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.

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.

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.

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.

The clinical data of 13 patients with esophageal dissecans superficials (EDS) induced by paraquat (PQ) in Qilu Hospital from March 2016 to April 2019 were analyzed retrospectively. EDS usually occurs on the 3rd to 9th day after taking poison, and the esophageal mucosa is different in size, color and character, in 10 cases of death, 1 case of pharyngeal pain basically disappeared on the 19th day after EDS onset, but died on the 27th day after taking poison, and 9 cases of death survived 5~19th days after taking poison, the overall cure rate was low; The pharyngeal pain symptoms of 3 surviving patients basically disappeared on day 15, 16 and 17 of EDS, and all patients had no discomfort after eating, and were cured gradually.

The clinical data of 13 patients with esophageal dissecans superficials (EDS) induced by paraquat (PQ) in Qilu Hospital from March 2016 to April 2019 were analyzed retrospectively. EDS usually occurs on the 3rd to 9th day after taking poison, and the esophageal mucosa is different in size, color and character, in 10 cases of death, 1 case of pharyngeal pain basically disappeared on the 19th day after EDS onset, but died on the 27th day after taking poison, and 9 cases of death survived 5~19th days after taking poison, the overall cure rate was low; The pharyngeal pain symptoms of 3 surviving patients basically disappeared on day 15, 16 and 17 of EDS, and all patients had no discomfort after eating, and were cured gradually.

Objective: To investigate an occupational hazardous gas poisoning incident caused by gas leakage in the process of hazardous waste treatment. Methods: An investigation was conducted on a case of occupational acute hazardous gas poisoning caused by waste treatment gas leakage in Shandong province in December 2017. Meanwhile, the clinical data of 5 cases of poisoning patients were analyzed, and the accident related poison test report and other relevant data were analyzed. Results: The incident was caused by the toxic waste did not do labeling work, the workers' protection measures were not in place, the illegal operation and the blind rescue, resulting in a total of 5 people died on the spot, 12 people were hospitalized with poisoning. Among them, 5 patients admitted to our hospital showed varying degrees of damage to the nervous system and respiratory system. After active treatment, they all got better and were discharged. Conclusion The poisoning is mainly caused by hydrogen sulfide dichloromethane hydrogen cyanide gas leakage serious production liability accident, clinical main performance for the nervous system circulatory system respiratory system and other system damage.

Objective: To report a case of rat poison with multiple hemorrhage after trauma. Methods: The clinical data of a case of rodenticide poisoning with hemorrhage as the first symptom admitted to a third-class a hospital in July 2018 were analyzed and summarized. Results: This patient is a rodent drug poisoning patient with hemorrhage as the first symptom.The disease was diagnosed as bromohamelin and bromadiolone poisoning through the analysis of poison detection because the rodent drug was taken in the market and the history of taking poison was concealed. The patient was given active comprehensive treatment of vitamin K1 and other drugs for clinical cure. Conclusion For patients with clinically unexplained hemorrhage, the possibility of rodenticide poisoning should be considered and the toxicant detection should be improved actively.

Objective: To explore the acute toxicity of Diquat in mice and to calculate the median lethal dose (LD₅₀) of Diquat to rats and observe the pathological changes of tissues and organs in rats with different concentrations of Diquat. Methods: Diquat solution of 50 mg/kg was prepared freshly with 1 000 mg of Diquat and dilute the solution with water to a total of 20 ml. A total of 99 healthy adult male Wistar rats were randomly divided into part one, part two and control groups. In the first part, 36 rats were randomly divided into 4 groups: 100 mg/kg group, 200 mg/kg group, 300 mg/kg group and 400 mg/kg group, which were treated with 100 mg/kg, 200 mg/kg, 300 mg/kg and 400 mg/kg of Diquat solution by gavage, respectively. The death and symptoms of poisoning after intragastric administration were recorded, and the maximum tolerated dose and absolute lethal dose were measured. In the second part, 54 rats were randomly divided into 6 groups: 200 mg/kg group, 220 mg/kg group, 240 mg/kg group, 260 mg/kg、280 mg/kg group and 300 mg/kg group, whichwere treated with 200 mg/kg, 220 mg/kg, 240 mg/kg, 260 mg/kg, 280 mg/kg and 300 mg/kg of Diquat solution by gavage, respectively. The survival of rats in different concentration of Diquat was observed and the LD₅₀ was calculated by Excel processing the formula of Koch's method. The control group were given equal volume water under the same experimental conditions. And moreover, the lungs, kidneys, hearts, livers, and brain tissues were collected and fixed by formaldehyde, embedded by paraffin, and sectioned for histopathological light microscopy. Results: The maximum tolerated dose was 240 mg/kg and the absolute lethal dose was 300 mg/kg. The LD₅₀ of Diquat for Rats was 280.58 mg/kg. The high-dose group had significantly more organ damage than the low-dose group after diquat poisoning. Conclusion The determination of the half-lethal dose of diquat, at the same time observed multiple organs damaged in rats after the diquat quickly poisoned. Kidneys, lungs and heart might be the main organ which was heavily damaged. With the extension of observation time, the organ damage of rats exposed to small doses gradually stabilized.

Objective: To investigate a poisonous mushroom poisoning incident and analyze its clinical data. Methods: Investigate a poisonous mushroom poisoning incident in a place in Shandong in July 2018, at the same time, the clinical data of 2 cases of mushroom poisoning were analyzed and summarized. Results: The incident was caused by a poisoning incident caused by residents eating poisonous mushrooms. The poisonous mushroom in this incident was identified as a scaled white goose cream. Two patients with poisoning developed gastrointestinal symptoms such as nausea and vomiting, abdominal pain and diarrhea, and liver damage occurred later. After active rescue and treatment, one patient was discharged from hospital, and the other patient developed acute pulmonary embolism during the treatment. He was discharged after interventional thrombolysis and follow-up treatment. Conclusion After investigation, the incident was caused by the ingestion of poisonous mushrooms mainly based on the scalloped white goose cream. After active treatment, they were cured and discharged.