Antisperm antibodies (ASA) in sera from 59 couples of infertility were studied by ELISA, the positive rate was 32.20%, in which 20.34% females and 11.86% males. (P

Objective To investigate the relationship of radiation dose with the volume and late toxicity of the sternocleidomastoid muscle ( SM) in patients with nasopharyngeal carcinoma. Methods SM was divided into upper part and lower part based on the lower edge of cricoid cartilage. Patients were divided into three groups according to the prescribed dose for clinical target volume at the lower neck ( CTV2 ) ( 0, 54,60 Gy) . The dosimetric parameters included Dmean , V66 , and V60 for the upper, lower, and whole SM. SM was delineated and the volume was calculated on computed tomography images in the treatment planning system before and at 6, 12, and 18 months after treatment. The anteroposterior and transversal diameters of SM at C3?C4 , C4?C5 , C5?C6 , and C6?C7 levels were measured and recorded. Late toxicity of neck skin and SM was evaluated according to the Common Terminology Criteria for Adverse Events V4 .0 criteria. Between?group comparison was made by t?test or Kruskal?Wallis non?parametric test. Between?group comparison of the sample rate was made by one?way analysis of variance. The correlation analysis was made by Spearman correlation. Results There were significant difference in SM volume between the three time points after treatment ( P=0. 000) . At 12 or 18 months after treatment, the volume of SM wasignificantly reduced ( P=0. 000,0. 000);the reduction in SM volume was significantly correlated with V66 of the SM and the upper SM ( P=0. 015,0. 020) . At 18 months after treatment, SM fibrosis was significantly correlated with V60 of the upper SM ( P=0. 030);the fibrosis of neck skin was significantly correlated with the Dmean and V60 of the upper SM ( P=0. 029,0. 005) . Conclusions In order to prevent the incidence of the fibrosis of neck skin and SM, the dose homogeneity should be as high as possible, while the number of hot spots should be as small as possible.

Objective To establish and evaluate a reliable and highly reproducible neonatal rat model of hyper-bilirubinemia and to provide an experimental basis for research of kernicterus and related mechanism of neuroinjury.Meth-ods Sixty 7-day old SD rats (28 male and 32 female) were used in this study.Three doses of phenylhydrazine hydrochlo-ride (25, 50, and 75 mg/kg) were intraperitoneally injected respectively to the neonatal rats to establish models of hyper-bilirubinemia induced by hemolysis.The control group was set up at the same time.48 hours after the experimental treat-ment, the bilirubin in blood and brain tissue, neuron-specific enolase (NSE) of brain tissue, and hemoglobin were detec-ted to evaluate the models.Results Compared with the control group, the bilirubin in the blood and brain tissue and the brain tissue NSE in the three experimental groups were significantly higher than that in the control group (P<0.05), while hemoglobin content was significantly lower than that in the control group (P<0.05).The bilirubin of blood and brain tis-sue and brain tissue NSE in the 50 mg/kg and 75 mg/kg dose phenylhydrazine hydrochloride groups were significantly high-er than that of the 25 mg/kg dose group ( P<0.05) , while hemoglobin content was significantly lower than that of the 25 mg/kg dose group ( P<0.05 ) .There were no significant differences between the 50 mg and 75 mg dose groups ( P>0.05).Conclusions Intraperitoneal injection of phenylhydrazine hydrochloride can be used to produce neonatal rat mod-els of hyperbilirubinemia, mimicking the clinical features of this disease, and 50 mg/kg of phenylhydrazine hydrochloride is the best concentration.It is an ideal method to establish newborn rat models of hyperbilirubinemia.

Objective To establish the newborn rhesus monkey model of hemolytic hyperbilirnbinemia and provide an experimental basic model for research of hyperbilirubinemia.Methods Sixteen 3-day old newborn rhesus monkeys were divided into experimental group and control group,with 8 newborn rhesus monkeys in each group.Eight newborn rhesus monkeys in experimental group were treated with intravenous injection of l0 g/L phenylhydrazine hydrochloride (50 mg/kg) to establish model of homolytic hyperbilirubinemia.The newborn rhesus monkeys in control group were treated with intravenous injection of 9 g/L saline at the same time.Twenty-four hours and 48 hours after the experimental treatment,the bilirubin in blood was detected to evaluate the models,and the clinical manifestations of newborn rhesus monkeys with hyperbilirubinemia were recorded by using monitoring equipment.The brain slices were made to evaluate the model in 1 dead monkeys of experimental group.Results The newborn rhesus monkey of experimental group showed obvious skin,sclera jaundice and hemoglobinuria.The serum total bilirubin [(252.76 ± 63.42) μmol/L],unconjugated bilirubin[(165.85 ±44.93) pmol/L] and conjugated bilirubin [(87.16 ±21.22) μmol/L] in the experimental group were significantly higher than those [(20.62 ± 5.72) μmol/L,(7.93 ± 2.31) μmol/L,(12.51 ± 3.53) μmol/L] in the control group,and the differences were statistically significant (t =14.581,13.881,14.040,all P ＜ 0.01).The level of hemoglobin [(47.18 ± 10.09) μmol/L] in the experimental group was significantly lower than that of the control group [(136.85 ± 13.48) μmol/L],and the difference was statistically significant (t =-21.308,P ＜ 0.01).The results of pathological showed brain edema,rupture and eosinophilic and bilirubin deposition in the basal nuclei,and necrosis appeared in some severe parts.And there were different degrees of retardation and coordination disorders in the experimental group(s) newborn rhesus monkeys,but gradually returned to normal in 4 months later.Conclusion Intravenous injection of phenylhydrazine hydrochloride can be used to produce newborn rhesus monkey models of hemolytic hyperbilirubinemia.

Aged ; Chlorpyrifos ; Dermatitis, Occupational ; etiology ; Female ; Humans ; Insecticides ; poisoning ; Middle Aged ; Organophosphate Poisoning ; complications

Acute Disease ; Adult ; Humans ; Male ; Occupational Diseases ; Phosgene ; poisoning

Objective: To study the therapy of cordyceps-astragalus-salvia miltiorrhiza in treating acute lung injury and pulmonary interstitial fibrosis induced by paraquat poisoning. Methods: All 120 adult Wister male rats were randomly assigned to three groups, the paraquat poisoning group (rats were intragastric administration paraquat 50 mg/kg body weight once at the beginning) , the cordyceps-astragalus-salvia miltiorrhiza therapy group (rats were given cordyceps-astragalus-salvia miltiorrhiza 90 mg/kg body weight intragastric administration half an hour after paraquat was given, then the same dose was given once a day) ; control group (rats were intragastric administration with physiological saline) . At 7th, 14th, 21st, and 28th day rats were sacrificed postanesthetic respectively after paraquat exposure, sample of lung tissue, bronchoalveolar lavage (BAL) , and venous blood were collected. GSH, SOD, TNF-α, TGF-β1, and HYP in plasma, bronchoalveolar lavage (BAL) , and the lung homogenates were determined. Optical microscope was performed to examine pathological changes in lung. Results: Each experimental time point paraquat group and the treatment group rats serum SOD content significantly lower than the control group (P<0.05) . Each experimental time point the treatment group rats serum SOD levels increased significantly than that of paraquat group (P<0.05) . Each experimental time point paraquat group rats serum GSH content significantly lower than that of the control group (P<0.05) . Treatment group rats 7 days time GSH content significantly lower than that of the control group (P<0.05) . Treatment group 21 days, 28 days GSH content was increased significantly than that of the paraquat group (P<0.05) . Each experimental time point paraquat group rats alveolar lavage SOD content was significantly lower than that of the control group (P<0.05) . Treatment group 7 days, 14 days time SOD content was significantly lower than that of the control group (P<0.05) , Treatment group 21 days, 28 days SOD content was increased significantly than that of the paraquat group (P<0.05) . Each experimental time point paraquat group and the treatment group rats alveolar lavage GSH content significantly were lower than that of the control group (P<0.05) . Treatment group days 14 and 21 days, 28 days GSH content was increased significantly than that of the paraquat group (P<0.05) . Each experimental time point paraquat group rats alveolar lavage TNF α levels was higher than that of the control group (P<0.05) . Treatment group 7 days, 14 days the rat alveolar lavage TNF α levels was higher than that of the control group (P<0.05) . Treatment group 21 days, 28 days TNF α content significantly was decreased than that of paraquat group (P<0.05) . Paraquat group days 14 and 21 days, 28 days HYP content was significantly higher than that of control group (P<0.05) . Treatment group 21 days HYP content was significantly higher than that of control group (P<0.05) . Treatment group 28 days time HYP content in lung tissue of rats was significantly decreased than that of the paraquat group (P<0.05) . Each experimental time point paraquat group rat lung tissue (tissue homogenate) TGF-β1 content was higher than that of the control group, the difference was statistically significant (P<0.05) . Under optical microscope, the tissue damage of lung was aggravated, and reduced after cordyceps-astragalus-salvia miltiorrhiza was administrated. Conclusion Cordyceps-astragalus-salvia miltiorrhiza can reduce inflammation factor releasing, and relieve lung injury. It has therapeutic effect on lung injury induced by paraquat poisoning.

Objective: To establish to paraquat poisoning acute lung injury animal model to study the therapeutic effect of Salvia polyphenols acid salt of paraquat-induced acute lung injury. Methods: Adult male Wister rats 120, were randomly divided into three groups: the paraquat exposure group, the start of the experiment to give a one-time 20% paraquat dope orally 50 mg/kg body weight of rats; salvianolate treatment group, the start of the experiment paraquat to give a one-time 20% the stock solution orally 50 mg/kg body weight of rats, and then given daily intraperitoneal injection of 200 mg/kg body weight of rats salvianolate; blank control group was given the same amount normal saline. The exposure group, the treatment group and control group rats were sacrificed after anesthesia in the 3rd, 7th, 14th, 21st day from the beginning of the experiment respectively, and taken out and preserved venous blood specimens and lung tissue to be tested. Venous detection heme oxygenase-1 (HO-1) , the lung tissue detection heme oxygenase-1 (HO-1) , hydroxyproline (HYP) . And do biopsy specimens from some of the lung tissue, HE and Masson staining observed by optical microscope. Results: Compared with control group, model group 7, 14, 21 days had elevated levels of serum and lung tissue HO-1 (all P<0.05) ; Treatment group 3, 7, 14, 21 days increased (all P<0.05) , and 3, 7, 14 days is higher than the model group (compared with model group, P<0.05) . Compared with control group, treatment group 3 days and model group, 14, 21 days HYP content in lung tissue increased significantly (all P<0.05) ; 21 days, compared with model group, HYP content of treatment group reduce obviously, the difference was statistically significant (P<0.05) . Optical microscope observation, lung tissue damage and aggravated with the experimental increase in the number of days, inflammatory cell infiltration, alveolar septal fibrosis gradually formed. The treatment group experimental animal lung tissue to reduce inflammation, lung fibrosis relief. Conclusion Paraquat (50 mg/kg body weight) to fill the stomach can be induced model of acute lung injury in the rats. The serum HO-1 expression and HO-1, HYP content in lung tissue increased obviously in model rats. Salvia miltiorrhiza polyphenols acid salt to a certain degree and stage influenced the expression of HO-1 and HYP, relieve acute lung injury and pulmonary fibrosis, has certain curative effect in the treatment of paraquat poisoning.

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 analyze the microdeletion and microduplication characteristics of pathogenic copy number variations (pCNVs) and clinical phenotypes in children with neurodevelopmental disorders, and to clarify the genetic pathogenic cause of children with neurodevelopmental disorders.Methods:Children who were identified as neurodevelopment disorders such as global developmental delay and mental disorder, by next generation sequencing-based whole genomic copy number variation testing from January 2017 to November 2019 at the First Affiliated Hospital of Anhui Medical University were enrolled, and the clinical phenotypes and pCNVs were reviewed analyzed.Results:There were 36 pCNVs in total 31 children, consisting of 24 microdeletion segments (66.67%)and 12 microduplication segments (33.33%), with sizes ranging from 320.00 kb to 93.26 Mb (mean 11.33 Mb). pCNVs frequently occurred in chromosome 15 , chromosome 8 and chromosome X, there were 9 children with 9 pCNVs in chromosome 15(25.00%), 3 children with 5 pCNVs in chromosome 8(13.89%)and 3 children with 4 pCNVs in chromosome X(11.11%) .The mainly clinical manifestations were motor disorder (30 children, 96.77%), mental disorder (22 children, 70.97%), speech development delay(22 children, 70.97% )accompanied by the malformation(11 children, 35.48%), abnormal face(11 children, 35.48%) and epilepsy(8 children, 25.81%), multisystem abnormalities generally exist in one individual.Conclusion:This study demonstrates the clinical utility of whole genome CNVs testing in the genetic diagnosis of children with neurodevelopment disorders.Genetic pathogenesis of children with neurodevelopmental disorders can be revealed by the analysis of pCNVs.