Методические указания по обучению чтению английской специальной литературы

ФЕДЕРАЛЬНОЕ ГОСУДАРСТВЕННОЕ БЮДЖЕТНОЕ

ОБРАЗОВАТЕЛЬНОЕ УЧРЕЖДЕНИЕ

ВЫСШЕГО ПРОФЕССИОНАЛЬНОГО ОБРАЗОВАНИЯ

«МОСКОВСКАЯ ГОСУДАРСТВЕННАЯ АКАДЕМИЯ ВЕТЕРИНАРНОЙ

МЕДИЦИНЫ И БИОТЕХНОЛОГИИ им. К. И. СКРЯБИНА»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ПО ОБУЧЕНИЮ

ЧТЕНИЮ АНГЛИЙСКОЙ СПЕЦИАЛЬНОЙ ЛИТЕРАТУРЫ.

( «Биология» и «Биотехнология»)

Москва 2012

ФЕДЕРАЛЬНОЕ ГОСУДАРСТВЕННОЕ БЮДЖЕТНОЕ ОБРАЗОВАТЕЛЬНОЕ УЧРЕЖДЕНИЕ ВЫСШЕГО ПРОФЕССИОНАЛЬНОГО ОБРАЗОВАНИЯ

«МОСКОВСКАЯ ГОСУДАРСТВЕННАЯ АКАДЕМИЯ ВЕТЕРИНАРНОЙ

МЕДИЦИНЫ И БИОТЕХНОЛОГИИ им. К. И. СКРЯБИНА»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ПО ОБУЧЕНИЮ

ЧТЕНИЮ АНГЛИЙСКОЙ СПЕЦИАЛЬНОЙ ЛИТЕРАТУРЫ

ДЛЯ БАКАЛАВРОВ И МАГИСТРОВ

ПО НАПРАВЛЕНИЯМ ПОДГОТОВКИ

«Биология» и «Биотехнология»

Москва 2012

УДК 4 И (Англ.) (07)

Киселева указания для обучения чтению английской специальной литературы для бакалавров и магистров по направлениям подготовки «Биология» и «Биотехнология» - М.

ФГБОУ ВПО МГАВМиБ им. , 2с.

Книга для чтения представляет собой сборник оригинальных текстов по современным проблемам биологии, вирусологии, молекулярной биологии, биохимии и некоторым другим проблемам.

Цель данного учебного пособия заключается в том, чтобы развить у студентов навыки чтения английской специальной литературы.

Каждый текст сопровождается рядом упражнений для закрепления специальной лексики и грамматических конструкций, характерных для языка научной прозы.

Учебное пособие предназначается для бакалавриата и магистратуры – по направлениям подготовки «Биология» и «Биотехнология».

Рецензия

На «Методические указания по обучению чтения

английской специальной литературы».

(Специальность 020400 – «БИОЛОГИЯ»)

Автор: П.

Рецензируемые методические указания предназначены для работы в студенческой аудитории (уровни дипломированный специалист, магистр) по специальности 020400 – «Биология».

Целью пособия является выработка у студентов навыков и умений чтения специальных текстов по биологии, вирусологии, молекулярной биологии, биохимии с целью извлечения профессионально значимой информации.

По своему содержанию рукопись пособия соответствует своему содержанию. В структуру пособия входят 16 аутентичных текстов, взятых автором из современных научных периодических журналов, издаваемых в Великобритании и США. Тексты сопровождаются серией упражнений, целью которых является закрепление терминологической лексики и грамматических конструкций, характерных для языка научной прозы.

В пособии представлены задания, предусматривающие различные формы взаимодействия студентов и способствующие развитию иноязычных речевых умений разных уровней, определяемых спецификой их будущей профессиональной деятельности.

Данное пособие рекомендуется к опубликованию.

Доцент кафедры английского

Языка МИОО

Предисловие.

Сборник представляет собой ряд оригинальных текстов по современным вопросам биологии, вирусологии, молекулярной биологии, биохимии и некоторым другим биологическим проблемам.

В работу включено 16 текстов, связанных с различными проблемами биологии. Тексты выбраны из различных научных периодических журналов, издаваемых в Великобритании и США в течение последних лет.

Прежде всего, внимание уделено проблемам, которые связаны с клеточной и молекулярной биологией, с проблемой метаболизма живого организма. Кроме того, в текстах речь идет о возникновении некоторых заболеваний, связанных с нарушением метаболизма. Пособие даёт довольно подробную информацию об истории происхождения эпидемий инфлюэнцы и о контроле над ними, о вирусе инфлюэнцы и его характере. Затрагиваются некоторые проблемы нервной системы.

После каждого текста даны упражнения, с помощью которых будут легче усваиваться специальная лексика и грамматические конструкции, часто употребляемые в научной литературе на английском языке.

Цель пособия – ознакомить студентов с некоторыми современными проблемами биологии, публикуемыми на английском языке, и способствовать развитию навыков чтения оригинальной специальной литературы.

A new home for metabolic research.

Welcome to the first issue of “Cell Metabolism”, the newest addition to the Cell Press family of journals. Our mission is to bring you the most timely and exciting research focusing on homeostas.

As we are reminded in uncounted introductions to papers and reviews, obesity is becoming epidemic worldwide. Indeed, obesity and other maladies of nutritional excess and modern stress levels, such as diabetes, atherosclrosis, and hypertension, are increasingly important health threats. Also contributing to the increased prevalence of these diseases are lengthened lifespans, made possible by improvements in health care and living conditions. Aging populations in turn have prompted a growing interest in longevity research and age-associated conditions such as osteoporosis. These topics and the underlying biology as represented by (but certainly not limited to) basic studies of mitochondrial function, metabolite homeostasis, and cell signaling, are a main focus of “Cell Metabolism”.

In the past, these topics were often addressed through classic physiology studies, today, the advent of modern molecular biology techniques (including gene cloning) transgenic and vector-mediated gene delivery, generation of strains bearing targeted mutations, and high-throughput analyses) has ignited conceptual advances by leaps and bounds. Molecular biology has also underlined the commonalities tying together disparate systems; a diabetes or aging researcher will need to read about work carried out in yeast, worms, flies, and fish as well as the usual mouse and human.

EXERCISES

Ex.1. Fill in the blanks the suitable words.

1) Obesity is becoming … worldwide.

2) Contributing made possible by improvements in … .

3) Aging populations have prompted a growing interest in… .

4) These topics were often addressed through … .

5) A diabetes or aging researcher will need to read about work

6) carried out in… .

.

Ex.2. Translate into Russian. Note the use of “ing-forms”. What are they?

1)…to bring you exciting research focusing on homeostasis.

2)…obesity is becoming epidemic worldwide.

3)…contributing to the increased prevalence of these diseases.

4) …improvements in health care and living conditions.

5) Aging populations have promped a growing interest.

6)…the underlying biology represented by basic studies of mitochondrial function, metabolic homeostasis and cell signaling are main.

7)…the advent of modern molecular biology techniques ( including gene cloning) has ignited conceptual advances.

8)… generation of strains bearing targeted mutations.

9) Molecular biology has also underlined the commonalities tying together disparate systems.

Ex.3. Answer the questions.

1) What is “Cell Metabolism”?

2) What is the task of this new journal?

3) What kinds of diseases will be mentioned in this issue?

4) What modern techniques are used nowadays?

Lipin, a lipodystrophy and obesity gene.

Considerable inroads have been made in the last decade toward identifying and characterising obesity genes expressed in adipose tissue and the hypothalamus. This has led to the formulation of the adipose-hypothalamic axis as a mechanism by which the CNS senses and regulates adipose tissue mass in the periphery. The hypothalamus receives input from afferent adiposity signals, notably leptin, which communicate the status of body fat stores. These signals subsequently act to modulate energy balance to maintain a predetermined level of adiposity. In addition substantial attention has focused on the neural circuitry upon which these peripheral signals act. This has led to the identification of a plethora of neurotransmitters and receptor systems with demonstrated and potential roles in regulating food intake and energy expenditure.

Efforts have also been applied to identify gene defects underlying conditions of insufficient adipose tissue, as is observed in lipodystrophy. As lypodystrophy and obesity represent extreme ends of the adiposity spectrum, it raises the question of whether genes whose deficiency leads to lipodystrophy may also promote obesity when overexpressed. Consistent with this possibility is the demonstration that some forms of congenital lipodystrophy in humans result from defects in genes with roles in adipogenesis and fat synthesis storage. However, it is unknown whether genes such as these, which function directly in the adipose tissue, can also cause obesity. Here we demonstrate that lipin, which is expressed primarily in peripheral tissues, possesses this capacity, causing lipodystrophy in its absence and promoting obesity when its levels are enhanced.

Lipin, which is encoded by the Lpin1 gene, was identified through positional cloning as the gene mutated in the fatty liver dystrophy (fld) mouse. Null mutation in lipin in these animals confers lipodystrophy, characterized by severe deficiency in adipose tissue mass, development of insulin resistance, and a progressive peripheral neuropathy. Lipin is expressed at high levels in metabolically active tissues such as adipose tissue and skeletal muscle and has been shown to interact with proteins having a putative role in nucleocytoplasmic transport in yeast, consistent with its nuclear localization in mammalian cells. It is unclear by examining lipin deficiency whether elevated lipin levels could promote increased adiposity. In addition, the function of lipin in skeletal muscle, where it is expressed at levels comparable to those in adipose tissue, has not yet been explored. To better understand the effect of lipin levels in adipose tissue and skeletal muscle on fat mass and energy metabolism, we have generated and characterized transgenic mouse models with enhanced lipin expression in either mature adipocytes or skeletal muscle.

EXERCISES

Ex.1 Write derivatives from the same root and do the translation.

To regulate, to add, to lead to, to receive, to apply, to promote,

to store, to develop, to resist, to progress, to compare, to explore.

Ex.2 Fill in the blanks the suitable words and translate the sentences

.into Russian.

1) These signals act to modulate … to maintain a predetermined level of adiposity.

2) Substantial attention has focused … upon which these peripheral signals act.

3) Efforts have also been applied … gene defects underlying conditions of insufficient adipose tissue.

4) Some forms of congenital lipodystrophy in humans result from … in genes.

5) Lipin, which is expressed primarily in … … possesses this capacity.

6) Lipin is expressed … in metabolically active tissues.

7) It is unclear whether elevated lipin levels could … increased adiposity

Ex. 3. Pay attention to the combinations of two nouns. Translate them into

Russian.

Adiposity signals, body fat stores, energy balance, food intake, energy expenditure, gene defects, adiposity spectrum, fat synthesis storage, adipose tissue mass, insulin resistance, lipin deficiency, lipin levels, fat mass and energy metabolism.

Ex.4 Answer the questions.

1) What can be called a mechanism by which adipose tissue

mass in the periphery is regulated?

2) What is the role of the hypothalamus in information the body about the status of its fat stores?

3) What acts to modulate energy balance to maintain a predetermined level of adiposity?

4) What helps to regulate food intake and energy expenditure?

5) What can cause obesity?

6) What did the scientist generate transgenic mouse models for?

7) What are metabolically active tissues?

ABCG1: How critical for cholesterol transport.

The amount of cholesterol that is carried in the plasma in the form of high density lipoproteins (HDL-C) is an important predictor of atherosclerotic disease. Although there are some nuances overall it is abundantly clear has been the reason for this association. Many mechanisms have been proposed, but the facilitation of so-called “reverse cholesterol transport” to the liver, in particular from macrophage foam cells in atheromas, has emerged as the dominant hypothesis. Members of the ATP binding cassette (ABC) transmembrane transporter family have come under scrutiny as possibly playing an important role in the process. The author explores the role of ABCG1 in cholesterol transport, using both gene knockout and transgenic techniques in mice, along with in vitro studies. The results are surprising and should prompt the reservation of judgment regarding the metabolic significance of reverse cholesterol transport to mature HDL.

ABC transportes came to the attention of HDL biologists through the discovery of the role of ABCA1. An extreme form of hereditary low HDL-C, was found to stem from the absence of the ABCA1 gene product, a protein important for the formation of HDL, through its initial lipidation of apolipoproteins. However, ABCA1 does not significantly mediate cholesterol efflux to mature HDL, and hereditary variation in the ABCA1 gene appears to have (modest) significance in determining HDL levels only in individuals with the very lowest levels.

Another ABC transporter, ABCG1, was subsequently suggested to be involved in cholesterol efflux to mature HDL. A large body of in vitro evidence was subsequently marshaled in support of such a view.

Even on a very high-cholesterol diet (21% fat and 1.25% cholesterol), there was no difference in plasma lipoprotein levels between knockout and control animals. However, knockout mice on this diet did have grossly visible pleural plaques, and histological analysis revealed markedly increased pleural and subpleural with phospholicrophages with prominent accumulation of neutral lipid, including cholesteryl ester and triglycerides along with phospholipids.

Multinucleated giant cells and many foam cells containing cholesterol clefts were observed, along with lymphocyte accumulation. Increased neutral lipid was also observed in hepatocytes and Kupffer cells. In older chowfed animals, modest pleural but no hepatocyte, lipid accumulation was observed. However, hepatic fatty acid synthesis pathways were induced. In transgenic mice overexpressing ABCG1, levels of cholesteryl esters in pleura and liver were decreased compared to wild-type controls, again without a plasma lipoprotein phenotype. No atherosclerosis data were presented.

On the basis of these studies we may now be confident that ABCG1 is responsible for much of the cholesterol efflux that utilizes mature HDL as an acceptor, certainly in the case of macrophages. In addition, while similar genes may play some contributory role, ABCG1 is clearly an important overall mediator of total cholesterol efflux from macrophages in some tissues, particularly under conditions of cholesterol excess. Surprisingly however, despite the persuasive evidence that it mediates cholesterol efflux to HDL, ABCG1 does not appear to be a determinant of the plasma HDL level, the variable whose correlation with coronary heart disease risk ultimately lay behind these studies. Of course, there are likely many determinants of atherosclerotic risk whose effect is independent of plasma lipoprotein levels. However, whether the level of expression of ABCG1 is one such variable remains unknown, and the presentation of data on this subject is eagerly awaited. Until then, the importance for atherosclerotic risk both of ABCG1 and, more generally, of macrophage cholesterol efflux to mature HDL will remain open questions.

Comment:

Foam-cells (cholesterol crystals, stromal red blood cells) – холестероловые кристаллы, остовные красно-кровяные клетки;

мертвые липидно-нагруженные макрофаги.

ABCA1 – ген

ABCG1 – ген, маркер кардиоваскулярного риска

ABC – транспортеры (маркеры множественной лекарственной резистентности )

Kupffer cells – клетки Купфера (купферовские клетки печени)

The ATP (adenosine triphosphate)

EXERCISES

Ex.1 Fill in the blanks with suitable words (or combinations of words) and translate them into Russian.

1) At least in macrophages, ABCG1 is responsible for much of the … .

2) The amount of cholesterol that is carried in the plasma in the form of … is an important predictor of atherosclerotic disease.

3) Facilitation of so-called “reverse cholesterol transport” to the … emerged as the dominant hypothesis.

4) The author explored the role of ABCG1 in …, using both gene knockout and transgenic techniques in mice.

5) Hereditary variation in the ABCA1 gene appears to have (modest) … in determining HDL levels only in individuals with the very lowest levels.

6) Knockout mice on this diet did have grossly visible … .

7) Multinucleated giant cells and many foam cells containing … were observed.

8) While similar genes may play some … ,ABCG1 is clearly an important overall mediator.

Ex.2 Write out all the sentences with “ing-forms” from the text. Translate them. State whether they are gerunds, nouns, or participles.

Ex.3 Answer the questions.

1) What is an important predictor of atherosclerotic disease?

2) What is the important role in cholesterol transport?

3) How did ABC transportes come to the attention of HDL biologists?

4) Was there any difference in plasma lipoprotein levels between knockout and control animals being on a very high-cholesterol diet?

5) What happened to knockout mice on this high-cholesterol diet?

6) What else was observed along with lymphocyte accumulation? (… and in hepatocytes?) And what about in older chowfed animals?

7) What atherosclerotic risk is still remained open questions?

A new way to keep your weight down.

Almost always, obesity is an obligate prerequisite for the development of type 2 diabetes mellitus. Loss of well known lipid phosphatase appears to prevent insulin- resistant diabetes in mice by removal of a positive regulator of adiposity.

In recent years, a substantial amount of attention has been directed toward understanding type 2 diabetes mellitus (T2DM), both because of the disease’s profound impact on health care as well as the intrinsically fascinating problem of how an efficient homeostatic mechanism can be so considerably disrupted by lifestyle changes. T2DM, formerly known as adult-onset diabetes, is the most common cause of hyperglycemia, which is believed to result when increasing resistance to the actions of the hormone insulin is accompanied by the failure of the pancreatic βcell to keep pace with the augmented needs for insulin secretion. Thus, a reasonable strategy to alleviate the symptons of T2DM would be to enhance insulin’s action in classical target tissues such as muscle and fat, and this is precisely the mechanism used by the commonly prescribed thiazolidinedione class of drugs. However, this action of thiazolidinediones was discovered by chance, and current efforts to develop novel therapeutics are guided by more rational approaches, since it is generally believed that it is easier to develop an inhibitor drug than an activator one, a logical focus is pathways that antagonize or terminate insulin signaling. Phosphorylation of both proteins and phospholipids is essential to insulin signaling, making the prospect of inhibiting the enzymes that remove the critical phosphates an attractive strategy for drug development. The scientists find a much milder phenotype in which increased insulin sensitivity is obvious only when mice are placed on a high-fat diet, a manipulation that increases fat cell mass and promotes insulin resistance. In fact, even in experimental model systems, discerning whether alterations in insulin responsiveness are direct or a consequence of leanness is often a challenge.

EXERCISES

Ex.1 Translate the given sentences into Russian, paying attention to the Complex Subject.

1) Obesity is supposed to be an obligate prerequisite for the development of type 2 diabetes mellitus.

2) Loss of well known lipid phosphatase appears to prevent insulin

-resistant diabetes

3) A substantial amount of attention is likely to have been directed

toward understanding type 2 diabetes mellitus.

4) T2DM is the most common cause of hyperglycemia which is believed

to result when increasing resistance to the actions of the hormone

insulin.

5) This action of thiazolidinediones proves to have been discovered by chance.

6) Phosphorylation of both proteins and phospholipids are sure to be essential to insulin signaling.

Ex.2 Fill in the blanks the suitable words and translate the sentenses.

1) Almost always, obesity is an obligate prerequisite for the

… of type 2 diabetes mellitus.

2) In recent years, a substantial … of attention has been directed

toward understanding T2DM.

3) A reasonable strategy to alleviate the symptoms of T2DM

would be to … insulin’s action in classical target tissues

4) This action of thiazolidinediones was … by chance.

5) It is easier to develop an inhibitor … than an activator one.

Ex.3 Answer the questions.

1) Is there any prerequisite for the development of T2DM?

2) Why is T2DM formerly known as adultonset diabetes?

3) What is a reasonable strategy to alleviate the symptoms of T2DM?

4) What happens to insulin sensitivity when mice are placed on a high-fat diet?

A potential link between muscle peroxi – some

proliferatior – activated receptor – a signaling

and obesity – related diabetes.

We are witnessing the emergence of a pandemic of obesity, metabolic syndrome, and type2 diabetes mellitus. Numerous studies have shown an intriguing link between muscle lipid accumulation related to caloric excess and the development of insulin resistance. However, the mechanisms linking altered muscle lipid metabolism to the development of insulin resistance and type2 diabetes remain unclear. Recent evidence indicates that intracellular lipid intermediates trigger cellular events that perturb insulin signaling. Increased import and oxidation of fatty acids into insulin target tissues such as skeletal muscle could also lead to reciprocal reductions in glucose utilization through events downstream or independent of the insulin-signaling pathway. Recently, we found that the expression of PPAR[1] and its target genes is increased in the diabetic heart. Transgenic mice with cardiac-specific overexpression of PPAR exhibit increased fatty acid uptake and oxidation and reciprocal inhibition of glucose uptake and utilization. We sought to determine whether chronic activation of the PPAR pathway leads to similar metabolic derangements in other major insulin target tissues, thus influencing the development of systemic insulin resistance and glucose intolerance. To explore the possibility, PPAR gain-of-function and loss-of-function studies were performed in mice. We found that the activity of the skeletal muscle PPAR pathway is directly linked to the development of insulin resistance, glucose intolerance and diabetes. Surprisingly, our results indicate that an intact PPAR regulatory pathway is necessary for the coupling of obesity and insulin resistance.

EXERCISES

Ex.1 Find in the text sentences with these words. Translate them paying attention to the structure of these words:

intracellar, intermediates, downstream, uptake, glucocorticoid pathway, derangements, overexpression.

Ex.2 Find the omitted words in the text and fill in the blanks with them.

1) We are witnessing the … of a pandemic of obesity.

2)There is a link between … accumulation related to caloric excess.

3)Increased import and oxidation of … could also lead to reciprocal reductions in glucose utilization.

4)The expression of PPAR and its target genes is increased in the …

5)Our results indicate that an intact PPAR regulatory pathway is necessary for the coupling of … .

Ex.3 Answer the questions.

1) Is the mechanism linking altered muscle lipid metabolism to the development of insulin resistance still unclear?

2) What serves a critical role in the gene regulatory control of cellular lipid metabolic pathway?

3) What did transgenic mice with cardiac-specific overexpression of PPAR exhibit?

4) I’d like to know whether chronic activation of the PPAR pathway leads to similar metabolic derangements in other major insulin target tissues?

5) What is the activity of the skeletal muscle PPAR pathway directly linked to?

Cellular iron: Ferroportin is the only way out.

Iron, an essential nutrient, is used in proteins that store and transport oxygen and catalyze redox reactions. In vertebrates, most iron in the body is destined for hemoglobin. When iron absorption from the diet is not sufficient to compensate for iron losses, hemoglobin production decreases, resulting in anemia. Not only is iron deficiency deleterious, but iron excess is also. Uncomplexed iron catalyzes the production of reactive oxygen species which cause cellular injury and cell death. In hereditary hemochromatoses, unrestrained iron absorption from the diet leads to the deposition of excess iron in the liver and other organs, with consequent organ damage and functional failure. In this issue of “Cell Metabolism”, the scientists use generic means to demonstrate the unique and nonredundant function of the cellular iron exporter ferroportin in maintaining extracellular iron homeostasis.

Cellular iron homeostasis assures adequate iron supply for the varying metabolic needs of individual cells, as long as extracellular iron concentrations remain in the normal range. Iron circulates in plasma or extracellular fluid complexed with transferring. Cells take up iron –transferrin by transferrin receptor –mediated endocytosis and store iron predominantly in cytoplasmic ferritin.

Organismal iron homeostasis has apparently evolved to maintain a stable concentration of iron-transferrin in plasma and extracellular fluid. This requires the coordinated control of three major iron flows into the plasma transferring compartment: iron absorption from the environment (maternal plasma iron in the fetus and intestinal dietary iron after birth), movement of iron out of storage in the liver, and recycling of the iron content of senescent cells (predominantly red blood cells) by macrophages. To maintain stable extracellular iron concentrations, the inflow of iron into plasma transferring must balance the outflow, which is dominated by the iron requirements of red cell hemoglobin production in the bone marrow. Additional smaller outflows supply the needs of other cells, and the rest enters into storage in hepatocytes.

Influences other than the concentration of iron-transferrin also regulate iron flows. Anemia and hypoxia stimulate iron absorption and recycling thus providing more iron for compensatory erythropoiesis. Moreover, both iron absorption and recycling are inhibited during infections, presumably to deprive invading pathogens of extracellular iron. Despite the potential for great complexity, the regulatory system that has emerged from recent studies is surprisingly simple and elegant. The single iron regulatory hormone, hepcidin, controls iron flows out of the cells and into the plasma transferring compartment by binding to a unique cellular iron exporter, ferroportin, and inducing its endocytosis and degradation. Ferroportin is found in all the tissues where major iron flows are regulated, including duodenal enterocytes, placental trophoblast, macrophages, and hepatocytes.

In the current study, total deficiency of ferroportin in mammals is also embryonic lethal, almost sertainly because the developing embryo cannot import iron across the maternal-fetal interface (extraembryonic visceral endoderm, placenta). If this early defect is selectively circumvented by conditionally deleting ferroportin in all tissues except the maternal-fetal interface, the embryo survives to birth but the newborn mouse rapidly develops severe iron deficiency as it begins to depend on intestinal absorption of iron. The mice also display defects in the release of iron from hepatic storage and in the recovery of iron from recycled red cells. As indicated by abundant trapped iron in intestinal enterocytes, macrophages, and hepatocytes, all these cells are unable to export cytoplasmic iron to plasma in the absence of ferroportin.

The iron-exporting tissues and cells have no significant alternative to the ferroportin iron efflux pathway and provides further support for the fundamental role of the hepcidin-ferroportin interation in systemic iron homeostasis. This interaction is also the key to understanding the pathogenesis of hereditary hemochromatosis. The excessive intestinal iron absorption characteristic of this group of diseases results from inappropriately high ferroportin activity either because of hepcidin deficiency or, less commonly, because of the insensitivity of mutated ferroportin to hepcidin. At the other end of the spectrum of iron disorders, anemia of inflammation develops when the cytokine-induced hepcidin internalizes and degrades ferroportin on iron-exporting cells, most notably macrophages. Recycled iron is trapped, decreasing the plasma concentration of iron and limiting hemoglobin production in developing erythrocytes in the bone marrow.

EXERCISES

plete the following sentences from the text

1) Most iron in the body is destined for … .

2) In hereditary hemochromatoses, unrest – rained iron absorption from the diet leads to … .

3) Additional smaller outflows supply the needs of other cells, and …

4) Anemia and hypoxia stimulate iron absorption and recycling thus… .

5) …, the regulatory system, that has emerged from recent studies is…

6) The mice also display defects … and in the recovery of iron from recycled red cells.

7) This interaction is also the key to understanding … .

EX 2. Translate the following sentences into English.

1) У позвоночных наибольшее количество железа в теле предназначается для гемоглобина.

2) Не только дефицит железа вреден, но и избыток также.

3) Гомеостаз железа в организме поддерживает стабильную концентрацию трансферрина в плазме и внеклеточной жидкости.

4) Несмотря на скрытую огромную сложность регуляторная система – удивительно проста и элегантна.

Ex.3.Translate into Russian. Note the use of “ing-forms”.What are they?

1)  When iron absorption from the diet is not sufficient…,resulting in

anemia.

2) Cellular iron homeostasis assures adequate iron supply for the varying metabolic needs of individual cells.

3) Iron circulates in plasma or extracellular fluid complexed with transferring.

4) Anemia and hypoxia stimulate iron absorption and recycling thus

providing more iron for compensatory erythropoiesis.

5) This interaction is also the key to understanding the pathogenesis of hereditary hemochromatosis.

6) This early defect is selectively circumvented by conditionally deleting ferroportin in all tissues.

Ex.4.Anwer the followring questions.

1) Why is total deficiency of ferroportin in mammals almost sertainly embryonic lethal?

2) What happens to the newborn mouse if the embryo survives to birth?

3) What group of diseases can break out due to inappropriately high ferroportin activity?

4) In what cases does hemoglobin production decrease?

5) What are three major iron flows into the plasma transferring compartments?

6) Where are red cells hemoglobin produced?

7) What stimulates iron absorption and recycling to provide more iron for compensatory erythropoiesis?

The prepared mind of the worm.

We humans can use our foresight and intelligence to prepare for hard times ahead. Examples range from Biblical times, when Joseph used premonition and prophecy to guide Egypt through famine, to the modern application of public policy to guide consumption of global resources. But how do simpler creatures cope with adversity, and what can we learn from them. The recent biochemical purification of a pheromone signaling imminent starvation from the roundworm c. elegans[2] represents a significant advance in our understanding of these phenomena.

Most living creatures can in fact sense their surroundings and make forecasts that amount to a life or death decision. A key skill, honed during evolution, is predicting food availability and calculating the odds of reproductive success. This depends not only on the individual and its environment but also on the population at large, which directly competes for available resources. When times are good, many organisms shoot for rapid reproduction. When times are bad, the organism must gamble: either wait (and risk that your neighbor will forge ahead) or go for it. However, waiting it out is hardly passive: it demands metabolic, developmental, and behavioral adaptations that permit the organism to survive impending adversity. Importantly, these adaptations are associated with stress resistance, metabolic efficiency, and longevity, and the dissection of such programs in organisms as diverse as yeast, worms, flies, and mice has led to important insights into the biology of aging.

C. elegans has a remarkable intelligence to sense its environment and its neighbours and prophesize accordingly. Salient environmental cues include an unidentified component in the worm’s bacterial food (possibly a carbohydrate), dietary cholesterol, temperature, and a constitutively secreted compound called dauer pheromone, an indicator of population density. A rich environment enhances reproductive growth, and in these favorable conditions, C. elegans’development from embryo through four larval stages (L1-L4) to reproductive adults is rapid, a matter of three days. Thereafter, self-fertilizing hermophrodites will produce broods of about zoo progeny and live another two weeks. In unfavorable conditions and high concentrations of dauer pheromone, worms will divert development to an alternate sexually immature third larval stage known as the dauer diapause. Preparation for diapause includes a shift to fat and carbohydrate storage, remodding of organs, recycling of cellular components through autophagy, and a behavioral change from solitary to social feeding. Dauer larvae themselves are nonfeeding, resistant to desiccation, oxidative, and thermal stress, and notably long lived. They lie still but remain responsive to prodding, cluster together in liquid drops to minimize desiccation and rear their heads in search of some means of opportunistic transport. Upon return to favorable conditions, they will mature to normal reproductive adults. The transformation is truly remarkable.

A dissection of diapause has shown that it is largely the prepared mind of the worm that perceives the environment, integrates various cues and computes the organismal decisions. Specific sensory and interneurins relay commitments throughout the body. Elegant work from a large number of laboratories reveals phyletically ancient endocrine systems that coordinate this process.

But we know relatively little about the exact environmental cues and their sensors. Among them, the dauer pheromone is the most potent inducer of diapause and perhaps best predictor of starvation. Pheromones are secreted chemicals that signal or elicit behavioral responses, typically between members of a species.

In the bigger picture what are the roles of pheromones in regulating mammalian life history choices? Pheromones are critical regulators of mating behaviors and female estrus in mammals, perhaps including humans. There are even reports of crowding pheromones that inhibit mating and delay puberty in feral mice, not unlike the worm. It is striking that in both worms and mammals, pheromones are detected by specific sensory neurons and can impinge on conserved central endocrine systems to influence developmental and behavioral responses associated with reproduction. Although much of our behavior is governed by visual cues, is it not conceivable that pheromones also influence our population behavior and signal the human condition?

EXERCISES

Ex.1 Find the omitted words or word combinations in the text.

1) How do simpler creatures … adversity?

2) Most living creatures can in fact sense their surroundings and make forecasts …

3) A key skill is predicting … .

4) C. elegans has a remarkable intelligence … its environment.

5) Worms will divert development to an alternate … third larval stage.

6) Upon return to favorable conditions, they will … to normal reproductive adults.

7) The dauer pheromone is the most potent … .

Ex.2 Translate into English.

1) Это зависит не только от индивидуума и его окружения, но также от популяции в целом.

2) Когда времена – благоприятны, многие организмы «распускаются» (развертываются) для быстрого размножения

3) Богатая окружающая среда увеличивает репродуктивный рост. 4)При возвращении к благоприятным условиям они дозреют до нормальных способных к репродукции взрослых.

4)Феромоны являются решающими регуляторами поведения спаривания.

5)И у червей и у млекопитающих феромоны обнаруживаются специальными (особыми) чувствительными нерврыми клетками.

Ex.3 Answer the questions.

1) How long is worm’s development from embryo through four larval stages to reproductive adults?

2) What does a key skill, honed during evolution, to predict and to calculate the odds of reproductive success depend on?

3) What does waiting for good times demand as we know that it is hardly passive?

4) What will worms do in unfavorable conditions and high concentrations of dauer pheromone?

5) What does preparation for diapause include?

6) How do dauer larvae behave themselves being in diapause?

7) What is the dauer pheromone?

Development of a combined selective enrichment

method and polymerase chain reaction (PCR)

assay for sensitive detection of Salmonella in

food samples.

Salmonellosis is one of the most important public health problems in many countries. The incidence of human diseases caused by food-borne pathogens, such as salmonella serovars has continually increased despite initiatives on the part of the food industries and federal regulatory agencies (mainly in the USA). In fact, changes in lifestyle as more meals are eaten outside the home, have increased the opportunities for transmission of this pathogenic bacterium through foods.

The standard technique recommended by the Association of Official Analytical Chemists (AOAC) and included in the Food and Drug Administration’s Bacteriological Analytical Manual (BAM) for the isolation of Salmonella from food samples consists of a 24 h selective enrichment, 24-48 h selective plating, and biochemical and serological confirmation of suspect colonies. The net result is a slow procedure, requiring 5-7 days for the complete detection of Salmonella in food samples.

Many recent studies have been concerned with the reduction of the time required for diagnosis. Alternative new methods using rapid cultural techniques, enrichment serology, antibody-based immunoassays, fluorescent antibody staining and DNA hybridization have been developed for the detection of Salmonella in pure cultures and food samples. However, limitations of some systems (lack of sensitivity, specificity or both) have prevented their general acceptance as alternative detection assays.

The polymerase chain reaction (PCR) has been used as an alternative method for confirmation of suspect Salmonella colonies after isolation and for detection of clinical and environmental samples. A recent study demonstrated the possibility of using PCR for Salmonella detection in meat samples. However the detection of this pathogen in foods remains difficult, mainly due to the presence of inhibitors and other microorganisms. In this study, we describe the development of a PCR assay complete to a selective enrichment method for the detection of small numbers of Salmonella cells in artificially multi-contaminated food samples.

EXERCISES.

Ex.1 Translate into English.

1) Сальмонелёз – одна из наиболее важных проблем национального здоровья во многих странах.

2) Увеличились изменения в стиле жизни, так как пища

съедается вне дома.

3) Возросла благоприятная возможность для передачи этой патогенной бактерии через пищу.

4) Многие недавние исследования касаются сокращения времени, требуемого для диагностики.

5) Недавнее исследование продемонстрировало возможность использования цепной реакции полимеразы (PCR -the polymerase chain reaction) для выявления сальмонеллы в образцах мяса.

Ex.2 Answer the questions.

1) Has the incidence of human diseases caused by food-born pathogens continually increased?

2) What organizations recommended the standard technique for the isolation of Salmonella?

3) What new alternative methods have been developed for the detection of Salmonella?

4) As what has the PCR been used after isolation and for detection of clinical and environmental samples?

5) What did a recent study demonstrate?

6) Why does the detection of this pathogen in foods remain difficult?

Ex.3. Say if the statements are false or true or there is no information in

text.

1) The detection of Salmonella in food samples is simple and quick process.

2) The PCR is the common method for detection of Salmonella colonies.

3) The food industries are seriously anxious of food-borne pathogens.

Protozoan and metazoan communities treating

a simulated petrochemical industry wastewater

in a rotating disc biological reactor.

The microfauna of adhered biofilms treating a simulated petrochemical plant wastewater was investigated in relation to the organic loading and the toxicity. Experiments in a six-compartment laboratory rotating biological reactor were performed at organic loading of O.99, 1.38 and 1.97 g/i. day. The concentration of organic compounds in the artificial wastewater (phenol, acetophenone and styrene), toxicity of the wastewater, number of representative types of microfauna, their biomass and species diversity were monitored along the reactor. During this study 25 species were identified and attributed to seven classes of the three types sareomastigophora, ciliophora and nemathelminthes. Eight species from 18 ciliates have been reported in the literature as being commonly found inhabitants of aerobic wastewater treatment plants. An inverse, relationship between the number of microfauna representatives and the organic loading was found. The presence of the most common species was related to the reactor operating conditions. A correlation between the toxicity of the wastewater measured by the Paramecium express-test and the distribution and abundance of microfauna was established. This express-test made it possible to predict the biological quality of the biofilm of activated sludge. Therefore, it is recommended as one of the control parameters to monitor systems of biological wastewater treatment.

Petrochemical industry wastewater treatment is one of the anthropogenic spheres where specific communities of microflora and microfauna are formed under the stressful influences of toxicity, lack of easily utilized nutrients, high values of organic and hydraulic loading and fluctuations of temperature and pH. The microflora, due to their primary importance in the process of initial destruction of organics, as well as their abilities to utilize a broad spectrum of compounds, appear as the primary component of the trophic chain Protozoa, the main consumers of bacteria, keep the suspended bacterial mass at low levels, thereby reducing the cause of secondary contamination of wastewater treatment plant effluents. Biofilm and activated sludge fauna are very sensitive to toxins, as compared to the microflora. This is why protozoa and metazoan have been suggested as indicators of effluent quality for activated sludge, trickling filter and rotating biological contactor bioreactors. The relationship between the number of ciliates and their species and physico-chemical variables measured in wastewater is stated. All the investigations have been concerned with the treatment of municipal wastewater or wastewater from the food or pharmaceutical industries. No data have yet been published concerning the microfauna of biofilms involved in petrochemical wastewater treatment. This present report is of general interest for properties of petrochemical wastewater compounds such as toxicity, mutagenicity and resistance to biological destruction.

According to the literature, a commonly used method for the evaluation of treatment process stability is microscopic observation of different protozoan species or key groups. We assumed that the observed responses of the test Paramecium are similar to those that would be exhibited by the microfauna in activated sludge used to treat the same wastewater. Our previous results showed an inverse relationship between the toxicity of treated wastewaters typical of the petrochemical industry and the member of microfauna in the activated sludge, as well as the biological treatment process efficiency in general.

The major objectives of this paper were:(i) to investigate the diversity of protozoan and metazoan populations of different specialized biofilms developed in the compartments along the length of the reactor in relation to the loading of the toxic contaminants; (ii) to determine the correlation between the toxicity of the wastewater measured by the express-test using Paramecium caudatum and the performance of the microfauna communities of the biofilms.

EXERCISES.

Ex.1 Complete the sentences according to the text and translate them.

1) A simulated petrochemical plant wastewater was investigated in relation to the … .

2) The concentration of organic compounds in the artificial wastewater … was monitored along the reactor.

3) The microflore appears as the primary component of … , the main … bacteria.

4) Protozoa and metazoan have been suggested as indicators of … for activated sludge.

5) All these investigations have been concerned with … .

6) Our previous results showed an inverse … between the … .

Ex.2 Translate into English.

1) Их биомасса и видовое разнообразие испытывались в реакторе.

2) Было обнаружено обратное соотношение между большим количеством представителей микрофауны и органической нагрузкой.

3) Присутствие большинства распространенных видов связано с действующими в реакторе условиями.

4) Этот экспресс-тест предсказал биологическое качество биоплёнки активированного осадка.

5) Констатируются отношения между большим количеством ресничных и их видов и физико-химических переменных измеренных в сточных водах.

Ex.3 Answer the questions.

1) How many species were identified and attributed to seven classes of the three types sareomastigophora, ciliophora and nemathelminthes?

2) What is one of theanthropogenic spheres where specific communities of microflora and microfauna are formed?

3) What are the main consumers of bacteria?

4) Why have protozoa and metazoan been suggested as indicators of effluent quality for activated sludge?

5) What have all these investigations been concerned with the treatment of municipal wastewater?

6) What are the observed responses of the test Paramecium similar to microfauna in activated sludge used to treat the same wastewater?

The origin and control of pandemic influenza.

In 1918 an epidemic of influenza killed 2O million people worldwide. Spanish flu, as it was called, was a horrific disease. The flu would start with headackes, muscular pain, and fever. These would be rapidly followed by vomiting, dizziness, labored breathing, and profuse sweating. Sometimes purple blisters would appear on the skin, and often blood would spurt out of the nose from hemorrhages in the lungs. Some of the victims of this dreadful, sudden, and unexpected illness went into violent fits of coughing. Death often followed, sometimes only hours after the first symptoms appeared.

Influenza viruses infect a number of different animals, and some of these viruses can cause very serious disease indeed, particularly in domesticated chickens and turkeys. Avian influenza viruses sometimes rapidly kill these birds, with 1OO percent mortality, and the symptoms resemble, at least to some extent, those of the Spanish flu in 1918. You can imagine, therefore, the concern felt when, in late 1997, a virulent bird flu virus, which had never before been seen in man, started infecting and killing people in Hong Kong. This virus, designated H5N1, killed six of the 18 people it infected. The virus seems to have been transmitted to people from infected chickens in the live bird markets, but so far there has been no evidence that the virus had learned how to spread from person to person. But there is also no reason to suppose that this might not happen, some time in the future. Killing off all the chickens in Hong Kong seems to have stopped the epidemic, at least for the time being. What could be done to control such a virulent influenza virus which, if it took off, would spread through today’s crowded communities with explosive violence? Vaccines probably could not be prepared in time, and the two anti-flu drugs available at the moment, amantadine and rimantadine, not only have undesirable side effects, but mutant viruses, resistant to these drugs, develop very rapidly.

Recently, a new approach to preventing and treating influenza in humans has been tested in clinical trials. These trials involved compounds that inhibit an enzyme on the virus (called neuraminidase) which the virus needs in order to complete its replication cycle in the body. These compounds are not vaccines, which prime the body’s immune system, instead, they act directly on the virus itself to stop it replicating, in much the same way antibiotics act to prevent the replication of susceptible bacteria.

EXERCISES.

Ex.1 Translate into Russian.

1) The virus seems to have been transmitted to people from infected chickens.

2) Killing off all the chickens in Hong Kong seems to have stopped the epidemic, at least for the time being.

Ex.2 Write out all the sentences with “ing-forms” from the text.

State whether they are gerund, nouns or participles.

Ex.3 Translate into English.

1) Испанка была страшной болезнью.

2) Смерть часто следовала иногда спустя лишь несколько часов после того как появились первые симптомы.

3) Некоторые из этих вирусов могут вызвать очень серъезную болезнь особенно у домашних цыплят и индеек.

4) Симптомы напоминали до некоторой степени симптомы испанки в 1918 году.

5) Опасный вирус птичьего гриппа начал поражать и убивать людей в Гонк Конге.

6) Вакцина возможно не могла быть приготовлена вовремя.

Ex.4 Answer the questions.

1) How many people were killed by the epidemic of influenza in 1918.

2) What was this epidemic called?

3) What are the first symptoms of the flu?

4) Can the flu infect a number of different animals?

5) When did the virulent bird flu start infecting and killing people?

6) How was the virus in Hong Kong designated?

7) Could this virus spread from person to person?

8) Why were the two anti-flu drugs available at that moment undesirable?

9) Has a new approach to treating influenza in humans been tested recently?

10) What does the virus need in order to complete its replication cycle in the body?

The Virus.

Viruses, unlike bacteria, can only grow inside living cells, using much of the cellular machinery to make thousands of new virus particles. This intimate relationship between virus and cell has made the development of anti-viral drugs very difficult, since many of the substances which “kill” the virus will also kill the host cell.

Unlike most viruses, which are regular in shape, flu virus particles may exist as long, spaghetti-like filaments, round balls, or any shape in between. They consist of a lipid membrane inside which is the genome of the virus, associated with five different viral proteins. Flu therefore belongs to the “enveloped” group of virosus. The influenza virus genome consists of eight separate pieces of ribonucleic acid (RNA) of negative sense each of which specifies the amino acid sequence of one ( and sometimes two) of the virus’s proteins. This segmented nature of the RNA allows different flu viruses to easily “mate” with each other, forming hybrid progeny viruses with bits of RNA from each parent virus.

Stuck onto the lipid envelope of the virus, like pins in a pincushion, are two glycoprotein molecules which play a vital role in the life-cycle of the virus. One of these surface “spikes” is a triangular, rod-shaped molecule called hemagglutinin, and one of its functions is to attach the virous to cells by way of specific receptors on the cell. The name hemagglutinin was originally used because the virus was found to agglutinate red blood cells, and this formed the basis of an assay for flu viruses. If the cell is a host cell which the virus is about to infect, instead of a red blood cell (which the virus cannot infect), the hemagglutinin spike will attach the virus to the cell through receptors on the cell, containing sialic acid, and then fuse the cell membrane with the membrane of the virus, allowing the RNA of the virus to get inside the cell and instruct the cell to make thousands of new virus particles.

The other “spike” on the surface of the virus is a mushroom-shaped enzyme, called neuraminidase. This enzyme removes the sialic acid receptors from the host cell (and from other newly made virus particles), and allows the virous to escape from the cell in which it grew and spread in the body to infect other cells. If this neuraminidase is blocked in some way, then the virus particles pile up in great clumps on the cell surface, unable to go anywhere, and the infection is effectively terminated.

EXERCISES.

Ex.1 Complete the following sentences from the text.

1) Viruses can only grow … .

2) Flu belongs to the “enveloped” … .

3) Different flu viruses form hybrid progeny viruses with bits of … from each parent virus.

4) The name hemagglutinin was originally used because … .

5) This enzyme removes the sialic acid receptors from … .

6) If this neuraminidase is blocked in some way, then … .

Ex.2 Translate into English.

1) Геном вируса гриппа состоит из восьми отдельных частиц рибонуклеиновой кислоты.

2) Одна из функций молекулы гемагглютинина-а – прикрепить вирус к клеткам.

3) Это сформировало основу образца для вирусов гриппа.

4) Другая “игла” на поверхности вируса – энзим грибовидной формы, называемый ньюраминидаза.

5)Этот энзим позволяет вирусу совершить побег из клетки, в которой он вырос.

Ex.3 Answer the questions.

1) Why is it very difficult to develop anti-viral drugs?

2) What form may flu virus particles exist?

3) Where is the genome of the virus?

4) What allows different flu viruses to easily “mate” with each other?

5) What plays a vital role in the life-cycle of the virus?

6) How can molecule hemagglutinin attach the virus to cells?

7) How did this molecule get its name “hemagglutinin”?

8) What does the RNA of the virus do as soon as it gets inside the cell?

The Influenza Virus keeps changing all the time.

There are two distinct kinds of influenza, types A and B. These two groups of the flu viruses have similar structures, but all of the A virus proteins are completely different from those of the B viruses as far as recognition by the immune system goes. It is flu A which infects pigs, horses, seals, whales, and many kinds of birds, as well as humans, while flu B has been found only in people.

Type A flu can be subdivided further into subtypes, according to how their hemagglutinin (H) and neuraminidase (N) antigens are recognized by antibodies. So far, 15 different H and nine different N antigens have been discovered, and Type A influenza viruses are made up of various combinations of these such as H1N1, H3N2, H5N1, and so on. Of these, H1N1, H2N2, H3N2, and, recently, H5N1 have been found to infect people. Many other combinations of H and N have been found in animal flu viruses. If you catch the flu, or receive flu vaccine, antibodies are formed in your body to the virus’s proteins. Some of these antibodies recognize small areas (epitops) on the hemagglutinin and neuraminidase of the virus. If the same virus then attemptes to reinfect you, those antibodies will bind tightly to its hemagglutinin and prevent the virus from infecting cells in the respiratory tract. You have developed immunity to that flu virus. With most viruses, that is the end of the story. In the case of measles, mumps, or smallpox, for example, infection or vaccination with these viruses results in immunity which may last all your life. These are stable viruses and change very little, if at all, over the years.

The influenza virus, on the other hand, is changing all the time. Major antigenic “shifts” occur in influenza Type A from time to time. In these “new” flu viruses suddenly appear in the human population. The first human influenza virus, isolated in 1933, was designated H1N1. This remained until 1957, when a new virus, H2N2, suddenly appeared in China. No one had any immunity to this new virus and it caused a pandemic of Asian flu. Other pandemic known to have occurred in this century were Spanish flu in 1918, Hong Kong flu in 1968, and Russian flu in 1977.

Between these shifts, the virus undergoes a series of small changes in its two surface proteins, H and N, called “drift”. What is the molecular basis of “shift” and “drift”? In the early 196Os it was thought that each virus contained a number of hemagglutinin antigens common to strains of the type, and that strain variation represented rearrangement of these antigens either quantitatively or spatially.

This was too small to code for more than a very few proteins, and so antigenic variation had to occur by some other mechanism. We therefore selected antigenic mutants of a couple of influenza viruses in the laboratory by passaging the viruses several times in the presence of sublimiting concentrations of neutralizing antibodies. We had already developed techniques for isolating hemagglutinin molecules from the wild-type and mutant viruses and also by this time had perfected a method for comparing the amino acid sequences of flu virus proteins. Nowadays methods are available for rapidly and accurately determining the sequences of very small amounts of proteins; but in 197O such techniques had not been fully developed. We used a method called “peptide mapping” in which the proteins were digested with trypsin to give a mixture of small peptides. These peptides were then separated by two-dimensional electrophoresis and chromatography, and stained to give a two-dimensional pattern or “map”. Identical proteins gave identical peptide maps. Proteins with one or two differences in their sequence gave slightly different maps, while proteins which differed greatly gave vastly different peptide maps.

When we looked at peptide maps of hemagglutinin molecules from the “escape mutants” (antigenic variants which escaped neutralization by antibody), we saw that while most of the spots were in the same location, one or two had shifted dramatically. This was the first indication that antigenic drift occurred by small changes in the amino acid sequences of the surface antigens of the virus. These experiments proved that drift results from mutations in the pieces of RNA coding the hemogglutinin and neuraminidase. These in turn cause small changes in the regions (epitopes) on the H and N molecules which bind antibodies, so that these antibodies can no longer bind and the virus is able to “escape” and cause an infection in a previously immune person.

EXERCISES.

Ex.1 Translate into English.

1) Эти две группы вируса гриппа имеют подобную структуру.

2) Все белки вируса А совершенно отличны от белков вируса В.

3) Грипп А поражает свиней, лошадей, тюленей, китов и многие виды птиц, так же как и людей, в то время как грипп В был обнаружен (найден) только у людей.

4) Если вы схватили грипп или получили вакцину против гриппа, в вашем теле образуются антитела к белкам вируса.

5) У вас развился иммунитет против вируса этого гриппа.

6) Эти вирусы устойчивы и изменяются очень мало, если вовсе не изменяются, на протяжении лет.

Ex.2 Fill in the blanks with the suitable words.

1) Type A flu can be subdivided … subtypes, … to how their hemagglutinin (H) and neuraminidase (N) antigens are recognized by …

2) If the same virus then attemptes to reinfect you, those … will bind tightly to its hemagglutinin and prevent the virus … infecting cells in the respiratory tract.

3) The influenza virus is changing … .

4) No one had any immunity to this new virus and it … a pandemic of Asian flu.

5) Nowadays methods are available … rapidly and accurately determining the … of very small amounts of proteins.

Ex.3 Answer the questions.

1) How many different H and different N antigens were discovered and give us the examples what combinations of them are made up?

2) Infection or vaccination from what diseases results in immunity which may last all your life?

3) When was the first human influenza virus isolated and was it designated?

4) When did a new virus H2N2 appear in China?

5) What pandemic of flu can you call?

6) What do we call “drift”?

7) What techniques for rapid and accurate determining the sequences of very small amounts of proteins were used in 1970 and how was that method called?

Where Do the New Viruses come from?

What is the origin of the “new” viruses which cause the major influenza pandemics? How would one go about trying to find out where these viruses come from? Why do they always seem to come from China?

In February 1957, a virus suddenly appeared somewhere along the road between Kutsing and Kweiyang in southern Chine which was quite unlike the H1N1 viruses previously causing flu infections in that region. The virus was designated H2N2 and caused a major pandemic of Asian flu. Where had the virus come from?

In July 1968, again in China, another “new” virus made its appearance. This virus had the same neuraminidase (N2) as the old Asian flu viruses, but the hemagglutinin was so different from that of the Asian flu virus that antibodies to the Asian (H2) hemagglutinin did not bind at all to the new hemagglutinin. The virus was therefore called H3N2 and it caused the Hong Kong flu pandemic of 1968. Again we used peptide mapping to examine the sequences of the Asian (H2) and Hong Kong (H3) hemagglutinins. It was immediately clear that the two hemagglutinins differed greatly in their amino acid sequence and that there was no way one could have arisen from the other by mutation in such a short period of time. The Hong Kong H3 hemagglutinin had to have come from somewhere else. But where? And how?

At an international virology conference in Budapest, we heard that the hemagglutinin in flu viruses from ducks and horses cross-reacted antigenically with the hemagglutinin of the Hong Kong virus. We then showed, by peptide mapping, that H molecules from Hong Kong flu and from a duck influenza virus were very similar in amino acid sequence. It was now clear how the Hong Kong virus had originated: the new virus was a reassortant (hybrid) virus with the N2 spike from the “old” Asian flu virus and the “new” H3 spike from an animal or bird flu virus.

Later, more sophisticated sequence analyses confirmed these findings and showed that the Asian H2N2 virus was also a hybrid virus.

Why do these hybrid viruses always seem to arise in Chine? One possibility is the close contact between people, poultry, and pigs in this country, increasing the chances for reassortant events between viruses to occur. However, conditions like this do exist elsewhere in the world, and it remains a mystery why China should be the birthplace of flu. It is clear that the recent H5N1 bird flu virus, which infected 18 people and caused six deaths in Hong Kong at the end of 1997, was not a hybrid virus (all its RNA segments were of avian virus origin), and it may be that other factors will allow certain animal influenza viruses to cross the species barrier and infect people.

There is no doubt that mutations in a fairly harmless flu virus can turn it into a killer.

The flu team at St. Jude children’s Research Hospital in Memphis examined the virus before and after it became virulent.

Although drift occurs in both flu A and B, the major shifts have only been seen in flu A. Possibly this is because the influenza Type A virus is found in a variety of hosts, while flu B has only ever been found in human infections.

EXERCISE.

Ex.1 Complete the following sentences from the text.

1) The virus was designated … and it caused a major … of Asian flu.

2) This virus had the same neuraminidase (N2) as the … .

3) We used … to examine the sequences of the Asian (H2) and Hong Kong (H3) hemagglutinins.

4) There was no way one could have arisen from the other by … in such a short period of time.

5) We then showed, by peptide mapping, that H molecules from Hong Kong flu and from a duck influenza virus were very … in amino acid sequence.

6)It remains a mystery why China should be the … of flu.

7) There is no doubt that mutations in a fairly harmless flu virus can … a killer.

8) Flu B has only ever been found in … .

Ex.2 Answer the questions.

1) What virus suddenly appeared in southern China in February 1957?

2) Where did a new virus cause flu pandemic of 1968? What was its name?

3) What became immediately clear when we used peptide mapping to examine the sequences of the Asian and Hong Kong hemagglutinins? E

4) What did we hear about cross-reacted antigenically at an international virology conference in Budapest?

5) How did the Hong Kong virus originate?

6) What hybrid viruses can you call?

7) What kind of conditions can cause the rise of hybrid viruses?

8) What makes a fairy hamless flu virus turn into a killer?

9) Why were the major shifts seen in flu A?

Ex.3. Choose what statement is the true answer to the questions.

Why do the major influenza pandemics come from Asia? What is the origin of flu virus both flu A and B?

1) Is it because of the close contact between people, poultry and pigs in

China?

2) It is because of mutations and drift in both flu A and B.

3) Birds are the carriers of flu virus.

Warren McCulloch’s search for the logic

of the Nervous system.

The 194Os saw the beginning of the computer age, building on the logical investigations of the 193Os and leading to the development of artificial intelligence in the 196Os and of neurally-inspired paradigms for neurally inspired methods of adaptive, parallel computing in the 198Os and 199Os. Among the key players in these developments was the neurologist Warren Sturgis McCulloch with Walter Pitts he showed how to formalize the brain as a network of neurons viewed as logical processing elements – a key element in the definition of the classical computer architecture based on stored programs that was devised by John von Neumann, and in the cybernetics of Norbert Wiener. With the addition of learning rules built on the ideas of Depald Hebb and Frank Rosenblatt, this formalization also led to the resurgence of artificial neural networks as a new computing technology from the mid-198Os onwards, a resurgence coupled with that in the computational modeling of the brain, thus closing the circle back to McCulloch was concerned with computer technology, as is reflected in his concerns for reliable computing from unreliable neuronlike elements and for redundant, distributed computing by larger modules. However, throughout his life he was driven less by the demands of technology than by the quest to understand how we think. Specific experimental techniques were always secondary to the basic questions: what is the logic of thought? What is a person? What is a man that he may know a number? As a young man worrying about the fundamental questions of philosophy, metaphysics, and epistemology, McCulloch set himself the goal of developing an “experimental epistemology”: how can one really understand the mind in terms of the brain? More particularly, he sought to discover “ A Logical Calculus Immanent in Nervous Activity”. The present paper will seek to provide some sense of McCulloch’s search for the logic of the nervous system, but will also show that his papers contain contributions to experimental epistemology which provide great insight into the mechanisms of nervous system function without fitting into the mold of a logical calculus. Moreover, McCulloch was not only a scientist but also a storyteller poet, and memorable “character”.

EXERCISES.

Ex. 1 Write out all the sentences with “ing-forms” from the text.

State whether they are gerunds, nouns or participles.

Ex.2 Complete the following sentences from the text and

translate them into Russian.

1) Warren McCulloch showed how to … the brain as a network of neurons.

2) This formalization led to the … of artificial neural networks.

3) Throughout his life he was driven less by the … than by the quest to understand how we think.

4) How can one really understand the mind … the brain?

5) His paper contains … to experimental epistemology.

Ex.3 Answer the questions.

1) What do we call the beginning of the computer age?

2) Who are the key players in the development of computing?

3) What is a key element in the definition of the classical computer architecture based on stored programs?

4) What did this formalization lead to?

5) What were McCulloch’s concerns?

6) What were the most important basic questions for McCulloch?

7) What did he seek to discover?

8) Do his papers contain contribution to experimental epistemology which provide great insight into the mechanisms of nervous system function?

Unesco Global Network for Molecular

and Cell Biology (MCBN)

Unesco stands for United Nations Educational, Scientific and Cultural Organisation: science occupies a central position not only in its acronym but also in its activities.

At the end of the 198Os two facts had become definite: that cell and molecular biology play a central role in science, and that networking had developed into a new dimension of knowledge. Most of the nonpolitical problems that afflict the world occur in the developing countries. Among these are malnutrition, environmental pollution, uncontrolled population growth, immune-deficiencies and the spreading of viral, bacterial and protozoan infections diseases. It was also recognized that all these problems are associated with areas investigated by molecular and cell biology. During the past several decades we have witnessed spectacular progress in the application of knowledge derived from basic biological sciences to solving problems in a wide variety of areas of great importance to human welfare: vaccinations, nutritional and hygienic measures, disease prevention and birth control represent milestones in solving these problems in countries with highly developed technology.

It is likewise obvious that the rest of the world has not felt an appreciable impact of these solutions. Prospective researchers in the field of cell and molecular biology often leave for more promising horizons, producing a regrettable brain drain.

Although the two types of countries require different solutions, the goal is the same: to help in the development of sustainable scientific growth, adapted to the local needs, based on local initiatives, and not imposed from the outside.

Loss of science is equivalent to the loss of rationality. It leads to the loss of opportunities to discover talent, it is ultimately associated with impoverishment of ideas of people and financial opportunities. Such a situation leads to the logic of confrontation rather than the logic of peace. Science is a tool for peace.

The best local approach to maintain the life of science is to concentrate local talent in centres of scientific excellence. The establishment of similar molecular and cell biology centres of excellence in various regions of the world will provide a reservoir of talent and expertise to allow opportunities for the training of researchers from developing countries. The MCBN centres will initiate, stimulate, and facilitate the exchange of ideas, people, expertise and skills, and are encouraged to share facilities with other network member laboratories. This provides an opportunity for experts in molecular and cell biology to carry out short working visits to all regions of the world to promote MCBN network activities and to support programs in Universities and other scientific organizations. The Network implements other activities including lectures and technical advice by senior specialists to laboratories that may require such assistance, transfer of knowledge and recently available technical information. The first of these centres has been created in Warsaw Poland. A feasibility study is being made for a similar institute in Africa, in Nairobi, Kenya.

The trump card in this game is UNESCO itself: a UNESCO of great tradition with newly acquired credibility and weight provided by the recent guidance of its Director General, Federico Mayor.

EXERCISES.

Ex.1 Complete the sentences taken from the text. Translate them.

1) All nonpolitical problems are … with areas investigated by molecular and cell biology.

2) Prospective researchers in the field of cell and molecular biology often … .

3) Such a situation leads to the logic of confrontation rather than … .

4) The MCBN centres will initiate, stimulate, and facilitate the exchange of … .

5) The Network implements other activities including … .

Ex.2 Translate into English.

1) Наука занимает центральное положение не только в акрониме, но также в своей деятельности.

2) Клеточная и молекулярная биология играет центральную роль в науке.

3) Большинство неполитических проблем в мире случаются в развивающихся странах.

4) Потеря науки эквивалентна потери здравого смысла.

5) Наука – инструмент мира.

6) Первый из этих центров был создан в Варшаве.

Ex.3 Answer the questions.

1) What became definite in the area of science at the end of the 1980s?

2) What are nonpolitical problems to be solved?

3) What problems are being solved on the basis of biological sciences serving to human welfare?

4) What is the problem of brain drain?

5) What is the goal of establishing scientific centres in different countries?

6) What does loss of science lead to?

7) What will molecular and cell biology centres provide?

8) In which way can the Network help in all regions of the world?

9) Where else can similar institutes be established?

10) Who is the director of UNESCO?

Control of the production of individual

fusicoccins at different dissolved

oxygen concentrations.

The regulatory effect of different concentrations of dissolved oxygen on the production of fusicoccins by the fungus F. usicoccum amygdali Del was studied. The maximum output of total fusicoccins was obtained by using a profiled dissolved oxygen tension (DOT) regime, in which the DOT was maintained at 15-20% during the whole fermentation shortened the fusicoccins production phase. The fermentation performance at a low DOT (5-8%) inhibited both the accumulation of biomass and the production of fusicoccins. At high DOT (40-50%), an accelerated accumulation of the biomass with an expressed autolysis of mycelia took place, and the production of fusicoccins was lowered. The qualitative composition of individual fusicoccins varied substantially at different DOTs.

Oxygen is one of the main limiting gaseous substrates in the microbial synthesis processes. It is known that an intensive mixing of the medium and the maintenance of a high level of oxygen saturation leads to a high concentration of biomass whereas oxygen limitation can enhance the production of certain metabolities. For example, the production of bialaphos, a herbicide, by Streptomyces hygroscopicus was increased in highly productive strains under a low oxygen partial pressure. Conversly the formation of cephalosporin C was enhanced at a high oxygen concentration, while penicillin formation was increased by a low level of dissolved oxygen.

Fusicoccins (FCs) are glucosides of tricyclic diterpene differing, in their chemical structure by the number of acetyl groups their positions, the extent of the oxidation of the aglycone moiety, as well as by their physiological activity. More than 40 naturally occurring and chemically modified FCs have been described.

In the fermentation of FCs by the fungus Fusicoccum amygdale, it was shown that different cultivation conditions such as the composition of the fermentation media, pH, the cultivation time, temperature, the aeration regime, and illumination affected the production of different individual FCs.

The productivity of the shear-sensitive fungus F. amygdali causes problems of mass transfer for its metabolite biosynthesis. F. amygdali is rather sensitive to mixing, as it grows in the form of large mycelial agglomerates with long peripheral hyphae with a proportion of filamentous mycelium. Previously, different constant and stepwise regulated mixing regimes using turbine agitators were tested in an attempt to provide effective mass transfer during the FCs production phase to avoid damaging effects on the mycelium. The replacement of turbine agitators with counterflow impellers improved the oxygen transfer efficiency significantly, provided the formation of a more productive morphology of F. amygdali, and increased the concentrations of the biomass and FCs. In the present work, we investigated the dissolved oxygen concentration as the main variable for process control, assuming that aeration creates considerably less shear damage.

EXERCISES.

Ex.1 Complete the following sentences taken from the text.

1) The maximum output of total fusicoccins was obtained by … .

2) The qualitative composition of individual fusicoccins varied … .

3) The production of bialaphos, a herbicide, was increased in … .

Ex.2 Translate into English.

1) Кислород является одним из главных лимитирующим газовым субстратом в процессах микробиологического синтеза.

2) Высокая концентрация биомассы может быть вызвана интенсивным смешением среды и сохранения раствора с высоким уровнем кислорода.

3) Образование пенициллина увеличилось с помощью низкого уровня растворённого кислорода.

4) Было описано более чем 40 естественно встречающихся и химически модифицированных фьюзикоксинов (FCs).

5) Продуктивность чувствительного среза гриба вызывает проблему переноса массы на его метаболитный биосинтез.

Ex.3 Answer the questions.

1) What was studied on the production of fusicoccins by the fungus?

2) What did the fermentation performance at a low DOT (dissolved oxygen tension) inhibite?

3) Where does an intensive mixing of the medium lead to?

4) What do fusicoccins differ in?

5) What are the most studied FCs and what are their characteristics?

6) What are different cultivation conditions in the fermentation of FCs by the fungus?

Text

Metabolism is the sum of all the chemical reactions that take place within every single cell of a living organism, providing energy for vital processes and synthesizing new organic material.

Metabolic reactions are of two sorts. Some are anabolic reactions, which use energy to build complex molecules from simple molecules. The others are catabolic reactions, which make chemical energy available in the course of breaking down complex molecules into simpler molecules.

In order to carry on its life processes, every organism takes from its environment “free”, or “useful”, energy, i. e. energy that is capable of performing work in the conditions of uniform temperature and pressure which characterize the interior of a cell. The organism eventually returns to its environment an equivalent amount of energy, much of it in the biologically unusable form of heat. All the energy used by living organisms derives ultimately from the sun. Photosynthetic plants use solar energy directly to synthesize organic compounds from inorganic constituents, e. g. carbon dioxide, water, and digesting photosynthetic organisms (or organisms that have digested photosynthetic organisms), nonphotosynthetic organisms obtain nutrients – mostly proteing, carbohydrates, and lipids – that serve them both as indirect sources of solar energy and as materials from which to synthesize their organic constituents.

In all organisms, the cellular reactions involved in metabolism make use of a particular energy – transferring compound – adenosine triphosphate (ATP). ATP releases energy when it is reduced; i. e., when it drops its phosphate groups to become first adenosine diphosphate (ADP) and then adenosine monophosphate (AMP). As ATP is reconstructed from these intermediate compounds, energy is stored. During anabolic reactions, which require energy, ATP is reduced; during catabolic reactions, which yield energy, ATP is synthesized. Every cellular chemical reaction is mediated by a specific enzyme (a protein that initiates and provides a site for a reaction between substances, without itself being chemically changed in the reaction). By their availability or unavailability as catalysts for chemical reactions, these enzymes regulate anabolism and catabolism. The first phase of the liberation of chemical energy from food occurs mainly in the digestive tract in animals and is mostly a preliminary to catabolism; large food moleculas are broken down into a number of relatively smaller molecules. Thus, proteins are broken down into the 20 or so amino acids of which they are composed, carbohydrates are broken down into simple sugars, and lipids into fatty acids and glycerols. The products of the first phase enter into the cells, where they are incompletely oxidized (by removal of hydrogen atoms or electrons). This incomplete oxidation constitutes the second phase of energy liberation, the key products of which are three carbon compounds – acetyl coenzyme A, oxaloacetate, and α-oxoglutarate. The details of the third and final phase of energy release from food were first elucidated by Sir Hans Krebs in 1937; in it, the products of the second phase combine and pass through a sequence of reactions (called the Krebs cycle, or tricarboxylic acid (TCA cycle) that results ultimately in the reformation of oxaloacetate and the production of two molecules of carbon dioxide (terminal respiration). Hydrogen atoms removed from intermediate products of this cycle are passed along a chain of carriers, eventually combining with oxygen to form water. Energy is released as the hydrogen atoms pass down the carrier chain; this energy is used to synthesize many moleculas of ATP. This method of ATP synthesis, which requires oxygen, is called oxidative phosphorylation. Yeasts and certain other microorganisms do not produce ATP by oxidative phosphorylation; instead, they use intermediate products of the second phase of energy liberation as hydrogen acceptors. The end products of this process, which is called fermentation, are ethyl alcohol or lactic acid. Fermentation does not require oxygen, but it results in the synthesis of substantially less ATP than is achieved via oxidative phosphorylation. Fermentation also occurs in animal muscle cells when energy needs outstrip the cell’s supply of oxygen.

The catabolic process begins with proteins, carbohydrates, and lipids and has as its rather indefinite end products the interconvertible intermediary compounds of the Krebs cycle. Anabolism begins with intermediate compounds and has as its end products the proteins, carbohydrates, lipids, and other large moleculas that make up the tissues of the organism. Although certain chemical reactions and intermediary products (e. g. acytyl coenzyme A) occur in both processes, the catabolism and anabolism of a specific compound are not achieved through reversals of the same chemical pathway.

Control over the rate of metabolic processes results from the greater or lesser production of the enzymes involved. Fine control results from the property of some of these enzymes (called pacemaker enzymes) whereby interaction with certain molecules other than their substrates (the substances they catalyze) causes them to modify their catalytic activity. The moleculars that cause these modulations interact with the pacemaker enzymes at sites other than their active sites (those where they react with their substrates), These interfering moleculars may be ATP or other products of the metabolic process to which the enzyme contributes, or they may be substances involved in another metabolic process. In any case, their availability to interact with the enzyme is an indication of the degree to which the reaction catalyzed by the enzyme may at a given moment be necessary to or superfluous in maintaining the metabolic balance of the organism.

Information about metabolic pathways is obtained in various ways. Organisms whose metabolisms are unbalanced (through either stress or disease) may accumulate abnormal quantities of particular metabolites (chemical substances involved in metabolism), a situation that will often be indicative of metabolic processes within the organism. Information as to metabolic pathways may also be obtained by feeding an or - ganism nutrient compounds containing isotopes and then monitoring the isotopic atoms as they pass through and out of the organism. It is through the use of isotopes that rates of degeneration and reconstruction of the various tissues in the human body are known (e. g. proteins in liver cells are replaced every five days, though the liver cells themselves last several months; proteins in muscle and brain tissue last much longer than do liver proteins). Important information linking enzyme-substrate pairs has been gained by the use of laboratory-bred mutants; these animals, genetically unable to synthesize particular metabolic enzymes accumulate the substrate of that enzyme in their cells.

Metabolic diseases arise from nutritional deficiencies, especially of vitamins or proteins; in connection with diseases of the endocrine system, the liver, or the kidneys; or as a result of genetic defects.

EXERCISES.

Ex.1 Read the text; make a plan of it and head it.

Ex. 2 Answer the questions.

1) What is metabolism?

2) What are metabolic reactions?

3) Where do living organisms derive all their energy?

4) In what cases can we speak about ATP (adenosine triphosphate) reduced or synthesized?

5) What is a specific enzyme and what does it do?

6) How many phases of the liberation of chemical energy are there?

7) What occurs after the first phase of the liberation of chemical energy?

8) What is called the Krebs cycle?

9) What are the pathways of the catabolic and anabolic processes?

10) How can information about metabolic pathways be obtained?

Ex.3. Say if the statements are false or true or there is no information in the text.

1) Energy released from food occurs in several stages.

2) Fermentation is not connected with the process energy liberation.

3) Excess storage of fat in liver cells may be the result of heavy feeding.

Использованная литература:

1)The New Encyclopedia Britannica, v.8, p. 55. Metabolism.

2) Cell Metabolism, v. 1 January, 2005

№ 1,

№ 2,

№ 3.

3) Perspectives … winter 2000.

4)Veterinarian. Iowa State University.

v.63 Spring 2001, №.1.

v.43, № 1, 1999.

v.43, № 2 , 2000.

5)World Journal of Microbiology and biotechnology.

1997, v. 13 , Number 1-6.

London. Philodelphia.

[1] PPAR – the peroxisome proliferator-activated receptor family - семья перикисно возрастающе-активирован

ного рецептора.

[2] The roundworm c. elegans – аскариды