bluuebunny/crossref_metadata_2025_split huggingface dataset:
Arginase II Restricts Host Defense toHelicobacter pyloriby Attenuating Inducible Nitric Oxide Synthase Translation in Macrophages
Authors: Lewis Nuruddeen D. , Asim Mohammad , Barry Daniel P. , Singh Kshipra , de Sablet Thibaut , Boucher Jean-Luc , Gobert Alain P. , Chaturvedi Rupesh , Wilson Keith T. 
Published: January 2010

AbstractHelicobacter pylori infection of the stomach causes peptic ulcer disease and gastric cancer. Despite eliciting a vigorous immune response, the bacterium persists for the life of the host. An important antimicrobial mechanism is the production of NO derived from inducible NO synthase (iNOS). We have reported that macrophages can kill H. pylori in vitro by an NO-dependent mechanism, but supraphysiologic levels of the iNOS substrate l-arginine are required. Because H. pylori induces arginase activity in macrophages, we determined if this restricts NO generation by reducing l-arginine availability. Inhibition of arginase with S-(2-boronoethyl)-l-cysteine (BEC) significantly enhanced NO generation in H. pylori-stimulated RAW 264.7 macrophages by enhancing iNOS protein translation but not iNOS mRNA levels. This effect resulted in increased killing of H. pylori that was attenuated with an NO scavenger. In contrast, inhibition of arginase in macrophages activated by the colitis-inducing bacterium Citrobacter rodentium increased NO without affecting iNOS levels. H. pylori upregulated levels of arginase II (Arg2) mRNA and protein, which localized to mitochondria, whereas arginase I was not induced. Increased iNOS protein and NO levels were also demonstrated by small interfering RNA knockdown of Arg2 and in peritoneal macrophages from C57BL/6 Arg2−/− mice. In H. pylori-infected mice, treatment with BEC or deletion of Arg2 increased iNOS protein levels and NO generation in gastric macrophages, but treatment of Arg2−/− mice with BEC had no additional effect. These studies implicate Arg2 in the immune evasion of H. pylori by causing intracellular depletion of l-arginine and thus reduction of NO-dependent bactericidal activity.
FcγRIIB Inhibits the Development of Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient Mice
Authors: Zhao Ming , Wigren Maria , Dunér Pontus , Kolbus Daniel , Olofsson Katarina E. , Björkbacka Harry , Nilsson Jan , Fredrikson Gunilla Nordin 
Published: January 2010

Abstract
The immune processes associated with atherogenesis have received considerable attention during recent years. IgG FcRs (FcγR) are involved in activating the immune system and in maintaining peripheral tolerance. However, the role of the inhibitory IgG receptor FcγRIIB in atherosclerosis has not been defined. Bone marrow cells from FcγRIIB-deficient mice and C57BL/6 control mice were transplanted to low-density lipoprotein receptor-deficient mice. Atherosclerosis was induced by feeding the recipient mice a high-fat diet for 8 wk and evaluated using Oil Red O staining of the descending aorta at sacrifice. The molecular mechanisms triggering atherosclerosis was studied by examining splenic B and T cells, as well as Th1 and Th2 immune responses using flow cytometry and ELISA. The atherosclerotic lesion area in the descending aorta was ~5-fold larger in mice lacking FcγRIIB than in control mice (2.75 ± 2.57 versus 0.44 ± 0.42%; p &lt; 0.01). Moreover, the FcγRIIB deficiency resulted in an amplified splenocyte proliferative response to Con A stimulation (proliferation index 30.26 ± 8.81 versus 2.96 ± 0.81%, p &lt; 0.0001) and an enhanced expression of MHC class II on the B cells (6.65 ± 0.64 versus 2.33 ± 0.25%; p &lt; 0.001). In accordance, an enlarged amount of CD25-positive CD4 T cells was found in the spleen (42.74 ± 4.05 versus 2.45 ± 0.31%; p &lt; 0.0001). The plasma Ab and cytokine pattern suggested increased Th1 and Th2 immune responses, respectively. These results show that FcγRIIB inhibits the development of atherosclerosis in mice. In addition, they indicate that absence of the inhibiting IgG receptor cause disease, depending on an imbalance of activating and inhibiting immune cells.
Functionally Significant Differences in Expression of Disease-Associated IL-7 Receptor α Haplotypes in CD4 T Cells and Dendritic Cells
Authors: Hoe Edwin , McKay Fiona C. , Schibeci Stephen D. , Gandhi Kaushal , Heard Rob N. , Stewart Graeme J. , Booth David R. 
Published: January 2010

Abstract
Common genetic variants of IL-7 receptor α (IL-7Rα) have recently been shown to affect susceptibility to multiple sclerosis (MS) and type 1 diabetes, and survival following bone marrow transplantation. Transcription of the gene produces two dominant isoforms, with or without exon 6, which code for membrane-bound or soluble IL-7Rα, respectively. The haplotypes produce different isoform ratios. We have tested IL-7Rα mRNA expression in cell subsets and in models of T cell homeostasis, activation, tolerance, and differentiation into regulatory T cell/Th1/Th2/Th17, memory, and dendritic cells (DCs) under the hypothesis that the conditions in which haplotype differences are maximal are those likely to be the basis for their association with disease pathogenesis. Maximal differences between haplotypes were found in DCs, where the ligand is mainly thymic stromal lymphopoietin (TSLP). The MS-protective haplotype produces a much lower ratio of soluble to membrane-bound receptor, and so potentially, DCs of this haplotype are more responsive to TSLP. The TSLP/IL-7Rα interaction on DCs is known to be critical for production of thymic regulatory T cells, and reduced production of these cells in MS susceptibility haplotypes may be a basis for its association with this disease. IL-7Rα mRNA expression varies greatly through cell differentiation so that it may be a useful marker for cell states. We also show that serum levels of soluble receptor are much higher for the MS susceptibility haplotype (p = 4 × 10−13). Because signaling through IL-7Rα controls T cell regulation, this haplotype difference is likely to affect the immunophenotype and disease pathogenesis.
Differential Effector Pathways Regulate Memory CD8 T Cell Immunity against Plasmodium berghei versus P. yoelii Sporozoites
Authors: Butler Noah S. , Schmidt Nathan W. , Harty John T. 
Published: January 2010

Abstract
Malaria results in &gt;1,000,000 deaths per year worldwide. Although no licensed vaccine exists, much effort is currently focused on subunit vaccines that elicit CD8 T cell responses directed against Plasmodium parasite liver stage Ags. Multiple immune-effector molecules play a role in antimicrobial immunity mediated by memory CD8 T cells, including IFN-γ, perforin, TRAIL, Fas ligand, and TNF-α. However, it is not known which pathways are required for memory CD8 T cell-mediated immunity against liver stage Plasmodium infection. In this study, we used a novel immunization strategy to generate memory CD8 T cells in the BALB/c mouse model of P. berghei or P. yoelii sporozoite infection to examine the role of immune-effector molecules in resistance to the liver stage infection. Our studies reveal that endogenous memory CD8 T cell-mediated protection against both parasite species is, in part, dependent on IFN-γ, whereas perforin was only critical in protection against P. yoelii. We further show that neutralization of TNF-α in immunized mice markedly reduces memory CD8 T cell-mediated protection against both parasite species. Thus, our studies identify IFN-γ and TNF-α as important components of the noncytolytic pathways that underlie memory CD8 T cell-mediated immunity against liver stage Plasmodium infection. Our studies also show that the effector pathways that memory CD8 T cells use to eliminate liver stage infection are, in part, Plasmodium species specific.
Synthesis of
Tert
‐Butyl (1

S

,2

S

)‐2‐Methyl‐3‐Oxo‐1‐Phenylpropylcarbamate by Asymmetric Mannich Reaction
Authors: Woon Yang Jung , Chandra Pan Subhas , List Benjamin 
Published: January 2010

Abstract

Tert‐
Butyl phenyl(phenylsulfonyl)methylcarbamate

(
E
)‐
tert‐
Butyl benzylidinecarbamate

Carbamic acid,
N‐
[(1
S,
2
S
)‐2‐methyl‐3‐oxo‐1‐phenylpropyl]‐1.1‐dimethylethyl ester
Synthesis of Pyrazolo[1,5‐
a
]Pyridines Via Azirines: Preparation of 2‐(3‐Bromophenyl)‐6‐(Trifluoromethyl)Pyrazolo[1,5‐
a
]Pyridine
Authors: Greszler Stephen , Stevens Kirk L. 
Published: January 2010

Abstract

3'‐Bromoacetophenone

Sodium hydride

2‐Chloro‐5‐(trifluoromethyl)pyridine

Trifluoracetic anhydride
2‐(2,2‐Dibromoethenyl)‐Benzenamine
Authors: Bryan Christopher , Aurregi Valentina , Lautens Mark 
Published: January 2010

Abstract

2‐Nitrobenzaldehyde

Tetrabromomethane

Triisopropyl phosphate

Sodium carbonate

Benzene, 1‐(2,2‐dibromoethenyl)‐2‐nitro

Benzenamine, 2 (2,2‐dibromoethenyl)‐
Preparation of (

S

)‐4‐Isopropyl‐

N

‐Propanoyl‐1,3‐Thiazolidine‐2‐Thione
Authors: Gálvez Erik , Romea Pedro , Urpí Fèlix 
Published: January 2010

Abstract

(
S
)‐Valinol

Carbon disulfide

(
S)‐
4‐Isopropyl‐1,3‐thiazolidine‐2‐thione

n‐
Butyllithium

Propanoyl chloride

(
S)‐
4‐Isopropyl‐
N‐
propanoyl‐1,3‐thiazolidine‐2‐thione
Stereoselective Synthesis of
anti
α‐Methyl‐β‐Methoxy Carboxylic Compounds
Authors: Gálvez Erik , Romea Pedro , Urpí Fèlix 
Published: January 2010

Abstract

(
E)‐
2‐Methyl‐3‐phenylpropenal

Trimethyl orthoformate

(
E)‐
3,3‐Dimethoxy‐2‐methyl‐1‐propenylbenzene

(
S)
‐4‐(1‐Methylethyl)‐3‐(1‐oxopropyl)2‐thiazolidinethione

Diisopropylethylamine

Titanium tetrachloride

(4
S)
‐3‐[(2
R,
3
S,
4
E)‐
3‐Methoxy‐2,4‐dimethyl‐1‐oxo‐5‐phenyl‐4‐pentenyl]‐4‐(1‐methylethyl)‐2‐thiazolidinethione

N,O‐
Dimethylaminopyridine

Triethylamine
Enantioselective Oxidation of an Alkyl Aryl Sulfide: Synthesis of (

S

)‐(–)‐Methyl

P

‐Bromophenyl Sulfoxide
Authors: Drago Carmelo , Walker Emma‐Jane , Caggiano Lorenzo , Jackson Richard F. W. 
Published: January 2010

Abstract

(S
)
(‐)‐2‐(
N‐
3,5‐Diidosalicyliden)amino‐3,3‐dimethyl‐1‐butanol

(L)‐( + )‐
tert‐
Leucinol

3,5‐Diiodosalicyladehyde

(
S)
‐(‐)‐
p‐
Bromophenyl methyl sulfoxide

Vanadyl acetylacetonate

p‐
Bromophenyl methyl sulfide
Synthesis of 2‐[3,3'‐Di‐(
Tert
‐Butoxycarbonyl)‐Aminodipropylamine]‐4,6,‐Dichloro‐1,3,5‐Triazine as a Monomer and 1,3,5‐[
Tris
‐Piperazine]‐Triazine as a Core for the Large Scale Synthesis of Melamine (Triazine) Dendrimers
Authors: Chouai Abdellatif , Venditto Vincent J. , Simanek Eric E. 
Published: January 2010

Abstract

3,3'‐Diaminodipropylamine

2‐(
tert
‐Butoxycarbonyloxyamino)2‐phenylacetonitrile

Cyanuric chloride

N‐(tert
‐Butoxycarbonyl)‐piperazine

N,N‐D
iisopropyl ethylamine

2‐[3,3'‐Di‐(
tert
‐butoxycarbonyl)‐aminodipropylamine]‐4,,6‐dichloro‐1,3,5‐triazone

1,3,5‐[Tris‐piperazine]‐triazine
Large Scale, Green Synthesis of a Generation‐1 Melamine (Triazine) Dendrimer
Authors: Chouai Abdellatif , Venditto Vincent J. , Simanek Eric E. 
Published: January 2010

Abstract

2‐[3,3'‐Di‐(
tert‐
butoxycarbonyl)‐aminodipropylamine]‐4,6‐dichloro‐1,3,5‐triazine

1,3,5‐[Tris‐piperazine]‐triazine

G1‐[N(CH
2
CH
2
CH
2
NHBoc)
2
]
6
‐Cl
3

G1‐[N(CH
2
CH
2
CH
2
NHBoc)
2
]
6
‐piperidine
Preparation of (

S

)‐2‐Allyl‐2‐Methylcyclohexanone
Authors: Mohr Justin T. , Krout Michael R. , Stoltz Brian M. 
Published: January 2010

Abstract

Pimelic acid

Allyl alcohol

p‐
Tolunesulfonic acid monohydrate

Diallyl pimelate

Iodomethane

Allyl 1‐methyl‐2‐oxocyclohexanecarboxylate

Tris(dibenzylideneacetone) dipalladium(0)

(
S)‐tert‐
ButylPHOX

(
S
)‐2‐Allyl‐2‐methylcyclohexanone

Sodium acetate

Semicarbazide hydrochloride

(
S
)‐2‐Allyl‐2‐methylcyclohexylidiene)hydrazinecarboximide
One‐Pot Multicomponent Preparation of Tetrahydropyrazoloquinolinones and Tetrahydropyrazoloquinazolinones
Authors: Glasnov Toma N. , Kappe C. Oliver 
Published: January 2010

AbstractTriethylamine5‐Phenyl‐1H‐pyrazol‐3‐amineDimedonep‐Tolualdehyde7,7‐Dimethyl‐3‐phenyl‐4‐p‐tolyl‐6,7,8,9‐tetrahydro‐1H‐pyrazolo[3,4‐b]‐quinolin‐5(4H)‐oneChlorotrimethylsilane
(3

R

,7

a
S

)‐3‐(Trichloromethyl)Tetrahydropyrrolo[1,2‐

C

]Oxazol‐1(3

H

)‐One: An Air and Moisture Stable Reagent for the Synthesis of Optically Active α‐Branched Prolines
Authors: Artman Gerald D. , Rafferty Ryan J. , Williams Robert M. 
Published: January 2010

Abstract

(
S
)‐Proline

2,2,2‐Trichloro‐1‐ethoxyethanol

(3
R
,7
aS
)‐3‐(Trichloromethyl)tetrahydropyrrolo[1,2‐
c
]oxazol‐1(3
H
)‐one

Sodium

Acetyl chloride

(
R
)‐Methyl 2‐allylpyrrolidine‐2‐carboxylate hydrochloride
Vinylation with Inexpensive Silicon‐Based Reagents: Preparation of 3‐Vinylquinoline and 4‐Vinylbenzophenone
Authors: Denmark Scott E. , Butler Christopher R. 
Published: January 2010

Abstract

4‐Vinylbenzophenone

3‐Vinylquinoline

1.3.5.7‐Tetramethyl‐1,3,5,7‐tetravinylcyclotetrasiloxane

Palladium tris(dibenzylideneacetone)

2‐(Di‐t
ert‐
butylphosphino)biphenyl
Low Pressure Carbonylation of Epoxides to β‐Lactones
Authors: Kramer John W. , Treitler Daniel S. , Coates Geoffrey W. 
Published: January 2010

Abstract

1,2‐Epoxy‐3‐phenoxypropane

[N,N'‐
Bis(3,5‐di‐
tert‐
butylsalicylidene)‐1,2‐phenylenediamino‐chromium‐di‐tetrahydrofuran]tetracarbonylcobaltate(1)

Carbon monoxide
Tetrakis(Dimethylamino)Allene
Authors: Fürstner Alois , Alcarazo Manuel , Krause Helga 
Published: January 2010

Abstract

Dichlormethylen‐dimethyliminium chloride

Dimethyl acetamide

1,3‐Dichloro‐1,3‐bis(dimethylamino)propenium chloride

Diethylamine

1,1,3,3,‐Tetrakis(dimethylamino)propenium tetrafluoroborate

Sodium amide

Tetrakis(dimethylamino)allene
Efficient One‐Pot Synthesis of Bis(4‐
Tert
‐Butylphenyl) Iodonium Triflate
Authors: Bielawski Marcin , Olofsson. Berit 
Published: January 2010

Abstract

Bis(4‐
tert‐
butylphenyl)iodonium triflate

Iodine

Tert‐
Butylbenzene

M‐
Chloroperbenzoic acid

Trifluoromethanesulfonic acid
Pd
(0)‐Catalyzed Diamination of
trans
‐1‐Phenyl‐1,3‐Butadiene with
Di
‐
tert
‐Butyldiaziridinone as Nitrogen Source
Authors: Du Haifeng , Zhao Baoguo , Shi Yian 
Published: January 2010

Abstract

Di‐
tert‐
butylurea

Tert‐
Butylamine

Triethylamine

Triphosgene

Di‐
tert‐
butyldiaziridinone

Tert‐
Butyl hypochlorite

Potassium
tert‐
butoxide

Trans‐
1,3‐Di‐
tert‐
butyl‐4‐phenyl‐5‐vinyl‐imidazolidin‐2‐one

(
E)‐
1‐Phenyl‐1,3‐butadiene

Tetrakis(triphenylphosphine)palladium
Synthesis of 4,5‐Dimethyl‐1,3‐Dithiol‐2‐One
Authors: Chandrasekaran Perumalreddy , Donahue James P. 
Published: January 2010

Abstract

O‐
Isopropyl
S‐
3‐Oxobutan‐2‐yl dithicarbonate

2‐Butanone

Potassium
O‐
isopropylxanthate

4,5‐Dimethyl‐1,3‐dithiol‐2‐one
B‐Protected Haloboronic Acids for Iterative Cross‐Coupling
Authors: Ballmer Steven G. , Gillis Eric P. , Burke Martin D. 
Published: January 2010

Abstract

N‐
Methyliminodiacetic acid

Iminodiacetic acid

Formalin

Formic acid

4‐Bromophenylboronic acid

Palladium(II) acetate

(2‐Biphenyl)dicyclohexylphosphine

p‐
Tolylboronic acid
Holoprosencephaly due to numeric chromosome abnormalities
Authors: Solomon Benjamin D. , Rosenbaum Kenneth N. , Meck Jeanne M. , Muenke Maximilian 
Published: January 2010

AbstractHoloprosencephaly (HPE) is the most common malformation of the human forebrain. When a clinician identifies a patient with HPE, a routine chromosome analysis is often the first genetic test sent for laboratory analysis in order to assess for a structural or numerical chromosome anomaly. An abnormality of chromosome number is overall the most frequently identified etiology in a patient with HPE. These abnormalities include trisomy 13, trisomy 18, and triploidy, though several others have been reported. Such chromosome number abnormalities are almost universally fatal early in gestation or in infancy. Clinical features of specific chromosome number abnormalities may be recognized by phenotypic manifestations in addition to the HPE. Published 2010 Wiley‐Liss, Inc.
Parental perspectives on living with a child with HoPE
Authors: Stashinko Elaine E. , Harley Leslie A. , Steele Roxanne A. , Clegg Nancy J. 
Published: January 2010

AbstractThis article describes the experiences and perceived needs of a small cohort of parents of children with holoprosencephaly (HPE). The factors that are important to the lives of children vary across families and stages of development. As children living with HPE grow and change, parents adapt their goals and expectations to reflect their child's now and future state. Relevant literature is integrated within the discussion to support recommendations for care. © 2010 Wiley‐Liss, Inc.
Non‐genetic risk factors for holoprosencephaly
Authors: Johnson Candice Y. , Rasmussen Sonja A. 
Published: January 2010

AbstractHoloprosencephaly (HPE) is a congenital defect of the brain characterized by incomplete cleavage of the embryonic forebrain into left and right hemispheres. Although a substantial proportion of cases of HPE can be attributed to genetic abnormalities, the etiology in many cases remains unknown, with non‐genetic risk factors believed to be important contributors. Due to the low birth prevalence of this defect, it has proven difficult to conduct studies of sufficient size to identify risk factors with certainty. This article provides a summary of non‐genetic risk factors for HPE that have been investigated in case reports and case series, animal studies, and epidemiologic studies, including maternal illnesses, therapeutic and non‐therapeutic exposures, nutritional factors, and sociodemographic factors. The article also highlights challenges in study design and further areas for research to better understand the etiology of HPE. Published 2010 Wiley‐Liss, Inc.
Holoprosencephaly and ectrodactyly: Report of three new patients and review of the literature
Authors: Keaton Amelia A. , Solomon Benjamin D. , van Essen Anthonie J. , Pfleghaar Kathleen M. , Slama Michael A. , Martin Judith A. , Muenke Maximilian 
Published: January 2010

AbstractHoloprosencephaly (HPE) and ectrodactyly represent congenital malformations of the developing forebrain and developing digits, respectively. The combination of these conditions is rare, with only 15 cases known to date (12 previously reported, and 3 new cases described here). While the findings in these patients overlap with previously described genetic conditions, the similarity in phenotypes among these patients has led to the establishment of a at least one distinct syndrome: HPE, ectrodactyly, and bilateral cleft lip‐palate syndrome (OMIM 300571). There has been great interest in identifying a genetic cause for the findings in patients with HPE and ectrodactyly; however the cause(s) of this rare association still remain unknown. Published 2010 Wiley‐Liss, Inc.
Management of children with holoprosencephaly
Authors: Levey Eric B. , Stashinko Elaine , Clegg Nancy J. , Delgado Mauricio R. 
Published: January 2010

AbstractHoloprosencephaly (HPE) is the most common malformation of the embryonic forebrain in humans. Although HPE occurs along a continuous spectrum, it has been categorized into four types from most severe to least severe: alobar, semilobar, lobar, and middle interhemispheric (MIH) variant. Facial malformations are often associated with HPE and usually correlate with the severity of brain malformation. With the most severely affected newborns, there is a high mortality rate in the first month of life, however, with milder forms of HPE, the majority survive beyond infancy. The Carter Centers for Brain Research in Holoprosencephaly and Related Malformations have enrolled 182 living children in a prospective research study. Based on previously published reports using this database, reports from other investigators, as well as our experience and personal observations, the range of developmental, neurological, and medical problems found in children with HPE is described in this article. Virtually all children with HPE have some developmental disability and the severity correlates with the severity of the brain malformation on neuroimaging. Common medical problems include hydrocephalus, seizures, motor impairment, oromotor dysfunction with risk of poor nutrition and aspiration, chronic lung disease, gastroesophageal reflux, constipation, hypothalamic dysfunction with disturbed sleep–wake cycles and temperature dysregulation, as well as endocrine dysfunction. Diabetes insipidus in particular is found in about 70% of children with classic HPE. Recommendations for management of these problems are given based on experiences of the authors and familiarity with the literature. © 2010 Wiley‐Liss, Inc.
Roles of bone morphogenetic protein signaling and its antagonism in holoprosencephaly
Authors: Klingensmith John , Matsui Maiko , Yang Yu‐Ping , Anderson Ryan M. 
Published: January 2010

AbstractHoloprosencephaly (HPE) is the most common malformation of the forebrain, resulting from a failure to completely septate the left and right hemispheres at the rostral end of the neural tube. Because of the tissue interactions that drive head development, these forebrain defects are typically accompanied by midline deficiencies of craniofacial structures. Early events in setting up tissue precursors of the head, as well as later interactions between these tissues, are critical for normal head formation. Defects in either process can result in HPE. Signaling by bone morphogenetic proteins (BMPs), a family of secreted cytokines, generally plays negative roles in early stages of head formation, and thus must be attenuated in multiple contexts to ensure proper forebrain and craniofacial development. Chordin and Noggin are endogenous, extracellular antagonists of BMP signaling that promote the normal organization of the forebrain and face. Mouse mutants with reduced levels of both factors display mutant phenotypes remarkably analogous to the range of malformations seen in human HPE sequence. Chordin and Noggin function in part by antagonizing the inhibitory effects of BMP signaling on the Sonic hedgehog and Nodal pathways, genetic lesions in each being associated with human HPE. Study of Chordin;Noggin mutant mice is helping us to understand the molecular, cellular, and genetic pathogenesis of HPE and associated malformations. © 2010 Wiley‐Liss, Inc.
Management of the hernial sac in inguinal hernia repair
Authors: Stylianidis G , Haapamäki M M , Sund M , Nilsson E , Nordin P 
Published: January 2010

AbstractBackgroundThere is no consensus on the best management of the indirect hernial sac in groin hernia surgery. The aim of this study was to investigate to what extent different management options are associated with reoperation for recurrence.MethodsThis study used data from the Swedish Hernia Register. Surgeons registered whether the indirect hernial sac was managed by division (leaving the distal part in place), excision or invagination.ResultsAn indirect hernia was found in 48 433 operations; the sac was excised in 49·5 per cent, invaginated in 37·6 per cent and divided in 12·9 per cent of operations. The 5-year cumulative reoperation incidence was 1·7 per cent for hernial sac excision, 1·7 per cent for division and 2·7 per cent for invagination. For indirect hernia repair, the relative risk of reoperation for recurrence was 0·63 (95 per cent confidence interval 0·51 to 0·79) for excision of the sac and 0·72 (0·53 to 0·99) for division compared with invagination. Lichtenstein repair combined with hernial sac excision had a 5-year cumulative reoperation incidence of only 1·0 per cent.ConclusionExcision of the indirect hernial sac in inguinal hernia repair is associated with a lower risk of hernia recurrence than division or invagination.