In this paper, the clinical data of a case of accidental poisoning of dimethylformamide in a traffic accident was analyzed. The patient was trapped in the driving room, his limbs were soaked in dimethylformamide for a long time, and dimethylformamide was inhaled at the same time. After 4 days of treatment in a local hospital, he was transferred to the Department of Poisoning & Occupational Diseases, Emergency Medicine of Qilu Hospital of Shandong University for treatment. The main clinical manifestation of the patient was liver damage and intractable abdominal pain, which was cured by active treatment.
Male ; Humans ; Dimethylformamide ; Abdominal Pain ; Occupational Diseases/complications* ; Poisoning

Fish bile poisoning may damage human liver and kidney, causing degeneration and necrosis. Can also damage brain cells and heart muscle, resulting in nervous system and cardiovascular system lesions. This paper reports a case of a patient who developed multiple organ dysfunction syndrome (MODS) after oral administration of fish bile with Xiexin folk prescription for eye disease. In January 2020, he went to the poisoning and occupational diseases department of the emergency department of Qilu hospital. After receiving hemoperfusion, continuous renal replacement therapy (CRRT) and symptomatic support treatment, the patient was improved and discharged. CRRT combined with HP is one of the rapid and effective methods for the treatment of acute fish bile poisoning.
Animals ; Gallbladder ; Hemoperfusion ; Humans ; Kidney ; Liver ; Male ; Multiple Organ Failure ; Poisoning/complications*

Allyl alcohol is an intermediate widely used in industrial production activities, which has caused many occupational damage in China. In this paper, the data of a case of skin damage and clinical cure of inhalation pneumonia caused by occupational allyl alcohol exposure were analyzed and summarized. The patient accidentally inhaled large amounts of allyl alcohol at work and had skin exposure, which was mainly manifested as aspiration pneumonia, respiratory failure, eye damage and skin bullae. After short-term hormone shock therapy, mechanical ventilation, infection prevention, local treatment and other comprehensive treatment, the patient was clinically cured. This case suggests that chemical pneumonia and respiratory failure may be caused by inhalation of allyl alcohol, and skin bullae may be caused by skin contact. Early treatment and hormone use should be emphasized.
Blister ; Hormones ; Humans ; Pneumonia ; Propanols ; Respiratory Insufficiency

Adult ; Femur Head Necrosis ; chemically induced ; drug therapy ; Glucocorticoids ; therapeutic use ; Humans ; Male ; Paraquat ; poisoning

Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Male ; Paraquat ; poisoning

OBJECTIVETo investigate the role of store-operated calcium channels (SOCs) in primary hepatocytes under conditions of calcium overload and ethanol-induced injury.

METHODSThe in vitro model of chronic ethanol-induced hepatocyte injury was established using primary hepatocytes isolated from Sprague-Dawley rats. Ethanol-induced changes (24, 48 and 72 h; 50, 100, 200, 400 and 800 mmol/L) in expression of the SOCs proteins stromal interaction molecule 1 (STIM1) and calcium release-activated calcium channel protein 1 (Oria1) were detected by qualitative PCR analysis (mRNA) and western blotting (protein). The possible role of these two SOCs proteins in the ethanol-induced extracellular calcium influx and related liver cell injury was determined by treating the cell system with various channel blockers (EGTA, La3+, and 2-APB). Cell viability was determined by MTT assay and cytosolic free calcium ion concentration was determined by flow cytometry.

RESULTSAfter 24 h of exposure to 0 (untreated) to 800 mM/L ethanol, the cell viability was reduced in a concentration-dependent manner. The 400 mmol/L concentration of ethanol decreased cell viability by 57.34% +/- 2.34%. and was chosen for use in subsequent experiments. Compared with the untreated control cells, the ethanol-treated cells showed significantly up-regulated mRNA and protein expression of both STIM1 and Orai1 at all times examined, suggesting that the ethanol-stimulated expression of STIM1 and Orai1 could persist for at least 72 h. The ethanol treatment induced increase in cytoplasmic calcium levels was significantly (and similarly) reduced by co-treatment with any of the three channel blockers.

CONCLUSIONChronic ethanol exposure can increase the expression of STIM1 and Orai1 in primary liver cells, suggesting that ethanol may increase extracellular calcium influx by up-regulating expression of these SOCs protein molecules, ultimately aggravating liver cell damage.

Animals ; Calcium ; metabolism ; Calcium Channel Blockers ; pharmacology ; Calcium Channels ; metabolism ; Calcium-Binding Proteins ; metabolism ; Cell Survival ; Cells, Cultured ; Ethanol ; adverse effects ; Hepatocytes ; drug effects ; metabolism ; Male ; Membrane Glycoproteins ; metabolism ; Primary Cell Culture ; Rats ; Rats, Sprague-Dawley ; Stromal Interaction Molecule 1

OBJECTIVETo investigate the clinical significance of dynamic changes of blood urea nitrogen (BUN), serum creatinine (Cr), serum cystatin (Cys C) and urinary protein on renal injury with paraquat poisoning.

METHODSAccording to the clinical manifestation and curative effect, the clinical information was analyzed retrospectively in 35 cases of acute paraquat poisoning, survival after eight weeks as the standard. Poisoning patients were taken a fasting blood 5 ml and the middle of urinary on the 1st day, 3rd day, 7th day, 14th day, 21st day and 8 weeks after the poisoning. Then the levels of serum BUN, Cr, Cys C and urinary protein were detected by automatic biochemistry analyzer. 30 cases healthy subjects were randomly selected as normal control group, and discharged kidney disease and other diseases of urinary system history. The same laboratory subjects have been done.

RESULTSThe level of serum Bun, Cr, Cys C of survival group increased significantly compared with control group within 21 days (P < 0.05). The level of serum BUN, Cr Cys C decreased on the 14th day. The decreased level of serum Cys C was lower than that of serum BUN and Cr. The renal function of 29 cases among 35 cases survival patients recovered on 21st day. The renal function of 31 cases among 35 cases survival patients recovered 8 weeks late. The positive rate of urinary protein of survival patients was high in the early intoxication (76.9%).

CONCLUSIONSerum Cys C is sensitive indicator to reveal the kidney injury on paraquat poisoning patients and have higher value of clinical applications in the diagnosis of the kidney injury of paraquat poisoning, which sensitivity is higher than serum BUN and Cr. The kidney injury caused by paraquat poisoning is reversible.

Acute Kidney Injury ; blood ; chemically induced ; Adolescent ; Adult ; Blood Urea Nitrogen ; Case-Control Studies ; Creatinine ; blood ; Cystatin C ; blood ; Female ; Humans ; Male ; Middle Aged ; Paraquat ; poisoning ; Young Adult

Objective To observe dynamically the CD11b,CD11c and CD54 in patients with acute cerebral infarction (ACI),to find out the change pattern and the effect of HBO on the change pattern,to illustrate the protective effects of HBO on cerebrovascular lesion in patients with ACI,and to explore the correlation between the CD1 1b,CD1 1c and CD54 before therapy and near and long-term effects on neurological recovery.Methods Sixty-four cases of ACI were divided into the HBO + routine therapy group (31 cases) and the therapy control group with only routine therapy (33 cases).CD11b,CD11c and CD54 in the subjects of both groups were measured in 72 hours,and on the 7th,10th,12th and 20th days respectively following acute infarction,and neural functional damage scores (NDS) were also evaluated at the same time.CD1 1b,CD11c and CD54 of the subjects in the normal control group (25 cases) were also measured by taking blood samples from peripheral veins.Results The expression of CD11b,CD11c and CD54 in the HBO group and the control group increased obviously within 72 hours of onset,and reached peak value within 72 hours.No significant differences could be seen between the two groups (P ＞ 0.05).Then,the above data declined on the 7th day.CD11b,CD11c in the HBO group maintained at peak level for7 days,while those in the control group maintained for 10 days.CD54 peak value kept for 10 days in the HBO group,while peak value maintained for 12 days in the therapy control group.Correlation analysis and linear regression analysis indicated that NDS on the 20th day (short-term curative effect) and NDS within half a year and a year (long-term effect) were 97.2％,96.7％,97.6％ respectively,which could be explained with the up-regulation of CD11b and/or CD1 1c and/or CD54 and other related factors.Conclusions The duration of peak levels of CD11 b,CD1 1 c and CD54 in ACI patients could be shortened,following hyperbaric oxygen therapy.HBO might intervene in the changing process of intercellular adhesion molecule,shorten the duration of abnormal time,reduce their expression,protect ACI patients and reduce the adhesion of leukocytes.The expression of CD11b,CD11c and CD54 could predict the severity and prognosis of the disease,interfere with the short or long- term curative effects on the patients before therapy and reduce the damage of blood vessels.In addition,they could provide scientific basis for the regulation and control of CD11b,CD11c and CD54 expression,and the early development of a comprehensive treatment profile of the disease.

Objective To observe dynamically the CD11b,CD11c and CD54 in patients with acute cerebral infarction (ACI),to find out the change pattern and the effect of HBO on the change pattern,to illustrate the protective effects of HBO on cerebrovascular lesion in patients with ACI,and to explore the correlation between the CD1 1b,CD1 1c and CD54 before therapy and near and long-term effects on neurological recovery.Methods Sixty-four cases of ACI were divided into the HBO + routine therapy group (31 cases) and the therapy control group with only routine therapy (33 cases).CD11b,CD11c and CD54 in the subjects of both groups were measured in 72 hours,and on the 7th,10th,12th and 20th days respectively following acute infarction,and neural functional damage scores (NDS) were also evaluated at the same time.CD1 1b,CD11c and CD54 of the subjects in the normal control group (25 cases) were also measured by taking blood samples from peripheral veins.Results The expression of CD11b,CD11c and CD54 in the HBO group and the control group increased obviously within 72 hours of onset,and reached peak value within 72 hours.No significant differences could be seen between the two groups (P ＞ 0.05).Then,the above data declined on the 7th day.CD11b,CD11c in the HBO group maintained at peak level for7 days,while those in the control group maintained for 10 days.CD54 peak value kept for 10 days in the HBO group,while peak value maintained for 12 days in the therapy control group.Correlation analysis and linear regression analysis indicated that NDS on the 20th day (short-term curative effect) and NDS within half a year and a year (long-term effect) were 97.2％,96.7％,97.6％ respectively,which could be explained with the up-regulation of CD11b and/or CD1 1c and/or CD54 and other related factors.Conclusions The duration of peak levels of CD11 b,CD1 1 c and CD54 in ACI patients could be shortened,following hyperbaric oxygen therapy.HBO might intervene in the changing process of intercellular adhesion molecule,shorten the duration of abnormal time,reduce their expression,protect ACI patients and reduce the adhesion of leukocytes.The expression of CD11b,CD11c and CD54 could predict the severity and prognosis of the disease,interfere with the short or long- term curative effects on the patients before therapy and reduce the damage of blood vessels.In addition,they could provide scientific basis for the regulation and control of CD11b,CD11c and CD54 expression,and the early development of a comprehensive treatment profile of the disease.

OBJECTIVETo observe the change of cytokine interleukin IL-1 beta, IL-6, IL-10, tumor necrosis factor-alpha (TNF-alpha) occurred in acute paraquat (PQ) poisoning rats and to investigate the mechanism of acute lung injury caused by paraquat (PQ) poisoning.

METHODSAll 72 healthy adult Wistar rats were random assigned into normal control groups, paraquat high dose group (120 mg/kg), paraquat middle dose (60 mg/kg) group, paraquat low dose group (30 mg/kg). Three observing periods of time included 8, 24, 72 h and the standards of TNF-alpha, IL-1 beta, IL-6, IL-10 were determined.

RESULTSEvery index of the PQ group was significantly higher than that in the NS group at the same period of time (P<0.05 or P<0.01). In the 72 h group, the high dose group was significantly higher than the middle and low dose group (P<0.05), and there was no significantly difference between the middle and low dose group (P>0.05). For the comparison of index in the same dose group, the group of 72 h was much higher than 8 h group and 24 h group (P<0.05), and there was no difference between the 8h group and 24 h group (P>0.05).

CONCLUSIONThe cytokine may play an important role in paraquat-induced acute lung tissue injury.

Acute Disease ; Animals ; Cytokines ; blood ; Disease Models, Animal ; Female ; Interleukin-10 ; blood ; Interleukin-1beta ; blood ; Interleukin-6 ; blood ; Male ; Paraquat ; poisoning ; Rats ; Rats, Wistar ; Tumor Necrosis Factor-alpha ; blood