Pricing contingent convertibles: a general framework for application in practice

The first contingent convertibles (CoCo) were issued in 2009, but, to date, the academic community has not given much attention to practical issues of pricing them. Combining various aspects from existing theoretical and practical literature, this paper first presents a CoCo pricing framework that allows a flexible and comprehensible valuation of real-world equity or TIER-1 ratio-triggered CoCos. The model is based on the assumption that the issuer's total asset value follows a Brownian motion, that book values reflect fair economic values in the case of financial distress, and that there is a linear relationship between straight equity and TIER-1 ratios. The pricing methodology is then applied to the Credit Suisse Buffer Capital Note issued in February 201

Glucocorticosteroid-induced spinal osteoporosis: scientific update on pathophysiology and treatment

Glucocorticosteroid-induced osteoporosis (GIOP) is the most frequent of all secondary types of osteoporosis. The understanding of the pathophysiology of glucocorticoid (GC) induced bone loss is of crucial importance for appropriate treatment and prevention of debilitating fractures that occur predominantly in the spine. GIOP results from depressed bone formation due to lower activity and higher death rate of osteoblasts on the one hand, and from increased bone resorption due to prolonged lifespan of osteoclasts on the other. In addition, calcium/phosphate metabolism may be disturbed through GC effects on gut, kidney, parathyroid glands and gonads. Therefore, therapeutic agents aim at restoring balanced bone cell activity by directly decreasing apoptosis rate of osteoblasts (e.g., cyclical parathyroid hormone) or by increasing apoptosis rate of osteoclasts (e.g., bisphosphonates). Other therapeutical efforts aim at maintaining/restoring calcium/phosphate homeostasis: improving intestinal calcium absorption (using calcium supplementation, vitamin D and derivates) and avoiding increased urinary calcium loss (using thiazides) prevent or counteract a secondary hyperparathyroidism. Bisphosphonates, particularly the aminobisphosphonates risedronate and alendronate, have been shown to protect patients on GCs from (further) bone loss and to reduce vertebral fracture risk. Calcitonin may be of interest in situations where bisphosphonates are contraindicated or not applicable and in cases where acute pain due to vertebral fracture has to be managed. The intermittent administration of 1-34-parathormone may be an appealing treatment alternative, based on its documented anabolic effects on bone resulting from the reduction of osteoblastic apoptosis. Calcium and vitamin D should be a systematic adjunctive measure to any drug treatment for GIOP. Based on currently available evidence, fluoride, androgens, estrogens (opposed or unopposed) cannot be recommended for the prevention and treatment of GIOP. However, substitution of gonadal hormones may be indicated if GC-induced hypogonadism is present and leads to clinical symptoms. Data using the SERM raloxifene to treat or prevent GIOP are lacking, as are data using the promising bone anabolic agent strontium ranelate. Kyphoplasty performed in appropriately selected osteoporotic patients with painful vertebral fractures is a promising addition to current medical treatmen

BIOARTS IN SCIENCE-CITYSCAPES ETHNOGRAPHIC FRAGMENTS OF THE NEUROWORLD

Ph.DDOCTOR OF PHILOSOPH

Chemical characteristics of tsunami-affected groundwater and lagoon on the east coast of Sri Lanka

Previous studies have shown that groundwater on the east coast of Sri Lanka was heavily impacted by salinization due to the Dec. 26, 2004 tsunami. This study follows up on these initial studies to investigate the effect of the onset of the first rainy season after the tsunami on groundwater quality in the same areas. The results show that approx. 620 mm of rain falling between September and November 2005 improved the water quality with respect to salinity, decreasing the average well water salinity levels from 1250 to 950 μS/cm. A slight elevation in salinity levels in flooded vs. non-flooded wells (1240 vs. 780 μS/cm) in November indicated prolonged salinity impacts in the tsunami-affected areas. As opposed to salinity, groundwater quality deteriorated significantly with the first rains following the dry season with respect to nutrient content. Average well nitrate concentration was doubled (from 7.7 to 17.0 mg/l), with number of wells exceeding the WHO standard of 50 mg/l increasing from 2 to 9% with the rains

Host plant dependent disease progression of the microsporidian parasite Nosema tyriae on Cinnabar moth larvae

Tyria jacobaeae was introduced as a biological control agent to control the noxious weed Jacobea vulgaris. Eventually introduced to the Cascade mountain range of Oregon, T. jacobaeae has been found to feed on Senecio triangularis, a native plant closely related to J. vulgaris. Nosema tyriae is a parasitic fungus under the phylum Microspora (Microsporidians) and Tyria jacobaeae is the main host of the parasite (Canning et Al. 1999). Microsporidia infections of insect larvae exhibit slowed development, and increased mortality in both the larval and pupal stages. Nutritional content of the host plant has been shown to increase the effect of the pathogen N. tyriae on T. jacobaeae. This increase can lead to greater mortality and decreased insect performance of T. jacobaeae on its non-target host S. triangularis (McEvoy et Al. 2008). The objective of this study was to determine the difference between pathogen infection levels on the two host plants T. jacobaeae and S. triangularis. Based on previously documented higher mortality rates on S. triangularis (McEvoy et al. 2008), our hypothesis was that pathogens would multiply faster on S. triangularis than J. vulgaris and that the infection levels would increase in later stages with more time post-inoculation, and with greater spore dosages. Host plant had no significant effect on levels of N. tyriae (intercept: χ² =30.2, df=1, P = 0.52) or disease progression (slope: χ² =1.09, df=1, P = 0.9). The effect of dose on disease progression was not significant (slope: χ² =3.4, df=1, P = 0.82), while the effect of dose on disease levels was marginally significant (intercept: χ² =212.6, df=1, P = 0.09)

«Sat fats»: Sind Milch, Butter und Käse rehabilitiert?

In den letzten Jahren hat sich in der Ernährungsforschung wieder vermehrt die Meinung durchgesetzt, dass Milchprodukte und die darin enthaltenen «Sat fats» (saturated fatty acids, gesättigte Fettsäuren) weniger schädlich sind als einst angenommen und auch durchaus einen positiven, gesundheitlichen Nutzen haben können, wenn massvoll genossen. Laut aktuellstem Forschungsstand gibt es keinen Grund, Milch, Butter und Käse gänzlich aus den Kühlschränken zu verbannen

Gastric lactobezoar - a rare disorder?

Gastric lactobezoar, a pathological conglomeration of milk and mucus in the stomach of milk-fed infants often causing gastric outlet obstruction, is a rarely reported disorder (96 cases since its first description in 1959). While most patients were described 1975-1985 only 26 children have been published since 1986. Clinically, gastric lactobezoars frequently manifest as acute abdomen with abdominal distension (61.0% of 96 patients), vomiting (54.2%), diarrhea (21.9%), and/or a palpable abdominal mass (19.8%). Respiratory (23.0%) and cardiocirculatory (16.7%) symptoms are not uncommon. The pathogenesis of lactobezoar formation is multifactorial: exogenous influences such as high casein content (54.2%), medium chain triglycerides (54.2%) or enhanced caloric density (65.6%) of infant milk as well as endogenous factors including immature gastrointestinal functions (66.0%), dehydration (27.5%) and many other mechanisms have been suggested. Diagnosis is easy if the potential presence of a gastric lactobezoar is thought of, and is based on a history of inappropriate milk feeding, signs of acute abdomen and characteristic features of diagnostic imaging. Previously, plain and/or air-, clear fluid- or opaque contrast medium radiography techniques were used to demonstrate a mass free-floating in the lumen of the stomach. This feature differentiates a gastric lactobezoar from intussusception or an abdominal neoplasm. Currently, abdominal ultrasound, showing highly echogenic intrabezoaric air trapping, is the diagnostic method of choice. However, identifying a gastric lactobezoar requires an investigator experienced in gastrointestinal problems of infancy as can be appreciated from the results of our review which show that in not even a single patient gastric lactobezoar was initially considered as a possible differential diagnosis. Furthermore, in over 30% of plain radiographs reported, diagnosis was initially missed although a lactobezoar was clearly demonstrable on repeat evaluation of the same X-ray films. Enhanced diagnostic sensitivity would be most rewarding since management consisting of cessation of oral feedings combined with administration of intravenous fluids and gastric lavage is easy and resolves over 85% of gastric lactobezoars. In conclusion, gastric lactobezoar is a disorder of unknown prevalence and is nowadays very rarely published, possibly because of inadequate diagnostic sensitivity and/or not yet identified but beneficial modifications of patient management

ost in promiscuity? An evolutionary and biochemical evaluation of HSD10 function in cardiolipin metabolism

Multifunctional proteins are challenging as it can be difficult to confirm pathomechanisms associated with disease-causing genetic variants. The human 17β-hydroxysteroid dehydrogenase 10 (HSD10) is a moonlighting enzyme with at least two structurally and catalytically unrelated functions. HSD10 disease was originally described as a disorder of isoleucine metabolism, but the clinical manifestations were subsequently shown to be linked to impaired mtDNA transcript processing due to deficient function of HSD10 in the mtRNase P complex. A surprisingly large number of other, mostly enzymatic and potentially clinically relevant functions have been attributed to HSD10. Recently, HSD10 was reported to exhibit phospholipase C-like activity towards cardiolipins (CL), important mitochondrial phospholipids. To assess the physiological role of the proposed CL-cleaving function, we studied CL architectures in living cells and patient fibroblasts in different genetic backgrounds and lipid environments using our well-established LC–MS/MS cardiolipidomic pipeline. These experiments revealed no measurable effect on CLs, indicating that HSD10 does not have a physiologically relevant function towards CL metabolism. Evolutionary constraints could explain the broad range of reported substrates for HSD10 in vitro. The combination of an essential structural with a non-essential enzymatic function in the same protein could direct the evolutionary trajectory towards improvement of the former, thereby increasing the flexibility of the binding pocket, which is consistent with the results presented here