Analisis Adduct DNA Setelah Pemberian Natrium Nitrit Dan Dimetilamin Secara Berulang Pada Tikus

Nitrosodimethylamine is a carcinogenic compound which can be formed from the reaction of nitrite and dimethylamine that is found in food. Nitrosodimethylamineis activated in liver and alkylates the DNA base and producing a DNA adductssuch as O6-methylguanine and N7-methylguanine that have a role incarcinogenesis. In this research, DNA was isolated from rat’s blood which waspreviously given nitrosodimethylamine’s precursor, sodium nitrite anddimethylamine. DNA adducts can be obtained from hydrolysis in hydrochloricacid 0.1 N for 30 minutes at 7000C. Then the adducts were analyzed using High Performance Liquid Chromatography (HPLC), with a strong cation exchangecolumn (Supelcosil LC-SCX, 5 μm, 250 x 4.6 mm), mobile phase consisting ofammonium phosphate with a final concentration of 40 mM, pH 3.00, flow rate 1.5mL/minute, column temperature 30oC and detected at exitation wavelength 286 nm and emission wavelength 366 nm. This method gave an acceptable validation result according to accuracy and precicion test results that fulfill the requirementand linear calibration curve with a quantitation limit of 22,5403 ng/mL. Rats were divided into six groups that two groups were given nitrosodimethylamine aspositive control, three groups were given prekursor, and the other was normalcontrol.Blood samples were collected in 1,2 and 4 hour after last induced. Aftergiving sodium nitrite 110 mg/kg bw and dimethylamine (1:5) orally for a week,N7-methylguanine and O6-methylguanine had not been detected in rat’s blood

Meningkatkan Hasil Belajar Siswa Pada Mata Pelajaran Sains Melalui Penggunaan Alat Peraga Di Kelas V SDN 1 Dolong A

Penelitian ini merupakan penelitian tindakan kelas. Penelitian ini dilakukan dalam dua siklus dengan tujuan meningkatkan hasil belajar siswa dengan menggunakan alat peraga di kelas V SDN 1 Dolong A. Subyek penelitian ini adalah siswa kelas V SDN 1 Dolong A yang berjumlah 32 orang terdiri dari 15 orang laki-laki dan 17 orang perempuan. Hasil penelitian pada siklus I menunjukkan rata-rata hasil observasi aktivitas siswa diperoleh persentase 71,87% dengan kategori baik, persentase aktivitas guru 77% kategori baik, persentase daya serap klasikal 56,63% dan tuntas klasikal sebesar 71,87%. Pada siklus II diperoleh rata-rata persentase aktivitas siswa sebesar 87,5% dengan kategori sangat baik, persentase aktivitas guru 90,38% kategori sangat baik, persentase daya serap klasikal 80% dan persentase tuntas klasikal sebesar 85%. Hal ini telah memenuhi indikator keberhasilan yang telah ditetapkan dengan nilai rata-rata hasil belajar minimal 70 dan ketuntasan klasikal sudah mencapai indikator keberhasilan minimal 80%

Diversity-based Attribute Weighting for K-modes Clustering

Categorical data is a kind of data that is used for computational in computer science. To obtain the information from categorical data input, it needs a clustering algorithm. There are so many clustering algorithms that are given by the researchers. One of the clustering algorithms for categorical data is k-modes. K-modes uses a simple matching approach. This simple matching approach uses similarity values. In K-modes, the two similar objects have similarity value 1, and 0 if it is otherwise. Actually, in each attribute, there are some kinds of different attribute value and each kind of attribute value has different number. The similarity value 0 and 1 is not enough to represent the real semantic distance between a data object and a cluster. Thus in this paper, we generalize a k-modes algorithm for categorical data by adding the weight and diversity value of each attribute value to optimize categorical data clustering

Broad targeting of resistance to apoptosis in cancer

Apoptosis or programmed cell death is natural way of removing aged cells from the body. Most of the anti-cancer therapies trigger apoptosis induction and related cell death networks to eliminate malignant cells. However, in cancer, de-regulated apoptotic signaling, particularly the activation of an anti-apoptotic systems, allows cancer cells to escape this program leading to uncontrolled proliferation resulting in tumor survival, therapeutic resistance and recurrence of cancer. This resistance is a complicated phenomenon that emanates from the interactions of various molecules and signaling pathways. In this comprehensive review we discuss the various factors contributing to apoptosis resistance in cancers. The key resistance targets that are discussed include (1) Bcl-2 and Mcl-1 proteins; (2) autophagy processes; (3) necrosis and necroptosis; (4) heat shock protein signaling; (5) the proteasome pathway; (6) epigenetic mechanisms; and (7) aberrant nuclear export signaling. The shortcomings of current therapeutic modalities are highlighted and a broad spectrum strategy using approaches including (a) gossypol; (b) epigallocatechin-3-gallate; (c) UMI-77 (d) triptolide and (e) selinexor that can be used to overcome cell death resistance is presented. This review provides a roadmap for the design of successful anti-cancer strategies that overcome resistance to apoptosis for better therapeutic outcome in patients with cancer

Extramedullary myeloma in an HIV-seropositive subject. Literature review and report of an unusual case

Myeloma is characterized by monoclonal bone marrow plasmacytosis, the presence of M-protein in serum and/or in urine and osteolytic bone lesions. HIV-seropositive subjects with myeloma are younger at the time of diagnosis of the tumour and usually the myeloma has a more aggressive clinical course than it does in HIV-seronegative subjects

A Test of Highly Optimized Tolerance Reveals Fragile Cell-Cycle Mechanisms Are Molecular Targets in Clinical Cancer Trials

Robustness, a long-recognized property of living systems, allows function in the face of uncertainty while fragility, i.e., extreme sensitivity, can potentially lead to catastrophic failure following seemingly innocuous perturbations. Carlson and Doyle hypothesized that highly-evolved networks, e.g., those involved in cell-cycle regulation, can be resistant to some perturbations while highly sensitive to others. The “robust yet fragile” duality of networks has been termed Highly Optimized Tolerance (HOT) and has been the basis of new lines of inquiry in computational and experimental biology. In this study, we tested the working hypothesis that cell-cycle control architectures obey the HOT paradigm. Three cell-cycle models were analyzed using monte-carlo sensitivity analysis. Overall state sensitivity coefficients, which quantify the robustness or fragility of a given mechanism, were calculated using a monte-carlo strategy with three different numerical techniques along with multiple parameter perturbation strategies to control for possible numerical and sampling artifacts. Approximately 65% of the mechanisms in the G1/S restriction point were responsible for 95% of the sensitivity, conversely, the G2-DNA damage checkpoint showed a much stronger dependence on a few mechanisms; ∼32% or 13 of 40 mechanisms accounted for 95% of the sensitivity. Our analysis predicted that CDC25 and cyclin E mechanisms were strongly implicated in G1/S malfunctions, while fragility in the G2/M checkpoint was predicted to be associated with the regulation of the cyclin B-CDK1 complex. Analysis of a third model containing both G1/S and G2/M checkpoint logic, predicted in addition to mechanisms already mentioned, that translation and programmed proteolysis were also key fragile subsystems. Comparison of the predicted fragile mechanisms with literature and current preclinical and clinical trials suggested a strong correlation between efficacy and fragility. Thus, when taken together, these results support the working hypothesis that cell-cycle control architectures are HOT networks and establish the mathematical estimation and subsequent therapeutic exploitation of fragile mechanisms as a novel strategy for anti-cancer lead generation