Nuclear accumulation of annexin A2 contributes to chromosomal instability by coilin-mediated centromere damage.

Most human cancers show chromosomal instability (CIN), but the precise mechanisms remain uncertain. Annexin A2 is frequently overexpressed in human cancers, and its relationship to tumorigenesis is poorly understood. We found that annexin A2 is overexpressed in the nuclei of CIN cells compared with cells with microsatellite instability (MIN). Ectopic annexin A2 expression in MIN cells results in a high level of aneuploidy and induces lagging chromosomes; suppression of annexin A2 in CIN cells reduces such CIN signatures with apoptosis of highly aneuploid cells. Ectopic expression of annexin A2 in MIN cells reduces the expression of centromere proteins. Conversely, annexin A2-knockdown in CIN cells increases the expression of centromere proteins. Moreover, the endogenous expression levels of centromere proteins in CIN cells were greatly reduced compared with MIN cell lines. The reduced expression of centromere proteins likely occurred due to aberrant centromere localization of coilin, a major component of the Cajal bodies. These results suggest that nuclear accumulation of annexin A2 has a crucial role in CIN by disrupting centromere function.

Lamin B2 prevents chromosome instability by ensuring proper mitotic chromosome segregation.

The majority of human cancer shows chromosomal instability (CIN). Although the precise mechanism remains largely uncertain, proper progression of mitosis is crucial. B-type lamins were suggested to be components of the spindle matrix of mitotic cells and to be involved in mitotic spindle assembly; thus, B-type lamins may contribute to the maintenance of chromosome integrity. Here, using a proteomic approach, we identified lamin B2 as a novel protein involved in CIN. Lamin B2 expression decreased in colorectal cancer cell lines exhibiting CIN, as compared with colorectal cancer cell lines exhibiting microsatellite instability (MIN), which is mutually exclusive to CIN. Importantly, lamin B2 knockdown in MIN-type colorectal cancer cells induced CIN phenotypes such as aneuploidy, chromosome mis-segregation and aberrant spindle assembly, whereas ectopic expression of lamin B2 in CIN-type colorectal cancer cells prevented their CIN phenotypes. Additionally, immunohistochemical analysis showed a lower expression of lamin B2 in cancer tissues extracted from patients with sporadic colorectal cancer (CIN-type) than that from patients with hereditary non-polyposis colorectal cancer (HNPCC; MIN type). Intriguingly, mitotic lamin B2 in MIN cancer cells was localized outside the spindle poles and mitotic lamin B2 localization was diminished in CIN cancer cells, suggesting an important role of lamin B2 in proper mitotic spindle formation. The obtained results suggest that lamin B2 maintains chromosome integrity by ensuring proper spindle assembly and that its downregulation causes CIN in colorectal cancer.

Apolipoprotein C-1 maintains cell survival by preventing from apoptosis in pancreatic cancer cells.

Pancreatic cancer still remains one of the most lethal diseases and establishment of new therapy is needed. The purpose of this study is to find novel factors involved in pancreatic cancer progression by proteomic approach. We compared pre- and postoperative serum protein profiling obtained from pancreatic cancer patients who had curative pancreatectomy using surface-enhanced laser desorption ionization time-of-flight mass spectrometry. The peak intensity levels of both 6630 and 6420 Da were significantly higher in the preoperative serum than in the postoperative serum (P<0.002). Sequential amino acid analysis identified these proteins to be apolipoprotein C-1 (ApoC-1). The high level of ApoC-1 in preoperative serum significantly correlated with poor prognosis. Furthermore, ApoC-1 was abundantly expressed in pancreas neoplastic epithelium, and was detected in the culture medium of the pancreatic cancer cell line in vitro, which suggests that cancer cells secrete ApoC-1. Inhibition of ApoC-1 expression by short interfering RNA suppressed cell proliferation and induced apoptosis of pancreatic cancer cells. The specific expression of ApoC-1 and its role in preventing from spontaneous apoptosis in pancreatic cancer cells suggest that ApoC-1 contributes to the aggressiveness of pancreatic cancer and will be useful as a new therapeutic target.

Chromosome instability and kinetochore dysfunction.

Chromosomal instability (CIN) has been recognized as a hallmark of human cancer and is caused by continuous chromosome missegregation during mitosis. Proper chromosome segregation requires a physical connection between spindle microtubules and centromeric DNA and this attachment occurs at proteinaceous structures called kinetochore. Thus, defect in kinetochore function is a candidate source for CIN and the generation of aneuploidy. Recently, a number of kinetochore components have been shown to be mutated and/or aberrantly expressed in human cancers, which suggests an important role of kinetochore for CIN and carcinogenesis. In this article, we will discuss about how kinetochore dysfunction causes CIN and might lead to the development of cancer.

Gene expression of 5-fluorouracil metabolic enzymes in hepatocellular carcinoma and non-tumor tissue.

5-fluorouracil (5-FU) is a basic agent used in chemotherapy. The aim of this study is to investigate the gene expression of 5-FU anabolic and catabolic enzymes in hepatocellular carcinoma (HCC) and non-tumor tissue, respectively to increase our knowledge of resistant mechanisms to 5-FU in HCC. The relative mRNA level of orotate phosphoribosyltransferase (OPRT), ribonucleotide reductase (RNR), dihydropyrimidine dehydrogenase (DPD) and target enzyme thymidylate synthase (TS), were analyzed in 30 matched samples of HCC (T) and non-tumor tissue (NT) using quantitative RT-PCR. The expression of OPRT, RNR-M1, RNR-M2 and TS is significantly higher in T compared with in NT (1.3-fold increase, 1.6-fold, 7.1-fold, 1.9-fold, respectively), but that of DPD showed no difference between T and NT. Our results show that HCC should not be treated with 5-FU alone because of its instability in liver.

Vascular-pedicled costal cartilage graft for the treatment of subglottic and upper tracheal stenosis.

BACKGROUND/PURPOSE: Free costal cartilage graft for the treatment of subglottic and tracheal stenosis is widely used, but postoperative granulation formation is a problem. To reduce the risk of granulation formation after free costal graft, a new operation of costal cartilage graft with vascular pedicle was introduced. METHODS: A vascular pedicled fifth costal cartilage graft is prepared using internal thoracic artery and vein and intercostal artery and vein as a vascular pedicle. The prepared graft is brought to the upper trachea. The anterior wall of cricoid is split, and the costal cartilage graft is implanted to the split part and tracheostomy. Extubation on the next day is possible if the general condition of the patient permits. RESULTS: In 3 cases of subglottic or upper tracheal stenosis, this operation was performed. All the patients had tracheostomy made during early infancy. The postoperative course was uneventful, and all the patients were extubated soon after the operation. No granulation tissue was observed by postoperative bronchoscopic examinations. CONCLUSIONS: Costal cartilage graft with vascular pedicle is a safe and useful new operation for the treatment of subglottic and upper tracheal stenosis. There also is a possibility of using this procedure for the treatment of long segment tracheal stenosis.

Inhibition of subgenomic hepatitis C virus RNA in Huh-7 cells: ribavirin induces mutagenesis in HCV RNA.

Hepatitis C virus (HCV) infection is a major problem throughout the world. Combination therapy of interferon (IFN) and ribavirin is the best treatment for eradication at present, but the mechanism is not completely understood. We used the HCV replicon system to investigate this mechanism. The effects of six drugs (UDCA, glycyrrhizin, TJ-9, bezafibrate, ribavirin, and alpha-IFN 2b) on HCV subgenomic RNA (genotype 1b, NS5B 415Y) were examined by reverse transcription polymerase chain reaction, cloning and sequencing. The HCV replication was inhibited by alpha-IFN 2b (7.39-13.2% at 10 U/mL, 3.29-6.12% at 100 U/mL, 1.3-4.86% at 1000 U/mL) and by ribavirin (4.36-13.9% at 100 microg/mL), but not by the other drugs at 24-72 h after treatment. Furthermore, the combination treatment was superior to IFN monotherapy and to ribavirin monotherapy at 72 h post-treatment. Sequence analyses of the double-stranded RNA-activated protein kinase (PKR)-binding domain and flanking regions within the HCV NS5A region revealed that the total numbers of substitutions caused by ribavirin (n = 36) or combination treatment (n = 57) were more than those of IFN alone (n = 5) and controls (n = 6). The HCV replicon system is the most efficient system for HCV replication and is an excellent choice for testing anti-HCV drugs and disinfectants. Our results further suggested that the combination of alpha-IFN 2b and ribavirin might induce mutations, and inhibit HCV RNA synthesis in hepatocytes to a greater extent than ribavirin monotherapy.

Establishment of a clonal human mesenchymal cell line that retains multilineage differentiation capacity from a spinal hamartoma.

We isolated a single-cell-derived cell line from a spinal hamartoma, a which occurred in a newborn boy and was associated with a rudimentary limb. The maternal cells (HHC-7) differentiated into osteoblasts, chondrocytes, adipocytes, and skeletal muscles when they were cultured in differentiation-inducing media specific to each mesenchymal cell. We isolated a single-cell-derived clonal cell line (Clone K) after transfection with SV40 T antigen. These cells expressed CD73 and CD117, while being negative for expression of CD45. Clone K cells cultured in an osteogenic differentiation medium increased ALP activity and expressed mRNAs for Runx2 and osteocalcin. Treatment with rhBMP-2 induced Clone K cells to differentiate into both osteoblasts and chondrocytes. These cells expressed mRNAs for Sox9 and aggrecan in addition to osteogenic markers. Culture in an adipogenic differentiation medium induced Clone K cells to differentiation into adipocytes, which expressed mRNAs for PPARgamma2 and a2P. Clone K cells cultured in a serum-depleted medium generated desmin-positive cells and expressed MyoD1 mRNA. Clone K cells exhibited numerous alpha-smooth muscle actin-positive cells; however, treatment with rhBMP-2 decreased their number. Clone K cells, transplanted with a carrier containing rhBMP-2 into the muscles of SCID mice, generated ectopic endochondral bone formation. In these tissues, several osteoblasts and chondrocytes expressed SV40 T antigen, indicating their Clone K cell origin. Thus, Clone K cells are useful tools for analyzing the characteristics of human multipotential mesenchymal progenitors.

Endoscopic SIS injection into the lower oesophageal sphincter in dogs.

AIM: To determine the usefulness of endoscopically-delivered small intestinal submucosa (SIS) as a scaffold in enhancing the lower oesophageal sphincter (LOS) pressures. METHODS: Six dogs were endoscopically injected--four with the SIS and two with its glycerin carrier. Manometry was performed prior to injection and every four weeks post-op. RESULTS: Adequate and site correct injections were made in four dogs. In one dog, significant augmentation of pressures were obtained at four weeks. None had significant changes in pressure at eight weeks, differences in length at either four or eight weeks or significant differences in the thickness of the examined layers. Four of the six had capillary cushions on pathological examination. The dog injected with the carrier had a loose and disorganise collection, while the others were well organised. CONCLUSION: SIS is a biologically compatible material. Lack of an animal model for gastro-oesophageal reflux disease (GORD) makes determining the ability of injections of SIS to combat reflux problematic.

Characterization of fission yeast cohesin: essential anaphase proteolysis of Rad21 phosphorylated in the S phase.

Cohesin complex acts in the formation and maintenance of sister chromatid cohesion during and after S phase. Budding yeast Scc1p/Mcd1p, an essential subunit, is cleaved and dissociates from chromosomes in anaphase, leading to sister chromatid separation. Most cohesin in higher eukaryotes, in contrast, is dissociated from chromosomes well before anaphase. The universal role of cohesin during anaphase thus remains to be determined. We report here initial characterization of four putative cohesin subunits, Psm1, Psm3, Rad21, and Psc3, in fission yeast. They are essential for sister chromatid cohesion. Immunoprecipitation demonstrates stable complex formation of Rad21 with Psm1 and Psm3 but not with Psc3. Chromatin immunoprecipitation shows that cohesin subunits are enriched in broad centromere regions and that the level of centromere-associated Rad21 did not change from metaphase to anaphase, very different from budding yeast. In contrast, Rad21 containing similar cleavage sites to those of Scc1p/Mcd1p is cleaved specifically in anaphase. This cleavage is essential, although the amount of cleaved product is very small (<5%). Mis4, another sister chromatid cohesion protein, plays an essential role for loading Rad21 on chromatin. A simple model is presented to explain the specific behavior of fission yeast cohesin and why only a tiny fraction of Rad21 is sufficient to be cleaved for normal anaphase.

The preoperative predictability of the short esophagus in patients with stricture or paraesophageal hernia.

BACKGROUND: Esophageal shortening is a known complication of advanced gastroesophageal reflux disease that may preclude a tension-free antireflux procedure. A retrospective analysis was performed to test the accuracy of preoperative testing. METHODS: From September 1993 to December 1998, 39 patients underwent esophageal mobilization with intraoperative length assessment. Patients were selected on the basis of irreducible hiatal hernia, stricture formation, or both. Patients in the upright position with a fixed hiatal hernia larger than 5 cm on an esophagram were considered to have a short esophagus. Manometric length two standard deviations below the mean for height was considered abnormally short. RESULTS: In 31 patients, intraoperative mobilization was sufficient to allow the gastroesophageal junction to lie 2 cm below the diaphragmatic crus, so no esophageal-lengthening procedure was required. Eight patients with a short esophagus required an esophageal-lengthening procedure after complete mobilization. Two patients subsequently underwent intrathoracic migration of the gastroesophageal junction (GEJ), with recurrence of symptoms and required gastroplasty during the second surgery. An esophagram had a sensitivity of 66% and a positive predictive value of 37%, whereas manometric length had a sensitivity of 43% and a positive predictive value of 25% for the diagnosis of short esophagus. The preoperative endoscopic finding of either a stricture or Barrett's esophagus was the most sensitive test for predicting the need for a lengthening procedure. CONCLUSIONS: Manometry and esophagraphy are not reliable predictors of the short esophagus. Additional tests and/or tests combined with other parameters are needed.

Left side thoracoscopically assisted gastroplasty: a new technique for managing the shortened esophagus.

Laparoscopic antireflux surgery is the procedure of choice for gastroesophageal reflux disease (GERD). However, many clinicians have reservations about its application in patients with complicated GERD, notably those with esophageal shortening. In this report, we present our experience with the laparoscopic management of the shortened esophagus. A total of 235 patients with primary GERD underwent laparoscopic antireflux procedures, 38 of whom were suspected preoperatively to have a shortened esophagus. Of the 235 patients, 8 (3.4%) needed a left thoracoscopically assisted gastroplasty in addition to laparoscopic Toupet repair (n = 4) or Nissen fundoplication (n = 4). Complications included pleural effusion (n = 1), pneumothorax (n = 2), and minor atelectasis (n = 1). The average hospital stay was 3 days. Results were satisfactory in 7 of 8 patients, with a mean follow-up of 20.2 months (range, 9-34 months). The surgical management of the shortened esophagus is difficult. However, the role of minimally invasive techniques is justified. Early results are appealing, with less morbidity, satisfactory control of GERD related symptoms, and a shortened hospital stay.

Persistent dysphagia after laparoscopic vagotomy.

BACKGROUND: Laparoscopic vagotomy represents a new and less invasive treatment for peptic ulcer disease, but the problem of postvagotomy dysphagia has not been solved. The aim of this study was to determine the etiologic factors related to long-term laparoscopic postvagotomy dysphagia. METHODS: Two female and 11 male patients with a mean age of 48.5 years who underwent laparoscopic vagotomy were investigated retrospectively. Preoperative diagnosis included duodenal ulcer resistant to medical treatment, gastric hypersecretion, gastric outlet obstruction, cholelithiasis, and gastroesophageal reflux disease (GERD). Ten patients underwent laparoscopic highly selective vagotomy, and three patients had laparoscopic truncal vagotomy with gastrojejunostomy or pyloroplasty. Nine of these patients had a Nissen fundoplication in conjunction with the vagotomy. RESULTS: The median long-term follow-up period was 47 months. Two patients complained of severe dysphagia, one of moderate dysphagia, and two of mild dysphagia. Neither type of vagotomy nor an additional fundoplication was correlated with the severity of postoperative long-term dysphagia. Severity of postoperative dysphagia was associated with severity of preoperative dysphagia (r = 0.752, p = 0.003) but not with heartburn (r = 0.358, p = 0.531) or regurgitation (r = 0.024, p = 0.938). The cause of preoperative dysphagia varied; however, all of these patients had GERD and consequent esophageal lesions. CONCLUSION: Preexisting dysphagia appears to play an integral role in persistent postoperative dysphagia. Care must be taken to construct a loose fundoplication in patients with dysphagia.

Does the duration of gastroesophageal reflux disease and degree of acid reflux correlate with esophageal function? A retrospective analysis of 768 patients.

To reconfirm that the duration of symptoms is not associated with esophageal motility in patients with gastroesophageal reflux disease (GERD), esophageal manometric data from 768 patients with GERD were retrospectively analyzed with relation to the duration of symptoms. GERD was defined by positive acid reflux test results monitored by ambulatory 24-hour pH monitoring. Correlation of the duration of symptoms with esophageal body pressures, the presence of dysmotility determined by simultaneous waves, average resting pressure of the lower esophageal sphincter (LES), and abdominal and overall lengths of the LES were statistically analyzed. The median duration of the symptoms was 60 months (range, 1-600). Duration of symptoms was not associated with contraction pressures of the esophageal body at 3 and 8 cm above the LES (r = -0.070 and -0.063, respectively). There was no correlation between LES pressures, LES lengths, or the percentage of simultaneous waves and duration of symptoms. Stricture formation is related to decreased distal esophageal function in GERD patients. In conclusion, the duration of GERD has little influence on esophageal body and LES function.

Surgery for achalasia: 1998.

Technical controversies abound regarding the surgical treatment of achalasia. To determine the value of a concomitant antireflux procedure, the best antireflux procedure, the correct length for gastric myotomy, the optimal surgical approach (thoracic or abdominal), and the equivalency of minimally invasive surgery, a literature review was carried out. The review is based on 23 articles on open transabdominal or transthoracic myotomy, 14 articles on laparoscopic myotomy, and four articles on thoracoscopic myotomy. Postoperative results of traditional open thoracic or transabdominal myotomy as determined by symptomatology were better with fundoplication than without fundoplication. The incidence of postoperative reflux as proved by pH monitoring was high in patients who had an open transabdominal myotomy without fundoplication. The type of antireflux procedure used and the length of gastric myotomy had little effect on results. The results of transthoracic Heller myotomy do not require a concomitant fundoplication. Laparoscopic and thoracoscopic myotomy had excellent results at short-term follow-up. A fundoplication must be added if the myotomy is performed transabdominally. A randomized prospective study is required to determine the best fundoplication and the extent of gastric myotomy. Although minimally invasive surgery for achalasia has excellent initial results, longer follow-up in a larger population of patients is needed.

Correlations between esophageal diseases and manometric length: a study of 617 patients.

The purpose of this study was to measure the length of the esophagus and assess its relationship to sex, weight, age, height, and various esophageal disorders. A retrospective analysis was undertaken of 617 esophageal manometric studies, which included 51 normal control subjects (27 males and 24 females) and 566 patients (297 males and 269 females) with esophageal disorders (50 with achalasia, 6 with diffuse esophageal spasm, 64 with strictures, 38 with nutcracker esophagus, 398 with gastroesophageal reflux disease [GERD] with positive 24-hour pH monitoring, and 66 with possible GERD but negative 24-hour pH monitoring). Manometry was performed in all of them by the station pull-through technique. The length of the esophagus was defined as the distance between the proximal end of the upper esophageal sphincter and the distal end of the lower esophageal sphincter. In the control group the mean (+/- standard deviation) length of the esophagus was 28.3 +/- 2.41 cm. In patients with esophageal disorders the mean length of the esophagus was 28.0 +/- 2.87 cm. Length of the esophagus is related to height but not to weight, sex, age, diffuse esophageal spasm, or nutcracker esophagus. Achalasia is associated with a longer esophagus, and GERD is associated with a shorter esophagus. Stricture is associated with a shorter esophagus, but this is in part due to the association between stricture and GERD. Patients with possible GERD but negative 24-hour pH monitoring have an esophageal length similar to that of GERD patients with positive 24-hour pH monitoring. Patients with GERD and stricture formation showed esophageal shortening in shorter patients. Achalasia, GERD, and GERD with stricture formation influence esophageal length. GERD-related strictures shorten the esophagus more significantly in short patients.

Fission yeast condensin complex: essential roles of non-SMC subunits for condensation and Cdc2 phosphorylation of Cut3/SMC4.

The condensin complex in frog extracts, containing two SMC (structural maintenance of chromosomes) and three non-SMC subunits, promotes mitotic chromosome condensation, and its supercoiling activity increases during mitosis by Cdc2 phosphorylation. Here, we report that fission yeast has the same five-member condensin complex, each of which is essential for mitotic condensation. The condensin complex was purified and the subunits were identified by microsequencing. Cnd1, Cnd2, and Cnd3, three non-SMC subunits showing a high degree of sequence conservation to frog subunits, are essential for viability, and their gene disruption leads to a phenotype indistinguishable from that observed in cut3-477 and cut14-208, known mutations in SMC4 and SMC2-like subunits. Condensin subunits tagged with GFP were observed to alter dramatically their localization during the cell cycle, enriched in the nucleus during mitosis, but cytoplasmic during other stages. This stage-specific alteration in localization requires mitosis-specific phosphorylation of the T19 Cdc2 site in Cut3. The T19 site is phosphorylated in vitro by Cdc2 kinase and shows the maximal phosphorylation in metaphase in vivo. Its alanine substitution mutant fails to suppress the temperature-sensitive phenotype of cut3-477, and shows deficiency in condensation, probably because Cut3 T19A remains cytoplasmic. Therefore, direct Cdc2 phosphorylation of fission yeast condensin may facilitate its nuclear accumulation during mitosis.

Manometric and radiographic verification of esophageal body decompensation for patients with achalasia.

BACKGROUND: Although morphologic, radiographic, and manometric features of achalasia have been well defined, it has not been established by careful retrospective analysis whether achalasia is a progressive disorder resulting in complete decompensation. STUDY DESIGN: To verify the hypothesis that achalasia is a progressive disease, we retrospectively investigated manometric, radiographic, and symptomatic data in patients with achalasia. Sixty-three patients (36 women and 27 men) with a median age of 44 years (range 11 to 79 years) were evaluated. The duration of symptoms ranged from 1 to 442 months, with a median of 48 months. Patients were divided into four groups according to the duration of symptoms: 36 patients with less than 5 years, 11 with 5 to 10 years, 9 with 10 to 15 years, and 7 with 15 years or more. RESULTS: Contraction pressures of the esophageal body decreased significantly at every level when the duration of symptoms increased (p < 0.04). The percentage of simultaneous waves in the esophageal body rose as the duration of symptoms increased. All waves were synchronous in every patient who had had symptoms for more than 15 years. The maximal width of the esophageal body measured on esophagram became greater with an increase in the duration of symptoms, but this measurement did not reach statistical significance (p = 0.063). The tortuosity of the esophagus, measured by the maximal angle of the esophageal axis, was significantly greater in patients with a longer duration of symptoms (p < 0.02). The type of symptoms was not associated with the duration of symptoms. CONCLUSIONS: Achalasia is a progressive disease, as verified by manometric and radiographic findings. The classification of esophageal motor function expressed by amplitude of contraction pressure and angle of tortuosity is objective and useful. Classification of achalasia by duration of symptoms may be important in treatment selection and effectiveness.

A new form of access for endo-organ surgery. The initial experience with percutaneous endoscopic gastrostomy.

BACKGROUND: Intraluminal gastric surgery provides a new treatment option for various disease processes. This study assesses the safety of a new large-diameter percutaneous endoscopic gastrostomy (PEG) for intraluminal surgery. METHODS: Investigators at six institutions were asked to complete a standard questionnaire to assess the difficulties associated with the assembly and introduction of the PEG, plus intraoperative and postoperative problems related to placement of the device. RESULTS: In terms of assembly; 1.9% of respondents reported difficulty obtaining complete vacuum of the balloon tip, and 3.8% had difficulty fitting the graduated dilator to the balloon-tipped cannula. Difficulties associated with introduction of the PEG included disengagement of the dilator from the balloon-tipped cannula (0%), extraction of the dilator-port assembly (0%), difficult PEG pullout (1.9%), abdominal wall bleeding (0%), and difficult PEG dilator separation (7.5%). Intraoperatively, 7.5% of respondents reported inadequate skin bolster fitting, 1.9% had CO(2) leakage into the peritoneal cavity, 0% had inadvertent PEG extraction, and 0% reported injury to the esophagus, colon, or small intestine. Postoperatively, there was a 9.4% rate of wound infection, a 1.9% rate of gastrocutaneous fistula, and a 1.9% rate of esophageal, colon, or small intestine injury. CONCLUSIONS: The large-diameter PEG is safe and effective for endo-organ surgery. Additional preventive measures for PEG site infection should be investigated.

A combined laparoscopic-endoscopic method of assessment to prevent the complications of short esophagus.

As antireflux surgery has been used increasingly for gastroesophageal reflux disease (GERD), a need has arisen for an accurate method to assess esophageal length. There are a number of preoperative tests that can help surgeons to establish the presence of a short esophagus, but intraoperative assessment after esophageal mobilization is the standard method. In this era of laparoscopic surgery, the surgeon mobilizes the esophagus extensively from the abdomen and then determines if mobilization is sufficient. We report an intraoperative technique that combines laparoscopic with endoscopic methods to determine the position of the gastroesophageal junction. Because two physicians are required, there is additional operating room time, resulting in increased costs. However, these costs are offset by the assurance that the complications of the short esophagus can be avoided. With experience, modifications were made, resulting in the technique described herein.