Application of Robotics in Orthodontics: A Systematic Review.

Robotics has various applications in dentistry, particularly in orthodontics, although the potential use of these technologies is not yet clear. This review aims to summarize the application of robotics in orthodontics and clarify its function and scope in clinical practice. Original articles addressing the application of robotics in any area of orthodontic practice were included, and review articles were excluded. PubMed, Google Scholar, Scopus, and DOAJ were searched from June to August 2023. The risk of bias was established using the risk of bias in non-randomized studies (ROBINS) and certainty assessment tools following the grading of recommendations, assessment, development, and evaluation (GRADE) guidelines. A narrative synthesis of the data was generated and presented according to its application in surgical and non-surgical orthodontics. The search retrieved 2,106 articles, of which 16 articles were selected for final data synthesis of research conducted between 2011 and 2023 in Asia, Europe, and North America. The application of robotics in surgical orthodontics helps guide orthognathic surgeries by reducing the margin of error, but it does not replace the work of a clinician. In non-surgical orthodontics, robotics assists in performing customized bending of orthodontic wires and simulating orthodontic movements, but its application is expensive. The articles collected for this synthesis exhibited a low risk of bias and high certainty, and the results indicated that the advantages of the application of robotics in orthodontics outweigh the disadvantages. This project was self-financed, and a previous protocol was registered at the PROSPERO site (registration number: CRD42023463531).

Colonic Electrical Stimulation for Chronic Constipation: A Perspective Review.

Chronic constipation affects around 20% of the population and there is no efficient solution. This perspective review explores the potential of colonic electric stimulation (CES) using neural implants and methods of bioelectronic medicine as a therapeutic way to treat chronic constipation. The review covers the neurophysiology of colonic peristaltic function, the pathophysiology of chronic constipation, the technical aspects of CES, including stimulation parameters, electrode placement, and neuromodulation target selection, as well as a comprehensive analysis of various animal models highlighting their advantages and limitations in elucidating the mechanistic insights and translational relevance for CES. Finally, the main challenges and trends in CES are discussed.

Stability and Reversible Oxidation of Sub-Nanometric Cu5 Metal Clusters: Integrated Experimental Study and Theoretical Modeling.

Sub-nanometer metal clusters have special physical and chemical properties, significantly different from those of nanoparticles. However, there is a major concern about their thermal stability and susceptibility to oxidation. In situ X-ray Absorption spectroscopy and Near Ambient Pressure X-ray Photoelectron spectroscopy results reveal that supported Cu5 clusters are resistant to irreversible oxidation at least up to 773 K, even in the presence of 0.15 mbar of oxygen. These experimental findings can be formally described by a theoretical model which combines dispersion-corrected DFT and first principles thermochemistry revealing that most of the adsorbed O2 molecules are transformed into superoxo and peroxo species by an interplay of collective charge transfer within the network of Cu atoms and large amplitude "breathing" motions. A chemical phase diagram for Cu oxidation states of the Cu5 -oxygen system is presented, clearly different from the already known bulk and nano-structured chemistry of Cu.

Ag5 nanoclusters with dual catalytic antiradical activities.

Silver nanoclusters of five atoms (Ag5) display outstanding catalytic activities for the deactivation of radicals. Using 2,2-diphenyl-1­picrylhydrazyl (DPPH) radical as a model system, we observed a fast radical reduction to DPPH anions using only [Ag5] 3 to 4 orders of magnitude less than [DPPH]. Moreover, nanoclusters remain stable at the end of the reaction, and can deactivate again DPPH radicals at the same rate, indicating that they act as anti-radical catalysts. The radical scavenger catalytic activity of Ag5 proceeds selectively through the oxidation of methanol (used to dissolve the radical) to formaldehyde, which is supported by DFT calculations. The obtained catalytic rate constants are almost 2 orders of magnitude higher than oxidases, and more than 4 orders of magnitude larger than graphene quantum dots. We also show that Ag5 not only catalyze the reduction of radicals but also their oxidation, promoting the inhibition of the autoxidation mechanisms of hydrocarbon polymers, which are very sensitive to the presence of radicals. For this purpose, thin films of two industrially relevant polymers (polyisoprene and acrylonitrile-butadienestyrene copolymer), were exposed to standard simulated photo-ageing conditions in the presence of Ag5. Using Attenuated Total Reflection-FTIR and DFT modeling we observed that, although Ag5 nanoclusters, with ≈ 15% surface coverage, do not totally inhibit the oxidation, they favour a decomposition that yields inactive products, in contrast with the more detrimental ketone formation pathway. These results not only open new possibilities for developing a post-process inhibition of polymer degradation, for which nowadays there are no efficient procedures, but also, they could be used as very efficient dual-redox catalytic radical scavengers for different industrial or biomedical purposes.

Binding of Al(iii) to synthetic RNA and metal-mediated strand aggregation.

Over the last few years, focused interest in aluminum has been heightened by recent studies regarding its health effects. Its possible relation with chronic diseases makes it convenient to address more in depth the reactivity of aluminum with biologically relevant molecules. The present work investigates the interaction of the aluminum ion with two synthetic RNAs, poly(rA) and poly(rU), through a detailed thermodynamic and kinetic study. The trivalent aluminum ion was kept in solution by complexation with the cacodylate anion, even at neutral pH, thus making the study with biological molecules feasible. The results obtained by spectrophotometry, circular dichroism, viscometry and thermal stability measurements indicate that aluminium strongly interacts with single and duplex RNA structures. The kinetic experiments point out that, even though cacodylate is required to keep the metal in solution, it actually inhibits the reaction of aluminum with RNA as it converts the metal into an unreactive dimer species. Notably, further interaction occurred in an excess of the aluminum/cacodylate complex, inducing aggregation of single-stranded RNAs. An analysis of the kinetic data has shown that the modes of aggregation of the two RNAs differ and such a difference can be ascribed to the diverse polynucleotide secondary structures. The observed stabilization of multiple-stranded systems by aluminum can serve as a model for future studies due to the interest aroused by this metal in the study of non-canonical nucleic acid structures.

Interstrand DNA covalent binding of two dinuclear Ru(ii) complexes. Influence of the extra ring of the bridging ligand on the DNA interaction and cytotoxic activity.

In this work, we report experimental and computational evidence for the intercalation into the DNA base-pairs of the free quinones quinizarin (Q) and naphthazarin (N) and the interstrand covalent binding of their p-cymene di-ruthenium(ii) complexes (Cl2Ru2X, with X = N, Q bridging ligands). The intercalation extent for the N complex was larger than that for Q, which is in good agreement with the higher relative contour length and melting temperature for the same CX/CDNA ratio and with the computational mean stacking distances between the ligand and the nearest base-pair (3.34 Å and 3.19 Å) for N and Q, respectively. However, the apparent binding constant of Q/DNA, two orders higher than that of N/DNA, indicates that the thermal stability of the X/DNA complex is more related to the degree of intercalation than to the magnitude of the binding constant. Cl2Ru2X complexes undergo aquation, forming the aqua-derivatives [(H2O)2Ru2X]2+. These can further bind covalently to DNA via interstrand crosslinking, through both Ru centres and two N7 sites of consecutive guanines, to give (DNA1,2)Ru2X complexes, by a mechanism similar to that of cisplatin. To the best of our knowledge, this type of interaction with dinuclear Ru(ii) complexes has not been reported hitherto. The experimental and computational results reveal that the number of rings of the aromatic moiety and the covalent binding to DNA play a key role in the behaviour of the quinones and their Ru(ii) derivatives. The cytotoxicity of the ligands and the corresponding Ru(ii) complexes was evaluated in MCF-7, A2780, A2780cis tumour cells and in the healthy cell line MRC-5. The cytotoxic activity was notable for N and negligible for Q. The IC50 values and the resistance (RF) and selectivity (SF) factors show that the Cl2Ru2N complex is the most promising among the four studied anticancer drugs.

Selectivity of a thiosemicarbazonatocopper(ii) complex towards duplex RNA. Relevant noncovalent interactions both in solid state and solution.

Thiosemicarbazones and their metal derivatives have long been screened as antitumor agents, and their interactions with DNA have been analysed. Herein, we describe the synthesis and characterization of compounds containing [CuL]+ entities (HL = pyridine-2-carbaldehyde thiosemicarbazone) and adenine, cytosine or 9-methylguanine, and some of their corresponding nucleotides. For the first time, crystal structures of adenine- and 9-methylguanine-containing thiosemicarbazone complexes are reported. To the best of our knowledge, the first study on the affinity thiosemicarbazone-RNA is also provided here. Experimental and computational studies have shown that [CuL(OH2)]+ entities at low concentration intercalate into dsRNA poly(rA)·poly(rU) through strong hydrogen bonds involving uracil residues and π-π stacking interactions. In fact, noncovalent interactions are present both in the solid state and in solution. This behaviour diverges from that observed with DNA duplexes and creates an optimistic outlook in achieving selective binding to RNA for subsequent possible medical applications.

Stabilization of Al(III) solutions by complexation with cacodylic acid: speciation and binding features.

Aluminium ions are believed to play a role in a number of neurological and skeletal disorders in the human body. The study of the biological processes and molecular mechanisms that underlie these pathological disorders is rendered a difficult task due to the wide variety of complex species that result from the hydrolysis of Al(3+) ions. In addition, this ion displays a pronounced tendency to precipitate as a hydroxide, so certain complexing agents should be envisaged to stabilize Al(III) solutions in near physiological conditions. In this work, we show that the common buffer cacodylic acid (dimethylarsinic acid, HCac) interacts with Al(III) to give stable complexes, even at pH 7. After preliminary analyses of the speciation of the metal ion and also of the ligand, a systematic study of the formation of different Al/Cac complexes at different pH values has been conducted. UV-Vis titrations, mass spectrometry NMR measurements and DTF calculations were performed to enlighten the details of the speciation and stoichiometry of Al/Cac complexes. The results altogether show that Al/Cac dimer complexes prevail, but monomer and trimer forms are also present. Interestingly, it was found that cacodylate promotes the formation of such relatively simple complexes, even under conditions where the polymeric form, Al13O4(OH)24(7+), should predominate. The results obtained can help to shed some light into the reactivity of aluminium ions in biological environments.

Anticancer activity and DNA binding of a bifunctional Ru(II) arene aqua-complex with the 2,4-diamino-6-(2-pyridyl)-1,3,5-triazine ligand.

The synthesis and full characterization of the new aqua-complex [(η(6)-p-cymene)Ru(OH2)(κ(2)-N,N-2-pydaT)](BF4)2, [2](BF4)2, and the nucleobase derivative [(η(6)-p-cymene)Ru(9-MeG)(κ(2)-N,N-2-pydaT)](BF4)2, [4](PF6)2, where 2-pydaT = 2,4-diamino-6-(2-pyridyl)-1,3,5-triazine and 9-MeG = 9-methylguanine, are reported here. The crystal structures of both [4](PF6)2 and the chloro complex [(η(6)-p-cymene)RuCl(κ(2)-N,N-2-pydaT)](PF6), [1](PF6), have been elucidated by X-ray diffraction. The former provided relevant information regarding the interaction of the metallic fragment [(η(6)-p-cymene)Ru(κ(2)-N,N-2-pydaT)](2+) and a simple model of DNA. NMR and kinetic absorbance studies have proven that the aqua-complex [2](BF4)2 binds to the N7 site of guanine in nucleobases, nucleotides, or DNA. A stable bifunctional interaction (covalent and partially intercalated) between the [(η(6)-p-cymene)Ru(κ(2)-N,N-2-pydaT)](2+) fragment and CT-DNA has been corroborated by kinetic, circular dichroism, viscometry, and thermal denaturation experiments. The reaction mechanism entails the very fast formation of the Ru-O-(PO3) linkage prior to the fast intercalation of the 2-pydaT fragment. Then, a Ru-N7-(G) covalent bond is formed at the expense of the Ru-O-(PO3) bond, yielding a bifunctional complex. The dissociation rate of the intercalated fragment is slow, and this confers additional interest to [2](BF4)2 in view of the likely correlation between slow dissociation and biological activity, on the assumption that DNA is the only biotarget. Furthermore, [2](BF4)2 displays notable pH-dependent cytotoxic activity in human ovarian carcinoma cells (A2780, IC50 = 11.0 µM at pH = 7.4; IC50 = 6.58 µM at pH = 6.5). What is more, complex [2](BF4)2 is not cross-resistant with cisplatin, exhibiting a resistance factor, RF(A2780cis), of 0.28, and it shows moderate selectivity toward the cancer cell lines, in particular, A2780cis (IC50 = 3.0 5 ± 0.08 µM), relative to human lung fibroblast cells (MRC-5; IC50 = 24 µM), the model for healthy cells.

Physical, behavioral, and psychological traits of gay men identifying as bears.

The Bear community exists as a subculture in reaction to the larger gay community. It rejects the normative idealized male beauty revered by mainstream gay men. While qualitative data document such self-identifiers as masculine-acting gay men who weigh more and have more body hair, there has to date been no quantitative analysis of this group's characteristics. In response, we conducted two large-scale studies of gay men identifying as Bears (n = 469) to survey their self-reported physical, behavioral, and psychological traits. Our studies indicated that Bears were more likely to be hairier, heavier, and shorter than mainstream gay men. They reported wanting partners who were hairier and heavier. They were less likely to reject sexual partners and the partners they did reject were more likely to be young or weigh too little (i.e., were not bearish). Bears were more likely than mainstream gay men to enact diverse sexual behaviors (e.g., fisting, voyeurism) and were comparatively more masculine. Bears had lower self-esteem but were no less (or more) hypermasculine than non-Bears. We concluded that Bears are intensely sexual. We speculate that Bears are viewed as less attractive than what is traditionally considered to be attractive. The partners they can attract may be limited and, in response to this limitation, they may be particularly attuned to seek out partners who will not reject them. This condition may produce the low self-esteem exhibited and may explain how the Bear culture developed to ensure that even the heaviest, hairiest, and/or shortest individual can partner. Future analyses of the community's health are warranted.

Interaction of thionine with triple-, double-, and single-stranded RNAs.

The interaction of thionine with triple, double, and single RNA helices has been fully characterized by thermodynamic and kinetic methods. The nature of the interaction of thionine with the synthetic polynucleotides poly(rU), poly(rA)·poly(rU), and poly(rA)·2poly(rU) has been studied at pH = 7.0 and 25 °C by UV absorbance, fluorescence, circular dichroism spectroscopy, viscometry, differential scanning calorimetry, and T-jump kinetic measurements. The results show that at I = 0.1 M thionine binds to a single poly(rU) strand, destabilizes the poly(rA)·2poly(rU) triplex by external binding, and intercalates into poly(rA)·poly(rU) with similar affinity to the thionine/DNA intercalated complex (Paul, P.; Kumar, G. S. J. Fluoresc. 2012, 22, 71-80). On the other hand, the differential scanning calorimetry measurements performed with thionine display a point in which the heat capacity remains unaltered, revealing the equilibrium of isothermal denaturation: thionine/poly(rA)·2poly(rU) + thionine ⇌ thionine/poly(rA)·poly(rU) + thionine/poly(rU), an outcome supported by the other techniques used. The denaturation equilibrium constant, K(D) (25 °C) = 522 M(-1), was evaluated from the affinity with the single, duplex, and triplex RNA.

Acetylcholine receptor antibodies in patients with pemphigus vulgaris: correlation with disease extent at the time of diagnosis and during follow-up.

Several studies have tried to determine the relationship between autoantibodies against the acetylcholine receptor and the development of pemphigus vulgaris. In this study, we observed that antibody levels against the acetylcholine receptor are mildly elevated in pemphigus vulgaris (PV), and significantly correlate with disease severity on the initial diagnosis and during follow up. However, it is not clear if these antibodies are just an epiphenomenon or a potential trigger of the known pathogenic process in PV.

Efficacy of ciprofloxacin and moxifloxacin against Nocardia brasiliensis in vitro and in an experimental model of actinomycetoma in BALB/c mice.

The efficacy of ciprofloxacin and moxifloxacin against Nocardia brasiliensis was evaluated by applying 25 mg of each drug/kg subcutaneously every 8 h in BALB/c mice infected with N. brasiliensis. A statistically significant difference was observed only with moxifloxacin. A moxifloxacin-trimethoprim-sulfamethoxazole combination was as active as when each compound was used alone.

Non-selective cyclooxygenase inhibition before periodic acceleration (pGz) cardiopulmonary resuscitation (CPR) in a porcine model of ventricular fibrillation.

Whole body periodic acceleration (pGz) along the spinal axis is a novel method of cardiopulmonary resuscitation (CPR). Oscillatory motion of the supine body in a horizontal fashion provides ventilation and blood flow to vital organs during cardiac arrest and pulsatile shear stress to the vascular endothelium. We previously showed in pigs that pGz-CPR affords better overall survival, post resuscitation myocardial function, and neurological outcomes compared to conventional chest compression CPR. pGz through pulsatile shear stress on the vascular endothelium elicits acute production of prostaglandins and endothelial-derived nitric oxide (eNO) in whole animal models and in vitro preparations. The salutary effects associated with pGz-CPR compared to chest compression CPR are in part related to endothelial-derived nitric oxide. Both eNO and prostaglandins are cardioprotective in ischemia reperfusion models. To differentiate between the roles of these mediators, indomethacin a non-selective cyclooxygenase inhibitor (COX) was used as a tool to investigate prostaglandin effects during pGz-CPR by acute outcomes of survival, cardioprotection and regional blood flows (RBF). Two groups of anesthetized, intubated pigs weighing 25-36kg were studied. Prior to electrical induction of ventricular fibrillation (VF) animals received equal volumes of either saline placebo Control (CONT) (n=9) or indomethacin (INDO), (n=8), (2mg/kg). After 3min of unsupported VF, both groups received 15min of pGz-CPR followed by pharmacologic and electrical attempts for resuscitation. Return of circulation (ROSC) to 3h occurred in (78%) in CONT and (63%) in INDO pretreated animals. There was no statistically significant difference in hemodynamics between groups at baseline or during the protocol. At baseline, INDO caused a decrease in brain RBF. Two hours after ROSC, INDO blunted the hyperemia response to brain and heart. Echocardiographic evidence of myocardial dysfunction was most notable for the INDO group in the wall motion score index (WMSI). After 3h of ROSC there was a 4-fold difference in both creatine phosphokinase (CPK) and Troponin I concentration between INDO and CONT. Therefore, non-specific acute inhibition of COX in part blunts the salutary effects of pGz-CPR. These data suggest that prostaglandins in part are involved in the cardio protection induced by pGz during CPR.

The effects of prostaglandin inhibition on whole-body ischemia-reperfusion in swine.

BACKGROUND: Prostaglandins (PGs), particularly PGE2 and PGI2, have a salutary effect on myocardial ischemia-reperfusion-induced myocardial damage. OBJECTIVE: We investigated acute PG synthesis inhibition on outcomes from whole-body ischemia-reperfusion injury using a well-characterized model of ventricular fibrillation (VF)-induced cardiac arrest in pigs. In addition, we assessed early postresuscitation myocardial function in survivors using echocardiography as well as a biochemical measure of myocardial tissue damage. METHODS: Twenty-six animals (weight range, 25-35 kg) received indomethacin (INDO; 2 mg/kg, nonselective cyclooxygenase (COX) 1 and 2 inhibitor), celecoxib (2 mg/kg; selective COX-2 inhibitor [COX-2-I]), or saline placebo 30 minutes before induction of VF. After 3 minutes of VF with no intervention, the animals received standard chest compression using an automated chest compression device (Thumper; Michigan Instruments, Grand Rapids, Mich) for 15 minutes. After 18 minutes of VF, a single dose of vasopressin and bicarbonate were administered and defibrillation attempted. Hemodynamics, regional blood flow, echocardiography, and serum troponin I measurements were performed before and after drug infusion or placebo, during cardiopulmonary resuscitation (CPR), and after return of spontaneous circulation (ROSC). RESULT: Return of spontaneous circulation to 180 minutes occurred in 9 of 10 animals receiving placebo, 7 of 8 animals given COX-2-I, and 3 of 8 animals given INDO (P = .01, placebo or COX-2-I vs INDO). Hemodynamics did not differ among groups over time. Indomethacin and COX-2-I attenuated the increase in regional blood flow in the heart and brain, observed in the placebo group, 30 minutes after ROSC. All 3 study groups had significant decrease in percentage of ejection fraction and fractional shortening after ROSC and significant increase in wall motion score index after ROSC. In the COX-2-I group, troponin I increased 9-fold compared with placebo, 180 minutes after ROSC. Whole-body ischemia-reperfusion and CPR significantly increased PGE2 and PGI2 levels. The latter were blunted by pretreatment with COX inhibition. CONCLUSION: These findings suggest that PGs have a critical role in myocardial function and viability during low-blood-flow states produced by CPR and possibly other low-blood-flow clinical conditions.

Nitric oxide synthase isoform inhibition before whole body ischemia reperfusion in pigs: vital or protective?

BACKGROUND: Nitric oxide (NO) is a critical regulator of vascular tone, and signal transduction. NO is produced via three unique synthases (NOS); endothelial (eNOS), and neuronal (nNOS) are both constitutively expressed and inducible (iNOS) produced primarily after stimulation. NO has been implicated during and after ischemia reperfusion injury as both a detrimental and cardioprotective mediator. Since cardiopulmonary resuscitation (CPR) in ventricular fibrillation (VF) is a model of whole body ischemia reperfusion injury, it provides an opportunity to assess the effects of NO from the three NOS isoforms. OBJECTIVE: To determine the differential role of nitric oxide synthase isoforms inhibition in ventricular fibrillation CPR and investigate whether inhibition of the NOS isoforms afford any cardioprotection in this model. METHODS: Thirty-two pigs, weight range 25-35 kg, were assigned to four groups of eight animals each. The animals were randomized to receive (1) N(G)-nitro-L-arginine methyl ester (LNAME), a non-selective endothelial nitric oxide synthase inhibitor, (2) 1-(2-trifluoromethylphenyl) imidazole (TRIM), a selective neuronal NOS inhibitor, (3) aminoguanidine (AMINOG), a selective inducible NOS inhibitor or (4) saline control (Control) in equal volumes, 30 min before induction of ventricular fibrillation (VF). After 3 min VF with no intervention, the animals received standard chest compressions using an automated chest compression device (Thumper) for 15 min. After 18 min of VF, single doses of vasopressin and bicarbonate were given and defibrillation attempted. Hemodynamics, regional blood flows, and echocardiography and were performed, before and after drug infusion, during CPR, and after return of spontaneous circulation (ROSC). RESULTS: ROSC for 3 h occurred in 5/8 (63%), 1/8 (13%), 0/8 (0%), and 6/8 (75%) in Control, LNAME, TRIM, and AMINOG treated animals, respectively. After infusion of LNAME, there was a significant increase from baseline in blood pressure [127+/-6 mmHg versus 169+/-3 mmHg, p<0.002] and coronary perfusion pressure [119+/-6 mmHg versus 149+/-6 mmHg, p<0.003]. During CPR, there were no differences among groups in hemodynamics or regional blood flow. In surviving animals, AMINOG had significantly better myocardial function (left ventricular ejection fraction, fractional shortening, and wall motion score index) than control or LNAME treated animals, and attenuated the post-resuscitation hyperemic response in heart and brain. CONCLUSIONS: Intact basal nNOS activity is vital for survival from whole body ischemia reperfusion injury. iNOS inhibition prior to ischemia reperfusion, protects myocardial function after ROSC and decreases myocardial and brain hyperemic response after ROSC.

Different roles of nitric oxide synthase isoforms in cardiopulmonary resuscitation in pigs.

The purpose of the present study was to identify the roles of the three nitric oxide synthase (NOS) isoforms on whole body ischemia-reperfusion injury during cardiopulmonary resuscitation (CPR) with periodic acceleration (pGz) in pigs. Thirty-two anesthetized pigs (27.6+/-3.4 kg) were monitored for hemodynamics and selected echocardiographic variables. Twenty minutes after NOS inhibition or placebo administration, ventricular fibrillation (VF) was induced and remained untreated for 3 min, followed by CPR with pGz for 15 min, plus 3 min of manual chest compressions and defibrillation attempt. Four groups were studied: (1) saline control; (2) L-NAME (non-selective NOS inhibitor); (3) aminoguanidine (inducible NOS inhibitor); (4) TRIM (neuronal NOS inhibitor). Return of spontaneous circulation (ROSC) to 180 min occurred in 6/8 controls, 4/8 L-NAME, 7/8 aminoguanidine, and 2/8 TRIM animals. The L-NAME group had significantly lower organ blood flow, impaired cardiac function, but higher vascular tone than control group. The aminoguanidine group had the highest organ blood flows and survival rate. Six out of eight TRIM treated animals had initial return of heartbeat; however, with impaired heart contractility and could not survive more than 20 min of ROSC. This study reveals the differential role of endogenous NO produced from the three NOS isoforms during pGz-CPR. Both endothelial and neuronal NOS derived NO show predominantly protective effects while inducible NOS derived NO plays a detrimental role in pGz-CPR. The present study has shown that cardiac arrest and resuscitation appears to be associated with a different expression of NOS isoforms which appear to affect resuscitation outcomes differently.

Treatment and prevention of atrial fibrillation with non-antiarrhythmic pharmacologic therapy.

Atrial fibrillation is one of the most frequent heart rhythm disturbances found in clinical practice. Anticoagulation, rate control, cardioversion, and ablative procedures have been the mainstay of treatment. The frequent recurrence of atrial fibrillation and the side effects when antiarrhythmic drugs are used have led to dissatisfaction with available treatment of this arrhythmia. Pharmacologic therapy with angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, statins, and perhaps aldosterone and calcium channel blockers may have a role in the prevention of atrial fibrillation onset and recurrence. We summarize the possible biologic mechanisms and the clinical observations supporting the use of non-antiarrhythmic medications in the prevention of atrial fibrillation.