Objective To determine the value of endoscopic ultrasonography (EUS)-guided fine needle aspiration biopsy (FNAB) for differential diagnosis of pancreatic lesions. Methods EUS was performed in 23 patients with pancreatic lesions detected by CT, MRI, or US to assess the shape, size, and position of the lesions and the status of lymph nodes metastasis. After excluding blood vessel between the lesions and the fine needle by EUS, EUS guided FNAB was carried out. Results All patients were performed EUS-guided FNAB and only 2 patients failed. Among the other 21 patients, cytology and pathology demonstrated tumors in 10 patients (pancreatic carcinoma, n=8; pancreatic cystadenoma, n=1; non functional neuroendocrine tumor, n=1). The results of EUS-guided FNAB were evaluated by surgery (n=16), or clinical follow-up (n=7). The sensitivity was 83%, and speciality was 100%, and no complication occurred. Conclusions EUS-guided FNAB is a safe and accurate method for differential diagnosis of pancreatic lesions.

Objective To determine the value of EUS- guided fine needle aspiration biopsy (FNAB)for the diagnosis of submucosal lesions.MethodsWe found 28 patients with upper gastrointestinal tract solid submucosal lesions by endoseopies. EUS was performed to assess the lesions arised from the specific layer of the wall and the lymph node metastasis. After excluding extrinsic normal tissues compressing the gastrointestinaltract, EUS guided FNAB were carried out. Results Among these patients, two were extrinsic normal tissues compressing the gastrointestinal tract and all other 26 patients were examined by EUS guided FNAB. EUS- guided FNAB failed in only 3 patients. Among the other 23 patients, cytology demonstrated malignant tumors in 4 patients(lymphoma, n=2; leiomyosarcoma, n=2) and benign lesions in 19 patients(leiomyoma, n=1;lipoma, n=1 ). The results of EUS-guided FNAB were validated by surgery (n=20), endoscopic treatment (n=1) or clinical follow-up (n=7). Conclusion EUS guided FNAB is a safe and accurate method for di-agnosis of submucosal lesions.

ObjectiveTo assess the surgical results and implications of clinicopathologic features on the prognosis of patients with hepatic matastases from gastric adenocarcinoma. MethodsNinety one of 834 patients with primary gastric cancer were diagnosed with synchronous ( n =79) or metachronous ( n =12)hepatic metastases. Twenty-one cases underwent hepatectomy for the metastasis. Results The actuarial 1-year, 3-year survival rates after hepatic resection were respectively 69% and 30%. Solitary and metachronous metastases were significant determinants for a favorable prognosis after hepatic resection. Pathologically, tumor pseudomembrane was found in 13 out of 21 patients which was associated with a favorable prognosis. ConclusionsSolitary and metachronous hepatic metastases from gastric cancer should be treated by a surgical approach which confers a good prognosis. The formation of pseudomembrane of the metastatic tumor predicts a favourable postoperative survival.

OBJECTIVETo explore the effect of zoledronate (ZOL) on the osteoclast adhesion and expression of integrin α(v) and β3 in vitro.

METHODSMice RAW264.7 cells were used for osteoclast differentiation in vitro, and osteoclastogenesis was examined by tartrate-resistant acid phosphatase (TRAP) staining and dentin resorption lacunae examination. The cells were then divided into 2 groups, the control group and ZOL treatment group (treated with 1 x 10(-6) mol · L(-1) ZOL for 2 d). The adhesion ability of osteoclasts and mRNA and the protein expressions of integrin α(v) and β3 were examined by crystal violet staining, real-time fluorescence quantitative polymerase chain reaction, Western blot analysis, and immunofluorescent chemistry.

RESULTSTRAP staining and dentin resorption lacunae examination revealed the formation of multi-nuclear osteoclasts. ZOL treatment significantly decreased the adhesion ability of osteoclasts (P < 0.01). In the ZOL-treated group, the mRNA levels of integrin α(v) and β3 were 0.66 ± 0.05 and 0.59 ± 0.08, respectively. In the control group, the mRNA levels of integrin α(v) and β3, were 1.01 ± 0.01 and 1.01 ± 0.02, respectively; these values were higher than those in the ZOL-treated group (P < 0.01). The protein level of integrin α(v) and β3 in the ZOL-treated group (31,934.84 ± 112.91 and 18,812.79 ± 194.13) was downregulated by approximately 39.19% and 40.17%, respectively, compared with those in the control group (52,517.81 ± 211.72 and 31,441.93 ± 456.87) (P < 0.01). Immunofluorescent examination showed that the fluorescent intensities of integrin α(v) and β3 in the ZOL-treated group (9.491 ± 0.748 and 4.744 ± 0.759) were also significantly decreased compared with those in the control group (15.159 ± 1.143 and 11.418 ± 1.095) (P < 0.01).

CONCLUSIONZOL significantly inhibits osteoclast adhesion and downregulates integrin α(v) and β3, expression, thus contributing to the ZOL-induced inhibition of osteoclast- mediated bone resorption.

Animals ; Bone Resorption ; Diphosphonates ; Gene Expression ; Imidazoles ; Integrin alphaV ; Mice ; Osteoclasts ; RNA, Messenger

Objective To study the effect of zoledronate (ZOL) on Ca2+/calmodulin-dependent kinase Ⅱ δ (CaMK Ⅱ δ) and down-stream gene expressions during osteoclast differentiation.Methods Mouse osteoclast precursors RAW264.7 cells were divided into the control group and ZOL group.The cells in both groups were induced with 50μg/L receptor activator of nuclear factor kappa B ligand (RANKL) and were harvested on 5 d,while the cells in ZOL group were also simultaneously treated with 1 × 10-6 mol/L ZOL for 2 d.Five days later,the cells were harvested and examined osteoclastogenesis,as well as gene expressions of CaMK Ⅱ δ,nuclear factor of activated T-cells cytoplasmic 1 (NFATc1),tartrate-resistant acid phosphatase (TRAP) and cell-sarcoma receptor coactivator (c-Src).Results The number of TRAP positive multinuclear osteoclasts,number and size of dentin absorption lacunae and area in the ZOL group were (20.0±3.2),(18.0±4.2) and (6 335.3± 1 043.2)μm2 respectively,which were significantly lower than (36.0 ± 8.4),(37.2 ± 5.0) and (11 636.2 ± 3 661.1) μm2 in the control group and decreased by 44.4 ％,51.6 ％ and 45.6 ％ respectively (P＜0.01).ZOL also significantly inhibited the gene expressions of CaMK Ⅱ δ,NFATc1,TRAP and c-Src,and the mRNA levels of these genes were decreased by 44.1％,49.0％,53.8％ and 49.6％ respectively,the protein level were decreased by 43.5 ％,32.2 ％,45.5 ％ and 48.0 ％ respectively.The immunofluorescent cytochemistry detection results showed the fluorescence intensity of CaMK Ⅱ δ,NFATc1,TRAP and c-Srcin in the ZOL group was significantly weakened when compared with the control group.Conclusion ZOL could significantly inhibit the osteoclast formation and bone absorption function,and down-regulates gene expressions of CaMK Ⅱ δ,NFATc1,TRAP and c-Src in osteoclast differentiation.

[ ABSTRACT] AIM:To study the expression profiles and the role of Ca 2+/calmodulin-dependent kinase II delta ( CaMKIIδ) during osteoclast differentiation .METHODS:Mouse RAW264.7 cells were induced by receptor activator of nuclear factor κB ligand ( RANKL) at 50μg/L for osteoclastogenesis .Tartrate-resistant acid phosphatase ( TRAP) staining and bone resorption lacunae examination were performed to verify osteoclast formation .The expression of CaMKIIδat mR-NA and protein levels was also determined by immunofluorescent cytochemistry , RT-qPCR and Western blot at days 0, 1, 3 and 5.RESULTS:TRAP positive multinuclear cells with bone resorption function were formed after 5 d of induction. The mRNA levels of CaMKIIδdetected by RT-qPCR were 1.028 ±0.041, 2.478 ±0.087, 10.524 ±1.284 and 42.914 ± 2.667 at days 0, 1, 3 and 5, respectively, while the protein levels of CaMKIIδ detected by Western blot were 0.762, 0.963, 1.802 and 3.136, respectively.The changes of protein level were also verified by immunofluorescence cytochemis -try, in which the fluorescence intensity increased in a time-dependent manner (P<0.05).CONCLUSION:The expres-sion of CaMKIIδincreases with the differentiation of osteoclasts .CaMKIIδmay play a key role in the osteoclastogenesis .

OBJECTIVETo explore the effect of zoledronate (ZOL) on osteoclast differentiation and expressions of transient receptor potential vanilloid 5 channel (TRPV5) and nuclear factor of activated T-cells cytoplasmic 1 (NFATc1).

METHODSRAW264.7 cells were divided into two groups for treatment with RANKL for 5 days (group A) or with additional ZOL treatment in the last 2 days of RANKL treatment (group B). Osteoclastogenesis of the cells and the mRNA and protein expressions of TRPV5 and NFATc1 after the treatments were examined.

RESULTSIn group B, the number of newly generated osteoclasts (≥ 3 nuclei), number and size of dentin resorption lacunaes were 29.0 ± 2.4, 24.8 ± 1.1, and 2 030.0 ± 165.7 µm², respectively, which were significantly lower than those in group A (56.5 ± 4.5, 49.3 ± 0.9, and 3 946.7 ± 367.5 µm², respectively, P<0.01). Fluorescent intensity of TRPV5 and NFATc1 were also significantly decreased in group B (P<0.01). Compared with those in group A, TRPV5 mRNA and protein expressions in group B were down-regulated by 50.4% and 37.8%, and those of NFATc1 by 68.0% and 48.4%, respectively (P<0.01).

CONCLUSIONZOL can significantly inhibit osteoclastogenesis and bone resorption, which may be attributed, at least partly, to ZOL-induced inhibition of TRPV5 and NFATc1 expressions.

Animals ; Bone Resorption ; Calcium Channels ; metabolism ; Cell Differentiation ; drug effects ; Cell Line ; Diphosphonates ; pharmacology ; Down-Regulation ; Imidazoles ; pharmacology ; Mice ; NFATC Transcription Factors ; metabolism ; Osteoclasts ; drug effects ; RANK Ligand ; pharmacology ; RNA, Messenger ; TRPV Cation Channels ; metabolism

To report two cases of type 1.5 split cord malformation (SCM), a subtype of SCM with combined characteristics of types I and II and to review the relevant literature and propose a new possible pathogenetic theory for type 1.5 SCM. A 52-year-old woman had hemicords within a single dural sac with a dorsal bony septum at the L5 level. A 9-year-old boy had hemicords within a single dural sac with a ventral bony septum and fibrous extension at the L3 level. Both patients underwent microsurgical treatments for removing the bony septum, detethering the spinal cord, and sectioning the filum terminale. The surgical procedure revealed an extradural partial bony septum and hemicords within an intact single dural sac in each patient. Both patients were discharged from the hospital without de novo nerve dysfunction. Published cases have validated that types I and II SCM can overlap. We recommend recent type 1.5 SCM as a normative terminology for this overlapping SCM and report two rare cases of this SCM. We propose an associated pathogenesis consisting of uneven distribution and regression to explain type 1.5 SCM. Furthermore, we postulate that the amount of condensing meninx primitiva might determine whether the left bony septum has fibrous extensions to the opposite dura in type 1.5 SCM.