Test of Perfomance ERK Hybrid Dryer with Biomass Furnace as Additional Heating System for Nutmeg Seed (Myristica SP.) Drying

Conventional drying depend on the weather. It was caused agricultural product damaged, and moldy attack. So we need hybrid dryer with a source of radiation and solar biomass to continuous drying and can be controlled.The aims of this research is test performance of ERK hybrid dryer to drying the nutmeg seed during the drying process. Experiments were conducted to determine the distribution of temperature in the dryer in condition with no material and material conditions. Input of energy derived from biomass combustion in the furnace (evening) and combination of biomass and radiation (during the day). Measurements of temperature and RH using a thermocouple CC and alcohol thermometer. Temperature and RH to be measured include temperature and RH in dryer with several measurement points representing the up, middle , bottom and inlet temperature, outlet temperature and ambient temperature measurements at intervals of 30 minutes. The results showed average temperature ranges between 42 ° C - 51 ° C and RH ranged between 50.96 % -55.65 % . Time of drying is used to dry nutmeg from the initial moisture content from 80.72 % wb to 9.67 % wb is 52 hours with an average drying rate is 7.8 % db / hour . The total energy used to heat and vaporize materials,water that is 290 499.9 kJ. Efficiency of drying system 8.63% and energy of drying required to water evaporated is 28520.62 kJ / kg. The result quality of product obtained color of nutmeg generally more uniform

Synthesis and bioevaluation of <i>N</i>,4-diaryl-1,3-thiazole-2-amines as tubulin inhibitors with potent antiproliferative activity - Fig 2

<p><b>Reagents and conditions.</b> (i) CS₂, Et₃N, Et₂O, 25°C; (ii) I₂, Et₃N, EtOAc, 0°C; (iii) NH₃·H₂O; (iv) CuBr₂, CHCl₃, EtOAc; (v) EtOH, MW 80°C; (vi) 1) CH₃I, DMF, 25°C or 2) Ac₂O, 50°C.</p

Effects of 10s on tubulin polymerization.

<p>Tubulin was pre-incubated for 1 min with <b>10s</b> at 2 μM, 10 μM, 25 μM and 50 μM, CA-4 at 0.5 μM, paclitaxel at 5 μM or vehicle DMSO (control) at room temperature before GTP was added to start the tubulin polymerization reactions. The reaction was monitored at 37°C.</p

Immunostaining of tubulin assembly in SGC-7901 cells.

<p>SGC-7901 cells were treated with <b>10s</b> (0.72 μM) for 48 h. Tubulin assembly was stained with FITC (left panel) and DAPI (middle panel). A merge of the two panels is shown on the right. Images were taken using a confocal microscope.</p

Antiproliferative activity of compounds 10a-v, CA-4 (2), Nocodazole (3) and SMART (5).

<p>Antiproliferative activity of compounds 10a-v, CA-4 (2), Nocodazole (3) and SMART (5).</p

We used a linear fitting curve to compare the predicted pIC50 values (modeled based on a known dataset of 21 defined compounds in SGC-7901 cells) with the experimental pIC50 values.

<p><i>y</i> = 0.992<i>x</i> + 0.007, <i>R</i> – <i>square</i> = 0.992.</p

Molecular structures of compounds 10a-v.

<p>Molecular structures of compounds 10a-v.</p

Synthesis and Bioevaluation of 3,6-Diaryl-[1,2,4]triazolo[4,3‑<i>b</i>] Pyridazines as Antitubulin Agents

A series of 3,6-diaryl-[1,2,4]­triazolo­[4,3-<i>b</i>]­pyridazines were designed as a class of vinylogous CA-4 analogues. The easily isomerized (<i>Z</i>,<i>E</i>)-butadiene linker of vinylogous CA-4 was replaced by a rigid [1,2,4]­triazolo­[4,3-<i>b</i>]­pyridazine scaffold. Twenty-one target compounds were synthesized and exhibited moderate to potent antiproliferative activity. The compound <b>4q</b> with a 3-amino-4-methoxyphenyl moiety as the B-ring, comparable to CA-4 (IC₅₀ = 0.009–0.012 μM), displayed the highly active antiproliferative activity against SGC-7901, A549, and HT-1080 cell lines with IC₅₀ values of 0.014, 0.008, and 0.012 μM, respectively. Tubulin polymerization experiments indicated that <b>4q</b> effectively inhibited tubulin polymerization, and immunostaining assay revealed that <b>4q</b> significantly disrupted tubulin microtubule dynamics. Moreover, cell cycle studies revealed that compound <b>4q</b> dramatically arrested cell cycle progression at G2/M phase in A549 cells. Molecular modeling studies showed that <b>4q</b> could bind to the colchicine binding site on microtubules

Novel Selective Estrogen Receptor Downregulators (SERDs) Developed against Treatment-Resistant Breast Cancer

Resistance to the selective estrogen receptor modulator tamoxifen and to aromatase inhibitors that lower circulating estradiol occurs in up to 50% of patients, generally leading to an endocrine-independent ER+ phenotype. Selective ER downregulators (SERDs) are able to ablate ER and thus, theoretically, to prevent survival of both endocrine-dependent and -independent ER+ tumors. The clinical SERD fulvestrant is hampered by intramuscular administration and undesirable pharmacokinetics. Novel SERDs were designed using the 6-OH-benzothiophene (BT) scaffold common to arzoxifene and raloxifene. Treatment-resistant (TR) ER+ cell lines (MCF-7:5C and MCF-7:TAM1) were used for optimization, followed by validation in the parent endocrine-dependent cell line (MCF-7:WS8), in 2D and 3D cultures, using ERα in-cell westerns, ERE-luciferase, and cell viability assays, with <b>2</b> (GDC-0810/ARN-810) used for comparison. Two BT SERDs with superior in vitro activity to <b>2</b> were studied for bioavailability and shown to cause regression of a TR, endocrine-independent ER+ xenograft superior to that with <b>2</b>

Interaction of oxidative stress and neurotrauma in ALDH2−/− mice causes significant and persistent behavioral and pro-inflammatory effects in a tractable model of mild traumatic brain injury

Oxidative stress induced by lipid peroxidation products (LPP) accompanies aging and has been hypothesized to exacerbate the secondary cascade in traumatic brain injury (TBI). Increased oxidative stress is a contributor to loss of neural reserve that defines the ability to maintain healthy cognitive function despite the accumulation of neuropathology. ALDH2-/- mice are unable to clear aldehyde LPP by mitochondrial aldehyde dehydrogenase-2 (Aldh2) detoxification and provide a model to study mild TBI (mTBI), therapeutic interventions, and underlying mechanisms. The ALDH2-/- mouse model presents with elevated LPP-mediated protein modification, lowered levels of PSD-95, PGC1-α, and SOD-1, and mild cognitive deficits from 4 months of age. LPP scavengers are neuroprotective in vitro and in ALDH2-/- mice restore cognitive performance. A single-hit, closed skull mTBI failed to elicit significant effects in WT mice; however, ALDH2-/- mice showed a significant inflammatory cytokine surge in the ipsilateral hemisphere 24 h post-mTBI, and increased GFAP cleavage, a biomarker for TBI. Known neuroprotective agents, were able to reverse the effects of mTBI. This new preclinical model of mTBI, incorporating significant perturbations in behavior, inflammation, and clinically relevant biomarkers, allows mechanistic study of the interaction of LPP and neurotrauma in loss of neural reserve