Inventarisasi Tanaman Peneduh Jalan Penjerap Timbal di Purwokerto

Tanaman peneduh jalan adalah tanaman yang berada di tepi jalan. Tanaman peneduh jalan memiliki dua fungsi yaitu sebagai estetika dan ekologis. Salah satu fungsi ekologis tanaman peneduh jalan adalah mengakumulasi bahan pencemar. Jenis pencemaran yang memerlukan penanganan secara sistematis dan komprehensif adalah pencemaran timbal (Pb). Pb banyak dihasilkan oleh aktivitas pembakaran bahan bakar minyak kendaraan bermotor. Jenis tanaman peneduh jalan yang berpotensi mengakumulasi Pb belum tereksplorasi sehingga dilakukan riset yang dapat menghasilkan database jenis spesies yang mampu mengurangi Pb di lingkungan. Tujuan penelitian adalah menginventarisasi jenis tanaman peneduh jalan penjerap Pb. Manfaat penelitian adalah mendapatkan jenis tanaman peneduh jalan yang berpotensi penjerap Pb. Metode penelitian yang digunakan adalah survai di 8 (delapan) jalan di wilayah Purwokerto. Sampel daun tanaman peneduh jalan diambil secara acak terpilih di sepanjang jalan tersebut. Hasil penelitian menunjukkan jenis-jenis tanaman peneduh jalan yang berpotensi menjerap Pb adalah Glodogan (Polyalthea longifolia), Angsana (Pterocarpus indicus), Filicium (Filicium decipiends), Ketapang (Terminalia catappa), Beringin (Ficus benjamina), Kupu-kupu (Bauhinia tomentosa), Puspa (Schima wallichii), Kenari (Canarium ovatum) dan Genitu (Chrysophyllum cainito)

Hybrid Graphene Oxide Based Ultrasensitive SERS Probe for Label-Free Biosensing

A metal nanoparticle attached to graphene oxide has the ability to open a new avenue of research with significant opportunities in the biomedical field. In this Letter, we report graphene oxide attached to a popcorn-shaped gold nanoparticle based hybrid SERS probe with ultrasensitive label-free sensing of HIV DNA and bacteria and provide its chemical fingerprint. Our SERS data with the hybrid material shows that it can be used for label-free detection of HIV DNA on the femto-molar level without any labeling. Experimental data with a novel SERS substrate show excellent reproducibility of the SERS signal. The current Letter demonstrates that the label-free SERS detection limit using a hybrid material can be as low as 10 CFU/mL for MRSA bacteria. The possible mechanism for very high sensitivity has been discussed

Local Structure Evolution and its Connection to Thermodynamic and Transport Properties of 1-Butyl-3-methylimidazolium Tetrafluoroborate and Water Mixtures by Molecular Dynamics Simulations

Our recently developed improved united atom force field shows a good quality to reproduce both the static and transport properties of neat ionic liquids (ILs). Combined with the TIP4P-Ew water model, the force field is used to simulate the mixture of 1-butyl-3-methylimidazolium tetrafluoroborate ([C₄mim]­[BF₄]) and water without further optimization to adjust any cross parameters. Liquid densities of the mixture are well predicted over the entire concentration range at temperatures from 298.15 to 353.15 K. Simulations also reproduce the positive values of excess volumes and excess enthalpies, as well as their increase with temperature. The simulated viscosities are in good agreement with experimental values, especially in the water-rich region. We found three distinct regions by analyzing the concentration dependent self-diffusion coefficients via Stokes–Einstein (SE) relation, indicating the mixture experiences significant microheterogeneity with the adding of water. This observation is well connected to the structure features obtained in simulations, such as radial distribution functions (RDFs), spatial distribution functions (SDFs) and water clustering analysis. At the water mole fraction (<i>x</i>₂) less than 0.2, most of the water molecules are isolated in the polar cation–anion network in ionic liquids. With the increase of <i>x</i>₂ from 0.2 to 0.8, large water cluster forms and eventually percolates the whole system. When <i>x</i>₂ > 0.8, ionic liquids show a moderate degree of aggregation (with maximum around 0.9 to 0.95) before the cations and anions are fully dissolved in water

Combination of 1, 9 PA and cetuximab induces apoptosis through downregulation of HIF-1α.

<p>(A) Induction of PARP cleavage by the combination of 1, 9 PA and cetuximab. A431, HN5, and DiFi cells were untreated or treated with cetuximab (10 nM for A431 and HN5 cells and 2 nM for DiFi cells for 16 h), 1, 9 PA (10 µM or 40 µM added the last hour before cell lysis), or both in 0.5% FBS culture medium. Cell lysates were prepared and analyzed by Western blotting with the antibodies shown. (B) Increased induction of apoptosis by the combination of 1, 9 PA and cetuximab. A431 cells were treated as described in (A). Cell lysates were prepared and analyzed by apoptosis ELISA. The relative absorbance values are plotted. The <i>p</i> value was <0.01 when comparing the level of apoptosis by 1, 9 PA alone (10 or 40 µM) or cetuximab alone with that of apoptosis by combination of the 2 agents (note: only the <i>p</i> values comparing 10 µM 1, 9 PA alone and in combination with cetuximab are shown). (C) Dependence of induction of apoptosis by the combination of 1, 9 PA and cetuximab on HIF-1α downregulation. A431neo and A431/HIF-1α-ΔODD cells were treated as indicated, and the cell lysates were prepared and analyzed as described in (A).</p

1, 9 PA enhances HIF-1α ubiquitination.

<p>(A). A431 cells were treated with 10 µM 1, 9 PA for indicated time period. Cell lysates were prepared for HIF-1α immunoprecipitation, followed by Western blotting of the immunoprecipitates with antibodies directed against ubiquitin (top), HIF-1α, and β-actin. (B) A431 cells were untreated or treated with 10 µM 1, 9 PA in the presence of 10 µM MG132 for 1 h in 0.5% FBS medium. HIF-1α was immunoprecipitated followed by Western blot analysis with an anti-HIF-1α antibody.</p

1, 9 PA downregulates HIF-1α independent of its JNK inhibitory function.

<p>(A) Temporal order and correlation of 1, 9 PA-induced HIF-1α downregulation and JNK inhibition, and the treatment-induced compensatory activation of Akt and Erk. A431 cells were treated with 5 µM 1, 9 PA in 0.5% FBS culture medium for the indicated time intervals. Cell lysates were then prepared for Western blotting with the antibodies shown. (B) Dose-dependent effects of 1, 9 PA on downregulating HIF-1α, inhibiting JNK, and activating Erk. A431 cells were exposed to increasing concentrations of 1, 9 PA for 16 h in 0.5% FBS culture medium at 37°C. Cell lysates were then prepared for Western blotting with the antibodies shown. (C) Independence of 1, 9 PA-induced HIF-1α downregulation from its JNK inhibitory function. A431 cells were treated with increasing concentrations of 1, 9 PA or 1-methyl-1, 9 PA for 1 h in 0.5% FBS culture medium. Cell lysates were then prepared for Western blotting with the antibodies shown. (D) No changes in HIF-1α level after activation or inhibition of JNK. A431 cells wert transiently transfected with a control vector or one of the constructs containing a constitutively active SEK1 S220E/T224D mutant (SEK1-CA), a dominant-negative SEK1 K129R mutant (SEK1-DN), or a dominant-negative MEKK1 K432M mutant (MEKK1-DN) overnight. Cell lysates were then prepared for Western blotting with the antibodies shown. (E) Compensatory activation of Erk after HIF-1α silencing in comparison with treatment by 1, 9 PA or 1-methyl-1, 9 PA. A431 cells were subjected to knockdown of HIF-1α with specific or control siRNA, or treated with 10 µM 1, 9 PA or 1-methyl-1, 9 PA for 16 h. Cell lysates were then prepared for Western blotting with the antibodies shown. (F) Downregulation of HIF-1α by 1, 9 PA in various cancer cell lines. Indicated cell lines were exposed to 10 or 40 µM 1, 9 PA for 1 h in 0.5% FBS culture medium. Cell lysates were then prepared for Western blotting with the antibodies shown.</p

Expression of HIF-1α/ΔODD mutant leads to cellular resistance to cetuximab without affecting cellular sensitivity to cetuximab-induced inhibition of EGFR signaling

<p><b>Copyright information:</b></p><p>Taken from "Responses of cancer cells with wild-type or tyrosine kinase domain-mutated epidermal growth factor receptor (EGFR) to EGFR-targeted therapy are linked to downregulation of hypoxia-inducible factor-1α"</p><p>http://www.molecular-cancer.com/content/6/1/63</p><p>Molecular Cancer 2007;6():63-63.</p><p>Published online 11 Oct 2007</p><p>PMCID:PMC2117021.</p><p></p> () A431neo and A431/HIF-1α/ΔODD cells were treated as indicated for 16 hours (overnight). Cell lysates were prepared and subjected to Western blot analysis with the indicated antibodies. () Cells were left untreated or treated with the indicated concentrations of cetuximab in culture with 0.5% FBS for 5 days. Relative cell numbers were measured by the MTT assay and are presented as a percentage of the untreated control. () A431neo and A431/HIF-1α/ΔODD cells (300 cells/dish) were cultured, with or without cetuximab (2 nM), for 9 days. After treatment, cells were fixed and the colonies were counted, as described in the Methods section

Downregulation of HIF-1α protein levels in cell lines with wild-type or mutated EGFR after treatment with cetuximab or gefitinib

<p><b>Copyright information:</b></p><p>Taken from "Responses of cancer cells with wild-type or tyrosine kinase domain-mutated epidermal growth factor receptor (EGFR) to EGFR-targeted therapy are linked to downregulation of hypoxia-inducible factor-1α"</p><p>http://www.molecular-cancer.com/content/6/1/63</p><p>Molecular Cancer 2007;6():63-63.</p><p>Published online 11 Oct 2007</p><p>PMCID:PMC2117021.</p><p></p> Cells from the indicated cell lines were treated with cetuximab or gefitinib overnight as described in Figure 4. After treatment, the cells were lysed, and equal amounts of cell lysates were subjected to Western blot analysis using antibodies directed against HIF-1α, as indicated. The level of β-actin served as the internal control for equal protein loading in each lane. The numeric values shown under each gel were derived from a densitometric analysis of the signals

Dose- and time-dependent responses of wild-type EGFR and tyrosine kinase domain-mutated EGFR cells to cetuximab and gefitinib treatment

<p><b>Copyright information:</b></p><p>Taken from "Responses of cancer cells with wild-type or tyrosine kinase domain-mutated epidermal growth factor receptor (EGFR) to EGFR-targeted therapy are linked to downregulation of hypoxia-inducible factor-1α"</p><p>http://www.molecular-cancer.com/content/6/1/63</p><p>Molecular Cancer 2007;6():63-63.</p><p>Published online 11 Oct 2007</p><p>PMCID:PMC2117021.</p><p></p> () Absolute cell numbers in each treatment group (control [DMSO]), 5 nM cetuximab, and 0.5 μM gefitinib, all in 0.5% FBS medium) were plotted against the duration of treatment. () The inhibition of cell proliferation after treatment with cetuximab was measured by an MTT assay and is shown as a percentage of the optical density value of control cells (untreated) for each concentration tested. () The inhibition of cell proliferation after treatment with gefitinib was measured as in () and is shown as a percentage of the optical density value of vehicle-treated cells (DMSO) for each concentration tested. Results are shown as the mean of five independent measurements, plus or minus the standard deviation (SD). The magnitude of some SDs was smaller than the symbol size; thus some bars do not appear in the figure

Effects of cetuximab and gefitinib treatment on the levels of total and phosphorylated EGFR and EGFR substrates in cell lines with wild-type and mutated EGFR

<p><b>Copyright information:</b></p><p>Taken from "Responses of cancer cells with wild-type or tyrosine kinase domain-mutated epidermal growth factor receptor (EGFR) to EGFR-targeted therapy are linked to downregulation of hypoxia-inducible factor-1α"</p><p>http://www.molecular-cancer.com/content/6/1/63</p><p>Molecular Cancer 2007;6():63-63.</p><p>Published online 11 Oct 2007</p><p>PMCID:PMC2117021.</p><p></p> Cells from the indicated lines were simultaneously switched to a culture medium containing 0.5% FBS and were either left untreated or treated with cetuximab (2 and 10 nM), vehicle, or gefitinib (0.1 and 0.5 μM) overnight (16 hours). A master medium containing either cetuximab or gefitinib was used in all cell lines. After treatment, the cells were lysed, and equal amounts of cell lysates were subjected to Western blot analysis using antibodies directed against total and phosphorylated EGFR (Y-1068) () and antibodies directed against phosphorylated ERK, Akt, and STAT3 as indicated (). The levels of β-actin and total ERK served as internal controls for equal protein loading in each lane in () and (), respectively. The numeric values under each gel were derived from a densitometric analysis of the signals