Adult ; Aluminum Silicates ; China ; epidemiology ; Female ; Humans ; Male ; Middle Aged ; Occupational Exposure ; adverse effects ; statistics & numerical data ; Quartz ; adverse effects ; analysis ; Silicosis ; epidemiology ; mortality

Objective To investigate the rule of the cerebral tissues aquaporin-4(AQP-4) expression in acute and chronic hepatic failure mice.To study the molecular biologic mechanism of the diffusion weighted imaging(DWI).Methods Sixty five male Sprague-Dawley rats were divided into 3 groups randomly,including acute(n=25),chronic hepatic failure(n=25)and control group(n=15). Thioacetamide(TAA)intraperitoneal injection produces the acute and chronic hepatic failure models.All rats in groups were examined with MR DWI.We Observed the distribution of abnormal signal on DWI.The DWI single values of top and lateral cortex of parietal lobe,peripheral region of lateral ventricle in the highest hyperintensity section of brain were measured.Blood ammonia values were examined.The pathologic and immuno-histochemistry and RT-PCR examination for brain specimen were performed.All date were analyzed with statistical methods.Results The mean values of blood ammonia were significantly different (P0.05).Conclusions Increase of the blood ammonia was the main cause for the brain energy metabolic abnormality and AQP-4 mRNA and protein expression.The hyperammonemia was the key factor in the occurrence and development of the hepatic brain edema.The abnormal findings in DWI signal could reflect the range and degree of the brain edema and AQP-4 protein expression.

Ralstonia metallidurans CH34 was isolated from the deposit of a znic factory .The degradation of phenol by R .metallidurans CH34 was investigated. The results showed that R . metallidurans CH34 possesses high ability to degrade phenol with the biodegradation rate constant of 0.33 . The optimal pH , temperature and volume of medium for phenol degradation are pH 7.0 , 30℃ , and 20%(v/v), respectively . In addition , this strain retains its ability to degrade phenol in the presence of high concentration of heavy metal ion .The sodium citrate , sodium succinate can enhance the degradation of phenol.

Objective To improve the effect of clinical diagnosis and treatment of acetabular fracture with a femoral nerve injury by analyzing the causes of femoral nerve injury following acetabular fractures.Methods From January 1996 to November 2004,146 cases of acetabular fractures were treated operatively.Six cases of them were complicated with femoral nerve injury.The causes of femoral nerve injury were analyzed on the basis of clinical manifestations,CT scan and 3-dimensional reconstruc- tion.All the cases were classified according to Letournel and Judet classification.Three cases had hema- toma compression (2 cases with double column fractures and 1 with transverse-posterior wall fractures);2 cases had femoral nerve injury caused by fracture fragments (1 case with anterior wall fracture following anterior hip dislocation,the another with old fracture of anterior column combined with fracture of superior ramus of pubis);and one case had anterior column fracture combined with fracture of wing of ilium,and the femoral nerve was injured by traction in operation.Clearance of hematoma,nerve tract decompression and epineuria solution were performed in 5 cases,and 1 case was treated conservatively.Results The average follow-up period was 1.8 years(ranging from 1 to 3 years).The muscle power of quadriceps fem- oris recovered from 1-2 grade before operation to 4-5 grade after operation in 5 cases.The function of ex- tensor knee and gait was normal.The function of sensory completely recovered in 4 cases.One case was followed up for 2 years,which showed the patient still suffered from hypoesthesia in the lower 2/3 of the thigh and the medial of the leg.One ease of traction injury was followed up for 1.2 years,showing the muscle power recovered to normal,but still presented with sensory disability.Conclusion Acetabular fractures associated with femoral nerve injury are rare.For complex acetabular fractures and severe trau- ma,attention should be given to the possibility of femoral nerve injury.Fragment stabbing and compres- sion of hematoma around iliopsoas muscle are the common causes of femoral nerve injury following ace- tabular fractures.Iatrogenic injury should not be ignored.

ObjectiveTo explore the effects of heat treatment and ultraviolet B (UVB) radiation alone or in combination on the expression of heat shock protein (HSP) 72 in human epidermal melanocytes.Methods Melanocytes were obtained from human foreskin,and subjected to primary culture.After 3 to 5 passages,the melanocytes were classified into 4 groups:control group (receiving no treatment),heat treatment group (treated with heat at 42 ℃ for 1 hour every day for 3 days),UVB group(irradiated with UVB at 50 mJ/cm2 daily for 3days),combination group(treated with heat at 42 ℃ for 1 hour followed by irradiation with UVB at 50 mJ/cm2daily for 3 days).After another 2- to 6-hour culture following the last treatment,melanocytes were collected and subjected to real time PCR and Western blot for the detection of HSP72 mRNA and protein expression,respectively.ResultsThe mRNA and protein expressions of HSP72 were significantly higher in the heat treatment group and combination group than in the control group (mRNA:6.584 ± 0.871 and 7.269 ± 0.454 vs.0.975 ± 0.089,both P ＜ 0.001; protein:2.022 ± 0.058 and 2.080 ± 0.045 vs.0.532 ± 0.033,both P ＜ 0.001 ),but was similar between the UVB group and control group (mRNA:0.832 ± 0.084 vs.0.975 ± 0.089,P ＞ 0.05;protein:0.546±0.021 vs.0.532 ± 0.033,P ＞ 0.05).The ANOVA of factorial design showed that neither heat treatment nor UVB irradiation had interaction effect on the mRNA or protein expression of HSP72 (F =2.106,1.399 respectively,both P ＜ 0.05).ConclusionsHeat treatment can cause an increase in the expression of HSP72,which may enhance the function of melanocytes and protect melanocytes from UVB induced damage.

ObjectiveTo investigate the effect of heat treatment combined with narrow band ultraviolet B(NB-UVB) on cultured normal human melanocytes in vitro.MethodsMelanocytes were isolated from the foreskin of normal human,cullured in vitro,and irradiated with NB-UVB of different doses(20,30,50,70,90,120 and 180 mJ/cm2).Then,MTT assay was performed to evaluate the proliferation and activity of melanocytes to determine the optimal dose of UVB for the next experiment.Melanocytes were classified into 3 groups to be treated with heat at 42 ℃ for 1 hour (heat group),irradiated with UVB at 50 mJ/cm2 (UVB group),or irradiated with UVB at 50 mJ/cm2 followed by heat treatment at 42 ℃ for 1 hour (combination group),daily for 3 successive days; those receiving no treatment served as the control.After 24-hour culture following the last treatment,tyrosinase activity was evaluated with L-dopa as the substrate,melanin content was detected by NaOH assay,and cell cycle stages were determined by flow cytometry.ResultsNB-UVB irradiation decreased the viability of melanocytes in a dose-dependent manner,and the optimum dose of UVB was 50 mJ/cm2.The tyrosinase activity of melanocytes was 0.244 ± 0.018 and 0.310 ± 0.015 respectively in the UVB group and combination group,and increased by 3.8％ (P ＜ 0.05) and 31.9％ (P ＜ 0.05) respectively compared with the control group (0.235 ± 0.018); the melanin content was 0.201 ± 0.016 and 0.286 ± 0.019,respectively in the UVB group and combination group,and increased by 17.5％ (P ＜ 0.05 ) and 67.3％ (P ＜ 0.05) compared with the control group (0.171 ± 0.016).In comparison with the control group,the percentage of melanocytes in G1 phase was decreased by 23.94％ in the UVB group(P＜ 0.05) and 33.51％ in the combination group(P ＜ 0.05),while that in S phase and G2 phase increased by 15.35％ (P ＜ 0.05 ) and 11.93％ (P ＜ 0.05),respectively in the UVB group,and 17.76％ (P ＞ 0.05) and 16.08％ (P ＞ 0.05),respectively in the heat group.ConclusionHeat treatment and NB-UVB can synergistically enhance the tyrosinase activity and accelerate melanogenesis,proliferation and differentiation,of melanocytes.

OBJECTIVETo evaluate the erectile and ejaculatory function of sacral tumor patients after sacral nerve root resection and investigate the relationship of erectile and ejaculatory dysfunction (EED) with the level of sacral nerve injury.

METHODSThis retrospective study included 47 male patients aged 16 to 63 (32.6 +/- 6.8) years treated by sacral tumor resection between January 2008 and August 2013. According to the levels of the sacral nerve roots spared in surgery, the patients were divided into four groups: bilateral S1-S3 (n=16), unilateral S1-S3 (n=21), unilateral S1-S2 (n=6), and unilateral S1 (n=4). The patients were followed up for 12 to 41 (27.2 +/- 10.9) months by questionnaire investigation, clinic review, and telephone calls about their erectile and ejaculatory function at 3, 6 and 12 months after surgery and in August 2013.

RESULTSIn the bilateral S1-S3 group, the incidence rates of EED were 31.25% (5/16), 25% (4/16), and 12.5% (2/16) at 3, 6, and 12 months respectively after surgery, with recovery of erectile and ejaculatory function in August 2013. The incidence rates of EED in the unilateral S1-S3 group were 85.71% (18/21), 71.43% (15/21), 52.38% (11/21), and 42.86% (9/21) at 3, 6 and 12 months and in August 2013, respectively; those in the unilateral S1-S2 group were 100% (6/6), 83.33% (5/6), 83.33% (5/6), and 66.67% (4/6) at the four time points; and those in the unilateral S1 group were all 100% (4/4). No statistically significant differences were found in the incidence rate of EED among the patients of different ages or tumor types (P > 0.05).

CONCLUSIONThe incidence of postoperative EED in male patients treated by sacral tumor resection is closely related to the mode of operation. Sparing the S3 nerve root at least unilaterally in sacral tumor resection is essential for protecting the erectile and ejaculatory function of the patient.

Adolescent ; Adult ; Ejaculation ; physiology ; Erectile Dysfunction ; epidemiology ; etiology ; Female ; Humans ; Incidence ; Male ; Middle Aged ; Organ Sparing Treatments ; Peripheral Nervous System Neoplasms ; surgery ; Postoperative Complications ; epidemiology ; Postoperative Period ; Retrospective Studies ; Sacrum ; Spinal Nerve Roots ; injuries ; surgery ; Surveys and Questionnaires ; Young Adult

Adult ; Female ; Humans ; Inhalation Exposure ; Male ; Middle Aged ; Paraquat ; poisoning

OBJECTIVEThe aim of this study was to investigate the expression of transforming growth factor-beta1 (TGF-beta1) and its signaling pathway molecules in oral squamous cell carcinoma (OSCC) and analyze the association between these factors and genesis and metastasis of OSCC.

METHODSThe express of TGF-beta1, TbetaRI, TbetaRII and Smad4, a pivotal downstream molecule of its signaling, in 10 normal oral mucosa tissues and 108 OSCC was detected by SP immunohistochemistry, and thier correlation with genesis and metastasis of OSCC were assessed.

RESULTSThe expressions of TbetaRII and Smad4 were lower in the tumors (34.3%, 38.9%) than those in the normal oral epithelium (80.0%, 100.0%, P < 0.05). The positive expression rates of TGF-beta1 and TbetaRI in the normal oral epithelium and OSCC were not significantly different (P > 0.05). There was an inverse correlation between TGF-beta1, Smad4, TbetaRII, TbetaRI expression and clinical stages (P < 0.01). The expression of TGF-beta1 was related with histological differentiation and tumor localization (P < 0.05). There was a relationship beteween Smad4 expression and histological differentiation and lymph node metastasis (P < 0.05). The expression of TbetaRII in the samples with lymph node metastasis was less than that in the ones without lymph node metastasis (P < 0.01), although there was no association between expression of TbetaRII and lymph node metastasis status.

CONCLUSIONThere is an important relationship between the abnormal TGF-beta1/Smad4 signal pathway and genesis and development of OSCC, while the low expressed Smad4 and TbetaRII may promote the metastasis of OSCC.

Carcinoma, Squamous Cell ; metabolism ; pathology ; Cell Membrane ; metabolism ; Cytoplasm ; metabolism ; Female ; Humans ; Lymphatic Metastasis ; Male ; Middle Aged ; Mouth Neoplasms ; metabolism ; pathology ; Neoplasm Staging ; Protein-Serine-Threonine Kinases ; metabolism ; Receptors, Transforming Growth Factor beta ; metabolism ; Signal Transduction ; Smad4 Protein ; metabolism ; Transforming Growth Factor beta1 ; metabolism

OBJECTIVETo investigate the inhibitory effect of transforming growth factor (TGF)-β₁ on oral squamous cell carcinoma (OSCC) Tb cell line.

METHODSCell counting method was used to examine the inhibitory effect of TGF-β₁ on Tb cell and flow cytometry (FCM) assay performed to measure the changes of cell cycle. Superarray was used to screen the changing expression of genes in TGF-β₁/Smads signaling pathway.RT-PCR method was used to detect the results of Superarray.

RESULTSTGF-β₁ showed significant inhibiting effect on OSCC Tb cell line. TGF-β₁ blocked the cell cycle at G₁ phase. The expression level of activin receptor-like kinase-1 (ACVRL-1), anti-mullerian hirmine (AMH), cyclim-dependent kinase inhibitor-2B (CDKN-2B) and transforming growth factor-beta-indnced factor (TGIF) was higer in the cells treated with TGF-β₁ than in control, while TDGF-1 expression was down-regulated. ACVRL-1 and CDKN-2B gene expression was consistent with the results of Superarray.

CONCLUSIONSTGF-β₁ can inhibit the growth of OSCC Tb cell line. The mechanism may be related to the regulation of cell cycle and the expression of ACVRL-1 and CDKN-2B in TGF-β₁-Smads signaling pathway.

Activin Receptors, Type II ; metabolism ; Anti-Mullerian Hormone ; metabolism ; Carcinoma, Squamous Cell ; pathology ; Cell Cycle Checkpoints ; Cell Line, Tumor ; Cyclin-Dependent Kinase Inhibitor p15 ; metabolism ; Humans ; Neoplasm Metastasis ; Signal Transduction ; Transforming Growth Factor beta1 ; pharmacology