Cellular and Molecular Medicine

Cardiovascular disease has become the main factor of death and birth defects in the world and also in Iran. New clinical studies have shown that early diagnosis of patients with coronary artery disease (CAD) can contribute to effective prevention or therapeutic structures, which reduce mortality or the next chance of cardiovascular events, and increase the quality of life. Most studies on CAD disease and its genetic risk factors so far, have been done excluding the Iranian population. PubMed was used to search for all relevant studies published on or before 2013 and rs3184504 was selected for association study for CAD. A total of 200 subjects with 100 cases and 100 controls were ultimately included in the analysis. Blood samples were collected and after DNA extraction the DNA analysis was performed by TaqMan Probe Real Time PCR to evaluate the association between candidate variant with the disease and some blood biochemical factors. Our study demonstrated that there was not a direct...

Familial adenomatous polyposis (FAP) is responsible for <1% of colorectal cancer (CRC) cases and is inherited an autosomal dominant trait. Patients generally present hundreds to thousands of adenomas and develop colorectal cancer by age 35- 40 if left untreated. Here we report four patients with germline frameshift mutation (small deletion) at exon 15 of adenomatous polyposis coli (APC) tumor suppressor gene. Peripheral blood samples were collected from patients and Exon 15 of the APC gene was studied by direct sequencing after genomic DNA extraction. Four frameshift mutations were detected. Two patients had 5 bp deletion, c.3927_3931delAAAGA and two siblings presented deletion at codon 849 (c.2547_2548delTA p.Asp849fsX62). This study was the first report of genetic screening in Iranian FAP patients. In contrast to other studies we revealed that one patient with mutation at codon 1309 had an attenuated phenotype.

Removing the bacteria, including Enterococcus faecalis, from the root canal is one of the important aims in endodontic treatment.We aimed to compare the antibacterial activity of Chlorhexidine with two natural drugs. The antibacterial activities of three different propolis extracts (alcohol concentrations: 0, 15, 40%) and Aloe vera gel on E. faecalis were compared using three methods: disk diffusion, microdilution and direct contact test. In addition to the above bacterium, the Aloe vera gel effect on Staphylococcus aureus and Streptococcus mutans was evaluated. Disk diffusion test revealed that propolis ethanolic extracts (the alcohol concentration of 15 and 40%) and Aloe vera gel have antibacterial activities but aqueous extract of propolis did not show any effect in this test. The MICs for propolis ethanolic extracts, Aloe vera gel and aqueous extract of propolis (0% alcohol) were 313 µg/ml, 750 µg/ml, 2250 µg/ml, and ≥ 500 µg/ml respectively, much higher than the Chlorhexidine o...

• Introduction• Reperfusion injury- Causes of reperfusion injury- Effects of reperfusion injury• Definition of postconditioning- Postconditioning algorithm• Protective effects of postconditioning- Infarct size reduction- Reduction of apoptosis- Reduction in endothelial dysfunction- Reduction in endothelial activation, and neutrophil adherence- Reduction of stunning- Anti-arrhythmic effects• Potentiality of postconditioning- Remote postconditioning- Pharmacological postconditioning- Postconditioning the human heart- Postconditioning in diseased hearts• Mechanisms involved in postconditioning- Passive mechanisms- Mechanical mechanisms- Cellular mechanisms- Active mechanisms (intramyocardiocyte mechanisms)- Triggers- Mediators- End effectors- Cardioprotection by pre- and post-conditioning is redox-sensitive• Conclusions• Introduction• Reperfusion injury- Causes of reperfusion injury- Effects of reperfusion injury• Definition of postconditioning- Postconditioning algorithm• Protective effects of postconditioning- Infarct size reduction- Reduction of apoptosis- Reduction in endothelial dysfunction- Reduction in endothelial activation, and neutrophil adherence- Reduction of stunning- Anti-arrhythmic effects• Potentiality of postconditioning- Remote postconditioning- Pharmacological postconditioning- Postconditioning the human heart- Postconditioning in diseased hearts• Mechanisms involved in postconditioning- Passive mechanisms- Mechanical mechanisms- Cellular mechanisms- Active mechanisms (intramyocardiocyte mechanisms)- Triggers- Mediators- End effectors- Cardioprotection by pre- and post-conditioning is redox-sensitive• ConclusionsIntroductionReperfusion injury- Causes of reperfusion injury- Effects of reperfusion injuryCauses of reperfusion injuryEffects of reperfusion injuryDefinition of postconditioning- Postconditioning algorithmPostconditioning algorithmProtective effects of postconditioning- Infarct size reduction- Reduction of apoptosis- Reduction in endothelial dysfunction- Reduction in endothelial activation, and neutrophil adherence- Reduction of stunning- Anti-arrhythmic effectsInfarct size reductionReduction of apoptosisReduction in endothelial dysfunctionReduction in endothelial activation, and neutrophil adherenceReduction of stunningAnti-arrhythmic effectsPotentiality of postconditioning- Remote postconditioning- Pharmacological postconditioning- Postconditioning the human heart- Postconditioning in diseased heartsRemote postconditioningPharmacological postconditioningPostconditioning the human heartPostconditioning in diseased heartsMechanisms involved in postconditioning- Passive mechanisms- Mechanical mechanisms- Cellular mechanisms- Active mechanisms (intramyocardiocyte mechanisms)- Triggers- Mediators- End effectors- Cardioprotection by pre- and post-conditioning is redox-sensitivePassive mechanismsMechanical mechanismsCellular mechanismsActive mechanisms (intramyocardiocyte mechanisms)TriggersMediatorsEnd effectorsCardioprotection by pre- and post-conditioning is redox-sensitiveConclusionsAbstractIschaemic preconditioning limits the damage induced by subsequent ischaemia/reperfusion (I/R). However, preconditioning is of little practical use as the onset of an infarction is usually unpredictable. Recently, it has been shown that the heart can be protected against the extension of I/R injury if brief (10–30 sec.) coronary occlusions are performed just at the beginning of the reperfusion. This procedure has been called postconditioning (PostC). It can also be elicited at a distant organ, termed remote PostC, by intermittent pacing (dyssynchrony-induced PostC) and by pharmacological interventions, that is pharmacological PostC. In particular, brief applications of intermittent bradykinin or diazoxide at the beginning of reperfusion reproduce PostC protection. PostC reduces the reperfusion-induced injury, blunts oxidant-mediated damages and attenuates the local inflammatory response to reperfusion. PostC induces a reduction of infarct size, apoptosis, endothelial dysfunction and activation, neutrophil adherence and arrhythmias. Whether it reduces stunning is not clear yet. Similar to preconditioning, PostC triggers signalling pathways and activates effectors implicated in other cardioprotective manoeuvres. Adenosine and bradykinin are involved in PostC triggering. PostC triggers survival kinases (RISK), including A t and extracellular signal-regulated kinase (ERK). Nitric oxide, via nitric oxide synthase and non-enzymatic production, cyclic guanosine monophosphate (cGMP) and protein kinases G (PKG) participate in PostC. PostC-induced protection also involves an early redox-sensitive mechanism, and mitochondrial adenosine-5′ -triphosphate (ATP)-sensitive K+ and PKC activation. Protective pathways activated by PostC appear to converge on mitochondrial permeability transition pores, which are inhibited by acidosis and glycogen synthase kinase-3β (GSK-3β). In conclusion, the first minutes of reperfusion represent a window of opportunity for triggering the aforementioned mediators which will in concert lead to protection against reperfusion injury. Pharmacological PostC and possibly remote PostC may have a promising future in clinical scenario.Ischaemic preconditioning limits the damage induced by subsequent ischaemia/reperfusion (I/R). However, preconditioning is of little practical use as the onset of an infarction is usually unpredictable. Recently, it has been shown that the heart can be protected against the extension of I/R injury if brief (10–30 sec.) coronary occlusions are performed just at the beginning of the reperfusion. This procedure has been called postconditioning (PostC). It can also be elicited at a distant organ, termed remote PostC, by intermittent pacing (dyssynchrony-induced PostC) and by pharmacological interventions, that is pharmacological PostC. In particular, brief applications of intermittent bradykinin or diazoxide at the beginning of reperfusion reproduce PostC protection. PostC reduces the reperfusion-induced injury, blunts oxidant-mediated damages and attenuates the local inflammatory response to reperfusion. PostC induces a reduction of infarct size, apoptosis, endothelial dysfunction and activation, neutrophil adherence and arrhythmias. Whether it reduces stunning is not clear yet. Similar to preconditioning, PostC triggers signalling pathways and activates effectors implicated in other cardioprotective manoeuvres. Adenosine and bradykinin are involved in PostC triggering. PostC triggers survival kinases (RISK), including A t and extracellular signal-regulated kinase (ERK). Nitric oxide, via nitric oxide synthase and non-enzymatic production, cyclic guanosine monophosphate (cGMP) and protein kinases G (PKG) participate in PostC. PostC-induced protection also involves an early redox-sensitive mechanism, and mitochondrial adenosine-5′ -triphosphate (ATP)-sensitive K+ and PKC activation. Protective pathways activated by PostC appear to converge on mitochondrial permeability transition pores, which are inhibited by acidosis and glycogen synthase kinase-3β (GSK-3β). In conclusion, the first minutes of reperfusion represent a window of opportunity for triggering the aforementioned mediators which will in concert lead to protection against reperfusion injury. Pharmacological PostC and possibly remote PostC may have a promising future in clinical scenario.