Antibiotic Efflux pumps in Prokaryotic Cells Assignment

1.  The types of membrane transporters are systematically organized in the prokaryotes and also found in eukaryotes with different characteristics, they include 2.A.1 Major Facilitator Super-family, 2.A.6 Resistance Nodulation Division, 2.A.7 Drug metabolite transporters, 2.A.17 Proton-dependent Oligopeptide transporter, 2.A.60 Organo Anion Transporter, 2.A.66 Multidrug Oligosaccharidyl-lipid Polysaccharide Flippase, 2.A.74 Multidrug Endosomal Transporter, 3.A.1 ATP Binding Cassette.
2.  Some of the major physiological mechanisms that the bacteria have developed to elude harmful molecules e.g. antibiotics and chemotherapeutic agents are the efflux pumps. These mechanisms were developed by the bacterial cells to expel toxic molecules found inside the cytosol and inside the cell. Some of these molecules might also include biological molecules. Other mechanisms along this are target modification and production of enzymes to neutralize antibiotics.
3.  The natural function of the membrane transporters is to facilitate the movement of molecules macro and micro molecules. This mostly may include biological molecules such as proteins and also other diffusible molecules that might enter the cell membrane of the bacteria. This is important for the cell to be able to maintain osmotic balance in the cytosol.
4. The major antibiotic transporters found in bacteria are Major Facilitator Super-family, ATP Binding Cassette, Resistance Nodulation Division, Small Multidrug Resistance and Multi-Antimicrobial Extrusion. The drugs acted on are not necessarily structurally or functionally related to each other. Due to the ability of the super-families to recognize different drugs that are not structurally similar, leads to the strain ability to develop cross-resistance that may be the genesis of multi-resistant strains an example P.aeruginosa.
5.  NO.  Different organisms have the capabilities of expressing more than one type of transporter that may be similar to one expressed by another organism. These transporters are known to occur in more than one species. This is because the efflux pumps are known to be located in the bacteria plasmids or transposons and are then spread to other organisms through conjugation.
6. A drug can be recognized by different pumps. An example of the drugs is the tetracycline, fluoroquinolones and chloramphenicols. However those drugs within the same class tend to be more specific in the type of pumps by which they are recognized.
7.  Efflux pumps by themselves are only known to have the ability to give only low or moderate resistance. This is because the natural resistance of many bacterias is dependent on the active systems inducible expression. It is also known that for the efflux pumps to confer high resistance corporation between them and other resistance mechanisms is paramount. An example is resistance in P.aeruginosa whose high resistance is result from combination of, the active efflux system MexAB OprM, the outer membrane barrier and AmpC -lactamase. Further the antibiotics play an important role in the expression of the efflux pump during gene transcription and it s the one that induces the efflux pump.
8. Since genetic characterization has been successfully employed in identifying efflux resistance mechanisms in some bacteria, it has been suggested that genotypic tests be used to identify new effective antimicrobial drugs. Having knowledge of the mechanisms used by these organisms to promote resistance in them, may help in developing new drugs that are not easily susceptible to the efflux pumps of the organisms, thus lowering the probability of resistance to the drugs. This is because the manufactured drugs will be able to minimize over expression of the pumps in the organisms and the development of poor substrate derivatives.
9.  The development of new antibacterial drugs will be dependent on the knowledge of the actions of the pumps on the detection of the different drug molecules. Despite the discovery of pump inhibitors used for therapy, it is important that the new drugs are designed in such a way that they are broad-spectrum inhibitors acting on both gram-negative and gram-positive bacteria of different phylogenetic families to evade rapid developing resistance.

Microbiology

a) Zoonosis is a normal disease of animals that can be transferred to humans with or without the help of diverse vectors.  b) Vectors are living transporters of infectious agents. They can transfer infectious agents like bacteria, viruses and protozoans to other animals and humans. Popular vectors are parasitic arthropods and domestic animals. c) Arthropod-borne diseases are diseases caused by infectious agents that arthropods served as vectors. Arthropods are invertebrate animals which have segmented bodies, possess exoskeletons and have jointed limbs. Some examples are arachnids, insects and crustaceans. d) Reservior hosts are main hosts of an infectious agent but they do not manifest the clinical symptoms of the disease and they can transfer the infectious agent to other animal hosts.
The ecological factors involved in the efficacy of WNV transmission to humans include climate change alterations in temperature abundance of avian species reservoir and, increased numbers of vectors.  Temperature is among the factors that highly influence the transmission and propagation of viruses in their different hosts. The alterations of temperature to that of the optimal temperature for transmission and replication of the virus can increase the incidence and intensity of disease.  Vast numbers of avian species reservoir and insect vectors could also magnify disease outbreaks.
The crow or Corvus spp. is an ideal indicator of West Nile Virus (WNV) to humans because of four reasons. First, they are easily infected by this virus and these infections have a high mortality rate. Second, crows are everywhere and they can be easily identified. Third, they are major sources of WNV infections because the virus intensively multiplies in the crows blood making it easy for mosquitoes to contact the virus and then infect humans. And fourth, its convenient to collect samples from crows because it does not consume any resources and great amount of time.
In order to calculate the point and interval approximations of WNV disease risk in an indivuals  country residence based on DCD 0.1 (dead crows per square mile), the Cochran-Mantel-Haenszel (CMH) option of the freq procedure in SAS System for Windows V8 was employed.  Comparison of WNV incidence risk between the areas with DCD reports and those without DCD reports was made through the application of CMH chi-square statistic. Since it takes about 2-14 days before WNV infection will manifest in human hosts, detach computations of CMH-pooled risk estimates for 3 exposure periods were done. These 3 exposure periods are two weeks prior to, one week prior to and the week of observance of WNV human cases.
Real time monitoring can be advantageous to the prevention of disease outbreaks. The information generated from this system can signal the prompt employment of numerous measures to prevent disease outbreaks in humans. On the other hand, real time disease monitoring is a very complexed system and various variables can influence its effectiveness.  Any negative influence from the variables involved can be detrimental to the systems effectiveness.  An example is its dependence on voluntary reports only, if absence of participants to report the sightings of dead crows occurs in a certain area, this would translate to failure of WNV human infection risk prediction in that area.
The factors that play a role in limiting the effectiveness of the Dead Crow Density (DCD) index as a predictor of potential human transmission cases are the variations in disease vector among the areas involved and the area residents participation in the reporting of the dead crow. Disease vectors are important in the zoonoses, transfer of infectious disease from animals to humans. Significant reduction in the number of vectors involve can also significantly lower the disease incidence and intensity. One limitation of DCD index then is its failure to consider the role of vectors in the transmission of disease. To reduce the impact of vectors in the study, a calculation variable for vectors could be included in the statistical analysis. Another limiting factor is the participation of people in reporting the sightings of dead crows. Low reporting participants translate into low specificity of the calculations. Hence, a solution is to educate and encourage the people to partake in the reporting.
The absence of reported human disease infections after a DCD e 0.1 can be due to vector variables or the human infections did not progress into a disease. Mosquitoes, which are vectors of the virus, might have been previously eliminated by mosquito control procedures. It is also possible that the mosquitoes did not feed on humans but instead fed on other animals. Another reason is not all viral infections lead to a clinical disease. Other infections only manifest as mild forms which are often undetected. Various factors like the high capability of the human hosts immune system can play a role in disease development.
Real time reporting systems like DCD index have great potential for the management of infectious diseases outbreaks. The establishment of real time reporting systems for other diseases can be of great significance to the health industry.  Given the time before the disease is transferred from the animal host to humans, various preventive and management measures can be prepared to minimize or eliminate the occurrence of infectious disease outbreaks in humans.

Running Head Physiological Changes During Human Exercise Lab Report

Body changes during different states are extremely complex evident from the many changes in observable respiratory variables resulting from the interaction between various organs, cells and systems. This projects seeks to determine the various physiological changes that takes place within an organisms body during exercise through the assessment of the respiratory rate, body temperature and other cardiovascular responses. Exercises often subject the human body to conditions that require compensatory adjustments, an aspect that can be determined through the observation of various body changes such as changes in body temperature, respiration rate, Skin temperature, and the blood pressure. During exercises for example, the heart rate will determine the number of heartbeats per unit and will often vary increasing during exercises, a state where the bodys needs for oxygen increases.
Other changes of interest during the experiment are inclusive of Tidal volume which will determine gas volume exchanges (O2 and CO2) during the exercise, respiratory rate, indicative of the changes in the number of breaths humans takes within certain time durations during exercise and the blood pressure which is a vital sign of the pressure exerted on the walls of the blood vessel by the circulating vessel.  Respiratory related observations will be extremely helpful in determining various body changes during exercise. Oxygen and Carbon Dioxide consumption and clearance levels respectively will be of great importance in defining respiration during exercises.
Respiration, a primary component of the mammalian physiology the process by which oxygen is transported from the clean air to the tissue cells and the carbon dioxide in the opposite direction, (Lister, Hoffman  Rudolph, 1997). Imperatively, individuals exhaled air that contains Carbon dioxide which is a waste product of the energy producing biochemical reaction that takes place within the cells during exercise. A number of studies have also indicated that ventilation increases considerably with the increase in lung ventilation received during sustained exercise, (Lister, Hoffman  Rudolph, 1997). The experiment is of great importance in a number of ways it will assist medial professional in diagnosis and tracking of medical conditions. It will also be of great interest to athletes assisting them to monitor physiological changes thereby gaining maximum efficiency from their training. Coaches, sports scientist and sports councils can also find the experiment beneficial in a number of ways. The experiment will also be of interest to the students of physiology and biological sciences and respiratory therapists.  
Hypotheses The experiment proposes to test the following hypotheses
1We hypothesize that the heart rate values will remain uniform at rest points, increase rapidly at the onset and throughout the exercise period, and drop rapidly during the recovery phase. 2 Carbon dioxide clearance is expected to remain on average at rest position, increase rapidly during the exercise before decreasing rapidly during the recovery phase.
3 It is also hypothesized that oxygen consumption is directly correlated to the levels of human activity, hence is expected to be low during rest, increase during the exercise and reduce rapidly during recovery. 4 Based on the expected temperature changes, we hypothesize that temperature and the body activity are directly correlated. Increase in body temperature with increase in the activity of the subjects during the exercise is expected. 5 Hemoglobin saturation is expected to remain constant during rest, increase during the exercise, decrease rapidly to the rest level during recovery before increasing with the increase of the recovery duration.
Method
Physiological changes in three human subjects aged between 18 and 21 were observed under laboratory conditions.  Critical to the experiment is the attainment of three sets of data representative of the rest, exercise and recovery conditions. At the outset, two measurements of the initial body conditions were taken at time zero and 3 minutes to determine the resting data points. The subjects were exercised on a treadmill, with its speed being progressively increased while data taken after every three minutes with the exercise phase lasting 9 minutes for all the three subjects. For the three sets of data, maximum heart rate for the experiment was specified as 177 and 172, 173 and 168, and 171 and 166 bmp for the male and female subjects beyond which the experiment was stopped.
The exercise heart rate was calculated and the values recorded this was necessary to predict the limits of the exercise since extremely high heart rates may endanger the health of the survivors besides being of an important indicator of respiratory changes during exercise. A number of instruments were used during the experiment the Spirometer was used to determine a variant data types inclusive of the CO2 Clearance, 02 Consumption. Values from the spirometer also aided in determining the tidal volume, respiration rate, vital capacity and the ventilation rate.  The heart rate monitor was used to determine the subjects heart rate while the blood pressures of the runners were measured using a mercury sphygmomanometer.
All the three subjects were seated during the collection of the resting data points which lasted for three minutes. The experiment did not have a control subject with the values from the rest position acting as the control to isolate the effect of exercise on the human body by holding constant variables comparative to those observed during the experiment. Two sets of recovery data were collected with the first one being collected three minutes with a reduced treadmill speed of 2 miles per hour while the second data set was collected when all the subjects were seated. It is imperative to note that a number of factors limited data collection only three sets of data rather than 7 were collected during the exercising phase since the heart rate of the subjects had reached critical limits.
This limited the calculation of other values such as the CO2 and 02 clearance, skin temperature, Hemoglobin saturation and systolic and diastolic blood pressure since the subjects could not continue with the experiments. Mean arterial pressure was determined to get the average of all pressure measured within specified time periods. To calculate mean arterial pressure, Systolic and Diastolic Blood pressure were applied in the formula
Mean Arterial Pressure (MAP)  (2Diastolic)  Systolic
                                 3
For example the first reading at rest position Systolic BP 112, Diastolic BP98
Applying the Formula, MAP (298) 112    102.6777 H 103
                    3
Oxygen consumption was obtained by calculating the difference between the amount of Oxygen delivered to peripheral tissues and the amount returning to the heart. Results
    There were significant variations in the data collected in all the three cases. For the first case involving male subject aged 21 years weighing73.6 kg and having72 inches in height with a resting heart rate of 63 bpm (noted as a non smoker), the heart rate increased to 1768, 191 and 204 within 3, 6 and 9 minutes of exercise. During recovery at a treadmill speed of 2 mph, the heart rate reduced to 144 before further reducing 3 minutes later to 64 at sitting position. Recoded tidal volumes were stable at 0.60 at sitting position, increasing to 1.00, 1.20 and 2.00 at 3, 6 and 9 minutes of exercise before reducing to 0.90 and 0.7. during the recovery phase. His respiration rate and ETC2 during times 0 and 3 minutes within the rest position were 30 and 25 and 40 and 72 respectively.
The respiratory rate was measured in breaths per minute. These later increased to 50 and 60, 65 and 65, 65 and 69 within 3, 9 and 9 minutes of exercise before reducing to 45 and 55 and 35 and 42 respectively during 3 and 6 minutes into the recovery phase.  For this subject, as a number of observable changes were made during the experiment. At rest for example, the subjects breath was easy, 3 minutes into the exercise, his breathing was still easy and running smooth however six minutes into the exercise, the subject was sweating lightly with his running difficult, his face also flushed. The subjects body temperature changes were also as expected with values averaging 34.75, 36 and 35 during rest, exercise and recovery phases respectively.
Fig. 1 Changes in Heart Rate

For the second male subject aged 19 years and weighing 72.48 kilograms with a height of 72 inches, the resting heart rate was determined at 75 bpm. The resting heart rate increased to 110 3 minutes within the sitting position, before increasing to 169, 171, 181, and 197 (bpm) within 3, 6, 9, and 12 minutes into the exercise respectively. The subjects tidal volumes were recorded as 9.60 and 1.00 at 0 and 3 minutes within the rest position. During exercise, the volume was observed as 1.00, 1.20, 1.30, and 1.60 (lbreath) within 3, 6, 9, and 12 minutes respectively. 2.20 and 1.60 (lbreath) were the observable tidal volume values during recovery.
Although the respiration rate for the subject was relatively stable at 25 breaths minute while in the rest position, this reduced to 18 breaths per minute 3 minutes into the exercise before increasing to 25 and 35 breaths per minute within 6 and 9 minutes into the exercise. Significant decrease occurred within 12 minutes into the exercise with the observable heart rate decreasing to 20 breaths per minute. During recovery phase, the recorded values were 20 and 15 at times 3 and 6 minutes respectively. Observable values of  O2 were 0.209 and 0.209 at 0 and 3 minutes during the rest position, 0.209, 0.213, 0.209 and 0.209 at 3, 6, 9 and 12 minutes respectively during the exercise. This averaged 0.209 during recovery.  
Fig. 2 Changes in carbon dioxide clearance

Data obtained for the third subject were on average, relatively low. The third subject was 18 years old, 66 cm in height and 65.6 kg in weight. The subject who was also a non smoker recorded a resting heart rate of 61 bpm although this increased to 69 bpm 3 minutes after the start first measurement. During the exercise, the subjects heart rate increased to 178, 123 and 208 3, 6 and 9 minutes into the exercise. During recovery, there were significant reductions in heart beat rate reducing to 163 and later to 68 at 3 and 6 minutes of recovery respectively. The subjects tidal volume were recorded as 0.60 and 1.00 at 0 and 3 minutes respectively during rest position, 1.00, 1.20, 1.30, and 1.60, at 3,6,9 and 12 minutes of exercise, and 2.20 and 1.60 at 3 and 6 minutes into the recovery phase.
Fig. 3 Changes in oxygen consumption

The following data were also observed andor calculated
Fig. 4 temperature
TimeSubject 1Subject 2Subject 3Resting Data points0 min3534353 min360.0234.534.5Exercise Data Points3 min---6 min---9 min-383612 min37--Recovery Data points3 min3737356 min353635Fig. 5 hemoglobin saturation
TimeSubject 1Subject 2Subject 3Resting Data points0 min9090903 min909090Exercise Data Points3 min---6 min---9 min-949212 min90--Recovery Data points3 min9090926 min909492Fig. 6 mean arterial pressure
TimeSubject 1Subject 2Subject 3Resting Data points0 min103790.023 min83790.02Exercise Data Points3 min--0.456 min--1.259 min-1032.4712 min104-Recovery Data points3 min77910.046 min95800.02
 Discussion and Conclusion
From the results above it is evident that both the Respiratory rate and the Body temperature increased during the exercise in all the three cases. It is also evident that the two variables are dependent upon the velocity of the treadmill hence the rate at which the body is moving.  Observations during resting are indicative of identical thresholds of panting with male heartbeats being higher than the female heartbeat. Heart rate observations for the three subjects support the hypothesis since it significantly increased although on average, all the three participants exhibited accepted levels of fall in heart rate after the exercise (Above 50 bpm). It has been observed that delayed fall in heart rate after exercise may be an important prognostic marker, (Powers,  Jackson, 2008).
Lister, Hoffman  Rudolph (1997) for example affirms that less than 30 bpm reduction one minute after the stop of exercise may be indicative of an impending heart attack, however, values of more than 50 bpm indicated a relatively healthy heart.  Results on oxygen consumption levels also supported out hypothesis with values remaining low during rest, increasing rapidly from the onset of exercise before stabilizing.  Temperature increase during exercise was expected since theoretically it is estimated that in excess of 70 of the energy that powers human muscles is lost as heat thereby leading to an increase in the body temperature, (Zheng, Sun, Li et al., 2008). There was also a direct correlation between increases in body temperature and the heart rate an observation that can be explained by the fact that the heart has to increase its pumping speed to ensure that the heat is pumped from the muscles to the skin surface for evaporation and cooling, (Evans  Meredith, et. al.1986).
The relationship between tidal volume and carbon dioxide clearance is also evident with carbon dioxide clearance decreasing with the increase in speed. Hemoglobin saturation is expected to remain constant during rest, increase during the exercise, decrease rapidly to the rest level during recovery before increasing with the increase of the recovery duration. This was an indication that for all the three subjects, the volume of oxygen per volume of blood increased with exercise an observation that can be explained by the bodys need of additional oxygen during exercise.  Conclusively, the data recorded strongly supported our hypotheses, indicative of the subjects relative health statuses
Significant deviations are expected based errors. Human error in taking values such as temperature values, timing could probably lead to deviations. Since certain values such as the MAP were estimates, the results were not exact hence were a probable cause of deviations. From the values obtained, the mean arterial pressure could be more valid comparative to a single value of systolic or diastolic blood pressure hence medical professionals should aim at calculating this value.  Additionally, they should check on the rate at which this value falls since if MAP falls significantly below 60 mmHg, then an individuals blood flow is not optimal.

The controversial debate and urban mythology

The controversial debate and urban mythology that links the use of cellular phones and power transmission lines as possible causes of cancer and brain tumors is a sensitive rhetoric that needs proper scientific analysis since this subject has direct impacts on public health. Such pseudoscience results in real economic cost and unnecessary psychological stress to individuals who dont have to experience such disturbances.
Before drawing conclusions on such pseudo sciences, researchers need to come up with substantial evidence to disapprove or support the question since power lines and use of mobile phones have become more common in the public domain.
Several studies can be done to establish the facts on the relationship between cancer and cell phones. A biological approach can be used to deduce the impacts of emissions  radiation from mobile phones on living cells either on animals or in laboratory test tubes (Novella, 2007). If there is any observable effect, then this deduction can be correlated to human tissues. This may however be misleading since the analogy may not always be correct (Novella, 2007).
Scientific evidence on this question may also be gathered using epidemiological studies which try to precisely establish any viable relationship between brain cancer and mobile phone use. This kind of approach may however turn out to be practically impossible since singling out the exact parameter of interest, in this case mobile phone use and correctly determining its relationship to another parameter i.e. cancer may not be achievable( Novella, 2007).
However, some controversies in the medical spheres related to this pseudo science are still emerging with time. According to the meta- analysis and research conducted by Dr. Khurana Vini, a U.S. based Neurosurgeon early this year, some forms of brain tumors result after an exposure to cell phone radiations for more than a decade. He (Dr. Khurana) disregarded most of the existing contradictory evidence since it was gathered or conducted on primary exposure periods of less than ten years. Some medical researchers also advice that children should not be allowed to use gadgets at a relatively early age due to fears that their thin skulls have the potential of permitting more radiation, more than what their brains can dissipate and thus may have a direct biological impact on their overall growth and development( Khurana, 2009).
Apart from cancer, other unconfirmed reports in this domain link several other health woes such as Leukemia and other blood diseases, reproductive problems and birth defects, fatigue, decreased libido, depression, sleeping problems, hormonal imbalances, and heart diseases among others.
Cell Phone Use and Associated Signals Do Not Lead to Cancer
No matter how much the cell phones are used, the chances of them causing cancer are totally unexpected. Cancer is usually caused by any destruction on the human DNA either by ionizing emissions from X-rays or Ultra Violet emissions, Chemical causes and carcinogens such as inhalation of tobacco smoke, or particular viruses that end up modifying the DNA make ups of an individual(Rankin, 2006). The microwave energy has the capacity of distorting chemical bonds but still have insufficient energy to mage the DNA. The normal light energy is also much greater than the microwave energy and yet it has never been reported to cause any form of cancer. The radiation emissions from cellular phones and their respective base stations are usually much less than the above two cases and thus there is no substantial fact that can link them to cancer and other related diseases (Rankin, 2006). This fact also applies with the misleading beliefs that transmission and high voltage power lines and microwave stoves lead to cancer.
Arguments fronted by Dr. Khurana, a U.S. based neurosurgeon that exposure to mobile phone radiations for a consecutive period of up to 10 or so years are still facing negative criticism. The outcome of the decade long Swedish research study, as reported in the American Journal of Epidemiology clearly disputes Dr. Khuranas findings. The Swedish carried out a population- based case- control study that lasted 10 years (i.e. 1998  2008) so as to verify or discredit the urban mythology that long-term exposure to cell phone radiations could result to brain cancer and related diseases. After the study was concluded in the year 2008, it was established that increased use of these gadgets for such periods do not in any way result to brain tumors regardless of the handset type. A similar study conducted in Denmark for a period of 21 years starting from 1982 to 2003, as published in the Journal of the National Cancer Institute, 2004 also gave similar results like those of the Swedish report. In Denmark, up to 430,000 cases of mobile phone users were traced all through the period to establish any signs of brain cancer. No substantial evidence linking tumor risk and mobile telephone exposure among either long-term or short- term users. Since Denmark maintains a computerized national cancer database and all cell phone service providers maintain subscriber records, the researchers used these two resources to establish any relations on the cell phone  cancer subject. Only a negligible number was revealed in the study as published in the Journal of the National Cancer Institute, 2004. Contrary to the misleading assumption that increased mobile phone use leads to cancer, the Denmark study revealed a negligible rate of brain tumor development among the long term cellular phone users. There was also no association between the part of the head where brain tumors develop and the side on which the phone is regularly used.
There is no known medical fact that correctly links mobile telephone Base Stations (transmitting stations) and cellular phone use with brain tumors and other associated health hazards(Karl, 2009). Such fears are usually based on rumors widely spread by the media. A recent story about the safety of mobile phone use in one of Australias leading magazine, The Sydney Morning Herald reported quite misleading and frightening phraseology on the subject matter. This magazine cited an organization referred to as the Environmental Working Group which allegedly released a relationship of radiation emissions from particular mobile handsets e.g. the Motorola and the Blackberry which emit more radiations than those of their competitors.
The assumption that high radiations emitted by these handsets are directly related to brain cancer is in reality misleading (Karl, 2009). This is because many laymen in the medical field ignorantly associate the word radiation with dangerous rays emitted from radioactive elements such as plutonium and uranium. Not all forms of radiation cause cancer except the gamma ray emissions. There is therefore no health danger posed by cell phone use and transmission stations simply because the signals and radiations emitted are weak and not in position to cause observable damages in the human DNA molecules and thus no chances of cancer arising. Mobile phone emissions are usually in the microwave range of 1800MHz, which is 650MHz less than the working frequency of microwave stoves (Karl, 2009). The transmission capacity of any given mobile phone is approximately 1 Watt (Geek, 2008) and the signals emitted by these gadgets are relatively low energy radiations in the range of 800  960 MHz. A cordless phone is likely to operate at frequencies equal to or slightly higher than 2.5 GHz. Electromagnetic radiations only ionize when they reach a frequency higher than 3000THz and can not destroy DNA before attaining this frequency. The only way the electromagnetic waves can result to cancer is through heating to very high temperatures (Geek, 2008) which is unattainable since these gadgets consume extremely low power (1Watt) which can hardly penetrate the human skin and thus there are no chances of cancer or tumors resulting from continuous use of these communications gadget( Geek, 2008).
Like many other current health and scientific debates, the controversies surrounding the subject on mobile phones and their alleged relationship to cancer is surrounded by some levels of pseudoscience (Novella, 2008). Other research scientists, the likes of Arthur Firstenberg end up quoting several doubtful scientific allegations about mobile phones without providing proper citations in their quest to convince the public on dangers related to mobile phone use. The procedures suggested by Firstenberg in his research could not yield any viable results when numerous repeats of the procedures were carried out in subsequent studies (Novella, 2008).
Other negative allegations correlating mobile phone use and exposure to the radio frequency radiations emitted by their base stations and associated power lines are also spread by entrepreneurs with selfish minds out to make individual gains(Novella, 2008). Such business men are usually the manufacturers and retailers of devices that have the capacity to shield one fro harmful mobile phone radiation. Some of these devices often sound technological, but with no observable effect or may even end up completely shielding mobile phone emissions at the expense of the wireless signals behind their principles of operation(Novella, 2008).
Though the research is still on going on the possible impacts of long-term use of mobile phones, it is often advisable to acquire mobile gadgets that do not necessarily have to be near the head when making or receiving calls to minimize the magnitude of the radiation you get exposed to while working. Use of gadgets that support blue tooth or those with headsets should be encouraged. Such advanced gadgets can also have the added advantage of minimizing deaths and road accidents since they do not interfere with the drivers concentration whenever he receives or makes a call.
Relationship between Emissions from Power Lines and Cancer
Electromagnetic fields can be regarded as the magnitude of force with both magnetic and electric components usually linked with electric charge in motion. No individual scientific study has conclusively gathered accurate evidence on the relationship between emissions from power lines and possible health hazards e.g. cancer.
In as much as there are numerous reports of children living within the vicinity of high voltage transmission stations developing strange illnesses (Neal, 1996), several scientific evidences from the American National Council on Radiation Protection link the electromagnetic fields emitted from such stations to be the main causes of cancer and other associated diseases. This is based on the fact that electromagnetic fields have the capacity of inhibiting body hormones such as melatonin which in turn distort sleep patterns in adults and increase leukemia cases in children (Neal, 1996). Many studies have previously indicated that the relation between cancer and high electromagnetic fields may take several years before the effect is clearly pronounced. Such bodily disorders usually come about after a relatively lengthy process of continuous worsening of conditions within the body before eventually culminating into a dreadful disease. Electromagnetic field radiations often begin destroying body tissues immediately after the exposure. Though it may take long before symptoms become defined, the damage is always in the process.
Contrary to early assumptions that electromagnetic fields posed no health hazard, experimental researches have proved otherwise (Neil, 1996). According to such experiments, weak electromagnetic fields have the ability of completely distorting the brain chemistry, inhibiting the immune system and the production of body hormones such as melatonin, a hormone which plays a major role in fighting several kinds of tumors (Neal, 1996).
Such studies have however resulted in many controversies, based on the case-control study carried out in Los Angeles, California, two sets of 230 children under the age of 10 was used. The correlation between leukemia and electromagnetic field exposures was evaluated. Individual measurements at several positions outside and inside households including the bedrooms were done. Information concerning the frequency of use of electrical gadgets in each household was collected and other varying factors regulated. As a result, households with high current configuration had double cases of leukemia and no relation was directly established with measured electromagnetic radiation (Neal, 1996).
Extremely high- current, huge- voltage conducting power lines located approximately 400metres away have the capacity to generate strong magnetic fields with strengths much higher than average domestic ambient levels. Overhead street power lines, 30metres above the ground can also create huge electro magnetic fields and for internal domestic wiring this field can extend to a distance of up to 1 meter. In the above three cases, the amount of current transmitted plays a key role in determining the magnitude of the magnetic field.
Quite a number of experiments related to this subject have in the past been carried out using animals such as mice and rats exposed to high electromagnetic fields for reasonably long periods (Neal, 1996). Some of these animals have been placed under such conditions for their entire life spans and but none has contracted cancer following such exposures. Several generations of animals raised under such laboratory conditions have also on the contrary not indicated any sign of birth disorders or defects in their immune system.
Without any animal information to back such claims that cancer can be caused by electromagnetic fields and no substantial physical process to explain the possible effects on the body, the only reliable information may be obtained from epidemiology (Neal, 1996).  For the several cancer cases, most medical specialists and researchers have formulated hypothesis that malignant cancer and tumors develop in at least two phases (Novella, 2007). The first stage is referred to as the initiation whereby an external agent damages a given cells DNA. Since electromagnetic radiations usually have inadequate strength to break chemical and molecular bonds, researchers are putting more effort in the second phase i.e. promotion in order to establish possible ways in which magnetic field can cause cancer by making cells to undergo abnormal mutations (Novella, 2007). 
Some studies also indicate that electromagnetic field radiations may lead to cancer by prying with the normal transmission and transfer of calcium across cell membranes (Neal, 2009). This kind of interference in turn ends up inhibiting major biological processes e.g. cell growth and multiplication, egg fertilization and reflex muscle actions. Electromagnetic fields also affect a cells capacity to synthesize hormones and inhibit other biological processes that directly affect growth (Novella, 2009).
In a different study conducted in Sweden, several medical researchers and expatriates assessed the overall prolonged exposure of individuals living within the vicinity of high- voltage power transmission lines (Neal, 1996). Several spot measurements of the electromagnetic field strengths in individual households were taken. The accuracy of the measurements were then confirmed using computerized models that could relate the field strength emitted by individual lines to the wiring networks, average distance of the power lines, and the amount of current each line was carrying at that particular instant(Neal, 1996). This research was conducted for about two consecutive decades and the finding was that any kind of exposure to electromagnetic fields regardless of their strength could result in cancer, more specifically chronic myeloid and acute leukemia (Neal, 1996).
Most scientists have since failed to clearly establish the mechanism in which electromagnetic fields produced by power lines induce or inhibit biological and metabolic reactions (Neal, 1996).Based on the fact that there is no known scientific or epidemiological evidence that clearly shows a direct or indirect relationship between cancer and the magnetic field strength and any viable method by which magnetic fields can stimulate cancer, huge uncertainty still surround this pseudo science.
Conclusion
It is not clearly understood how the notion relating cell phone use and cancer got into the public domain since currently, despite the many on going medical studies, there is no proven evidence that establishes any relationship on the subject. Most people are currently facing many challenges that need to be attended to.
This means that formulating and later spreading imaginary health hazards and related pseudo science has both the effects of diverting ones attention from real issues and desensitizing individuals to possible warnings about similar, but genuine dangers.  If the assumption that mobile phone use leads to cancer, then presently, there ought to be extremely numerous reported brain cancer cases since mobile phone use has become an extremely common mode of communication in the world in the last 15 or so years.
In as much as mobile phone signals have not yet been proved to cause cancer and other related complications, several research findings have indicated that electromagnetic field radiations, no matter how weak they are can result to cancer and other dreaded diseases such as leukemia and heart diseases.
Unlike emissions and radiations from cellular phones and their associated transmission which can be totally shielded using aluminum foils(Geek, 2008), there is no known element that can shield electromagnetic radiations no matter how weak they are from penetrating any material. Maximum caution and preventive measures should therefore be taken by people who live near power distribution stations e.g. through relocations so as to minimize any chances of cancer developing in their body.
The lack of clarity on the above subject should be treated with utmost care in case further research comes up with contradicting results. It is therefore advisable to take preventive measures when using these gadgets for your own safety. Excessive exposure to base station radio waves and mobile phone use should be minimized or regulated probably using headsets that could increase the distance between ones brain and these gadgets.
For total credibility, government sponsored independent agencies and concerned public health ministries should invest more in doing research related to cancer and emissions from power lines and mobile telephones for the sake protecting innocent citizens. In conducting such studies, concerned power distribution companies and mobile telephone service providers should not be involved so as to minimize chances of sabotage and biasness of the results. As a concluding remark, independent organizations with thorough knowledge of the above subject should be involved in conveying accurate and updated information to the public in order to create awareness.

Respiratory functions affected by Leptins

Leptin is a protein produced by adipose tissues that circulate in the brain and interact with the receptors in the hypothalamus to inhibit eating.  Importance of this peptide is demonstrated by profound obesity exhibited by the ob/ob mouse (C57BL/6J-Lep(ob)) which is unable to produce functional leptin. The measurement of respiratory functions in this mouse shows that profound obesity is associated with impaired respiratory mechanics and depressed respiratory control, particularly during sleep. Leptin may act as growth factor in the lung as well as neuro-hormonal modulator of central respiratory control mechanisms. Human obesity is associated with more variable leptin levels for a given degree of adiposity.  Thus, relative deficiency in leptin, or a leptin resistance, may play a role in obesity-related breathing disorders such as obesity hypoventilation syndrome (OHS) or obstructive sleep apnea (OSA).

Respiratory functions affected by leptins
Obesity has taken a form of epidemic in several developed countries and it is continuously rising (Mokdad AH et al. 2001). Several diseases are associated with the obesity, one of most important of which is respiratory function impairment. It can cause airway depression and impaired activity of upper airway tract muscles especially during sleep can cause obstructive sleep apnoea in >50% of obese patients (body mass index >30 kg/m2) (Punjabi NM et al. 2002) whereas severe obesity (body mass index >40 kg/m2) can cause depression of the respiratory pump muscles during wakefulness, resulting in CO2 retention and the syndrome of obesity hypoventilation (OHS) (Berger KI et al. 2001). Similar phenomenon has been observed in animal models of obesity such as the ob mouse (C57BL/6J-Lepob). It is proposed that a constellation of respiratory complications are attenuated with leptin (i.e. protein product of the ob gene) replacement.

Leptin is a satiety producing hormone secreted by adipocytes (Friedman JM and Halaas JL 1998) that provides a common link between obesity and respiratory depression. Initial study demonstrated that complete impairment of leptin signaling in genetically obese ob/ob mice significantly reduced the ventilatory response to hypercapnia during wakefulness (Tankersley C, Kleeberger S, Russ B, Schwartz A, and Smith P 1996). Subsequent clinical studies have shown that both OSA and OHS are associated with the most common form of impaired leptin signaling in humans, namely leptin resistance (Ip MS, Lam KS, Ho C, Tsang KW, and Lam W. et al. 2000).

Thus animal and human studies both shows that leptin resistance or deficiency may cause depressed hypercapnic sensitivity especially during sleep. Central effect of leptin on satiety and metabolism is predominantly through arcuate nucleus in hypothalamus. The anorexigenic effects of leptin occur primarily through activation of melanocortin 4 (MC4) receptors and inhibition of neuropeptide Y (NPY) in the hypothalamus. Putatively, MC4 and NPY pathways could impact on respiratory control via neural connections between the hypothalamus and respiratory control centers in the medulla (Glass MJ, Chan J, and Pickel VM 2002).Thus impairment of MC4 pathways or activation of NPY pathways in the hypothalamus could contribute to the respiratory depression associated with impaired leptin signaling.
The combination of leptin deficiency and profound weight gain in adult ob/ob mice can produce marked changes in respiratory mechanics (Tankersley, C.G., O'Donnell, C. and Daood, M.J., 1998. ). Ob/ob mouse shows that the profound obesity is associated with impaired respiratory mechanics and depressed respiratory control, particularly during sleep. Moreover, wild type mice with diet-induced obesity have normal respiratory function associated with markedly elevated leptin levels. Human obesity, similar to obesity in wild type mice, also causes an elevation in circulating leptin. But it does not show any tight relations, it is moreover variable in nature.

Methodology
Animals- Twelve mutant obese C57BL/6J-Lepob male mice, 22 C57BL/6J male mice, 7 mutant Ay male mice from Jackson Laboratory (Bar Harbor, ME), 9 NPY-deficient transgenic male mice (NPY-/-), and 9 littermates (NPY+/+),were used in this study.

Sleep/wake state was assessed from EEG and EMG recordings. Wakefulness is characterized by low-amplitude high-frequency (10-20 Hz) EEG waves and high levels of EMG activity as compare to sleep states. Non-rapid eye movement (NREM) sleep is characterized by high-amplitude, low-frequency (2-5 Hz) EEG waves and an EMG activity less than during wakefulness. Rapid eye movement (REM) sleep was characterized by low-amplitude; mixed-frequency (5-10 Hz) EEG waves, although the predominant pattern was a fixed amplitude theta frequency consistent with hippocampal theta rhythm. During REM sleep, the EMG activity was either equal to or less than that seen during NREM sleep but was always less than that seen during wakefulness.

Ventilation was measured during wakefulness and NREM and REM sleep in response to a range of hypercapnic gases (0, 3, 5, and 8% CO2 in 40% O2 to ensure no hypoxic stimulus) and hypoxic gases (15% O2 and 10% O2 in 3% CO2 to eliminate hypoxia-induced hypocapnia). Least squares linear regression analysis was used to calculate HCVR (slope of the relationship between E and inspired CO2) and HVR (slope of the relationship between E and inspired O2) during wakefulness and NREM sleep. Data for the HVR are not presented during REM sleep due to the absence of sustained periods of REM sleep during hypoxic exposure.

Experimental groups-Comparisons of ventilatory control parameters were made between mice in three separate series of experiments: 1) wild-type lean C57BL/6J mice of 30 g of weight maintained on a regular ad libitum chow diet (WT30), wild-type C57BL/6J mice maintained on a high-fat diet (49% fat; 5.8 kcal/g) for 16 wk to develop diet-induced obesity with 40 g of weight (WT40), C57BL/6J-Lepob mice of 40 g of weight maintained on a regular ad libitum chow diet (OB40), and C57BL/6J-Lepob mice of 60 g of weight maintained on a regular ad libitum chow diet (OB60); 2) NPY-/- and NPY+/+ mice maintained on a regular ad libitum chow diet; and 3) Ay and weight-matched wild-type C57BL/6J mice maintained on a high-fat diet (Ay control).

Plasma leptin determination-Arterial blood (1-1.2 ml) was obtained from direct cardiac puncture under iso-flurane anesthesia. Serum leptin levels were measured with a mouse leptin radioimmunoassay kit from Linco Research (St. Charles, MO).

Statistical analyses- Data were analyzed by using Crunch 4 (Crunch Software; Oakland, CA), and results for E, HCVR, and HVR are shown as means ± SE. Statistical significance between groups was derived within each sleep/wake state by using ANOVA with Newman-Keuls post hoc analyses where appropriate.

Results
VE and HVR in leptin-deficient mice- In the OB40 group, baseline VE had a trend to be lower than in weight-matched obese wild-type mice (WT40 group) during wakefulness (P = 0.06) and was significantly lower during NREM sleep (37.5 ± 2.7 vs. 55.8 ± 3.1 ml/min, P < 0.05;  and REM sleep (36.4 ± 3.6 vs. 61.2 ± 3.8 ml/min, P < 0.05). This difference in baseline VE between the OB40 and WT40 strain was entirely due to a significantly lower VT in the leptin deficient mice. The OB60 mice had significantly higher levels of  VE at baseline than OB40 mice due to larger VT across all sleep/wake stages . However, when VE was corrected per body weight, there was no difference between the two groups. Similarly, in C57BL/6J mice, VE and VT were higher in the WT40 mice than in the WT30 mice, and the difference was no longer present when VE was corrected per body weight. There was no statistically significant difference in the HVR or hypoxia-induced changes in VT and f during either wakefulness or NREM sleep between all four groups of mice, regardless of the presence or absence of leptin deficiency and obesity.

HVR and HCVR in NPY-deficient mice - Body weight and serum leptin levels (2.1 ± 0.1 vs. 2.6 ± 0.2 ng/ml) were similar between NPY-/- and NPY+/+ mice. There was no significant difference in either baseline respiratory frequency, VT, E, or the HVR between the two strains across all sleep/wake states. During hypercapnic challenge in wakefulness, the NPY-/- animals exhibited an elevated HCVR (P < 0.05) compared with wild-type littermates due to a trend to a larger increase in VT. There was no difference in the HCVR between the two groups of mice in NREM and REM sleep.

HVR and HCVR in Ay mice - The elevated body weight in both Ay and control mice was associated with high leptin levels that tended to be greater in Ay (29.0 ± 4.9 ng/ml) than in control mice (21.2 ± 1.3 ng/ml) but did not reach statistical significance (P = 0.13). Baseline VE was significantly lower in Ay mice compared with control mice across all sleep/wake stages . Low levels of E in Ay mice could be attributed to both smaller VT and f than in control animals. The HVR was identical in both strains. During NREM sleep, Ay mice exhibited a significant depression of the HCVR compared with control mice, which was entirely due to smaller increases in VT. During wakefulness and REM sleep, the HCVR was similar between strains ( Vsevolod Y. Polotsky et al.2004).


There are several outcomes of this study. This study shows relationship between levels of leptin and interruption of leptin signaling pathways (MC4 and NPY) on respiratory control. Some new findings which are concluded from this study are baseline VE is decreased in both leptin-deficient mice and Ay mice with disrupted MC4 pathways but not in NPY-/- mice. This reduction in baseline VE in leptin-deficient and Ay mice is likely due to the reduced basal metabolic rate reported in these strains (Breslow MJ et al. 1999).
Second-the HCVR (hypercapnic ventilatory responsiveness), which is depressed by leptin deficiency (O'Donnell CP et al.1998) and restored by leptin replacement in ob/ob mice during sleep, is also depressed by the MC4 blockade in Ay mice during NREM sleep.

Third, the HVR (hypoxic ventilatory response) is not affected by leptin deficiency, MC4 blockade, or NPY deficiency, suggesting that 1) the effect of leptin on ventilatory control is specific for CO2-sensing neurons located in medulla and 2) leptin deficiency does not impact on the sensing of hypoxia either centrally by the medullary receptors or peripherally by the carotid bodies.

Baseline VE-It is confirmed from this study that leptin deficiency is associated with decrease in baseline VE more during sleep as compare to wakefulness. It is due to centrally mediated reduction in metabolic rate present in the leptin-deficient mice. It also proves that action of leptin is mediated via both MC4 and NPY pathways (Erickson JC, Hollopeter G, and Palmiter RD 1996).

Central leptin signaling pathways and respiratory control-leptin deficiency leads to marked suppression of the HCVR. Leptin replacement caused large increases in baseline VE and significantly increased the HCVR during NREM and REM sleep, independent of weight, metabolism, and food intake.

Leptin and human respiratory control
Human respiratory control and leptin relationship is different to that found in ob/ob mice. Based on the findings in mice obese individuals can be on risk by two mechanisms-
when plasma and CSF leptin levels are low (Caro and Schwartz 1996);
when plasma leptin levels are high, but CSF leptin levels are proportionately low
The ob/ob mouse reproduces the primary clinical features of OHS. A clear rationale exists for investigating the relationship between leptin and the respiratory pump muscles in obese humans. In OSA, sleep is the factor that predisposes the upper airway to collapse (Gastaut et al., 1965). As noted above, the effects of leptin on ventilatory control in mice were more pronounced during sleep than wakefulness ( O’Donnell et al., 1999). Assuming that leptin can influence the upper airway in sleeping humans, this would suggest that the presence of elevated leptin levels in the CNS might protect against OSA.

It is noted that absence of leptin in ob/ob mice does not cause observable collapse of upper airway but it does not exclude the possibility of leptin relation with airway in humans because of three reasons. First, the minute cross-sectional area of the mouse upper airway may produce mechanical stability, since, according to the law of Laplace, the wall tension required to maintain a given trans-mural pressure decreases in proportion to the radius.

Second, the neuronal circuitry controlling upper airway collapsibility (upper airway muscles) or CO2 retention (diaphragmatic pump muscles) may differ between mice and humans. Third, the distribution of leptin receptors in humans in areas of the CNS controlling upper airway and pump muscles may not be comparable to that of the mouse. Thus relationship between leptin levels and respiration in humans is a matter of further research.

It is also noted that gender plays an important role in development of sleep apnoea disorders. In women, for the same BMI incidence of sleep apnoea is lower than that of males with same leptin levels. This may be explained by presence of different sex hormones that might play a protective role in development of sleep disorders. (Camargo et al. 1998).


In summary above study shows a relationship between leptin levels and respiratory control. Insufficient leptin levels in obese individuals may cause Obesity hypo-ventilation syndrome. This effect of leptin is more profound during sleep, which shows that it plays a role in development of sleep apnea disorders. Leptin deficiency control on respiration is specific to hypercapnia only and is not related to hypoxia. Thus leptin deficiency does not impact on central or peripheral chemoceptors that senses hypoxia.  It is also concluded that effect of leptin on respiration is dependent on hypothalamic pathway. Leptin receptors are also abundant in the nucleus of the solitary tract and other centres in the medulla involved in respiratory responses to CO2 and pH.  Human obesity is most commonly related with elevated leptin levels called as leptin resistance. Thus leptin resistance in obese individuals can cause sleep apnoea.

The Theory of Evolution


In 1859, Charles Darwin published The Origin of Species which formed the foundation for one of the most controversial theories in the history of mankind. Darwin argued and provided substantial evidence to the effect that all organisms had originated from the same source. Although Darwin did not refer to the phenomenon as evolution, referring to it as ‘common descent with modification’ instead, Darwin explained how organisms had originated from simple creatures to evolve to the complex creatures seen today in a process that took million of years (Ayala, 2008: 322).

Darwin based his evidence of evolution on his discovery of what is today referred to as natural selection which seemed to hold true of all species. The lives of organisms are normally characterized by competition against other members of the species for food, water and other resources, and against an ever-changing environment. Darwin observed that to ensure their survival, organisms constantly adapted their structural, behavioral and psychological characters to the prevailing conditions. This adaptation “refers to the process by which natural selection modifies the phenotype and generates traits whose effects facilitate the propagation of genes” (Andrews, Gangestad & Matthews, 2002: 491).

According to Darwin, evolution by natural selection was the result of some members of the species developing “fitter phenotypes” which helped them adapt better to their environment. Organisms which could not adapt to their environments died off or disperse, leaving only those which could adapt (Kikvidze & Callaway, 2009: 402; Fowler, T. & Kuebler, D. 2007; 57). This was referred to as survival for the fittest, the fittest being not necessarily the strongest or the largest members of a species but the one which was able to adapt to its environment as it changed. Darwin’s discovery of natural selection has been employed by plant and animal breeders to produce ‘sports’ through selective breeding. By controlling the breeding process of the plants and animals to ensure that fertilization occurs only between members with the desired qualities, breeders have been able to produce mutations of the original breeds which bear the desired traits.
Darwin noted that one of the consequences of the natural process of selection is that organisms tend to develop “adaptive organs and functions” which help the organisms to fit better into their environments. In short, these “organisms exhibit design” which tips chances of survival in their favour, making them more adaptive than organisms which do not develop these variations (Ayala, 2008: 324; Kikvidze & Callaway, 2009: 401). A classic example of design is the separation of the thumb from the other fingers on the human hand and among some of the higher primates. The stronger thumb helps the organisms to grip things better than primates whose hands lack the thumb. According to Darwin, design occurs “gradually and cumulatively, step-by-step, promoted by the reproductive success of individuals with incrementally more adaptive elaborations” (Ayala, 2008: 324). However, the design of actual living things is rarely perfect as the process of developing these adaptive features takes thousands or millions of years, yet the environment changes frequently and mostly unpredictably. This means that while an organism is developing features to help it adapt to a particular environmental change, more changes occur in the environment.

Among the most unrelenting critics to the Darwinian thheory of evolution are Christian who believe that the universe was created by a Supreme God. Among the Christians are those who see no conflict between the Darwinian theory of evolution and creationism. In short, there are those who accept both theories. This group of Christians has faulted the theory of evolution because it is based on the notion that creation comes with “interference with, or dispensation of, natural laws, and that ‘creation’ must be accompanied by arbitrary or unorderly phenomena” (Mivart, 2009: 4). These Christians have argued that the basis on which the conflict between creationism and evolution is founded is based not on factual information.
Critics have also pointed that even after moving the theory, Charles Darwin was noted to doubt it and its applicability, suggesting that he may not have been sufficiently confident of his own work. Darwin was noted saying:
But then with me the horrid doubt always arises whether the convictions of man's mind, which

has been developed from the mind of the lower animals, are of any value or at all trustworthy. Would any one trust in the convictions of a monkey's mind, if there are any convictions in such a mind? (Darwin, 1881).
Darwin’s critics have pointed to this ‘doubt’ as part of the evidence that the theory is unable to either explain some of the phenomena it should, or  Darwin had reasons not to explain some of the phenomena.

Antibiotics


Antibiotics:
Antibiotics are the drugs which are prescribed by the physician to fight against infection caused by microorganisms.Antibiotics are documented as agents to treat illnesses. But there are instances when antibiotics are specified by physicians to prevent infections.

Usually antibiotics are given prophylactically in certain medical conditions only, like when a person has transplanted heart valves or damaged heart valves. These people are more prone to develop cardiac heart valves infections even with minor surgeries ( Reese, Betts & Gumustop, 2000). This is due to the lodging of bacteria from other sites of the body through the blood stream into the abnormal/diseased heart valves during the surgical process. The physicians therefore prescribe antibiotics propylactically to people with heart valves problems who are even undergoing dental surgeries.Antibiotics are also prescribed to indivisuals who are immunocompromised especailly people who have AIDS and are also preferred in patients undergoing chemotherapy and radiation therapy.Persons who are immunocompetent are also sometimes prescribed antibiotics before a major surgery like bowel surgery. People travelling to third world countries are given prophylactical antibiotics to prevent them from prevailing illnesses in the third world countries, like diarrhea.

It is recommended that it should only be the physician right to decide whther antibiotics is needed by the indivisual for the infection or not. In ordinary infections, it is not advisable to start antibiotics at all.It should be concised that the improper and excessive use of antibiotics lead to antimicrobial resistance ( Reese, Betts & Gumustop, 2000).

Overuse and development of resistance
 Antibiotics are not recommended for a normal cold, because antibiotics only work against fighting infections caused by bacteria. Viruses cause illnesses such as a soar throat cold or flu. Antibiotics do not cure infections caused by viruses and should not be taken in these cases. It is advised that a cold or the flu be allowed to run its natural course. The average cold or flu lasts up to two weeks or more. If the symptoms persist for more than four weeks then it would be wise to consult the physician. In most instances, antibiotics either kill bacteria (bacteriocidal drugs) or cause their growth to come to a halt (bacteriostatic drugs). However, in some situations, certain bacterium grows stronger than the antibiotic coverage and the drug is unable to be effective aginst them. These strains of bacteria are called “resistant,” as they are in fact resistant to antibiotics.

Usually resistance to antibiotics develops when a person has taken antibiotics either too often or improper dosages (Cunha, 2009). Another form of mistreat is by patients who insist antibiotics prescriptions from their physicians. Remarkably, many doctors concede to misguided patients who stipulate antibiotics to treat colds and other viral infections that cannot be cured by these antibiotics. Due to the malpractices, there are certain bacterias which are resistant to various antibiotics and are termed as 'multi-drug resistant.’ Though we cannot completely stop resistance from occurring, we can slow down its progress and hinder its spread.Patients and physicians must take additional care, caution and consideration while making use of the antibiotics.

Individually if there is no serious infection in the body and we don’t require antibiotics, we should not take them. Many infections are cured without antibiotics and it is not at all compulsory to use antibiotic in minor ailments. Bacteria are becoming increasingly resistant and there aren't too many new antibiotics in the pipeline (Gallagher, 2008). It is therefore strongly recommended to use antibiotics optimally in order to seize the emerging bacterial resistance. The people need to be informed that by not using the antibiotic unnecessarily, the drugs will more likely to work when it is needed at the time of serious bacterial infections.

The future of antibiotics
The future of antibiotic is desolate. There is a marked decrease in the indurty of Research and development and without extensive researches and preventive practices; the risk of resistance against antimicrobial drugs can not be addressed. The processes by which bacteria exhibit resistance to antimicrobials are usually drug inactivation or modification, alteration of target site, alteration of metabolic pathway and reduced drug accumulation.