Akustické vlastnosti slovního přízvuku ve čtené české anglictině

klíčová slova: česká angličtina, cizí přízvuk, slovní přízvuk, přízvučná slabika, trvání, f0, akustické vlastnosti. Tato studie zkoumá akustické vlastnosti slovního přízvuku v české angličtině. První kapitola vysvětluje problém cizího přízvuku z různých úhlů pohledu. Dále se zabývá různými vlivy na pociťovanou sílu cizího přízvuku. Závěrem je, že chybná realizace slovního přízvuku má jistě negativní vliv jak na hodnocení mluvčího tak na srozumitelnost řeči (Benrabah, 1997; Hahn, 2004; Cutler, 1984). V druhé kapitole porovnáváme výsledky studií, které zkoumaly mluvčí různých jazyků a předkládáme všeobecnou teorii osvojování akustických vlastností slovního přízvuku. Zajímají nás především f0 a trvání. Tato teorie, založená na hypotéze rysů (feature hypothesis) (McAllister et al., 2002 v Lee, Guion & Harada, 2006), říká, že jazyky, jejichž systém slovního přízvuku se podobá angličtině (např. holandština a arabština), používají akustické vlastnosti užívané v jejich rodném jazyce. Oproti tomu mluvčí jazyků s nekontrastivním slovním přízvukem (např. vietnamština a čeština) dávají přednost těm akustickým vlastnostem, které jsou v jejich rodném jazyce fonologicky aktivní na úrovni segmentů. Mluvčí vietnamštiny, tónového jazyka, preferují f0 před trváním vokálu (Nguyen, 2003), takže pro mluvčí češtiny,...key words: Czech English, foreign accent, word stress, word accent, stressed syllable, duration, f0, acoustic cues. This study investigates the acoustic properties of word stress in Czech English. The notion of foreign accent is introduced and its drawbacks are presented. Further on the various influences on the perceived degree, or strength, of foreign accent are discussed. Faulty realization of word stress is identified as one of the factors that contribute to unintelligibility of non-native speech (Benrabah, 1997; Hahn, 2004; Cutler, 1984). In Chapter 2 we compare the results of studies that used speakers of a variety of languages and form a basic theory on the acquisition of acoustic cues to word stress. We are mostly interested in f0 and duration. This theory, based on the feature hypothesis (McAllister et al., 2002 in Lee, Guion & Harada, 2006), states that languages that have a similar stress system to that of English (Dutch, Arabic) use their native cues to signal word stress, while non-contrastive languages (Vietnamese, Czech) prefer cue/s that are phonologically active on segmental level in their native language. Speakers of Vietnamese, a tone language, were found to prefer f0 over duration (Nguyen, 2003), so for Czech, a language that uses phonological vowel duration, it is expected that...Institute of PhoneticsFonetický ústavFaculty of ArtsFilozofická fakult

The endothelin antagonist bosentan: Hemodynamic effects during normoxia and hypoxic pulmonary hypertension in pigs

AbstractIn this study, we investigated the hemodynamic effects and receptor-blocking properties of the nonselective endothelin antagonist bosentan in pigs during normoxia and acute hypoxia. Hypoxic pulmonary hypertension was induced by decreasing the fraction of inhaled oxygen to 0.1. In a control group of pigs, hemodynamic parameters proved to be stable through 2 hours of hypoxia. Infusions of endothelin-1, endothelin-3, and sarafotoxin 6c into the pulmonary artery resulted in pulmonary and systemic vasoconstriction during normoxia, whereas endothelin administration during hypoxic pulmonary hypertension resulted in pulmonary vasodilation. After administration of bosentan, the vasopressor effect of endothelin-1 during normoxia was significantly attenuated and the pulmonary vasodilatory effect of endothelin-1 during hypoxia was reduced. Furthermore, the development of hypoxic pulmonary hypertension was significantly reduced by bosentan. In contrast, bosentan did not influence the pulmonary vasopressor response to the thromboxane mimic U-46619. We therefore conclude that vasopressor endothelin receptors seem to be activated by endogenous endothelin released during hypoxia, leading to an increase in the pulmonary vascular tone. (J THORAC CARDIOVASC SURG 1996;112:890-7

Personal comorbidities and their subsequent risks for liver, gallbladder and bile duct cancers

Many environmental risk factors for hepatobiliary cancers are known but whether they are associated with specific cancer types is unclear. We present here a novel approach of assessing standardized incidence ratios (SIRs) of previously diagnosed comorbidities for hepatocellular carcinoma (HCC), gallbladder cancer (GBC), cholangiocarcinoma (CCA) and ampullary cancer. The 13 comorbidities included alcohol and nonalcohol related liver disease, chronic obstructive pulmonary disease, gallstone disease, viral and other kinds of hepatitis, infection of bile ducts, hepatic and other autoimmune diseases, obesity and diabetes. Patients were identified from the Swedish Inpatient Register from 1987 to 2018, and their cancers were followed from 1997 onwards. SIRs for HCC were 80 to 100 in men and women diagnosed with hepatitis C virus and they were also >10 in patients diagnosed with hepatitis B virus, other kind of hepatitis, hepatic autoimmune disease and nonalcohol related liver disease. Many of these risks, as well as alcohol related liver disease, were either specific to HCC or were shared with intrahepatic CCA. For GBC, CCA and ampullary cancer infection of bile ducts was the main risk factor. Gallstone disease, nonhepatic autoimmune diseases and diabetes were associated with all hepatobiliary cancers. The limitations of the study include inability to cover some rare risk factors and limited follow-up time. Many of the considered comorbidities are characterized by chronic inflammation and/or overt immune disturbance in autoimmune diseases. The results suggest that local chronic inflammation and a related immune disturbance is the carcinogenic trigger for all these cancers.Peer reviewe

Familial Risks for Liver, Gallbladder and Bile Duct Cancers and for Their Risk Factors in Sweden, a Low-Incidence Country

Simple Summary Familial risk of cancer implies that two or more family members are diagnosed with the same cancer. This may be due to the genes or environmental factors that family members share. Familial risk for liver and gallbladder cancer is about 2.7 which means that when one family member is diagnosed with these cancers other family members have 2.7 times higher risk of being diagnosed with the same cancers compared to families were no member is yet diagnosed with these cancers. Risk between spouses is entirely due to shared environmental factors and for liver cancer there is a small risk. The most important way to prevent these cancers is to avoid their risk factors, alcohol, smoking and overweight, and to seek medical care for diabetes and liver infections. We used the Swedish Cancer Registry data to address familial risks for concordant (same) and discordant (different) hepatobiliary cancers, including their associations with any other cancers and with known risk factors. Risks were also assessed between spouses. The analysis covered Swedish families and their cancers between years 1958 and 2018. Adjusted familial risks were expressed as standardized incidence ratios (SIRs). Familial SIRs for concordant hepatocellular carcinoma (HCC) were 2.60, and for gallbladder cancer they were at the same level (2.76). Familial risk was also found for intrahepatic bile duct cancer and for female extrahepatic bile duct cancer. HCC was associated with lung and cervical cancers; extrahepatic bile duct and ampullary cancers were associated with colon and pancreatic cancers, suggesting Lynch syndrome. Among spouses, hepatobiliary cancer was associated with HCC, stomach, pancreatic, cervical and upper aerodigestive tract cancers. Among risk factors, family members diagnosed with alcohol-related disease showed association with HCC. The observed familial risks for hepatobiliary cancers were relatively high, and considering the poor prognosis of these cancers, prevention is of the utmost importance and should focus on moderation of alcohol consumption, vaccination/treatment of hepatitis viral infections and avoidance of overweight and other risk factors of type 2 diabetes.Peer reviewe

Familial Risks for Liver, Gallbladder and Bile Duct Cancers and for Their Risk Factors in Sweden, a Low-Incidence Country

Simple Summary Familial risk of cancer implies that two or more family members are diagnosed with the same cancer. This may be due to the genes or environmental factors that family members share. Familial risk for liver and gallbladder cancer is about 2.7 which means that when one family member is diagnosed with these cancers other family members have 2.7 times higher risk of being diagnosed with the same cancers compared to families were no member is yet diagnosed with these cancers. Risk between spouses is entirely due to shared environmental factors and for liver cancer there is a small risk. The most important way to prevent these cancers is to avoid their risk factors, alcohol, smoking and overweight, and to seek medical care for diabetes and liver infections. We used the Swedish Cancer Registry data to address familial risks for concordant (same) and discordant (different) hepatobiliary cancers, including their associations with any other cancers and with known risk factors. Risks were also assessed between spouses. The analysis covered Swedish families and their cancers between years 1958 and 2018. Adjusted familial risks were expressed as standardized incidence ratios (SIRs). Familial SIRs for concordant hepatocellular carcinoma (HCC) were 2.60, and for gallbladder cancer they were at the same level (2.76). Familial risk was also found for intrahepatic bile duct cancer and for female extrahepatic bile duct cancer. HCC was associated with lung and cervical cancers; extrahepatic bile duct and ampullary cancers were associated with colon and pancreatic cancers, suggesting Lynch syndrome. Among spouses, hepatobiliary cancer was associated with HCC, stomach, pancreatic, cervical and upper aerodigestive tract cancers. Among risk factors, family members diagnosed with alcohol-related disease showed association with HCC. The observed familial risks for hepatobiliary cancers were relatively high, and considering the poor prognosis of these cancers, prevention is of the utmost importance and should focus on moderation of alcohol consumption, vaccination/treatment of hepatitis viral infections and avoidance of overweight and other risk factors of type 2 diabetes.Peer reviewe

Second Primary Cancers After Liver, Gallbladder and Bile Duct Cancers, and These Cancers as Second Primary Cancers

Background: Second primary cancers (SPCs) are important clinically as they may negatively influence patient survival and they may tell about therapeutic side effects and general causes of cancer. Population-based literature concerning SPCs after hepatobiliary cancers is limited and here we assess risks of SPCs after hepatocellular cancer (HCC), and cancers of the gallbladder, bile ducts and ampulla of Vater. In reverse order, we consider the risk of hepatobiliary cancers as SPCs after any cancer. Methods: We used standardized incidence ratios (SIRs) to estimate bidirectional relative risks of subsequent cancers associated with hepatobiliary cancers. Cancer diagnoses were obtained from the Swedish Cancer Registry from years 1990 through 2015. Results: We identified 9997 primary HCCs, 1365 gallbladder cancers and 4721 bile duct cancers. After HCC, risks of four SPCs were increased: gallbladder (SIR = 4.38; 95% confidence interval 1.87-8.67), thyroid (4.13; 1.30-9.70), kidney (2.92; 1.66-4.47) and squamous cell skin (1.55; 1.02-2.26) cancers. In reverse order, HCC as SPC, in addition to the above cancers, associations included upper aerodigestive tract, esophageal, small intestinal and bladder cancers and non-Hodgkin lymphoma. For gallbladder and bile duct cancers, associations were found with small intestinal and pancreatic cancers. Conclusion: The results suggested that HCC is associated with two types of SPC, one related to shared environmental risk factors, such as alcohol, exemplified by upper aerodigestive tract and esophageal cancer, and the other related to immune dysfunction, exemplified by squamous cell skin cancer. SPCs associated with gallbladder and bile duct cancers suggest predisposition to mutations in the mismatch repair gene MLH1.Peer reviewe