Cobalt–carbon/silica nanocomposites prepared by pyrolysis of a cobalt 2,2′-bipyridine terephthalate complex for remediation of cationic dyes

Recently, carbon nanostructures have attracted interest because of their unique properties and interesting applications. Here, CoC@SiO₂-850 (3) and CoC@SiO₂-600 (4) cobalt–carbon/silica nanocomposites were prepared by solid-state pyrolysis of anthracene with Co(tph)(2,2′-bipy)·4H₂O (1) complex in the presence of silica at 850 and 600 °C, respectively, where 2,2′-bipy is 2,2′-bipyridine and tph is the terephthalate dianion. Moreover, Co(μ-tph)(2,2′-bipy) (2) was isolated and its X-ray structure indicated that cobalt(ii) has a distorted trigonal prismatic coordination geometry. 2 is a metal–organic framework consisting of one-dimensional zigzag chains within a porous grid network. 3 and 4 consist of cobalt(0)/cobalt oxide nanoparticles with a graphitic shell and carbon nanotubes embedded in the silica matrix. They were characterized by scanning electron microscopy (SEM), transmission electron microscopy (TEM), powder X-ray diffraction (XRD), Brunauer–Emmett–Teller (BET), Raman spectroscopy, and X-ray photoelectron spectroscopy (XPS). XPS revealed that the nanocomposites are functionalized with oxygen-containing groups, such as carboxylic acid groups. In addition, the presence of metallic cobalt nanoparticles embedded in graphitized carbon was verified by XRD and TEM. The efficiency of 3 for adsorption of crystal violet (CV) dye was investigated by batch and column experiments. At 25 °C, the Langmuir adsorption capacity of 3 for CV was 214.2 mg g⁻¹ and the fixed-bed column capacity was 36.3 mg g⁻¹. The adsorption data were well fitted by the Freundlich isotherm and pseudo-second-order kinetic model. The adsorption process was spontaneous and endothermic.

A cobalt–carbon@silica nanocomposite was synthesized from a cobalt 2,2′-bipyridine terephthalate complex and its adsorption behavior towards crystal violet dye was tested using batch and column techniques.     

Antitumour activity of rhinacanthone against Dalton's ascitic lymphoma

The antitumour activity of Rhinacanthone (3,4-dihydro-3,3-dimethyl-2H-naphtho-[1,2-B] pyran-5,6-dione) has been evaluated against Dalton's ascitic lymphoma (DAL) in Swiss albino mice. A significant enhancement of mean survival time of tumour bearing mice and peritoneal cell count in normal mice was observed with respect to the control group. When these Rhinacanthone treated animals underwent i.p. inoculation with DAL cells, tumour cell growth was found to be inhibited. After 14 d of inoculation, Rhinacanthone was able to reverse the changes in the haemotological parameters, protein and packed cellular volume consequent to tumour inoculation.     

Synthesis of novel 3-butyl-2-substituted amino-3H-quinazolin-4-ones as analgesic and anti-inflammatory agents

A variety of novel 3-butyl-2-substituted amino-3H-quinazolin-4-ones were synthesized by reacting the amino group of 3-butyl-2-hydrazino-3H-quinazolin-4-one with various aldehydes and ketones. The title compounds were investigated for analgesic, anti-inflammatory and ulcerogenic index activities. The compound 3-butyl-2-(1-methylbutylidene-hydrazino)-3H-quinazolin-4-one (AS3) emerged as the most active analgesic agent. Compound 3-butyl-2-(1-ethylpropylidene-hydrazino)-3H-quinazolin-4-one (AS2) emerged as the most active anti-inflammatory agent and is moderately more potent when compared to the reference standard diclofenac sodium. Interestingly, the test compounds showed only mild ulcerogenic potential when compared to aspirin.     

Survivin deficiency leads to imparalization of cytokinesis in cancer cells

Background: Survivin has been implicated in cancer progression and is known to be over-expressed in a variety of human malignancies. Positive regulation of survivin expression provides a connecting link between cell cycle and tumorigenesis or perhaps tumour maintenance. Methods: An experiment was designed to analyse survivin expression in cell lines (MCF 7, Zr751, A549, HepG2) using SDS-PAGE, Western blots, RT-PCR, AGE and heamatoxylin-eosin staining were done. Results: SDS-PAGE revealed the presence of 16.5 kDa protein. Subsequent western Blot and cytological analysis showed down-regulation of survivin expression in cancer cells. Conclusion: Therefore, the study allows the conclusion that survivin is essential for proper chromosome segregation and cytokinesis. It seems reasonable to suspect that abnormal expression or function of survivin might contribute to multinucleated and apoptotic conditions.     

Selective activation of angiotensin AT2 receptors attenuates progression of pulmonary hypertension and inhibits cardiopulmonary fibrosis

Background and Purpose

Pulmonary hypertension (PH) is a devastating disease characterized by increased pulmonary arterial pressure, which progressively leads to right-heart failure and death. A dys-regulated renin angiotensin system (RAS) has been implicated in the development and progression of PH. However, the role of the angiotensin AT₂ receptor in PH has not been fully elucidated. We have taken advantage of a recently identified non-peptide AT₂ receptor agonist, Compound 21 (C21), to investigate its effects on the well-established monocrotaline (MCT) rat model of PH.

Experimental Approach

A single s.c. injection of MCT (50 mg·kg⁻¹) was used to induce PH in 8-week-old male Sprague Dawley rats. After 2 weeks of MCT administration, a subset of animals began receiving either 0.03 mg·kg⁻¹ C21, 3 mg·kg⁻¹ PD-123319 or 0.5 mg·kg⁻¹ A779 for an additional 2 weeks, after which right ventricular haemodynamic parameters were measured and tissues were collected for gene expression and histological analyses.

Key Results

Initiation of C21 treatment significantly attenuated much of the pathophysiology associated with MCT-induced PH. Most notably, C21 reversed pulmonary fibrosis and prevented right ventricular fibrosis. These beneficial effects were associated with improvement in right heart function, decreased pulmonary vessel wall thickness, reduced pro-inflammatory cytokines and favourable modulation of the lung RAS. Conversely, co-administration of the AT₂ receptor antagonist, PD-123319, or the Mas antagonist, A779, abolished the protective actions of C21.

Conclusions and Implications

Taken together, our results suggest that the AT₂ receptor agonist, C21, may hold promise for patients with PH.     

Synthesis, analgesic, anti-inflammatory, ulcerogenic index and antibacterial activities of novel 2-methylthio-3-substituted-5,6,7,8-tetrahydrobenzo (b) thieno[2,3-d]pyrimidin-4(3H)-ones

A variety of novel 2-methylthio-3-substituted-5,6,7,8-tetrahydrobenzo (b) thieno[2,3-d]pyrimidin-4(3H)-ones have been synthesized by reacting (2-methylthio-4-oxo-3H-5,6,7,8-tetrahydrobenzo (b) thieno[2,3-d]pyrimidin-3-yl)dithiocarbamic acid methyl ester (5) with a variety of amines. The starting material dithiocarbamate (5) was synthesized from 2-amino-3-carbethoxy-4,5,6,7-tetrahydrobenzo (b) thiophene (1) by a novel innovative route. The title compounds were investigated for analgesic, anti-inflammatory, ulcerogenicity index and antibacterial activities. While the test compounds exhibited significant activity, the compounds 1-methyl-3-(2-methylthio-4-oxo-3H-5,6,7,8-tetrahydrobenzo (b) thieno[2,3-d]pyrimidin-3-yl)thiourea (A1), 1-dimethyl-3-(2-methylthio-4-oxo-3H-5,6,7,8-tetrahydrobenzo (b) thieno[2,3-d]pyrimidin-3-yl)thiourea (A2), 1-diethyl-3-(2-methylthio-4-oxo-3H-5,6,7,8-tetrahydrobenzo (b) thieno[2,3-d]pyrimidin-3-yl)thiourea (A3) and 1-pyrrolidinyl-3-(2-methylthio-4-oxo-3H-5,6,7,8-tetrahydrobenzo (b) thieno[2,3-d]pyrimidin-3-yl)thiourea (A4) showed more potent analgesic activity and the compounds 1-dimethyl-3-(2-methylthio-4-oxo-3H-5,6,7,8-tetrahydrobenzo (b) thieno[2,3-d]pyrimidin-3-yl)thiourea (A2), 1-diethyl-3-(2-methylthio-4-oxo-3H-5,6,7,8-tetrahydrobenzo (b) thieno-[2,3-d]pyrimidin-3-yl)thiourea (A3) and 1-pyrrolidinyl-3-(2-methylthio-4-oxo-3H-5,6,7,8-tetrahydrobenzo (b) thieno[2,3-d] pyrimidin-3-yl)thiourea (A4) showed more potent anti-inflammatory activity than the reference standard diclofenac sodium.