EXMENES DE INGLES II FACULTAD DE BIOQUIMICA Y CS.

BIOLGICAS
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% ris of dying! and in "#$% alone! variola&s last year in the wild! it infected some
"0 million people. 'y now! the destructionists say! people will have lost their immunity to variola! and no
containment facility is "00% safe against accidental escape of the virus or terrorist attac. If there were an
outbrea today! about a million people could die or go blind from the disease in the several months it would
tae to get enough vaccine produced! says (hendon. If researchers want to study the virus! he adds! they
can use cloned variola )*+ or the nucleotide se,uences 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 e-ists 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 ris 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 +I)0.
0hould 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. 'ut it is a hypothetical call as to how useful that information would be.
'iological )efense 1stablishments argue that with no international mechanism for verifying if a
state has clandestine stocs of variola! no potential defense against possible future biological threats can be
planned. 2hat if such state changes the virus slightly! so that the e-isting vaccine is ineffective3. 0amples
of the original live virus would be needed to develop rapid tests for smallpo- virus attacs as well as new
vaccines.
2ith the death sentence on variola growing ever more complicated! 245 62orld 4ealth
5rgani7ation8 is resigned to a long fight. 0ays 9umate! This is too important a matter to settle by a simple
ma:ority.
0cience! vol 2$%
1) Traduzca el text!
") I#d$%ue &$ la& &$'u$e#te& a($r)ac$#e& &# *erdadera& (al&a&!
a8 1l virus de la viruela podr;a ser <til en la investigaci=n de drogas contra el 0ida.
b8 >as probabilidades de ,ue una persona infectada viva son del 20 al 40%.
c8 *o e-isten mecanismos internacionales para el control de los stocs del virus de la viruela.
d8 *o es posible usar el )*+ del virus de la viruela clonado para investigaciones.
e8 1l virus de la viruela se considera un virus peligroso para su uso en investigaci=n
+) Ex,#'a clara - .re*e)e#te/
a8 Tres argumentos a favor de la erradicaci=n del virus de la viruela.
b8 Tres argumentos en contra de su erradicaci=n.
0) Selecc$#e la alter#at$*a crrecta 1de acuerd c# el text)
a8 1l virus de la viruela I) (ue exter)$#ad ttal)e#te II) (ue c#trlad III) ex$&te2 ,er e#
la.ratr$&!
b8 1n el caso de un nuevo brote de viruela I) td& ,dr3a)& re&$&t$r la $#(ecc$4# II) #ad$e ,dr3a
re&$&t$r la $#(ecc$4# III) 5a.r3a )uc5a& )uerte&!
c8 >a informaci=n ,ue se perder;a destruyendo al virus I) e& $),re&c$#d$.le II) # e& $),re&c$#d$.le
III) # &e &a.e!
d8 I) Ex$&te# II) N ex$&te# III) Se e&t6# $#*e&t$'a#d otras formas de reali7ar estudios basados en el
virus de la viruela.
e8 I) E& ,&$.le II) N e& ,&$.le III) Tal *ez &e ,ueda e#c#trar alg<n lugar de donde el virus no
pueda escapar.

") CANCER/ A FAILURE OF IMMUNITY7
The theory that declining immunocompetence is an underlying factor in the causation of both
aging and cancer is appealing but raises some notty issues. The concept is based on several assumptions?
that tumor cells carry specific antigens@ that competent immune systems recogni7e 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.
Aroponents of this theory claim that the increased incidence of cancer in older people could be
e-plained by age.associated tumors. Bnlie tumors that are induced in e-perimental animals by chemicals
or viral agents! most human tumors have wea or no demonstrable tumor antigens. Curthermore! when
being profoundly immunocompromised! as in infection with 4ID 64uman immunodeficiency virus! the
virus that causes +I)08 or after corticosteroid therapy to prevent organ transplant re:ection! the tumors
patients develop are usually lymphomas 6cancer of the lymphatic system8 or the form of sin cancer called
9aposi&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 e-pected that elderly people would have primarily tumors of types similar to those seen in other
immunodeficiency states! which simply is not the case.
2hy then! do older people have more cancer3 +lthough there seems to be no single e-planation!
several contributing factors have been identified. Aerhaps the most important is time. The process of
carcinogenesis is comple- and has many steps! only now being elucidated at a genetic level. In humans the
se,uence of events in carcinogenesis is best understood for colon cancer. + 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. 5ther easily biopsied cancers 6such as cervical! lung! prostate! and breast8 may soon be
shown to have similar se,uential pathogeneses.
1)Traduzca el text!
") Real$ce u# .re*e re&u)e# c# la& $dea& ce#trale& de cada ,6rra(!
+) I#d$%ue &$ la& &$'u$e#te& a($r)ac$#e& &# *erdadera& (al&a&/
a8>os tumores humanos presentan gran cantidad de ant;genos tumorales.
b8>as secuencias de patogEnesis del cFncer de mama y colon son distintas.
c8>os tumores mFs comunes en pacientes inmunocomprometidos son los linfomas.
d8>os estudios reali7ados en ratas no son claros respecto al origen del cFncer de colon.
0) C#te&te .re*e)e#te la& &$'u$e#te& ,re'u#ta&/
a8 GH=mo la teor;a propuesta e-plica el desarrollo del cFncer3
b8 GHuFl es el factor mFs importante ,ue conduce al desarrollo de cFncer en gente mayor3
c8 1numere tres tumores ,ue se desarrollen mFs com<nmente en esas personas.
d8 GIuE tipos de cFncer se desarrollan mas com<nmente en pacientes con corticoterapia3
+) MICRO8IAL TOXINS
T5e #ature ( tx$#&
Jost of our nowledge of microbial to-ins has come from wor on pathogenic
bacteria! for the search for bacterial to-ins began shortly after the discovery of the role
bacteria had as ethiological agents for human disease. 'y "K#0 the to-ins 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 in:ected into e-perimental animals.
2hat autopsies revealed was that these animals showed the characteristic lesions
associated with the specific natural infection. The to-ic substances .which proved to be
heat.labile and are now nown to be proteins. were termed exotoxins, for they were
present in the medium! although not associated with the bacterial cells.
+ number of other pathogenic bacteria have been subse,uently shown by comparable
methods to produce e-oto-ins that have specific effects! yet filtrates which had been
prepared from cultures of many important pathogens failed to show to-icity. This led to
the e-amination of the bacterial cells themselves 6which had been illed by heat8 as
possible to-ic agents. *ot only did such e-periments show that the cells of nearly all
Gram-negative pathogenic bacteria are intrinsically toxic but heat.illed cells of many
non.pathogenic (ram.negative bacteria were shown to have similar effects. The heat.
stable to-ins with which the cells of (ram.negative bacteria were associated came to be
nown as endotoxins. Jany years of intensive study were re,uired to reveal their
nature and cellular origin@ it is now nown that endotoxins are lipopolysaccharide-
protein complexes, which derive from the outer layers of the cell walls of Gram-
negative bacteria.
The e-amination 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 anthra- and plague! for which this approach had failed to reveal any
significant to-ic product.
The to-ins of both organisms were later found to be comple-es of two or more
substances! each of which was non.to-ic by itself but which together acted
sinergistically to produce a to-ic effect. 0uch nowledge allowed the assay systems for
the to-ins to be refined to such an e-tent that .in each case. it became possible to
establish the production of to-in by cultures of bacteria in vitro.
1) Traduzca e&te text
") S$#tet$ce .re*e)e#te l& ,u#t& ,r$#c$,ale& de l& %ue 5a.la el text!
+) Re&,#da e&ta& ,re'u#ta&/
a8 H=mo fue ,ue se descubri= la e-istencia de las to-inas de Horynebacterium difteriae y
Hlostridium tetani3
b8 IuE significa el tErmino e-oto-ins3
c8 Todas las bacterias producen e-oto-ins3 1-plicar.
d8 IuE caracter;sticas tienen las endoto-ins3
e8 H=mo act<an las to-inas de anthra- y plague3
0) Mar%ue c# 1X) la& rac$#e& %ue ex,re&a# $#(r)ac$4# c#te#$da e# el text!
a8 +lgunas to-inas son estables al calor! pero otras no.
b8 >as endoto-inas y las e-oto-inas tienen diferente composici=n.
c8 >os clostridios forman esporos ,ue pueden sobrevivir por largo tiempo.
d8 >os agentes causantes de antra- y plague tuvieron ,ue ser estudiados de una forma
diferente al resto.
e8 >os mEtodos de aislamiento de to-inas son e-tremadamente comple:os y lentos.
0) T9E TOPOLO:Y OF WALL AN; MEM8RANE SYNT9ESIS
)uring 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 e-tension
of the area of both wall and membrane. 2ith 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 ma:or wall polymers are all mediated by en7ymes which are
nown to be locali7ed in the cell membrane! yet it is not nown whether these en7ymes
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 pree-isting wall and membrane
fabric. Jany e-periments designed to e-amine this ,uestion have been performed! often
with conflicting results. It is important to eep in mind that secondary displacement of
newly incorporated materials may occur. Cor e-ample! the plasticity of the cell
membrane and the outer wall layer of (ram.negative bacteria could cause an apparently
random distribution of newly synthesi7ed components! even if they were initially
incorporated at specific points. The same effect would result from a rapid turnover of
wall or membrane constituents. Honse,uently! evidence for locali7ed growth of walls or
membranes is incontrovertible! whereas evidence that suggests random incorporation is
often ambiguous.
In the streptococci! (ram.positive bacteria with spherical cells! clear evidence for a
locali7ed e,uatorial region of wall growth has been obtained by the use of antisera
specifically directed against wall constituents. The antiserum! which is con:ugated with
a fluorescent dye! is used to coat the cells for them to be made intensely and uniformly
fluorescent. )uring subse,uent growth in the presence of non.fluorescent antisera! the
poles of the cells remain intensely fluorescent for several generations and new non.
fluorescent wall areas are progressively inserted between the old wall material as
growth proceeds. Thus! during e-ponential growth of streptococci! wall synthesis is
highly locali7ed! and the walls are not secondarily modified. 4owever it has also been
shown that! when the growth of streptococci is prevented by inhibition of protein
synthesis 6either by specific aminoacid deprivation or by chloramphenicol treatment8!
the synthesis of wall material continues and results in a progressive thicening of the
wall over its entire surface.
1) Traduzca e&te text
") ;$.u<e cada u#a de la& eta,a& de la d$*$&$4# celular de&cr$,ta&!
a8 b8 c8 d8
+) ;$'a &$ l& &$'u$e#te& e#u#c$ad& &# *erdader& (al&&
a8 1n la s;ntesis de algunos componentes de la pared celular intervienen
en7imas.
b8 *o se conoce con e-actitud d=nde estFn locali7adas estas en7imas.
c8 >a membrana celular :uega un importante papel en la s;ntesis de algunos
componentes de la pared celular.
d8 >as en7imas participan de las primeras etapas de s;ntesis de fosfol;pidos y
mon=meros.
e8 Todav;a no se conoce cuFl es la distribuci=n de esas en7imas.
0) Re&,#da e&ta& ,re'u#ta&
a8 0eLale en el te-to y tradu7ca una definici=n de streptococo
b8 Aara ,uE se usa un antisuero fluorescente3
c8 IuE se ha ,uerido demostrar con la utili7aci=n de antisueros fluorescentes3
d8 1l uso de ciertos antibi=ticos! ,uE efecto produce en relaci=n con la pared celular
de los estreptococos3