Objective To investigate the imaging appearances of non-ossifying fibromas in healing stage and its clinical value.Methods The imaging features of non-ossifying fibroma in healing stage in 10 cases followed-up clinically(2 cases of them were verified by pathology after operation) were analyzed. All of the cases were examined by radiography,4 cases were examined by CT, 1 case underwent MRI. Results All of the cases were located in long bone of lower extremity. 8 cases were in tibia,2 cases were in femur. 5 cases were shown as homogeneous sclerosis,lucent areas were presented in sclerotic foci in 5 cases. 5 cases were unchangeable after followed-up 1 to 4 years .Conclusion The non-ossifying fibroma is being sclerotic stabilized foci after puberty , no operation is necessary for the healed form non-ossifying fibroma.

Objective To investigate the effect of high dose mifepristone and high dose progesterone in the treatment of patients with endometrial carcinoma and to explore the possible mechanisms associating with them Methods Thirty untreated patients diagnosed as endometrial carcinoma through dilation and curettage of the uteri were divided into 3 groups at random Each group was given medroxyprogesterone acetate(MPA),(500 mg/day) or mifepristone(MIF),(100 mg/day)or MIF(100 mg/day)+ MPA(500 mg/day)for 5 days respectively On the sixth day, hysterectomy was performed on these patients The endometrial cancer specimen of post hysterectomy was compared with the one of pre administrating The morphologic changes of the endometrial cancer cells were observed through light microscope Immunohistochemistry assay (SP method) was applied to determine the localization and immunoreactive intensity of proliferating cell nuclear antigen(PCNA), estrogen receptor (ER), progesterone receptor (PR), B cell leukemia lymphoma 2 (bcl 2), bcl 2 associated X protein(bax) and CD 44 v6 Results Better differentiation degree and active excretion were observed in all of the post hysterectomy endometrial specimen In the same time, apoptosis of carcinoma cells was observed The most significant changes were seen in the MIF+MPA group In the MPA group,the pre treatment and post treatment expression of PR(2 9?1 1,1 6?0 8),ER(2 8?0 9,1 4?0 9),PCNA(0 84?0 10,0 60?0 12),bcl 2(0 236?0 089,0 157?0 981) and CD 44 v6 (4 6?1 8,2 5?1 9) were all decreased(all P 0 05) In the MIF+MPA group, the expression of PR(3 2?1 0,0 8?0 8),ER(2 7?0 9,0 7 ?0 9 ),PCNA(0 81?0 09,0 25?0 09),bcl 2(0 225?0 091,0 066?0 009)and CD 44 v6(4 5?1 9,2 7?1 6) were all decreased(all P

Objective CD44, a cell surface glycoprotein, plays an important role in tumor growth and glycolysis.The aim of this study was to investigate the effects of neutralizing CD44 antibodies on the growth and glycolytic metabolism of B16 cells in melanoma in vitro.Methods B16 cells were treated with control antibodies (50 μg/mL) or different concentrations of CD44 antibodies (2, 10, and 50 μg/mL) for 24 hours, followed by examination of the activation of the AKT pathway in the B16 cells by Western blot.Then the tumor cells were also treated with control antibodies (50 μg/mL) or CD44 antibodies (50μg/mL) after pretreated with API-2 (4 μmol/L) in a parallel test.After 48 hours of treatment, the expression of lactate dehydrogenase A (LDHA) in the B16 cells and the level of lactate in the culture supernatant were detected by immunofluorescence and colorimetry, respectively.Lastly, the B16 cells were treated with control antibodies (50μg/mL), API-2 (4 μmol/L), CD44 antibodies (50μg/mL), or API-2 + CD44 antibodies for 96 hours, followed by measurement of the proliferation of the cells by MTT and their apoptosis by AO/EB and AnnexinV staining.Results In comparison with the control antibody group, the level of AKT phosphorylation (p-AKT) in the B16 cells showed a concentration-dependent increase in the 2, 10, and 50 μg/mL CD44 antibody groups (1.00±0.25 vs 2.51±0.32, 3.89±0.46, and 4.07±0.42, P<0.01), and the expression of LDHA was increased by (2.13±0.24) times, with the lactate level in the culture supernatant significantly elevated from (35.32±3.24) to (56.34±8.19) mmol/L (P<0.01) after 96 hours of treatment with 50 μg/mL CD44 antibodies.Treatment with API-2+CD44 antibodies, however, suppressed the increase in the LDHA expression and reduced the level of lactate.Compared with the control antibody group, the proliferation rate of the B16 cells was markedly decreased in the API-2, CD44 antibody, and API-2+CD44 antibody groups ([103±12.91] vs [84.87±19.35], [71.35±16.23], and [41.16±9.15]%, P<0.05), while the apoptosis rate remarkably increased ([5.23±0.96] vs [13.65±4.27], [19.21±3.53], and [43.21±7.87]%, P<0.01).Conclusion Neutralizing the function of CD44 in the B16 cells in vitro can inhibit the growth of the cells and promote AKT-mediated glycolytic metabolism, while suppressing the AKT pathway may enhance the antitumor activity of the CD44 antibody.

10.3969/j.issn.2095-4344.2013.26.002

Objective To investigate the feasibility of adrenal sparing surgery for selected renal cell carcinoma (RCC), since the necessity of routine adrenalectomy during radical nephrectomy for RCC has been challenged in recent years.Methods 178 patients underwent perifascial nephrectomy in a 16-year period. Of these patients, 96 had ipsilateral adrenal gland preserved during nephrectomy and 82 underwent concomitant adrenalectomy. 75 excised adrenal specimens were examined pathologically. Disease specific survival rates were assessed according to the pathological stage of the tumors.Results Of the 75 patients, 53 presented a macroscopically normal adrenal gland without patho- histological changes. The other 22 patients were suspected to have adrenal metastasis intraoperatively, while only 5 of them were confirmed to have adrenal involvement by histopathology. Two patients in the adrenal gland preservation group developed ipsilateral adrenal recurrence and synchronous or metachronous contralateral adrenal metastasis during follow-up, although both were documented to have a normal-appearing adrenal gland intraoperatively. Five patients with adrenal metastasis and 2 patients with adrenal recurrence had large renal tumors. The survival difference among subgroups of patients undergoing adrenalectomy or with adrenal gland left in situ was not statistically significant.Conclusion Adrenal sparing surgery could be done for patients with small renal tumors along with macroscopically normal ipsilateral adrenal glands.

Objective To investigate the dosimetric advantages of proton and heavy ion radiotherapy ( particle radiotherapy) for liver cancer adjacent to gastrointestinal tract. Methods Ten patients with liver cancer adjacent to gastrointestinal tract receiving radiotherapy were recruited in this study. The prescription was first given with 50 Gy ( RBE )/25 fractions to planning target volume 1 ( PTV-1 ) using proton irradiation,and then administered with 15 Gy ( RBE)/5 fractions to PTV-2 using carbon-ion irradiation. A simultaneous integrated boost regime was established using the same variables and prescription. The organ at risk ( OAR) constraints were referred to RTOG 1201. All plans were performed for dose evaluation after qualifying the OAR constraints. Results The dose coverage of 95％ of the prescribed dose ( V95) for PTV-1 from the photon plan (97.15％±4. 27％),slightly better than (96.25±6. 69％) from the particle plan (P=0. 049).The V95 of PTV-2 from the particle plan was (94.6％±6. 22％),comparable to (95.12％±3. 49％) from the photon plan (P=0. 277).The integral dose of Body-PTV-1 delivered by the particle plan was merely 39. 9％ of that delivered by the photon plan. The mean liver-GTV dose from the particle plan was only 81. 8％ of that from the photon plan. The low-dose irradiation to the stomach and duodenum from the particle plan was significantly lower than that from the photon plan. Conclusions The dose to the liver-gross tumor volume ( GTV) is the main factor limiting the increase of total dose to the tumors. When the absolute GTV in the liver is relatively large,particle radiotherapy can maintain comparable dose coverage to the tumors as the photon radiotherapy whereas significantly reduce the dose to the liver-GTV.

Thirteen compounds were isolated from the stem bark of Bombax ceiba L. by silica gel, and Sephadex LH-20 column chromatography. Their structures were identified by spectroscopic analysis as: lupeol(1), lupeone(2), betulinic acid(3), zeorin(4), oleanolic acid(5), 3-oxooleanolic acid(6), cleomiscosin A(7), (±)-lyoniresinol(8), desmosterol(9), stigma-3, 6-dione(10), (+)-lasiodiploidin(11), aurantiamide acetate(12), and(2S, 3S, 4R, 10E)-2-［(2R)-2-hydroxytetracosanoylamino］-10-octadecene-1, 3, 4-triol(13). Among them, compounds 3, 4, 6, 7-13 were isolated from this plant for the first time.

Fear memories are temporarily suppressed after repeated retrieval, a phenomenon known as memory extinction.How to reduce or even eliminate fear memory is the key to the treatment of fear related diseases such as post-traumatic stress disorder(PTSD). A single extinction training based on Pavlov's fear regulation task could only inhibit the expression of conditioned fear memory traces, but it could not eliminate the acquired conditioned fear memory. However, according to the reconsolidation theory based on memory, the retrieval-extinction paradigm has a more lasting effect on the erasure and rewriting of fear memory, and can effectively prevent the return of fear memory. Studies have shown that extraction-regression is closely related to a variety of neurotransmitter receptors such as glutamate receptor(GluR), dopamine receptor(DAR), L-type voltage-gated calcium channels(LVGCs) and cannabinoid. Moreover, its effect is closely related with factors such as retrieval-extinction memory stage. At present, most of the researches on extracted boundary conditions only stay at the level of behavior, with little understanding and exploration on the level of molecular mechanism. From the perspective of molecular neurobiology, with different stages of memory and different types of receptors and molecular mechanisms, this research reviewed the mechanisms of retrieval-extinction in recent years.It provided valuable signaling pathways, molecular targets and research directions for the treatment of fear-related diseases such as PTSD.

Objective To investigate whether human RhoA is modified by SUMO. Methods Overlap extension PCR and double digestion technique were used to construct the eukaryotic expression vector pcDNA3-3flag-RhoA, which was identified by sequencing. The plasmid was transfected into HEK293T cells and its expression was detected by Western blotting. Immunofluorescence assay was used to detect whether RhoA is co-localized with SUMO. Co-Immunoprecipitation was used to detect whether RhoA is modified by SUMO. Results The recombinant plasmid pcDNA3-3flag-RhoA was successfully constructed and verified. Western blotting showed that the recombinant plasmid pcDNA3-3flag-RhoA expressed abundant fusion protein in HEK293T cells. Immunofluorescence showed that RhoA was co-localized with SUMO2/3 but not with SUMO1. Co-immunoprecipitation verified that RhoA was modified by SUMO2/3 but not SUMO1. Conclusion Human RhoA is modified by SUMO2/3 and probably participates in the regulation of axon regrowth after nervous system injury.

Objective To investigate whether human RhoA is modified by SUMO. Methods Overlap extension PCR and double digestion technique were used to construct the eukaryotic expression vector pcDNA3-3flag-RhoA, which was identified by sequencing. The plasmid was transfected into HEK293T cells and its expression was detected by Western blotting. Immunofluorescence assay was used to detect whether RhoA is co-localized with SUMO. Co-Immunoprecipitation was used to detect whether RhoA is modified by SUMO. Results The recombinant plasmid pcDNA3-3flag-RhoA was successfully constructed and verified. Western blotting showed that the recombinant plasmid pcDNA3-3flag-RhoA expressed abundant fusion protein in HEK293T cells. Immunofluorescence showed that RhoA was co-localized with SUMO2/3 but not with SUMO1. Co-immunoprecipitation verified that RhoA was modified by SUMO2/3 but not SUMO1. Conclusion Human RhoA is modified by SUMO2/3 and probably participates in the regulation of axon regrowth after nervous system injury.