Monday, February 6, 2017

There are thousands of opportunistic infections for now though lets just look at five 

  1. Entamobiasis  
  2. Blastocystic hominis
  3. Giardia Intestinalis
  4. Dientamoeba Fragilis
  5. Trichomonas vaginalis
first lets define opportunistic infections ,An opportunistic infection ia one where in the parasite /protozoan takes advantage of the host weakened or compromised immune system. In other words the  parasite may have been in the host/individual and does not seem to affect the host harmfully until the host is most vulnerable.

Entamoeba histolytica is the first such protist that we will look at.
Histo= tissue  lytica=dissolves
the life cycle,mode of transmission ,prevalence or distribution,treatment,identification,problems it causes .

the life cycle is a rather simple one. the cyst is ingested accidentally it further develops into a more prefound mature cyst  this process is called excystation then its becomes a trophozoite, followed by multiplication increased in number of trophozoites and cysts.

how is this infection usually acquired is probably the question  , the answer is easy bad plumbing ,drinking contaminated water with eggs or  trophozoites ,filth flies are also carriers they may pitch on your food and contaminate it with eggs or trophozoite .close living environment may also advance the process of transmission. reservoir hosts such as pigs and dogs should be monitored carefully to decrease the process of transmission.

prevalence and distriobution  entamoeba histolytica is spread worldwide it  however affects mostly developing countries  .it is the 3rd most cause of parasitic death only malaria and visceral leishmaniasis comes before it .Its responsible for 70,000-100,000 deaths per year.It is not common in the caribbean  but its affects central american countries , it affects mostly travellers ,homesexual men

identification of the problem , entamoeba hystolitica  can distroy the liver , lungs ,(brain and skin rare cases ) the protist feels on the enteric mucosa  lining the large intestine in the process protelytic enzyme is released which break down or dissolves the tissue  note Histo=tissue lytica=dissolving in the process abscess can take place on the liver  .abscess this is when tissue is swollen and is infected with pus.note this often causes ulceration of the liver and lung tissue .the infected lung and liver tissues have pus contaminated with trophozoites which will only make the condition worst.

dysenery will take place as well the patient will have bloody diarrhea , persons infected have gross fatigue they will pass 15/20 stool per day.there are three different stage of infection
1 benign  3  invasive  3 chronic stage

in benign stage the persons shows little to no symptoms and are considered to be in good standing

in invasive stage the trophozoites are within the large intestine or colon and start to cause ulceration and abscess of body tissues

chronic stage is when the liver , lungs  neurologic and in rare case the skin can be affected .

 iodinoquinol in  early stages

metabendazole in chronic stages .

laboratory test for infection

stool analysis to find egg of entamoeba histolytica  or trophozoites of entamoeba histolytica  note the size should be an average of 10-15 um .

Blastocystic hominis

there has been many debate as to whether blastocystic hominis is actually infectious or whether it has caused any serious problems .
blastocystic hominis is believed to cause nausea , watery diarrhea , vomiting ,abdominal pain and excess flatulence have been reported.

Image result for blastocystis hominis

Giardiasis Intestinalis
Image result for giardiasis intestinalis cycle

Giardiasis intestinalis  , laboratory analysis  alternate method of analysing the protozoan .

giardiasis is considered to be common  , the method of transmission is mainly due to drinking contaminated water infected with the cyst or trophozoites of the giardiasis intestinalis.
the trophozoites are between 10-18 um  they contain up to four pair of flagellates 

the cyst are usually between 10-12 um in size they contain from 2 to 4 pairs of flagella ,

giardiasis is known worldwide its distribution is without a doubt recognised as well in 2013 there was  250m cases reported to be symptomatic giardiasis  its not known to cause any serious fatalities but it gives gross discomfort 

persons will experience bloating,nausea ,vomiting,abdominal pain,diarrhea  .in jamaica there is < 5% prevalence  its also known as travellers disease  beavers are the reservoir host in usa .

there are two stages of giardiasis acute and chronic stage 

Acute stage 1
        persons experience ;vomiting,nausea ,diarrhea 

chronic stage  3
 persons experience malabsorption of fats and vitamin b12   the perosn will experience drained energy and vitality

 metronidazole is the drug of choice

 Laboratory analysis

stool smear containing cysts or trophozoites

 dudonial fluid may contain trophozoites

alternate immunoassay enzyme used to test for antigen of giardiasis

Trichomonas vaginalis 

mode of transmission ,treatment,prevention ,laboratory testing, distribution/prevalence,method of reproduction ,describe the protozoan.

trichomonas vaginalis is a parasite that have of it shapes like a pear the other half  is flat it  has four pair of flagella anteriorly and one posterior flagellum .It also contains a single nucleus .the trophozoites are between 15-18um

Trypanosomas is less than <5% on the normal female population and it is also as high as 70% among prostitutes and inmates
trypanosomas is highly contagious and is spread through direct contact its dosent have a cyst stage

trypanosomas vaginalis reproduce through the process of binary fission rather longitudinal binary fission. thgis is also favoured by low acidity . hence the protozoan changes the ph of the female genital environment .

extreme conditions would be yellowish conspicious foul smelling discharge from female genitals which in some cases are frothy.

dependent damage to the epithelium of infected organ
 Severe case 
infertility in women and cervical erosion

associated with the increased risk of acquiring HIV-1 which is related to the inflammation of gental tract.

smear of vaginal discharge  if trophozoites are found within the vaginal fluid then that person has trichomonas vaginalis



works for both male and female.

use condoms
vinegar douche can prevent infection of disease.
Opportunistic helminth infection


There are more than one helminths but one of the most undestimated and dangerous type is the  Schistosomiasis

the cycle ,little detail of how the schistosome funstions  where they are found ,the types and what they cause to happen to persons infected , treatment ,prevention and contol .

Schistosomes have a cycle the eggs are found when the egg matures it releases miracidia which finds a host which is mostly aquatic or amphibious snails ,the miracidia penetrates the snails skin . The snail releases  sporozoites that  develop into the cercaria the cercaria loses its tail  then further develops inside a host which is usually human the  cercaria gets caught up in the blood flow and is brought to portal blood in liver and develops into adult. the adult then releases the eggs in either urine or stool

the schistoma functions in different ways the cercarial schistosomes (free living swimming form) has an acidophillic head and a basophillic  tail . the acidophillic(-ve) head Post acetabular gland  secretes a sticky mucus when it comes into contact with a host skin ,it then dissolves into the skin of that individual.the basophillic tail Pre acetabular gland secretes collagenase  and the tail drops off from the cercarial schistosomes ,now its called a schistosomule.
unencysted metacercaria.

there are three types of schistosomes these are S. mansoni, S.haematobium and S.japonicum.

S.Mansoni has eggs that are have hooks , there are two forms of infection Acute and intermediate-chronic stage .In the acute stage  there is a onset of nausea , vomiting diarrhoea  as well as fever.This fever is called katayama ,katayama is caused because of the onset of female laying eggs five weeks after infection and granuloma formation around eggs trapped in the liver and intestinal walls.granulaoma formation is induced by cell -mediated immunity
high eosinophilia ,less than 1/3 of the eggs excape into the intestine when symptoms occurs they manifest themselves in nausea , headache ,irritating coughing (migrating larvae or escaped eggs)in extreme cases diarrhea accompanied with blood.

intermediate to chronic cases
there are thousands of eggs trapped in the tissues

intestinal schistosomiasis 

the pathogenic reaction is a cellular , granulomatous inflammation around eggs trapped in the intestinal tissues,with subsequent fibrosis.The large intestine shows the most severe legions.

Hepatosplenic Schistosomiasis 

the pathology is similar to that seen in the intesine with granulomatous inflammation around eggs trapped in the hepatic portal vein  and liver , leading to fibrosis and hepatosplenic disease .

portal hypertension  may result in ascites (accumulation of fluids in the abdomenal cavaties and rupture of the oesaphageal varices.

Schistosomiasis   S.Mansoni eggs are 150um long  eggs have terminal spines.


The adult form of these parasites are normally found in the bladder or in the uterus . when the female lays 1000s of eggs they are calcified and are trapped in the tissues . eggs are often passed in the urine
thousands of eggs are passed in urine and causes problems such as;

  • bladder ulceration
  • difficulty urinating 
  • frequent  urination
  • haematuria (blood in urine)- urinary schistomiasis
on rare occassions eggs are passed in the liver and causes granuloma formation as well ,however it is much less severe.


its practically the same as S.mansoni except for the case where it has a higher fecundity than s.mansoni  .Hence it is more severe in almost all aspects

the eggs are small 80um times 65um these species of the parasites has the smalles eggs ,the eggs also lacks terminal spines  these species can also cause stunt growth in host that they infects .this occurs when eggs get trapped in the hypothalamus of the infected organism .

there are a few species of schistomiasis that have there definitive host but get caught up in the wrong host and therefore meet a dead end because they have or rather cannot develop to maturation within another organism .One such case is the species of schistosomiasis that normally infects birds ,when these organisms affect individual which are not direct host such as human a condition occurs that is known as swimmers itch.

this gives discomfort to the victim ,rash appears soon as the skin is penetrated larvae are dying some already dead this causes hypersensitivity  and painful rash.

Opportunistic protist and helminths infections

Thursday, January 26, 2017

Title:                   Aggression hormones and how it affects  brain development

Introduction:  The objective is to figure out how aggression affects the development of the brain. Pain frustrations, harsh treatments, personality traits e.g. type- A personality with extreme competitive behaviour, high testosterone levels are all seen as triggers that affect aggression. From various finding however it could be seen that there was indeed a correlation between aggression and brain development. It was discovered that persons that have high aggression tends to also have reduce, brain symmetry, amygdala, cortical thickness etc.
It was concluded that it was not just hormones that causes aggression, and in-depth analysis from research findings suggests that aggressive individuals are more victims of poorly developed brain. These individuals themselves probably should not be held accountable for their actions.

Body:                   It is believed that noradrenergic activation is related to social challenges; this in turn affects aggression on different levels. The hormonal, symapthic and autosomous nervous system as well as the Central nervous system (CNS) are mainly affected by the nervous system. Noradrenergic is a hormone and neurotransmitter that is synthesised in the brain, it is release directly in the blood stream and goes to noradrenergic receptors that prepares the body for fight/Flight. Catecholamines are also thought to be responsible for metabolic preparation for prospective fights, somatic effects control the sympathic system this involves increase in blood pressure and heart rate (Makara & Kruk, 1998).
These increases causes a feedback into the nervous system and affects fight readiness, the CNS noradrenalic system on the other hand decreases pain perception, enhance attention, and improves olfactory recognition. Alpha two (α 2) adrenoceptors are indispensable for aggression,β adrenoceptors is thought to control adaptability  of aggression response (Makara & Kruk, 1998) hence noradrenergic activation slightly affects aggression .The central noradrenaline along with the sympatho-adrenal system works together to prepare animal to be effective in a  fight situation and helps the organism to endure the effects caused by fights. They can control neural processes, they have the ability to relate the aggression and can manipulate behaviour for a given circumstances.
Recent studies have suggested that neurotransmitters, hormones, cytokine, growth hormones and enzymes are all factors that aid in the signalling of molecules that influences aggression (Nelson & Chiavatto, 2001).Serotonin (5-HT) which is a part of the brain neurotransmitter system, is primarily the main molecular determinant of inter-male aggression. Other neurotransmitter seems to work indirectly than directly. When slight modulation of (5H-T) levels, receptor sub-type activation density and binding affinity was performed. It was noted that these changes affected aggression.
From the investigations it can be seen that hormones and neurotransmitters which causes noradrenergic activation vaguely affects aggression. If there is any damage to the brain or poor development such as reduction, then it is safe to assume that the secretion of hormones will be affected. Especially due to the fact that hormone noradrenergic norepinephrine is synthesised in the brain itself. The question however is how does brain development affects aggression, so far trends suggest that it directly affects aggression.

The neural circuit is composed of several regions of the prefrontal cortex, amygdala, hippocampus, medial preoptic area, hypothalamus, anterior cingulated cortex, insular cortex and other interconnection which is involved in emotional regulation. Structural or functional abnormalities in one or more of these regions or in the inter-connections among them can increase. The brain system mediates aggression appears to be fairly constant among mammals, many details of the regulatory pathways are species specific (Nelson & Chiavatto, 2001). One such example is the Syrian hamster which exhibits c- fos immune-activity, in the medial amygdala in the medial amygdala, bed nucleus of the stria terminalis (BST), ventrolateral hypothalamus and dorsolateral part of periaqueductal gray (PAG) after displaying offensive aggression towards an intruder.
Nitric oxide was seen as a modulating neurotransmitter. This helps to stimulate aggression, especially in mice (Nelson & Chiavatto, 2001). Argenine vasopressin (AVP) is another hormone that plays an important role in aggression and other social behaviour .AVP on aggression is centred in the anterior hypothalamus (AH), when microinjection of AVP took place into the (AH) in combination with (5-HT) receptor, the receptor showed that only 5-HT receptor activation was inhibited, it was hence discovered that AVP facilitated aggression.
Histamine  findings proved that intracerebroventricular histamine , when administered decreases 5-HT levels in the hypothalamus of rats .Thus the receptor nullifies the aggression that mice would normally exhibit (Nelson & Chiavatto, 2001).MAOA monoamine oxidase A also contributes to aggression because they alter neurotransmitter levels,MAOA is mainly found in catecholaminergic neurons in the brain. Studies have proven that inhibition of MAOA correlates with reduced aggression in isolated male mice.
From the scientific evidence it can be expressed that aggression is stimulated by a wide array of hormones and chemical compound found in the brain. Nitric oxide stimulates aggression, histamine was found to nullify the effects of aggression .MAOA is found to be in the catecholaminergic neuron , from the studies it can be seen that brain development and aggression is intertwined .It was even determined that MAOA causes reduction of aggression in mice.
Foot shock of mice’s also increases aggression, this is a result of increased 5-HT level. Humans when treated with MAO enzymes as a pharmacological inhibitor express no change in regards to aggression. The indolamine serotonin (5-HT) is the most prevalent neurotransmitter associated with aggression, in a wide range of species including human. It has proven to be difficult to know the precise role of the (5-HT) and how it affects the execution of aggressive behaviour (de Boer & Koolhaas, 2005).It is well known that some 5-HT 1a and 5-HT 1b aid in the reduction of aggression behaviour without even slowing motor function. Systemic injections of anti-aggressive dosage of 5-HT 1a and 5-HT 1brobustly release due to inhibitory actions located near dendrite, and terminal auto receptors respectively.
 Experiment conducted on rats confirmed that systemic administration of drugs, acting on selective agonists (which are substances that initiate a physiological response when combined with a receptor).It was shown that both 5-HT 1a and 5-HT 1b expressed anti-aggressive effects in resident rats (de Boer & Koolhaas, 2005).Studies conducted with positron emission topography have revealed that human brain undergoes a period of postnatal maturation that is more protracted than previously expected. The highest amount of glucose metabolism is found in the primary sensory and motor cortex. Cingulate cortex, thalamus, brain stem, cerebellar vermis and hippocampus region.
It was seen that within 2-3 months, glucose utilization increases in the parental, temporal and visual cortex. Within 6-12 months, glucose utilization significantly increases in frontal cortex. The metabolic change is due to rising of various behaviours during early years in life. The metabolic change is due to rising of various behaviour during early years in life.
The cerebral cortex goes through a glynamic course of metabolic maturation that persist until late adolescent to teenage years (16-18).Firstly there is an increase in the rates of glucose utilization from birth to about four years, at this point the child cerebral cortex uses over twice as much glucose than adult (Chungani ,M.D. 1998).In brain development there was a significantly more rapid development occurring in the occipital lobes than in other region. Infants with brain abnormalities had a significant increase in cortical thickness and a significant decrease in cortical folding. These were more apparent at forty weeks, males are more likely than females to show aggression across species, ages and situations proves that these differences may be partly influenced by early hormones.
 Aggression based on studies were done with adrenal hyperplasia (CAH), those exposed to high levels of androgen in the prenatal and early postnatal periods, had higher aggression scores that the controls used. Cerebrospinal fluid levels of the major central metabolites of serotonin (5HT), norepinephrine (NE) and dopamine (DA) - 5 Hydroxyindoleacetic acid (5HIAA), 3-Methoxy-4 hydroxy phenyglycol (MHPG) and homovanillic acid (HIV) independentlyscored history and showed significant negative correlation with 5HIAA and a significant positive correlation with MHPG. Testosterone cannot be overlooked as a hormone which is correlated with aggression, testosterone is a hormone that causes elevated levels of aggression .Testosterone causes elevated amount of aggression both in males and females.
 It has been discovered that males that are more symmetrical are exposed to higher levels of testosterone than other individuals that are less symmetrical. Also males that are more symmetrical are also more aggressive than others  (Hyatt and Caron 2011).It can be seen that hormones especially (testosterone) significantly control aggression  (Streissguth , PHD, et al. 1991).When testosterone was injected in varying species of animals, whether the individual was a male or female resulted in an increase in aggression.
 In chimpanzee species it was shown that dominant socially high- ranking males exhibit high aggression and likewise high testosterone levels (Muller & Wrangham, 2004).In human it operates differently, there are things such as competition example male-male competition (Archer,2006:Hignr,R Ramenofsky when social status is challenge there is an elevated amount of testosterone that is released, this automatically leads to more aggression. In American criminal justice a person can be exempted from prosecution if it is proven that the prosecutor is legally insane. That is because a mental condition may influence the behaviour of an individual; this is due to the fact that the defendant might not understand the wrongfulness of the act they have committed.
1998 case study old kid kindle ,It was shown that ‘kip’ shot and killed his parent ,he then brought the gun to school where he killed two more people and injured 25 more before being disarmed. Brain imaging showed that kip kindle could be not sanity by reason of insanity, small cavities were found in kindle’s frontal lobe.This however didn’t prove to be enough evidence to support the fact that it was an abnormality that altered his behaviour in any way. Hence ‘kip’ was sentenced to 111 years in prison without parol, another case studies M ‘Naughten 1843 UKHLJ16 House of lords.
 Daniel M Naughten attempted to kill the Prime Minister, Sir Robert Peel, but instead shot and killed Edward Drummond the Prime Minister’s secretary. M’ Naughten was suffering from insane delusion at the time of killing. From this the House of Lords formulated the M naughten’s rules which apply in determining whether a person should escape criminal liability on the grounds of being insane.Experts after critically evaluating the situation suggested that M naughten showed fast deterioritation in his reasoning ability. The defendant had no comprehension of the act he committed, further medical research indicates that patients with selective damage to PFC can often know right from wrong but still be unable to act on such knowledge.
Difference in PFC may also be caused by other variables, including levels of education and alcoholism. There are patterns that emerge for the amygdale, where damage can results in increased or decreased aggression. Growing number of research gives good reason why some brain dysfunction can affect the probability of different kinds of criminal behaviour. It must be noted that there are no concrete biological markers genetic or physiological that can predict behaviours, Violence arise from a symphony of factors. One main finding is brain development and how it affects aggression from research finding (Hyatt & Caron, 2011) it was revealed that there is a more in depth, analysis that must be taken into consideration when addressing the effects of aggression on the brain development.
It was discovered that persons that have conduct disorder, such as;  aggression , destruction of property , deceitfulness etc ,had a reduction in grey matter (Hyatt & Caron, 2011).The goal is to determine if brain regions implicate emotion processing shows structural alterations in adult with conduct disorder. Using voxy based morphometer which is a neuroimaging analysis technique that investigate focal differences in the brain anatomy the grey matter volume was compared shown to be reduction in grey matter volume in comparison to healthy control subjects. Not only was there reduction in grey matter but results showed significant reduction in bilateral, anterior, interior cortex and left amygdala.
 In other words the aggressive behaviour seemed to stem from a deeper cause which is developmental abnormalities of the brain itself. Close inspection of neurodevelopment theories suggests that early expression of conduct abnormalities have a high likelihood to continue into adulthood, acting as a stepping stone for antisocial personality disorder or psychopathy.GI –Gyrification index measures cortical folding, this method was best used to cement the belief that conduct disorder patients had brain deficiencies. The hypothesis was correct and it was proven that there was in deed a correlation between brain development and conduct disorder, which is the venting of aggression.
Conduct disordered patients compared with control subjects, expressed reduced cortical thickness and folding (Hyatt & Caron, 2011) .Thinner cortex was located primarily in posterior brain regions, including left superior temporal lobes, parietal lobes, temporal parietal junction, and precuneus.From the finding it could be seen that not only did person that showed aggressive behaviour had a reduction in the grey matter but also reduction, in the size of the amygdala, cortical thickness and folding. Cortical thickness and folding reduction hence forth was used as the marker for brain abnormalities in persons that expressed aggressive or conduct disorder.
These researches causes one to think even more if aggressive behaviour root cause is actually abnormalities of the brain, then maybe one should look on brain development and factors that affects brain development, and at what stage of a person life does most of their brain developed. Research have proved using PET (Positive emission topography) that the human brain undergoes a protracted (longer than anticipated) time for development after postnatal maturation (Harry M.D, 1998).PET have indicated using degree of glucose metabolism, the functional activity present in primary sensory and motor cortex .At 2-3 months of age, glucose utilisation increased in temporal, parietal lobes as well as visual cortex; basal ganglia and cerebral hemispheres (Harry M.D, 1998).
Within 6-12 months glucose utilisation increased in the frontal cortex, this is responsible for the various behaviour in the first year of life. The investigation showed that metabolic maturation persist until age 16-18, however most maturation takes place between the moment of conception up to  about age 4.That’s when maturation and glucose maturation is most dominant, after age 10 there is a decline in glucose utilisation and hence brain development. From the various research it is evident that most development, takes place in early onset of life.
 Evidence have pointed to factors such as; brain plasticity following injury as well as critical period of maximal learning as key factor for differences in brain development .The purpose of these investigation is to clearly show the correlation of aggression with brain development and to figure out how what brain development have to do with brain abnormalities .Brain plasticity is said to be the extraordinary behaviour necessary for adaptation, modification and change in structure and function following changes within the body or the external environment .From the definition a child’s brain is considered to be more adaptive than that of adults and can hence learn at a faster rate, as well as recover from brain injury.
 Examination of brain plasticity has analysed and proved that, brain development passes series of development starting with neurogenesis, and processing to neural migration, synaptogenesis, pruning and myelin formation. Principles that basically affect brain plasticity are affected by environmental events like; sensory stimuli, psychoactive drugs, gonadal hormones, parental child relationships, peer relationships, peer relationships, early stress, intestinal flora and diet (Kolb PHD & Gibb PHD, 2011).Environmental stimuli influences maturation and differentiation, uncertainty causes the brain to overproduces neuron if  there is deficiency in some . The brain has a parallel system in which unnecessary cells are removed by cell death and synaptic pruning .

The stimuli from the environment determine how reduction takes place, these stimuli causes brain plasticity. Brain plasticity can be both a good and a bad thing, because consistent cell loss causes reduction in cortical thickness over time (Kolb PHD & Gibb PHD, 2011). That is the cortical becomes thinner in caudal rostral, which develops around age two and continues to about age 20.The fact finding evidence has displayed the structure of how aggression , starts from early age development rather than something that manifest overnight.
The wasting of the cortical thickness begins from rather and early neonatal to post neonatal stage, because of environmental stimuli such as diet, stress and more. In the long run it is these factors that further affect how an individual brain and behavioural pattern is different from the control healthy population. Environmental factors that causes pre and post neonatal to have wasting taking place in the cortical thickness are; stress, neglect, diet and more for this purpose we will look at these few. Diet, fetal nutrition deprivation is a strong programming stimulus, testing shows that it correlates with disease later on in life.
One instance is over nutrition can be deleterious to the health of the offspring, it can result in metabolic syndrome that can lead to diabetes two or obesity if persist to adulthood (Armilage & Taylor, 2005). Note programming or plasticity doesn’t change, it may be an adaptation but it is short sighted. It doesn’t known the condition of the future and prepare neonatal based on past environment or stimulus .This is what causes deletion of what is probably and advantageous characteristics , and also  has  the disadvantage of short sightedness .Some environmental condition are short term and the effects  of foetal changes continues into adult stages of the individual.
For mothers that are pregnant, she becomes the environment of the foetus, if she is under stress in any way she will release cortisol. The foetus is not mature and cortisol is known to affect the pre-frontal cortex, it is toxic to neural development. Evidence suggest that aggression may actually be caused directly from the environment (mother in the case of foetus -neonatal), that influence how one’s brain develop from an early stage in life. Studies have even proven that increase in cortisol level may even cause one’s loss of symmetry in and poor development of the brain (Streissguth , PHD, et al. 1991).
Hypothalamus releases cortisol, if cortisol in the blood becomes too concentrated then pre frontal acts as a negative feedback and indigenous opioids and endorphins are released to regulate of negate the effects of the excess cortisol.
Conclusion: It was evident that poorly developed brain was the common factor for persons that showed increased episodes of aggression, than controlled group. Case studies of persons that committed felony and criminal offence reported that some persons that committed heinous acts, after doing brain scan it was revealed that most of these individuals had  reduce amygdala ,tumours and damage to the pre-frontal cortex. These findings required deeper investigation, these revealed than these damages were mainly caused by the environment in which a foetus and or baby is brought up in .That is considering that between the ages 0-4 majority brain development take place (Kolb PHD and Gibb PHD 2011).Thus it is confirmed that increased aggression is mainly caused by the adaptive nature of the human body for survival (brain plasticity).
Brain plasticity and programming is beneficial but it also has negative implication of short sightedness. Some environmental changes are only temporary, but brain plasticity causes deletions of possibly important genes causing and individual to be more vulnerable. This vulnerability may cause reduction in brain mass, neurons, amygdala etc. Hence causing personality disorder such as psychopathy, conduct disorder and aggressive outburst. Brain abnormalities can induce increase in aggressive behaviour.
Acknowledgement: This research was supported partially by a wide array of journal articles listed in the reference. It is with a wholesome gratitude that I give my thanks, the expertise greatly assisted in the completion and comprehension of the research. I would like to thank C.J, Hyatt and H .E. Caron in illuminating how cortical thickness and folding occur, Kolb, PHD .B and Gibbs, PHD .R in explaining how brain plasticity works.
I would also like to thank Dr. Hyslop for giving a very understanding concise lecture on factors that affect aggression. I would also like to thank my colleague Gabriel Walters for outlining the construct of the research when I needed it most.


Armilage, J. A., & Taylor, P. D. (2005). Experimental models of development programming consequence of exposure to an energy rich diet during development, 3-8.
Harry M.D, C. T. (1998). Studies of ceebralglucose utilisation with PET. A critical period of brain development , 184-188.
Hyatt, C. J., & Caron, H. E. (2011). Misconduct the causes. Cortical Thickness and folding deficits in conduct disordered adolescents, 207-213.
Kolb PHD, B., & Gibb PHD, R. (2011). Brain Plasticity . Brain plasticity and behaviour in the developing brain , 265-274.
de Boer, Sietse F, and Jaap M Koolhaas. 5-HT1A and 5-HT1B receptor agonists and aggression: A pharmacological, 2005: 126-139.
Makara, J, and M R Kruk. "Aggression and how it affects the brain." Catecholaminergic Involvement in the Control of, 1998: 85-97.
Nelson, Randy J, and Silvana Chiavatto. "Aggression hormones." Molecular basis of aggression, 2001: 713-717.
Chungani ,M.D., Harry T. A Critical period of Brain development:Studies of cerebral glucose .Utilization with Pet. Detroit ,Michigan: American Health Foundation, 1998.
Streissguth , PHD, Ann Pytkowics, Jon M . MD Aase, Clarren K ,MD Sterling, and Sandra P Randels. 1991. "Brain development ." Fetal alcohol syndrome in adolescents and adults. 265-269.

Aggression and how it affects brain development

Thursday, October 29, 2015

You are probably here because you have encountered a website that pops up a dialog box or some other form of annoying modal widget preventing you from accessing the content of the website. Usually these dialogs will ask you to either register to their website, complete some kind of offer or to complete a survey before you can proceed to the website. The dialog usually contains a tinted background over the website's content preventing you from selecting or viewing anything else on the website. It usually looks something like this:

This can sometimes be very annoying, as you can see the dialog blocks us from accessing any of the content behind it. In this particular website the modal dialog shows up when it detects that we have visited the website more than once. I am going to show you a little trick to remove this signup dialog so we can access the websites content so the end result should look like this:


The methods can vary between web browsers, so just to make this clear we will be working with the Google Chrome browser this method will also work with other major browsers such as Firefox. Open your browser and go to the website containing the popup dialog. Ensure the the page is completely loaded before proceeding. In case we will be using this link. This is what the webpage currently looks like.


Hover you mouse over any of the dark background regions and right-click on the region. A menu consisting of a list of options should popup. It should now look something like this. The red star indicates the region that was right-clicked.


Select the 'Inspect Element' option from the menu list that popped up. A small window should show up showing lines of HTML code. You won't need to know what the codes mean but if you look closely you will see that a line of code has been automatically highlighted.


Now click on the line of code that has been highlighted and hit the delete button on your keyboard. This will remove the tinted dark background covering the website. Your end result should look something like this.


Now if there are still objects covering the content of the webpage you can just repeat steps 1 through to step 4 but this time instead of right-clicking the dark background you would instead right-click the object that is currently on the webpage that you want to remove. In our case the background has been removed however the signup dialog is still present. So to remove the signup dialog, going through the steps again, we would hover our mouse over the signup dialog (going as close as possible to one of its ends) and then right-click. Select the 'Inspect Element' option. The window containing the HTML code will popup. Click on the line of code that is highlighted and hit delete. You will repeat the steps until all objects blocking the webpage are removed. This is the end result after removing the signup dialog.

Simple Trick to Bypass Website Dialog Blocking Content

Tuesday, October 20, 2015

While there are a large number of drag-and-drop software and websites out there that will allow you to  create stunning diagrams only a select few take into consideration diagrams that involve software development. As such key components required to create class diagrams, sequence diagrams, use cases and other forms of software modeling diagrams are usually absent. Here I have compiled for you a list of websites that allow you to create UML diagrams.


If you're looking for a website that gets straight to the point, one that doesn't require registration then this is the website for you. You can either save your diagrams to google drive, One Drive, drop box or even to your computer/ device. This website allows you to select predefined components from specific categories to complete your diagrams. You can select components from UML diagrams, entity relationship diagrams, flow charts, basic shapes and arrows.


Creately has a clean user interface packed with amazing tools to get you up and running and creating stunning UML diagrams in minutes. Creately has over a hundred templates from which you can choose to start creating your diagram. With Creately you can design sequence diagrams, class diagrams and use case diagrams. Creately also allows you to connect with collaborators and draw diagrams in real-time. While this website has a free version there are some restrictions such as you will only be able to create one(1) project and only (5) diagrams. To remove these limits please refer to their pricing plans to see if there is a package that suits your budget.


Yet another astonishing web app that allows you to create UML diagrams. This website allows you to create a free account with a few restrictions. You are limited to only 5 diagrams and 2 MB of free storage so if you thing you'll need more room to draw then consider upgrading your free account when you register. To begin drawing just simply hit the large orange button that says "Start Drawing" you can begin immediately. In addition to UML you can also create Flow charts, Venn diagrams and other technical drawings.


Cacoo is another UML design website that offers free as well as paid packages for creating diagrams. This website also has a large number of templates and tools that you can choose from to start building your diagrams. Along with the usual UML and flow chart tools you can also create other diagrams such as database diagrams, sitemap diagrams and wire-frame diagrams. Cacoo also allows you to choose from a wide range of languages and is therefore used by many persons and companies across the globe.

This is yet another stunning website that has a friendly user interface for creating diagrams. Diagrams can easily be created by just clicking any of the tools in the left sidebar. Clicking on the tools in the sidebar will generate the respective components in the drawing in the center bar as well as generating a code that you can easily edit to your liking. No need to drag-and-drop, re-size or move around any object on the diagram, just simply edit the code or add your own code and the diagram will be generated automatically.

Websites to Create UML Diagrams for Your Software Online

Friday, October 16, 2015

There are numerous amounts of movies and T.V series centered around technology and particularly technologies that can think like humans. Machines that are capable of performing like humans are referred to as Artificially  Intelligent machines. Movie directors have developed creative story lines that brings fictional A.I technologies to life through movies. Here I have compiled a large list of A.I. movies that you can watch:


This movie involves a man, Theodore Twombly, a writer who was recently involved in a break-up, gets his hands on an amazingly complex operating system. The OS named Samantha is surprisingly very smart and funny. As the movie continues Theodore develops a deep loving relationship with his new operating system. As he learns new things about her she also seeks to learn things about him and also develops feelings for him.

I, Robot

This movie features Will Smith as a detective in a world soon to be overrun by robots. In this world robots are in every household they are treated like any other personal product. The movie starts with Smith investigating a murder that he thinks was carried out by one of the robots. Robots are programmed to obey and protect humans so when the unlikely suspect in a murder case turns out to be a robot, humans become fearful for their lives.


Wall-e a waste disposal robot is the last robot alive and spends his days doing exactly what e as programmed to do to clean up the earth. Wall-e kept doing this until he came across another robot that was sent back to earth named Eve. Eve was sent back to earth to determine if the planet habitable enough for the humans to return. Wall-E follows eve across the galaxy and together they embark on an amazing adventure. 

Artificial Intelligence (2001)

This is a movie about a little boy, David,  who found out why he was always different from other kids, he was a robot. In this world humans live along-side robots or "mechas". David partners with an energetic mecha, Gigolo Joe to discover what he can do. David was originally created to replace a son. David seeks ways to become more realistic to gain the love he seeks from his mother. David is the first robot build that is capable of love.

Ex Machina

A software programmer, Gleeson, wins a competition where the prize involves him evaluating an A. I robot's intelligence. Gleeson gets to spend some time at secret location where he is introduced to the robot Ava. The robot appears physically attractive and is capable of reasoning beyond anything Gleeson has ever seen. Gleeson is warned by the robot not to trust her creator, Nathan. Initially Ava shows signs of consciousness and even flirts with Gleeson a bit.

A.I(Artificial Intelligence) Movies List

Yard Life © 2015 - Designed by Templateism