Dynamic intraligamentary stabilization versus conventional ACL reconstruction: A matched study on return to work

PurposeThe dynamic intraligamentary stabilization (DIS) technique is based on a different treatment approach than ACL reconstruction in that it intends to promote self-healing of the ligament. It is only recommended for acute injuries (<21 days). The purpose of the present study was to compare DIS and ACLR with respect to the extent of work incapacity, revision rates, secondary arthroscopies, and treatment costs during recovery.MethodsThe study was a post-hoc analysis of prospectively collected data in the Swiss National Accident Insurance Fund (SUVA) database. All registered DIS cases treated until 31 December 2012 were included in the study. ACLR cases were matched to DIS cases using a propensity score approach and analysed in a follow-up period of 2 years after injury. Paired Student’s T-test and the Chi-square test were used to compare the outcome measures.ResultsAll 53 DIS patients were matched to an ACLR pair. The mean time period from injury to surgery was 14 days for DIS and 50 days for ACLR (p < 0.001). Overall work incapacity was 13% for DIS and 17% for ACLR resulting in a difference of nearly 1 month of absence from work (p = 0.03). The course of postoperative work incapacity was very similar between the groups, while the work incapacity prior to surgery lower in the DIS group. We found no difference in treatment costs, secondary arthroscopies and revision rates.ConclusionDIS patients benefited from nearly one month shorter absence from work than ACLR patients. This difference is likely related to the early surgical timing that is recommended for DIS. Since no differences were found between DIS and ACLR in terms of treatment costs, secondary arthroscopies and revision rates, the study supports the choice of DIS as an additional treatment option for acute ACL injuries. Further comparative studies are proposed to improve the evidence about optimal timing and best practice in ACL treatment.     

Repair of a Vaginal Evisceration Following Colpocleisis Utilizing an Allogenic Dermal Graft

Vaginal evisceration following colpocleisis is a very rare event and, to our knowledge, there has only been one previous case report. An 86-year-old woman presented to the Emergency Department with acute onset of abdominal pain occurring following a bowel movement. Six months previously, she had undergone a colpocleisis for recurrent vaginal vault prolapse. On presentation to the emergency room, she was noted to have 60 cm of necrotic small bowel protruding through her vaginal introitus. She was taken to the operating room for resection of the small bowel and closure of her colpocleisis. The closure of the vaginal defect was difficult and required a vaginal approach employing an allogenic dermal graft. This was accomplished and the patient had an uneventful recovery and was discharged home. At 18 months followup, she has had no complication or recurrence. Evisceration following colpocleisis is a rare event, but can be very difficult to manage and we suggest consideration of employing a graft to reinforce the repair.     

Differential expression of hMLH1 in sporadic human colorectal cancer tumors and distant metastases

Somatic defects in the mismatch repair system constitute an important pathway in colorectal carcinogenesis. We have examined the expression of mismatch repair proteins in sporadic stage IV colorectal tumors and their derived metastases. Sporadic tumors were further examined for differences in expression between the tumor transition zone and the invasive front. Expression of hMSH2, hMLH1, and hPMS2 was screened immunohistochemically in 92 stage IV tumors and derived liver metastases. In cases with loss of mismatch repair protein expression, lymph node metastases were also examined. Clinicopathological parameters and Ki‐67 staining indexes were evaluated and compared. Four tumors displayed a complete loss of hMLH1/hPMS2 expression at the transition zone; however, three of these expressed both proteins at the invasive front and in liver and lymph node metastases. A further four were predominantly hMLH1/hPMS2 negative at the transition zone, but with distinct subclones of hMLH1/hPMS2‐expressing cells at the transition zone. All of these tumors expressed hMLH1/hPMS2 at the invasive front and in liver metastases, with three also expressing hMLH/hPMS2 in lymph node metastases. No significant difference in the proliferative index was observed for the hMLH1/hPMS2‐compromised group. In stage IV tumors re‐expression of hMLH1/hPMS2 occurred, leading to different patterns of expression within the primary tumor and between tumor and metastases. This may have functional importance for the chemosensitivity of metastases compared to the primary tumor.     

ERCC1 Asn118Asn polymorphism as predictor for cancer response to oxaliplatin-based chemotherapy in patients with advanced colorectal cancer

Objective: To assess whether the polymorphism of ERCC1 Asn118Asn (C→T) had effects on cancer response to chemotherapy and outcome in Chinese patients treated with oxaliplatin as first-line chemotherapy regimen for advanced colorectal cancer.Methods: ERCC1 Asn118Asn polymorphism was analyzed in 99 patients with stages Ⅲ and Ⅳ advanced colorectal cancer treated with oxaliplatin-based chemotherapy.For all of the patients, ERCC1 Asn118Asn genotype was analyzed for associations with treatment response and time to disease progress (TTP).Results: The allele frequencies of the ERCC1 gene codon 118 were C/C 50.51% (50/99), C/T 41.41% (41/99), T/T 8.08% (8/99), respectively.Patients with C/C genotype showed higher response rate than those with C/T T/T (OR = 3.764, 95% CI: 1.310-10.813).The median TTP of all patients was 7 months (95% CI: 5.569-8.431).Patients with C/C genotype showed a median TTP of 10 months (95% CI:8.924-11.076), which was longer than 5 months (95% CI: 4.424-5.576) in patients with C/T T/T genotypes.Conclusion:Our results showed a link between ERCC1 Asn118Asn genetic polymorphism and cancer response to oxaliplatin-based chemotherapy and time to disease progress in Chinese patients with advanced colorectal cancer.ERCC1 Asn118Asn genotyping may be of predictive benefit in selecting treatment regimen for advanced colorectal cancer.     

胃癌组织hMLH1启动子甲基化是造成其蛋白表达降低的主要原因

目的：通过研究胃癌中错配修复基因hMLH1启动子区5CpG岛甲基化及蛋白表达情况，探讨hMLH1启动子Ⅸ甲基化对蛋白表达的影响及在胃癌发病中的作用。方法：收集诊断明确且未经放化疗的胃癌手术切除标本41例及同病例癌旁黏膜。应用免疫组化SP法检测标本hMLH1蛋白表达情况。应用甲基化特异性PCR（MSP）榆测标本hMLH1启动子区甲基化情况。结果：胃癌组与癌旁组，hMLH1蛋白阳性表达率分别为58．54％（24／41）和80．49％（33／41）（P〈0．05）；启动子甲基化率分别为80．49％（33／41）和24．39％（10／41）（P〈0．05）；完全甲基化率分别为41．46％（17／41）和19．51％（8／41）（P〈0．05）；部分甲基化率分别为39．02％（16／41）和4．88％（2／41）（P〈0．05）。无论胃癌组织还是癌旁组织，完全甲基化病例均出现hMLH1蛋白表达缺失，部分甲基化病例和启动子未甲基化病例均有hMLH1蛋白表达。hMLHI基因启动子甲基化率与胃癌患者性别、年龄、癌组织分化程度、浸润深度和淋巴结转移均无明显相关性（P〉0．05）。结论：hM—LH1基因启动子甲基化是导致hMLH1蛋白表达降低的主要原因；胃黏膜hMLH1蛋白表达降低有助于胃癌的预警。     

XRCC2基因多态性与肺癌易感性关系的研究

目的：探讨中国北方人群中XRCC2基因C41657T、G4234C多态性与肺癌的关系。方法：应用PCR-RFLP方法检测199例肺癌患者和200例正常人的XRCC2 C41657T及G4234C多态位点，比较两组之间等位基因及基因型频率分布及其与肺癌的关系。结果：肺癌患者XRCC2 C41657T多态位点的CC、CT、TT基因型和C、T等位基因频率分布与健康对照组相比差异均无统计学意义（P〉0．05）。G4234C多态位点的GG、GC、CC基因型和G、C等位基因频率分布与健康对照组相比差异也均无统计学意义（P〉0．05）。两多态性位点联合分析显示，肺癌患者与健康对照组的4个单体型分布亦无统计学差异（P〉0．05）。以病理类型、吸烟状况和年龄进行分层分析显示，XRCC2 C41657T多态位点可能与腺鳞癌和不吸烟人群的肺癌发病风险相关；与C／C基因型相比，携带T等位基因的基因型（C／T＋T／T）可显著增加腺鳞癌的发病风险（OR为2．95，95％CI=1．15—7．59）；而C／T基因型可显著增加不吸烟组人群中肺癌的发病风险（OR为2．12，95％CI=1．05-4．27）。对于XRCC2 G4234C多态位点，与G／G基因型相比，G／C基因型和携带C等位基因的基因型（G／C＋C／C）可显著增加小细胞肺癌的发病风险（OR为2．82和2．82；95％CI=1．15～6．91和1．17～6．76）；G／C基因型或与C／C基因型相加可显著增加年龄≥60岁的人群中肺癌的发病风险（OR为2．29和2．37；95％CI=1．11—4．72和1．16—4．88）。结论：对于XRCC2 C41657T多态位点，携带T等位基因的基因型可能增加腺鳞癌的发病风险，C／T基因型可能增加不吸烟者患肺癌风险；XRCC2 G4234C多态位点，G／C基因型或携带C等位基因可能增加小细胞肺癌的发病风险和老年人（年龄≥60岁）患肺癌的风险。     

COX-2抑制剂NS-398对肝癌细胞放射增敏作用的实验研究

目的探讨环氧合酶-2（COX-2）抑制剂NS-398对肝癌细胞系HCC-9810的放射增敏作用及其机制。方法MTT实验测定NS-398对肝癌细胞系HCC-9810细胞毒性;成克隆实验检测NS- 398对HCC-9810的放射增敏作用;电镜观察细胞形态学改变;流式细胞仪（FCM）分析细胞凋亡率;逆转录聚合酶链反应（RT-PCR）、FCM观察Bcl-2、Bax mRNA及蛋白表达。结果NS-398对HCC-9810细胞毒性呈现浓度、时间依赖性。10μmol/L NS-398作用24 h细胞增殖抑制率仅为3%,由D_q计算增敏比（SER）为1．29,细胞存活曲线“肩区”减小。NS-398处理HCC-9810细胞后放射诱导凋亡的敏感性增高,Bax mRNA和蛋白表达上调,呈NS-398剂量依赖性关系,而Bcl-2表达无明显变化,Bax/ BcL-2比值增高。结论NS-398对肝癌细胞系HCC-9810有放射增敏作用,且可能是通过上调Bax基因表达增强放射诱导凋亡作用及抑制亚致死损伤修复实现的。     

靶向ERCC1 RNA干扰对人肺腺癌细胞顺铂耐药的逆转

目的:探讨利用RNA干扰技术切除修复交叉互补基因1(excision repair cross-completion gene 1,ERCC1)逆转耐顺铂(cisplatin,CDDP)人肺腺癌细胞A549/CDDP的耐药性。方法:(1)常规体外培养A549/CDDP细胞,以脂质体包裹的ERCC1-siRNA转染细胞,转染浓度分别为100、200、300 nmol/L,并设空白转染、Lip转染对照组,观察转染效果。(2)采用免疫组化SABC法及RT-PCR法分别检测肿瘤细胞转染siRNA后ERCC1基因和蛋白的表达。(3)MTT法检测肿瘤细胞耐药指数,观察ERCC1靶向siRNA逆转A549/CDDP细胞顺铂耐药的效果。结果:(1)Lip组、siRNA-neg组转染效率分别为(56.38±9.82)%、(63.54±4.87)%,SiRNA-ERCC1①组、siRNA-ERCC1②组、siRNA-ERCC1③组转染效率分别为(43.62±6.08)%、(65.85±9.61)%和(78.93±4.86)%。(2)针对ERCC1的siRNA转染A549/CDDP后,细胞ERCC1 mRNA及蛋白表达均下调,siRNA-ERCC1(300 nmol/L)组效应最强,分别下降至(11.19±6.82)%和(20.88±6.57)%(P<0.01)。(3)A549/CDDP细胞转染后耐药倍数减为6.05、4.64、2.94,空载体对照组细胞的耐药倍数为9.6。结论:RNA干扰技术封闭ERCC1基因可较大程度逆转耐顺铂人肺腺癌细胞的耐药性,且呈一定的浓度依赖性;ERCC1基因可作为逆转肺癌耐药治疗的有效靶点。