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Части речи. Имя прилагательное.

Части речи. Имя прилагательное.

 

Общее значение: признаковость

 

Классификация: подразделяются на относительные и качественные

 

Грамматические категории: качественные прилагательные имеют степени сравнения, образуемые либо синтетически, либо аналитически в зависимости от количества слогов в слове.

 

Характерные синтаксические позиции: определение и предикатив. Есть прилагательные, которые могут занимать обе синтаксические позиции, есть только атрибутивные (mere, sheer, utter); есть только предикативные (glad, able, afraid, alive, alike).

 

Морфологические особенности: многие прилагательные образованы от других частей речи  при помощи суффиксов:

 

Суффикс

Прилагательные

-able

Comfortable, expensive, talkative

-ible

Sensible, visible, susceptible

-ant

Elegant, predominant, arrogant

-ent

Dependent, intelligent, innocent

-al

Cultural, musical, medical

-ic

Atomic, scientific, heroic

-ish

Childish, foolish, brownish

-ive

Attractive, expensive, talkative

-ful

Careful, useful, skilful

-less

Careless, helpless, useless

-ly

Brotherly, deadly, friendly

-ous

Dangerous, curious, anxious

-y

Dirty, dusty, sleepy

 

Многие английские прилагательные совпадают по своей форме с причастиями настоящего или прошедшего времени, т.е. образованы суффиксами –ed  и  -ing.

 

Задание 1. Ознакомьтесь с фрагментом текста и найдите в нем относительные и качественные прилагательные. Образуйте степени сравнения качественных прилагательных.

 

Задание 2. Обратите внимание на выделенные –ed  и –ing формы. Какими частями речи они являются? Чем вы руководствовались при отнесении их к той или иноф части речи?

 

Fibrosis

An accumulation in the liver of connective tissue resulting from an imbalance between production and degradation of the extracellular matrix and accentuated by the collapse and condensation of preexisting fibers.

Etiology

Fibrosis is a common response to hepatocellular necrosis or injury, which may be induced by a wide variety of agents, eg, any process disturbing hepatic homeostasis (especially inflammation, toxic injury, or altered hepatic blood flow) and infections of the liver (viral, bacterial, fungal, and parasitic). Numerous storage disorders resulting from inborn errors of metabolism are often associated with fibrosis, including lipid abnormalities (Gaucher's disease); glycogen storage diseases (especially types III, IV, VI, IX, and X); alpha1-antitrypsin deficiency; storage of exogenous substances, as seen in iron-overload syndromes (hemochromatosis) and copper storage diseases (Wilson's disease); accumulation of toxic metabolites (as in tyrosinemia, fructosemia, and galactosemia); and peroxisomal disorders (Zellweger syndrome). Numerous chemicals and drugs cause fibrosis, especially alcohol, methotrexate, isoniazid, oxyphenisatin, methyldopa, chlorpromazine, tolbutamide, and amiodarone. Disturbances of hepatic circulation (eg, chronic heart failure, Budd-Chiari syndrome, veno-occlusive disease, portal vein thrombosis) and chronic obstruction to bile flow can lead to fibrosis. Lastly, congenital hepatic fibrosis is an autosomal recessive malformation.

Pathogenesis

The normal liver is made up of hepatocytes and sinusoids distributed within an extracellular matrix composed of collagen (predominantly types I, III, and IV) and noncollagen proteins, including glycoproteins (eg, fibronectin, laminin) and several proteoglycans (eg, heparan sulfate, chondroitin sulfate, dermatan sulfate, hyaluronate). Fibroblasts, normally found only in the portal tracts, can produce collagen, large glycoproteins, and proteoglycans.

Other liver cells (particularly hepatocytes and fat-storing [Ito], Kupffer, and endothelial cells) also can produce extracellular matrix components. Fat-storing cells, located beneath the sinusoidal endothelium in the space of Disse, are precursors of fibroblasts, capable of proliferating and producing an excess of extracellular matrix. The development of fibrosis from active deposition of collagen is a consequence of liver cell injury, particularly necrosis, and inflammatory cells. The precise factors released from these cells is not known, but one or more cytokines or products of lipid peroxidation are likely. Kupffer cells and activated macrophages produce inflammatory cytokines. New fibroblasts form around necrotic liver cells; increased collagen synthesis leads to scarring. Fibrosis may derive from active fibrogenesis and from impaired degradation of normal or altered collagen. Fat-storing cells, Kupffer cells, and endothelial cells are important in the clearance of type I collagen, several proteoglycans, and denatured collagens. Changes in these cells' activities may modify the extent of fibrosis. For the histopathologist, fibrous tissue may become more apparent from passive collapse and condensation of preexisting fibers.

Thus, increased synthesis or reduced degradation of collagen results in active deposition of excessive connective tissue, which affects hepatic function: (1) Pericellular fibrosis impairs cellular nutrition and results in hepatocellular atrophy. (2) Within the space of Disse, fibrous tissue accumulates around the sinusoids and obstructs the free passage of substances from the blood to the hepatocytes. (3) Fibrosis around hepatic venules and the portal tracts disturbs hepatic blood flow. Venous resistance across the liver increases from portal vein branches to sinusoids and finally to hepatic veins. All three routes can be involved.

The fibrous bands that link portal tracts with central veins also promote anastomotic channels: Arterial blood, bypassing the normal hepatocytes, is shunted to efferent hepatic veins, which further impairs hepatic function and can accentuate hepatocellular necrosis. The extent to which these processes are present determines the magnitude of hepatic dysfunction: eg, in congenital hepatic fibrosis, large fibrous bands involve predominantly the portal regions but usually spare the hepatic parenchyma. Congenital hepatic fibrosis thus presents as portal hypertension with preserved hepatocellular function.