Pancreatic cancer is a highly malignant tumor of digestive tract which early diagnose is very difficult and has low rate of surgical resection of advanced pancreatic cancer. However, the rate of postoperative recurrence and metastas is high. Its prognosis is poor. To improve the prognosis of pancreatic cancer , it is necessary to improve its early diagnosis and effective prediction of postoperative recurrence and metastasis. In recent years, with the development of proteomics, the early diagnosis of pancreatic cancer and its early diagnosis of recurrence and metastasis was possible. Wsing proteomics technology for protein differences screening, isolation and identification is conductive to early detection of pancreatic proteome changes and establishment of the markers for early diagnosis, and recurrence and metastasis of pancreatic cancer.

Objective To investigate the expression of apolipoprotein E (ApoE) and complement C4b1 in pancreatic carcinoma and study its significance. Methods Immunohistochemistry was used to detect the expression of ApoE and C4b1 protein in 38 cases of pancreatic carcinoma tissues and adjacent normal pancreatic tissues, and RT-PCR was used to detect the expression of ApoE and C4b1 mRNA in 20 cases of pancreatic carcinoma tissues and adjancent normal pancreatic tissues. The relevance of ApoE and C4b1 expressions to the biological features of pancreatic carcinoma were analyzed. Results The positive rates of ApoE and C4b1 expressions are 86.8% (33/38) and 76.3% (29/38) in pancreatic carcinoma, respectively,which were significantly higher than those in normal pancreatic tissues [42.1% (16/38) and 26.3% ( 10/38 ),P ＜ 0.01]. The positive rates of ApoE and C4b1 expressions [78.3% ( 18/23 ) and 73.9% ( 17/23 )] in patients with metastasis were significantly higher than in those without metastasis [(33.3% (5/15) and 40.0%(6/15), P ＜ 0.05). Significantly higher expressions of ApoE and C4b1 mRNA were noted in pancreatic carcinoma(4.83 ± 0.65 and 7.94 ± 0. 95 ) than those in the normal pancreatic tissue ( 1.78 ± 0.74and 1.22 ±0.57, P ＜ 0.01 ), and patients with metastasis showed significantly higher expression of ApoE and C4b1 mRNA (5.05 ±0.71 and 8.24 ± 1.07) than those without metastasis (4.42 ±0.25 and 7.39 ±0.15,P ＜ 0.05). Conclusions ApoE and C4b1 were highly expressed in pancreatic cancer, and may be closely related with lymph node metastasis.

Objective To investigate the expressions of complements 3 (C3), 4B1 (C4B1) and apolipoprotein E (ApoE) in pancreatic cancer and relations with TNM staging and lymph node metastasis of pancreatic cancer. Methods Thirty-eight pancreatic cancer biopsy specimens, 20 fresh pancreatic cancer specimens and 20 adjacent normal tissues of pancreatic cancer were collected. The expressions of C3, C4B1, ApoE in pancreatic cancers and normal pancreatic tissues were detected by immunohistochemistry and Western-Blot, the positive expression rates of C3, C4B1, ApoE and the differences in gray scale were also observed. Their association with pancreatic cancer TNM staging and lymph node metastasis were analyzed by SPSS 13.0. Results The expression rates of C3, C4B1, ApoE in pancreatic cancer were 73.68% (28/38), 86.84%(29/38) and 76.31% (33/38) respectively, higher than those in normal pancreatic tissues which were 42.11% (16/38), 26.32% (10/38) and 42.11% (16/38) accordingly, the differences were statistically significant (χ2 was 7.77, 19.01, 16.6, and P value were 0.01, 0.00, 0.00 respectively). The gray scale of C3, C4B1 and ApoE in pancreatic cancer were 1.63±0.28,1.25±0.18 and 2.57±0.22 respectively, higher than those in normal pancreatic tissue (0.88±0.19,0.65±0.13,1.28±0.24 respectively), the differences were statistically significant (t value were 9.93,11.81,17.71 and all P value were 0.00, respectively). There was no association between C3 and TNM staging or lymphatic metastasis of pancreatic cancer. C4B1 and ApoE were closely related with TNM stage and lymph node metastases. The expressions of C4B1 and ApoE in stage Ⅱ to Ⅳ pancreatic cancer or with lymphatic metastasis were significantly higher than those in stage Ⅰpancreatic cancer and those without lymph node metastasis. Conclusion C3, C4B1 and ApoE were all highly expressed in pancreatic cancer. C3 was only involved in early event in pancreatic cancer, not related with development of pancreatic cancer. C4B1 and ApoE were involved in tumor growth and metastasis.

Malignant lymphoma of the maxillary sinus is very rare. A case of diffuse large B-cell lymphoma (DLBCL) of the left maxillary sinus is presented here. A 59-year-old man came to our hospital complaining of swelling under the left lower eyelid without any other symptoms. Imaging examination including CT and MRI detected a tumor in the left maxillary sinus. The tumor was invasive into left orbit. The biopsy revealed a diffuse large B-cell lymphoma. The tumor cells were positive to CD20, CD79a, CD45. In conclusion, a very rare case of DLBCL of the maxillary sinus was reported.
Humans ; Lymphoma, Large B-Cell, Diffuse ; Male ; Maxillary Sinus ; Middle Aged ; Paranasal Sinus Neoplasms

Objective To investigate the association of C3 and ApoE expressions with lymph node metastasis and clinical pathological stage of human pancreatic cancer. Methods Immunohistochemistry was used to detect the expression of C3 and ApoE in pancreatic cancer's tissues and normal pancreatic tissues,and the relevance of C3 and APoE expressions to the metastasis of pancreatic cancer was analyzed. Results The positive rates of C3 and ApoE expressions were 73.68% and 86.84% in pancreatic cancer,significantly higher than those in normal pancreas tissues (42.11% and 42.11%, P＜0.01 ). The positive rate of C3 expressions in pancreatic cancer of lymph node metastasis was 56.52%, in those without lymph node metastasis was 46.67% (P=0.741). The positive rate of C3 expressions in pancreatic cancer of stage Ⅰ was 57.14%, in those of stage Ⅱ - Ⅳ was 77.42% (P=0.194). The positive rate of ApoE expressions in pancreatic cancer of lymph node metastasis was 78.26%, significantly higher than those without lymph node metastasis (33. 33%, P＜0.01). The positive rate of ApoE expressions in pancreatic cancer of stage Ⅰ was 57. 14%, significantly lower than those of stage Ⅱ - Ⅳ (93.55%, P ＜0.05 ). Conclusions C3 and ApoEare all overexpressed in pancreatic cancer. C3 is not related with tumor's lymph node metastasis and clinical stages, may be marker for early diagnosis of pancreatic cancer. ApoE is closely related with tumor' s development, may reflect the biological behavior of pancreatic cancer.

To determine appropriate surgical methods and flaps to apply plastic surgery of facial defects. Several plastic methods were introduced progressively to eight cases. From simple to complex, we discussed the direct suture, relaxation suture, Z-flap, flap-footed, combined or multiple flaps, and free flap method to decrease the tension in wounds. The skin and flaps were successful in all eight cases and healed the wounds. It is important to choose appropriate surgical techniques and flaps to repair facial injuries.
Face ; surgery ; Facial Injuries ; surgery ; Free Tissue Flaps ; Humans ; Reconstructive Surgical Procedures ; Skin ; Wound Healing

ObjectivesTo investigate the effects of 5-aza-2-deoxycytidine(5-Aza-dC),a methylation inhibitor,on the expression and methylation of tissue factor pathway Inhibitor (TFPI-2) gene in PANC1 cell line of pancreatic cancer.MethodsPANC1 cell lines were treated with different dosages of 5-Aza-dC ( 1× 10-7,5 × 10-7,1× 10 -6 mol/L).The status of TFPI-2 methylafion and expressions of TFPI-2 mRNA and protein were determined by MSP,RT-PCR,and Western blot.Results TFPI-2 gene CpG island was completely methylated,and there was no expression of TFPI-2 mRNA and protein without 5-Aza-dC treatment.After treatment with different dosages of 5-Aza-dC( 1 × 10-7,5 × 10 -7,1 × 10-6 mol/L),TFPI-2 gene CpG hypermethylation was reversed from incomplete methylated to complete non-methylated.The relative expressions of TFPI-2 mRNA were 0.211± 0.087,O.327 ± 0.068,0.609 ± 0.017; and the relative expressions of TFPI-2 protein were O.429 ± O.121,O.675 ± O.044,1.132 ± O.124 in a dose-dependent manner ( P ＜0.05 ).ConclusionsThe hypermethylatien of promoter region may be the primary reason for TFPI-2 gene expression down-rogtdation and inactivation.5-Aza-dC may reverse the hypermethylation of TFPI-2 gene,and induce the m-expression of TFPI-2 mRNA and protein.

Objective To analyze the results in neonatal hearing screening,and then to make diagnosis and intervention for neonates with hearing problems as soon as possible.Methods From January 2004 to December 2008,7 064 newborns at Shanghai East Hospital received hearing screening by distortion product oto-acoustic emissions (DPOAE) 2～4 days after birth.Re-screening tests were performed for infants who failed the initial screening 42 days after birth.Those newborns who failed again received further audiologic diagnostic evaluations 3 months afterwards.Results Among 7 064 cases screened,out of 6 412 normal newborns,579 (9.03%)failed the initial screening,and 38 (7.41%)failed re-screening.129 cases of the other 652 (19.79%) newborns in NICU failed the initial screening,and 20 cases (18.69%) failed re-screening.There were statistical differences between the passing rates of the two groups (P

AIM:To investigate the effects of down-regulation of protein kinase C (PKC) on the activity of storeoperated Ca2 + channels (SOC) and the proliferation of airway smooth muscle cells (ASMCs). METHODS:Rat bronchial smooth muscle cells were isolated and cultured. Fluo-3 /AM fluorescence was measured by laser confocal microscope to assessing intracellular Ca2 +. Downregulation of PKC activity was achieved by incubation of ASMCs with PKC activator phorbol-12-myristate-13-acetate (PMA,10 ?mol/L) or phorbol 12,13 -dibutyrate (PDBu,1 ?mol/L) for 24 h. The proliferation of ASMCs was assayed by calculating the reduction rates of Alamar blue. RESULTS:Down-regulation of PKC activity by longterm exposure of PMA or PDBu inhibited the proliferation of ASMCs,the similar results were obtained by using PKC inhibitor chelerythrine. Both downregulation of PKC activity and inhibition of PKC activity by chelerythrine reduced Ca2 + entry through SOC channels. Low concentration of PMA (0. 1 ?mol/L) promoted the proliferation of ASMCs,and this effect was inhibited by SOC blocker SKF-96365. CONCLUSION:Inhibition or down -regu-lation of PKC activity results in the inhibition of SOC channels,suggesting that PKC is involved in the activation of these channels. Ca2 + entry through SOC channels might contribute to PKC-promoted proliferation of ASMCs.

Store-operated Ca(2+) channels (SOCs) are plasma membrane Ca(2+) permeable channels activated by depletion of intracellular Ca(2+) store. Ca(2+) entry through SOCs is known as store-operated Ca(2+) entry (SOCE), which plays an important role in the functional regulation of airway smooth muscle cells (ASMCs). Protein kinase C (PKC) has been shown to have an activating or inhibiting effect on SOCE, depending on cell types and PKC isoforms that are involved. In ASMCs, the effect of PKC on SOCE has not been elucidated so far. In this study, the role of PKC in the activation of SOCE in rat ASMCs was examined by using Ca(2+) fluorescence imaging technique. The results showed that acute application of PKC activators PMA and PDBu did not affect SOCE induced by the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) inhibitor thapsigargin. The non-selective PKC inhibitor chelerythrine significantly inhibited thapsigargin- and bradykinin-induced SOCE. RT-PCR assay identified PKCα, δ and ɛ isoforms in rat ASMCs. PKCα-selective inhibitor Gö6976 and PKCɛ-inhibiting peptide Epsilon-V1-2 had no effect on SOCE; by contrast, PKCδ-selective inhibitor rottlerin attenuated SOCE dramatically, suggesting that PKCδ was the major PKC isoform involved in the activation of SOCE in ASMCs. Moreover, PKC down-regulation by extended exposure to high doses of PMA or PDBu also reduced SOCE, confirming the essential role of PKC in the activation of SOCE in ASMCs. In addition, PKC down-regulation did not influence the expression of stromal interaction molecule 1 (STIM1) and Orai1, two elementary molecules in the regulation and activation of SOCs. These results identified PKCδ as an essential PKC isoform involved in the activation of SOCE, and confirmed that PKC regulates the function of ASMCs in a SOCE-dependent manner.