An Intrusion Detection System by K-means Cluster Algorithm, which is unsupervised machine learning, can predict whether data are normal or abnormal (intrusion). We can make a model by K-means cluster, forming the given data as two or eight different cluster groups, which is called training data. Based on the model (trained data), we can predict whether new data are normal or abnormal.
First, we calculate the distance from each cluster center to the most outer location, which is called the threshold in the cluster. We can then calculate the distance from each cluster center to a new data location. If the latter value is less than the threshold, it is normal. Otherwise, it is abnormal.
You have to simulate two group clusters and eight group clusters and compare them in terms of detection ratio. From the new data, we already know whether data are normal or attack. We can calculate your intrusion detection algorithmâs accuracy.
Submission: 1) intrusion detection system algorithm, 2) a screenshot of the accuracy from the algorithm. As you know, the given data have eight dimensions, so we cannot plot our result in two dimensional domains. We can choose third and fourth columns data and plot the cluster points as third for x axis and the forth for y axis. 3) A screenshot of plotting in two dimensions.
Sample Solution
Dynamic Foundation: MDM2 SNP309 (rs2279744) is a solitary nucleotide T>G polymorphism present in the primary intron of the MDM2 quality and a negative controller of p53 tumor silencer protein. The discoveries propose that MDM2 309TG polymorphism might be a hazard factor for a few tumors. This investigation analyzed clinical relationship of thyroid tumors with SNP309 in Iranian-Azeri populace. Techniques: In present examination, 107 thyroid disease patients and 156 malignant growth free control were gotten from Iranian-Azeri populace. Genomic DNA including of fringe blood and tumor tests was extricated by salting out methodology. The MDM2 SNP309 genotyping was completed by polymerase chain response single strand conformational polymorphism (PCR-SSCP) measure. All investigations were directed by spss programming with Chi-squared(?2) test and the P G, polymorphism Presentation The grouping of the entire human genome was finished in 2001 [1], and Approximately 6.5 million SNPs (single nucleotide polymorphisms) have been identified in human qualities. Contingent upon where a SNP happens, it may have various outcomes at the phenotypic level. SNPs are situated in the coding locales of qualities that change the capacity or structure of the encoded proteins and in non-coding areas of the genome, and have no direct known impact on the phenotype of a person. These distinctions could add to a large number of the individual highlights that portray us as one of a kind. Likewise, in light of the fact that they happen at a generally high recurrence in the genome (around one SNP for each 1000 bp), SNPs can be utilized as markers for these increasingly significant hereditary changes. 89% of the investigated SNPs are situated in an exon and 11 % in an intron [2,3]. Thyroid disease (TC) is the most widely recognized harm of the endocrine framework and records for around 2.1% of all malignancies analyzed around the world. The thyroid disease has a 4.4% commonness in ladies and a 1.3% predominance in men. The male-to-female proportion was roughly 1: 3.5, while the unrefined rate for men was 1.9/100,000 and that for ladies was 6.6/100,000. Thyroid malignancy is the ninth most regular disease (2.1% all things considered) in ladies [4]. The rate pace of thyroid malignant growth in the two ladies and men is increasing[5]. Essential thyroid tumors are delegated generous or threatening, which start from follicular and parafollicular (or c-cells) epithelial cells. Generous tumors containing follicular adenoma and threatening tumors are contained papillary, follicular, medullary and anaplastic carcinomas. The follicular cells convert iodine into thyroxine (T4) and triiodothyronine (T3) and incorporate papillary, follicular and anaplastic carcinomas and Follicular adenoma. The parafollicular or C-cells, which discharge calcitonin, contain medullary carcinoma [6]. Between thyroid tumors, papillary thyroid disease speak to roughly 80% of every single thyroid danger [7]. Some molecularbiomarkersinvolved inthyroid tumorsincludep53, RET, BRAF, RET/PTC ,RAS, PAX8/PPAR? and NTRK1 [8]. The human homologue of the mouse twofold moment 2 (MDM2 or HDM2) quality locatedon chromosome 12q13-14 with 491 amino acids long and 12 exons comprise of twotranscriptional advertisers, constitutive advertiser and p53-responsive intronic advertiser [9, 10, 11]. MDM2 oncoprotein actsa basic regul-atory job for some, tumor-related qualities that are significant for cell-cycle control, for example, the P53 [12]. The p53 quality is transformed in about half of every single human malignancy [13]. P53 is a tumor silencer quality, which is associated with different pathways, including apoptosis, DNA fix, cell cycle capture and senescence [14]. MDM2 and TP53 control each other through a criticism circle [15]. P53 initiates MDM2 on the transcriptional level while MDM2 communicates through its N-terminal space with a a-helix present in the transactivation area of p53 with high fondness and hinders its, subsequently, sets it up for proteolytic debasement at the ubiquitination pathway [16]. The general recurrence of MDM2 quality intensification in human tumors is around 7.2% [17]. An ongoing report has demonstrated that a MDM2 single nucleotide polymorphism in the primary intron with a T to G change at the nucleotide 309 in the p2 advertiser area of MDM2, so that, The nearness of the freak G-allele in cells containing SNP 309 GG builds the liking of the transcriptional activator stimulatory protein 1 (Sp1), that controls the basal degrees of MDM2 mRNA and protein in these cells not in T/T wild cells. These more significant levels of mdm2 in cells with the GG SNP309 alleles decrease the p53 apoptotic reactions that happen in individuals because of DNA harm and other ecological dangers while in cells with the TT SNP309 alleles can increment p53 protein levels after a pressure signal. Along these lines, in certain people with a G/G genotype at SNP309, the level of cells experiencing apoptosis or cell cycle capture in light of genotoxic stress is low [18, 19]. The MDM2 SNP309 polymorphism has been related with a few malignancies, including gastric carcinoma [20], non-little cell lung disease [21], endometrial disease [22], Colorectal Cancer [23], Hepatocellular Carcinoma [24], and bladder malignant growth [25]. Conversely, no expanded hazard was watched for bosom disease [26,27], ovarian malignant growth [28], prostate malignancy [29]. In the present investigation, the relationship between the MDM2 SNP309 polymorphisms and thyroid tumors chance in the Iranian-Azeri was analyzed. Materials and Methods Examples study and gathering In this investigation our patient gathering including of 107 subjects who were determined to have thyroid malignant growth (age go: 14-81 and mean age: 39.3) were qualified for this examination. All patients with histologically affirmed essential thyroid malignancy. Control gathering were chosen haphazardly from 156 solid subjects with no family ancestry of malignancy (age run: 19-79 and mean age: 40.9). An institutionalized survey from the control gathering, including data on age, sexual orientation, family ancestry of types malignancy, smoking and liquor utilization history was finished for everybody. Educated assent was earned from all members. All cases and controls were ethnic Azari from northwest of Iran. The investigation convention was approvedby the Ethics Committee of Tabriz University of the Medical Sciences research focus (www.tbzmed.ac.ir/Research). Fringe blood and tissue tests weretaken from patients who experienced medical procedure at Nour-Nejat and Emam-Reza clinics of Tabriz-Iran, from 2008 to 2012. DNA extraction and PCR intensification Fringe blood tests were kept in vials containing ethylene-diamine-tetra-acidic corrosive (EDTA), an anticoagulant. Genomic DNA was removed from 5ml the entire blood blended in with anticoagulant utilizing salting out technique as depicted [30] and afterward put away at â 20 until further use. The 194 bp piece including of the T to G polymorphic site in the intronic advertiser of MDM2 district was enhanced utilizing explicit groundworks forward: 5′-CAAGTTCAGACACGTTCCGA-3′ and invert: 5′-TCGGAACGTGTCTGAACTTG-3′. PCR was performed in a 25 µl response blend containing 1µl layout DNA (20-50ng), 2.5µl PCR cushion (10x), 0.5µl dNTPs (10mM), 0.75µl of every preliminary (10pmol), 0.85µl Mgcl2 (50mM), 18.45µl sterile refined H2O and 0.2µl Taq DNA polymerase (5unit/µl), (Cinnagen, Iran). PCR enhancement was done in a warm cycler (Sensoquest, GmbH, Germany). The accompanying cycling conditions were: an initialdenaturation at 95°C for 5 min pursued by 35 cycles of denaturation at 95 °C for 30 s, toughening at 59°C for 30 s and lengthening at 72°C for 30 s and a last expansion at 72°C for 10 min. SSCP profiles For sscp investigation, 4ml of the intensified pcr item added to 6ml of denaturing stacking color arrangement with a proportional volume containing (95 % formamide, 10 mM NaOH, 20 mM EDTA, 0.05 % bromophenol blue and 0.05 % xylene cyanol). The arrangement was quickly vortexed and The all out blend were denatured by warming at 95°C for 10 min and each example blend was promptly snap-cooled on ice before stacking onto the vertical electrophoresis set. 5µl of each pcr item test are stacked onto a non-denaturing 10% polyacrylamide gel comprised of (5 ml acrylamideâbisacrylamide arrangement (40 %) (38:2), 3.5 ml TrisâBorateâEDTA cushion (TBE.5x), 13.5 ml deionized-refined H2O, 300 µl ammonium persulfate (10 %, crisply arranged) and 30 µl tetramethylethylenediamine). At that point gel was kept running in 0.6x TBE cradle for 15-17h under a steady voltage and temperature 100v cm/l and 4°c utilizing a vertical electrophoretic mechanical assembly (Akhtarian, Iran) and a power provider (Apelex, France). One of the undenatured PCR items as negative control and a 50-bp DNA stepping stool (atomic size marker; Fermentas, USA) were stacked into the gel wells. After electrophoresis, the gel was silver recolored to the accompanying way: The gel was submerged in a plate containing arrangement 1 (4ml outright ethanol 10% and 2ml acidic corrosive 5% with refined water to a last volume of 400 mL was come to; fixing arrangement) and the plate was put over a shaker to blend for 10 minutes (this progression was performed multiple times). At that point the arrangement 1 was expelled, and the arrangement is a recently fabricated 2 (0.1% silver nitrate) was included for 15-20 minutes. After, the arrangement 2 was spilled out and quickly was washed gel with deionized water. Toward the end, the newly fabricated arrangement (3 gr NaOH, 20 ml formal>
Dynamic Foundation: MDM2 SNP309 (rs2279744) is a solitary nucleotide T>G polymorphism present in the primary intron of the MDM2 quality and a negative controller of p53 tumor silencer protein. The discoveries propose that MDM2 309TG polymorphism might be a hazard factor for a few tumors. This investigation analyzed clinical relationship of thyroid tumors with SNP309 in Iranian-Azeri populace. Techniques: In present examination, 107 thyroid disease patients and 156 malignant growth free control were gotten from Iranian-Azeri populace. Genomic DNA including of fringe blood and tumor tests was extricated by salting out methodology. The MDM2 SNP309 genotyping was completed by polymerase chain response single strand conformational polymorphism (PCR-SSCP) measure. All investigations were directed by spss programming with Chi-squared(?2) test and the P G, polymorphism Presentation The grouping of the entire human genome was finished in 2001 [1], and Approximately 6.5 million SNPs (single nucleotide polymorphisms) have been identified in human qualities. Contingent upon where a SNP happens, it may have various outcomes at the phenotypic level. SNPs are situated in the coding locales of qualities that change the capacity or structure of the encoded proteins and in non-coding areas of the genome, and have no direct known impact on the phenotype of a person. These distinctions could add to a large number of the individual highlights that portray us as one of a kind. Likewise, in light of the fact that they happen at a generally high recurrence in the genome (around one SNP for each 1000 bp), SNPs can be utilized as markers for these increasingly significant hereditary changes. 89% of the investigated SNPs are situated in an exon and 11 % in an intron [2,3]. Thyroid disease (TC) is the most widely recognized harm of the endocrine framework and records for around 2.1% of all malignancies analyzed around the world. The thyroid disease has a 4.4% commonness in ladies and a 1.3% predominance in men. The male-to-female proportion was roughly 1: 3.5, while the unrefined rate for men was 1.9/100,000 and that for ladies was 6.6/100,000. Thyroid malignancy is the ninth most regular disease (2.1% all things considered) in ladies [4]. The rate pace of thyroid malignant growth in the two ladies and men is increasing[5]. Essential thyroid tumors are delegated generous or threatening, which start from follicular and parafollicular (or c-cells) epithelial cells. Generous tumors containing follicular adenoma and threatening tumors are contained papillary, follicular, medullary and anaplastic carcinomas. The follicular cells convert iodine into thyroxine (T4) and triiodothyronine (T3) and incorporate papillary, follicular and anaplastic carcinomas and Follicular adenoma. The parafollicular or C-cells, which discharge calcitonin, contain medullary carcinoma [6]. Between thyroid tumors, papillary thyroid disease speak to roughly 80% of every single thyroid danger [7]. Some molecularbiomarkersinvolved inthyroid tumorsincludep53, RET, BRAF, RET/PTC ,RAS, PAX8/PPAR? and NTRK1 [8]. The human homologue of the mouse twofold moment 2 (MDM2 or HDM2) quality locatedon chromosome 12q13-14 with 491 amino acids long and 12 exons comprise of twotranscriptional advertisers, constitutive advertiser and p53-responsive intronic advertiser [9, 10, 11]. MDM2 oncoprotein actsa basic regul-atory job for some, tumor-related qualities that are significant for cell-cycle control, for example, the P53 [12]. The p53 quality is transformed in about half of every single human malignancy [13]. P53 is a tumor silencer quality, which is associated with different pathways, including apoptosis, DNA fix, cell cycle capture and senescence [14]. MDM2 and TP53 control each other through a criticism circle [15]. P53 initiates MDM2 on the transcriptional level while MDM2 communicates through its N-terminal space with a a-helix present in the transactivation area of p53 with high fondness and hinders its, subsequently, sets it up for proteolytic debasement at the ubiquitination pathway [16]. The general recurrence of MDM2 quality intensification in human tumors is around 7.2% [17]. An ongoing report has demonstrated that a MDM2 single nucleotide polymorphism in the primary intron with a T to G change at the nucleotide 309 in the p2 advertiser area of MDM2, so that, The nearness of the freak G-allele in cells containing SNP 309 GG builds the liking of the transcriptional activator stimulatory protein 1 (Sp1), that controls the basal degrees of MDM2 mRNA and protein in these cells not in T/T wild cells. These more significant levels of mdm2 in cells with the GG SNP309 alleles decrease the p53 apoptotic reactions that happen in individuals because of DNA harm and other ecological dangers while in cells with the TT SNP309 alleles can increment p53 protein levels after a pressure signal. Along these lines, in certain people with a G/G genotype at SNP309, the level of cells experiencing apoptosis or cell cycle capture in light of genotoxic stress is low [18, 19]. The MDM2 SNP309 polymorphism has been related with a few malignancies, including gastric carcinoma [20], non-little cell lung disease [21], endometrial disease [22], Colorectal Cancer [23], Hepatocellular Carcinoma [24], and bladder malignant growth [25]. Conversely, no expanded hazard was watched for bosom disease [26,27], ovarian malignant growth [28], prostate malignancy [29]. In the present investigation, the relationship between the MDM2 SNP309 polymorphisms and thyroid tumors chance in the Iranian-Azeri was analyzed. Materials and Methods Examples study and gathering In this investigation our patient gathering including of 107 subjects who were determined to have thyroid malignant growth (age go: 14-81 and mean age: 39.3) were qualified for this examination. All patients with histologically affirmed essential thyroid malignancy. Control gathering were chosen haphazardly from 156 solid subjects with no family ancestry of malignancy (age run: 19-79 and mean age: 40.9). An institutionalized survey from the control gathering, including data on age, sexual orientation, family ancestry of types malignancy, smoking and liquor utilization history was finished for everybody. Educated assent was earned from all members. All cases and controls were ethnic Azari from northwest of Iran. The investigation convention was approvedby the Ethics Committee of Tabriz University of the Medical Sciences research focus (www.tbzmed.ac.ir/Research). Fringe blood and tissue tests weretaken from patients who experienced medical procedure at Nour-Nejat and Emam-Reza clinics of Tabriz-Iran, from 2008 to 2012. DNA extraction and PCR intensification Fringe blood tests were kept in vials containing ethylene-diamine-tetra-acidic corrosive (EDTA), an anticoagulant. Genomic DNA was removed from 5ml the entire blood blended in with anticoagulant utilizing salting out technique as depicted [30] and afterward put away at â 20 until further use. The 194 bp piece including of the T to G polymorphic site in the intronic advertiser of MDM2 district was enhanced utilizing explicit groundworks forward: 5′-CAAGTTCAGACACGTTCCGA-3′ and invert: 5′-TCGGAACGTGTCTGAACTTG-3′. PCR was performed in a 25 µl response blend containing 1µl layout DNA (20-50ng), 2.5µl PCR cushion (10x), 0.5µl dNTPs (10mM), 0.75µl of every preliminary (10pmol), 0.85µl Mgcl2 (50mM), 18.45µl sterile refined H2O and 0.2µl Taq DNA polymerase (5unit/µl), (Cinnagen, Iran). PCR enhancement was done in a warm cycler (Sensoquest, GmbH, Germany). The accompanying cycling conditions were: an initialdenaturation at 95°C for 5 min pursued by 35 cycles of denaturation at 95 °C for 30 s, toughening at 59°C for 30 s and lengthening at 72°C for 30 s and a last expansion at 72°C for 10 min. SSCP profiles For sscp investigation, 4ml of the intensified pcr item added to 6ml of denaturing stacking color arrangement with a proportional volume containing (95 % formamide, 10 mM NaOH, 20 mM EDTA, 0.05 % bromophenol blue and 0.05 % xylene cyanol). The arrangement was quickly vortexed and The all out blend were denatured by warming at 95°C for 10 min and each example blend was promptly snap-cooled on ice before stacking onto the vertical electrophoresis set. 5µl of each pcr item test are stacked onto a non-denaturing 10% polyacrylamide gel comprised of (5 ml acrylamideâbisacrylamide arrangement (40 %) (38:2), 3.5 ml TrisâBorateâEDTA cushion (TBE.5x), 13.5 ml deionized-refined H2O, 300 µl ammonium persulfate (10 %, crisply arranged) and 30 µl tetramethylethylenediamine). At that point gel was kept running in 0.6x TBE cradle for 15-17h under a steady voltage and temperature 100v cm/l and 4°c utilizing a vertical electrophoretic mechanical assembly (Akhtarian, Iran) and a power provider (Apelex, France). One of the undenatured PCR items as negative control and a 50-bp DNA stepping stool (atomic size marker; Fermentas, USA) were stacked into the gel wells. After electrophoresis, the gel was silver recolored to the accompanying way: The gel was submerged in a plate containing arrangement 1 (4ml outright ethanol 10% and 2ml acidic corrosive 5% with refined water to a last volume of 400 mL was come to; fixing arrangement) and the plate was put over a shaker to blend for 10 minutes (this progression was performed multiple times). At that point the arrangement 1 was expelled, and the arrangement is a recently fabricated 2 (0.1% silver nitrate) was included for 15-20 minutes. After, the arrangement 2 was spilled out and quickly was washed gel with deionized water. Toward the end, the newly fabricated arrangement (3 gr NaOH, 20 ml formal>