportion of direct action (ray particles directly destroy biological molecules such as DNA and indirect action (radical-mediated oxidative damage) in the damage caused by X-ray and proton irradiation of lung cancer cells.Methods:Unirradiated human lung adenocarcinoma A549 cells and human large cell lung cancer NCI-H460 cells were cultured in media containing 0, 0.125, 0.25, 0.5, 0.75 mol/L dimethyl sulfoxide (DMSO) for 1 h to obtain plating efficiency (PE) values, thereby determining whether DMSO affected cell survival. Following pretreatment with each DMSO concentration, cells were exposed to X-ray irradiation at physical doses of 2, 4, 6, 8 Gy and proton irradiation at equivalent doses of 2, 4, 6, 8 GyE, respectively. Survival fractions (SF) and maximum protection (MP) values were calculated to evaluate the effects of varying DMSO concentrations on post-irradiation cell survival and to quantify the contribution of indirect radiation damage mechanisms (higher MP indicates greater indirect effect contribution). PE, SF, and MP values were determined using clonogenic assays. Comparisons among multiple groups were performed using one-way ANOVA followed by Tukey's multiple comparison, and comparisons between irradiation groups were analyzed using independent samples t-tests. Results:The PE of unirradiated cells treated with varying DMSO concentrations showed no statistically significant differences. Following pretreatment at different DMSO concentrations and subsequent irradiation with X-rays or protons, the protective effect of DMSO reached saturation at 0.5 mol/L. At this concentration, comparison of the average MP values across 4 radiation doses revealed: In A549 cells, the MP value was 54.21%±1.73% for X-ray irradiation group and 39.69%±0.72% for proton irradiation group ( t=16.82, P<0.001); in NCI-H460 cells, the MP value was 52.04%±1.00% for X-ray irradiation group and 41.31%±0.70% for proton irradiation group ( t=10.19, P<0.001). Conclusions:Under biologically equivalent doses, proton irradiation demonstrates greater reliance on direct effects in lung cancer cells killing compared with X-ray irradiation.

Objective:To establish the model of acute kidney injury (AKI), search for more sensitive and reliable biomarkers.Methods:In April 2018, 100 male Wister rats aged 6 to 8 weeks were selected and randomly divided into experimental group (n=90) and control group (n=10). The experimental group was given Diachalefin (140 mg/kg body weight) by intragastric administration, while the control group was given saline intragastric administration. Ten rats in the experimental group were killed 0.5 h, 2 h, 6 h, 24 h, 3 d, 7 d, 14 d, 21 d and 28 d after intragastric administration, respectively. Serum creatinine (Cr), urea nitrogen (BUN) and uric acid (UA) were detected by automatic biochemical analyzer with 5 ml of blood from inferior vena cava puncture. Serum neutrophil gelatinase-associated lipid carrier protein (NGAL), kidney damage molecule-1 (KIM-1) and transforming growth factor-β1 (TGF-β1) levels were determined by enzyme-linked immunosorbent assay (ELISA). The data between groups were compared using two independent sample t tests.Results:The renal tissue structure of rats in the control group was not significantly abnormal, while the renal tissue cell damage of rats in the experimental group was obvious, which gradually increased with the extension of time in the early stage, and gradually recovered in the later stage. UA in experimental group reached its peak at 24 h after exposure and was still higher than that in control group at 14 d ( P<0.05), Cr reached its peak at 7 d, and then gradually decreased, and there was no statistical significance between experimental group and control group at 28 d ( P>0.05). BUN increased at 6 h after exposure and reached the highest value at 7~14 d ( P<0.05). Blood NGAL increased at 0.5 h after exposure, reached its peak at 24 h, continued to increase at 3, 7 and 14 days ( P<0.05), and began to decrease at 21 days. KIM-1 began to increase at 0.5 h, continued to peak at 24 h, 3 and 7 d after exposure, and began to decrease at 14 d, but it was still higher than that in control group ( P<0.05). There was no significant difference in TGF-β1 at each time point ( P>0.05). Western blot assay results: Compared with control group, there was no significant difference in the expression level of TGF-β1 in kidney tissue of experimental group ( P>0.05). NGAL increased gradually from 2 h and was higher at 7 and 14 d, with statistical significance ( P<0.05). KIM-1 increased at 2 h, decreased at 6 and 24 h, and increased again at 3 and 7 d. Conclusion:NGAL and KIM-1 can be used as early diagnostic biomarkers for diquat-induced acute kidney injury.

This article analyzed the clinical data of a patient with acute benzene poisoning caused by oral ingestion of 100 ml of pure benzene. The patient presented with multiple organ dysfunction syndrome, manifested as consciousness disorders, abnormal coagulation function with hematuria, and delayed liver injury. After comprehensive treatment including fluid replacement, diuresis, protection of vital organs, and nutritional support, the patient was discharged after recovery. Poisoning caused by oral administration of large doses of benzene is rare. Analyzing the diagnosis and treatment process of this patient can enhance clinicians' understanding of acute benzene poisoning, provide empirical references for the clinical treatment of such poisoning patients, and improve their survival rate as much as possible.

Automotive antifreeze, being colorless and odorless, can easily cause acute poisoning if ingested. Acute poisoning can lead to damage to the central nervous system, digestive system, and kidney function, and may even result in death. This article analyzes the clinical data, diagnostic and therapeutic processes, and outcomes of two patients admitted to the Department of Poisoning and Occupational Diseases, Emergency Medicine of Qilu Hospital, Shandong University, who suffered acute poisoning due to ingesting antifreeze. The findings aim to provide a reference for clinicians in the diagnosis and treatment of antifreeze poisoning.

This article analyzes the treatment process of a patient with respiratory failure caused by occupational acute acetonitrile poisoning. Due to operational errors, the patient's body was sprayed with a large amount of acetonitrile liquid, leading to the absorption of acetonitrile through the skin and resulting in acute poisoning. The clinical manifestations were nervous system and respiratory system damage, accompanied by severe lactic acidosis. After active comprehensive treatments such as tracheal intubation, mechanical ventilation, continuous renal replacement therapy (CRRT) , and glucocorticoids, the patient basically recovered. The treatment process of this patient indicates that early identification and correct first aid of acetonitrile poisoning are the keys to improving prognosis and can provide a reference for the handling of similar clinical cases.

Automotive antifreeze, being colorless and odorless, can easily cause acute poisoning if ingested. Acute poisoning can lead to damage to the central nervous system, digestive system, and kidney function, and may even result in death. This article analyzes the clinical data, diagnostic and therapeutic processes, and outcomes of two patients admitted to the Department of Poisoning and Occupational Diseases, Emergency Medicine of Qilu Hospital, Shandong University, who suffered acute poisoning due to ingesting antifreeze. The findings aim to provide a reference for clinicians in the diagnosis and treatment of antifreeze poisoning.

This article analyzes the treatment process of a patient with respiratory failure caused by occupational acute acetonitrile poisoning. Due to operational errors, the patient's body was sprayed with a large amount of acetonitrile liquid, leading to the absorption of acetonitrile through the skin and resulting in acute poisoning. The clinical manifestations were nervous system and respiratory system damage, accompanied by severe lactic acidosis. After active comprehensive treatments such as tracheal intubation, mechanical ventilation, continuous renal replacement therapy (CRRT) , and glucocorticoids, the patient basically recovered. The treatment process of this patient indicates that early identification and correct first aid of acetonitrile poisoning are the keys to improving prognosis and can provide a reference for the handling of similar clinical cases.

Objective:To compare the relative proportion of direct action (ray particles directly destroy biological molecules such as DNA and indirect action (radical-mediated oxidative damage) in the damage caused by X-ray and proton irradiation of lung cancer cells.Methods:Unirradiated human lung adenocarcinoma A549 cells and human large cell lung cancer NCI-H460 cells were cultured in media containing 0, 0.125, 0.25, 0.5, 0.75 mol/L dimethyl sulfoxide (DMSO) for 1 h to obtain plating efficiency (PE) values, thereby determining whether DMSO affected cell survival. Following pretreatment with each DMSO concentration, cells were exposed to X-ray irradiation at physical doses of 2, 4, 6, 8 Gy and proton irradiation at equivalent doses of 2, 4, 6, 8 GyE, respectively. Survival fractions (SF) and maximum protection (MP) values were calculated to evaluate the effects of varying DMSO concentrations on post-irradiation cell survival and to quantify the contribution of indirect radiation damage mechanisms (higher MP indicates greater indirect effect contribution). PE, SF, and MP values were determined using clonogenic assays. Comparisons among multiple groups were performed using one-way ANOVA followed by Tukey's multiple comparison, and comparisons between irradiation groups were analyzed using independent samples t-tests. Results:The PE of unirradiated cells treated with varying DMSO concentrations showed no statistically significant differences. Following pretreatment at different DMSO concentrations and subsequent irradiation with X-rays or protons, the protective effect of DMSO reached saturation at 0.5 mol/L. At this concentration, comparison of the average MP values across 4 radiation doses revealed: In A549 cells, the MP value was 54.21%±1.73% for X-ray irradiation group and 39.69%±0.72% for proton irradiation group ( t=16.82, P<0.001); in NCI-H460 cells, the MP value was 52.04%±1.00% for X-ray irradiation group and 41.31%±0.70% for proton irradiation group ( t=10.19, P<0.001). Conclusions:Under biologically equivalent doses, proton irradiation demonstrates greater reliance on direct effects in lung cancer cells killing compared with X-ray irradiation.

Objective:To establish the model of acute kidney injury (AKI), search for more sensitive and reliable biomarkers.Methods:In April 2018, 100 male Wister rats aged 6 to 8 weeks were selected and randomly divided into experimental group (n=90) and control group (n=10). The experimental group was given Diachalefin (140 mg/kg body weight) by intragastric administration, while the control group was given saline intragastric administration. Ten rats in the experimental group were killed 0.5 h, 2 h, 6 h, 24 h, 3 d, 7 d, 14 d, 21 d and 28 d after intragastric administration, respectively. Serum creatinine (Cr), urea nitrogen (BUN) and uric acid (UA) were detected by automatic biochemical analyzer with 5 ml of blood from inferior vena cava puncture. Serum neutrophil gelatinase-associated lipid carrier protein (NGAL), kidney damage molecule-1 (KIM-1) and transforming growth factor-β1 (TGF-β1) levels were determined by enzyme-linked immunosorbent assay (ELISA). The data between groups were compared using two independent sample t tests.Results:The renal tissue structure of rats in the control group was not significantly abnormal, while the renal tissue cell damage of rats in the experimental group was obvious, which gradually increased with the extension of time in the early stage, and gradually recovered in the later stage. UA in experimental group reached its peak at 24 h after exposure and was still higher than that in control group at 14 d ( P<0.05), Cr reached its peak at 7 d, and then gradually decreased, and there was no statistical significance between experimental group and control group at 28 d ( P>0.05). BUN increased at 6 h after exposure and reached the highest value at 7~14 d ( P<0.05). Blood NGAL increased at 0.5 h after exposure, reached its peak at 24 h, continued to increase at 3, 7 and 14 days ( P<0.05), and began to decrease at 21 days. KIM-1 began to increase at 0.5 h, continued to peak at 24 h, 3 and 7 d after exposure, and began to decrease at 14 d, but it was still higher than that in control group ( P<0.05). There was no significant difference in TGF-β1 at each time point ( P>0.05). Western blot assay results: Compared with control group, there was no significant difference in the expression level of TGF-β1 in kidney tissue of experimental group ( P>0.05). NGAL increased gradually from 2 h and was higher at 7 and 14 d, with statistical significance ( P<0.05). KIM-1 increased at 2 h, decreased at 6 and 24 h, and increased again at 3 and 7 d. Conclusion:NGAL and KIM-1 can be used as early diagnostic biomarkers for diquat-induced acute kidney injury.

This article analyzed the clinical data of a patient with acute benzene poisoning caused by oral ingestion of 100 ml of pure benzene. The patient presented with multiple organ dysfunction syndrome, manifested as consciousness disorders, abnormal coagulation function with hematuria, and delayed liver injury. After comprehensive treatment including fluid replacement, diuresis, protection of vital organs, and nutritional support, the patient was discharged after recovery. Poisoning caused by oral administration of large doses of benzene is rare. Analyzing the diagnosis and treatment process of this patient can enhance clinicians' understanding of acute benzene poisoning, provide empirical references for the clinical treatment of such poisoning patients, and improve their survival rate as much as possible.