Penerapan Teknologi General Packet Radio Service Pada Sistem Monitoring Sepeda Motor

General Packet Radio Service (GPRS) merupakan sistem transmisi berbasis paket untuk Global System for Mobile (GSM). Pengembangan sistem keamanan menggunakan GPRS merupakan salah satu bidang yang terus mengalami pembaharuan terutama di negara Indonesia dimana keamanan masih menjadi salah satu fokus dalam perbaikan. Tingkat keamanan kendaraan terutama sepeda motor di Indonesia masih sangat kurang terjamin, hal ini menjadi latar belakang tugas akhir ini dirancang. Alat ini dirancang untuk dapat memberikan informasi tentang keberadaan sepeda motor baik dalam informasi kehilangan maupun informasi posisi kendaraan. Data mengenai informasi kehilangan akan dikirimkan langsung ke Handphone pengguna dengan transmisi GSM dan data mengenai informasi posisi berupa data lintang dan bujur akan dikirimkan menuju database yang dibuat dengan menggunakan MySQl melalui GPRS serta dapat diakses menggunakan website dengan halaman utama menggunakan HyperText Markup Language (HTML) dan koneksi dengan Google Maps API. Peta dasar yang dinamis membuat akurasi yang lebih baik antara data pelacakan dengan penandaan posisi pada peta. Data mengenai posisi akan didapat melalui Global Positioning System (GPS) yang kemudian data tersebut akan diolah menjadi data yang siap dikonversikan pada peta dan dalam bentuk sebuah marker

SNP-SNP interaction analysis of NF-kappa B signaling pathway on breast cancer survival

In breast cancer, constitutive activation of NF-kappa B has been reported, however, the impact of genetic variation of the pathway on patient prognosis has been little studied. Furthermore, a combination of genetic variants, rather than single polymorphisms, may affect disease prognosis. Here, in an extensive dataset (n = 30,431) from the Breast Cancer Association Consortium, we investigated the association of 917 SNPs in 75 genes in the NF-kappa B pathway with breast cancer prognosis. We explored SNP-SNP interactions on survival using the likelihood-ratio test comparing multivariate Cox' regression models of SNP pairs without and with an interaction term. We found two interacting pairs associating with prognosis: patients simultaneously homozygous for the rare alleles of rs5996080 and rs7973914 had worse survival (HRinteraction 6.98, 95% CI= 3.3-14.4, P=1.42E-07), and patients carrying at least one rare allele for rs17243893 and rs57890595 had better survival (HRinteraction 0.51, 95% CI= 0.3-0.6, P = 2.19E-05). Based on in silico functional analyses and literature, we speculate that the rs5996080 and rs7973914 loci may affect the BAFFR and TNFR1/TNFR3 receptors and breast cancer survival, possibly by disturbing both the canonical and non-canonical NF-kappa B pathways or their dynamics, whereas, rs17243893-rs57890595 interaction on survival may be mediated through TRAF2-TRAIL-R4 interplay. These results warrant further validation and functional analyses.Peer reviewe

Association of the CHEK2 c.1100delC variant, radiotherapy, and systemic treatment with contralateral breast cancer risk and breast cancer-specific survival

Background: Breast cancer (BC) patients with a germline CHEK2 c.1100delC variant have an increased risk of contralateral BC (CBC) and worse BC-specific survival (BCSS) compared to non-carriers.Aim: To assessed the associations of CHEK2 c.1100delC, radiotherapy, and systemic treatment with CBC risk and BCSS.Methods: Analyses were based on 82,701 women diagnosed with a first primary invasive BC including 963 CHEK2 c.1100delC carriers; median follow-up was 9.1 years. Differential associations with treatment by CHEK2 c.1100delC status were tested by including interaction terms in a multivariable Cox regression model. A multi-state model was used for further insight into the relation between CHEK2 c.1100delC status, treatment, CBC risk and death. Results: There was no evidence for differential associations of therapy with CBC risk by CHEK2 c.1100delC status. The strongest association with reduced CBC risk was observed for the combination of chemotherapy and endocrine therapy [HR (95% CI): 0.66 (0.55-0.78)]. No association was observed with radiotherapy.Results from the multi-state model showed shorter BCSS for CHEK2 c.1100delC carriers versus non-carriers also after accounting for CBC occurrence [HR (95% CI): 1.30 (1.09-1.56)].Conclusion: Systemic therapy was associated with reduced CBC risk irrespective of CHEK2 c.1100delC status. Moreover, CHEK2 c.1100delC carriers had shorter BCSS, which appears not to be fully explained by their CBC risk.Peer reviewe

No evidence that protein truncating variants in BRIP1 are associated with breast cancer risk: implications for gene panel testing.

BACKGROUND: BRCA1 interacting protein C-terminal helicase 1 (BRIP1) is one of the Fanconi Anaemia Complementation (FANC) group family of DNA repair proteins. Biallelic mutations in BRIP1 are responsible for FANC group J, and previous studies have also suggested that rare protein truncating variants in BRIP1 are associated with an increased risk of breast cancer. These studies have led to inclusion of BRIP1 on targeted sequencing panels for breast cancer risk prediction. METHODS: We evaluated a truncating variant, p.Arg798Ter (rs137852986), and 10 missense variants of BRIP1, in 48 144 cases and 43 607 controls of European origin, drawn from 41 studies participating in the Breast Cancer Association Consortium (BCAC). Additionally, we sequenced the coding regions of BRIP1 in 13 213 cases and 5242 controls from the UK, 1313 cases and 1123 controls from three population-based studies as part of the Breast Cancer Family Registry, and 1853 familial cases and 2001 controls from Australia. RESULTS: The rare truncating allele of rs137852986 was observed in 23 cases and 18 controls in Europeans in BCAC (OR 1.09, 95% CI 0.58 to 2.03, p=0.79). Truncating variants were found in the sequencing studies in 34 cases (0.21%) and 19 controls (0.23%) (combined OR 0.90, 95% CI 0.48 to 1.70, p=0.75). CONCLUSIONS: These results suggest that truncating variants in BRIP1, and in particular p.Arg798Ter, are not associated with a substantial increase in breast cancer risk. Such observations have important implications for the reporting of results from breast cancer screening panels.The COGS project is funded through a European Commission's Seventh Framework Programme grant (agreement number 223175 - HEALTH-F2-2009-223175). BCAC is funded by Cancer Research UK [C1287/A10118, C1287/A12014] and by the European Community´s Seventh Framework Programme under grant agreement number 223175 (grant number HEALTH-F2-2009-223175) (COGS). Funding for the iCOGS infrastructure came from: the European Community's Seventh Framework Programme under grant agreement n° 223175 (HEALTH-F2-2009-223175) (COGS), Cancer Research UK (C1287/A10118, C1287/A 10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007, C5047/A10692, C8197/A16565), the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 16 CA148065 and 1U19 CA148112 - the GAME-ON initiative), the Department of Defense (W81XWH-10-1- 0341), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund. This study made use of data generated by the Wellcome Trust Case Control consortium. Funding for the project was provided by the Wellcome Trust under award 076113. The results published here are in part based upon data generated by The Cancer Genome Atlas Project established by the National Cancer Institute and National Human Genome Research Institute.This is the author accepted manuscript. The final version is available from BMJ Group at http://dx.doi.org/10.1136/jmedgenet-2015-103529

Cardiomyocite Contractility,Calcium handling and Endothelial Function in a mouse model of Type II Diabetes and the Metabolic Syndrome

Diabetes, obesity and dyslipidemia are associated with a significant increase in cardiovascular morbidity and mortality, caused by cardiomyopathy, vasculopathy and their consequences. The prevalence of affected patients is still increasing, resulting in a major health care problem.14.0pt;margin-left:0cm;text-align:justify;line-height:150%;text-autospace:ideograph-numeric" align="left">The existence of a primary diabetic cardiomyopathy, in the absence of an ischemic or hypertensive cardiomyopathy is at least partially related to alterations in cardiomyocyteproperties. Although it has been shown in vivo that cardiac dysfunctionis aggravated in the metabolic syndrome and characterized by additionalfeatures, -.1pt">changes in intrinsic properties of cardiomyocytes have not been studied in mice with the metabolic syndrome (MetS). 14.0pt;margin-left:0cm;text-align:justify;line-height:150%;text-autospace:ideograph-numeric" align="left">Diabeticangiopathy is characterized by abnormalities in vascular wall morphology and altered vascular reactivity. It is currently unclear whether the dyslipidemia and hypertension, associated with diabetes type II in MetS, worsen these diabetes-induced alterations in vascular function.-.1pt"> 14.0pt;margin-left:0cm;text-align:justify;line-height:150%;text-autospace:ideograph-numeric" align="left">-.1pt">Concerning therapy, 150%">hypocaloric diet and ACE-inhibitors arecurrently the golden standard in the treatment of cardiovascular complications in patients with diabetes mellitus type II and the metabolic syndrome. .5pt">However, most studies are performed with both entities in one group, exhibiting a large pathological and clinical variance-.1pt">. ideograph-numeric" align="left">-.1pt">This study was designed tline-height:150%;letter-spacing:-.1pt">o gain further insight into the mechanisms contributing to cardiovascular dysfunction in the metabolic syndrome and to.5pt"> study more in detail the effect of ACE-inhibitors and hypocaloric dieton cardiovascular function in d150%">iabetes type II and the metabolic syndrome.5pt">, as separate entities. ideograph-numeric" align="left">Cardiomyocyte function and Ca2+ handling in a mouse model of the metabolic syndrome. We have shown that cardiomyocyte function and Ca2+ handling are impaired in DKO mice (the used model of the metabolic syndrome), associated with reduced contractile reserve, compared to ob/ob mice. ACE-inhibition, but not weight reduction, can restore cardiomyocyte relaxation and β-adrenergic responsiveness. These data indicate that the in vivo features of cardiomyopathy in the metabolic syndrome can at least partially be explained by alterations in intrinsic cardiomyocyte properties and Ca2+ handling. Secondly, they indicate that dyslipidemia and/or hypertension in typeII diabetic mice aggravate cardiomyocyte dysfunction.14.0pt;margin-left:0cm;text-align:justify;line-height:150%;text-autospace:ideograph-numeric" align="left">Vascular reactivity in a mouse model of themetabolic syndrome.DKO mice show a more pronounced impairment of acetylcholine-induced vasorelaxation, compared to ob/ob. This effect is mainly NO-mediated and can be restored by ACE-inhibition and hypocaloric diet. In contrast, response to bradykinin is equally reduced in both genotypes and is not influenced by ACE-inhibition. These data suggest that dyslipidemia and hypertension aggravate NO-mediated endothelium-dependentrelaxation in type II diabetic mice, reversible by ACE-inhibition and diet. In contrast, these features prevent further worsening of bradykinin-induced vasorelaxation in type II diabetic mice. This effect might be mediated via endothelial COX-2 and can not be restored by ACE-inhibition.14.0pt;margin-left:0cm;text-align:justify;line-height:150%;text-autospace:ideograph-numeric" align="left">Taken together, this study shows that dyslipidemia and hypertension aggravate cardiovascular dysfunction in vitro in type II diabetic mice. ACE-inhibiton and hypocaloric diet can improve this impaired cardiovascular function.status: publishe

Betrouwbaarheid van het MoistureMeterD Compact toestel en de pitting test ter evaluatie van weefselvocht in patiënten met borstkanker-gerelateerd lymfoedeem

status: publishe

Revisie van de Lymf-ICF vragenlijst voor borstkanker-gerelateerd lymfoedeem van het bovenste lidmaat (Lymph-ICF-UL): betrouwbaarheid en validiteit

status: publishe