3-Methylglutaconic Aciduria Research

3-Methylglutaconic Aciduria Research A distinct type of 3-methylglutaconic aciduria due to a mutation in the Translocase of Inner Mitochondrial Membrane 50 (TIMM50) gene Abstract BACKGROUND: 3-methylglutaconic aciduria biochemically characterized by increased urinary excretion of 3-methylglutaconic acid result from defective leucine metabolism and disorders affecting mitochondrial function though in many cases the cause remains unknown. Recently mutations in mitochondrial TIMM50 gene has been reported in four patients from two unrelated families. We report additional mutations in TIMM50 gene in 6 individuals from two unrelated consanguineous families with a distinctive type of 3-methylglutaconic aciduria. METHODS:Â  We report on three patients of South Asian ancestry with intractable epilepsy, microcephaly, developmental delay, visual deficit spastic quadriplegia and three Caucasian patients of eastern European origin with intellectual disability with or without seizure. Metabolic testing revealed mild lactic acidosis and excretion of large amount of 3-methylglutaconic acid in urine in all patients. Full exome sequencing was performed using genomic DNA isolated from one surviving patient, two healthy siblings and both parents of South Asian family. Exome sequencing was also performed for Caucasian patients of eastern European origin. RESULTS:Â  Exome sequencing identified two homozygous mutation Gly372Ser and Iso392Thr mutations in the gene TIMM50. There were no other candidate alterations in exome that could explain the phenotype in the proband. The mutations are located in the conserved C-terminal domain of the Tim50 protein that interacts with the N-terminal domain of the Tim23 protein in the intermembrane space and regulates mitochondrial protein import of presequence-containing polypeptides Both parents are heterozygous. CONCLUSION: Given the phenotypic similarilty of the patients from two unrelated families and an earlier report of mutations in additional family, we conclude that TIMM50 gene mutation results in a novel mitochondrial disorder with 3-methyl glutaconic aciduria. INTRODUCTION 3-methylglutaconic aciduria (MGCA), an increase in urinary 3-methylglutaconic acid or 3-methylglutaric acid, can be a nonspecific finding in mitochondrial disorders, organic aciduria, urea cycles disease, neuromuscular disorders. but is a consistent abnormality of 3-methylglutaconyl-CoA hydratase deficiency and patients with mutations in TAZ, SERAC1, OPA3, DNAJC19 and TMEM70 gene1. These genes all encode mitochondrial membrane or membrane related proteins. In 3-methylglutaconyl-CoA hydratase deficiency due to mutation in AUH gene , 3-methylglutaconic acid derives from 3-methylglutaconyl CoA (3MG CoA), an intermediate in leucine catabolism1. It has been proposed that in other disorders, 3-methylglutaconic acid derives from aberrant isoprenoid shunting from cytosol to mitochondria via mevalonate pathway or redirection of mitochondrial acetyl CoA toward production of 3MGA due to an increase in the intra-mitochondrial NADH/NAD+ ratio resulting from mutation induced impairment in electron transport chain or Kreb cycle function 2. Examples of mitochondrial include Barth syndrome, a cardioskeletal myopathy with neutropenia, abnormal mitochondria and MGCA. Barth syndrome is caused by X-linked recessive mutations in the TAZ gene which encodes the mitochondrial membrane localized transacylase involved in the maturation of cardiolipin. Autosomal recessive mutations in the OPA3 gene (OMIM: 606580), the mouse ortholog of which encodes a mitochondrial inner membrane protein of unknown function, cause MGCA3 (OMIM: 258501), a neuroopthalmologic syndrome characterized by early-onset bilateral optic atrophy and later-onset spasticity, extrapyramidal dysfunction and cognitive deficit. MGCA5 (OMIM: 610198) is yet another form of MGCA caused by autosomal recessive mutations in the DNAJC19 gene (OMIM: 608977) and in addition to increased urinary excretion of 3-methylglutaconic acid, patients present with infancy or childhood onset dilated cardiomyopathy, microcytic anemia, mild muscle weakness and ataxia. Many patients die of cardiac failure. The DNAJC19 gene encodes the human homolog of the yeast Tim14 which is a part of the Tim23 mitochondrial protein import machinery and hasbeen shown to interact with the mtHsp70 in an ATP-dependent manner to regulate Tim23 function (Davey, 2006). WE report a distinct type of 3-methylglutaconic aciduria resulting from a mutation in mitochondrial TIMM50 gene in 3 sibs from a consanguineous family. We initially reported these xases in abstract form. Recently two different mutations in mitochondrial TIMM50 gene have been reported in four patients with 3 methylglutaconic aciduria, epilepsy, severe intellectual disability and lactic acidosis. Subjects Family 1 Family 1 has three affected sibs of South Asian ancestry with intractable epilepsy, microcephaly, developmental delay, visual deficit spastic quadriplegia. Two affected sibs died unexpectedly when they were visiting families in a remote area of a South Asian country. Metabolic testing had revealed large amount of 3-methylglutaconic acid in urine in all three affected sibs. The patients have a healthy brother and a healthy sister. Mother and father are first cousins. Detailed clinical history, imaging, EEG and metabolic testing were obtained for all affected persons. Full exome sequencing was performed using genomic DNA isolated from one surviving patient, two healthy siblings and both parents. Patient IV-1. Patient IV-1 was the first born child of the parents and was born at 36 weeks gestation after a normal pregnancy and delivery. Her weight at birth was 1.99 kg. Her weight, height and head circumference were always below 5th centile. She also had asthma and frequent episodes of pneumonia presumably due to aspiration, but the family refused G-tube placement. She was severely delayed. She never sat, stand or spoke. She has poor head control, truncal hypotonia but very brisk tendon jerks and sustained clonus. Funduscopy revealed bilateral optic atrophy. She developed seizures at 1 year of age. EEG revealed multifocal spikes arising from both hemispheres. She was treated with phenobarbital and Zonegran but family was noncompliant with medications. She continued to have daily myoclonic jerks. MRI at 2.5 and 5 years of age showed increased T2 signal in basal ganglia and periventricular white matter, brain atrophy, prominent ventricle, increased extraxial fluid. Normal liver en zymes and blood count, normal blood and CSF glucose and a serum ammonia of 21. Several serum lactate levels were mildly elevated. Lactate 2.8, 4.5 (Pyruvate 0.23), 5.4 (normal 0.7 to 2.1) Lactate to pyruvate ratio 20:1. Urine organic acid analysis revealed very high lactic acid, 3-methylglutaconic acid, and 3-methylglutaric acid. Muscle biopsy revealed only scattered atrophic muscle fibers on electron microscopy. Respiratory chain enzyme activities were within normal limits. She died at 7.5 years of age apparently due to complications from an infection while she was visiting families in a remote area of a South Asian country. Patient IV-4 was twin A born at 36 weeks gestation after an uncomplicated twin pregnancy. Her weight, height and head circumference were always below 5th centile. She was severely delayed. She never sat, stand or spoke. She has poor head control, truncal hypotonia but very increased reflexes and spasticity in the limbs. At nine-month-of age, she started to experience several episodes of eye fluttering and body jerking. Her EEG reved slow background, poor sleep architecture and frequent multifocal spike and sharp wave activities coming from both the left and right hemispheres. Her seizures were treated with Zonegran and was poorly controlled but parents refused more aggressive treatment of seizures. Metabolic testing revealed mild elevation of lactate and moderate increase of 3 methylglutaconic, 3 methylglutaric acids in urine. A brain MRI at 11-month-of age revealed diffuse volume loss supratentorially with prominent sulci and extraaxial fluid spaces, mild enlargement of the ventricl es and patchy signal abnormalities in the basal ganglia bilaterally, especially involving the caudate nuclei and putamen. On spectroscopy with voxel placed in the right basal ganglia with short and long TE, there was a lactate peak which inverted on long TE spectrum. Also, the NAA peak was low with NAA to creatinine being 1.15 on short echo and 1.29 on long echo spectrum. Also, the choline was elevated with choline/creatine ratio being 1.00 on short echo and 1.41 on long echo images. She died at 1.5 years of age apparently due to complications of an infection while she was visiting families in a remote area of a South Asian country. Patient IV-5 is a 13 year old female of South Asian ancestry, with 3-methylglutaconic aciduria intractable epilepsy, microcephaly, developmental delay, visual deficit and spastic quadriplegia. She was born at 36 weeks gestation after an uncomplicated twin pregnancy. She was twin B and stayed in NICU for 18 days for feeding issues. Her weight was 1.4 kg and she was not intubated. Patient first presented with seizures at 3 months of age with eyelid fluter and jerking of extremities. Her initial EEG revealed multifoal spikes. Initial biochemical evaluation revealed normal serum and CSF glucose, normal ammonia and liver enzymes. Serum lactate and CSF lactate 4.24 mmol were mildly elevated . Lactate was 2.7. Ammonia 25. Serum amino increased alanine 43.6 micromol/dl (9.9-34.5). Csf lactate 4.24 mmol. CSF alanine 7 micromol/dl (0.6 -4.7). There were also mild elevations of serum and CSF valine, leucine, isoleucine and alanine and lysine. Urine organic analysis revealed moderate increase of 3 methylglutaconic, 3 methylglutaric, glutaric, adipic, suberic, and sebacic acids. MRI of brain at 11 months of age revealed severe atrophic changes involving gray and white matter, predominantly of the cerebrum. Grossly abnormal signal is seen in the basal ganglia, particularly the caudate nucleus and the putamen with relative sparing of the globus pallidus and thalamus. A recent MRI (at age 13 years) reveals severe but stable atrophic changes of the gray and white matter of the supra and infratentorial brain, stable white matter changes of the putamen, caudate nucleus and periventricular white matter, Scattered diffusion restriction in the retrotrigonal white matter, compatible with active demyelination and atrophic changes of the optic nerves. Her seizures were treated with with Keppra, Lamictal, Zonegran and Onfi. She also receives carnitine. She continues to have brief episodes of whole body stiffening each week, but the family was also not very compliant with medications. He r current EEG shows slow background for age, poorly formed sleep spindles indicatvie of diffuse neuronal dysfunction, frequent multifocal interictal spike and wave suggests increased risk of seizures arising from multiple foci and hypsarrhythmia in sleep . She has failure to thrive despite G-tube feeding. At 12 years of age, G-tube was placed due to history of aspirations. Height, weight and head circumference below 5th centile. She is severely delayed. She is nonverbal and never learned to sit independently, stand or walk. She recognizes family members, responds to their voice and looks and smiles at them. Her fundoscopy shows mild optic atrophy. She has bilateral esotropia and dysconjugate gaze. She has poor head control and truncal hypotonia, but her limbs are spastic and her tendon reflexes are very brisk. Family 2 Patient V:1 was the first son of Caucasian consanguineous parents (IV:4 and IV:5) of Eastern European origin. Within the context of an organic acid and amino acid study in young and adult subjects with non-syndromic developmental delay and intellectual disability, he was investigated at the age of 17 years and presented with a developmental language disorder (involving semantic, syntactic, and pragmatic components of the linguistic system), emotional and communicative problems (fearful, aggressive, and loner), and hyperactivity. On neuropsychological testing he showed a short attention span. The child was born at term after an uneventful pregnancy and his birth weight was 2.9 kg. At 4 months of age he was affected by myoclonic jerks that were controlled by administration of valproic acid and lamotrigine. Developmental delay was observed starting from the middle of the first year of life, accompanied by decreased muscle tone. He could walk without support only at 6 years. At last medi cal exam, the patient showed a reduced muscle mass (height 148 cm, Z-score 3.43; weight 38 kg, Z-score 4.21; BMI 17.1 kg/m2, Z-score 2.02) and a head circumference of 51 cm (Z-score 2.76). Due to refusal of parents, no brain imaging studies could be performed. Fundoscopic examination was normal. Laboratory tests, including creatine phosphokinase (CPK), liver enzymes and plasma amino acids, were normal. The profile of urinary organic acids showed a large peak of 3-methylglutaconic acid (113 mmol/mol creatine) and a slightly increased level of 3-methylglutaric acid (17 mmol/mol creatinine). Patient V:3 was the younger brother of V:1, the third child of IV:4 and IV:5. He was investigated at the age of 11 years and presented with a clinical phenotype (developmental delay and intellectual and behavioral disorder) similar to that of his brother. The pregnancy and early postnatal course was unremarkable and birth weight was 3.1 kg. At 3 months he received valproic acid and lamotrigine to control tonic seizures with sudden stiffening movements of arms and legs. The boy walked independently at 4 years. When he was 9 years, his growing parameters were: height 119 cm (Z-score 2.47), weight 22 kg (Z-score 1.91), BMI 15.5 kg/m2 (Z-score 0.38), and head circumference 48 cm (Z-score 3.52). Neuropsychological exam revealed mental retardation and impaired communicative skills, including poor language abilities (few repetitive words with no sentences). Occasionally, the patient is aggressive. Ophthalmologic examination revealed left esotropia. High levels of 3-methylglutaconic acid (15 5 mmol/mol creatine) were identified in urine, together with smaller amounts of 3-methylglutaric acid (22 mmol/mol creatinine). Patient V:5 was the second son of consanguineous parents (IV:9 and IV:10) related to those of patients V:1 and V:3. The girl was delivered by cesarean section because of growth arrest at 37 week. The neonate showed no external malformations. Birth weight was 2.1 kg. In the following years, the clinical phenotype was characterized by delayed developmental milestones, nocturnal enuresis, severe cognitive impairment, speech retardation, and lack of communicative skills. Results of the electroencephalogram were normal. No brain imaging data are available. On a few occasions, levels of ammonia and lactic acid were found to be slightly elevated, but these results could not be confirmed by repeated blood analyses. Plasma levels of amino acids are within normal range. Fundoscopic examination was normal up to 7 years, but since then there is evidence of mild bilateral optic atrophy. Urine levels of of 3-methylglutaconic acid and 3-methylglutaric acid were 176 mmol/mol creatine and 29 mmol/mol creatinine, respectively. DISCUSSION Deleterious Nature of the TIMM50 gene alteration: TIMM50 NM_001001563 c.1114G>A p.G372S The p.G372S variant (also known as c.1114G>A), located in coding exon 9 of the TIMM50 gene, results from a G to A substitution at nucleotide position 1114. The glycine at codon 372 is replaced by serine, an amino acid with somewhat similar properties. The alteration is not observed in healthy cohorts: Based on data from the NHLBI Exome Sequencing Project (ESP), the TIMM50 c.1114G>A alteration was not observed among 6,503 individuals tested. Allele frequency data for this nucleotide position are not currently available from the 1000 Genomes Project and the alteration is not currently listed in the Database of Single Nucleotide Polymorphisms (dbSNP). Though some variants may appear to be rare due to database-specific ethnic underrepresentation, rare missense alleles commonly exhibit a deleterious effect on protein function (Kryukov, 2007; Tennessen, 2012). The altered amino acid is conserved throughout evolution: The G372 amino acid position is completely conserved in eukaryotes all th e way from the yeast Saccharomyces cerevisiae to humans (Mokranjac, 2003). The alteration is predicted deleterious by in silico models: The p.G372S alteration is predicted to be probably damaging and deleterious by PolyPhen and SIFT in silico analyses, respectively. The amino acid is located in a functionally important protein domain: The p.G372S alteration is located in the conserved C-terminal domain of the Tim50 protein that interacts with the N-terminal domain of the Tim23 protein in the inter membrane space and regulates mitochondrial protein import of presequence-containing polypeptides (Geissler, 2002; Yamamoto, 2002; Guo, 2004). The alteration cosegregated with disease in the family herein: Co-segregation analysis revealed that this alteration is present in a heterozygous form in the mother, father and brother, and absent in the sister. Based on the available evidence, the TIMM50 c.1114G>A (p.G372S) alteration is classified as a likely pathogenic mutation. The TIMM50 gene is not currently known to underlie Mendelian disease (aka clinically novel). The TIMM50 gene function is consistent with the probands clinical presentation: The Translocase of Inner Mitochondrial Membrane 50 (TIMM50) gene (OMIM: 607381) is located on human chromosome 19q13.2 and consists of 11 exons. It encodes the Tim50 protein, a 353 amino acid 40 kDA homolog of the yeast Tim50 protein that functions as an integral part of the mitochondrial Tim23 protein import machinery by linking protein translocation across the outer and inner mitochondrial membranes. This interaction was confirmed by the coprecipitation of Tim50 with an antibody against Tim23 (Geissler, 2002; Yamamoto, 2002; Guo, 2004). The authors further confirmed that the C-terminal domain of Tim50 is located in the inter-membrane space (IMS) where it stably binds to the segment of Tim23 that spans the IMS and regulates its function. Nuclear encoded mitochondrial proteins are synthesized in the cytosol and subsequently imported into the mitochondria through the function of translocators, the TOM complex of the outer mitochondrial membrane (OMM), and the Tim23 and Tim22 complexes of the inner mitochondrial membrane (IMM) (Jensen, 2002). While the Tim22 complex is involved in the transport and insertion of proteins lacking the presequence into the inner membrane, the Tim23 complex is required to process and insert presequence-containing precursor proteins. The IMM generates a proton motive force that is critical for cellular energy synthesis (Stock, 2000) and the permeability barrier of the IMM needs to be maintained during the transport of proteins through the pore-forming Tim23 protein associated with other IMM proteins such as Tim14 (human DNAJC19), Tim17, Tim21, Tim44 and Tim50. Using various yeast IMM protein mutants, Meinecke et al. (2006) demonstrated that tim17 and tim21 mutant mitochondria displayed membra ne potential values that were comparable to wild type mitochondria, whereas tim50 mutant mitochondria showed a drastic reduction of the membrane potential. Further functional studies revealed that the Tim23 channel is tightly regulated by Tim50 in its inactive state to maintain the IMM permeability barrier and is opened only when presequence-containing polypeptide chains need to be translocated into the mitochondrial matrix or the inter membrane space (IMS). Loss of Tim50 function in yeast led to cellular growth arrest and reduced cell viability (Mokranjac, 2003). Knockdown to Tim50 expression in cultured human cells using RNA mediated interference resulted in an increase in the release of cytochrome c and apoptosis in response to cell death stimuli (Guo, 2004). A 50 kDa isoform of the human mitochondrial TIM50, TIM50a, consisting of 456 amino acids has been found to localize in nuclear speckles, specifically in the Cajal bodies, and interact with small nuclear ribonuclear proteins (snRNPs), the coilin protein and the Survival of Motor Neurons (SMN) protein (Xu, 2005) which has been implicated in Spinal Muscular Atrophy (SMA). The protein sequences of the mitochondrial TIM50 and the nuclear TIM50a are identical with the exception of additional 103 amino acids at the N-terminal of TIM50a that are the result of an alternative translational start sequence. This additional N-terminal sequence in TIM50a is thought to contain a putative nuclear localization sequence that allows the Tim50a isoform to display a nucleus specific localization. Based on their results, Xu et al. hypothesized that Tim50a might be involved in the regulation of snRNP biogenesis and possibly the function of the nuclear SMN protein encoded by the SMN1 gene. One of our patien ts had mulsle biopsy. Although there were atrophic changes, no neuropthic pattern was seen. Reference List (1) Wortmann SB, Kluijtmans LA, Rodenburg RJ et al. 3-Methylglutaconic acidurialessons from 50 genes and 977 patients. J Inherit Metab Dis 2013;36:913-921. (2) Ikon N, Ryan RO. On the origin of 3-methylglutaconic acid in disorders of mitochondrial energy metabolism. J Inherit Metab Dis 2016;39:749-756. Legends Legend to Figure 1 Five-generations pedigree of the family with mild 3-methylglutaconic aciduria in which the TIMM50 p.(Ile293Thr) was identified. Subjects V:1, V:3, and V:5 (filled symbols) are patients suffering from intellectual disability and increased urinary excretion of 3-methylglutaconic acid. They are born to consanguineous parents and homozygous for the TIMM50 c.1011T>C mutation predicting the replacement of isoleucine 293 with threonine in the encoded protein. The mutation was inherited by a common ancestor (either I:1 or I:2) and has been identified in the heterozygous state in the clinically and biochemically unaffected subjects III:3, III:4, III:9, IV:2, IV:4; IV:5; IV:9, IV:10, and V:2.

HTML and Web Site Construction :: essays research papers

Chapter 1 Planning   Ã‚  Ã‚  Ã‚  Ã‚  When you plan your web page you start by writing everything down on paper. Write what you want your web page to say, show, and do. To make a map of the links you will be using, write a circle in the center of a new sheet of paper and write HOME in it. Then draw lines to other circles that say the names of your sub pages. Later you will learn how to link your home page to your sub pages. Chapter 2 Starting your front page   Ã‚  Ã‚  Ã‚  Ã‚  First we want to have a simple text program to use. Go to START programs Accessories NOTEPAD. Notepad is the only program I found to work for html. After you are in notepad type the following. - this will start an html document   Ã‚  Ã‚  Ã‚  Ã‚   - starts the header   Ã‚  Ã‚  Ã‚  Ã‚  - title that you see at top left corner on screen   Ã‚  Ã‚  Ã‚  Ã‚  - ends title   Ã‚  Ã‚  Ã‚  Ã‚  - ends header   Ã‚  Ã‚  Ã‚  Ã‚  - starts the body ( the guts )   Ã‚  Ã‚  Ã‚  Ã‚  - ends the body   Ã‚  Ã‚  Ã‚  Ã‚  - ends html document ( IMPORTANT )   Ã‚  Ã‚  Ã‚  Ã‚  After the 1st tag, type the name you want to appear in the upper left corner of your screen. This will put whatever you typed ( between the two title tags ) up in the upper left corner of your screen. Note: Make sure that you type in between the two title tags. If you don’t you won’t see the title on the screen.   Ã‚  Ã‚  Ã‚  Ã‚  TIME TO SAVE! After you finish typing your title click on the file option menu at the top of the screen. Once there, click â€Å"save as†. Save the document to a new 3  ½Ã¢â‚¬  floppy as home.htm. You must save it .htm or your internet browser will not open. If you are done saving it go to â€Å"my computer† on the desktop and click on 3  ½ floppy ( A: ) Then click on home.htm. When the file opens up look at the upper left hand corner of your screen. There you should see your title. To edit the web page and add more stuff, click on view ( at top of screen ) then click source. Notepad should open up with the codes you typed earlier. After you are done editing go to file save. Then go back to your web page and click REFRESH. This should refresh the screen to what you just typed. Chapter 3 Text, centering, coloring, and font   Ã‚  Ã‚  Ã‚  Ã‚  To enter text into your web page, all you need to do is type what you want any where in between the two tags.

Effects of Identity Theft on Social Networking Sites

This research is important because of the rowing risks of Identity Theft, as the blob sites and social networking sites Users population increase, Identity theft crimes also increases. This may help the students to focus on their studies, knowing that they are safe from Identity theft criminals because nowadays, social networking sites are used in sharing information that may help them in their studies. The study is concerned with the various personalities of the student, this is one way to release and expose their creativity to provide interactive materials in preventing identity theft.This is to warn the Users about Identity Theft. This study is conducted for the users to be aware in these existing crimes. This can develop the values of an individual which shows care in their fellow users that can be a victim of identity theft. Being a contributor in decreasing the identity theft in social networking sites deserves honor in the country, it can be not as formal as expected, but it g ives moral to the country. With this research, contributors started to be professionals by sharing their efforts and knowledge to help the country fight against Identity theft.Theft is an unusual act of human being which results too rime that intentionally creates huge problem in our society. Theft builds a serious damage in reputations and accounts in users of computer system, personal properties of users may and can be steal anytime by the fraudsters. Identity Theft is an epidemic which is rising in our society, it affects everybody even the newbie which are new users and adequate users, Criminals for many years improved materials to get easy access in stealing. Identity theft is a serious crime that defrauds millions of dollars from innocent victims.Identity Theft exists because of the advance ways of doing crimes which result to inhuman to inhuman nature act. There are instances that Identity Theft crimes are unrecognized by users that's why criminals are more pursuing the act o f stealing that builds a broken system in our computer society. The effects of Identity Theft really change each and every member of Social Networking Sites, Identity Theft creates damage which is not limited in financial problems, and psychologically users were also affected because of the improper use of their identity that tends to destroy their reputation.Social Networking Sites were also affected; there would be less numbers of users because they are afraid of Identity theft which ends to break rules and security and system in Social Networking sites. If there are mounting problems for sure there would be more alternative solutions for their kind of increasing problem, through implementing rules and laws would be more accurate and flexible in building a strong security and social networking sites and other websites.Security operators and administrators in Internet will also play a big role in preventing and decreasing Identity theft. Since there are different kinds of Theft tha t are existing in our country, students must be aware in these existing crimes to prevent more hilarious situations. Technology was developed because of humans high intellectual abilities and they can create either epidemic crime of precautionary measures in existing crimes. Many people are innocent in fraudsters and criminals that's why they need to improve their knowledge when it comes to cautions about Identity Theft.Unimplemented laws result in increasing crimes that's why it should be release as soon as possible to prevent existing crimes. If we minimize Identity Theft there would be a solid computer system which can be attain through knowledge sharing to the users. Definition of Identity Theft Identity theft is a crime. Identity Theft and Identity fraud are terms used to refer to all types of crime in which someone wrongfully obtains and uses another person's personal data in some way that involves fraud or deception, typically for economic grain stated by the U. S.Department of Justice. With enough information about an individual, a criminal can take over that individual's identity to conduct wide range of crimes like fraudulent use of telephone calling cards, or obtaining other goods or privileges which the criminal might be denied if he were to use his real name. Identity Theft is â€Å"an absolute epidemic†, according to Robert Ellis Smith, a respected privacy author and advocate. It affects everybody, and there is very little you can do to prevent it and, I think, worst of all-?you can't detect it until it's probably too late. Some law-enforcement authorities call identity theft â€Å"the fastest growing crime across the country right now†. In fact, identity theft is the most called-about subject on the Privacy Rights Clearinghouses telephone hotlist. (http:// www. Identifying. Org/). In many cases, a victim's losses may include not only out-of- octet financial losses, but substantial additional financial costs associated with trying t o restore his reputation in the community and correcting erroneous information for which the criminal is responsible. (http://www. ]justice. Gob/criminal/ fraud/websites/theft. HTML) Coming from the answer of Anna Marie Estonia, a sophomore IBIS student of PUT, Identity Theft is a form of stealing someone's identity in which someone pretends to be someone else by assuming that person's identity, typically in order to access resources or obtain credit and other benefits in that person's name. Therefore, the researcher concludes that Identity Theft is a Technological act of Theft, this involved High Technological objects Oriented Materials which are used in stealing. As our Technology develops many crimes were developed as well because of the improper use of internet and computer system.Identity Theft implies the low security in accessing internet and other online sites which can cause devastation in other users. Many cases were not yet settled with regards to this manner and many imp lemented subscriptions were in act to support the anti-Latinity Theft in Social Networking Sites which can help many recent and future users. The Concept of Social Networking Sites More and more, people are turning to the Internet to keep in touch with friends, family and colleagues. Social networking sites (SONS), make staying involved quicker, easier – and more fun – than ever before.However, Social Networking Sites have drawbacks. These relate to privacy. While you can protect yourself, you can't control what others post about you – a growing concern as employers are beginning to search out information about new and potential employees. As there are few erasers to fraudulent usage, there is significant risk of misrepresentation. A user should also monitor the terms of use for SONS – they have been known to change without notice. People have also been known to become addicted, spending so much of their time on these sites that their real lives suffer. 5 minute Guide to Social Networking Sites) Social Networking sites are social network sites as web-based services that allow individuals to construct a public or semi-public profile within a bounded system; articulate a list of other users with whom they share a connection, and view ND traverse their list of connections and those made by others within the system. (http://]CM. Indiana. Du/via/issues/Boyd. Ellison. HTML) There are dating sites, friendship sites, and sites with a business purpose and hybrids that offer a combination of these. Globally, hundreds of millions of people have Joined one or more social sites. Whom. PCMCIA. Com) From the response of Noel Angelo Magellan, Social Networking Sites are more likely a virtual place where people in the world can communicate and interact with each other socially and as explained by Christine Marie Tyson, Social Networking ties are used for communicating our love ones in other places in the world, our long lost friends, used for worldw ide meetings and many more. In short, communicating people's lives to another person around the world. Example of this sites are Faceable, Twitter, Renee, Webb, mayday and many more.To sum it up, Social Networking Sites are made for the purpose of social interaction – connecting and communicating with one another around the world through internet. Describing the Cases of Identity Theft Law enforcement agencies have developed new methods and new relationships to catch the bad guys in cyberspace. Some cases include Reshipping and Pushing. Reshipping is an operation in which conspirators or unwitting accomplices in the United States are hired to receive packages of electronic or other merchandise bought with fraudulent or stolen credit cards, and then repackages the merchandise for shipment, usually abroad.By the time the merchant finds out that the credit card was fraudulent, the merchandise is already in another country. Pushing is the act of attempting to steal passwords and financial information by posing as a trustworthy person or business in a seemingly official (spoofed) electronic communication. Daniel Larkin, Fighting Online Crime) It may seem that there are some countries like the United States and Australia which have already enacted laws that pertain to the prosecution of identity theft related crimes. The Philippines however, being one of the largest Faceable populations in the world -? is also one of the many countries without a law to protect its citizens from online identity theft. Clogging is one of the many online problems involving identity theft. A Kellogg is software that tracks your keystrokes and records them so that a hacker can go back later and see what sites you visited, what information you submitted and more. Gallopers work invisibly in the background and are impossible to detect without security software. (www. Agro. H) As explained by Christine Marie Tyson, cases of identity theft nowadays can do anything like, chatting with strangers to get close with them, pushing, hack one's account in order to get some benefits of their victims, impersonates someone else in order to conceal their own true identity, getting somebody else's photos and information through social networking sites and portray or imitate the identity of the victim. To summarize the discussion, the one thing that all of these attacks have in common though is the very thing that binds social networks together: trust.We need to become far more aware of the value of our personal information and importantly the information we have about your friends. Effects of Identity Theft in Social Networking Sites The growing popularity of social networking sites (SONS) among the Internet users demands an introspection of personal and social behavior of human beings. Today 1. 5 billion people across the world have their profiles in social networking sites. SONS becomes a reason for anxiety and addiction.The beginning of social networking sites started to make contacts with people and build a network of healthy relationship in the society. But now it seems offering cybernetics's a great advantage to target victims. (International Journal of Business and Social Science) As stated by Risk Ferguson, Senior Security Adviser of Trend Micro, â€Å"With explosive growth and user populations of this order it's hardly surprising that these services also appear to be coming of age as attack platforms for cybernetics's. Web 2. With its user-generated, rich, interactive content and social networking with its interlinked trust-based networks of people and groups, offer cybernetics's great scope for leveraging the capabilities offered, both to disseminate traditional forms of mallard through new channels and also to carry out social engineering attacks for the purposes of target profiling or identity theft†. (http:// hosted. Personalities. Com/358216/affection/1746500010/cybercafà ©/) Based on the answer of Paul Francis del Rosaries, †Å"It can affect the site's popularity.Some people would probably quit using the site if their image or identity were used in ways that they did not know about. The site would have reduced users which would also affect their income rate. Because social networking sites usually depends on how many users they have on their site for example is the â€Å"Faceable†. † To sum up, with limited government oversight, industry standards or incentives to educate users on security, privacy and protecting your identity, users are then exposed to identity theft and fraud.Additionally, these platforms have terabytes of confidential user information and are likely vulnerable to outside (or inside) attack. Although the issue is not yet in the mainstream conscious, it may well e sooner or later. Cyber laws have to be fortified with advancement of rules as if violators cannot escape committing a crime, at the cost of societal value. Ways on how Identity Theft can be avoided As with any cri me, you can't guarantee that you will never be a victim, but you can minimize your risk These are some of the tips that can make you and your family, safe on social networking sites : 1) Change the profile privacy now.Keep your information accessible only to people in your friend list. 2) Don't post very personal information on the profile. It includes your email ‘d, date of birth, contact number, mom address and information about your family members. Just like in the real world, it is not possible to completely protect oneself from a crime like identity theft. But there are many safeguards you can adopt to protect your identity. 1 Protect your wallet. Some people keep a lot of stuff in their wallet – credit card charge slips, deposit slips, and all IDs, including their ASS and TIN cards.Minimize your risk by keeping items with personal information in a safe place home. 2. ) Protect your computer. Use anti-virus software, as well as firewall and anti- spare software. Th is will help deter criminals' efforts in stealing your personal information. Coming from the answer of Mark Angelo Menace, mostly, celebrities are the victims of Identity theft and it can be avoided in a form or way of privacy. Celebrities should have privacy in other aspects of their life. In the side of the poser or the theft, self-discipline is the best way to avoid this.Another is, other people can report cases like Identity theft. Overall, people should be contented on who they are and what they have and with that there will be no more cases like these. As a conclusion, these are many ways in minimizing Identity Theft; we Just eave to implement it and continue to maintain the security of our computer system. The simplest way in minimizing this increasing numbers on thieves in Identity theft crisis is by Just being responsible enough in our belongings. Minimizing Identity theft will lead to a better computer system.

Learning Theory Classical Conditioning Of Observational...

Abstract Research indicates that development of friendships begins in preschool ages 3 to 5. As communication skills increase, the desire to develop close friendships also increases during preadolescence and adolescence. Ability to develop communication skills that are conducive to forming close friendships determines the kind and an on occasion the number of friendships an individual has. Individual approaches to friendship are linked to attachment style (self esteem and interpersonal trust). Once these friendships are developed, do they influence individual social interactions? Yes, close friendships have influence on social interactions such as social activity level, mood, weight, political views, new friends, health, mortality, etc., which can be explained through the social learning theory; classical conditioning of observational learning. There has also been much empirical investigation examining selection and socialization effects with results indicating influences on a wide variety of attitudes and behaviors. There is also growing evidence of influence on health throughout an individual’s life. Introduction † Do close friendships influence social interactions?† I will begin by defining the term close friendships to ensure the meaning being used is understood. Close friendships are defined as a relationship in which two people spend a great deal of time together, interact in a variety of situations, and provide mutual emotional support (Text Book); TheShow MoreRelatedClassical Conditioning And Operant Conditioning1492 Words   |  6 Pages To expand upon the concepts of the two forms of conditioning listed above, three additional principals not previously listed for the sake of convenience are present in both forms of conditioning; these three principals-extinction, spontaneous recovery, and stimulus discrimination-are among the number of basic principals of conditioning that are found in most forms of conditioning. To explain, Extinction refers to the process by which the steady weakening or diminishment of a conditioned responseRead MoreLearning Experience Paper : Smoking Cessation Essay1185 Words   |  5 Pages Learning Experience Paper: Smoking Cessation Throughout one’s lifetime, an individual undergoes a magnitude of various learning experiences, all of which serve as a shaping agent, consequently forming personality traits that are unique to each human being. Examining this fact further, what does learning mean, precisely? Namely, the definition of learning is the resulting change in behavior or knowledge that occurs through experienceRead MoreBehaviorism And Social Learning Theory1531 Words   |  7 Pages Behaviorism and social learning theory are examples of two mechanistic theories that focus on explaining children’s behavior. Social learning theory emphasizes observational learning and imitation. On the other hand, behaviorism is rooted in focusing on how the environment impacts development. The environment shapes the child’s development as the child strives to adapt to the environment. Both theories deal with explaining behavior and consist of similarities, but are composed of different elementsRead MoreBehaviorism Theory And Social Cognitive Theory1082 Words   |  5 PagesLearning perspective also known as behavioral perspective is a theory that is apprehensive with how a person’s behavior changes because of their environment and experiences. The learning perspective has two theories; behaviorism and social-cognitive learning theory. Furthermore, behaviorists do not invoke the mind to explain behavior; they prefer to stick to what they can observe and meas ure directly: acts and events that happen in the environment (Carole Wade, 2008). In this essay the followingRead MorePros and Cons of Spanking996 Words   |  4 PagesThe theory of discipline has been debated for decades. Arguments over how it should be carried out and how harsh it should be has been discussed. One aspect of discipline has been shoved into the dark, the effect on the child. No matter how much it is spoken of children remember what happened to them in their childhood. Whether they were pleasant or not can lead to problems later in life. One debate that shall soon be settled deals with the spanking of children. Some will agree that there is nothingRead MoreClassical Conditioning, Operant Conditioning, and Observational Learning664 Words   |  3 PagesOur understanding of classical conditioning, operant conditioning, and observational learning has allowed us to unlock many of the answers we sought to learn about human behavior. Classical conditioning is a technique of behavioral training, coined by Ivan Pavlov, which basically states that an organism learns through establishing associations between different events and stimuli. This helps us understand human behavior in an assortment of ways. It makes it clear that almost everything we do isRead MoreEssay on Behavioral Learning Theories887 Words   |  4 PagesBehavioral Learning Theories Most theorists agree that learning occurs when experience causes a change in a persons knowledge or behavior . Behaviorists emphasize the role of environmental stimuli in learning and focus on the behavior, i.e., an observable response. Behavioral theories are based on contiguity, classical and operant conditioning, applied behavior analysis, social learning theory and self-regulation/cognitive behavior modification. Early views of learning were contiguityRead MoreThe Theory Of Classical Conditioning929 Words   |  4 PagesDiscussion 5 1. Define: Classical Conditioning is learning theory based on the assumption that the learning process occurs due to associations between an environmental stimulus and a natural occurring stimulus, as indicated in our textbook. This learning theory was developed by John Watson. He proposed that this theory is able to explain human behavior. Watson also assumed that our environment shapes our personality as a whole. His ideas were influenced by the findings of Ivan Pavlov, a RussianRead MoreClassical Vs. Classical Conditioning1295 Words   |  6 Pages Classical Conditioning Behaviorism Classical conditioning is a type of learning through which an organism learns to associate one stimulus with another. It can also be known as respondent conditioning. The stimulus is any event or object in the environment to which an organism responds. The components of classical conditioning are as follows: Unconditioned response (UR) which is a response that is elicited by an unconditioned stimulus without prior learning. Unconditioned Stimulus (US)Read MoreSummary of a New Board Game for Children Essay839 Words   |  4 Pagesgoal line in whichever (non-harmful way) the winner see fits. Definition of Theories and Techniques There a quite a number of theories and techniques that have been utilized in designing this game. An example will be self-efficacy, a concept under the social cognitive theory. The concept of self-efficacy was developed from a larger theory known as Social Cognitive Theory which later on developed into Social Cognitive Theory (Bandura A., 1994). Albert Bandura has noted that an individual’s skills such