Radiation-induced brain injury is a neurological injury caused by radiation therapy of head and neck tumors. The pathogenesis is still unclear. It is hypothesized that immune cells play an important role in radiation-induced brain injury. The excessive activation of microglia in the central nervous system and the migration of peripheral immune cells into the brain collectively promote the incidence and development of radiation-induced brain injury. In this article, the immunological mechanism underlying the radiation-induced brain injury was reviewed.

Objective To evaluate the protective effect of astragaloside Ⅳ against ultraviolet B (UVB)-induced photodamage to human HaCaT keratinocytes,and to investigate its mechanisms.Methods Culturedimmortalized human HaCaT keratinocytes were divided into four groups:blank control group receiving untreated,UVB group irradiated with 50 mJ/cm2 UVB,astragaloside Ⅳ group treated with astragaloside Ⅳ,UVB + astragalosideⅣ group treated with astragaloside Ⅳ for 24 hours before and after 50 mJ/cm2 of UVB radiation.The concentration ofastragaloside Ⅳ ranged from 10 to 200 mg/L in cell proliferation assay,and according to the results of proliferationassay,20 mg/L was determined as the optimal concentration in the other assays.At 24 hours after UVB radiation,cellcounting kit-8 (CCK8) assay was performed to evaluate cellular proliferative activity,flow cytometry to determineintracellular reactive oxygen species (ROS) levels,and Western blot to measure the expression levels of p53,p38,matrix metalloproteinase-9 (MMP-9) and high mobility group Al (HMGA-1) protein in HaCaT cells.ResultsCompared with the control group,astragaloside Ⅳ at 10 and 20 mg/L had no inhibitory effect (F =1.32,P ＞ 0.05),while astragaloside Ⅳ at 50,100 and 200 mg/L showed significantly inhibitory effect (F =20.20,P ＜ 0.05),on theproliferation of HaCaT cells.In addition,cellular proliferative activity in the UVB group was significantly lower thanthat in the control group (F =99.00,P ＜ 0.01).Compared with the UVB group,cellular proliferative activityincreased to different degrees in HaCaT cells treated with both UVB and astragaloside Ⅳ of 10-200 mg/L (F =19.08,P ＜ 0.01),with the strongest increase observed in those treated with UVB and astragaloside Ⅳ of 20 mg/L.Further experiments revealed reduced intracellular ROS levels in the UVB + astragaloside Ⅳ (20 mg/L) groupcompared with the UVB group (t =21.12,P ＜ 0.01).Western blot assay showed that the expression levels of p53,p38,MMP-9 and HMGA-1 protein were significantly higher in the UVB group than in the control group (all P ＜0.01),but significantly lower in the UVB + astragaloside Ⅳ (20 mg/L) group than in the UVB group (all P ＜ 0.01).Conclusion Astragaloside Ⅳ can effectively protect keratinocytes from UVB-induced photodamage.

OBJECTIVE: To analyze the role and significance of pepsin and pepsinogen in the pathogenesis of OME in children. METHOD: Pediatric patients with otitis media aged 2-8 years who enrolled in our department of the hospital from May of 2012 to December of 2012 were set as experimental group (38 cases, 48 ears) which should be underwent tympanic membrane puncture/tube insertion. Meanwhile, pediatric patients waiting for cochlear implant without otitis media (10 ears), were set as control group. Middle ear lavage fluid and plasma samples from the two groups were collected and detected using enzyme-linked immune method for pepsin and pepsinogen. RESULT: The concentrations of pepsin and pepsinogen in the middle ear lavage fluid of OME group [(48.8 ± 415.99) ng/ml and 676.32 ± 336.71)ng/ml] were significantly higher than those in the control group [(8.20 ± 4.59)ng/ml and (77.27 ± 50.33) ng/ml] (P < 0.01). Meanwhile, the concentration of pepsinogen in the middle ear lavage of OME patients was significantly higher than that of plasma (P < 0.01). The concentration of pepsin in the middle ear lavage fluid from the dry ear subgroup was lower than those in the serum ear and mucous ear subgroups (P < 0.01), but there was no significant difference about concentrations of pepsinogen among the dry ear, serum ear and mucous ear subgroups (P > 0.05). CONCLUSION Pepsin and pepsinogen in the middle ear cavity of OME patients maybe originated from laryngopharyngeal reflux (LPR), indicating that LPR is associated with the pathogenesis of OME in children.
Child ; Child, Preschool ; Ear, Middle ; metabolism ; Enzyme-Linked Immunosorbent Assay ; Humans ; Laryngopharyngeal Reflux ; physiopathology ; Otitis Media with Effusion ; metabolism ; Pepsin A ; metabolism ; Pepsinogen A ; metabolism ; Tympanic Membrane ; surgery

OBJECTIVETo get a complete cDNA sequence of B2 and evaluate the correlation on structure and expression between B2 and insulin like growth factor binding protein related protein 1 (IGFBP-rP1) in colorectal carcinomas, paired normal tissues, adenomas, tissues adjacent to the tumor, and colorectal carcinoma cell lines.

METHODS5'RACE (rapid amplification of cDNA end) was applied to get the sequence of the 5' end of B2. Semi-quantitative RT-PCR and immunohistochemistry were used to detect the expression of B2 in colorectal cancer tissues and cell lines (SW480, SW1116, SW620, HCT8, CoLo205 and LoVo).

RESULTSA sequence of 1,125 bp was obtained by combining the sequence from 5'RACE product and the known sequence of B2. It shared 1,122/1,125 identities with IGFBP-rP1. At the level of mRNA, the expression of B2/IGFBP-rP1 was high in colorectal carcinomas, moderate in adenomas and tissues adjacent to tumor, low in normal tissues (P < 0.05). Five cell lines except SW480 showed no expression of B2/IGFBP-rP1. A significant difference was obtained in the immunoreactivity of B2/IGFBP-rP1 between normal tissue and cancer (P < 0.05). In 28.9% (22/76) samples, cancer cells locating at the invasive front of cancer nest had a stronger staining of B2/IGFBP-rP1 than those surrounding the lumen. These samples had also an increased frequency of lymph node metastases, increased depth of invasion and a stronger staining of B2/IGFBP-rP1 than in other samples (P < 0.05).

CONCLUSIONSB2 is the same gene as IGFBP-rP1. Overexpression of B2/IGFBP-rP1 may play an important role in the initiation and promotion of colorectal cancer. Its overexpression in invading tumor cells may be linking with an increased potential of invasion.

Adenocarcinoma ; metabolism ; secondary ; Adenoma ; metabolism ; pathology ; Aged ; Cell Line, Tumor ; Colonic Neoplasms ; metabolism ; pathology ; Female ; Humans ; Insulin-Like Growth Factor Binding Proteins ; biosynthesis ; genetics ; Lymphatic Metastasis ; Male ; Middle Aged ; Neoplasm Invasiveness ; RNA, Messenger ; genetics ; Rectal Neoplasms ; metabolism ; pathology ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVETo evaluate the efficacy and toxicity of the combined therapy with oxaliplatin and capecitabine (XELOX) in patients with advanced or recurrent gastric cancer.

METHODSForty-one patients with previously untreated advanced or recurrent gastric cancer received intravenous infusion of oxaliplatin at the dose of 130 mg/m(2) on day 1 and oral administration of capecitabine at 1000 mg/m(2) twice a day on days 1-14. The chemotherapy was repeated every 2 weeks for a median of 4 cycles.

RESULTSTwo of 41 patients achieved a complete response, and 15 had partial responses, with an overall response rate of 41.5%. Stable disease was observed in 11 patients and progressive disease in 9. The median time to progression and overall survival was 6.2 months and 11.8 months. All the 41 patients were evaluated for toxicity according to NCI criteria, 4 showed grade 3-4 neural toxicity, 4 had hematological toxicity and 3 had hand-foot syndrome.

CONCLUSIONThe XELOX regimen shows good efficacy with an acceptable toxicity profile in advanced or recurrent gastric cancer patient.

Adult ; Aged ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Deoxycytidine ; analogs & derivatives ; therapeutic use ; Female ; Fluorouracil ; analogs & derivatives ; therapeutic use ; Humans ; Male ; Middle Aged ; Neoplasm Recurrence, Local ; drug therapy ; Stomach Neoplasms ; drug therapy ; pathology

TMTP1, a 5-amino acid peptide NVVRQ, obtained by using the flagella peptide library screening in our previous studies, can be used for the labeling of malignant in situ and metastatic lesions, and even micro-metastases. In this study, TMTP1 was assessed for its ability to specifically target the malignant hematopoietic cells and metastatic lesions of hematological malignancies. FITC-TMTP1 was chemically synthesized. Immunofluorescence assay and competitive test were carried out to determine the specific binding capacity of TMTPl to hematological malignant cell lines, including HL60, k562, SHI-1, Jurkat, Raji, El-4 and umbilical cord blood mononuclear cells. Mononuclear cells were isolated from the bone marrow of healthy subjects and patients with chronic myeloid leukemia. Then the cells were co-clutured with TMTP1 or scrambled peptides and the binding and affinity of TMTP1 peptide to the primary cells of hematological malignancies were flow cytometrically analyzed. The binding specificity of TMTP1 to target hematological malignancies was measured in vivo by intravenous injection of FITC-conjugated TMTP1 into El-4 lymphoma-bearing mice. The results showed that TMTP1 specifically bound to the cells of a series of hematological malignancies, including HL60, k562, Jurkat, Raji, El-4 and chronic myeloid leukemia primary cells but not to bone marrow mononuclear cells from healthy subjects. By contrast, TMTP1 could bind to the metastatic foci of lymphoma originating from the EL-4 cell line while the scrambled peptide failed to do so. Moreover, the occult metastases could be identified, with high specificity, by detecting FITC-TMTP1. We are led to conclude that TMTP1, as a novel tumor-homing peptide, can serve as a marker for primary malignant and metastatic lesions for the early diagnosis of hematological malignances and a carrier of anticancer drugs for cancer treatment.

TMTP1,a 5-amino acid peptide NVVRQ,obtained by using the flagella peptide library screening in our previous studies,can be used for the labeling of malignant in situ and metastatic lesions,and even micro-metastases.In this study,TMTP1 was assessed for its ability to specifically target the malignant hematopoietic cells and metastatic lesions of hematological malignancies.FITC-TMTP 1 was chemically synthesized.Immunofluorescence assay and competitive test were carried out to determine the specific binding capacity of TMTPI to hematological malignant cell lines,including HL60,k562,SHI-1,Jurkat,Raji,El-4 and umbilical cord blood mononuclear cells.Mononuclear cells were isolated from the bone marrow of healthy subjects and patients with chronic myeloid leukemia.Then the cells were co-clutured with TMTP1 or scrambled peptides and the binding and affinity of TMTP1 peptide to the primary cells of hematological malignancies were flow cytometrically analyzed.The binding specificity of TMTP 1 to target hematological malignancies was measured in vivo by intravenous injection of FITC-conjugated TMTP1 into El-4 lymphoma-bearing mice.The results showed that TMTP1 specifically bound to the cells of a series of hematological malignancies,including HL60,k562,Jurkat,Raji,El-4 and chronic myeloid leukemia primary cells but not to bone marrow mononuclear cells from healthy subjects.By contrast,TMTP1 could bind to the metastatic foci of lymphoma originating from the EL-4 cell line while the scrambled peptide failed to do so.Moreover,the occult metastases could be identified,with high specificity,by detecting FITC-TMTP1.We are led to conclude that TMTP1,as a novel tumor-homing peptide,can serve as a marker for primary malignant and metastatic lesions for the early diagnosis of hematological malignances and a carrier of anticancer drugs for cancer treatment.

OBJECTIVETo evaluate the inhibitory effect of recombinant adenovirus carrying human endostatin gene (Ad-endo) on the growth of human pancreatic carcinoma xenograft in nude mice.

METHODSThe expression of endostatin in human pancreatic carcinoma Capan-2 cells was examined by RT-PCR after infection with Ad-endo. The supernatants of Capan-2 cells were collected after 48 h of infection with Ad-endo as the conditioned medium for human umbilical vein endothelial cells (HUVECs), whose proliferation in vitro was assayed. Capan-2 cell xenografts were established to determine the antitumoral effects of Ad-endo in vivo. The intratumoral microvessel density (MVD) was evaluated using CD31 staining.

RESULTSThe expression of endostatin gene was detected by PT-PCR in infected Capan-2 cells. The conditioned medium from Ad-endo-infected cells significantly inhibited HUVEC proliferation (P<0.05). Ad-endo significantly suppressed the growth of Capan-2 tumor xenografts in nude mice (P<0.05), and the MVD decreased significantly in the treated tumor (P<0.05) as compared with that in the control group.

CONCLUSIONAdenovirus carrying human endostatin gene produces inhibitory effects on the growth of human pancreatic carcinoma tumors in nude mice.

Adenoviridae ; genetics ; metabolism ; Angiogenesis Inhibitors ; metabolism ; pharmacology ; Animals ; Endostatins ; biosynthesis ; genetics ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Neovascularization, Pathologic ; genetics ; Pancreatic Neoplasms ; blood supply ; pathology ; therapy ; Recombinant Proteins ; biosynthesis ; genetics ; pharmacology

Objective To study the reproductive biology of Chinese herbal medicine Polygonatum cyrtonema Hua. Methods The flowering habit of P. cyrtonema was observed and recorded regularly. The pollen viability at different flowering periods was detected by TTC. The stigma activity at different flowering periods was measured by the benzidine-hydrogen peroxide method. The hybridization index was estimated and pollen-ovule ratio was calculated. The breeding system of P. cyrtonema was determined by six different artificial pollination treatments. Results The flower buds of P. cyrtonema appeared at April 5. They bloomed at April 10 and fruited early in May, flowering about 30–40 days. The pollen began to have viability since the anthers were not cracked, and loss viability after flowers withered. The pollen viability at the bloom day was about 73.06%±5.19%. The stigmas began to have activity before flowers opening and lost it when the flowers began to decline. The hybridization index was 4, so the breeding system of P. cyrtonema Hua was partly self-compatible and xenogamy needing pollinator according to Dafni's standard.The pollen-ovule ratio was 1799.20±445.54,therefore the breeding system of P.cyrtonema Hua was facultative xenogamy according to Cruden's standard. The results of artificial pollination experiments showed that P. cyrtonema Hua had three breeding methods,including apomixis,selfing and outcrossing.The fruit setting rate of P. cyrtonema Hua was greatly influenced by external conditions such as strong wind and rain.Generally,P.cyrtonema Hua had a low fruit-set percentage because of obvious flower and fruit dropping. The natural fruit setting rate was only 17.46%. Conclusion The coexistence of apomixes, sexual and asexual reproduction in P. cyrtonema are the survival strategy adapting to different habitat types.

OBJECTIVETo explore the role of sorafenib in reversing multidrug resistance (MDR) in hepatoma BEL-7402/FU cells and its possible mechanisms.

METHODSMTT colorimetric assay was used to obtain the dose-response curve of sorafenib in BEL-7402/FU cells, and flow cytometry performed to assess the effect of sorafenib on Rho123 concentration in the cells. The optimal dose of sorafenib for cell treatment was determined according to the results of MTT assay and flow cytometry. MTT assay was employed to evaluate the effect of sorfenib on the cytotoxicity of the antitumor drugs, flow cytometry performed to determine the expression of cell membrane transport protein (P-gp), and RT-PCR used to detect mdr1 gene expression in the cells treated with sorafenib at the optimal dose.

RESULTSSorafenib at the concentration of 4 micromol/L, efficiently reversed the MDR of the cells with minimal side effects. At the concentration of 4 micromol/L, sorafenib partially reversed the drug resistance of BEL-7402/FU cells to ADM, 5-FU, GEM and DDP, with reversal indexes of 2.98, 7.16, 1.99 and 10.08, respectively. Treatment of the cells with 4 micromol/L, sorafenib also partially down-regulated P-gp expression in BEL-7402/FU cells, and caused a reduction of mdr1 gene expression by 27.3% in comparison with the control cells.

CONCLUSIONSorafenib can reverse MDR in human hepatoma cells probably in association with down-regulation of mdr1 gene expression and increased accumulation of the chemotherapeutic agents in the cells.

ATP-Binding Cassette, Sub-Family B, Member 1 ; genetics ; metabolism ; Antineoplastic Agents ; pharmacology ; Benzenesulfonates ; pharmacology ; Cell Line, Tumor ; Down-Regulation ; drug effects ; Drug Resistance, Multiple ; drug effects ; Drug Resistance, Neoplasm ; drug effects ; Humans ; Liver Neoplasms ; genetics ; Niacinamide ; analogs & derivatives ; Phenylurea Compounds ; Pyridines ; pharmacology