In re Kagenvaema: An End-Run Around the “Applicable Commitment Period”

(Excerpt) Imagine a debtor who lives in New York State, where the median household income for 2007 was approximately $53,000. The debtor is a doctor and receives$80,000 of income from the hospital where she works. The good doctor, however, has gotten in over her head. She purchased a gigantic home she could not afford, has too many student loans to pay back, and regrets buying that expensive car. Her credit card debt is staggering, and she incurs thousands of dollars each month in interest and fees. She decides she can no longer handle the financial pressure and wants to file for Chapter 13 bankruptcy. However, because her income exceeds the median income in New York, the doctor is classified as an above-median income debtor, which requires a debtor to propose a repayment plan that lasts five years. The doctor is not thrilled about the prospect of subjecting herself to the five-year bankruptcy period, particularly because she has been offered a lucrative position as a partner in a prestigious medical practice. She decides to defer the offer because she does not want to increase her income during the time she is in bankruptcy and therefore have to pay more to her unsecured creditors. After filing for bankruptcy, she determines that, due to the amount of debt held by her secured creditors, her projected disposable income amounts to zero or a negative number. As a result, she is not subject to the five-year commitment period and proposes a plan to repay her unsecured creditors for 2 years. The plan is confirmed, although it guarantees the unsecured creditors recover only a fraction of the debt owed to them. After the two years has ended, she accepts a position with the medical practice and now receives $200,000 per year in compensation. The unsecured creditors, however, would not enjoy in her increased income because the bankruptcy period has ended. Is this a fair result? According to the Ninth Circuit, there is nothing wrong with increasing secured debt or deferring income as a means of cheating unsecured creditors out of their money

Chromosome 1q21.2 and additional loci influence risk of spontaneous coronary artery dissection and myocardial infarction

Spontaneous coronary artery dissection (SCAD) is a cause of myocardial infarction Here, the authors present a genome-wide association study of SCAD, finding an association at 1q21.2 which potentially affects expression of ADAMTSL4

Pituitary Adenylate Cyclase-activating Polypeptide (PACAP)/PAC1HOP1 Receptor Activation Coordinates Multiple Neurotrophic Signaling Pathways: Akt ACTIVATION THROUGH PHOSPHATIDYLINOSITOL 3-KINASE γ AND VESICLE ENDOCYTOSIS FOR NEURONAL SURVIVAL*

MAPK and Akt pathways are predominant mediators of trophic signaling for many neuronal systems. Among the vasoactive intestinal peptide/secretin/glucagon family of related peptides, pituitary adenylate cyclase-activating polypeptide (PACAP) binding to specific PAC1 receptor isoforms can engage multiple signaling pathways and promote neuroprotection through mechanisms that are not well understood. Using a primary sympathetic neuronal system, the current studies demonstrate that PACAP activation of PAC1HOP1 receptors engages both MAPK and Akt neurotrophic pathways in an integrated program to facilitate neuronal survival after growth factor withdrawal. PACAP not only stimulated prosurvival ERK1/2 and ERK5 activation but also abrogated SAPK/JNK and p38 MAPK signaling in parallel. In contrast to the potent and rapid effects of PACAP in ERK1/2 phosphorylation, PACAP stimulated Akt phosphorylation in a late phase of PAC1HOP1 receptor signaling. From inhibitor and immunoprecipitation analyses, the PACAP/PAC1HOP1 receptor-mediated Akt responses did not represent transactivation mechanisms but appeared to depend on Gαq/phosphatidylinositol 3-kinase γ activity and vesicular internalization pathways. Phosphatidylinositol 3-kinase γ-selective inhibitors blocked PACAP-stimulated Akt phosphorylation in primary neuronal cultures and in PAC1HOP1-overexpressing cell lines; RNA interference-mediated knockdown of the receptor effectors attenuated PACAP-mediated Akt activation. Similarly, perturbation of endocytic pathways also blocked Akt phosphorylation. Between ERK and Akt pathways, PACAP-stimulated Akt signaling was the primary cascade that attenuated cultured neuron apoptosis after growth factor withdrawal. The partitioning of PACAP-mediated Akt signaling in endosomes may be a key mechanism contributing to the high spatial and temporal specificity in signal transduction necessary for survival pathways