Nueva ley polaca de grupos de sociedades. Un análisis crítico.

This article presents and critically analyses the amendment of the Polish Commercial Companies Code, which entered into force in October 2022 and introduced, among others, the provisions of art. 211 to 2116 and art. 4 § 1 point 51 CCC, which regulate the new Polish law on groups of companies. The new legal institutions, including the binding order of the controlling company, are discussed, pointing out their shortcomings and practical problems.Este artículo presenta y analiza críticamente la modificación del Código de Sociedades Mercantiles polaco, que entró en vigor en octubre de 2022 e introdujo, entre otras, las disposiciones de los artículos 211 a 2116 y del artículo 4 § 1 punto 51 CSM, que regulan la nueva ley polaca de grupos de sociedades. Se debaten las nuevas instituciones jurídicas, incluido la orden vinculante de sociedad dominante, señalando sus deficiencias y problemas prácticos

Novel KCNQ1 mutations in patients after myocardial infarction

Background: Patients after myocardial infarction (MI) are at greater risk of sudden cardiac death (SCD) than people in the overall population. The aim of this study was to detect mutations, including intronic ones, in the KCNQ1 gene coding for proteins of cardiac potassium channels and evaluate their possible effects on the clinical course in patients after MI. Methods: The study group was composed of 100 Polish patients after MI, which included 27 women (mean age 69 years) and 73 men (mean age 67 years). All patients underwent clinical examinations and genetic tests. The genetic test results have been correlated with the clinical data. The following parameters have been chosen as endpoints for this survey: sudden cardiac arrest (SCA) or SCD, complex ventricular arrhythmia, QT interval and QT dispersion values assessed during 24-hour Holter ECG monitoring in relation to ventricular arrhythmias as well as the minimum and maximum heart rate (HR) observed during the examination. Results: Six new mutations in the KCNQ1 gene: C2505734T, A2753831C in exons and C2505846A, G2753881A, T2755854C, T2755875G in introns. Detected intronic mutations in patients after MI were related to a worse clinical course and frequent occurrence of SCA. Conclusions: The novel intronic mutations may have a significant influence on the clinical course of the disease. (Cardiol J 2008; 15: 252-260

Daily levels of sex hormones in 15 subfertile women formulate a menstrual cycle profile predominant with progesterone secretion

Introduction: Changes in sex hormone secretions during the menstrual cycle may affect fertility. It has been shown that a prematurely raised progesterone (P4) level after therapeutic injection of human chorionic gonadotropin caused changes in endometrial gene expression and lowered the pregnancy rate. The aim of the present study was to investigate the complete menstrual patterns of P4 together with its derivatives testosterone (T) and oestradiol (E2) in subfertile women during their natural cycles. Material and methods: Daily serum levels of P4 (ng/mL), T (ng/mL), E2 (pg/mL), and sex hormone binding protein (SHBG, nmol/L) were measured throughout a single 23–28-day menstrual cycle in 15 subfertile women aged 28–40 years with patent oviducts and normospermic partners. Knowing SHBG levels, the free androgen (FAI) and free oestrogen (FEI) indexes were calculated for each cycle day in each patient. Results: Baseline (cycle day one) levels of luteinising hormone (LH), thyroid stimulating hormone (TSH), P4, and T were comparable with reference intervals for a normal cycle, whereas follicle stimulating hormone (FSH), E2, and SHBG exceeded those. During cycles, the levels of P4 correlated positively with E2 levels (r = 0.38, p < 0.05, n = 392) an  negatively with T (r = –0.13, p < 0.05, n = 391). T correlated negatively with E2 (r = –0.19, p < 0.05, n = 391). Menstrual cycle phases were hidden. The curve of the mean/median daily levels of P4 rose prematurely, was parallel with the E2 rise, and culminated closely, but with more than 4 times greater amplitude of P4 (2571% of baseline levels in day 16) than of E2 (580% in day 14). In turn, the curve of T declined in a U-shaped manner with a nadir (–27%) on day 16. Averaged daily levels of FEI, but not FAI, varied significantly between 23 and 26 days long and the 27–28-day cycles. Conclusions: 1. Throughout the entire menstrual cycle length in subfertile women, P4 secretion predominates quantitatively over secretions of the remaining sex hormones when menstrual cycle phases are hidden. 2. The rise of E2 secretion is in parallel with the P4 rise, but with 4 times lower amplitude of E2. 3. T secretion declines and is inversely related to both P4 and E2 secretions. 4. Changes in E2 bioavailability are related to menstrual cycle length.

Genome-wide analysis and expression profiling of calcium-dependent protein kinases in potato (Solanum tuberosum)

Calcium-dependent protein kinases (CDPKs or CPKs), unique to plants and some protists, are involved in growth and developmental processes as well as in defence against diverse environmental stresses. CDPKs are encoded by multi-gene families. Despite extensive studies of the CDPKs in many species, information about the evolutionary history and expression patterns of the CDPK family in the staple crop potato (Solanum tuberosum) remains poorly known. In this study, we performed bioinformatics analysis of the potato whole genome sequence and identified 23 potential CDPK genes. These genes are located in eleven, of twelve, potato chromosomes. Based on the phylogenetic tree and gene structures, the CDPKs were divided into four subfamilies. To determine their expression, reverse transcription quantitative polymerase chain reaction (RT-qPCR) analysis was carried out for the CDPK genes in different organs of potato such as young and mature leaves, stems, young shoots, roots, stolons, swollen stolons, flowers and tubers. The CDPKs were expressed in all the organs analysed, but their expression patterns varied greatly. The expression of some CDPKs was strongly organ specific, for example StCPK13 and StCPK18 was found only/ mostly in flowers. In Solanum genotypes differing in resistance to Phytophthora infestans, the expression and activity of CDPKs increased in response to a P. infestans elicitor with different kinetics and intensity. The expression levels and activity of the CDPKs correlated positively with the level of the resistance. Our results support earlier suggestion that CDPKs are involved in potato organ development and defence against stresses. We provide new information about the CDPK gene family in the potato and a perspective on its evolutionary history and biological roles of the individual kinases

Concepts of independence and impartiality of the judiciary in the light of regulations and case-law

W artykule podjęto próbę analizy pojęć niezawisłości sędziów, niezależności sądów oraz bezstronności sądu. Przedstawiono uregulowania prawne oraz wykładnię sądów i trybunałów na poziomie krajowym i europejskim posiłkując się przy tym poglądami doktryny. Celem opracowania jest zaproponowanie uporządkowania narracji w przedmiocie rozumienia wskazanych terminów – na podstawie dotychczasowej judykatury. Terminy „niezawisłość”, „niezależność” i „bezstronność” są nie tylko doniosłe teoretycznie i praktycznie, ale obecnie żywo dyskutowane i nic nie wskazuje na to, aby w najbliższym czasie uległo to zmianie. Rozważenie znaczenia terminów i zaproponowanie ich rozgraniczenia niesie za sobą konsekwencje dla funkcjonowania całego systemu prawa.The article deals with an issue of understanding of the concepts indicated in the title which are subject of interpretation of courts and tribunals at a national and European level. The aim of the analysis is to find out how the above phrases are understood and to propose a way to organize them. The proper meaning of the terms: “independence”, and “impartiality” is not only theoretically and practically significant, but is also currently under discussion. The consideration of these terms is therefore of fundamental importance for the functioning of the entire legal system

Towards Understanding Human Mitochondrial Leucine Aminoacylation Identity

International audienceSpecific recognition of tRNAs by aminoacyl-tRNA synthetases is governed by sets of aminoacylation identity elements, well defined for numerous prokaryotic systems and eukaryotic cytosolic systems. Only restricted information is available for aminoacylation of human mito-chondrial tRNAs, despite their particularities linked to the non-classical structures of the tRNAs and their involvement in a growing number of human neurodegenerative disorders linked to mutations in the corresponding tRNA genes. A major difficulty to be overcome is the preparation of active in vitro transcripts enabling a rational mutagenic analysis, as is currently performed for classical tRNAs. Here, structural and aminoacylation properties of in vitro transcribed tRNA Leu(UUR) are presented. Solution probing using a combination of enzymatic and chemical tools revealed only partial folding into an L-shaped structure, with an acceptor branch but with a floppy anticodon branch. Optimization of aminoacylation conditions allowed charging of up to 75% of molecules, showing that, despite its partially relaxed structure, in vitro transcribed tRNA Leu(UUR) is able to adapt to the synthetase. In addition, mutational analysis demonstrates that the discriminator base as well as residue A14 are important leucine identity elements. Thus, human mitochondrial leucylation is dependent on rules similar to those that apply in Escherichia coli. The impact of a subset of pathology-related mutations on amino-acylation and on tRNA structure, has been explored. These variants do not show significant structural rearrangements and either do not affect aminoacylation (mutations T3250C, T3271C, C3303T) or lead to marked effects. Interestingly, two variants with a mutation at the same position (A3243G and A3243T) lead to markedly different losses in aminoacylation efficiencies (tenfold and 300-fold, respectively)

Artykuł oryginalnyZwiązek pomiędzy polimorfizmami w genach SCN5A, KCNQ1 i KCNE1 a złożonymi komorowymi zaburzeniami rytmu u chorych po zawale serca

Background: Post-MI patients are highly susceptible to sudden cardiac arrest (SCA) and sudden cardiac death (SCD) resulting from ventricular arrhythmia (VA). The search for new clinical predictors to identify those patients who are at the highest risk of these events is therefore essential. Numerous data indicate that the presence of polymorphisms and mutations in the cardiac ion channel genes SCN5A, KCNQ1 and KCNE1 might serve as such a predictor. Since genetic alterations in these genes underlie congenital long QT syndrome (LQTS), which is associated with an increased occurrence of arrhythmic complications and SCD, we decided to verify how alterations in these genes contribute to QT interval abnormalities and consequently to VA, SCA and SCD in post-MI patients. Aim: To detect single nucleotide polymorphisms (SNP) in SCN5A, KCNQ1 and KCNE1 of post-MI patients, and to assess whether they are related to electrophysiological markers of cardiac arrhythmia (QT interval) and the clinical course. Method: The study group consisted of 100 patients (27 females, mean age 69 years) with documented MI 3 months before enrolment. All patients underwent baseline and (after 12 months) control examinations encompassing history, physical examination, basic laboratory analysis, resting 12-lead ECG, 24-hour 12-lead Holter ECG monitoring and echocardiography. Genetic tests were performed during baseline examination. Results: In post-MI patients two exonic polymorphisms, H558R in SCN5A and S38G in KCNE1, and two intronic ones, in KCNQ1, were detected. H558R was associated with an increase in QT dispersion (QTd) at minimum and maximum heart rate and QT interval prolongation before premature ventricular beats (PVB), whereas S38G and intronic polymorphisms were related to an increase in QTd before PVB. None of the above polymorphisms was related to complex VA, SCA or SCD. Conclusion: The above polymorphisms were associated with abnormal repolarisation phase patterns in post-MI patients, which manifested in QT interval prolongation and QTd increase. There was no relationship between these polymorphisms and complex VA, SCA or SCD. The results show that not only exonic alterations but also intronic ones may affect the phenotype.Wstęp: Wysokie zagrożenie nagłym zatrzymaniem krążenia (NZK) i nagłym zgonem sercowym (NZS), u podłoża którego leżą groźne komorowe zaburzenia rytmu (KZR), u chorych po zawale serca skłania do poszukiwania nowych wskaźników klinicznych, które z dużym prawdopodobieństwem pozwoliłyby na wyodrębnienie spośród nich osób o najwyższym ryzyku tych zdarzeń sercowych. Coraz więcej doniesień wskazuje, że obecność mutacji i polimorfizmów w genach sercowych kanałów jonowych SCN5A i KCNQ1, KCNE1 może stanowić właśnie taki wskaźnik. Ponieważ zmiany w tych genach mogą powodować wrodzone zespoły wydłużonego odstępu QT, który związany jest ze zwiększoną częstością występowania powikłań arytmicznych i NZS, postanowiono sprawdzić, w jakim stopniu zmiany w tych genach przyczyniają się do nieprawidłowości odstępu QT, a tym samym złożonych KZR, NZK i NZS u chorych po zawale serca. Cel: Celem badania w tej grupie chorych było poszukiwanie zmian w genotypie w postaci polimorfizmów pojedynczych nukleotydów (ang. single nucleotide polymorphism, SNP) w genach SCN5A, KCNQ1 i KCNE1. Następnie ocena, czy stwierdzone zaburzenia genetyczne mają związek z elektrofizjologicznym markerem ryzyka zaburzeń rytmu serca, jak odstęp QT, oraz ocena związku pomiędzy stwierdzonymi zmianami w genotypie a klinicznym przebiegiem choroby: złożonymi KZR, NZK i NZS. Dodatkowo sprawdzano, czy zmiany w intronach genów mogą wpływać na przebieg kliniczny. Metodyka: Badaniem objęto 100 osób z populacji polskiej z udokumentowanym przebytym co najmniej przed 3 mies. zawałem serca. U wszystkich pacjentów przeprowadzono badanie wstępne i po 12 mies. kontrolne. Obejmowały one wywiad, badanie przedmiotowe, podstawowe badania laboratoryjne, spoczynkowe badanie EKG, 24-godzinne monitorowanie EKG metodą Holtera oraz badanie echokardiograficzne. W okresie badań wstępnych wykonano badania genetyczne. W analizie statystycznej korelowano dane genetyczne z danymi klinicznymi. Wyniki: U chorych po zawale serca w egzonach: genu SCN5A wykryto polimorfizm H558R, genu KCNE1 – S38G, natomiast w intronach genu KCNQ1 dwa polimorfizmy. Polimorfizm H558R związany był ze zwiększoną dyspersją QT w czasie wolnych i szybkich rytmów serca i z wydłużeniem odstępu QT przed przedwczesnymi pobudzeniami komorowymi, podczas gdy polimorfizmy S38G i intronowe ze zwiększoną dyspersją QT przed przedwczesnymi pobudzeniami komorowymi. Żaden z powyższych polimorfizmów nie był związany ze złożonymi KZR, NZK i NZS. Wnioski: Powyższe polimorfizmy u chorych po zawale serca związane były z nieprawidłowym przebiegiem fazy repolaryzacji, czego najwyraźniejszym przejawem było wydłużanie się odstępu QT i zwiększenie dyspersji QT. Nie wykazano związku polimorfizmów w tych genach ze złożonymi KZR, NZK ani NZS. Uzyskane wyniki wskazują, że nie tylko zmiany w egzonach, ale i w intronach mogą mieć wpływ na fenotyp