Volume 89  ·   Issue 48  ·  2009

In the world, there are nearly 1.2 million cases of colorectal cancer annually, ranking 4th among malignant tumors in men and 3rd among malignant tumors in women ~ ([1]). According to the estimation of the American Cancer Society, there were 146 970 new cases of colorectal cancer in the United States in 2009, and 49 920 patients died of colorectal cancer ~ ([2]). In China, the age-standardized incidence of colorectal cancer in 2002 was 13.6/100,000 in men and 9.2/100,000 in women ~ ([3]).

I. Background Blood glucose monitoring is an important part of diabetes management. The results of blood glucose monitoring are helpful to evaluate the degree of glucose metabolism disorder in diabetic patients, formulate hypoglycemic programs, reflect the effect of hypoglycemic treatment and guide the adjustment of treatment programs. Patients' self-blood glucose monitoring (SMBG) is the basic form of blood glucose monitoring, while glycosylated hemoglobin (HbAlc) is the gold standard to reflect the long-term blood glucose control level. However, both HbAlc and SMBG have certain limitations.

Objective To discuss the causes of common complications of ureteroscopy and how to prevent them. Methods A total of 768 cases of common complications of ureteroscopy were retrospectively analyzed from February 2004 to February 2009. Results The intra-operative complications were failed entry ( n = 6, 0. 78% ) , ureterostoma injury and ureterostoma submucosa pseudocana ( n = 12, 1. 56% ) , ureteral perforation ( n = 16, 2. 08% ) , stone displacement ( n = 13 , 1. 87% ) and ureteral mucosa evulsion ( n = 3, 0. 39% ). And the post-operative complications were lumbago or renal colic ( n = 11, 1. 43% ) , infection ( n = 9, 1. 17% ) and severe hematuria ( n = 5 , 0. 65% ) . Conclusion Skillful operative techniques and strict indications are key to reducing complications of ureteroscopy.

Objective To discuss the methods of surgical treatment and their timing choices of cervical lymphangioma. Methods A retrospective review of 53 patients with cervicofacial lymphangioma were treated surgically from July 1990 to December 2008. The age at operation was from 6. 5 months to 41 years old (median age was 2 years old and 3 months). Eighteen (34.0%) lesions were located in the suprahyoid region and 35 ( 66. 0% ) lesions in the infrahyoid region. The diameter of lesion ranged from 3. 3 to 8. 2 cm (average: 4.4 cm). Neck mass was the sole symptom for 77. 4% (41/53) cases. Nine patients presented with life-threatening complications including intracystic hemorrhage in 2 cases/times, infection and rapid increase in tumor size in 5 cases/times, dysphagia in 2 cases/times and respiratory obstruction in 4 cases/times. Color Doppler ultrasound was used to diagnose all patients pre-operatively. Computed tomography (CT) was used in 11 cases and magnetic resonance imaging (MRI) in 21 cases for differential diagnosis. Results The patients were treated by complete resection in 34 cases and subtotal resection in 8 cases. But partial resection in 11 (20. 8% ) cases developed a residual or recurrent lesion within 9 months to 5 years post-operation, including 7 cases in suprahyoid region and 4 cases in infrahyoid region. The rate of residual or recurrent lesions was significantly higher in the suprahyoid region (7/18 ) than that in the infrahyoid region (4/35) ( χ~2,P< 0. 05 ) . The peri-operative complications were paralyses of mandibular branch of facial nerve, Homer's syndrome, secondary hemorrhage, fluid collection at resection site, local infection and parotid fistula in 1 case respectively. Respiratory distress caused by edema of tongue was present in 2 cases. All of them were cured conservatively. The pathological diagnosis was confirmed as capillary lymphangioma in 19 cases and cystic lymphangioma in 34 cases. Conclusion The localization and extent of cervical lymphangioma are the most important determining factors for a successful surgical resection. Although complete excision is the ideal treatment for cervicofacial lymphangioma, this should not be attempted if lesions are too large and neighboring structures liable to injury. The surgeons should be aware of the limitations and potential surgical complications in certain instances.

Objective To investigate the determinants of long-term survival for ampulla of Vater carcinoma treated by pancreaticoduodenectomy. Methods A total of 77 patients with ampulla of Vater carcinoma undergoing pancreaticoduodenectomy were reviewed. Kaplan-Meier method was used to analyze the survival rate. Independent t test was used for statistical comparison and COX regression model for mullivariate analysis. Results No patient died as a result of surgery. The overall 5-year survival was 40. 7%. Univariate analysis showed that perioperative serum carcinoembryonic antigen ( CEA ) level ( P = 0. 012 ) , tumor invasion depth ( P = 0. 000) , UICC stage ( P = 0. 000) and tumor size ( P = 0. 001) were significant prognostic factors of ampulla of Vater carcinoma; in multivariate analysis, only the tumor size (P = 0.000) was an independent prognostic factor of ampulla of Vater carcinoma. Conclusion Pancreaticoduodenectomy is associated with significant survival. Tumor size is the most important influencing factor of outcome after pancreaticoduodenectomy; in addition, perioperative serum CEA level, tumor invasion depth and UICC stage may also influence the survival rate, there exists a need for further follow-up studies.

Objective To investigate a new velopharyngoplasty (VPP), including its anatomic character and its mechanism of remodeling of oral-pharynx cavity for treating obstructive sleep apnea hypopnea syndrome ( OSAHS). Methods Two cases of soft palate were dissected in adult male cadavers. And the model of VPP was established to further observe its technical characteristics. A total of 85 OSAHS patients were studied by PSG. And all cases received velopharyngoplasty (VPP) and follow-ups. Ten cases were selected for CT scanning of palatal pharyngeal cavity and CT workstation was employed for imaging measurements. Results The measured parameters of pharyngeal palate included soft palate length, maximal thickness of soft palate, soft palate to posterior pharyngeal edge of free space, parapharyngeal space (distance between tonsils) , uvula length, width of uvula base, velopharyngeal cross-sectional area and cross-sectional area of angina. All these parameters had a significantly difference between pre-operation and post-operation [(37. 8±5.5)mm vs (27.0 ±4. 1)mm,( 13. 3 ±2. 2) mm vs (9. 3 ±2. 5) mm, (7. 1 ±2. 8) mm vs (10. 3 ± 1.7)mm,(45.2±25.5)mm~2 vs (135. 3 ±26.4)mm~2,(2. 0 ±21. 8)mm~2 vs (208.4 ± 15. 9)mm~2]; however there was no significant difference in retropharyngeal wall thickness[(6. 8 ±2. 9)mm vs (7.0 ±2. 5) mm]. Conclusion VPP remodels palatopharyngeal region through the design of incision, the management of pharyngopalatine arch tonsillectomy and the suture of laterapharynx mucisae. This surgical procedure can obviously upgrade the velum palatinum, enlarge the oropharyngeal airway effectively. It is a significant modified-UPPP surgical technique.

Objective To investigate the role of heme oxygenase-1 (HO-1) in the oxidative stress damage of intestinal mucosa barrier disruption in patients with malignant obstructive jaundice (MOJ). Methods Fifteen jaundiced patients with malignant biliary obstruction undergoing endoscopic retrograde cholangiopancreatography ( ERCP) examination or treatment were enrolled. The control group was comprised of 10 healthy subjects with gastroscopy and 10 patients with non-jaundiced biliary obstruction. Patients were subjected to duodenal biopsy to assess the intestinal oxidative stress as estimated by lipid peroxidation ( malondialdehyde) and activity of superoxide dismutase (SOD). Apoptosis of epithelial cell was examined by TdT-mediated dUTP-biotin nick end labeling. Immunohislochemistry and Western blotting were employed to examine the distribution and expression of HO-1 proteins in intestinal mucosa. Results MOJ jaundiced patients presented high levels of intestinal oxidative stress with a significantly increased level of lipid peroxidation[(1. 79 ±0. 24) vs (1.09 ±0.28) vs (1. 18 ±0.32) nmol ·mg~(-1) · prot~(-1), P=0. 041] and a decreased SOD activity [(303±10)vs (398 ±11) vs (406 ± 11 )nmol · mg~(-1) · prot~(-1), P=0.017]. The apoptotic rate of intestinal epithelial cells was significantly higher in jaundiced group than in non-jaundiced control group. Apoptotic index was (69. 1 ± 5. 9) % , (28. 6 ± 3. 5) % and (10. 2 ± 2. 5) % respectively (P<0. 01). The staining of HO-1 was predominantly localized in cytoplasm. In jaundiced patients, HO-1 was obviously elevated than those in the control group (HO-1 optical density 0. 28 ±0. 04 vs 0. 20 ±0. 04 vs 0. 13 ±0. 05) ( P < 0. 01 ) . Similar outcomes were obtained by quantitative analysis of Western blotting images [HO-1/GAPDH (10.7±0.7)% vs (7.6±0.5)% vs (3. 9 ±0. 4)% ,P <0. 01]. Conclusion MOJ induces intestinal oxidative stress and it may be a key contributing factor to intestinal barrier failure in the patient population. HO-1 protein level is rising with the progression of obstruction. Perhaps HO-1 has a protective effect upon MOJ through anli-oxidative damage.

Objective To review and investigate the relationship of geneotype and phenotype in Chinese patients with Gaucher disease ( GD) . Methods The samples were first screened for known mutations as reported previously in Chinese population. Long chain PCR and nested PCR were employed to amplify the segments of glucocerebrosidase functional gene in patients with unknown mutant alleles. The products of nested-PCR were subjected to DNA sequencing to detect the new mutations. Results Forty kinds of mutations were detected in this panel of patients. The L444P mutation was the most common one accounting for 33. 0% of mutant alleles. It was followed by F213I, N188S, V375L and M416V. Conclusion There are at least 40 mutations in Chinese GD patients. The spectrum of mutation is significantly different from that in Caucasians. 70% of mutant alleles have been characterized. It becomes feasible to make clinical and prenatal diagnoses through gene analysis.

Objective To construct a high-throughput suspension microarray for detecting the hotspot gene mutations of p53 , pl6, retinoblastoma ( Rb) and epidermal growth factor receptor ( EGFR) and to investigate the significance of this multimarker panel in molecular diagnosis of non-small-cell lung cancer (NSCLC). Methods The specific probes of normal or mutated sequences targeting the hotspot mutation sites of p53, pl6, Rb and EGFR were designed and immobilized to carboxylated Luminex microspheres (micro-beads). Genomic DNA was extracted from 65 specimens of cancer tissues and 20 adjacent normal lung tissues. p53, pl6, Rb and EGFR genes were amplified by PCR, hybridized with the specific probes on the beads and measured using Luminex 100. Results The single gene mutations of p53, p16, Rb or EGFR in NSCLC specimens were 53. 8% (35/65), 20.0% (13/65), 7.7% (5/65) or 35.4% (23/65) respectively. The para-tumor normal tissue specimens were 5.0% (1/20), 5.0% (1/20), 0 and 0 respectively. For combined detections of four genes, the sensitivity, specificity and accuracy were 81. 5% (53/65) , 90.0% (18/20) and 83. 5% (71/85) respectively. The mutation rates of this panel in stage Ⅰ , stage Ⅱ and stage Ⅲ were 78.3% (18/23), 80.0% (16/20) and 86.4% (19/22) respectively. Conclusions A high-throughput suspension microarray with a higher specificity and sensitivity has been built. It may be used to simultaneously detect the gene mutations of p53, pl6, Rb or EGFR in NSCLC specimens. This suspension microarray is helpful to improve the sensitivity of molecular diagnosis of NSCLC and guide the molecular targeting therapy of NSCLC.

Objective To investigate the effect of Gefitinib on insulin sensitivity in rats of type-2 diabetes and its mechanism. Methods Normal Wistar rats were fed with high sucrose-fat diet for 1 month and then injected intraperitoneally with streptozotocin ( STZ) . The rats satisfying the definity of type-2 diabetes were divided into 3 groups and given control solution (0. 9%NaCl) , low-dose Gefitinib and high-dose Gefitinib for 8 days, respectively. Body weights, FBG and FINS were recorded before, just after and 7 days after administration, respectively. After the second round of administration executed the rats and got the livers from rats. Compared the expression of insulin receptor substrate-1 ( IRS-1) and phosphatidylinositol-3-kinase (PI3K) genes in liver among the 3 groups with semi-quantitative Reverse Transcription-Polymerase Chain Reaction( PCR). Results Normal Wistar rats fed with high sucrose-fat diet for 1 month and then injected intraperitoneally with STZ could establish type-2 diabetes model. After administration,insulin sensitivity index (ISI) of Gefitinib groups were significantly increased compared with control group (2. 96 ± 1. 38 vs 0. 92 ±0. 20,P <0. 05). There Were no significant difference between the two dose groups(2. 95 ±1.51 vs 2. 96 ±1. 38, P>0. 05). 7 days after administration, the improved ISI did not change (2. 03 ±0.72 vs 2. 99 ± 0. 63, P > 0.05). Body weights of the 3 goups had no significant difference. The expression of IRS-1 gene significantly decreased in Gefitinib groups compared with control group [(3.3 ±1.5)% vs ( 6. 3 ± 2. 4 ) % P <0. 05] and with no obvious difference between the two dose groups [(3. 3 ±1.5)% vs (3. 2 ± 1. 8)% , P > 0. 05] , while the expression of PI3K gene significantly increased in Gefitinib groups compared with control group [( 1. 27 ± 0. 73 ) % vs ( 0. 41 ± 0. 24 ) % , P < 0. 05] also with no obvious difference between the two dose groups [(1. 27 ± 0. 73) % vs (1. 43 ± 0. 71) % , P > 0. 05]. Conclusions Gefitinib can improve insulin sensitivity in rats of type-2 diabetes. 2 t_(1/2) after administration, the effect still existed. The effect probably due to the increase of PDK/Akt pathway of insulin signaling, and had no relationship withbody weight in our study dose range.

Objective To investigate the impact of polyethylene glycols( PEG) upon islet survival in homogeneous murine islet transplantation and understand the impact of PEGylation in combination with rapamycin upon anti-rejection therapy in homogeneous mice islet transplantation. Methods The subcutaneously pre-vascularized STZ-induced diabetic mice treated with transplanted islets of BALB/c mice were randomly divided into 6 groups: Group A with normal mice islets; Group B with PEG-packed islets; Group C with normal mice islets and 1. 5 mg · kg~(-1)· d~(-1) rapamycin; Group D with PEG-packed islets and 1. 5 mg · kg~(-1) · d~(-1)rapamycin; Group E with normal mice islets and 3 mg · kg~(-1) · d~(-1) rapamycin; Group F with PEG-packed islets and 3 mg · kg~(-1) · d~(-1) rapamycin. The post-transplantation blood glucose was monitored. Transplanted islets were analyzed by H&E and insulin immunostain. Results The survival time in group B was significantly prolonged as compared with group A (P<0. 01). The survival time in group C were (35. 0 ±3. 1 )d and groups D, E, F had survival of up to 6 weeks. Transplantation sites of group A were observed with a more abundant infiltration of immune cells than group B. And the unmodified islets in group A were completely destroyed after transplantation. Insulin-positive islet cells were not detected at the entire transplantation site in group A while the presence was found at the transplantation site in group B. Conclusion PEG-packed islets can significantly improve the survival time of transplanted islets. When combined with rapamycin, it can reduce the dose of rapamycin.

Objective To obtain the evidence of fibrotic resolution in fatty liver by changing the diet and to clarify the mechanism of hepatocyte proliferation inhibition in rat with fatty liver fibrosis. Methods (1) Nonalcoholic steatohepatitis with advanced fibrosis was induced in rats by giving them a methionine-choline-deficient diet (MCDD) for 10 weeks ( group M). A melhionine-choline-control diet ( MCCD) instead of MCDD was given for the last 2 weeks to the experimental group( group R). (2) Fibrosis and inflammation were determined by tissue staining. The activation of hepatic stellate cells and Kupffer cells were determined by immunostaining, immunoblot or quantitative RT-PCR respectively. (3) Hepatocytic apoptosis and proliferation were determined by TUNEL and BrdU staining respectively. Expressions of IL-6, STAT3, JNK-1, c-Jun, p21 , C/EBPα, HNF6 and HGF-alpha were evaluated by quantitative RT-PCR and immunoblot to clarify the mechanism of hepatocytic proliferation inhibition. Results (1) Changing the diet from MCDD to MCCD triggered the reduction of fat in hepatocytes and a decrease in inflammatory response. (2) The regression of fibrosis was accompanied by the disappearance of activated stellate cells and macrophages. ( 3 ) Compared with control group ( group C) , hepatocytic apoptotic number increased significantly in group M (68 ±16 vs 40 ± 8,P <0. 05) and the ratio of hepatocytic proliferation/apoptosis decreased markedly in group M (0. 10 ± 0. 03 vs 0. 19 ± 0.03, P < 0. 01 ); compared to group M, hepatocytic apoptotic number decreased significantly in group R (48 ± 6, P < 0. 05 ) and hepatocytic proliferation number and the ratio of hepatocytic proliferation/apoptosis increased markedly in group R (17.2±4.4 vs7.5 ±3.0, 0.41 ±0.09 vs 0. 10±0.03 respectively, P<0.01). (4) Compared with group C, the mRNA level of IL-6, JNK-1, c-Jun, C/EBPa, p21 and HNF6 mRNA decreased significantly (0. 34 ± 0.18 vs 1.33 ±0.44, 0.41 ±0.11 vs 0.83 ±0.26, 0.19 ±0.03 vs 1.53 ±1.2, 1.94 ±0.64 vs 4.51 ±1.15, 0. 34 ±0.20 vs 1.30 ±0.75, 0.47 ±0.21 vs 0. 92 ±0. 16 respectively, P <0.05 or P <0.01) , and protein level of IL-6, STAT3, JNK-1, c-Jun, C/EBPa, P21 and HNF6 also decreased significantly in liver fibrotic stage (P <0. 05 or P <0. 01) while only IL-6, JNK-1 and p21 recovered immediately after a changed diet from MCDD to MCCD (P <0. 05 or P <0.01). Conclusion Food intake is a very important factor for controlling the fatty status and pathology of liver. Hepatocytic proliferation inhibition is associated with the arrested G_o-S phasic transition in fatty liver fibrosis and the up-regulated expression of IL-6, JNK-1 and p21. These factors play a very important role in the recovery of fatty liver fibrosis.

Objective To study the preventive effect of recombinant polypeptide of N-terminal heparin-binding domain of fibronectin on hepatic failure induced by endotoxin in mice. Methods The 40 hepatic failure Balb/C mice were established by intraperitoneal injection of lipopolysaccharide ( LPS) and d-galactosamine(GalN). The mice were randomly divided into two groups,one for polypeptide treatment, the othe for saline treatment. Another 20 mice were used as normal control. Half hour prior to , 1,2 ,and 3 hours after injection of LPS and GalN, the rhFNHN-29 polypeptide (10 mg/kg) was injected through the tail vein of mice. The same volume of saline was given to the saline treated group and the normal control group. Six hours after the injection of LPS and GalN, 250 μl blood was taken from the eye vein of each mouse for plasma TNFα testing, and 72 hours after the injection, mortality rates of the mice of different groups were observated. The liver, lung, heart, kidney, and brain tissues of the survival mice were examined for histopathology after 72 hours . The Liver tissue was also examined for electron micrograph and for mRNA expression of TNFα, IL-1 β, IL-6 by RT-PCR. Results The 72 hours mortality rates in saline-treated and polypeptide treated-mice were 70% and 15% respectively (P < 0. 01 ) . The histopathology showed that necrosis occurred less on the hepatocytes of polypeptide treated mice than on the saline treated ones. The ultrastructure of hepatocyte under the electron microscope showed that cell apparatus of saline treated mice were destroyed and cytoplasm become loose. The expression level of TNFα,IL-l β,IL-6 mRNA on hepatocytes in polypeptide treated mice was significantly lower( 1. 26 ± 0. 37,0. 98 ± 0. 21,0. 43 ± 0. 17,87. 43 ± 16. 7 respectively) than that in the saline treated ones(1.98 ±0. 56,1. 24 ± 0. 35,0. 64 ± 0. 25 and 236. 11 ± 32.7, respectively) (P<0. 01). Similarly, the plasm TNFα level(87.43 ±16.7 ) in polypeptide treated group was significantly lower than that(236. 11 ±32. 7 ) in the saline treated group(P <0. 01). Conclusion The rhFNHN-29 polypeptide can prevent and treat hepatic failure induced by endotoxin . The mechanism by which the polypeptide takes the effect may involve its ability to down-regulate expression of those inflammative factors such as TNFα, IL-1β, IL-6.

Objective To study the in vitro accumulation of ~(18)F-FHBG, its in vivo distribution and ~(18)F-FHBG PET-CT imaging for reporter gene (HSVl-tk) in nude mice with a xenograft of breast adenocarcinoma Methods The in vitro uptake of ~(18)F-FHBG in tumor cells of T47D and T47D-tk and the distribution of ~(18)F-FHBG in normal Kunming mice and nude mice with breast adenocarcinoma xenograft were detected by well-type γ counter. Reporter gene PET-CT imaging with ~(18)F-FHBG was performed in nude mice with a xenograft of breast adenocarcinoma. And the expression location of HSVl-tk gene could be monitored by observing the in vitro and in vivo accumulation of ~(18)F-FHBG. Results The in vitro uptake of ~(18)F-FHBG in T47D-tk cells (143. 67 dpm/10~4 ± 5. 82 dpm/10~4 cells) was significantly higher than that in T47D cells (2.23 dpm/10~4 ± 0.23 dpm/10~4 cells) at 60 and 120 min post-injection ( P < 0. 001 ) and reaches a plateau at 60 min. In normal Kunming mice, ~(l8)F-FHBG was mainly distributed in liver, intestine, kidney and bladder while there was no obvious radioactive accumulation in brain. F-FHBG accumulated at a significantly higher level in T47D-tk tumors than in T47D tumors and its accumulation yielded the best image effect at 2 h by PET-CT imaging in nude mice. Conclusion The in vitro uptake of ~(18)F-FHBG in T47D-tk cells is significantly higher than that in T47D cells. ~(18)F-FHBG is mainly excreted by digestive tract and urinary tract in mice. It agrees with the expression pattern of HSVl-tk gene. ~(18)F-FHBG can determine the localization of HSVl-tk gene expression in an efficient way. This study will offer a monitoring method and scientific base for ~(18)F-FHBG reporter gene imaging and HSV1 -tk gene therapy in tumors.

A 54-year-old male was admitted to the respiratory ward of our hospital on January 11, 2009 due to intermittent fever for 8 months, dyspnea for 5 months, headache, nausea and vomiting for 5 days. This was the fourth time that the patient was admitted to our hospital and the third time that he was admitted to our ward. He had suffered from type 2 diabetes for more than 10 years, and his personal and family history were not special.

autoimmune disease (AID) is a disease state caused by the immune system responding to its own components due to the impairment of normal immune tolerance function. At present, its diagnosis mostly depends on the detection of autoantibodies in serum, but due to its lack of specificity and sensitivity, early diagnosis and individualized treatment of AID become difficult for clinicians. Therefore, it is necessary to deeply study the pathogenesis of AID and determine the target of autoantibodies-autoantigen, so as to seek more sensitive diagnostic methods and formulate more effective and targeted treatment and even prevention programs.

allo-hematopoietic stem cell transplantation (allo-HSCT) may cure hematological malignant diseases, but HSCT needs to find donors with HLA compatibility, so that the body can develop immune tolerance to foreign antigens (non-self) and make the transplantation successful.Therefore, the ideal hematopoietic stem cell transplantation can only be carried out between autologous or identical twins.

Pulmonary hypertension is a kind of malignant pulmonary vascular disease characterized by pulmonary arteriole vascular remodeling, which often leads to death due to the progressive increase of pulmonary vascular resistance and eventually leads to right heart failure ~ ([1]). In recent years, there are more and more data on the protective role of estrogen in pulmonary vascular system, because it can weaken the function damage of pulmonary vascular endothelial cells and smooth muscle cells caused by various stimuli, and is beneficial to improve vascular remodeling and vasodilation. In addition, anti-inflammatory and calcium pump inhibition methods also play a certain role, but the specific mechanism is not fully understood at present. The mechanism of estrogen protective effect on pulmonary vascular system and its therapeutic prospect are reviewed in this paper.

Released by the World Health Organization in Geneva on 27 October 2009<Global Health Risks>report, pointing out that these health risks are a major contributor to death and disease burden, suggesting that controlling global health risks could prevent millions of premature deaths.