62 research outputs found

    Natural history of asymptomatic pancreatic cystic neoplasms

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    AbstractBackgroundThe management of asymptomatic pancreatic cysts is controversial and indications for excision are based on pathology and natural history.ObjectivesThis study aimed to examine outcomes of asymptomatic lesions using a protocol based on size and cyst fluid analysis.MethodsAsymptomatic cysts were identified from a prospectively maintained database. Sequential cross‐sectional imaging studies were assessed, and results of endoscopic ultrasound‐guided aspiration were co‐analysed.ResultsA total of 338 asymptomatic patients underwent evaluation. Overall, 84 cysts were <1.5 cm and 254 were ≥1.5 cm in diameter. Median patient follow‐up was 5.1 years [interquartile range (IQR): 4.1–6.9 years]. In the group in which cysts measured <1.5 cm in diameter, median cyst size was 1.0 cm (IQR: 0.6–1.2 cm) at presentation and increased to 1.2 cm (IQR: 0.7–1.6 cm) during follow‐up. Five (6.0%) patients underwent resection, all within 2 months of presentation. In the group in which cysts measured ≥1.5 cm in diameter, median cyst size was 2.5 cm (IQR: 2.0–3.4 cm) at presentation and increased to 2.7 cm (IQR: 3.0–4.2 cm). A total of 63 (24.8%) patients underwent resection. Surgery was performed with 2 months in 53 (84.1%) patients, within 12 months in four (6.3%) patients and at >12 months post‐presentation in six (9.5%) patients. A total of 70.6% of resected specimens were identified as malignancies or mucinous lesions.conclusionsAsymptomatic cysts of <1.5 cm in diameter can safely be followed by imaging and are expected to undergo little change. A quarter of all asymptomatic cysts measuring ≥1.5 cm are appropriately resected based on imaging and cyst fluid analysis

    Parvovirus Minute Virus of Mice Induces a DNA Damage Response That Facilitates Viral Replication

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    Infection by DNA viruses can elicit DNA damage responses (DDRs) in host cells. In some cases the DDR presents a block to viral replication that must be overcome, and in other cases the infecting agent exploits the DDR to facilitate replication. We find that low multiplicity infection with the autonomous parvovirus minute virus of mice (MVM) results in the activation of a DDR, characterized by the phosphorylation of H2AX, Nbs1, RPA32, Chk2 and p53. These proteins are recruited to MVM replication centers, where they co-localize with the main viral replication protein, NS1. The response is seen in both human and murine cell lines following infection with either the MVMp or MVMi strains. Replication of the virus is required for DNA damage signaling. Damage response proteins, including the ATM kinase, accumulate in viral-induced replication centers. Using mutant cell lines and specific kinase inhibitors, we show that ATM is the main transducer of the signaling events in the normal murine host. ATM inhibitors restrict MVM replication and ameliorate virus-induced cell cycle arrest, suggesting that DNA damage signaling facilitates virus replication, perhaps in part by promoting cell cycle arrest. Thus it appears that MVM exploits the cellular DNA damage response machinery early in infection to enhance its replication in host cells

    Paracentral Acute Middle Maculopathy in the Setting of New Onset Giant Cell Arteritis

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    Paracentral acute middle maculopathy (PAMM) is a condition in which ischemia of the deep retinal capillary plexus causes distinctive hyperreflective lesions in the inner nuclear layer on high resolution SD-OCT
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