On the homeomorphism groups of manifolds and their universal coverings

Let $\mathcal H_c(M)$ stand for the path connected identity component of the group of all compactly supported homeomorphisms of a manifold $M$. It is shown that $\mathcal H_c(M)$ is perfect and simple under mild assumptions on $M$. Next, conjugation-invariant norms on \H_c(M) are considered and the boundedness of $\mathcal H_c(M)$ is investigated. Finally, the structure of the universal covering group of $\mathcal H_c(M)$ is studied.Comment: 19 page

Non-cognitive Values: A Warrant of the Rationality and Responsibility of Science

Although the presence of cognitive values in science has been accepted for half a century, until recently it was claimed that the presence of non-cognitive values threatened the rationality and objectivity of science and it was a sign of a scientist’s weakness. This view appeared to be correct when cognitive and non-cognitive values were treated dichotomously, and science was seen as a set of theories and procedures. The analysis of science as a social practice shows however that this dichotomy cannot be maintained and that the scientist, when planning and conducting research, makes assumptions which include value judgments encompassing certain non-cognitive values. Ignoring the presence of non-cognitive values does not secure objectivity and rationality of science. On the contrary, since they are constitutive elements of scientific research, pretending that they do not work in research exposes science to ideologization. Rational subordination of science to them becomes a vehicle and a warrant of not only rationality but also objectivity and social responsibility of science. This in turn allows us to restore the proper place of science in culture.Although the presence of cognitive values in science has been accepted for half a century, until recently it was claimed that the presence of non-cognitive values threatened the rationality and objectivity of science and it was a sign of a scientist’s weakness. This view appeared to be correct when cognitive and non-cognitive values were treated dichotomously, and science was seen as a set of theories and procedures. The analysis of science as a social practice shows however that this dichotomy cannot be maintained and that the scientist, when planning and conducting research, makes assumptions which include value judgments encompassing certain non-cognitive values. Ignoring the presence of non-cognitive values does not secure objectivity and rationality of science. On the contrary, since they are constitutive elements of scientific research, pretending that they do not work in research exposes science to ideologization. Rational subordination of science to them becomes a vehicle and a warrant of not only rationality but also objectivity and social responsibility of science. This in turn allows us to restore the proper place of science in culture

AKADEMICKA NAUKA PRZEMYSŁOWA I JEJ NORMY PRICE

Ćwierć wieku temu John Ziman sformułował tezę, iż nauka akademicka i nauka przemysłowa stapiają się w jeden system nauki postakademickiej i zarazem postprzemysłowej, w którym Mertonowskie normy nauki akademickiej wyrażone akronimem CUDOS (communism, universalism, disinterestedness, organized scepticism) ustępują miejsca normom nauki przemysłowej wyrażonym akronimem PLACE (proprietary, local, authoritarian, commissioned, expert). W niniejszym artykule bronię tezy, iż ów system wyewoluował w system akademickiej nauki przemysłowej, której normy można wyrazić akronimem PRICE: patron relevant, innovative, competitive, econometrical. Reformowanie nauki akademickiej okazuje się wobec tego także jej re-normowaniem w zakresie i etyki, i organizacji badań. Źródłem owej transformacji jest utożsamienie wiedzy z towarem. Etyka badań naukowych przekształca się w etykę produkcji wiedzy, a instytucje naukowe to producenci wiedzy, która staje się „towarem epistemicznym”, gdy jest na tenże fragment zapotrzebowanie jako na coś, co zaspokaja potrzeby „konsumentów”. Naukowcy są zaś elementem procesu produkcji wiedzy, a sam ten proces podlega kalkulacjom rynkowym. Nie podważa to epistemicznej wartości danego projektu badawczego i jego wyników, ale prowadzi do kontrowersyjnych konsekwencji, m.in. do fragmentaryzacji i aspektualizacji wiedzy, związania kierunków badawczych z interesami podmiotów władzy i ignorowania krytyki transformatywnej. W rezultacie niekiedy to, co było w nauce Mertonowskiej traktowane jako zagrożenie czy wykroczenie przeciwko etosowi nauki okazuje się racjonalnym zachowaniem przedsiębiorcy funkcjonującego na rynku dóbr i usług epistemicznych. Akademicka nauka przemysłowa nie jest też w stanie pełnić w społeczeństwie ról poza-instrumentalnych (kształtowania światopoglądu, wspierania społecznej racjonalności, dostarczania niezależnych ekspertów), które pełniła nauka akademicka. Próby zapobiegania tym problemom czy zagrożeniom będą zaś z góry skazane na niepowodzenie, ponieważ środki zaradcze są oparte na innym rozumieniu wiedzy

Somatic comorbidity in Polish patients with epilepsy

A wide spectrum of somatic and psychiatric disorders occurs frequently in patients with epilepsy, which adds to the burden of this disease. The aim of the study was to estimate the prevalence and risk factors of somatic comorbidities and analyze somatic comedication in adult patients with epilepsy. This study involved patients with epilepsy treated in university epilepsy clinic. Data on epilepsy, antiepileptic drugs (AEDs), somatic comorbidities, and their treatment were collected from a structured interview and from medical records. The sample population consisted of 636 patients (mean age, 35.3 years); 380 (59.7%) were female and 241 (37.9%) had well‑controlled epilepsy. At least 1 comorbid somatic condition was found in 216 patients (34%). The most prevalent somatic comorbidities were cardiovascular diseases, allergies, migraine, hyperlipidemia, thyroid disorders, and chronic lower respiratory diseases. Furthermore, 200 patients (31.4%) were prescribed at least 1 medication for somatic disorders. Logistic regression analysis revealed several independent risk factors for the occurrence of somatic comorbidities: older age, shorter duration of epilepsy, lower seizure frequency, and lower number of AEDs. Somatic comorbidities and comedication with non‑AEDs were found in one‑third of the relatively young cohort of adult patients with epilepsy. Patients with pharmacoresistant epilepsy may be at risk of underdiagnosis and undertreatment of somatic comorbidities. The presence of comorbidities may have implications for the diagnosis and treatment of seizure disorder and coexisting condition

Insulinopodobny czynnik 3 - nowy hormon związany z zespołem policystycznych jajników?

Introduction: The aim of this study was to find a correlation between insulin-like factor 3 (INSL3) and androgens: androstenedione (A), free testosterone (fT), and total testosterone (T), in two groups of polycystic ovary syndrome (PCOS) women: those with a body mass index (BMI) lower than 25 kg/m2 and those with a BMI higher than 25 kg/m2. The association between INSL3 and other serum parameters: luteinising hormone (LH), follicle-stimulating hormone (FSH), dehydroepiandrosterone sulphate (DHEA-S), sex hormone binding globulin (SHBG) and glucose and insulin were also investigated. Material and methods: The study group comprised 37 PCOS women aged 27 &#177; 4 years. The control group consisted of 34 healthy, premenopausal women (aged 24.2 &#177; 1.2) with regular menses and no signs of hyperandrogenism. There were 27 PCOS women of normal weight (BMI < 25 kg/m2), and ten overweight individuals (BMI &#8805; 25&#8211;30 kg/m2). Correlations between level of INSL3 and LH, FSH, T, fT, A, DHEA-S, SHBG, metabolic tests, height, weight, and WHR (waist-to-hip ratio) were also investigated. Results: PCOS women showed non-significantly higher levels of INSL3 compared to the healthy controls (64.6 &#177; 27.7 and 62.7 &#177; 20.0 ng/mL, respectively). However, we identified very strong correlations between INSL3 and androstenedione (r = 0.48, p = 0.0115), and free (r = 0.44, p = 0.0108) and total testosterone (r = 0.46, p = 0.0057) in the PCOS subgroup with a BMI of < 25 kg/m2. There was no statistically significant correlation between INSL3 and LH in any subject of the PCOS group, nor between INSL3 and FSH, DHEA-S, glucose, basal insulin concentration or HOMA-IR. Conclusions: We found a positive correlation between INSL3 and androgens in PCOS women, especially those with a BMI of < 25 kg/m2. This may play a key role in PCOS pathophysiology. (Endokrynol Pol 2012; 63 (5): 356-361)Wstęp: Celem pracy była analiza zależności między stężeniem insulinopodobnego czynnika 3 a stężeniami androgenów: androstendionu (A), wolnego testosteronu (fT) oraz całkowitego testosteronu (T) u kobiet z zespołem policystycznych jajników (PCOS), z uwzględnieniem wskaźnika masy ciała (BMI). Przedmiotem badania był także związek między INSL3 a hormonem luteotropowym (LH), folikulotropowym (FSH), siarczanem dehydroepiandrosteronu (DHEA-S), białkiem wiążącym hormony płciowe (SHBG) oraz stężeniami glukozy i insuliny. Materiał i metody: Badaną grupę stanowiło 37 kobiet z PCOS, średnia wieku 27 &#177; 4 lat. Grupę kontrolną stanowiły 34 zdrowe kobiety (średnia wieku 24,2 &#177; 1,2 roku) z regularnymi miesiączkami, bez objawów hiperandrogenizacji. Kobiety z PCOS podzielono na grupy pod względem masy ciała; grupę z prawidłową masą ciała tworzyło 27 kobiet, natomiast z nadwagą i otyłością - 10 badanych. Analizie poddano także zależności między stężeniem INSL3 i stężeniami LH, FSH, T, fT, A, DHEA-S, SHBG, glukozy i insuliny oraz wskaźniki antropometryczne (wzrost, masa ciała, wskaźnik talia-biodra). Wyniki: U kobiet z PCOS wykazano wyższe stężenie INSL3 w porównaniu z grupą kontrolną (64,6 &#177; 27,7 i 62,7 &#177; 20,0 ng/mL, odpowiednio). Wykazano silną zależność między stężeniem INSL3 a stężeniem androstendionu (r = 0,48; p = 0,0115), wolnego (r = 0,44; p = 0,0108) i całkowitego testosteronu (r = 0,46; p = 0,0057) w grupie kobiet z PCOS o prawidłowej masie ciała. Nie wykazano zależności między stężeniem INSL3 a stężeniami LH, FSH, DHEA-S, stężeniem glukozy, insuliny oraz wskaźnikiem insulinooporności HOMA. Wnioski: Wykazano związek między stężeniem INSL3 a androgenemią u kobiet z PCOS, szczególnie silnie wyrażoną u kobiet z prawidłową masą ciała, co może być istotne w patofizjologii PCOS. (Endokrynol Pol 2012; 63 (5): 356-361

ACE inhibitor therapy: Possible effective prevention of new-onset atrial fibrillation following cardiac surgery

Background: Atrial fibrillation (AF) is a common complication after coronary artery bypass grafting (CABG). The aims of the study were to assess possible predictors and identify modes of prevention of new-onset AF following coronary surgery. Methods: Retrospective clinical and statistical analysis was made of the medical records of 217 patients who had undergone coronary surgery. Results: AF occurred in 28% (61/217) of the patients. In univariate analysis the age of the patients with AF was higher (p = 0.0033), they had a longer history of coronary disease (p = 0.0417) and more had > 3 grafts (p < 0.05). Low ejection fraction (< 40%) was also a risk factor of arrhythmia (p < 0.0001). In multivariate regression analysis two independent predictors of AF were identified: no ACE inhibitor treatment before surgery (p = 0.0005) and age > 60 years (p < 0.01). Patients with AF had a higher mean heart rate after the procedure: 115 &#177; 34 vs. 78 &#177; 21/min (p < 0.0005). Patients treated with ACE inhibitors before and after surgery had a lower incidence of AF than non-treated patients: 8% vs. 48% (p < 0.0001) and 4% vs. 61%, p < 0.0001) respectively. Beta-blocker treatment before and after surgery resulted in a lower incidence of AF: at 23% vs. 75% (p < 0.001) and 19% vs. 96% (p < 0.0001), respectively. Conclusions: No ACE inhibitor therapy before surgery, advanced age, low ejection fraction, high post-procedure heart rate, duration of coronary disease and the number of grafts (corresponding to the length of the procedure) were found to be strong probable predictors of AF following cardiac surgery. ACE inhibitor therapy may be effective in the prevention of newonset AF. Treatment based on individual variables is crucial for proper treatment and to diminish the risk of arrhythmia. (Cardiol J 2007; 14: 274-280

Comparison of mutation profile between primary phyllodes tumors of the breast and their paired local recurrences

Phyllodes tumor of the breast (PTB) is a rare neoplasm and accounts for 0.2-2.0% of breast cancer in women. Histopathological diagnosis of the tumor is difficult, and histological features do not always predict the course of the disease and the risk of progression. Pathogenesis and molecular biological characteristics as well as PTB prognostic factors are unknown. In search for genetic factors affecting PTB progression, 10 patients were analyzed for whom material from the primary tumor and local recurrence was available. DNA isolated from paraffin blocks was sequenced using the next-generation sequencing method (NGS). In 4 pairs, consisting of primary tumor and local recurrence, probably pathogenic/pathogenic variants were detected, and in three pairs they were observed in the CDKN2A gene, while other variants were found in PTEN and TP53 genes. NGS results indicate that the above-mentioned variants are hereditary, which suggests that the CDKN2A gene might be involved in cancerogenesis of PTB. Additionally, the selected pathogenic variant of EGFR gene was exclusively detected in one recuurent tumor, which might suggest the involvement of this gene in the mechanism of progression. In order to determine if this variant is associated with progression, the frequency of this mutation should be examined in larger group of malignant and borderline tumors

Inflammatory Proteins HMGA2 and PRTN3 as Drivers of Vulvar Squamous Cell Carcinoma Progression.

Current knowledge on the biology of squamous cell vulvar carcinoma (VSCC) is limited. We aimed to identify protein markers of VSCC tumors that would permit to stratify patients by progression risk. Early-stage tumors from patients who progressed (progVSCC) and from those who were disease-free (d-fVSCC) during follow-up, along with normal vulvar tissues were examined by mass spectrometry-based proteomics. Differentially expressed proteins (DEPs) were then verified in solid tissues and blood samples of patients with VSCC tumors and vulvar premalignant lesions. In progVSCC vs. d-fVSCC tumors, the immune response was the most over-represented Gene Ontology category for the identified DEPs. Pathway profiling suggested bacterial infections to be linked to aggressive VSCC phenotypes. High Mobility Group AT-Hook 2 (HMGA2) and Proteinase 3 (PRTN3) were revealed as proteins predicting VSCC progression. HMGA2 and PRTN3 abundances are associated with an aggressive phenotype, and hold promise as markers for VSCC patient stratification. It appears that vulvovaginal microflora disturbances trigger an inflammatory response contributing to cancer progression, suggesting that bacterial rather than viral infection status should be considered in the development of targeted therapies in VSCC