Acute Ethanol Exposure Suppresses the Repair of O6-Methylguanine DNA Lesions in Castrated Adult Male Rats

Alcohol has clearly been associated with an increase of cancers in numerous tissues, including the respiratory tract, colon, rectum, liver, but especially the esophagus, larynx, pharynx, and mouth. Alcohol alone has not been shown to be a mutagen until it is converted to acetaldehyde and, therefore, alcohol presumably acts as a cocarcinogen. Previous data has shown that alcohol concentrations of 2% or greater inhibits DNA repair, and in light of the widespread consumption of alcoholic beverages with alcohol contents ranging from 4 to 5% (beer and wine coolers) to 50% (whiskey), interest in determining the mechanism(s) responsible for alcohol-induced carcinogenesis has heightened. Although previous studies, in intact rats, have investigated the effects of chronic alcohol exposure on some aspects of DNA repair, we have begun to address the effects of acute or "binge" alcohol exposure on mammalian DNA repair. Toward this end, we report the inhibition of O⁶-methylguanine-DNA methyltransferase (MGMT) by a single intraperitoneal injection of 30% ethanol in adult male castrated rats. This inhibition lasted for at least 24 hr. We also observed a dose-response effect of ethanol on MGMT activity, again only in the castrated rats. The finding of ethanol's effect on MGMT activity in castrated and not intact rats implies a hormonal component of MGMT DNA repair response, which has only been alluded to in past research.     

Phosphorylative respiratory activity of mitochondria isolated from the left and right ventricles of rabbit hearts following partial pulmonary trunk occlusion

Right ventricular hypertrophy was produced by placing a spiral Monel metal clip around the pulmonary trunks of rabbits causing a sustained 67% occlusion of the vessel. The operation produced a doubling of right ventricular weight, by 13 days post-surgery, which persisted throughout the post-operative period studied (13 to 84 days); only a slight increase in left ventricular free wall weight was observed. Isolated mitochondria exhibited region-specific changes with time in state 3 Qo₂. Thirteen days after operation, the state 3 Qo₂ of right ventricular mitochondria was depressed to about 85% of controls. Thereafter, respiration increased fairly sharply, peaking at just above control values by 40 days post-operation. Finally, it declined abruptly to about 70% of controls by 84 days. A very different pattern of change was observed when left ventricular mitochondrial respiratory activities were examined. Thirteen days after the operation, state 3 Qo₂ was elevated somewhat above controls. Thereafter, it declined linearly and gradually, dropping to about 85% of controls by 84 days.     

Effect of glucagon on cardiac conduction in man

His bundle electrograms were obtained in 26 patients before and after intravenous administration of glucagon (50 μg/kg). The group consisted of 4 patients with normal conduction and 22 patients with conduction disease. The P-A interval, measured in all patients, was 35 ± 1.4 msec (mean ± standard error of the mean) before and 30 ± 1.5 msec after infusion of glucagon (P < 0.001). The mean A-H interval during sinus rhythm in all patients and during pacing at 100/min in 21 patients was, respectively, 97 ± 6.0 msec and 114 ± 6.4 msec before, and 96 ± 6.0 msec and 114 ± 6.6 msec after infusion of glucagon (not significant). The mean H-V interval in 25 patients was 48 ± 2.6 msec before and 49 ± 2.0 msec after infusion of glucagon (not significant). The mean sinus rate and sinus recovery times were, respectively, 73 ± 3.0 beats/min and 1,025 ± 42.0 msec before and 81 ± 3.0 beats/min and 919 ± 27.0 msec after infusion of glucagon (P < 0.001 and < 0.01). Functional and effective refractory periods were measured (In milliseconds) with use of the atrial extrastimulus technique. The mean atrial functional and effective refractory periods (21 patients) were, respectively, 273 ± 11.6 and 252 ± 12.0 before and 256 ± 10.0 and 238 ± 9.6 after infusion of glucagon (P < 0.001 and < 0.01). Mean atrloventricular (A-V) nodal functional refractory period (22 patients) and effective refractory period (15 patients) were 465 ± 22.0 and 404 ± 33.0 before and 457 ± 23.0 and 395 ± 32.0 after the infusion (not significant). The mean effective refractory period of the His-Purkinje system (2 patients) was 440 ± 45.0 before and 425 ± 55.0 after infusion of glucagon (not significant).In summary, glucagon increased sinus nodal automaticity, as manifested by an increase in sinus rate and decrease of sinus nodal recovery time, and improved intraatrial conduction as manifested by a reduction of the P-A interval and atrial functional and effective refractory periods. Glucagon had no effect on A-V nodal or intraventricular conduction.     

Prevention of atherosclerosis

Primary prevention instituted early in life offers the most promising opportunity to affect morbidity and mortality of atherosclerosis. This conclusion is inevitable because of the sudden catastrophic nature of the first event in many patients and the demonstration of advanced pathologic changes in those who are symptomatic. There is little evidence that advanced lesions regress.A prerequisite to the achievement of the goal of primary prevention is the training of “preventive cardiologists” dedicated to accumulating new data and utilizing information now available for the design and implementation of such programs in the young. A scientific approach to primary prevention requires documentation of the basic mechanism of the cause and progression of plaque formation. This information is not presently available. However, it is now possible to identify children at high risk of premature development of complication of the disease utilizing known risk factors and their tendency to familial aggregation. A plan for identification and management of such children is outlined. As new data become available one can anticipate changes in methods of detection and management with a view toward improving results in primary prevention.     

Improved bone regeneration through amniotic membrane loaded with buccal fat pad-derived MSCs as an adjuvant in maxillomandibular reconstruction

BackgroundHuman amniotic membranes (HAMs), as a biological membrane with healing, osteogenic, and cell therapy potential, has been in the spotlight to enhance the outcomes of treating bone defects. Present study aims to clinically assess the potential of HAM loaded with buccal fat pad-derived stem cells (BFSCs) as an osteogenic coverage for onlay bone grafts to maxillomandibular bone defects.Materials and methodsNine patients with jaw bone defects were enrolled in the present study. The patients were allocated to two study groups: Iliac crest bone graft with HAM coverage (n = 5), and Iliac bone grafts covered with HAM loaded with BFSCs (n = 4). Five months following the grafting and prior to implant placement, cone beam computed tomography was performed for radiomorphometric analysis.ResultsThe mean increase in bone width was found to be significantly greater in the HAM + BFSCs group (4.42 ± 1.03 mm versus 3.07 ± 0.73 mm, p < 0.05). Further, the changes in vertical dimension were greater in the HAM + BFSCs group (4.66 ± 1.06 mm versus 4.14 ± 1.03 mm, p > 0.05).ConclusionCombined use of HAM with mesenchymal stem cells may enhance bone regeneration specifically in the horizontal dimension. Moreover, this methodology reduces the amount of harvested autogenous bone and diminish secondary bone resorption.     

Industrial separation of oxygen isotopes by oxygen distillation

¹⁸O‐labeled water (Water‐¹⁸O) is a widely used starting material of ¹⁸F‐labeled diagnostic agents in positron emission tomography (PET). Conventionally, Water‐¹⁸O has been separated from other stable oxygen isotope species (¹⁶O, ¹⁷O) by water distillation or nitric oxide distillation. However, conventional methods are costly and may have safety issues. In 2004, we developed the first unit of our novel oxygen isotope separation process by cryogenic oxygen distillation to overcome these issues. To meet the needs of the market, we built a second unit in 2013 and a third in 2016. We are now operating three commercially viable separation units with a total capacity of 600 kg of Water‐¹⁸O per year.     

Catechol‐O‐methyltransferase gene val158met polymorphism and depressive symptoms during early childhood

Catechol‐O‐Methyltransferase (COMT) is a critical regulator of catecholamine levels in the brain. A functional polymorphism of the COMT gene, val158met, has been linked to internalizing symptoms (i.e., depression and anxiety) in adolescents and adults. We extended this research by investigating whether the val158met polymorphism was associated with childhood symptoms of depression and anxiety in two independent samples of young children (Ns = 476 and 409). In both samples, preschool‐aged children were genotyped for the COMT val158met polymorphism. Symptoms of psychopathology were assessed via parent interviews and primary caregiver reports. In both samples, children homozygous for the val allele had higher levels of depressive symptoms compared to children with at least one copy of the met allele. Our findings extend previous research in older participants by showing links between the COMT val158met polymorphism and internalizing symptoms in early childhood. © 2013 Wiley Periodicals, Inc.     

Photodynamic therapy effect on cell growth inhibition induced by Radachlorin and toluidine blue O on Staphylococcus aureus and Escherichia coli: An in vitro study

IntroductionPhotodynamic therapy is an innovative treatment modality, which is appropriate for tumor detection and for the treatment of cancer as well as nontumoral diseases, such as psoriasis (2), bacterial and viral eradication.Material and methodEffect of two photosensitizer (toluidine blue O (TBO) and Radachlorin was investigated on Staphylococcus Aureus ATCC 25923 (American Type Culture Collection) and Escherichia coli (ATCC 25922).ResultsPDI by TBO caused S. aureus 5.83 log10 killing (P.Value < 0.0001) and reduce 0.08 log 10 in E. coli (P.Value = 0.321). PDI by Radachlorin^® reduce 0.17 log 10 in E. coli (P.Value < 0.0001) and S. aureus showed 6.1 log 10 colony count reduction.ConclusionWithin the limitation of this in vitro study, we can conclude that both PS have the same effect on S. aureus and E. coli with good inhibition effect on S. aureus and partial inhibition effect E. coli.