Information Content of Equity Analyst Reports

This paper investigates the market reaction to the information released in security analyst reports. It shows that the market reacts significantly and positively to changes in recommendation levels, earnings forecasts, and price targets. While changes in price targets and earnings forecasts both provide information to the market, revisions in price targets have a larger and more significant impact than comparable revisions in earnings forecasts. The text of the report is also a significant source of information as it provides the justifications supporting an analyst's summary opinion. When all of this information is considered simultaneously, some of it, notably the earnings forecasts, is subsumed. The results further show that analysts correctly predict price targets slightly over 50% of the time. Finally, the valuation methodology used does not seem to be correlated with either the market's reaction or the analyst's accuracy.

The Market for Borrowing Corporate Bonds

This paper describes the market for borrowing corporate bonds using a comprehensive data set from a major lender. The cost of borrowing corporate bonds is comparable to the cost of borrowing stock, between 10 and 20 basis points, and both have fallen over time. Factors that influence borrowing costs are loan size, percentage of inventory lent, rating, and borrower identity. There is no evidence that bond short sellers have private information. Bonds with Credit Default Swaps (CDS) contracts are more actively lent than those without. Finally, the 2007 Credit Crunch does not affect average borrowing costs or loan volume, but does increase borrowing cost variance

The Market for Borrowing Corporate Bonds

This paper describes the market for borrowing corporate bonds using a comprehensive dataset from a major lender. The cost of borrowing corporate bonds is comparable to the cost of borrowing stock, between 10 and 20 basis points per year. Factors that increase borrowing costs are loan size, percentage of inventory lent, rating, and borrower identity. Trading strategies based on cost or amount of borrowing do not yield excess returns. Bonds with corresponding CDS contracts are more actively lent than those without. Finally, the 2007 Credit Crunch did not affect average borrowing cost or loan volume, but increased borrowing cost variance.

Plug-in Plan Tool v3.0.3.1

The role of PLUTO (Plug-in Port UTilization Officer) and the growth of the International Space Station (ISS) have exceeded the capabilities of the current tool PiP (Plug-in Plan). Its users (crew and flight controllers) have expressed an interest in a new, easy-to-use tool with a higher level of interactivity and functionality that is not bound by the limitations of Excel. The PiP Tool assists crewmembers and ground controllers in making real-time decisions concerning the safety and compatibility of hardware plugged into the UOPs (Utility Outlet Panels) onboard the ISS. The PiP Tool also provides a reference to the current configuration of the hardware plugged in to the UOPs, and enables the PLUTO and crew to test Plug-in locations for constraint violations (such as cable connector mismatches or amp limit violations), to see the amps and volts for an end item, to see whether or not the end item uses 1553 data, and the cable length between the outlet and the end item. As new equipment is flown or returned, the database can be updated appropriately as needed. The current tool is a macroheavy Excel spreadsheet with its own database and reporting functionality. The new tool captures the capabilities of the original tool, ports them to new software, defines a new dataset, and compensates for ever-growing unique constraints associated with the Plug-in Plan. New constraints were designed into the tool, and updates to existing constraints were added to provide more flexibility and customizability. In addition, there is an option to associate a "Flag" with each device that will let the user know there is a unique constraint associated with it when they use it. This helps improve the safety and efficiency of real-time calls by limiting the amount of "corporate knowledge" overhead that has to be trained and learned through use. The tool helps save time by automating previous manual processes, such as calculating connector types and deciding which cables are required and in what order

Nature of the current-induced insulator-to-metal transition in Ca2_2RuO4_4 as revealed by transport-ARPES

The Mott insulator Ca$_2$RuO$_4$ exhibits a rare insulator-to-metal transition (IMT) induced by DC current. While structural changes associated with this transition have been tracked by neutron diffraction, Raman scattering, and x-ray spectroscopy, work on elucidating the response of the electronic degrees of freedom is still in progress. Here we unveil the current-induced modifications of the electronic states of Ca$_2$RuO$_4$ by employing angle-resolved photoemission spectroscopy (ARPES) in conjunction with four-probe transport. Two main effects emerge: a clear reduction of the Mott gap and a modification in the dispersion of the Ru-bands. The changes in dispersion occur exclusively along the $XM$ high-symmetry direction, parallel to the $b$-axis where the greatest in-plane lattice change occurs. These experimental observations are reflected in dynamical mean-field theory (DMFT) calculations simulated exclusively from the current-induced lattice constants, indicating a current driven structural transition as the primary mechanism of the IMT. Furthermore, we demonstrate this phase is distinct from the high-temperature zero-current metallic phase. Our results provide insight into the elusive nature of the current-induced IMT of Ca$_2$RuO$_4$ and advance the challenging, yet powerful, technique of transport-ARPES.Comment: 8 pages, 4 figure

Pleurotomy with subxyphoid pleural drain affords similar effects to pleural integrity in pulmonary function after off-pump coronary artery bypass graft

Background: Exacerbation of pulmonary dysfunction has been reported in patients receiving a pleural drain inserted through the intercostal space in comparison to patients with an intact pleura undergoing coronary artery bypass grafting (CABG). Evidence suggests that shifting the site of pleural drain insertion to the subxyphoid position minimizes chest wall trauma and preserves respiratory function in the early postoperative period. the aim of this study was to compare the pulmonary function parameters, clinical outcomes, and pain score between patients undergoing pleurotomy with pleural drain placed in the subxyphoid position and patients with intact pleural cavity after off-pump CABG (OPCAB) using left internal thoracic artery (LITA).Methods: Seventy-one patients were allocated into two groups: I (n = 38 open left pleural cavity and pleural drain inserted in the subxyphoid position); II (n = 33 intact pleural cavity). Pulmonary function tests and clinical parameters were recorded preoperatively and on postoperative days (POD) 1, 3 and 5. Arterial blood gas analysis and shunt fraction were evaluated preoperatively and in POD1. Pain score was assessed on POD1. To monitor pleural effusion and atelectasis chest radiography was performed routinely 1 day before operation and until POD5.Results: in both groups a significant impairment was found in lung function parameters until on POD5. However, no significant difference in forced vital capacity and forced expiratory volume in 1 second were seen between groups. A significant decrease in partial pressure of arterial oxygen and an increase in shunt fraction values were observed on POD1 in both groups, but no statistical difference was found when the groups were compared. Pleural effusion and atelectasis until on POD5 were similar in both groups. There were no statistical differences in pain score, duration of mechanical ventilation and postoperative hospital stay between groups.Conclusion: Subxyphoid insertion of pleural drain provides similar effects to preserved pleural integrity in pulmonary function, clinical outcomes, and thoracic pain after OPCAB. Therefore, our results support the hypothesis that once pleural cavities are incidentally or purposely opened during LITA dissection, subxyphoid placement of the pleural drain is recommended.Universidade Federal de São Paulo, Escola Paulista Med, Pirajussara Hosp, Dept Med,Cardiol Discipline, BR-04024002 São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, São Paulo Hosp, Dept Med,Cardiol Discipline, BR-04024002 São Paulo, BrazilUniversidade Federal de São Paulo, Physiotherapy Sch, Dept Human Movement Sci, BR-11060001 Santos, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, São Paulo Hosp, Dept Med,Pneumol Discipline, BR-04039002 São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Pirajussara Hosp, Dept Med,Cardiovasc Surg Discipline, BR-04024002 São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, São Paulo Hosp, Dept Med,Cardiovasc Surg Discipline, BR-04024002 São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Pirajussara Hosp, Dept Med,Cardiol Discipline, BR-04024002 São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, São Paulo Hosp, Dept Med,Cardiol Discipline, BR-04024002 São Paulo, BrazilUniversidade Federal de São Paulo, Physiotherapy Sch, Dept Human Movement Sci, BR-11060001 Santos, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, São Paulo Hosp, Dept Med,Pneumol Discipline, BR-04039002 São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Pirajussara Hosp, Dept Med,Cardiovasc Surg Discipline, BR-04024002 São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, São Paulo Hosp, Dept Med,Cardiovasc Surg Discipline, BR-04024002 São Paulo, BrazilWeb of Scienc

Novel SPG11 mutations in Asian kindreds and disruption of spatacsin function in the zebrafish

Autosomal recessive hereditary spastic paraplegia with thin corpus callosum (HSP-TCC) maps to the SPG11 locus in the majority of cases. Mutations in the KIAA1840 gene, encoding spatacsin, have been shown to underlie SPG11-linked HSP-TCC. The aim of this study was to perform candidate gene analysis in HSP-TCC subjects from Asian families and to characterize disruption of spatacsin function during zebrafish development. Homozygosity mapping and direct sequencing were used to assess the ACCPN, SPG11, and SPG21 loci in four inbred kindreds originating from the Indian subcontinent. Four novel homozygous SPG11 mutations (c.442+1G>A, c.2146C>T, c.3602_3603delAT, and c.4846C>T) were identified, predicting a loss of spatacsin function in each case. To investigate the role of spatacsin during development, we additionally ascertained the complete zebrafish spg11 ortholog by reverse transcriptase PCR and 5′ RACE. Analysis of transcript expression through whole-mount in situ hybridization demonstrated ubiquitous distribution, with highest levels detected in the brain. Morpholino antisense oligonucleotide injection was used to knock down spatacsin function in zebrafish embryos. Examination of spg11 morphant embryos revealed a range of developmental defects and CNS abnormalities, and analysis of axon pathway formation demonstrated an overall perturbation of neuronal differentiation. These data confirm loss of spatacsin as the cause of SPG11-linked HSP-TCC in Asian kindreds, expanding the mutation spectrum recognized in this disorder. This study represents the first investigation in zebrafish addressing the function of a causative gene in autosomal recessive HSP and identifies a critical role for spatacsin during early neural development in vivo

ELF5 suppresses estrogen sensitivity and underpins the acquisition of antiestrogen resistance in luminal breast cancer.

We have previously shown that during pregnancy the E-twenty-six (ETS) transcription factor ELF5 directs the differentiation of mammary progenitor cells toward the estrogen receptor (ER)-negative and milk producing cell lineage, raising the possibility that ELF5 may suppress the estrogen sensitivity of breast cancers. To test this we constructed inducible models of ELF5 expression in ER positive luminal breast cancer cells and interrogated them using transcript profiling and chromatin immunoprecipitation of DNA followed by DNA sequencing (ChIP-Seq). ELF5 suppressed ER and FOXA1 expression and broadly suppressed ER-driven patterns of gene expression including sets of genes distinguishing the luminal molecular subtype. Direct transcriptional targets of ELF5, which included FOXA1, EGFR, and MYC, accurately classified a large cohort of breast cancers into their intrinsic molecular subtypes, predicted ER status with high precision, and defined groups with differential prognosis. Knockdown of ELF5 in basal breast cancer cell lines suppressed basal patterns of gene expression and produced a shift in molecular subtype toward the claudin-low and normal-like groups. Luminal breast cancer cells that acquired resistance to the antiestrogen Tamoxifen showed greatly elevated levels of ELF5 and its transcriptional signature, and became dependent on ELF5 for proliferation, compared to the parental cells. Thus ELF5 provides a key transcriptional determinant of breast cancer molecular subtype by suppression of estrogen sensitivity in luminal breast cancer cells and promotion of basal characteristics in basal breast cancer cells, an action that may be utilised to acquire antiestrogen resistance

The Genetic Basis of Hepatosplenic T-cell Lymphoma

Hepatosplenic T cell lymphoma (HSTL) is a rare and lethal lymphoma; the genetic drivers of this disease are unknown. Through whole exome sequencing of 68 HSTLs, we define recurrently mutated driver genes and copy number alterations in the disease. Chromatin modifying genes including SETD2, INO80 and ARID1B were commonly mutated in HSTL, affecting 62% of cases. HSTLs manifest frequent mutations in STAT5B (31%), STAT3 (9%), and PIK3CD (9%) for which there currently exist potential targeted therapies. In addition, we noted less frequent events in EZH2, KRAS and TP53. SETD2 was the most frequently silenced gene in HSTL. We experimentally demonstrated that SETD2 acts as a tumor suppressor gene. In addition, we found that mutations in STAT5B and PIK3CD activate critical signaling pathways important to cell survival in HSTL. Our work thus defines the genetic landscape of HSTL and implicates novel gene mutations linked to HSTL pathogenesis and potential treatment targets