Типологія синтаксичних конструкцій в німецькій та українській мовах

Німецька та українська мови є односистемними мовами: обидві належать до індоєвропейської мовної сім’ї. Спільні корені та тривалий період ізольованого розвитку, вказують на те, що вказані мови мають характеристики подібності та відмінності в своій внутрішній будові. Німецька та українська належать до синтетичного типу флективних мов. Це означає, що граматичне значення слів у них виражається, здебільшого, за допомогою системи флексій і реалізується в межах одного графічного слова. Але флективна система німецької мови бідніша, ніж у слов’янських мовах.Немецкий и украинский языки являются односистемными языками: оба принадлежат к индоевропейской языковой семье. Общие корни и длительный период изолированного развития, указывают на то, что указанные языки имеют характеристики сходства и различия в своем внутреннем строении. Немецкий и украинский принадлежат к синтетическому типу флективных языков. Это означает, что грамматическое значение слов в них выражается, в основном, с помощью системы флексий и реализуется в пределах одного графического слова. Но флективная система немецкого языка беднее, чем в славянских языках.German and Ukrainian are single-system languages: both belong to the Indo-European language family. Common roots and a long period of isolated development, indicate that these languages ​​have characteristics of similarity and differences in their internal structure. German and Ukrainian belong to the synthetic type of inflectional languages. This means that the grammatical meaning of words in them is expressed, mainly, with the help of a system of inflexions and is realized within a single graphic word. But the inflectional system of the German language is poorer than in the Slavic languages

Flow-chart of the subjects at risk of CD from south Italy.

<p>Characteristics, age and presence/absence of HLA-DQ2/DQ8 in a population at risk of CD (relatives of CD- and with CD-like symptoms subjects) attending the Department of Laboratory Medicine of the University of Naples Federico II/CEINGE-Center of Advanced Biotechnology (Naples, Italy) between 2003 and 2013.</p

Frequencies of HLA-DQ genotypes (A) and haplotypes (B) detected in 666 CD patients from south Italy.

<p>CD, celiac disease</p><p>^aGenotypes were based on the presence of the following haplotypes: DQ2.5 = DQA1*05-DQB1*02 (DRB1*03) alleles; DQ2.2 = DQA1*02-DQB1*02 (DRB1*07) alleles; DQ2.3 = DQA1*03-DQB1*02 (DRB1*04/09/11) alleles; DQ8 = DQA1*03-DQB1*0302 (DRB1*04) alleles</p><p>^bStatistically significant differences, <i>p</i><0.001 at χ² test between males (M) and females (F)</p><p>^cDQX refers to: DQ7 = DQB1*0301 (DRB1*11/12/X) alleles; DQ4, DQ5, DQ6 and DQ9, were assigned if DQB1*04, DQB1*05, DQB1*06 and DQB1*0303 alleles were present, respectively</p><p>^dStatistically significant differences, <i>p</i><0.05 at χ² test, between DQ2/DQ8 (+) and DQ2/DQ8 (-) CD patients</p><p>Frequencies of HLA-DQ genotypes (A) and haplotypes (B) detected in 666 CD patients from south Italy.</p

Frequencies of HLA-DQ genotypes (A) and haplotypes (B) detected in unaffected subjects (n = 4869) from south Italy.

<p>CD, celiac disease</p><p>^aGenotypes were based on the presence of the following haplotypes: DQ2.5 = DQA1*05-DQB1*02 (DRB1*03) alleles; DQ2.2 = DQA1*02-DQB1*02 (DRB1*07) alleles; DQ2.3 = DQA1*03-DQB1*02 (DRB1*04/09/11) alleles; DQ8 = DQA1*03-DQB1*0302 (DRB1*04) alleles</p><p>^bStatistically significant differences between CD-relatives (n = 3662) and with CD-like symptoms (n = 1207) subjects; <i>p</i><0.001 at χ² test</p><p>^cDQX refers to: DQ7 = DQB1*0301 (DRB1*11/12/X) alleles; DQ4, DQ5, DQ6 and DQ9, if DQB1*04, DQB1*05, DQB1*06 and DQB1*0303 alleles were present, respectively</p><p>^dStatistically significant differences, <i>p</i><0.001 at χ² test, between DQ2/DQ8 (+) and DQ2/DQ8 (-) unaffected subjects.</p><p>Frequencies of HLA-DQ genotypes (A) and haplotypes (B) detected in unaffected subjects (n = 4869) from south Italy.</p

Structural features of mutations p.Phe123Leu and p.Asp168Ala GCK.

<p>The structure of GCK in the closed form (PDB code: 1v4s) is represented by cyan ribbons. A) Mutation p.Phe123Leu. Phe123 is structured inside the hydrophobic core of the small domain. Yellow sticks represent hydrophobic residues that constitute the core. Phe123 and Leu123 are represented by red sticks (left and right panel, respectively). B) The sticks represent residue Thr168 and glucose. The right panels show a close-up view of the glucose-binding cleft for the wild-type (top) and for the Ala168 mutant (bottom).</p

Structural features of mutations p.His137Asp, p.Arg392Ser and p.Gly162Asp GCK.

<p>The structure of GCK in the closed form (PDB code:1v4s) is shown as cyan ribbons. A) p.His137Asp. Loop 141–144, which is involved in GKRP binding, is in red. His137 is at the end of the α3 helix. His137 is a capping residue of the helix, which is terminated by the interaction between side chain of His137 and Phe133. Asp137 (right) is not able to replace His137 interactions but adds a new interaction with Lys104. B) p.Gly162Asp. Yellow sticks represent hydrophobic residues that constitute the core. The location of Gly162 is marked in red (left of the panel). Asp162 is on the right of the panel. C) p.Arg392Ser. Residues Asp42, Glu236, Asn240 and Arg392 are represented by yellow sticks. H-bonds are shown in green. The wild-type enzyme and the p.Arg392Ser mutant are on the left and right of the panel, respectively.</p

Enzyme activities of the respiratory chain complexes I and IV evaluated in lymphocytes from mitochondrial diabetic patients (pt) and their mothers (m) bearing mtDNA variants in these complexes.

a<p>Pool is relative to 12 healthy control subjects.</p>b<p>Residual activity (%) was obtained by normalization of the enzyme activity firstly <i>vs</i> citrate synthase and then <i>vs</i> the healthy cont rol pool. ND: Not determined.</p

Clinical and metabolic characteristics of pediatric patients from Southern Italy with suspected mitochondrial diabetes (n = 11)^a.

a<p>Continuous variables are reported as median (2.5^th–97.5^th percentiles) and categorical variables as percentages;</p>b<p>BMI z score = Body mass index z score;</p>c<p>Mother and/or maternal relatives.</p

Familial (F) pedigrees of the suspected mitochondrial diabetes patients enrolled in the study.

<p>The inclusion criteria were: Diabetes+at least one of the following: A) maternal heritability of diabetes or Impaired Fasting Glucose (IFG) and/or hearing impairment and/or maculopathy in three consecutive generations (or in two if there were 2–3 affected subjects/family); B) neurosensorial hearing impairment; and C) maculopathy. In each square it's reported the presence of the criteria (A, B and/or C) in the probands.</p

Biochemical and phenotypic characteristics of the children affected by GCK MODY

a<p>BMI<i>z</i> scores: (calculated in children aged 2–18 years), see Materials and methods</p>b<p>FPG: Fasting plasma glucose; (impaired fasting glucose [IFG] = 5.6–6.9 mmol/L; diabetes mellitus [DM] = ≥7.0 mmol/L)</p>c<p>OGTT: Oral glucose tolerance test (normal glucose tolerance [NGT] <7.8 mmol/L; impaired glucose tolerance [IGT] = 7.8–11.0 mmol/L; DM = ≥11.1 mmol/L)</p>d<p>FPIR: First phase insulin response (reference value: ≥60.0 µU/ml)</p>e<p>HbA1c: glycosylated haemoglobin (reference value: 4.3–5.9%)</p>f<p>Not available because patient M002 was <2 years old</p>g<p>Not fasting nursling</p>n.a.<p>Not available</p