Cardiovascular Risk and Cardiovascular Events in Patients With Chronic Myeloid Leukemia Treated With Tyrosine Kinase Inhibitors

Background

Cardiovascular events (CVEs) have been observed in patients with chronic myeloid leukemia treated with second-generation tyrosine kinase inhibitors.

Do smokers have a different gingival crevicular fluid cytokine/chemokine profile than nonsmokers in clinically healthy periodontal sites? A systematic review and meta-analysis

Clinical Oral Investigations - Assessing the evidence and comparing the levels of cytokines in gingival crevicular fluid (GCF) of periodontal healthy sites of smokers and nonsmokers. Seven...     

Niacin inhibits carrageenan-induced neutrophil migration in mice

Several emerging lines of evidence support an anti-inflammatory role for nicotinic acid (niacin); however, its role in the regulation of leukocyte migration in response to inflammatory stimuli has not been elucidated until now. Herein, we have examined the effect of nicotinic acid on neutrophil recruitment in experimentally induced inflammation. We demonstrated that nicotinic acid treatment inhibited interleukin (IL)-8-induced, leukotriene (LT)B₄-induced, and carrageenan-induced neutrophil migration into the pleural cavity of BALB/c mice and reduced neutrophil rolling and adherence in a mouse cremaster muscle preparation. Surprisingly, nicotinic acid treatment increased the level of the neutrophil chemoattractant KC in response to carrageenan. These results suggest that nicotinic acid plays an important role in the regulation of inflammation due to its ability to inhibit the actions of the neutrophil chemoattractants IL-8 and LTB₄. Further inhibition of chemoattractants leads to impairment of leukocyte rolling and adherence to the vascular endothelium in the microcirculation of inflamed tissues.     

Behavior of two Leishmania infantum strains—evaluation of susceptibility to antimonials and expression of microRNAs in experimentally infected J774 macrophages and in BALB/c mice

Parasitology Research - Strains of the same Leishmania parasite species, isolated from different host organisms, may exhibit unique infection profiles and induce a change in the expression of...     

Fluoride toothpaste supplemented with sodium hexametaphosphate reduces enamel demineralization in vitro

Objective

The aim of this study was to evaluate the effect of fluoride dentifrices combined with sodium hexametaphosphate (HMP) on enamel demineralization in vitro.

Material and methods

Enamel bovine blocks were selected by initial surface hardness (SHi) and then divided into five experimental groups (n?=?12): placebo (without fluoride and without HMP); 1100 ppm F (1100F); and 1100F associated with HMP at 0.5 % (1100HMP0.5%), 1 % (1100HMP1%), and 2 % of HMP (1100HMP2%). Blocks were submitted to five pH cycles (demineralizing/remineralizing solutions) at 37 °C. After pH cycling, final surface hardness (SHf), percentage of surface hardness loss (%SH), integrated differential hardness (ΔIH), integrated loss of subsurface hardness (ΔKHN), and enamel firmly bound fluoride (F) were determined. Data were submitted to one-way ANOVA, followed by Student–Newman–Keuls test (p?<?0.05).

Results

Significant differences were observed among all groups regarding %SH and ΔKHN. 1100HMP1% promoted the lowest mineral loss among all groups (p?<?0.001), and led to significantly lower demineralization in the deeper regions of the subsurface lesion when compared with the other HMP-containing toothpastes (p?<?0.001). Significantly higher mineral loss was observed for 1100HMP2% when compared to the other fluoridated dentifrices, mainly in the outer part of the lesion (p?<?0.001). Enamel F uptake was similar for 1100F and 1100HMP1% but significantly reduced for other HMP concentrations.

Conclusion

The supplementation of a 1100-ppm F dentifrice with 1 % HMP promoted a higher inhibitory effect against enamel demineralization when compared to a dentifrice containing the same amount of fluoride in vitro.

Clinical relevance

This dentifrice could potentially be indicated to patients at high risk of caries.

     

Evaluation of the toxic and genotoxic potential of landfill leachates using bioassays

Landfill leachates are liquid effluents with elevated concentrations of chemical compounds that can cause serious environmental pollution. In the south of the state of Santa Catarina, Brazil, a sanitary landfill was installed that employs a system of anaerobic/facultative lagoons for the treatment of its leachate. The present work examined the toxic and genotoxic potential of untreated and treated landfill leachates using bioassays. The chemical, toxic, genotoxic and mutagenic properties of the untreated leachate and the treated leachate were determined. Examination of the chemical properties showed a marked decrease in parameters after treatment, as well as in toxicity towards all the organisms tested. The results of the comet assay demonstrated that both leachates showed genotoxicity in all of the organisms tested, indicating the persistence of genotoxic substances even after treatment. A significant decrease in micronucleated cells was detected in Geophagus brasiliensis exposed to the treated leachate compared to untreated.     

The phthalimide analogues N-3-hydroxypropylphthalimide and N-carboxymethyl-3-nitrophthalimide exhibit activity in experimental models of inflammatory and neuropathic pain

BackgroundPhthalimide analogues devoid of the glutarimide moiety exhibit multiple biological activities, thus making them candidates for the treatment of patients with different diseases, including those with inflammatory and painful disorders. In the present study, the activities of five phthalimide analogues devoid of the glutarimide moiety (N-hydroxyphthalimide, N-hydroxymethylphthalimide, N-3-hydroxypropylphthalimide, N-carboxy-3-methylphthalimide, N-carboxymethyl-3-nitrophthalimide) were evaluated in experimental models of acute and chronic inflammatory and neuropathic pain.MethodsThe phthalimide analogues were administered per os (po) in Swiss mice or Wistar rats. Nociceptive response induced by formaldehyde and mechanical allodynia induced by chronic constriction injury (CCI) of the sciatic nerve or intraplantar (ipl) injection of complete Freund’s adjuvant (CFA) were used as experimental models of pain.ResultsN-carboxymethyl-3-nitrophthalimide (700 mg/kg, -1 h) inhibited the second phase of the nociceptive response induced by the intraplantar injection of formaldehyde in mice. N-3-hidroxypropylphthalimide (546 mg/kg, -1 h) inhibited both phases of the nociceptive response induced by formaldehyde. Treatment of rats with N-carboxymethyl-3-nitrophthalimide (700 mg/kg) or N-3-hydroxypropylphthalimide (546 mg/kg) inhibited the mechanical allodynia induced by CCI of the sciatic nerve or ipl injection of CFA in rats. Intraperitoneal administration of the opioid antagonist naltrexone (10 mg/kg, -1.5 h) attenuated the antinociceptive activity of N-carboxymethyl-3-nitrophthalimide (700 mg/kg) in the model of nociceptive response induced by formaldehyde.ConclusionsN-3-hydroxypropylphthalimide and N-carboxymethyl-3-nitrophthalimide, two phthalimide analogues devoid of the glutarimide moiety, exhibited activities in different experimental models of pain, including models of chronic inflammatory and neuropathic pain.     

Cognitive impairment in antiphospholipid syndrome: evidence from animal models

Although antiphospholipid syndrome (APS) is a multisystem prothrombotic condition, its inflammatory nature has been increasingly recognized in recent years. Stroke and transitory ischemic attacks are the neurological manifestations included in APS criteria, however many other neurological involvements have been attributed to antiphospholipid antibodies (aPL), such as seizures, transverse myelitis, and cognitive impairment. In this article we will review evidence from animal model that explain the role of aPL in cognition.