Sergio Rodríguez-Reynoso

Bio: Sergio Rodríguez-Reynoso is an academic researcher from Mexican Social Security Institute. The author has contributed to research in topics: Nitric oxide & Ischemia. The author has an hindex of 6, co-authored 11 publications receiving 198 citations.

HLA-A and HLA-B allele frequencies in a mestizo population from Guadalajara, Mexico, determined by sequence-based typing

Abstract: HLA-A and HLA-B genes were typed by DNA sequencing in a mestizo population from Guadalajara, Jalisco, Mexico. Thirty-seven HLA-A and 51 HLA-B alleles were observed in 103 samples. The common typical Amerindian alleles (>5%) and haplotypes (>or=2.0%) found were A*02010101, *24020101, *310102, B*350101, and *4002, and A*310102-B*4002, A*240201-B*350101, and the typical European alleles were A*010101, *29010101, B*1402, B*180101, and A*020101-B*1402, A*020101-B*510101, and A*3002-B*180101. This reflects the blending of the two main parental populations of mestizos: Amerindian and Iberian. Mexicans were found to be relatively closer to the Portuguese than to Spaniards. This proximity may indicate a larger Portuguese influence in Mexicans than previously considered. Present data contribute to the understanding of the genetic structure in Mexico.

Arterial blood gas changes in New Zealand white rabbits during carbon dioxide-induced pneumoperitoneum.

Abstract: 398 Laparoscopic surgery has become commonplace in human adults and children where induction of pneumoperitoneum is required to attain adequate visibility. Several gases have been proposed for this purpose, but carbon dioxide is used in almost all laparoscopic interventions (1). Several physiologic alterations associated with mechanical and blood gasinduced changes have been reported in clinical and experimental studies after carbon dioxide-induced pneumoperitoneum (CDP). These include arterial and pulmonary hypertension, reduced lung compliance, increase in cardiac output, venous oxygen pressure, and venous saturation, in addition to acidemia, hyperkalemia, and hypercapnia (1–5). Use of these procedures in neonates is uncommon and has been reported by only a few groups (6, 7). Several animal species, mainly adult pigs (Sus scrofa), are routinely used by surgeons for training before attempting clinical procedures. On the basis of our experience, the rabbit is an appropriate species with which to obtain the skills needed for laparoscopic surgery in newborn humans, due to their similar size and abdominal anatomy. In the clinical and laboratory settings, we routinely use an intra-abdominal gas pressure of 8 mm Hg with 100% carbon dioxide to provide good visibility of internal structures (6, 7). This pressure has little or no effect on hemodynamics in normal healthy subjects (8, 9). Although the physiologic alterations related to induction of pneumoperitoneum during laparoscopy have been extensively studied in larger humans and animals, we were concerned that the proportionally larger volume of carbon dioxide used in small subjects could generate hypercapnia of greater clinical significance. Therefore, the blood gas status of New Zealand White (NZW) rabbits was studied during carbon dioxide pneumoperitoneum. The protocol was approved by the CIBO Research Committee, and all animals were treated in compliance with institutional and federal regulations. Twenty conventional NZW virgin does or bucks (Oryctolagus cuniculus), 2.5 to 3.5 kg of body weight, from

[Impact of vacuum-assisted closure management in deep neck abscesses].

Abstract: Background The presence of deep neck abscesses is potentially serious; they can lead to death in a short period of time. The vacuum-assisted closure (V.A.C.) therapy has been used in many areas of surgery for complex wound healing. This treatment modality has recently been considered in the field of head and neck surgery. Objective Evaluate the efficacy of healing therapy using V.A.C. therapy in deep neck abscesses. Material and methods Open-label trial. Patients with deep neck abscesses were included using V.A.C. therapy vs. conventional therapy. Cultures were taken before and during surgery, and prior to primary wound closure. The percentages of healing, viable tissue, wound healing time, and hospital stay were evaluated. Results A total of 18 patients were included. Affected neck spaces: submaxilar 29%, parapharyngeal 22%, submental 21% and masticatory 13%. The final postsurgical culture was negative in 78%. Viable tissue of the wound for the V.A.C. group was 42%, and for the control group was 36% (p = 0.025). Healing time was 22 ± 6 days and 38 ± 15.5, respectively (p = 0.01). The mean number of hospital stay was 12 days for both groups. Conclusions Therapy with V.A.C. is useful in the treatment of deep neck abscesses; it decreased healing time as a result of more viable tissue allowing suture closure of the wound in a shorter period.

Melatonin as an antioxidant: under promises but over delivers.

Abstract: Melatonin is uncommonly effective in reducing oxidative stress under a remarkably large number of circumstances. It achieves this action via a variety of means: direct detoxification of reactive oxygen and reactive nitrogen species and indirectly by stimulating antioxidant enzymes while suppressing the activity of pro-oxidant enzymes. In addition to these well-described actions, melatonin also reportedly chelates transition metals, which are involved in the Fenton/Haber-Weiss reactions; in doing so, melatonin reduces the formation of the devastatingly toxic hydroxyl radical resulting in the reduction of oxidative stress. Melatonin's ubiquitous but unequal intracellular distribution, including its high concentrations in mitochondria, likely aid in its capacity to resist oxidative stress and cellular apoptosis. There is credible evidence to suggest that melatonin should be classified as a mitochondria-targeted antioxidant. Melatonin's capacity to prevent oxidative damage and the associated physiological debilitation is well documented in numerous experimental ischemia/reperfusion (hypoxia/reoxygenation) studies especially in the brain (stroke) and in the heart (heart attack). Melatonin, via its antiradical mechanisms, also reduces the toxicity of noxious prescription drugs and of methamphetamine, a drug of abuse. Experimental findings also indicate that melatonin renders treatment-resistant cancers sensitive to various therapeutic agents and may be useful, due to its multiple antioxidant actions, in especially delaying and perhaps treating a variety of age-related diseases and dehumanizing conditions. Melatonin has been effectively used to combat oxidative stress, inflammation and cellular apoptosis and to restore tissue function in a number of human trials; its efficacy supports its more extensive use in a wider variety of human studies. The uncommonly high-safety profile of melatonin also bolsters this conclusion. It is the current feeling of the authors that, in view of the widely diverse beneficial functions that have been reported for melatonin, these may be merely epiphenomena of the more fundamental, yet-to-be identified basic action(s) of this ancient molecule.

Melatonin mitigates mitochondrial malfunction

Abstract: Melatonin, or N-acetyl-5-methoxytryptamine, is a compound derived from tryptophan that is found in all organisms from unicells to vertebrates. This indoleamine may act as a protective agent in disease conditions such as Parkinson's, Alzheimer's, aging, sepsis and other disorders including ischemia/reperfusion. In addition, melatonin has been proposed as a drug for the treatment of cancer. These disorders have in common a dysfunction of the apoptotic program. Thus, while defects which reduce apoptotic processes can exaggerate cancer, neurodegenerative disorders and ischemic conditions are made worse by enhanced apoptosis. The mechanism by which melatonin controls cell death is not entirely known. Recently, mitochondria, which are implicated in the intrinsic pathway of apoptosis, have been identified as a target for melatonin actions. It is known that melatonin scavenges oxygen and nitrogen-based reactants generated in mitochondria. This limits the loss of the intramitochondrial glutathione and lowers mitochondrial protein damage, improving electron transport chain (ETC) activity and reducing mtDNA damage. Melatonin also increases the activity of the complex I and complex IV of the ETC, thereby improving mitochondrial respiration and increasing ATP synthesis under normal and stressful conditions. These effects reflect the ability of melatonin to reduce the harmful reduction in the mitochondrial membrane potential that may trigger mitochondrial transition pore (MTP) opening and the apoptotic cascade. In addition, a reported direct action of melatonin in the control of currents through the MTP opens a new perspective in the understanding of the regulation of apoptotic cell death by the indoleamine.

A review of the molecular aspects of melatonin's anti-inflammatory actions: recent insights and new perspectives.

Abstract: Melatonin is a highly evolutionary conserved endogenous molecule that is mainly produced by the pineal gland, but also by other nonendocrine organs, of most mammals including man. In the recent years, a variety of anti-inflammatory and antioxidant effects have been observed when melatonin is applied exogenously under both in vivo and in vitro conditions. A number of studies suggest that this indole may exert its anti-inflammatory effects through the regulation of different molecular pathways. It has been documented that melatonin inhibits the expression of the isoforms of inducible nitric oxide synthase and cyclooxygenase and limits the production of excessive amounts of nitric oxide, prostanoids, and leukotrienes, as well as other mediators of the inflammatory process such as cytokines, chemokines, and adhesion molecules. Melatonin's anti-inflammatory effects are related to the modulation of a number of transcription factors such as nuclear factor kappa B, hypoxia-inducible factor, nuclear factor erythroid 2-related factor 2, and others. Melatonin's effects on the DNA-binding capacity of transcription factors may be regulated through the inhibition of protein kinases involved in signal transduction, such as mitogen-activated protein kinases. This review summarizes recent research data focusing on the modulation of the expression of different inflammatory mediators by melatonin and the effects on cell signaling pathways responsible for the indole's anti-inflammatory activity. Although there are a numerous published reports that have analyzed melatonin's anti-inflammatory properties, further studies are necessary to elucidate its complex regulatory mechanisms in different cellular types and tissues.

Melatonin: A novel protective agent against oxidative injury of the ischemic/reperfused heart

Abstract: This brief review summarizes the recently obtained evidence which illustrates the beneficial effects of the endogenously produced antioxidant, melatonin, in reducing tissue damage and reversing cardiac pathophysiology in models of experimental ischemia/reperfusion. The report also describes the actions of other antioxidants, especially vitamin E and antioxidative enzymes, in altering the degree of ischemia/reperfusion damage in the heart. Based on the data available, melatonin seems to have advantages over other antioxidants tested in terms of ameliorating the hypoxia and reoxygenation-induced damage. While the bulk of the studies that have used melatonin to overcome cardiac injury following transient arterial occlusion and subsequent reperfusion have used pharmacological doses to achieve protection, two recent reports have further shown that merely reducing endogenous circulating concentrations of melatonin (by surgical removal of a source of melatonin, i.e. the pineal gland) exaggerates the degree of injury and reduces survival of animals as a result of induced ischemia/reperfusion of the heart. These findings are consistent with observations in other organs where the loss of physiological concentrations of melatonin results in increased oxidative damage during hypoxia and reoxygenation. These findings have implications for the elderly since in the aged endogenous levels of melatonin are naturally reduced thereby possibly predisposing them to more severe cardiac damage during a heart attack. To date, the bulk of the studies relating to the protective actions of melatonin in reducing cardiac ischemia/reperfusion injury have used the rat as the experimental model. Considering the high efficacy of melatonin in limiting ischemia/reperfusion damage as well as melatonin's low toxicity, the studies should be expanded to include other species and models of cardiac ischemia/reperfusion. The results of these investigations would help to clarify the potential importance of the use of melatonin in situations of oxidative damage to the heart in humans.