513 research outputs found
A. H. M. Jones, Augustus
No full textFlam-Zuckermann Léa. A. H. M. Jones, Augustus. In: L'antiquité classique, Tome 41, fasc. 1, 1972. pp. 401-402
[Die Stolgebühren der Juden an die christliche Geistlichkeit im Hannoverland
No full textvon M. Zuckermann]Erinnerungsschrift zum hundertjährigen Geburtstage des Landrabbiners Dr. Samuel E. Meye
Communicating Anti-Semitism - Are the "Boundaries of the Speakable" Shifting?
No full textBergmann W, Heitmeyer W. Communicating Anti-Semitism - Are the "Boundaries of the Speakable" Shifting? In: Zuckermann M, ed. Antisemitismus - Antizionismus - Iraelkritik; Tel Aviver Jahrbuch für Deutsche Geschichte. Tel Aviver Jahrbuch für deutsche Geschichte. Vol 33. Göttingen: Wallstein; 2005: 72-89
Antiferromagnetism in amorphous alloys containing rare-earth atoms. I. The molecular field approximation
No full text The model of Harris, Plischke, and Zuckermann for random magnetic anisotropy in amorphous alloys is examined in the molecular field approximation for the case of antiferromagnetic exchange coupling. The existence of spin-flop transitions and a spin-glass-like magnetic susceptibility is established by numerical calculation. The results are discussed in connection with current theoretical and experimental work. </jats:p
Different significance of ret/PTC(1) and ret/PTC(3) rearrangements in thyroid carcinogenesis: lesson from two subgroups of patients with papillary thyroid carcinomas showing the highest incidence of ret/PTC activation
No full textDifferent Significance of ret/PTC1 and ret/PTC3 Rearrangements in Thyroid Carcinogenesis: Lesson from Two Subgroups of Patients with Papillary Thyroid Carcinomas Showing the Highest Incidence of ret/PTC Activation*
To the editor:
The recent paper by Thomas et al. (1) shows that: 1) ret/PTC activation plays a central role in the pathogenesis of papillary thyroid carcinomas (TCs) occurring in children from Ukraine and Belarus after the Chernobyl accident (60.7% of the Ukrainian and 51.3% of the Belarussian cases); and 2) these patients have an increased incidence of the ret/PTC3 isoform (ret fusion with RGF gene) vs. the more frequent ret/PTC1 (ret fusion with H4 gene). In particular, a strong correlation was observed between the ret/PTC3 isoform and the solid-follicular subtype of papillary TC, which was present in 46 of 67 cases. This morphological variant has been considered as evidence of a more malignant phenotype (2). Nineteen of the 24 ret/PTC-positive solid-follicular TCs harbored a ret/PTC3 rearrangement, whereas only 5 had a ret/PTC1 rearrangement.
The authors suggest that: 1) “there are good reasons to believe that there is a causal link between radiation exposure and ret/PTC rearrangements” because (a) the prevalence of ret/PTC in post-Chernobyl TCs is higher than the highest frequencies reported in the literature in nonexposed subjects (25–40%); (b) ionizing radiation can induce ret/PTC rearrangement “in vitro ” (3) and patients exposed to external radiation show a high frequency of ret/PTC rearrangements (4); and 2) “there is a strong correlation between the morphological subtype of papillary carcinoma and the type of ret rearrangement,” either in humans or transgenic animals. In fact, the targeted expression of ret/PTC1 to the thyroid gland caused the generation of TCs of the classic type (5), whereas ret/PTC3 mice developed aggressive TCs with a prevalent solid component, which were highly prone to metastasize to regional lymph nodes (6). The authors hypothesize that “although the ret component of the 2 chimeric proteins is identical, some functional differences between the two ret fusion partners may contribute to the different neoplastic phenotypes” (1). Thomas et al. (1) correctly acknowledge that whether ret/PTC activation is “linked primarily to the nature of the carcinogenetic agent (radiation or environmental factors) or the age of the patients (ranging between 6–18 yr in their series) remains to be determined.”
In the last 5 yr we have collected the largest series of a very rare subgroup of patients with papillary TCs, namely those associated with familial adenomatous polyposis (FAP), an inherited multitumoral syndrome due to germ-line mutations of the APC gene (7). Ninety-seven patients have been collected from the literature, and 15 personal cases, who had detection of the APC germ-line mutation, have been added (7).
Eight of nine of these patients (89%) had ret/PTC activation (8, 9). In particular, an unusual histological variant, the so-called cribriform variant, was very frequent (8), and the ret/PTC1 isoform was always found (9). All these patients were very young (mean age, 24 yr; range, 20–36 yr). All of them were followed up for long time (5–17 yr). A particularly indolent biological behavior was observed, which is in accordance with the low malignancy of the entire series (only 2 of 112 patients had distant metastases; Refs. 7 and 8). Interestingly, the only patient who, after lobectomy and isthmusectomy, had recurrence 17 yr after initial surgery, in addition to ret/PTC1, which was already present in the first tumor, also had ret/PTC3 both in the thyroid and in the regional lymph nodes. p53 mutations were concomitantly found in the thyroid tumoral tissue of this patient (8, 10).
The group of patients with FAP-associated (or genetically determined) TC confirms that young age [mean age, 24 yr (in our series)] is a quite constant finding in groups with a high rate of ret/PTC activation. Additional factors could be early detection, due to intensive screening of high-risk populations (siblings of an index case with FAP, subjects exposed to nuclear radiation) and/or small diameter of tumors (,1 cm in three of six subjects of the Italian series). On the contrary, there is less evidence that the histological variant is also predetermined by the type of ret/PTC isoform. In fact, some patients with ret/PTC1 had the solid variant, and some of those with ret/PTC3 had variants other than the solid one. In particular, among patients with FAP-associated TCs, three members of the same kindred with the same germ-line mutation of the APC gene and ret/PTC1 activation had three different variants: classic papillary, cribriform, and follicular, respectively (11).
Cumulative data in both groups of patients support the view that: 1) ret activation is highly prevalent in young subjects with small tumors or in patients belonging to special subgroups who are intensively screened for TC; 2) patients with ret/PTC1 isoform usually show an indolent behavior, whereas ret/PTC3 is associated with a more aggressive biological behavior (8, 10); 3) ret/PTC1 may coexist with ret/PTC3 in the same tumor; in particular, ret/PTC3 may develop with age or become more prevalent in patients with previous ret/PTC1 activation, and determine a more aggressive behavior; 4) the solid variant is usually, but not always, associated with ret/PTC3; and 5) whereas the link with radiation is evident in children from Belarus, it is not proven in FAP patients, even if patients from the latter subgroup could have a greater susceptibility to environmental radiation (12). In FAP patients APC mutations alone do not seem sufficient to cause TC (lack of loss of heterozygosity of the APC gene in the thyroid tumoral tissue) (8), but concomitant cofactors [modifier genes, sex-related factors (F:M 5 17:1) or environmental factors] are always required (12). A detailed genetic and clinicopathological analysis, also including long-term follow-up, of these two rare subgroups of patients with papillary TC, namely post-
Chernobyl and FAP associated, could give a better insight into the relative role of genetic and environmental factors in thyroid carcinogenesis
Antiferromagnetism in amorphous alloys containing rare-earth atoms. II. Monte Carlo studies
No full text The model of Harris, Plischke, and Zuckermann for random magnetic anisotropy in amorphous alloys is examined for the case of antiferromagnetic exchange coupling using Monte Carlo techniques. Initial magnetization curves, hysteresis loops, and coercive fields are obtained and compared with the results of the molecular field approach of Callen, Liu, and Cullen. The external magnetic field for spin-flip transitions is obtained and is discussed in relation to previous work by Ferrer and Zuckermann and Coqblin and Bhattacharjee. The results are discussed in the light of recent experimental work. </jats:p
Simulation of short-chain polymer collapse with an explicit solvent
No full textWe study the equilibrium behavior and dynamics of a polymer collapse transition for a system composed of a short Lennard-Jones (LJ) chain immersed in a LJ solvent for solvent densities in the range of rho=0.6-0.9 (in LJ reduced units). The monomer hydrophobicity is quantified by a parameter lambdais an element of[0,1] which gives a measure of the strength of attraction between the monomers and solvent particles, and which is given by lambda=0 for a purely repulsive interaction and lambda=1 for a standard LJ interaction. A transition from the Flory coil to a molten globule is induced by increasing lambda. Generally, the polymer size decreases with increasing solvent density for all lambda. Polymer collapse is induced by changing the hydrophobicity parameter from lambda=0 to lambdagreater than or equal to0.5, where the polymer is in a molten globule state. The collapse rate increases monotonically with increasing hydrophobicity and decreases monotonically with increasing solvent density. Doubling the length of the chain from N=20 to N=40 monomers increases the collapse time roughly by a factor of 2, more or less independent of the hydrophobicity and solvent density. We also study the effect of conformational restrictions on polymer collapse using a chain model in which the bond angles are held near 109.5degrees using a stiff angular harmonic potential, but where free internal rotation is allowed, and find that the collapse times increase considerably with respect to the fully flexible polymer, roughly by a factor of 1.6-3.5. This increase is most pronounced for high solvent densities. (C) 2002 American Institute of Physics.PT: J; CR: ALLEN MP, 1987, COMPUTER SIMULATION, P149 BYRNE A, 1995, J CHEM PHYS, V102, P573 CHAN HS, 1993, J CHEM PHYS, V99, P2116 CHANG RW, 2001, J CHEM PHYS, V114, P7688 CHU B, 1995, MACROMOLECULES, V28, P180 CREIGHTON TE, 1994, PROTEIN FOLDING CROOKS GE, 1999, PHYS REV E B, V60, P4559 DEGENNES PG, 1979, SCALING CONCEPTS POL DEGENNES PG, 1985, J PHYS LETT, V46, L639 DIJKSTRA M, 1994, J CHEM PHYS, V101, P3179 DIJKSTRA M, 1994, PHYS REV LETT, V72, P298 ESCOBEDO FA, 1996, MOL PHYS, V89, P1733 FRENKEL D, 1992, PHYS REV LETT, V68, P3363 GANAZZOLI F, 1995, MACROMOLECULES, V28, P5285 GRAYCE CJ, 1997, J CHEM PHYS, V106, P5171 GROSBERG AY, 1988, J PHYS-PARIS, V49, P2095 GROSBERG AY, 1993, MACROMOLECULES, V26, P4249 GROSBERG AY, 1994, STAT MECH MACROMOLEC HALPERIN A, 2000, PHYS REV E, V61, P565 IVANOV VA, 1998, J CHEM PHYS, V109, P5659 IVANOV VA, 2000, MACROMOL THEOR SIMUL, V9, P488 KAYAMAN N, 1999, MACROMOLECULES, V32, P8399 KHALATUR PG, 1998, EUR PHYS J B, V881, P5 KLUSHIN LI, 1998, J CHEM PHYS, V108, P7917 KUZNETSOV YA, 1995, J CHEM PHYS, V103, P4807 KUZNETSOV YA, 1996, J CHEM PHYS, V104, P3338 KUZNETSOV YA, 1999, J CHEM PHYS, V111, P3744 LUNABARCENAS G, 1996, J CHEM PHYS, V104, P9971 MA JP, 1995, J CHEM PHYS, V103, P2615 MARTYNA GJ, 1996, MOL PHYS, V87, P1117 NAKATA M, 1999, J CHEM PHYS, V110, P2703 NISHIO I, 1979, NATURE, V281, P208 NOGUCHI H, 2000, J CHEM PHYS, V113, P854 OSTROVSKY B, 1994, EUROPHYS LETT, V25, P409 OSTROVSKY B, 1995, BIOPHYS J, V68, P1694 PANDE VS, 1998, CURR OPIN STRUC BIOL, V8, P68 PITARD E, 1998, EUROPHYS LETT, V41, P467 PITARD E, 1999, EUR PHYS J B, V7, P665 POLSON JM, 1999, PHYS REV E, V60, P3429 POLSON JM, 2000, J CHEM PHYS, V113, P1283 SCHWEIZER KS, 1994, ADV POLYM SCI, V116, P1283 SCHWEIZER KS, 1997, ADV CHEM PHYS, V98, P1 SHAKHNOVICH EI, 1997, CURR OPIN STRUC BIOL, V7, P29 STOCKMAYER WH, 1960, MAKROMOL CHEM, V35, P54 SUEN JKC, 1997, J CHEM PHYS, V106, P1288 SWISLOW G, 1980, PHYS REV LETT, V44, P796 TANAKA G, 1995, MACROMOLECULES, V28, P1049 TIMOSHENKO EG, 1995, J CHEM PHYS, V102, P1816 TIMOSHENKO EG, 1995, PHYS REV E, V51, P492 TIMOSHENKO EG, 1996, PHYS REV E B, V54, P4071 TUCKERMAN M, 1992, J CHEM PHYS, V97, P1990 TUCKERMAN ME, 1990, J CHEM PHYS, V93, P1287 VANDERSCHOOT P, 1998, MACROMOLECULES, V31, P4635 WILLIAMS C, 1981, ANNU REV PHYS CHEM, V32, P433 YU JQ, 1992, MACROMOLECULES, V25, P1618 ZHU PW, 1997, J CHEM PHYS, V106, P6492; NR: 56; TC: 17; J9: J CHEM PHYS; PG: 11; GA: 541FBSource type: Electronic(1
Simulation of heteropolymer collapse with an explicit solvent in two dimensions
No full textMolecular dynamics simulations are used to study the equilibrium properties and collapse dynamics of a heteropolymer in the presence of an explicit solvent in two dimensions. The system consists of a single copolymer chain composed of hydrophobic (H) and hydrophilic (P) monomers, immersed in a Lennard-Jones solvent. We consider HP chains of varying hydrophobic number fraction n(H), defined as the ratio of the number of H monomers to the total number of monomers. We also consider homopolymer chains with a uniform variable degree of hydrophobicity lambda, which describes the hydrophobic-solvent interaction, and which ranges from hydrophilic (lambda=0) to hydrophobic (lambda=1). We investigate the effects of varying n(H) and lambda, the HP sequencing, and the solvent density on the equilibrium and collapse properties of the chain. For sufficiently high n(H), we observe a collapse transition for random copolymers from a stretched coil to a liquidlike globule upon a decrease in temperature; the transition temperature decreases with increasing n(H). The transition can also be induced at a fixed (and sufficiently low) temperature by varying n(H) for random copolymers or lambda for homopolymers. We find that polymer size varies inversely with solvent density. The rate of polymer collapse is found to strongly vary inversely with increasing n(H) and lambda for copolymers and homopolymers, respectively. Further, the collapse rates for these two cases are very close for n(H)=lambda, except at lower values (n(H)=lambda approximate to 0.5), where the homopolymers collapse more rapidly. At moderate densities (rho=0.5-0.7, in LJ reduced units), we find that random copolymers collapse more rapidly at low density and that this difference tends to increase with decreasing n(H). At fixed solvent density and n(H) we find the collapse rate differs little for random copolymers, and multi-block copolymers with equal n(H). Finally, the simulations suggest that copolymers tend to collapse by a uniform thickening rather than by first forming locally collapsed clusters which aggregate at longer time. The exception to this appears to be block-copolymers comprised of sufficiently long alternating H and P blocks. (C) 2000 American Institute of Physics. [S0021-9606(00)51027-7].PT: J; CR: ALLEN MP, 1987, COMPUTER SIMULATION, P149 BUGUIN A, 1996, CR ACAD SCI II B, V322, P741 BYRNE A, 1995, J CHEM PHYS, V102, P573 BYRNE A, 1997, PHYSICA A, V243, P14 CREIGHTON TE, 1994, PROTEIN FOLDING CROOKS GE, 1999, PHYS REV E B, V60, P4559 DAWSON KA, 1997, PHYSICA A, V236, P58 DEGENNES PG, 1985, J PHYS LETT, V46, L639 DOI M, 1986, THEORY POLYM DYNAMIC DUNWEG B, 1991, PHYS REV LETT, V66, P2996 GANAZZOLI F, 1995, MACROMOLECULES, V28, P5285 GAREL T, 1998, SPIN GLASSES RANDOM GROSBERG AY, 1988, J PHYS-PARIS, V49, P2095 HALPERIN A, 2000, PHYS REV E, V61, P565 KHOKHLOV AR, 1998, PHYSICA A, V249, P253 KHOKHLOV AR, 1999, PHYS REV LETT, V82, P3456 KLUSHIN LI, 1998, J CHEM PHYS, V108, P7917 KUZNETSOV YA, 1995, J CHEM PHYS, V103, P4807 KUZNETSOV YA, 1996, J CHEM PHYS, V104, P3338 KUZNETSOV YA, 1996, J CHEM PHYS, V105, P7116 MARTYNA GJ, 1996, MOL PHYS, V87, P1117 NAKATA M, 1997, PHYS REV E B, V56, P3338 OSTROVSKY B, 1994, EUROPHYS LETT, V25, P409 OSTROVSKY B, 1995, BIOPHYS J, V68, P1694 PANDE VS, 1998, CURR OPIN STRUC BIOL, V8, P68 PIERLEONI C, 1991, PHYS REV LETT, V66, P2992 PITARD E, 1999, EUR PHYS J B, V7, P665 SHAKHNOVICH EI, 1997, CURR OPIN STRUC BIOL, V7, P29 SHANNON SR, 1997, PHYS REV LETT, V79, P1455 TANAKA G, 1995, MACROMOLECULES, V28, P1049 THIRUMALAI D, 1995, J PHYS, V5, P1547 TIMOSHENKO EG, 1995, J CHEM PHYS, V102, P1816 TIMOSHENKO EG, 1996, PHYS REV E B, V54, P4071 TIMOSHENKO EG, 1998, PHYS REV E, V57, P6801 TUCKERMAN M, 1992, J CHEM PHYS, V97, P1990 TUCKERMAN ME, 1990, J CHEM PHYS, V93, P1287 VILLENEUVE C, 1997, MACROMOLECULES, V30, P3066 WANG XH, 1998, MACROMOLECULES, V31, P2972 WANG XH, 1999, MACROMOLECULES, V32, P4299 WU C, 1996, PHYS REV LETT, V77, P3053; NR: 40; TC: 11; J9: J CHEM PHYS; PG: 11; GA: 331MHSource type: Electronic(1
Simulation study of lateral diffusion in lipid-sterol bilayer mixtures
No full textWe employ off-lattice Monte Carlo simulations to study lateral diffusion in lipid-sterol bilayers using a two-dimensional model system which has been designed to simulate the experimental phase diagrams of both lipid-cholesterol and lipid-lanosterol systems. We focus on the effects of varying sterol concentration and temperature on the tracer diffusion coefficient, D, which characterizes the lateral motion of single tagged lipids in a bilayer. Generally. we find that increasing the cholesterol concentration suppresses D due to an increased conformational ordering of lipid chains. We argue that this effect competes with an increase in the average free area per lipid, which favours an increase in D. At temperatures close to the main transition temperature, the competition between the two effects leads to intriguing behavior of D. Overall, the model results are in excellent qualitative agreement with available experimental results for lipid-cholesterol mixtures. Additional studies of a model lipid-lanosterol system, for which experimental diffusion results are not available, predict that the presence of lanosterol has a smaller effect than cholesterol on reducing D relative to the pure lipid system. We conclude that. the molecular model employed contains the essential features required to describe many of the qualitative features of the lateral diffusion behavior in lipid-sterol systems.PT: J; CR: ALECIO MR, 1982, P NATL ACAD SCI-BIOL, V79, P5171 ALMEIDA PFF, 1992, BIOCHEMISTRY-US, V31, P6739 BLOCH K, 1991, CHOLESTEROL EVOLUTIO, P363 BLOOM M, 1988, CAN J CHEM, V66, P706 COHEN MH, 1959, J CHEM PHYS, V31, P1164 DAMMANN B, 1995, COMPUTER SIMULATION DEMEL RA, 1972, BIOCHIM BIOPHYS ACTA, V266, P26 DONIACH S, 1978, J CHEM PHYS, V68, P4912 FINEGOLD L, 1993, CHOLESTEROL MODEL ME FRENKEL D, 1996, UNDERSTANDING MOL SI, P103 GABDOULINE RR, 1996, J PHYS CHEM-US, V96, P15942 HANSEN JP, 1986, THEORY SIMPLE LIQUID IPSEN JH, 1987, BIOCHIM BIOPHYS ACTA, V905, P162 KORLACH J, 1999, P NATL ACAD SCI USA, V96, P8461 LADHA S, 1996, BIOPHYS J, V71, P1364 LINDBLOM G, 1994, PROG NUCL MAG RES SP, V26, P483 LINSEISEN FM, 1993, CHEM PHYS LIPIDS, V65, P141 MACEDO PB, 1965, J CHEM PHYS, V42, P245 MARCELJA S, 1974, BIOCHIM BIOPHYS ACTA, V367, P165 MERKEL R, 1994, J PHYS CHEM-US, V98, P4428 METROPOLIS N, 1953, J CHEM PHYS, V21, P1087 MOURITSEN OG, 1995, BIOPHYS CHEM, V55, P55 NEEDHAM D, 1988, BIOCHEMISTRY-US, V27, P4668 NEEDHAM D, 1989, BIOPHYS J, V55, P1001 NIELSEN M, 1996, PHYS REV E, V54, P6889 NIELSEN M, 1999, PHYS REV E B, V59, P5790 NIELSEN M, 1999, THESIS MCGILL U MONT NIELSEN M, 2000, EUROPHYS LETT, V52, P368 PARE C, 1998, BIOPHYS J 1, V74, P899 PINK DA, 1980, BIOCHEMISTRY-US, V19, P349 POLSON JM, 2000, UNPUB PRESTI FT, 1985, MEMBRANE FLUIDITY BI, V4, P97 ROBINSON AJ, 1995, BIOPHYS J, V68, P164 RUBENSTEIN JR, 1979, P NATL ACAD SCI USA, V76, P15 SANKARAM MB, 1991, P NATL ACAD SCI USA, V88, P8686 SMONDYREV AM, 1999, BIOPHYS J, V77, P2075 SMONDYREV AM, 1999, J CHEM PHYS, V110, P3981 SMONDYREV AM, 1999, J COMPUT CHEM, V20, P531 TANAKA K, 1999, LANGMUIR, V15, P600 THEWALT J, 1996, UNPUB THEWALT JL, 1992, BIOPHYS J, V63, P1176 TIELEMAN DP, 1997, BBA-REV BIOMEMBRANES, V1331, P235 TOCANNE JF, 1994, PROG LIPID RES, V33, P203 TROUARD TP, 1999, J CHEM PHYS, V110, P8802 TU K, 1995, BIOPHYS J, V69, P2558 TU KC, 1998, BIOPHYS J, V75, P2147 URBINA JA, 1995, BBA-BIOMEMBRANES, V1238, P163 VATTULAINEN I, 1997, PHYS REV LETT, V79, P257 VAZ WLC, 1992, COMMENTS MOL CELL BI, V8, P17 VIST MR, 1984, THESIS U GUELPH GUEL VIST MR, 1990, BIOCHEMISTRY-US, V29, P451 WU ES, 1977, BIOCHEMISTRY-US, V16, P3936 ZHELEV DV, 1993, BIOCHIM BIOPHYS ACTA, V1147, P89; NR: 53; TC: 21; J9: EUR PHYS J E; PG: 13; GA: 459EWSource type: Electronic(1
Comparison of Wirsung-jejunal duct-to-mucosa and dunking technique for pancreatojejunostomy after pancreatoduodenectomy
No full textBACKGROUND: Pancreato-enteric reconstruction after pancreatoduodenectomy (PD) is still a source of debate because of the high incidence of complications. Among the various types of pancreato-jejunostomies we don't know yet which is the best in terms of anastomotic failure and related complications rates. Wirsung-jejunal duct-to-mucosa anastomosis (WJ) and "dunking" pancreato-jejunal anastomosis (DPJ) are the two most used ones worldwide but conflicting results are reported. To determine which is the safer anastomosis and to define when an anastomosis should be preferred, we retrospectively reviewed two groups of patients who underwent WJ or DPJ. METHODS: Twenty-three patients underwent PD with WJ (n = 17) with dilated (WJD) (n = 9) or not-dilated Wirsung's duct (WJND) (n = 8) or with a DPJ (n = 6) over a 3-year period at a single institution. RESULTS: The complications rate was high in all groups of patients (33.3% in WJD, 37.5% in WJND and 66.7% in DPJ). A pancreatic fistula developed in one patient in each group (11.1% in WJD, 12.5% in WJND and 16.7% in DPJ). All these patients were managed conservatively. Anastomotic disruption took place in the WJ patients especially in the WJND group (n = 2) compared to the WJD (n = 1) (25% vs. 11.1%) or DPJ groups (0%): these three patients required a re-operation. Overall, the anastomotic defects were higher in patients who underwent WJND (37.5%), compared to WJD (22.2%) and to DPJ (16.7%). However, no statistical differences were found among the groups. Delayed gastric emptying (DGE) and total parenteral nutrition (TPN) along with anastomotic defects were responsible for a prolonged hospital stay. CONCLUSIONS: Our results were not able to demonstrate any statistical difference between the two different techniques in preventing anastomotic failure. WJ can represent a valid choice in case of a dilated duct and a firm, fibrotic enlarged gland that could not be properly invaginated in a small jejunal loop. DGE may occur in those patients who experienced an anastomotic failure and required a TPN regimen with a prolonged hospital stay
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