Reports said formaldehyde could induce the damages of organism and cause the peroxidation of lipids. Formaldehyde inhalation may significantly increase the tissue malondialdehyde concentration and decrease the activity of superoxide dismutase, catalase enzyme, glutathione peroxidase enzyme and the concentration of glutathione in the tissues with a dose-effect relationship. The possible mechanisms of oxidation lesion and the toxic effects of formaldehyde were discussed in the present paper.

Objective To investigate the serum level of C-reactive protein (CRP) in patients with cerebral infarction and its effect on the prognosis of brain infarction.Methods 113 patients (86 with thrombosis and 27 with lacunar infarction) and 48 healthy persons as control were enrolled in this study. The serum level and abnormal rate of CRP were determined. All the patients were scored by clinic neurological function deficit scale (NDS).Results The serum level of CRP in the patients with thrombosis was higher than that in the patients with lacunar infarction. It was also higher in the patients with lacunar infarction than in normal controls (all P

Objective To investigate the indoors air formaldehyde pollution in the human anatomy laboratory and its effects on students health. Methods AHMT method was used to determine the concentration of formaldehyde in the indoor air and to observe the students’ signs and symptoms in the near month. Results The level of formaldehyde in the air of human anatomy laboratory was higher than that of the control and was higher than national standard limit. The prevalence rate of eye symptoms(51.98%), nasal symptoms(58.91%), throat symptoms(48.02%), nausea and vomiting, psychiatric symptoms(68.32%) and cold liability (60.89%) in the exposed group was higher than those in the control group(P

OBJECTIVETo study the protective effects of N-acetylcysteine (NAC) against oxidative injury in the brain tissue of mice induced by decabromodiphenyl ether (PBDE-209) and the expression of mitogen activated protein kinase (MAPK)-related proteins in the hippocampus.

METHODSTwenty-one male BALB/c mice were randomly divided into three groups with seven mice in each group: solvent control group, PBDE-209 group with gavage of 500 mg/kg PBDE-209, and PBDE-209 +NAC group which received intraperitoneal injection of 100 mg/kg NAC 0.5 h before exposure to PBDE-209. Mice were sacrificed 6 weeks after exposure. Malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, and glutathione (GSH) level in the cerebral cortex, hippocampus, cerebellum, and striatum, as well as the protein expression of extracellular signal-regulated kinase (ERK), phosphorylated ERK (p-ERK), p38 MAPK (p38), and phosphorylated p38 (p-p38) in the hippocampus, were determined by Western blot.

RESULTSCompared with the hippocampal and cerebellar levels of MDA in control group [(4.91±1.60) and (2.42±1.41) nmol/mg pro] and PBDE-209+NAC group [(6.16±1.03) and (2.83±0.85) nmol/mg pro], the MDA levels in PBDE-209 group [(12.12±6.39) and (4.24±1.15) nmol/mg pro] were significantly increased (P < 0.05). The striatum MDA level in PBDE-209 group [(12.92±4.30) nmol/mg pro] was significantly increased as compared with that of the control group [(4.05±2.23) nmol/mg pro] (P < 0.05). The hippocampal SOD activity of PBDE-209 group [(59.29±37.09) U/mg pro] was reduced significantly as compared with those of the control group [(93.28±21.75) U/mg pro] and PBDE-209+NAC group [(98.92±21.54) U/mgpro] (P < 0.05). The GSH levels in the cerebral cortex, striatum, and cerebellum in PBDE-209 group [(40.98±13.19), (24.46±11.30), and (3.55±1.55) mg GSH/g pro] were significantly reduced as compared with those of the control group [(75.79±26.51), (44.52±13.15) and (8.01±3.23) mg GSH/g pro] and the PBDE-209+NAC group [(89.86±28.39), (39.01±9.05) and (10.34±2.58) mg GSH/g pro] (P < 0.05). Western blot results showed that the ratios of p-p38/p38 and p-ERK/ERK in the hippocampus were significantly higher in the PBDE-209 group than in the control group and PBDE-209+NAC group (P < 0.05).

CONCLUSIONAntioxidant NAC has a protective effect against PBDE-209-induced brain injury in mice to some extent, and reduces the expression of MAPK-related proteins.

Acetylcysteine ; pharmacology ; Animals ; Antioxidants ; metabolism ; pharmacology ; Brain ; drug effects ; metabolism ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Glutathione ; metabolism ; Halogenated Diphenyl Ethers ; toxicity ; Hippocampus ; metabolism ; Male ; Malondialdehyde ; metabolism ; Mice, Inbred BALB C ; Mitogen-Activated Protein Kinases ; metabolism ; Oxidation-Reduction ; Phosphorylation ; p38 Mitogen-Activated Protein Kinases ; metabolism

Objective To explore the value of prenatal echocardiography in diagnosis of fetal ventricular septal defect (VSD).Methods Prenatal echocardiography was performed on 3 826 fetuses,and the results were compared with those of postnatal echocardiography or autopsy findings.The diagnostic accuracy,misdiagnosis rate and missed diagnosis rate of prenatal echocardiography for VSD were calculated.Results Among 3 826 fetuses,VSD was found in 61 fetuses (61/3 826,1.59％) with prenatal echocardiography,including simple VSD in 36 fetuses (36/3 826,0.94％) and VSD complicated with other heart malformations in 25 fetuses (25/3 826,0.65 ％).According to the results of autopsy and postnatal echocardiography,the final diagnosis of VSD was found in 76 cases (76/3 826,1.99％),of which simple VSD was found in 51 cases (51/3 826,1.33 ％),VSD complicated with other heart malformations were found in 25 fetuses (25/3 826,0.65％).The diagnostic accuracy,missed diagnosis rate and misdiagnosis rate of simple VSD with prenatal echocardiography was 58.82％ (30/51),41.18％ (21/51) and 1.06‰ (4/3 775),respectively.The diagnostic accuracy,missed diagnosis rate and misdiagnosis rate of VSD complicated with other heart malformations with prenatal echocardiography was 96.00％ (24/25),4.00％ (1/25) and 0.26‰ (1/3 801),respectively.Conclusion Echocardiography has important clinical value in prenatal diagnosis of fetal VSD,which can provide important references for treatment plan and prognosis evaluation.

Polybrominated diphenyl ethers (PBDEs) was one of the most common brominated flame retardants, it has been widely used in products such as furnitures, polymer and plastical material, textiles, electronic products and building materials. PBDEs have potential effect such as neurodevelopmental toxicity, reproductive toxicity, thyroid toxicity, immunological toxicity, embryo toxicity, liver toxicity, teratogenicity and potential carcinogenicity. This paper was aimed to review the environmental exposure way, current level, neurotoxicity, neurodevelopmental toxicity and reproductive toxicity of PBDEs. In recent years, PBDEs has been detected in environment, wildlife animal and human body around the world, there were the significant differences of exposure levels of PBDEs. The most abundant congener were tetra-BDE or BDE-47, hexa-BDE or BDE-153, and deca-BDE or BDE-209. Prenatal exposure to PBDEs has great impact on the infants' neurodevelopmental function, induces changes in neuropsychological developmental behavior, decreases of congnition, motivation and attention. High levels of PBDEs have positive relationship with Luteinizing hormone levels, testis disfunction and children's cryptorchidism, and have negative relationship with sperm number and testis size.

Polybrominated diphenyl ethers (PBDEs) was one of the most common brominated flame retardants, it has been widely used in products such as furnitures, polymer and plastical material, textiles, electronic products and building materials. PBDEs have potential effect such as neurodevelopmental toxicity, reproductive toxicity, thyroid toxicity, immunological toxicity, embryo toxicity, liver toxicity, teratogenicity and potential carcinogenicity. This paper was aimed to review the environmental exposure way, current level, neurotoxicity, neurodevelopmental toxicity and reproductive toxicity of PBDEs. In recent years, PBDEs has been detected in environment, wildlife animal and human body around the world, there were the significant differences of exposure levels of PBDEs. The most abundant congener were tetra-BDE or BDE-47, hexa-BDE or BDE-153, and deca-BDE or BDE-209. Prenatal exposure to PBDEs has great impact on the infants' neurodevelopmental function, induces changes in neuropsychological developmental behavior, decreases of congnition, motivation and attention. High levels of PBDEs have positive relationship with Luteinizing hormone levels, testis disfunction and children's cryptorchidism, and have negative relationship with sperm number and testis size.

Objective : To analyze the risk factors for endophthalmitis requiring evisceration or enucleation. Methods : The charts of 121 eyes of 121 inpatients with endophthalmitis were retrospectively reviewed , and the group that required evisceration or enucleation (24 patients) with those that received salvaging therapies (97 patients) were compared. Age , sex , medication history , past medical history , clinical manifestation , Leukocyte counts and treatment progression were retrospectively analyzed. Results : Twenty four eyes( 19. 8% )underwent enucleation or evisceration. The proportion of corneal ulcerative endophthalmitis ( 33. 3% ) and endogenous endophthalmitis (25. 0% ) in evisceration or enucleation group was greater than that in the salvaging group ( 1. 0% , 4. 1% ) (P < 0. 001) . The group of eviscerated or enucleated eyes was older (P < 0. 05] , had poorer initial visual acuity [(2. 9 ± 0. 2) LogMAR vs (2. 3 ± 0. 5) LogMAR , P < 0. 001] , had longer duration before intervention ( 15. 8 d vs 4. 6 d , P < 0. 05) , and had more Leukocyte counts [( 12. 8 ± 5. 6) × 109/L vs (9. 1 ± 3. 3) × 109/L , P < 0. 005 ] . With Logistic regression analysis , corneal ulcer, endogenous endophthalmitis , initial vision , leukocyte counts , duration before intervention were the risk factor for evisceration or enucleation ( OR = 343. 283 , OR = 22. 608 , OR = 1 920. 384 , OR = 1. 341 , OR = 1. 167 ) . Conclusion The most common cause of evisceration or enucleation caused by infectious endophthalmitis are infections from corneal ulcer and from endogenous source. The risk factors for endophthalmitis requiring evisceration or enucleation would be considered to be corneal ulcer endophthalmitis , endogenous endophthalmitis , initial vision , leukocyte counts , and duration before intervention.

Objective To study changes in expression of claudin-11 and proteins related to mitogen-activated protein kinase (MAPK) signaling pathways, as well as the ultrastructure of the blood testis barrier(BTB), in male ICR mice exposed to decabromodiphenyl ether (BDE-209). Methods Fifty-two mice, 4 weeks of age, weighing 15-21 g, were provided with adaptive feeding for 1 week. Mice were randomly divided into 4 groups, named control, low-dose, medium-dose and high-dose groups. The treated groups received BDE-209, by intragastric gavage, at doses, respectively, of 100, 300 and 500 mg/kg. Mice were sacrificed after 6 weeks and organs harvested on ice, weighed and stored at-80 °C. The ultrastructure of testicular tissues was examined by electron microscopy. Western blotting was used to detect proteins related to the MAPK pathway, including p38 mitogen activated protein kinase (p38), phosphorylated p38 (p-p38), extracellular regulated protein kinase 1/2 (ERK1/2) , phosphorylated ERK1/2 (p-ERK1/2) , c-jun N-terminal kinase (JNK), phosphorylated JNK (p-JNK) and the BTB tight junction protein claudin-11. Analyze the difference between each groups. Results At sacrifice, the body weights in each treated group were compared with those in the control group weighing (41.14 ± 0.60) g. Compared with controls, body weights were significantly different (P<0.05) in the middle dose, at (39.97 ± 0.66) g and high dose, at (39.98± 0.55) g in control group. The coefficients of the testis were significantly lower (P<0.05) in each treated group than in controls, with values of (0.37±0.0)%, (0.31±0.05)% and (0.31±0.04)% for low- dose, medium-dose and high-dose groups, respectively. The epidymus coefficient values were also significantly lower than controls (P<0.05), with values of (0.16±0.06)%, (0.11±0.05)% and (0.07±0.03)%, respectively in the same three dose groups. Electron microscopy ultrastructure showed that, compared with the control group, the testes in the middle and high dose groups had closely connected fractures, cell edema and more vacuoles. Compared with in the control group, levels of p-p38 and p-JNK in testicular tissue were significantly increased (P<0.05). In the control group and in low-, medium- and high-dose groups, the p-p38/p38 ratios were 1.35±0.13, 3.46±0.10, 5.71±0.26 and 4.79±0.21, respectively. The corresponding p-JNK/JNK ratios were 2.07±0.0, 4.77±0.18, 3.63±0.06 and 4.85±0.15. Claudin-11 levels were significantly lower (P<0.05) than control values in each dosed group. The corresponding values in control, low-dose, medium-dose and high-dose groups were 8.33±0.36, 2.06±0.27, 3.37±0.27 and 1.55±0.19, respectively. Conclusion BDE-209 increased expression of proteins in the MAPK pathway and decreased expression of the BTB tight junction protein claudin-11 in testicular tissue. It also caused ultrastructural damage to the Sertoli cell BTB tight junctions.This suggested that BDE-209 might damage Sertolicells BTB through effects on the MAPK pathway.

Objective To study changes in expression of claudin-11 and proteins related to mitogen-activated protein kinase (MAPK) signaling pathways, as well as the ultrastructure of the blood testis barrier(BTB), in male ICR mice exposed to decabromodiphenyl ether (BDE-209). Methods Fifty-two mice, 4 weeks of age, weighing 15-21 g, were provided with adaptive feeding for 1 week. Mice were randomly divided into 4 groups, named control, low-dose, medium-dose and high-dose groups. The treated groups received BDE-209, by intragastric gavage, at doses, respectively, of 100, 300 and 500 mg/kg. Mice were sacrificed after 6 weeks and organs harvested on ice, weighed and stored at-80 °C. The ultrastructure of testicular tissues was examined by electron microscopy. Western blotting was used to detect proteins related to the MAPK pathway, including p38 mitogen activated protein kinase (p38), phosphorylated p38 (p-p38), extracellular regulated protein kinase 1/2 (ERK1/2) , phosphorylated ERK1/2 (p-ERK1/2) , c-jun N-terminal kinase (JNK), phosphorylated JNK (p-JNK) and the BTB tight junction protein claudin-11. Analyze the difference between each groups. Results At sacrifice, the body weights in each treated group were compared with those in the control group weighing (41.14 ± 0.60) g. Compared with controls, body weights were significantly different (P<0.05) in the middle dose, at (39.97 ± 0.66) g and high dose, at (39.98± 0.55) g in control group. The coefficients of the testis were significantly lower (P<0.05) in each treated group than in controls, with values of (0.37±0.0)%, (0.31±0.05)% and (0.31±0.04)% for low- dose, medium-dose and high-dose groups, respectively. The epidymus coefficient values were also significantly lower than controls (P<0.05), with values of (0.16±0.06)%, (0.11±0.05)% and (0.07±0.03)%, respectively in the same three dose groups. Electron microscopy ultrastructure showed that, compared with the control group, the testes in the middle and high dose groups had closely connected fractures, cell edema and more vacuoles. Compared with in the control group, levels of p-p38 and p-JNK in testicular tissue were significantly increased (P<0.05). In the control group and in low-, medium- and high-dose groups, the p-p38/p38 ratios were 1.35±0.13, 3.46±0.10, 5.71±0.26 and 4.79±0.21, respectively. The corresponding p-JNK/JNK ratios were 2.07±0.0, 4.77±0.18, 3.63±0.06 and 4.85±0.15. Claudin-11 levels were significantly lower (P<0.05) than control values in each dosed group. The corresponding values in control, low-dose, medium-dose and high-dose groups were 8.33±0.36, 2.06±0.27, 3.37±0.27 and 1.55±0.19, respectively. Conclusion BDE-209 increased expression of proteins in the MAPK pathway and decreased expression of the BTB tight junction protein claudin-11 in testicular tissue. It also caused ultrastructural damage to the Sertoli cell BTB tight junctions.This suggested that BDE-209 might damage Sertolicells BTB through effects on the MAPK pathway.