Some Textual and Factual Discrepancies in James Joyce's Ulysses: The Blooms’ Several “First Nights”

This essay investigates how in Ulysses James Joyce created several textual, biographical, temporal, and topographical discrepancies at the narrative origin of Leopold Bloom and Molly Tweedy’s life together. The textual and contextual evidence indicates that there were two (or possibly more) “first nights” ― different firsts on different evenings ― for the soon to be Blooms. This is one of the many instances in the book when the “facts” in the fiction ― as well as some of the seemingly analogous facts outside the novel ― do not cohere. The genetic study of this kind of temporal and spatial slippage in the book’s purportedly coherent texture challenges readers’ preconceptions about the fixity of the character’s life-stories in the narrative and uncovers some of the ways in which Joyce relied on the names and some facts derived from the lives of real people in a variety of often unexpected ways to create the life-stories of his fictional characters

Ulysses at 100

The year 2022 marked the 100th anniversary of the publication of Ulysses. The following reflections express different sentiments and thoughts about the novel that gave T. S. Eliot “all the surprise, delight, and terror that I can require.

Piroxicam and intracavitary platinum-based chemotherapy for the treatment of advanced mesothelioma in pets: preliminary observations

Malignant Mesothelioma is an uncommon and very aggressive tumor that accounts for 1% of all the deaths secondary to malignancy in humans. Interestingly, this neoplasm has been occasionally described in companion animals as well. Aim of this study was the preclinical evaluation of the combination of piroxicam with platinum-based intracavitary chemotherapy in pets. Three companion animals have been treated in a three years period with this combination. Diagnosis was obtained by ultrasonographic exam of the body cavities that evidenced thickening of the mesothelium. A surgical biopsy further substantiated the diagnosis. After drainage of the malignant effusion from the affected cavity, the patients received four cycles of intracavitary CDDP at the dose of 50 mg/m2 every three weeks if dogs or four cycles of intracavitary carboplatin at the dose of 180 mg/m2 (every 3 weeks) if cats, coupled with daily administration of piroxicam at the dose of 0.3 mg/kg. The therapy was able to arrest the effusion in all patients for variable remission times: one dog is still in remission after 3 years, one dog died of progressive disease after 8 months and one cat died due to progressive neoplastic growth after six months, when the patient developed a mesothelial cuirass. The combination showed remarkable efficacy at controlling the malignant effusion secondary to MM in our patients and warrants further investigations

'A French Homer in America: James Joyce, Henri Matisse and George Macy’s Limited Editions Club "Ulysses"'

On 6 December 1933, Judge John M. Woolsey of the Southern District Court of New York determined that Ulysses was not obscene and thus could be lawfully imported into the United States. By the end of the following month, Bennett Cerf, co-founder of Random House, had published the first authorized edition of James Joyce’s book in America. Then, on 22 October 1935, George Macy, the visionary director of the Limited Editions Club (LEC) in New York, a subscription-based fine arts book press, published his Ulysses with illustrations by Henri Matisse. Given its limited availability and cost—then and now—most people have never seen this monumental deluxe edition of Ulysses, and so very few people have actually tried to read it, but that is probably beside the point. The LEC Ulysses is one of the most iconic modernist books ever produced and it presented an avant-garde reimagining of Homer’s Odyssey in text and images for an American readership that may not have been quite prepared for it

The serine protease HtrA1 specifically interacts and degrades the tuberous sclerosis complex 2 protein

Hamartin and tuberin are products of the tumor suppressor genes TSC1 and TSC2, respectively. Mutations affecting either gene result in the tuberous sclerosis syndrome, a neurologic genetic disorder characterized by the formation of multiple benign tumors or hamartomas. In this study, we report the identification of TSC2, but not TSC1, as a substrate of HtrA1, a member of the human HtrA family proteins of serine proteases. We show the direct interaction and colocalization in the cytoplasm of HtrA1 and TSC2 and that HtrA1 cleaves TSC2 both in vitro and in vivo. Finally, we show that alterations in HtrA1 expression cause modifications in phosphorylation status of two downstream targets of TSC2: 4E-BP1 and S6K. Our data suggest that, under particular physiologic or pathologic conditions, HtrA1 degrades TSC2 and activates the downstream targets. Considering that HtrA1 levels are significantly increased during embryogenesis, we speculate that one of the targets of HtrA1 activity during fetal development is the TSC2-TSC1 pathway. ©2010 AACR

The serine protease HtrA1 specifically interacts and degrades the tuberous sclerosis complex 2 protein

Hamartin and tuberin are products of the tumor suppressor genes TSC1 and TSC2, respectively. Mutations affecting either gene result in the tuberous sclerosis syndrome, a neurologic genetic disorder characterized by the formation of multiple benign tumors or hamartomas. In this study, we report the identification of TSC2, but not TSC1, as a substrate of HtrA1, a member of the human HtrA family proteins of serine proteases. We show the direct interaction and colocalization in the cytoplasm of HtrA1 and TSC2 and that HtrA1 cleaves TSC2 both in vitro and in vivo. Finally, we show that alterations in HtrA1 expression cause modifications in phosphorylation status of two downstream targets of TSC2: 4E-BP1 and S6K. Our data suggest that, under particular physiologic or pathologic conditions, HtrA1 degrades TSC2 and activates the downstream targets. Considering that HtrA1 levels are significantly increased during embryogenesis, we speculate that one of the targets of HtrA1 activity during fetal development is the TSC2-TSC1 pathway

The serine protease HtrA1 specifically interacts and degrades the tuberous sclerosis complex 2 protein

Hamartin and tuberin are products of the tumor suppressor genes TSC1 and TSC2, respectively. Mutations affecting either gene result in the tuberous sclerosis syndrome, a neurologic genetic disorder characterized by the formation of multiple benign tumors or hamartomas. In this study, we report the identification of TSC2, but not TSC1, as a substrate of HtrA1, a member of the human HtrA family proteins of serine proteases. We show the direct interaction and colocalization in the cytoplasm of HtrA1 and TSC2 and that HtrA1 cleaves TSC2 both in vitro and in vivo. Finally, we show that alterations in HtrA1 expression cause modifications in phosphorylation status of two downstream targets of TSC2: 4E-BP1 and S6K. Our data suggest that, under particular physiologic or pathologic conditions, HtrA1 degrades TSC2 and activates the downstream targets. Considering that HtrA1 levels are significantly increased during embryogenesis, we speculate that one of the targets of HtrA1 activity during fetal development is the TSC2-TSC1 pathway. ©2010 AACR