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Cholinergic anti-inflammatory pathway (CAP) describes a neuronal-inflammatory reflex centered on systemic cytokine regulation by α7 nicotinic acetylcholine receptor (α7nAChR) activation of spleen-residue macrophage. However, the CAP mechanism attenuating distal tissue inflammation, inducing a low level of systemic inflammation, is lesser known. In this study, we hypothesized that CAP regulates monocyte accessibility by influencing their adhesion to endothelial cells. Using RNA-seq analysis, we identified that α1,3-Fucosyltransferase 7 (FucT-VII), the enzyme required for processing selectin ligands, was significantly downregulated by α7nAChR agonist among other cell-cell adhesion genes. The α7nAChR agonist inhibited monocytic cell line U-937 binding to P-selectin and adhesion to endothelial cells. Furthermore, α7nAChR agonist selectivity was confirmed by α7nAChR knockdown assays, showing that FUT7 inhibition and adhesion attenuation by the agonist was abolished by siRNA targeting α7nAChR encoding gene. Consistently, FUT7 knockdown inhibited the adhesive properties of U-937 and prevented them to adhere to endothelial cells. Overexpression of FUT7 also abrogated the adhesion attenuation induced by GTS-21 indicating that FUT7 inhibition was sufficient for inhibiting adhesion by α7nAChR activation. Our work demonstrated that α7nAChR activation regulates monocyte adhesion to endothelial cells through FUT7 inhibition, providing a novel insight into the CAP mechanism.

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) inflammatory pathway is a component of the innate immune system that recognizes cytosolic nucleic acids. The pathway has been implicated in several processes including aging, autoinflammatory conditions, cancer, and metabolic diseases. The cGAS-STING pathway represents a promising therapeutic target in a variety of chronic inflammatory diseases.

A 70-year-old woman underwent a renal biopsy due to nephrotic syndrome. She had suffered from nontuberculous mycobacterial infection (NTM) for 14 years. The patient was diagnosed as having membranoproliferative glomerulonephritis (MPGN) type 3 and immunoglobulin (Ig)-associated MPGN based upon LM/erythromycin and IF findings, respectively. In high-magnification imaging, electron-dense deposits showed immunotactoid glomerulopathy (ITG). There was no evidence of hematological cancer, and the patient improved after receiving treatments for NTM. To the best of our knowledge, this patient is the first to show an association between ITG and NTM. Although ITG is generally considered as related to lymphoproliferative disease, it is suggested that ITG is driven by bacterial infection and is a potential outcome of Ig-associated MPGN.

Background. Streptococcal toxic shock-like syndrome (TSLS) is a severe infection caused by group A hemolytic streptococcus. It is clinically characterized by rapidly progressive septic shock and multiple organ failure within just a few hours. TSLS presenting as primary peritonitis is rare, especially in a male. Herein, we report a case of TSLS in a male presenting with primary peritonitis, with a review of 25 cases in Japan. Case Presentation. A 51-year-old male was referred to our hospital with abdominal pain and hypotension. We made a preoperative diagnosis of peritonitis with septic shock and performed an emergency operation. Intraoperative findings indicated no marked origin of the peritonitis. Preoperative blood culture showed the presence of group A hemolytic streptococcus. The patient required intensive care involving artificial respiration, abdominal drainage and cytokine absorption therapy, and was discharged on postoperative day 25. Conclusion. TSLS in a male presenting as primary peritonitis is rare. Although this condition is a severe infection, it can be treated by multimodal therapy.

Background. Percutaneous endoscopic gastrostomy (PEG) is the standard modality for long-term enteral nutrition for patients with dysphagia. Compared with open gastrostomy, though PEG is an extremely safe procedure with fewer complications, there are severe cases due to anatomical features. For these cases, laparoscopic-assisted percutaneous endoscopic gastrostomy (LAPEG) is the optimal method. Case Presentation. A 52-year-old man had a disturbance in swallowing because of cerebral infarction. We attempted PEG under gastrointestinal fiberscope (GIF) and colon fiberscope inspection; however, the procedure was unsuccessful because it was impossible to move the transverse colon downward. We therefore attempted LAPEG to observe the stomach and other organs. Under laparoscopic observation, we diagnosed gastric volvulus, classified as the organo-axial type. For this reason, inserting the tube through the skin was very difficult. We easily corrected the gastric volvulus by using laparoscopic forceps and were finally able to place the PEG tube safely. Discussion. Gastric volvulus is rare in clinical practice. The treatment of gastric volvulus depends on whether mucosal ischemia is present. Endoscopic reduction of gastric volvulus is effective for many patients. Surgical treatment should be considered for patients with gastric volvulus that frequently recurs. In our patient, completely inserting the GIF was impossible; therefore, we could not correctly diagnose gastric volvulus. Laparoscopy-assisted PEG is a useful and safe technique for placing a gastrostomy tube in patients presenting with anatomical difficulties. Moreover, in our patient, gastropexy was performed with PEG. Therefore, LAPEG may be used to prevent the recurrence of gastric volvulus. Gastropexy is a useful option in LAPEG. Conclusions. Laparoscopy has the advantage of allowing a direct inspection of the stomach while gastrostomy is performed and may reveal complications to PEG insertion. Furthermore, in our patient, gastropexy was performed with PEG.

Acute kidney injury (AKI) and chronic kidney disease (CKD) are interconnected syndromes that represent a global public health challenge. Organelles play essential roles in a vast range of cell functions, and their damage is related to several kidney diseases. Organelles launch the stress signal or trigger the stress response, and organelles interact with each other through a phenomenon termed organelle crosstalk. The endoplasmic reticulum (ER) is a major organelle that controls protein synthesis, folding, and degradation via the unfolded protein response pathway. Renal pathogenic conditions, such as chronic hypoxia, induce a maladaptive unfolded protein response pathway (ER stress) in the kidney, leading to progression of AKI and CKD. Mitochondria have an essential role in producing adenosine triphosphate for maintaining the cellular/organelle functions, including protein homeostasis in the ER. Thus, mitochondrial dysfunction also can induce ER stress (altered protein homeostasis) and subsequent cellular damage. Recent evidence has shown that ER or mitochondrial dysfunction disrupts the organelle crosstalk between mitochondria and ER in the kidney. Such alterations of ER-mitochondria crosstalk might contribute to the progression of AKI to CKD. Mitochondrial injury induces aberrant tubular inflammation, which is one of the major fibrotic processes. We recently found that a novel tubular inflammatory pathway that is activated specifically by the interaction of mitochondrial DNA with the ER membrane molecule triggers the progression of tubular inflammation in AKI. Thus, there is accumulating evidence for the pathophysiologic importance of organelle crosstalk, especially mitochondria-ER crosstalk. Organelle stress and crosstalk can serve as potential therapeutic targets for the prevention of AKI-to-CKD transition.

Introduction Duodenal gastrointestinal stromal tumours (GIST) are rare. Therefore, difficulties are experienced when selecting the appropriate surgical procedure in patients with duodenal GISTs. This report presents the cases of three patients with duodenal GISTs who underwent wedge resection. This report would help surgeons identify clinical features and surgical procedures in patients with duodenal GISTs. Presentation of case Three patients were diagnosed with duodenal submucosal tumours. The first patient presented with melena, the second with postoperative anaemia, and the third with an incidental finding of a large abdominal tumour after presenting with ischaemic colitis. All tumours arose in the 2nd portion of the duodenum and measured 3.5, 3, and 9.2 cm, respectively. Wedge resection of the duodenum was performed in all patients. In patients one and two, simple closure of duodenal wall was performed after wedge resection. In patient three, side-to-side anastomosis with the jejunum was performed because a large area of the wall was removed using the wedge resection technique. Pancreatoduodenectomy was avoided in all patients. Recurrence was not noted in any patient. Discussion Since GISTs are not generally associated with lymph node metastasis, local resection with negative margins is sufficient to surgically manage patients with GISTs. Conclusion Our results indicated the effectiveness of performing wedge resection for duodenal GISTs not in close proximity to the ampulla of Vater. Moreover, less invasive procedures should be adopted in patients with duodenal GISTs., Highlights • GIST are derived from the intestinal cells of Cajal in the GIT and mesentery. • The occurrence of duodenal GIST is rare. • Complete wedge resection was performed for GIST at the 2nd portion of the duodenum. • Wedge resection is a feasible and safe surgical method for duodenal GISTs.

The relevance of primary cilia shortening in kidney disease and its pathomechanism are largely unknown. Tubular damage in acute kidney injury (AKI) is strongly associated with mitochondrial dysfunction. Thus, we investigated the interaction between primary cilia and mitochondria in cisplatin-induced AKI mouse models. We observed that the expression of intraflagellar transport 88 (IFT88), a ciliary maintenance protein, was decreased in the renal cortex following tubular damage due to cisplatin-induced AKI. This result was consistent with the decreased IFT88 expression in cisplatin-treated RPTEC/TERT1 cells (human primary proximal tubular cells) parallel to the shortening of primary cilia, suggesting a causative link between tubular damage and IFT88-mediated cilia regulation. To address the effect of impaired primary cilia with decreased IFT88 expression on tubular function, RPTEC/TERT1 cells treated with cisplatin and knocked down for IFT88 using siRNA (IFT88-KD) were assessed for phenotypic changes and mitochondrial metabolic function. Both cisplatin and IFT88-KD caused primary cilia shortening, downregulated mitochondrial oxidative phosphorylation capacity, and had defective fatty acid oxidation and decreased ATP production. Furthermore, IFT88 overexpression enhanced mitochondrial respiration, which partially counteracted cisplatin-induced defective fatty acid oxidation. These results are indicative of the contribution of IFT88 to mitochondrial homeostasis. Our findings suggest that tubular mitochondrial dysfunction in cisplatin-induced AKI is mediated, at least in part, by a decrease in IFT88 expression with primary cilia shortening. That is, tubular mitochondrial damage followed by tubular injury in AKI may occur through alteration of IFT88 expression and subsequent ciliary shortening in tubular cells.

Summary: Acute kidney injury (AKI) is characterized by mitochondrial dysfunction and activation of the innate immune system. The cyclic GMP-AMP synthase (cGAS) stimulator of interferon genes (STING) pathway detects cytosolic DNA and induces innate immunity. Here, we investigate the role of mitochondrial damage and subsequent activation of the cGAS-STING pathway using a genetically engineered animal model of cisplatin-induced AKI and cultured tubular cells. Cisplatin induced mtDNA leakage into the cytosol—probably through BCL-2-like protein 4 (BAX) pores in the mitochondrial outer membrane—in tubules, with subsequent activation of the cGAS-STING pathway, thereby triggering inflammation and AKI progression, which is improved in STING-deficient mice. STING knockdown in cultured tubular cells ameliorates inflammatory responses induced by cisplatin. mtDNA depletion and repletion studies support tubular inflammatory responses via the cGAS-STING signal activation by cytosolic mtDNA. Therefore, we conclude that mitochondrial dysfunction and subsequent activation of the mtDNA-cGAS-STING pathway is a critical regulator of kidney injury. : Acute kidney injury (AKI) is associated with tubular inflammation and mitochondrial dysfunction. Maekawa et al. reveal that tubular mitochondrial damage leads to mtDNA leakage into the cytosol, probably via BAX pores on the mitochondria, activating cGAS-STING signaling and subsequent tubular inflammation in cisplatin-induced AKI. Suppression of the STING ameliorates tubular inflammation and progression of AKI. Keywords: acute kidney injury, tubular cells, mitochondrial DNA, inflammation, cGAS-STING pathway, cisplatin nephrotoxicity

A phase II trial was conducted to investigate the benefit of oxaliplatin-based adjuvant chemotherapy in Japanese stage III colon cancer patients. Eligible patients were scheduled to receive 12 cycles of mFOLFOX6 or 8 cycles of CAPOX in adjuvant settings. The primary endpoint was the 3-year disease-free survival (DFS). Cox proportional hazards regression was performed to identify risk factors for a worse DFS. A total of 130 patients, including 73 patients receiving mFOLFOX6 and 57 patients receiving CAPOX, were enrolled from 16 institutions between April 2010 and April 2014. The 3-year DFS was 82.2%, exceeding the expected primary endpoint of 81.7%. The 3-year DFS tended to be higher in patients receiving mFOLOFOX6 than in those receiving CAPOX (mFOLFOX6, 86.3%; CAPOX, 76.9%; P = 0.06). The 3-year DFS rates did not differ markedly based on the risk stratification (T1/T2/T3 N1 vs. T4 or N2) indicated by the IDEA COLLABORATION study (P = 0.22). In the multivariate analysis, stage IIIC (P = 0.046) and early discontinuation (P

High-resolution numerical simulation has been performed to study aeroacoustic noise radiated from a turbulent boundary layer at freestream Mach number Ma = 0.3, which develops on a smooth flat plate and over a small forward-facing step. Sound waves radiated from the turbulent boundary layer on the flat plate are dominant in a very-low-frequency band and have characteristics of a linear sound source. The sound waves are observed in the far-field from the boundary propagate outside of the flow region where small hydrodynamic pressure fluctuations with a significant long-wavelength appear. The instantaneous hydrodynamic pressure fields that gradually develop or decay while moving downstream with the turbulent boundary layer are associated with the evolution of various vortical structures. The characteristics of the sound wave being a linear sound source and dominant in a very-low-frequency band are similar to those of the real high-speed train. The sound waves generated from the turbulent boundary layer over the forward-facing step with a height (SH) of SH/y+ ≅ 62 are significantly larger in a full frequency band than those radiated from the turbulent boundary layer on the flat plate. Numerical results of the turbulent boundary layer over the forward-facing step with a height of SH/y+ ≅ 30 show that the sound waves are dominant in the low-frequency band, and also step-specific sound waves are generated in the high-frequency band. Further, even if the step height is SH/y+ ≅ 7.5, the sound waves unique to the small step are generated in the high-frequency band.

We previously reported the first evidence of oncological benefits from a Japanese phase II trial of oxaliplatin-based adjuvant chemotherapy in patients with stage III colon cancer (the FACOS study). We herein report the long-term survival and persistent oxaliplatin-related peripheral sensory neuropathy (PSN) for patients enrolled in this trial. Patients were scheduled to receive the mFOLFOX6 or CAPOX regimen in the adjuvant setting. The five-year overall survival (OS) rate and persistent PSN were evaluated. A total of 130 patients (mFOLFOX6, n = 73; CAPOX, n = 57) were eligible. The 5-year OS rate was 91.4%. No significant difference in the OS rate was observed between regimens (mFOLFOX6, 94.4%; CAPOX, 87.4%; P = 0.25). The incidence of PSN during adjuvant treatment was 55.4% in grade 1 (G1), 30.0% in G2, and 4.6% in G3. No patients showed G3 PSN at 12 months, but G1 or G2 residual PSN after 5 years was observed in 21.8% (G1, 20%; G2, 1.8%). Updated results from the FACOS study support the benefits of oxaliplatin-based adjuvant chemotherapy in terms of the long-term survival among Japanese patients with stage III colon cancer. However, long-term persistent PSN occurs in about 20% of survivors, counterbalancing the favorable OS.

No difference in the gene methylation status of tumor-suppression genes between pancreatic cancer tissues and adjacent non-cancer tissues is observed. The present study investigated whether the promoter CpG islands of the cysteine dioxygenase 1 (CDO1), tachykinin precursor 1 (TAC1) and checkpoint with forkhead and ring finger domains (CHFR) genes were methylated in pancreatic cancer and adjacent non-cancerous pancreatic tissue in order to determine if they could be considered as markers for the detection of pancreatic cancer. A total of 38 Formalin-fixed and paraffin-embedded pancreatic adenocarcinoma tissues and their adjacent non-cancerous specimens from patients with pancreatic cancer, as well as 9 non-cancerous pancreatic samples from patients without pancreatic adenocarcinoma were obtained following surgical resection. The hypermethylation of CpG islands was detected using a methylation-specific quantitative PCR. The methylation values were calculated using the ∆Cq method and were expressed as 2-ΔCq. The 2-ΔCq value of the CDO1 promoter from pancreatic adenocarcinoma specimens was significantly higher compared with that of adjacent non-cancerous and tumor-free pancreatic tissues (P

Background: The management of gastric cancer patients who received gastrectomy and/or postoperative chemotherapy is of high importance. However, the safety and efficacy of chemotherapy in hemodialysis patients have not been established. In this study, we report 6 cases of hemodialysis patients who underwent gastrectomy for gastric cancer. Case Presentation: The presented cases included 5 men and 1 woman, with a mean age of 66.3 years (range, 59–74 years). All patients underwent standard laparotomy, with 3 of 6 patients (50%) experiencing postoperative complications. Three patients who did not experience any postoperative complications could receive subsequent chemotherapy. S-1 chemotherapy regimen and uracil and tegafur chemotherapy regimen were administered to 1 and 2 patients, respectively. These 3 patients did not experience any chemotherapy-related side effects. Among the 4 patients who received a diagnosis of pathologic stages II to III, 2 patients treated with postoperative chemotherapy achieved better prognoses than those who did not receive chemotherapy (mean, 25.5 versus 5.0 months). Discussion and Conclusion: Hemodialysis patients with gastric cancer who received gastrectomy exhibited a high morbidity rate. Postoperative chemotherapy can be performed immediately after surgery in patients who do not experience postoperative complications. S-1 regimen and uracil and tegafur regimen could be administered safely in hemodialysis patients. Postoperative chemotherapy may lead to a good prognosis in gastric cancer patients receiving hemodialysis.

Lipotoxicity plays an important role in the progression of chronic kidney damage via various mechanisms, such as endoplasmic reticulum stress. Several studies proposed renal lipotoxicity in glomerular and tubular cells but the effect of lipid on renal erythropoietin (EPO)-producing (REP) cells in the interstitium has not been elucidated. Since renal anemia is caused by derangement of EPO production in REP cells, we evaluated the effect of palmitate, a representative long-chain saturated fatty acid, on EPO production and the endoplasmic reticulum stress pathway. EPO production was suppressed by palmitate (palmitate-conjugated bovine serum albumin [BSA]) or a high palmitate diet, but not oleic acid-conjugated BSA or a high oleic acid diet, especially under cobalt-induced pseudo-hypoxia both in vitro and in vivo. Importantly, suppression of EPO production was not induced by a decrease in transcription factor HIF activity, while it was significantly associated with endoplasmic reticulum stress, particularly transcription factor ATF4 activation, which suppresses 3'-enhancer activity of the EPO gene. ATF4 knockdown by siRNA significantly attenuated the suppressive effect of palmitate on EPO production. Studies utilizing inherited super-anemic mice (ISAM) mated with EPO-Cre mice (ISAM-REC mice) for lineage-labeling of REP cells showed that ATF4 activation by palmitate suppressed EPO production in REP cells. Laser capture microdissection confirmed ATF4 activation in the interstitial area of ISAM-REC mice treated with palmitate-conjugated BSA. Thus, endoplasmic reticulum stress induced by palmitate suppressed EPO expression by REP cells in a manner independent of HIF activation. The link between endoplasmic reticulum stress, dyslipidemia, and hypoxia may contribute to development and progression of anemia in CKD.

Introduction: In rectal cancer, distal intramural spread may sometimes occur, but a maximum extent of distal spread of > 6 cm is very rare. Case Presentation: A 65-year-old Japanese male with an advanced rectal cancer tumor with para-aortic lymph node metastasis was admitted. We performed a low anterior resection with lymphadenectomy, but the intraoperative frozen-section analysis of margins revealed malignant cell positivity; we, therefore, performed an abdominoperineal resection. Pathological findings showed that the maximum extent of distal spread was 6 cm. After 12 courses of FOLFOX4 as adjuvant chemotherapy, abdominal computed tomography revealed whole lymph node metastases, including Virchow’s node. Though FOLFIRI + panitumumab was started, he was not eligible for additional chemotherapy after 10 cycles. Conclusion: An intraoperative frozen pathology examination was helpful for the additional resection, when unexpected distal spreading had occurred in rectal cancer. The evidence of a distal negative margin should not be underestimated.

Neuroendocrine carcinoma (NEC) of the colon is very rare, and squamous cell carcinoma (SCC) of colon cancer is rare. We recently treated a patient with both NEC and SCC that initially presented as multiple unresectable liver and lung metastases. A 68-year-old Japanese man was referred to our hospital because of diarrhea with descending colon cancer obstruction. He underwent a left colectomy. Based on immunohistochemistry results, we diagnosed mixed NEC and SCC, the primary lesion location of which was probably the lung in the final pathologic examination. He began systemic palliative chemotherapy with CDDP and CPT-11. After 3 months of treatment, shown the progressive disease, we started CDDP and VP-16. The patient was not eligible for additional chemotherapy after 2 months.

The prevalence of chronic kidney disease (CKD), characterized by progressive renal dysfunction with tubulointerstitial fibrosis, is increasing because of societal aging. Uremic toxins, accumulated during renal dysfunction, cause kidney damage, leading to renal deterioration. A recent metabolomic analysis revealed that plasma D-serine accumulation is associated with faster progression of renal dysfunction in CKD patients. However, the causal relationship and the underlying mechanisms remain unclear. Herein, we demonstrated that D-serine markedly induced cellular senescence and apoptosis in a human proximal tubular cell line, HK-2, and primary culture of human renal tubular cells. The former was accompanied by G2/M cell cycle arrest and senescence-associated secretory phenotype, including pro-fibrotic and pro-inflammatory factors, contributing to tubulointerstitial fibrosis. Integrated stress response mediated by the general control nonderepressible 2 played an important role in D-serine-induced tubular cell toxicity and pro-fibrotic phenotypes, accelerating CKD progression and kidney aging. D-serine upregulated the L-serine synthesis pathway. Furthermore, D-serine-induced suppression of tubular cell proliferation was ameliorated by L-serine administration, indicating that D-serine exposure induced an L-serine-deprived state in tubular cells, compensated by L-serine synthesis. Thus, this study unveils molecular mechanisms underlying D-serine-induced tubular damage and pro-fibrotic phenotypes, suggesting that D-serine is a uremic toxin involved in CKD pathogenesis.

Background In Japanese super aging society, there is a need to establish home dental care service supply system. Current situation of home dental care should be analyzed.Methods A cross-sectional survey was conducted using a self-administered postal questionnaire distributed to all members of Iwate Dental Association. Implementation of home and nursing home dental care, number of staffs of dental clinic and the contents of dental home care were analyzed. For the analysis, correspondence analysis, item response theory, and zero-inflated model were used.Results Among 354 dental clinics, 187 (52.8%) were implemented home dental care and 195 (55.1%) were implemented nursing home dental care. Dental clinics handle home dental care by part-time workers. Denture treatment and oral care was the common treatment of dental home care.Conclusion More than half of the dental clinics were not managed the home dental care. Infrastructure improvement is necessary for the sufficient supply of dental home care service.

Predicting malignancy is important for adequate adjuvant therapy in patients with cancer. Due to cancer being a genetic disease, the detection of gene mutations could be helpful in predicting the prognosis and efficacy of drugs. Gastric cancer is the fifth most common cancer and is the third leading cause of cancer associated mortality worldwide. Mutations in genes may correlate with clinical information in patients with gastric cancer after surgery and, therefore, may be useful for predicting the prognosis of this disease. In the present study, to assess the usefulness of a commercial sequencing panel, TruSeq® Amplicon-Cancer Panel (Illumina), using a next-generation sequencer (Illumina MiSeq), mutation analysis of fresh as well as formalin-fixed paraffin-embedded (FFPE) gastric cancer tissues was performed retrospectively. The study group comprised of 4 patients who underwent gastrectomy for gastric cancer. Cancer and normal stomach tissues were collected immediately following surgical removal. Thereafter, the specimens were fixed in 10% neutral formalin for 24–72 h. Normal and FFPE cancer tissues were histologically examined and confirmed. A total of 3 mutations were identified in the driver genes (KRAS, TP53 and APC) in cancer tissues from 2 of the 4 patients, using fresh samples. In addition, FFPE samples were analysed for the same tissues and the same results were obtained by setting the threshold for the percentage of the mutation rate to avoid detection of pseudo-positive mutations. In conclusion, the sequencing analysis using FFPE-derived DNA samples was successfully performed.

No difference in the gene methylation status of tumor-suppression genes between pancreatic cancer tissues and adjacent non-cancer tissues is observed. The present study investigated whether the promoter CpG islands of the cysteine dioxygenase 1 (CDO1), tachykinin precursor 1 (TAC1) and checkpoint with forkhead and ring finger domains (CHFR) genes were methylated in pancreatic cancer and adjacent non-cancerous pancreatic tissue in order to determine if they could be considered as markers for the detection of pancreatic cancer. A total of 38 Formalin-fixed and paraffin-embedded pancreatic adenocarcinoma tissues and their adjacent non-cancerous specimens from patients with pancreatic cancer, as well as 9 non-cancerous pancreatic samples from patients without pancreatic adenocarcinoma were obtained following surgical resection. The hypermethylation of CpG islands was detected using a methylation-specific quantitative PCR. The methylation values were calculated using the ∆Cq method and were expressed as 2−ΔCq. The 2−ΔCq value of the CDO1 promoter from pancreatic adenocarcinoma specimens was significantly higher compared with that of adjacent non-cancerous and tumor-free pancreatic tissues (P