Free-living wrist and hip accelerometry forecast cognitive decline among older adults without dementia over 1- or 5-years in two distinct observational cohorts.

The prevalence of major neurocognitive disorders is expected to rise over the next 3 decades as the number of adults ≥65 years old increases. Noninvasive screening capable of flagging individuals most at risk of subsequent cognitive decline could trigger closer monitoring and preventive strategies. In this study, we used free-living accelerometry data to forecast cognitive decline within 1- or 5-years in older adults without dementia using two cohorts. The first cohort, recruited in the south side of Chicago, wore hip accelerometers for 7 continuous days. The second cohort, nationally recruited, wore wrist accelerometers continuously for 72 h. Separate classifier models forecasted 1-year cognitive decline with over 85% accuracy using hip data and forecasted 5-year cognitive decline with nearly 70% accuracy using wrist data, significant improvements compared to demographics and comorbidities alone. The proposed models are readily translatable to clinical practices serving ageing populations.

Correction: LncRNA AFAP1-AS1 promotes growth and metastasis of cholangiocarcinoma cells.

[This corrects the article DOI: 10.18632/oncotarget.16880.].

OPA Interacting Protein 5 Antisense RNA 1 Expedites Cell Migration and Invasion Through FOXM1/ Wnt/ß-Catenin Pathway in Pancreatic Cancer.

BACKGROUND: Pancreatic cancer (PC) is a digestive tract malignancy with poor prognosis. Long noncoding RNA (lncRNA) OPA interacting protein 5 antisense RNA 1 (OIP5-AS1) was regarded to be correlated with human malignancy, working as tumor suppressor or promoter on the basis of tumor types. However, the function of OIP5-AS1 in PC remained unclear. AIMS: The study focused on the function and regulatory mechanism of OIP5-AS1 in PC. METHODS: OIP5-AS1 expression was assessed by the quantitative reverse transcription PCR (RT-qPCR) in tumor tissues and PC cell lines. 5-ethynyl-2'-deoxyuridine (EdU) incorporation and cell counting kit-8 (CCK-8) assays were applied to detect cell proliferation ability. Through wound healing and transwell assays, cell migration and invasion capacities were estimated. Flow cytometry analysis was performed to examine apoptosis capability of PC cells. RESULTS: OIP5-AS1 downregulating inhibited cell proliferation, migration, and invasion capacities, while promoting cell apoptosis rates. As a competing endogenous RNA (ceRNA), OIP5-AS1 competed with Forkhead Box M1 (FOXM1) for the binding sites on microRNA-320b (miR-320b). OIP5-AS1 was able to upregulate FOXM1 expression via silencing miR-320b. Furthermore, FOXM1 served as an activator of Wnt/ß-catenin pathway and mediated the effect of OIP5-AS1 on Wnt/ß-catenin pathway. CONCLUSION: OIP5-AS1 expedites the proliferative, migrated, and invasive capability of PC cells, while repressing cell apoptosis through regulating miRNA-320b/FOXM1 axis and FOXM1/Wnt/ß-catenin pathway in PC. OIP5-AS1 regulation on FOXM1/Wnt/ß-catenin pathway may offer novel efficient markers for PC treatments.

LncRNA RGMB-AS1 facilitates pancreatic cancer cell proliferation and migration but inhibits cell apoptosis via miR-574-3p/PIM3 axis.

Pancreatic cancer (PC) is among the most notorious malignancies worldwide. Long noncoding RNA (lncRNA) repulsive guidance molecule bone morphogenetic protein (BMP) coreceptor b antisense RNA 1 (RGMB-AS1) was an oncogene in glioma. However, the RGMB-AS1 function in PC remains largely unknown. Herein, quantitative real-time polymerase chain reaction was performed to analyze the expression of RGMB-AS1. We determined RGMB-AS1 influence on PC cell malignant behaviors via functional assays. Besides, we applied subcellular fractionation and fluorescence in situ hybridization (FISH) assays to confirm the cellular distribution of RGMB-AS1 in PC cells. We used mechanism assays to detect the regulatory axis of RGMB-AS1 in PC cells. Briefly, the level of RGMB-AS1 expression in PC cells was abnormally high. RGMB-AS1 knockdown impeded PC cell proliferation and migration, but induced cell apoptosis, and RGMB-AS1 overexpression led the opposite consequences. RGMB-AS1 acted as a competing endogenous RNA (ceRNA) to sequester miR-574-3p and thereby regulated Pim-3 proto-oncogene, serine/threonine kinase (PIM3) expression. Conclusively, our work revealed the cancer-promoting function of RGMB-AS1 in PC and that the regulatory mechanism of the RGMB-AS1/miR-574-3p/PIM3 axis might contribute to novel biomarker development in PC treatment.NEW & NOTEWORTHY RGMB-AS1 promotes PC cell proliferation, elevates PC cell migration capacity, inhibits PC cell apoptosis, and promotes PC cell proliferation and migration but inhibits cell apoptosis via targeting miR-574-3p. PIM3 is directly targeted by miR-574-3p.

Inhibition of PI3K/AKT signaling via ROS regulation is involved in Rhein-induced apoptosis and enhancement of oxaliplatin sensitivity in pancreatic cancer cells.

Several natural products have been demonstrated to both enhance the anti-tumor efficacy and alleviate the side effects of conventional chemotherapy drugs. Rhein, a main constituent of the Chinese herb rhubarb, has been shown to induce apoptosis in various cancer types. However, the exact pharmacological mechanisms controlling the influence of Rhein on chemotherapy drug effects in pancreatic cancer (PC) remain largely undefined. In this study, we found that Rhein inhibited the growth and proliferation of PC cells through G1 phase cell cycle arrest. Moreover, Rhein induced caspase-dependent mitochondrial apoptosis of PC cells through inactivation of the PI3K/AKT pathway. Combination treatment of Rhein and oxaliplatin synergistically enhanced apoptosis of PC cells through increased generation of intracellular reactive oxygen species (ROS) and inactivation of the PI3K/AKT pathway. Pre-treatment with the ROS scavenger N-acetyl-L-cysteine attenuated the combined treatment-induced apoptosis and restored the level of phosphorylated AKT, indicating that ROS is an upstream regulator of the PI3K/AKT pathway. The combination therapy also exhibited stronger anti-tumor effects compared with single drug treatments in vivo. Taken together, these data demonstrate that Rhein can induce apoptosis and enhance the oxaliplatin sensitivity of PC cells, suggesting that Rhein may be an effective strategy to overcome drug resistance in the chemotherapeutic treatment of PC.

Upregulation of METTL14 mediates the elevation of PERP mRNA N6 adenosine methylation promoting the growth and metastasis of pancreatic cancer.

BACKGROUND: Pancreatic cancer is one of the most lethal human cancers. N6-methyladenosine (m6A), a common eukaryotic mRNA modification, plays critical roles in both physiological and pathological processes. However, its role in pancreatic cancer remains elusive. METHODS: LC/MS was used to profile m6A levels in pancreatic cancer and normal tissues. Bioinformatics analysis, real-time PCR, immunohistochemistry, and western blotting were used to identify the role of m6A regulators in pancreatic cancer. The biological effects of methyltransferase-like 14 (METTL14), an mRNA methylase, were investigated using in vitro and in vivo models. MeRIP-Seq and RNA-Seq were used to assess the downstream targets of METTL14. RESULTS: We found that the m6A levels were elevated in approximately 70% of the pancreatic cancer samples. Furthermore, we demonstrated that METTL14 is the major enzyme that modulates m6A methylation (frequency and site of methylation). METTL14 overexpression markedly promoted pancreatic cancer cell proliferation and migration both in vitro and in vivo, via direct targeting of the downstream PERP mRNA (p53 effector related to PMP-22) in an m6A-dependent manner. Methylation of the target adenosine lead to increased PERP mRNA turnover, thus decreasing PERP (mRNA and protein) levels in pancreatic cancer cells. CONCLUSIONS: Our data suggest that the upregulation of METTL14 leads to the decrease of PERP levels via m6A modification, promoting the growth and metastasis of pancreatic cancer; therefore METTL14 is a potential therapeutic target for its treatment.

UV-Triggered Transient Electrospun Poly(propylene carbonate)/Poly(phthalaldehyde) Polymer Blend Fiber Mats.

This work reports the first transient electrospun nanofiber mat triggered by UV-irradiation using poly(propylene carbonate) (PPC)/poly(phthalaldehyde) (cPPA) polymer blends. The ability to trigger room temperature transience of nanofiber mats without the need for additional heat or solvent expands its utility in nonbiological fields, especially for transient electronic devices. The addition of a photo-acid-generator to the system, working in combination with UV light, provides an acid source to enhance degradation because both polymer backbones are acid-sensitive. Electrospinning enables the production of PPC/cPPA composite nanofiber mats capable of significant degradation upon exposure to UV radiation while maintaining relatively high mechanical properties. An acid amplifier, an autocatalytically decomposing compound triggered by acid, was used to generate more acid and accelerate nanofiber degradation. The electrospun fiber mats can be post-annealed to achieve an improved mat with a mechanical strength of ∼170 MPa.

LncRNA AFAP1-AS1 promotes growth and metastasis of cholangiocarcinoma cells.

We investigated the role of actin filament associated protein 1 antisense RNA1 (AFAP1-AS1) lncRNA in promoting cholangiocarcinoma (CCA). qRT-PCR analysis of patient samples showed that AFAP1-AS1 expression was higher in CCA tumors than matched adjacent non-tumor tissue. AFAP1-AS1 levels were also higher in CCA cell lines (HuCCT1 and TFK-1) than a normal biliary epithelium cell line (HIBEpic). AFAP1-AS1 knockdown in CCA cell lines using shAFAP1-AS1 reduced cell proliferation and colony formation in CCK-8 and colony formation assays, respectively. Cell cycle analysis demonstrated that AFAP1-AS1 knockdown resulted in G0/G1 cell cycle arrest and inhibition of S-G2/M transition compared to the controls. CCA cells transfected with shAFAP1-AS1 also exhibited reduced metastasis and invasiveness in Transwell and wound healing assays. This was further confirmed in xenograft experiments with nude mice using CCA cells transfected with shAFAP1-AS1 or control shRNA. AFAP1-AS1 knockdown cells produced smaller tumors, demonstrating that AFAP1-AS1 promotes tumor growth in vivo. AFAP1-AS1 knockdown also increased expression of actin filament associated protein 1 (AFAP1) and reduced cell stress filament integrity, as determined from western blot and immunofluorescence assays, respectively. These findings indicate that AFAP1-AS1 exerts oncogenic effects in CCA. We postulate that AFAP1-AS1 is a potentially useful diagnostic and prognostic biomarker and therapeutic target for CCA.

Transient Fiber Mats of Electrospun Poly(Propylene Carbonate) Composites with Remarkable Mechanical Strength.

Polymers with a triggered decomposition are attractive for an array of applications ranging from patterning to transient packaging materials, as well as for environmental protection. This work showed for the first time UV and thermally triggered transience in fiber mats using poly(propylene carbonate) (PPC) composites. The electrospun PPC-composite fiber mats combine excellent decomposition performance (because of the high surface to volume ratio) with high stiffness and thus represent a new class of materials enabling innovative applications, such as transient filter materials and short-time plant protection materials, as well as temporary lightweight materials for aerospace engineering. Thermally and UV-triggerable additives (protected acids or base) have been used in different concentrations to tune the transience performance of the fiber mats over a wide range (75-212 °C). The addition of organo-modified clay (OMMT) enhanced mechanical stability and prevented shrinkage at room temperature. Different annealing methods have been used to improve the mechanical properties even further (tensile strength = 2-12 MPa, Young's modulus = 55-747 MPa) making these fiber mats attractive for a broad field of applications. An Ashby plot of Young's modulus versus degradation temperature for electrospun fiber mats is shown, revealing much lower degradation temperatures with higher moduli for PPC composites compared to other electrospun polymers.

Simultaneous inhibition of the ubiquitin-proteasome system and autophagy enhances apoptosis induced by ER stress aggravators in human pancreatic cancer cells.

In contrast to normal tissue, cancer cells display profound alterations in protein synthesis and degradation. Therefore, proteins that regulate endoplasmic reticulum (ER) homeostasis are being increasingly recognized as potential therapeutic targets. The ubiquitin-proteasome system and autophagy are crucially important for proteostasis in cells. However, interactions between autophagy, the proteasome, and ER stress pathways in cancer remain largely undefined. This study demonstrated that withaferin-A (WA), the biologically active withanolide extracted from Withania somnifera, significantly increased autophagosomes, but blocked the degradation of autophagic cargo by inhibiting SNARE-mediated fusion of autophagosomes and lysosomes in human pancreatic cancer (PC) cells. WA specifically induced proteasome inhibition and promoted the accumulation of ubiquitinated proteins, which resulted in ER stress-mediated apoptosis. Meanwhile, the impaired autophagy at early stage induced by WA was likely activated in response to ER stress. Importantly, combining WA with a series of ER stress aggravators enhanced apoptosis synergistically. WA was well tolerated in mice, and displayed synergism with ER stress aggravators to inhibit tumor growth in PC xenografts. Taken together, these findings indicate that simultaneous suppression of 2 key intracellular protein degradation systems rendered PC cells vulnerable to ER stress, which may represent an avenue for new therapeutic combinations for this disease.

Blocking NF-κB Is Essential for the Immunotherapeutic Effect of Recombinant IL18 in Pancreatic Cancer.

PURPOSE: We sought to find new immune-based treatments for pancreatic cancer. EXPERIMENTAL DESIGN: We detected IL18 expression in plasma and specimens from patients with pancreatic cancer. We then investigated whether IL18 had a therapeutic effect for pancreatic cancer in vitro and in vivo and any underlying mechanisms. RESULTS: Higher plasma IL18 was associated with longer overall survival (OS), but higher IL18 in pancreatic cancer tissues was associated with shorter OS and increased invasion and metastasis. Recombinant IL18 alone had no antitumor effect in the syngeneic mice with orthotopically transplanted tumors and promoted tumors in immunocompromised mice; it also facilitated immune responses in vitro and in vivo by augmenting the activity of cytotoxic T cells and NK cells in peripheral blood and lymph nodes. However, IL18 promoted the proliferation and invasion of pancreatic cancer cells, in vitro and in vivo, through the NF-κB pathway. Nevertheless, by coadministrating IL18 with BAY11-7082, an NF-κB inhibitor, we were able to prevent the procancerous effects of IL18 and prolong the survival time of the mice. CONCLUSIONS: IL18 has both cancer-promoting and cancer-suppressing functions. Although its single-agent treatment has no therapeutic effect on pancreatic cancer, when combined with the NF-κB pathway inhibitor, IL18 improved survival in a murine pancreatic cancer model. Our study implies the possibility of a combinational immunotherapy that uses IL18 and targets NF-κB pathway. Clin Cancer Res; 22(23); 5939-50. ©2016 AACR.

Systematic review and meta-analysis of minimally invasive versus open approach for pancreaticoduodenectomy.

BACKGROUNDS AND OBJECTIVE: The technique of minimally invasive pancreatic surgeries has evolved rapidly, including minimally invasive pancreaticoduodenectomy (MIPD). However, controversy on safety and feasibility remains when comparing the MIPD with the open pancreaticoduodenectomy (OPD); therefore, we aimed to compare MIPD and OPD with a systemic review and meta-analysis. METHODS: Multiple electronic databases were systematically searched to identify studies (up to February 2016) comparing MIPD with OPD. Intra-operative outcomes, oncologic data, postoperative complications and postoperative recovery were evaluated. RESULTS: Twenty-two retrospective studies including 6120 patients (1018 MIPDs and 5102 OPDs) were included. MIPD was associated with a reduction in estimated blood loss (WMD -312.00 ml, 95 % CI -436.30 to -187.70 ml, p < 0.001), transfusion rate (OR 0.41, 95 % CI 0.30-0.55, p < 0.001), wound infection (OR 0.37, 95 % CI 0.20-0.66, p < 0.001) and length of hospital stay (WMD -3.57 days, 95 % CI -5.17 to -1.98 days, p < 0.001). Meanwhile, MIPD group has a higher R0 resection rate (OR 1.47, 95 % CI 1.18-1.82, p < 0.001) and more lymph nodes harvest (WMD 1.74, 95 % CI 1.03-2.45, p < 0.001). However, it had longer operation time (WMD 83.91 min, 95 % CI 36.60-131.21 min, p < 0.001). There were no significant differences between the two procedures in morbidities (p = 0.86), postoperative pancreatic fistula (p = 0.17), delayed gastric empting (p = 0.65), vascular resection (p = 0.68), reoperation (p = 0.33) and mortality (p = 0.90). CONCLUSIONS: MIPD can be a reasonable alternative to OPD with potential advantages. However, further large-volume, well-designed RCTs with extensive follow-ups are suggested to confirm and update the findings of our analysis.

Par3 regulates invasion of pancreatic cancer cells via interaction with Tiam1.

The conserved polarity complex, which comprises partitioning-defective proteins Par3, Par6, and the atypical protein kinase C, affects various cell-polarization events, including assembly of tight junctions. Control of tight junction assembly is closely related to invasion and migration potential. However, as the importance of conserved polarity complexes in regulating pancreatic cancer invasion and metastasis is unclear, we investigated their role and mechanism in pancreatic cancers. We first detect that the key protein of the conserved polarity complex finds that only Par3 is down-regulated in pancreatic cancer tissues while Par6 and aPKC show no difference. What is more, Par3 tissues level was significantly and positively associated with patient overall survival. Knocking-down Par3 promotes pancreatic cancer cells invasion and migration. And Par3 requires interaction with Tiam1 to affect tight junction assembly, and then affect invasion and migration of pancreatic cancer cells. Then, we find that tight junction marker protein ZO-1 and claudin-1 are down-regulated in pancreatic cancer tissues. And the relationship of the expression of Par3 and ZO-1 in pancreatic cancer tissue is linear correlation. We establish liver metastasis model of human pancreatic cancer cells in Balb/c nude mice and find that knocking down Par3 promotes invasion and metastasis and disturbs tight junction assembly in vivo. Taken together, these results suggest that the Par3 regulates invasion and metastasis in pancreatic cancers by controlling tight junction assembly.

Synergistic antitumor activity of withaferin A combined with oxaliplatin triggers reactive oxygen species-mediated inactivation of the PI3K/AKT pathway in human pancreatic cancer cells.

Application of oxaliplatin for the treatment of pancreatic cancer (PC) is restricted owing to its toxic side effects and drug resistance. We investigated how withaferin A (WA), a bioactive component isolated from the medicinal plant Withania somnifera, acts synergistically with oxaliplatin on human PC in vitro and in vivo. We found that WA enhanced oxaliplatin-induced growth suppression and apoptosis in PC cells dramatically through a mechanism involving mitochondrial dysfunction and inactivation of the PI3K/AKT pathway. Combination treatment resulted in significant accumulation of intracellular reactive oxygen species (ROS). Pretreatment of cells with the ROS scavenger N-acetylcysteine completely blocked the apoptosis induced by combination treatment, and recovered expression of AKT inactivation, which revealed the important role of ROS in apoptosis and AKT regulation. In vivo, combination therapy showed the strongest anti-tumor effects compared with single agents, without obvious additional toxicity. These results support the notion that combination treatment with oxaliplatin and WA could facilitate development of an effective strategy for PC treatment.

A new approach for Roux-en-Y reconstruction after pancreaticoduodenectomy.

BACKGROUND: Postoperative pancreatic fistula remains the most common complication of pancreaticoduodenectomy (PD) and is potentially lethal. It contributes significantly to prolonged hospitalization and mortality. In this study, we introduced a new technical approach, a modified Roux-en-Y reconstruction and evaluated its safety and feasibility. METHODS: We retrospectively reviewed the patients who had undergone PD with the modified Roux-en-Y reconstructive technique for periampullary malignancies from January 2011 to June 2012. The data on complications, hospital stay and outcomes after the modified Roux-en-Y reconstruction were analyzed. RESULTS: The reconstruction was performed in 171 patients, of whom 92 received pancreaticogastrostomy and 79 received pancreaticojejunostomy. The median duration of surgery was 4.0 hours (range 3.1-6.9) in all patients, and the median blood loss was 530 mL (range 200-2000). Sixty-nine patients were subjected to transfusions, with a median transfusion volume of 430 mL (range 200-1400). The median hospital stay of the patients was 14 days (range 11-38). Their operative mortality was zero and overall morbidity was 18.1% (31 patients). Only four patients (2.3%) developed pancreatic fistulas (grade A fistulas in two patients and grade B in two patients); no patients developed grade C fistula. None of the patients developed bile reflux gastritis. CONCLUSIONS: The modified Roux-en-Y reconstruction, which isolates biliary anastomosis from pancreatic, gastric or jejunal anastomosis, is a safe, reliable, and favorable technique. But it needs further investigation in randomized controlled trials.

[Typing and surgical treatment choice for pancreatic ductal stone].

OBJECTIVE: To explore the improvement of typing and reasonable surgical treatment for pancreatic ductal stone (PDS). METHODS: Totally 89 patients with pancreatic ductul stone treated underwent surgeries from January 2000 to December 2012 were involved into this study. There were 57 male and 32 female patients, the average age was (52 ± 23) years. According to the magnetic resonance cholangiopancreatography imaging and finding during surgery, pancreatolithiasis was classified into three types: type I, the stones were located in the main pancreatic duct; type II, the stones were located both in main and branch pancreatic duct; type III, the stones were diffusely scattered in the branch pancreatic duct; the position of PDS within pancreatic parenchyma were subtitled. In this group, 43 type I PDS were extracted with endoscopic papillotomy or endoscopic pancreatic sphincterotomy, or pancreatolithotomy plus pancreato-jejunal lateral anastomosis with wide anastomotic stoma; 39 type II cases were treated by pancreatolithotomy plus pancreato-jejunal lateral anastomosis or/and resection of pancreatic section; 7 type III PDS were managed with resection of pancreatic section. RESULTS: All surgeries were performed successfully. Among complications, 6 cases (6.7%) were pancreatic leakage which recovered after systematic non-surgical treatment, 2 cases (2.2%) were anastomotic bleeding which led to 1 death, 6 cases (6.7%) were residual pancreatolithiasis in branch pancreatic duct type. Seventy-eight patients were followed up for 6 to 131 months, 57 cases were still alive so far. Five cases were intermittent abdominal pain, 7 cases were diabetes resulted from 2 subtotal pancreatectomy and 5 distal pancreatectomy, 5 cases occurred pancreatolithiasis recurrence and 3 underwent secondary surgeries. CONCLUSIONS: The basis of this modified typing of pancreatolithiasis is the position of stone in pancreatic duct rather than pancreas parenchyma. It is more important and valuable for surgical principle of taking stones out completely and maintaining pancreatic function.

"Total arterial devascularization first" technique for resection of pancreatic head cancer during pancreaticoduodenectomy.

Integrated resection of the pancreatic head is the most difficult step in radical pancreaticoduodenectomy (RPD) in patients with the portal vein (PV) and superior mesenteric vein (SMV) invasion or oppression by the tumor. This study introduced a new idea and skill named the "total arterial devascularization first" (TADF) technique and its applications in RPD. Three arterial blood supplies of pancreatic head were obstructed before dissection of veins. The critical steps included exposure of the anterior surface of the abdominal aorta (AA) by completely transecting neural and connective tissue between superior mesenteric artery (SMA) and pancreatic mesounsinate, and transection of the mesounsinate from the origin of SMA to the root of the celiac trunk. From January 2012 through May 2013, a total of 58 patients with PV/SMV invasion or oppression underwent RPD using this technique. The median operative time was 5.1 h (ranging 4.5-8.1 h). The median intraoperative blood loss was 450 mL (ranging 200-900 mL). No intraoperative and postoperative bleeding of pancreatic head region occurred. Among the 58 patients, 21 were subjected to vessel lateral wall angiectomy or angiorrhaphy, and 10 to angiectomy and end-to-end anastomosis. The incidence of postoperative bleeding, postoperative pancreatic fistula and biliary fistula was 5.2%, 6.8%, and 1.7%, respectively. No patients died 3 months after operation. The TADF technique is a new method for intricate RPD and could improve the security of surgery and reduce intraoperative bleeding, which is expected to become standardized surgical approach for RPD.

A modified technique of end-to-end pancreaticojejunostomy with transpancreatic interlocking mattress sutures.

BACKGROUND: Postoperative pancreatic fistula (POPF) represents the most important cause of morbidity after pancreaticoduodenectomy (PD) and contributes to prolonged hospitalization and increased mortality rates. This study presents a new technique, which involves end-to-end pancreaticojejunostomy with transpancreatic interlocking mattress sutures, and evaluates its safety and reliability. METHODS: From January 2011 to May 2012, 79 patients with periampullary malignancies underwent PD by using this modified technique, and the morbidity and mortality rates were calculated. RESULTS: In this study, all cases recovered well from PD. Four transpancreatic interlocking mattress sutures were performed in 79 patients. The median duration of surgery was 3.9 hr (range 3.1-6.8), and the median time to perform pancreaticojejunostomy was 15.3 min (range 9-24). Overall, morbidity occurred in 16 patients (22.3%), and the causes included upper gastrointestinal bleeding (n = 2), biliary fistula (n = 1), pulmonary infection (n = 1), delayed gastric emptying (n = 1), abdominal abscess (n = 1, caused by PF), wound infection (n = 3), arrhythmia or myocardial infarction (n = 3), urinary tract infection (n = 2), and POPF (n = 2, 2.53%). One patient had grade A POPF, one had grade B POPF, and none of them had grade C POPF. No death occurred during surgery. CONCLUSION: The end-to-end pancreaticojejunostomy with transpancreatic interlocking mattress sutures is a simple, rapid, safe, and reliable technique with low POPF rate and low delayed massive hemorrhage rate.

Modified technique of pancreaticogastrostomy for soft pancreas with two continuous hemstitch sutures: a single-center prospective study.

Postoperative pancreatic fistula (POPF) remains a persistent problem after pancreaticoduodenectomy (PD), especially in the presence of a soft, nonfibrotic pancreas. To reduce the risk of POPF, pancreaticogastrostomy (PG) is an optional reconstruction technique for surgeons after PD. This study presents a new technique of PG for a soft, nonfibrotic pancreas with double-binding continuous hemstitch sutures and evaluates its safety and reliability. From January 2011 to June 2012, 92 cases of patients with periampullary malignancy with a soft pancreas underwent this technique. A modified technique of PG was performed with two continuous hemstitch sutures placed in the mucosal and seromuscular layers of the posterior gastric wall, respectively. Then the morbidity and mortality was calculated. This technique was applied in 92 patients after PD all with soft pancreas. The median time for the anastomosis was 12 min (range, 8-24). Operative mortality was zero, and morbidity was 16.3 % (n = 15), including hemorrhage (n = 2), biliary fistula (n = 2), pulmonary infection (n = 1), delayed gastric emptying (DGE; n = 5, 5.4 %), abdominal abscess (n = 3, one caused by PF), and POPF (n = 2, 2.2 %). Two patients developed a pancreatic fistula (one type A and one type B) classified according to the International Study Group on Pancreatic Fistula. The described technique is a simple and safe reconstruction procedure after PD, especially for patients with a soft and fragile pancreas.