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EXÁMENES DE INGLES II – FACULTAD DE BIOQUIMICA Y CS. BIOLÓGICAS
1) SMALLPOX VIRUS WINS STAY OF EXECUTION
The debate over what should be done with variola has been rumbling on for years. The chief
argument of those calling for destruction is that the virus is too dangerous to be allowed to “live”.
Infected people have a 20% to 40% risk of dying, and in 1967 alone, variola’s last year in the wild, it
infected some 10 million people. By now, the destructionists say, people will have lost their immunity to
variola, and no containment facility is 100% safe against accidental escape of the virus or terrorist attack.
“If there were an outbreak today, about a million people could die or go blind from the disease in the
several months it would take to get enough vaccine produced”, says Ghendon. If researchers want to
study the virus, he adds, they can use cloned variola DNA or the nucleotide sequences that have been
made of several strains of the virus’s genome. “ I cannot understand why anybody would want to study
the virus of a disease that no longer exists when there are micro-organisms emerging or re-emerging that
are real public health threats today ,” he says.
Those arguing against immediate destruction say that the slight risk of the virus escaping is
outweighed by the wealth of scientific information to be obtained from the live virus –about its virulence,
its pathogenic mechanisms, and its potential in screening drugs for other viral diseases, including AIDS.
Should variola be destroyed, some ecologists argue, it would also constitute the first deliberate
eradication of a biological species. “There is no doubt that some information will be irrevocably lost by
destroying the virus. But it is a hypothetical call as to how useful that information would be”.
Biological Defense Establishments argue that with no international mechanism for verifying if a
state has clandestine stocks of variola, no potential defense against possible future biological threats can
be planned. What if such state changes the virus slightly, so that the existing vaccine is ineffective?.
Samples of the original live virus would be needed to develop rapid tests for smallpox virus attacks as
well as new vaccines.
With the death sentence on variola growing ever more complicated, WHO (World Health
Organization) is resigned to a long fight. Says Kumate, “This is too important a matter to settle by a
simple majority”.
Science, vol 267
1) Traduzca el texto.
2) Indique si las siguientes afirmaciones son verdaderas o falsas.
a)
b)
c)
d)
e)
El virus de la viruela podría ser útil en la investigación de drogas contra el Sida.
Las probabilidades de que una persona infectada viva son del 20 al 40%.
No existen mecanismos internacionales para el control de los stocks del virus de la viruela.
No es posible usar el DNA del virus de la viruela clonado para investigaciones.
El virus de la viruela se considera un virus peligroso para su uso en investigación
3) Exponga clara y brevemente:
a) Tres argumentos a favor de la erradicación del virus de la viruela.
b) Tres argumentos en contra de su erradicación.
4) Seleccione la alternativa correcta (de acuerdo con el texto)
a) El virus de la viruela I) fue exterminado totalmente II) fue controlado III) existe, pero en
laboratorios.
b) En el caso de un nuevo brote de viruela I) todos podríamos resistir la infección II) nadie podría
resistir la infección III) habría muchas muertes.
c) La información que se perdería destruyendo al virus I) es imprescindible II) no es
imprescindible III) no se sabe.
d) I) Existen II) No existen III) Se están investigando otras formas de realizar estudios basados en
el virus de la viruela.
e) I) Es posible II) No es posible III) Tal vez se pueda encontrar algún lugar de donde el virus no
pueda escapar.
2) CANCER: A FAILURE OF IMMUNITY?
The theory that declining immunocompetence is an underlying factor in the causation of both
aging and cancer is appealing but raises some knotty issues. The concept is based on several
assumptions: that tumor cells carry specific antigens; that competent immune systems recognize these
antigens and destroy tumor cells; and that cancer would develop only if the immune response to
antigens on tumor cells were somehow muted or the individual were immunodeficient.
Proponents of this theory claim that the increased incidence of cancer in older people could be
explained by age-associated tumors. Unlike tumors that are induced in experimental animals by
chemicals or viral agents, most human tumors have weak or no demonstrable tumor antigens.
Furthermore, when being profoundly immunocompromised, as in infection with HIV (Human
immunodeficiency virus, the virus that causes AIDS) or after corticosteroid therapy to prevent organ
transplant rejection, the tumors patients develop are usually lymphomas (cancer of the lymphatic
system) or the form of skin cancer called Kaposi’s sarcoma rather than the broad spectrum of tumors –
e.g., lung, colon, breast, prostate- observed in older people. If immune senescence accounted for the
increasing incidence of cancer with age, it would be expected that elderly people would have primarily
tumors of types similar to those seen in other immunodeficiency states, which simply is not the case.
Why then, do older people have more cancer? Although there seems to be no single
explanation, several contributing factors have been identified. Perhaps the most important is time. The
process of carcinogenesis is complex and has many steps, only now being elucidated at a genetic level.
In humans the sequence of events in carcinogenesis is best understood for colon cancer. A series of five
to seven events that should occur for a tumor to develop, have been identified and some clinical stages
in the development of colon cancer. Other easily biopsied cancers (such as cervical, lung, prostate, and
breast) may soon be shown to have similar sequential pathogeneses.
1)Traduzca el texto.
2) Realice un breve resumen con las ideas centrales de cada párrafo.
3) Indique si las siguientes afirmaciones son verdaderas o falsas:
a)
b)
c)
d)
Los tumores humanos presentan gran cantidad de antígenos tumorales.
Las secuencias de patogénesis del cáncer de mama y colon son distintas.
Los tumores más comunes en pacientes inmunocomprometidos son los linfomas.
Los estudios realizados en ratas no son claros respecto al origen del cáncer de colon.
4) Conteste brevemente las siguientes preguntas:
a)
b)
c)
d)
¿Cómo la teoría propuesta explica el desarrollo del cáncer?
¿Cuál es el factor más importante que conduce al desarrollo de cáncer en gente mayor?
Enumere tres tumores que se desarrollen más comúnmente en esas personas.
¿Qué tipos de cáncer se desarrollan mas comúnmente en pacientes con corticoterapia?
3) MICROBIAL TOXINS
The nature of toxins
Most of our knowledge of microbial toxins has come from work on pathogenic
bacteria, for the search for bacterial toxins began shortly after the discovery of the role
bacteria had as ethiological agents for human disease. By 1890 the toxins of two
important human pathogens, Corynebacterium difteriae and Clostridium tetani had
been discovered, and a sterile filtrate which had been prepared from the fully grown
culture had been observed to cause death when injected into experimental animals.
What autopsies revealed was that these animals showed the characteristic lesions
associated with the specific natural infection. The toxic substances -which proved to be
heat-labile and are now known to be proteins- were termed exotoxins, for they were
present in the medium, although not associated with the bacterial cells.
A number of other pathogenic bacteria have been subsequently shown by comparable
methods to produce exotoxins that have specific effects, yet filtrates which had been
prepared from cultures of many important pathogens failed to show toxicity. This led
to the examination of the bacterial cells themselves (which had been killed by heat) as
possible toxic agents. Not only did such experiments show that the cells of nearly all
Gram-negative pathogenic bacteria are intrinsically toxic but heat-killed cells of many
non-pathogenic Gram-negative bacteria were shown to have similar effects. The heatstable toxins with which the cells of Gram-negative bacteria were associated came to
be known as endotoxins. Many years of intensive study were required to reveal their
nature and cellular origin; it is now known that endotoxins are lipopolysaccharideprotein complexes, which derive from the outer layers of the cell walls of Gramnegative bacteria.
The examination of the cells and culture filtrates of pathogenic bacteria which had
been grown in vitro led to the recognition of a number of microbial products that
damage the host, yet many important bacterial pathogens remained to be studied,
specially the causative agents of anthrax and plague, for which this approach had failed
to reveal any significant toxic product.
The toxins of both organisms were later found to be complexes of two or more
substances, each of which was non-toxic by itself but which together acted
sinergistically to produce a toxic effect. Such knowledge allowed the assay systems for
the toxins to be refined to such an extent that -in each case- it became possible to
establish the production of toxin by cultures of bacteria in vitro.
1) Traduzca este texto
2) Sintetice brevemente los puntos principales de los que habla el texto.
3) Responda estas preguntas:
a) Cómo fue que se descubrió la existencia de las toxinas de Corynebacterium difteriae y
Clostridium tetani?
b) Qué significa el término “exotoxins”?
c) Todas las bacterias producen “exotoxins”? Explicar.
d) Qué características tienen las “endotoxins”?
e) Cómo actúan las toxinas de “anthrax” y “plague”?
4) Marque con (X) las oraciones que expresan información contenida en el texto.
a)
b)
c)
d)
Algunas toxinas son estables al calor, pero otras no.
Las endotoxinas y las exotoxinas tienen diferente composición.
Los clostridios forman esporos que pueden sobrevivir por largo tiempo.
Los agentes causantes de antrax y plague tuvieron que ser estudiados de una forma
diferente al resto.
e) Los métodos de aislamiento de toxinas son extremadamente complejos y lentos.
4) THE TOPOLOGY OF WALL AND MEMBRANE SYNTHESIS
During the cell cycle of a bacterium the surface layers of the cell continuously
change in form. The increase in the volume of the cell is accompanied by an extension
of the area of both wall and membrane. With the onset of division, a vectorial change
in wall deposition occurs, the transverse septum beginning to grow inward, at right
angles to the cell wall, until it forms a complete septum separating the two daughter
protoplasts. Thereafter, the transverse septum peels apart into two layers, each of which
becomes the newly formed pole of one of the daughter cells.
The terminal steps in the synthesis of both phospholipids and he monomers destined
for incorporation into major wall polymers are all mediated by enzymes which are
known to be localized in the cell membrane, yet it is not known whether these enzymes
are concentrated at specific sites in the membrane or more or less evenly dispersed
over its surface.
The increase in the area of the wall and membrane that accompanies cell growth
might occur by the insertion of new material at specific growth points or by the
intercalation of new material at numerous sites in the preexisting wall and membrane
fabric. Many experiments designed to examine this question have been performed,
often with conflicting results. It is important to keep in mind that secondary
displacement of newly incorporated materials may occur. For example, the plasticity of
the cell membrane and the outer wall layer of Gram-negative bacteria could cause an
apparently random distribution of newly synthesized components, even if they were
initially incorporated at specific points. The same effect would result from a rapid
turnover of wall or membrane constituents. Consequently, evidence for localized
growth of walls or membranes is incontrovertible, whereas evidence that suggests
random incorporation is often ambiguous.
In the streptococci, Gram-positive bacteria with spherical cells, clear evidence for a
localized equatorial region of wall growth has been obtained by the use of antisera
specifically directed against wall constituents. The antiserum, which is conjugated with
a fluorescent dye, is used to coat the cells for them to be made intensely and uniformly
fluorescent. During subsequent growth in the presence of non-fluorescent antisera, the
poles of the cells remain intensely fluorescent for several generations and new nonfluorescent wall areas are progressively inserted between the “old” wall material as
growth proceeds. Thus, during exponential growth of streptococci, wall synthesis is
highly localized, and the walls are not secondarily modified. However it has also been
shown that, when the growth of streptococci is prevented by inhibition of protein
synthesis (either by specific aminoacid deprivation or by chloramphenicol treatment),
the synthesis of wall material continues and results in a progressive thickening of the
wall over its entire surface.
1) Traduzca este texto
2) Dibuje cada una de las etapas de la división celular descriptas.
a)
b)
c)
d)
3) Diga si los siguientes enunciados son verdaderos o falsos
a) En la síntesis de algunos componentes de la pared celular intervienen
enzimas.
b) No se conoce con exactitud dónde están localizadas estas enzimas.
c) La membrana celular juega un importante papel en la síntesis de algunos
componentes de la pared celular.
d) Las enzimas participan de las primeras etapas de síntesis de fosfolípidos y
monómeros.
e) Todavía no se conoce cuál es la distribución de esas enzimas.
4) Responda estas preguntas
a) Señale en el texto y traduzca una definición de streptococo
b) Para qué se usa un antisuero fluorescente?
c) Qué se ha querido demostrar con la utilización de antisueros fluorescentes?
d) El uso de ciertos antibióticos, qué efecto produce en relación con la pared celular
de los estreptococos?