Objective:To explore the clinical and pathological features of familial gastric cancer, and to get the early discovery and early treatment of it.Methods:Two kindreds of familial gastric cancer were followed up and their clinical and pathological features were analyzed.Results:Six patients with gastric cancer were found in the 2 kindreds.Autosomal dominant inheritance was observed in these cases.clinical and pathological features of familial gastric cancer were showed according to the document analysis:early onset;poor prognosis;patients suffer simultaneous or metachronous carcinoma;CDH1 germline mutation carriers had higher penetrance;pathologically, tumors are mostly diffuse infiltrative type with lower differentiated degree and earlier metastasis to lymphnodes;in one kindred,the sites of the lesions were relatively consistent.Conclusion:Familial gastric cancer has particular clinical and pathological features:early onset;poor prognosis;patients suffer simultaneous or metachronous carcinoma;CDH1 germline mutation carriers have higher penetrance; pathologically,tumors are mostly diffuse infiltrative type with lower differentiated degree and earlier metastasis to lymphnodes.

OBJECTIVETo investigate the expression level of high mobility group box-1 (HMGB1) in human colorectal cancer and its relation with different clinicopathological characteristics and prognosis of colorectal cancer patients.

METHODSImmunohistochemical method was used to detect the HMGB1 expression in tissue samples of 86 colorectal cancer patients and 32 normal colorectal tissue samples. Positive rates of HMGB1 expression were compared among different clinicopathological characteristics. Relation of HMGB1 expression with survival was analyzed.

RESULTSHMGB1 expression was mainly in colorectal cancer cell nucleus, with a few appearance of co-expression in nucleus and cytoplasm. Positive rate of HMGB1 expression in normal tissues was significantly lower than that in colorectal cancers [9.4% (3/32) vs. 66.3% (57/86), P=0.000], and it was much higher in large cancers, lower differentiation, invasion to outside serosa, advanced clinical stage and lymph node metastasis (all P<0.05), but was similar in terms of age and gender (P>0.05). Survival analysis showed that 3-year survival rate of patients with positive HMGB1 expression was significantly lower as compared to those with negative HMGB1 expression (56.1% vs. 85.7%, P=0.021), meanwhile it was significantly lower in patients with co-expression in nucleus and cytoplasm as compared to those with simple nuclear expression (41.4% vs. 75.0%, P=0.013).

CONCLUSIONSHMGB1 expression in colorectal cancer is high, and its positive rate increases with the low differentiation, invasion and metastasis. HMGB1 co-expression in nucleus and cytoplasm indicates poor prognosis of colorectal cancer patients.

Cell Nucleus ; Colorectal Neoplasms ; HMGB1 Protein ; Humans ; Lymphatic Metastasis ; Prognosis ; Survival Analysis ; Survival Rate

OBJECTIVETo compare the clinical short-term safety and efficacy between robotic right colectomy (RRC) and laparoscopic right colectomy(LRC) with meta-analysis.

METHODSA search of the Medline, Embase, Ovid, CNKI and WANFANG databases was performed for studies comparing clinical or oncologic outcomes of RRC with LRC before July 2014. The RevMan 5.2 software was used for meta-analysis. The operative time, estimated blood loss, length of hospital stay, conversion rate to open surgery, postoperative complications and related outcomes were evaluated.

RESULTSSix studies including 217 RRC cases and 400 conventional LRC cases were enrolled and analyzed. The meta-analysis showed that RRC had longer operative time (MD=48.05, 95% CI: 26.52 to 69.57, P<0.01), less estimated blood loss (MD=-17.74, 95% CI: -28.32 to -7.16, P=0.01), faster postoperative intestinal peristalsis recovery (MD=-0.79, 95% CI: -1.10 to -0.48, P<0.01), lower postoperative overall complications (OR=0.63, 95% CI: 0.42 to 0.93, P=0.02). Conversion rate and postoperative hospital stay between the two groups were not significantly different (all P>0.05).

CONCLUSIONCompared to LRC, RRC is associated with less estimated blood loss, faster postoperative intestinal peristalsis recovery, lower postoperative overall complications, and longer operative time.

Colectomy ; Humans ; Laparoscopy ; Length of Stay ; Operative Time ; Postoperative Complications ; Postoperative Period ; Robotic Surgical Procedures

Objective Learning the dynamic changes of serum new Buniavirus IgM antibody of fever with thrombocytopenia syndrome cases to cover the missing of early diagnosis method for new Buniavirus nucleic acid detecting negative cases,provide the basis for clinical diagnosis and correct treatment.Methods Select the confirmed cases that the first serologic test results for the new Buniavirus nucleic acid testing is positive and negative for IgM antibody test,reserve the consecutive serum samples from patients which is taken every other day until leaving hospital,use Mac-ELISA method to detect the serum specimens of the new Buniavirus IgM seroconversion time and dynamic changes,and calculate the percentage of seroconversion time and the average seroconversion time.Results The new Buniavirus IgM seroconversion time proportions of the serum of the 16 patients who meet the requirements of the study after the onset of disease:5 d:2/16;7 d:6/16;9 d:9/16;11 d:10/16;13 d:12/16;15 d:16/16,and the average seroconversion time is 10.25 ± 3.58 days.Conclusions The serum new Buniavirus IgM antibody of the 16 fever with thrombocytopenia cases can be conversed as early as five days after the onset of disease and the latest with 15 days,then the density of the patient's serum antibody gradually increases after 基金 DOI:10.3760/cma.j.issn.1003-9279.2014.04.00 seroconversion and until 30 days after the disease can still maintain a high level.The convalescent serum IgG antibody titer of the 16 patients is 4 times more than the acute phase.New Buniavirus IgM antibodies detection can be used as an auxiliary method of the early diagnosis of fever with thrombocytopenia syndrome cases.

Objective To design and produce serial shock tubes and further examine their application to experimental studies on blast injury.Methods Bio-medical engineering technique was used for the design and development of the serial shock tubes. One thousand four hundred and fifty nine animals (757 rats, 105 guinea pigs, 335 rabbits, 240 dogs and 22 sheep) were then used to test the wounding effects of the shock tubes.Results Three types of bio-shock tubes, that is, large-, medium- and small-scale shock tubes were made in our laboratory. The large-scale shock tube is 39 meters long; the inner diameter of the test section is 1 meter; and the maximum overpressure in the driving section is 10.3 MPa. A negative pressure could be formed by means of the reflected rarefactive wave produced by the end plate. The medium-scale shock tube is 34.5 meters long; the maximum overpressure in the driving section is 22 MPa; the test section is designed to be a knockdown, showing 5 basic types with inner diameter of 77 to 600 millimeters, which could be used for researches on overpressure, explosive decompression, underwater explosion, and so on. The small-scale shock tube is 0.5 meter long with the maximum endured overpressure of 68.6 MPa. Results from animal experiments showed that this set of shock tubes could induce various degrees of systemic or local blast injury in large or small animals. Conclusions This set of bio-shock tubes can approximately simulate typical explosive wave produced by nuclear or charge explosion, and inflict various degrees of blast injury characterized by stability and reproducibility. Therefore, they can meet the needs of blast research on large and small animals.

OBJECTIVETo inquire into the influence of silencing HMGB1 expression by small interfering RNA (siRNA) on cell growth, proliferation, invasion and metastasis of colorectal cancer LoVo cells both in vitro and in vivo.

METHODSLentivirus-mediated HMGB1 siRNA was transfected into LoVo cells to silence the HMGB1 expression. The HMGB1 mRNA and protein expression after siRNA transfection was detected by RT-PCR and Western blot. MTT assay was used to observe the cell proliferation and to draw a growth curve. Cell cycle was measured by flow cytometry. The ability of invasion and speed of cell migration were evaluated by transwell chamber invasion and cell scratch assay. The influence of HMGB1 silencing on the proliferation of LoVo cells in vivo was observed in LoVo tumor-bearing nude mice.

RESULTSLentivirus-mediated siRNA was successfully transfected into colorectal cancer cell line LoVo. The expression of HMGB1 mRNA and protein in the HMGB1-siRNA group were 0.24±0.04 and 0.21±0.03, respectively. Compared with the HMGB1-siRNA-Neg group (0.82±0.13, 1.15±0.18) and control group (0.93±0.15, 1.21±0.20), the difference was significant (P<0.05). MTT assay showed that the cell proliferation in the HMGB1-siRNA group was significantly inhibited when compared with that in the HMGB1-siRNA-Neg group and control group (P<0.05). Flow cytometry showed that the proliferation index (PI) of HMGB1-siRNA group was 38.27±1.32, significantly lower than 54.66±1.74 in the HMGB1-siRNA-Neg group and 57.43±1.29 in the control group (P<0.05). The transwell assay showed that the number of penetrated cells in the HMGB1-siRNA group was 14.0±3.5, significantly lower than 51.0±6.7 in the HMGB1-siRNA-Neg group and 68.0±5.3 in the control group (P<0.05). Similarly, the scrape wound recovered significantly slower in the HMGB1-siRNA group (83.61±23.21) µm than that in the other two groups (202.86±46.46) µm and (214.58±57.38) µm(P<0.05). The nude mouse xenograft tumor experiment showed that the final tumor volume was (521±34) mm3 in the HMGB1-siRNA group, significantly smaller than that in the HMGB1-siRNA-Neg group of (763±46) mm3 and control group of (802±51) mm3 (P<0.05).

CONCLUSIONSLentivirus-mediated HMGBl-siRNA can effectively inhibit the HMGB1 expression in colorectal cancer LoVo cells both in vitro and in vivo. HMGB1 gene silencing can slow the growth of colorectal cancer cells, extend the cell proliferation cycle, decrease their invasion and migration, and significantly inhibit the growth of xenograft tumor in nude mice.

Animals ; Cell Cycle ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Colorectal Neoplasms ; pathology ; therapy ; Gene Expression ; HMGB1 Protein ; genetics ; metabolism ; Humans ; In Vitro Techniques ; Lentivirus ; Mice ; Mice, Nude ; Neoplasm Invasiveness ; RNA Interference ; RNA, Messenger ; metabolism ; RNA, Small Interfering ; therapeutic use ; Transfection ; Tumor Burden

A case of ichthyosis follicularis,alopecia and photophobia syndrome caused by a novel mutation c.1165C＞T in the membrane-bound transcription factor protease site 2 (MBTPS2) gene was firstly reported.The proband presented with dry skin,congenital hairlessness,follicular keratotic papules,photophobia,epilepsy,and mental and motor retardation.Next-generation and Sanger sequencing analysis confirmed that the proband and his mother both had a c.1165C＞T (p.pro389Ser) mutation in exon 9 of the MBTPS2 gene.According to the clinical manifestations of the patient and genetic characteristics of the MBTPS2 gene mutation,the patient was diagnosed with ichthyosis follicularis,alopecia and photophobia syndrome.

Objective To inquire into the influence of silencing HMGB1 expression by small interfering RNA ( siRNA) on cell growth, proliferation, invasion and metastasis of colorectal cancer LoVo cells both in vitro and in vivo. Methods Lentivirus?mediated HMGB1 siRNA was transfected into LoVo cells to silence the HMGB1 expression. The HMGB1 mRNA and protein expression after siRNA transfection was detected by RT?PCR and Western blot. MTT assay was used to observe the cell proliferation and to draw a growth curve. Cell cycle was measured by flow cytometry. The ability of invasion and speed of cell migration were evaluated by transwell chamber invasion and cell scratch assay. The influence of HMGB1 silencing on the proliferation of LoVo cells in vivo was observed in LoVo tumor?bearing nude mice. Results Lentivirus?mediated siRNA was successfully transfected into colorectal cancer cell line LoVo. The expression of HMGB1 mRNA and protein in the HMGB1?siRNA group were 0. 24 ± 0. 04 and 0. 21 ± 0. 03, respectively. Compared with the HMGB1?siRNA?Neg group (0.82±0.13, 1.15±0.18) and control group (0.93±0.15, 1.21±0.20), the difference was significant ( P<0.05) . MTT assay showed that the cell proliferation in the HMGB1?siRNA group was significantly inhibited when compared with that in the HMGB1?siRNA?Neg group and control group (P<0.05). Flow cytometry showed that the proliferation index (PI) of HMGB1?siRNA group was 38.27± 1.32, significantly lower than 54.66±1.74 in the HMGB1?siRNA?Neg group and 57.43±1.29 in the control group (P<0.05). The transwell assay showed that the number of penetrated cells in the HMGB1?siRNA group was 14.0±3.5, significantly lower than 51.0±6.7 in the HMGB1?siRNA?Neg group and 68.0±5.3 in the control group (P<0.05). Similarly, the scrape wound recovered significantly slower in the HMGB1?siRNA group (83.61±23.21) μm than that in the other two groups (202.86±46.46) μm and (214.58±57.38) μm (P<0.05). The nude mouse xenograft tumor experiment showed that the final tumor volume was (521±34) mm3 in the HMGB1?siRNA group, significantly smaller than that in the HMGB1?siRNA?Neg group of (763± 46) mm3 and control group of (802±51) mm3(P<0.05). Conclusions Lentivirus?mediated HMGBl?siRNA can effectively inhibit the HMGB1 expression in colorectal cancer LoVo cells both in vitro and in vivo. HMGB1 gene silencing can slow the growth of colorectal cancer cells, extend the cell proliferation cycle, decrease their invasion and migration, and significantly inhibit the growth of xenograft tumor in nude mice.

Objective To inquire into the influence of silencing HMGB1 expression by small interfering RNA ( siRNA) on cell growth, proliferation, invasion and metastasis of colorectal cancer LoVo cells both in vitro and in vivo. Methods Lentivirus?mediated HMGB1 siRNA was transfected into LoVo cells to silence the HMGB1 expression. The HMGB1 mRNA and protein expression after siRNA transfection was detected by RT?PCR and Western blot. MTT assay was used to observe the cell proliferation and to draw a growth curve. Cell cycle was measured by flow cytometry. The ability of invasion and speed of cell migration were evaluated by transwell chamber invasion and cell scratch assay. The influence of HMGB1 silencing on the proliferation of LoVo cells in vivo was observed in LoVo tumor?bearing nude mice. Results Lentivirus?mediated siRNA was successfully transfected into colorectal cancer cell line LoVo. The expression of HMGB1 mRNA and protein in the HMGB1?siRNA group were 0. 24 ± 0. 04 and 0. 21 ± 0. 03, respectively. Compared with the HMGB1?siRNA?Neg group (0.82±0.13, 1.15±0.18) and control group (0.93±0.15, 1.21±0.20), the difference was significant ( P<0.05) . MTT assay showed that the cell proliferation in the HMGB1?siRNA group was significantly inhibited when compared with that in the HMGB1?siRNA?Neg group and control group (P<0.05). Flow cytometry showed that the proliferation index (PI) of HMGB1?siRNA group was 38.27± 1.32, significantly lower than 54.66±1.74 in the HMGB1?siRNA?Neg group and 57.43±1.29 in the control group (P<0.05). The transwell assay showed that the number of penetrated cells in the HMGB1?siRNA group was 14.0±3.5, significantly lower than 51.0±6.7 in the HMGB1?siRNA?Neg group and 68.0±5.3 in the control group (P<0.05). Similarly, the scrape wound recovered significantly slower in the HMGB1?siRNA group (83.61±23.21) μm than that in the other two groups (202.86±46.46) μm and (214.58±57.38) μm (P<0.05). The nude mouse xenograft tumor experiment showed that the final tumor volume was (521±34) mm3 in the HMGB1?siRNA group, significantly smaller than that in the HMGB1?siRNA?Neg group of (763± 46) mm3 and control group of (802±51) mm3(P<0.05). Conclusions Lentivirus?mediated HMGBl?siRNA can effectively inhibit the HMGB1 expression in colorectal cancer LoVo cells both in vitro and in vivo. HMGB1 gene silencing can slow the growth of colorectal cancer cells, extend the cell proliferation cycle, decrease their invasion and migration, and significantly inhibit the growth of xenograft tumor in nude mice.

Objective To investigate the expression level of high mobility group box-1 (HMGB1) in human colorectal cancer and its relation with different clinicopathological characteristics and prognosis of colorectal cancer patients. Methods Immunohistochemical method was used to detect the HMGB1 expression in tissue samples of 86 colorectal cancer patients and 32 normal colorectal tissue samples. Positive rates of HMGB1 expression were compared among different clinicopathological characteristics. Relation of HMGB1 expression with survival was analyzed. Results HMGB1 expression was mainly in colorectal cancer cell nucleus , with a few appearance of co-expression in nucleus and cytoplasm. Positive rate of HMGB1 expression in normal tissues was significantly lower than that in colorectal cancers [9.4%(3/32) vs. 66.3%(57/86), P=0.000], and it was much higher in large cancers, lower differentiation, invasion to outside serosa, advanced clinical stage and lymph node metastasis (all P<0.05), but was similar in terms of age and gender(P>0.05). Survival analysis showed that 3-year survival rate of patients with positive HMGB1 expression was significantly lower as compared to those with negative HMGB1 expression (56.1% vs. 85.7%, P=0.021), meanwhile it was significantly lower in patients with co-expression in nucleus and cytoplasm as compared to those with simple nuclear expression (41.4% vs. 75.0%, P=0.013). Conclusions HMGB1 expression in colorectal cancer is high, and its positive rate increases with the low differentiation, invasion and metastasis. HMGB1 co-expression in nucleus and cytoplasm indicates poor prognosis of colorectal cancer patients.