Incidental Portal Vein Aneurysm Found in a Patient with a Diaphragmatic Hernia and Evolving Gastric Volvulus

Rare and poorly described within the literature, a portal vein aneurysm (PVA) is defined as an abnormal vascular dilation of the portal vein exceeding 19 mm in patients with cirrhotic livers and 15 mm in patients with normal livers. Incidence has been estimated to be 0.06[percent] and fewer than 200 cases have been described in the literature1,4. We describe an incidental and asymptomatic PVA found in an 80-year-old Caucasian male presenting with evolving gastric volvulus in the context of a large diaphragmatic hernia. Computed tomography (CT) revealed displacement of abdominal contents and 37 mm aneurysm of the main portal vein (image 1,2). Because of the large size of our patients' malformation (37 mm), surgery was pursued in the form of aneurysmorrhaphy. There is a paucity of literature regarding the management of PVA - however the literature distinguishes between those with and without underlying portal hypertension. Notably, the patient was asymptomatic from this pathology and had no underlying portal hypertension. He was seen in an outpatient clinic two weeks after discharge and had fully recovered without any reported sequela or symptoms related to his vascular surgery.Ashkan Kashanchi (1), Yonatan Akivis (2), Anthony Scalzo (3) ; 1. Saint Louis University School of Medicine. 2. SUNY Downstate College of Medicine. 3. Saint Louis University School of Medicine, Departments of Pediatrics and Internal Medicine, Division of Toxicology, Division of Emergency Medicine, Department of Surgery.Includes bibliographical reference

Evidence for Persistence of Ectromelia Virus in Inbred Mice, Recrudescence Following Immunosuppression and Transmission to Naive Mice

Orthopoxviruses (OPV), including variola, vaccinia, monkeypox, cowpox and ectromelia viruses cause acute infections in their hosts. With the exception of variola virus (VARV), the etiological agent of smallpox, other OPV have been reported to persist in a variety of animal species following natural or experimental infection. Despite the implications and significance for the ecology and epidemiology of diseases these viruses cause, those reports have never been thoroughly investigated. We used the mouse pathogen ectromelia virus (ECTV), the agent of mousepox and a close relative of VARV to investigate virus persistence in inbred mice. We provide evidence that ECTV causes a persistent infection in some susceptible strains of mice in which low levels of virus genomes were detected in various tissues late in infection. The bone marrow (BM) and blood appeared to be key sites of persistence. Contemporaneous with virus persistence, antiviral CD8 T cell responses were demonstrable over the entire 25-week study period, with a change in the immunodominance hierarchy evident during the first 3 weeks. Some virus-encoded host response modifiers were found to modulate virus persistence whereas host genes encoded by the NKC and MHC class I reduced the potential for persistence. When susceptible strains of mice that had apparently recovered from infection were subjected to sustained immunosuppression with cyclophosphamide (CTX), animals succumbed to mousepox with high titers of infectious virus in various organs. CTX treated index mice transmitted virus to, and caused disease in, co-housed naïve mice. The most surprising but significant finding was that immunosuppression of disease-resistant C57BL/6 mice several weeks after recovery from primary infection generated high titers of virus in multiple tissues. Resistant mice showed no evidence of a persistent infection. This is the strongest evidence that ECTV can persist in inbred mice, regardless of their resistance status

CD1d-restricted NKT cells: an interstrain comparison

CD1d-restricted Va14-Ja281 invariant abTCR1 (NKT) cells are well defined in the C57BL/6 mouse strain, but they remain poorly characterized in non-NK1.1-expressing strains. Surrogate markers for NKT cells such as abTCR1CD42CD82 and DX51CD31 have been used in many studies, although their effectiveness in defining this lineage remains to be verified. Here, we compare NKT cells among C57BL/6, NK1.1-congenic BALB/c, and NK1.1-congenic nonobese diabetic mice. NKT cells were identified and compared using a range of approaches: NK1.1 expression, surrogate phenotypes used in previous studies, labeling with CD1d/a-galactosylceramide tetramers, and cytokine production. Our results demonstrate that NKT cells and their CD4/CD8-defined subsets are present in all three strains, and confirm that nonobese diabetic mice have a numerical and functional deficiency in these cells. We also highlight the hazards of using surrogate phenotypes, none of which accurately identify NKT cells,and one in particular (DX51CD31) actually excludes these cells. Finally, our results support the concept that NK1.1 expression may not be an ideal marker for CD1d-restricted NKT cells, many of which are NK1.1-negative, especially within the CD41 subset and particularly in NK1.1-congenic BALB/c mice

Innate immunity defines the capacity of antiviral T cells to limit persistent infection

Effective immunity requires the coordinated activation of innate and adaptive immune responses. Natural killer (NK) cells are central innate immune effectors, but can also affect the generation of acquired immune responses to viruses and malignancies. How NK cells influence the efficacy of adaptive immunity, however, is poorly understood. Here, we show that NK cells negatively regulate the duration and effectiveness of virus-specific CD4+ and CD8+ T cell responses by limiting exposure of T cells to infected antigen-presenting cells. This impacts the quality of T cell responses and the ability to limit viral persistence. Our studies provide unexpected insights into novel interplays between innate and adaptive immune effectors, and define the critical requirements for efficient control of viral persistence

Probing type Ia supernova properties using bolometric light curves from the Carnegie Supernova Project and the CfA Supernova Group

We present bolometric light curves constructed from multiwavelength photometry of Type Ia supernovae (SNe Ia) from the Carnegie Supernova Project and the CfA Supernova Group, using near-infrared observations to provide robust constraints on host galaxy dust extinction. This set of light curves form a well-measured reference set for comparison with theoretical models. Ejected mass and synthesized 56Ni mass are inferred for each SN Ia from its bolometric light curve using a semi-analytic Bayesian light curve model, and fitting formulas provided in terms of light curve width parameters from the SALT2 and SNOOPY light curve fitters. A weak bolometric width-luminosity relation is confirmed, along with a correlation between ejected mass and the bolometric light curve width. SNe Ia likely to have sub-Chandrasekhar ejected masses belong preferentially to the broad-line and cool-photosphere spectroscopic subtypes, and have higher photospheric velocities and populate older, higher mass host galaxies than SNe Ia consistent with Chandrasekhar-mass explosions. Two peculiar events, SN 2006bt and SN 2006ot, have normal peak luminosities but appear to have super-Chandrasekhar ejected masse