Omien osakkeiden takaisinostot tie ylisuuriin tuottoihin:totta vai tarua?

Tiivistelmä. Osingot on perinteisesti mielletty keinoksi jakaa yhtiöiden ylimääräisiä kassavarantoja omistajille. Yhdysvalloissa sallittiin omien osakkeiden takaisinostot 1980-luvulla. Takaisinostot ovat saavuttaneet kansainvälisesti suuren suosion yhtiöiden keskuudessa ylimääräisten kassavarantojen jakamisen keinona. Tämän Pro gradu -tutkielman tarkoituksena on selvittää, miten markkinat reagoivat lyhyellä aikajänteellä Helsingin pörssiin listattujen yhtiöiden omien osakkeiden takaisinostoihin. Aihetta on tutkittu aiemmin kansainvälisesti, jolloin on havaittu omien osakkeiden takaisinostojen aiheuttaneen positiivisen reaktion markkinoilla. Suomessa tehtyjen tutkimuksien tulokset ovat linjassa kansainvälisten tutkimuksien kanssa. Tässä Pro gradu -tutkielmassa tutkitaan omien osakkeiden takaisinostojen aloittamisilmoituksien vaikutusta Helsingin pörssiin listattujen yhtiöiden markkina-arvoihin aikavälillä 2010–2020. Tutkielman lopullisessa otoksessa aloittamisilmoituksia on yhteensä 128. Markkinoiden reaktiota tutkitaan aloittamisilmoituksien ympärillä. Tämän tutkielman tutkimusmenetelmä on tapahtumatutkimus, mikä auttaa havainnoimaan markkinoiden reaktiota ja ylisuurien tuottojen syntymistä. Tapahtumaikkuna pitää sisällään yhteensä 58 päivää. Tapahtumaikkuna sisältää yhdeksän päivää ennen omien osakkeiden takaisinostojen aloittamisilmoituksia ja 48 päivää aloittamisilmoituksien jälkeen. Aihetta tutkimalla saadaan havaintoja siitä, päteekö tehokkaiden markkinoiden keskivahvat ehdot Helsingin pörssissä. Tämän Pro gradu -tutkielman tulokset osoittavat, että Suomen osakemarkkinat ottavat omien osakkeiden takaisinostot positiivisesti vastaan, sillä ilmoituspäivänä ja tätä seuraavana kaupankäyntipäivänä havaitaan positiivisia ylisuuria tuottoja. Kumulatiiviset ylisuuret tuotot ovat myös positiivisia omien osakkeiden takaisinostojen aloittamisilmoituksien ympärillä. Tuloksien avulla voidaan myös todeta, että markkinat eivät ole aina tehokkaita Helsingin pörssissä keskivahvojen ehtojen näkökulmasta

Functional polymorphisms in the P2X7 receptor gene are associated with stress fracture injury

Context: Military recruits and elite athletes are susceptible to stress fracture injuries. Genetic predisposition has been postulated to have a role in their development. The P2X7 receptor (P2X7R) gene, a key regulator of bone remodelling, is a genetic candidate that may contribute to stress fracture predisposition. Objective: To evaluate the putative contribution of P2X7R to stress fracture injury in two separate cohorts, military personnel and elite athletes. Methods: In 210 Israeli Defence Forces (IDF) military conscripts, stress fracture injury was diagnosed (n=43) based on symptoms and a positive bone scan. In a separate cohort of 518 elite athletes, self-reported medical imaging scan-certified stress fracture injuries were recorded (n=125). Non-stress fracture controls were identified from these cohorts who had a normal bone scan or no history or symptoms of stress fracture injury. Study participants were genotyped for functional SNPs within the P2X7R gene using proprietary fluorescence-based competitive allele-specific PCR assay. Pearson Chi-square (χ2) tests, corrected for multiple comparisons, were used to assess associations in genotype frequencies. Results: The variant allele of P2X7R SNP rs3751143 (Glu496Ala- loss of function) was associated with stress fracture injury, while the variant allele of rs1718119 (Ala348Thr- gain of function) was associated with a reduced occurrence of stress fracture injury in military conscripts (P<0.05). The association of the variant allele of rs3751143 with stress fractures was replicated in elite athletes (P<0.05), whereas the variant allele of rs1718119 was also associated with reduced multiple stress fracture cases in elite athletes (P<0.05). Conclusions: The association between independent P2X7R polymorphisms with stress fracture prevalence supports the role of a genetic predisposition in the development of stress fracture injury

Exercise and bone health across the lifespan

With ageing, bone tissue undergoes significant compositional, architectural and metabolic alterations potentially leading to osteoporosis. Osteoporosis is the most prevalent bone disorder, which is characterised by progressive bone weakening and an increased risk of fragility fractures. Although this metabolic disease is conventionally associated with ageing and menopause, the predisposing factors are thought to be established during childhood and adolescence. In light of this, exercise interventions implemented during maturation are likely to be highly beneficial as part of a long-term strategy to maximise peak bone mass and hence delay the onset of age- or menopause-related osteoporosis. This notion is supported by data on exercise interventions implemented during childhood and adolescence, which confirmed that weight-bearing activity, particularly if undertaken during peripubertal development, is capable of generating a significant osteogenic response leading to bone anabolism. Recent work on human ageing and epigenetics suggests that undertaking exercise after the fourth decade of life is still important, given the anti-ageing effect and health benefits provided, potentially occurring via a delay in telomere shortening and modification of DNA methylation patterns associated with ageing. Exercise is among the primary modifiable factors capable of influencing bone health by preserving bone mass and strength, preventing the death of bone cells and anti-ageing action provided

In quest of genetic susceptibility to disorders manifesting in fractures:assessing the significance of genetic factors in femoral neck stress fractures and childhood non-OI primary osteoporosis

Abstract Osteoporosis is a bone disorder that leads to a reduction in bone volume, deterioration of bone microarchitecture and therefore increased fracture risk. Bone disorders such as osteoporosis commonly have both genetic and environmental components. Family and twin studies have shown the importance of genetics in bone formation and health, but most of the genetic factors contributing to bone formation are still largely unknown. The aim of this thesis was to search for and identify genetic factors that predispose to two different bone disorders manifesting in fractures, namely femoral neck stress fractures and childhood primary osteoporosis without features of OI (i.e. non-OI primary osteoporosis). Furthermore, in vitro studies were performed to elucidate the importance and mechanism of action of identified genetic factors in non-OI primary osteoporosis. By using candidate gene analyses we identified predisposing alleles, haplotypes and their interactions that increased the risk for femoral neck stress fractures in young male military conscripts. The conscripts lacking the CTR C allele and/or VDR C-A haplotype had a three-fold increased risk for femoral neck stress fractures compared to the carriers of both. Furthermore, conscripts carrying the LRP5 A-G-G-C haplotype had a three-fold increased risk for femoral neck stress fractures and in combination with VDR C-A haplotype a four-fold increased risk for stress fractures. These associations were mediated by low body weight and BMI. In the search for genetic factors of non-OI primary osteoporosis in children and adolescent, two novel mutations in LRP5 and two more variants in WNT3A and DKK1 were found in patients. The variants were also observed in the affected family members, but not in the control group. The effects of these variants were examined in in vitro studies and the results showed that some LRP5 mutations and the WNT3A variant might reduce bone formation by decreasing the canonical Wnt signalling activity.Tiivistelmä Osteoporoosi on luustosairaus, joka alentaa luuntiheyttä ja heikentää luun rakennetta ja siten lisää murtumien riskiä. Osteoporoosin kaltaiset luusairaudet ovat usein monitekijäisiä tauteja, joiden syntyyn vaikuttavat sekä perinnölliset että ympäristölliset tekijät. Perhe- ja kaksostutkimukset ovat osoittaneet perinnöllisten tekijöiden olevan tärkeitä luun muodostuksessa ja terveydessä, mutta nämä tekijät ovat kuitenkin vielä suurelta osin tuntemattomia. Tutkimustyön tavoitteena oli etsiä ja tunnistaa perinnöllisiä tekijöitä, jotka altistavat kahdelle luunmurtumina ilmenevälle sairaudelle: reisiluunkaulan rasitusmurtumille ja lasten primaariselle osteoporoosille. Lisäksi primaariselle osteoporoosille altistavien perinnöllisten tekijöiden merkitystä ja vaikutusmekanismeja tutkittiin in vitro- kokeilla. Reisiluunkaulan rasitusmurtumille altistavien alleelien, haplotyyppien ja näiden vuorovaikutusten tunnistamiseen käytettiin ehdokasgeenianalyysiä nuorten alokkaiden aineistossa. Potilailla, joilta CTR-geenin C-alleeli ja/tai VDR-geenin C-A haplotyyppi puuttuivat, oli kolminkertainen riski rasitusmurtumien syntyyn molempien geenimuotojen kantajiin verrattuna. Myös LRP5-geenin A-G-G-C haplotyypin kantajilla oli kolminkertainen riski rasitusmurtumiin ja VDR-geenin C-A haplotyyppi ja A-G-G-C yhdessä lähes nelinkertaistivat rasitusmurtumien riskin alokkailla. Näiden assosiaatioiden todettiin välittyvän alhaisen painon ja painoindeksin välityksellä. Lapsuudessa tai varhaisnuoruudessa puhkeavan primaarisen osteoporoosin perinnöllisten tekijöiden etsinnässä löydettiin kaksi uutta mutaatiota LRP5-geenistä ja yhteensä kaksi uutta muutosta WNT3A- ja DKK1-geeneistä. Uusien ehdokasgeenilöydösten osuutta primaarisen osteoporoosin syntyyn tukee se, että muutokset löydettiin potilaiden lisäksi heidän sairailta sukulaisiltaan eikä muutoksia havaittu kontrolliaineistoissa. Uusien mutaatioiden mahdollisia vaikutuksia tutkittiin in vitro-kokein, jotka osoittivat, että eräät LRP5-geenin mutaatiot ja WNT3A-geenin muutos alentavat kanonisen Wnt-signalointireitin aktiivisuutta ja voivat siten vähentää luunmuodostusta

New genetic variants in CYP2B6 and SLC6A support the role of oxidative stress in familial Ménière’s disease

Abstract The objective was to study the genetic etiology of Ménière’s disease (MD) using next-generation sequencing in three families with three cases of MD. Whole exome sequencing was used to identify rare genetic variants co-segregating with MD in Finnish families. In silico estimations and population databases were used to estimate the frequency and pathogenicity of the variants. Variants were validated and genotyped from additional family members using capillary sequencing. A geneMANIA analysis was conducted to investigate the functional pathways and protein interactions of candidate genes. Seven rare variants were identified to co-segregate with MD in the three families: one variant in the CYP2B6 gene in family I, one variant in GUSB and EPB42 in family II, and one variant in each of the SLC6A, ASPM, KNTC1, and OVCH1 genes in family III. Four of these genes were linked to the same co-expression network with previous familial MD candidate genes. Dysfunction of CYP2B6 and SLC6A could predispose to MD via the oxidative stress pathway. Identification of ASPM and KNTC1 as candidate genes for MD suggests dysregulation of mitotic spindle formation in familial MD. The genetic etiology of familial MD is heterogenic. Our findings suggest a role for genes acting on oxidative stress and mitotic spindle formation in MD but also highlight the genetic complexity of MD

System analysis and design of mmW mobile backhaul transceiver at 28 GHz

Abstract In the next generation of mobile network, 5G, mm-wave (mmW) communication is considered one of the main disruptive technologies to increase data rates and improve spectrum efficiency. Wireless backhaul with stationary or moving nodes is one of the best candidate use-cases. This paper provides a comprehensive analysis on the architecture and design of mmW transceiver with automatic gain control (AGC) for mobility management. The focus is on the RF component requirements, especially, power amplifiers, low-noise amplifier and antennas as well as on their impact on the link-budget. Results are provided based on real figures of commercial components

Integrated Proteomics Identified Up-regulated Focal Adhesion-mediated Proteins In Human Squamous Cell Carcinoma In An Orthotopic Murine Model

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