EJEMPLO DE “FICHAS BIBLIOGRÁFICAS” 

 
 
Como  les  comentaba,  existen  muchos  y  muy  diversos  formatos  para  las  fichas  bibliográficas,  sin 
embargo,  no  les  pido  que  usen  alguno,  únicamente  quiero  la  información  que  utilizaron  con  la 
respectiva referencia. Por ello, les muestro ejemplos de lo mínimo que necesitan. Si desean utilizar 
un formato más completo o complejo, lo pueden así hacer. 
 
 
1. ¿Cuáles son algunos ejemplos para las “fichas bibliográficas” solicitadas? 
 
 
 
“The search of novel effective antiviral agents for treatment of viral infections is a constant challenge 
for human health. Even when successful drugs have been developed and employed to combat well‐
known human pathogens, many current therapies face the difficulty of a high rate of genetic change 
exhibited  by  viruses,  enabling  the  selection  of  drug‐resistant  mutants.  This  shift  adds  to  the 
increasing  periodic  emergence  of  new  viral  pathogens  or  the  reemergence  of  old  ones  lacking  a 
reliable  drug  therapy.  Therefore,  the  finding  of  new  antiviral  approaches  is  a  continuously 
demanding effort.” 
 
Ludert, Juan Ernesto; Pujo, H. Flor, Arbiza, Juan (Editores); Human Virology in Latin America, From 
Biology to control; 2017, E.U.A. ; Springer International Publishing. 
 
 
 
 
“Multidrug resistance and multidrug tolerance
Numerous mechanisms of drug resistance have been described, and in most cases we have a good
understanding of these processes at the molecular level. The main types of resistance are target
modification by mutation; target modification by specialized enzymatic changes; target substitution,
such as expressing an alternative target; antibiotic modification or destruction;
antibiotic efflux; and restricted permeability to antibiotics9,10. It is interesting to note that all
of the theoretically logical possibilities of antibiotic resistance seem to have been realized in
nature. Importantly, all of these mechanisms accomplish the same aim, which is to prevent the
antibiotic from binding to its target (FIG. 2). Each of these resistance mechanisms allows cells to
grow at an elevated concentration of antibiotic. Bactericidal antibiotics kill the cell not by
inhibiting the target, but by corrupting its function to create a toxic product. Aminoglycoside
antibiotics kill the cell by interrupting translation, which produces misfolded toxic peptides11.
Beta-lactam antibiotics, such as penicillin, inhibit peptidoglycan synthesis, which activates, by
an unknown mechanism, autolysin enzymes present in the cell wall12.This leads to digestion of the
peptidoglycan by autolysins and cell death. Fluoroquinolones inhibit the ligase step of the DNA
gyrase and topoisomerase, without affecting the preceding nicking activity. As a result, the enzymes
are converted into endonucleases13.”

Lewis, Kim; PersisterCells, dormancy and infectious disease; Nature Reviews Microbiology,volumen 5,
enero 2007, pp 48-56.