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The article discusses the urgent need for a national crusade against atherosclerosis in Mexico due to the prevalence of chronic degenerative diseases like obesity, diabetes, and atherosclerotic diseases. The socioeconomic, political, and cultural changes in Mexico have led to a shift in epidemiological profiles, with cardiovascular diseases becoming the leading public health problems. The article highlights the importance of addressing dyslipidemia and other risk factors to combat the cardiovascular disease epidemic in Mexico. [Extracted from the article]

Caveolae are identifiable plasma membrane invaginations. The main structural proteins of caveolae are the caveolins. There are three caveolins expressed in mammals, designated Cav-1, Cav-2, and Cav-3. It has been postulated that Cav-1 acts as a scaffold protein for signaling proteins; these include ion channels, enzymes, and other ligand receptors like membrane-associated estrogen receptor (ER)[alpha] or ER[beta]. Caveolae-associated membrane proteins are involved in regulating some of the rapid estrogenic effects of 17[beta]-estradiol. One important system related to the activity of ER[alpha] and caveolae is the renin-angiotensin system. Angiotensin II (ANG II) has numerous actions in vascular smooth muscle, including modulation of vasomotor tone, cell growth, apoptosis, phosphatidylinositol 3-kinase (PI3K)/Akt activation, and others. Many proteins associated with caveolae are in close relation with the scaffolding domain of Cav-1 (82-101 amino acid residues). It has been proposed that this peptide may acts as a kinase inhibitor. Therefore, to explore the ability of Cav-1 scaffolding peptide (CSP-1) to regulate ANG 1I function and analyze the relationship between ER[alpha] and ANG II type 1 and 2 ([AT.sub.1] and [AT.sub.2]) receptors, we decided to study the effects of CSP-1 on ANG H-induced intracellular [Ca.sup.2+] kinetics and the effect of 17[beta]-estradiol on this modulation using human smooth muscle cells in culture, intracellular [Ca.sup.2+] concentration measurements, immuno- and double-immunocytochemistry confocal analysis of receptor expression, immunoblot analysis, and immunocoprecipitalion assays to demonstrate coexpression. We hypothesized that CSP-1 inhibits ANG II-mediated increases in intracellular [Ca.sup.2+] concentrations by interfering with intracellular signaling including the PI3K/Akt pathway. We also hypothesize that ATE receptors associate with Cav-1. Our results show that there is a close association of [AT.sub.1], [AT.sub.2], and [ER.sub.[alpha]] with Cav-1 in human medal smooth muscle cells in culture. CSP-1 inhibits ANG II-induced intracellular signaling. estrogen receptors; angiotensin type 1 and 2 receptors; phosphatidylinositol 3-kinase; intracellular signaling; tissue culture; angiotensin receptors

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Introduction: Head and neck cancer patients are at high risk of anorexia-cachexia syndrome and literature shows that Eicosapentaenoic acid (EPA) could regulate it. We aim to determine the EPA effect on body composition and pro-inflammatory markers in patients with head neck cancer. Materials and methods: A randomized single-blind placebo-controlled clinical trial was conducted in patients with head and neck squamous cell cancer who received a polymeric diet with 2 g of EPA or a standard polymeric diet for six weeks before antineoplastic treatment. We assessed body composition by bioelectrical impedance analysis and determined IL-1β, IL-6, TNF-α and IFN-γ, CRP, serum proteins, and blood count at baseline and at the end of the study. Results: 32 patients received EPA (2 g/day) and 32 became controls. A decrease in serum levels of IL-1β, IL-6, TNF-α, and IFN-γ was observed in the experimental group, as well as regulation of body weight (¡0.3 § 5.9 vs. ¡2.1 § 3.7), lean body mass (¡0.2 § 3.8 vs. ¡1.3 § 3.6), body fat mass (0.2 § 3.5 vs. ¡1.2 § 3.8), and quality of life (10 § 33 vs. 5 § 34). Conclusion: Supplementing with 2 g/day of EPA to head and neck cancer patient during antineoplastic treatment regulates serum pro-inflammatory cytokines, body weight, lean body mass, and improve quality of life. [ABSTRACT FROM AUTHOR]

Background: Leptin and insulin levels are key factors regulating fetal and neonatal energy homeostasis, development and growth. Both biomarkers are used as predictors of weight gain and obesity during infancy. There are currently no prediction algorithms for cord blood (UCB) hormone levels using Artificial Neural Networks (ANN) that have been directly trained with anthropometric maternal and neonatal data, from neonates exposed to distinct metabolic environments during pregnancy (obese with or without gestational diabetes mellitus or lean women). The aims were: 1) to develop ANN models that simulate leptin and insulin concentrations in UCB based on maternal and neonatal data (ANN perinatal model) or from only maternal data during early gestation (ANN prenatal model); 2) To evaluate the biological relevance of each parameter (maternal and neonatal anthropometric variables).Methods: We collected maternal and neonatal anthropometric data (n = 49) in normoglycemic healthy lean, obese or obese with gestational diabetes mellitus women, as well as determined UCB leptin and insulin concentrations by ELISA. The ANN perinatal model consisted of an input layer of 12 variables (maternal and neonatal anthropometric and biochemical data from early gestation and at term) while the ANN prenatal model used only 6 variables (maternal anthropometric from early gestation) in the input layer. For both networks, the output layer contained 1 variable to UCB leptin or to UCB insulin concentration.Results: The best architectures for the ANN perinatal models estimating leptin and insulin were 12-5-1 while for the ANN prenatal models, 6-5-1 and 6-4-1 were found for leptin and insulin, respectively. ANN models presented an excellent agreement between experimental and simulated values. Interestingly, the use of only prenatal maternal anthropometric data was sufficient to estimate UCB leptin and insulin values. Maternal BMI, weight and age as well as neonatal birth were the most influential parameters for leptin while maternal morbidity was the most significant factor for insulin prediction.Conclusions: Low error percentage and short computing time makes these ANN models interesting in a translational research setting, to be applied for the prediction of neonatal leptin and insulin values from maternal anthropometric data, and possibly the on-line estimation during pregnancy. [ABSTRACT FROM AUTHOR]

Introduction and objective: The aim of this communication is to describe the cardiovascular risk factors affecting a Mexican urban middle-class population. Methods: A convenience sample of 2602 middle class urban subjects composed the cohort of the Lindavista Study, a prospective study aimed to determine if conventional cardiovascular risks factors have the same prognosis impact as in other populations. For the baseline data, several measurements were done: obesity indexes, smoking, blood pressure, fasting serum glucose, total cholesterol, HDL-c, LDL-c and triglycerides. This paper presents the basal values of this population, which represents a sample of the Mexican growing urban middle-class. Results: The mean age in the sample was 50 years; 59% were females. Around 50% of the entire group were overweighed, while around 24% were obese. 32% smoked; 32% were hypertensive with a 20% rate of controlled pressure. 6% had diabetes, and 14% had impaired fasting glucose; 66% had total cholesterol=200 mg/dL; 62% showed HDL-c levels < 40 mg/dL; 52% triglycerides > 150 mg/dL, and 34% levels of LDL-c=160 mg/dL. Half of the population studied had the metabolic syndrome. Conclusion: These data show a population with a high-risk profile, secondary to the agglomeration of several cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

Objective. The objective of this study was to investigate the effect of bromocriptine (BEC) on left ventricular mass index (LVMI) and residual renal function (RRF) in chronic kidney disease (CKD) patients with type 2 diabetes (T2D). Research Design and Methods. A 6-month double-blind randomized controlled trial was conducted in 28 patients with T2D and stage 4 CKD with increased LVMI. Fourteen patients received BEC (2.5 mg, initially 1 tablet with subsequent increase to three times a day) and 14 received a placebo (PBO; initially 1 tablet with subsequent increase to three times a day). Cardiovascular changes were assessed by monitoring 24h ambulatory blood pressure, two-dimensional-guided M-mode echocardiography, and N-terminal brain natriuretic peptide (NT-proBNP) plasma levels. RRF was evaluated by creatinine clearance and cystatin-C plasma levels. Results. Both BEC and PBO groups decreased blood pressure--but the effect was more pronounced in the BEC group. Average 24h, diurnal and nocturnal blood pressures, and circadian profile showed improved values compared to the PBO group; LVMI decreased by 14% in BEC and increased by 8% in PBO group. NT-proBNP decreased in BEC (0.54 ± 0.15 to 0.32 ± 0.17 pg/mL) and increased in PBO (0.37 ± 0.15 to 0.64 ± 0.17pg/mL). Creatinine clearance did not change in the BEC group and decreased in the PBO group. Conclusions. BEC resulted in a decrease on blood pressure and LVMI. BEC also prevented the progression of CKD while maintaining the creatinine clearance unchanged. [ABSTRACT FROM AUTHOR]

Caveolae are identifiable plasma membrane invaginations. The main structural proteins of caveolae are the caveolins. There are three caveolins expressed in mammals, designated Cay-1, Cav-2, and Cav-3. it has been postulated that Cay-1 acts as a scaffold protein for signaling proteins; these include ion channels, enzymes, aiid other ligand receptors like membrane-associated estrogen receptor (ER)α or ERβ. Caveolae-associated membrane proteins are involved in regulating some of the rapid estrogenic effects of 17β-estradiol. One important system related to the activity of ERα and caveolae is the renin-angiotensin system. Angiotensin II (ANG II) has numerous actions in vascular smooth muscle, including modulation of vasomotor tone, cell growth, apoptosis, phosphatidylinositol 3-kinase (P13K)/Akt activation, and others. Many proteins associated with caveolae are in close relation with the scaffolding domain of Cay-1 (82-101 amino acid residues). It has been proposed that this peptide may acts as a kinase inhibitor. Therefore, to explore the ability of Cay-1 scaffolding peptide (CSP- 1) to regulate ANG II function and analyze the relationship between ERα and ANG II type 1 and 2 (AT1 and AT2) receptors, we decided to study the effects of CSP-I on ANG II-induced intracellular Ca2+ kinetics and the effect of 17β-estradiol on this modulation using human smooth muscle cells in culture, intracellular Ca2+ concentration measurements, immuno- and double-immunocytochemistry confocal analysis of receptor expression, immunoblot analysis, and immunocoprecipitation assays to demonstrate coexpression. We hypothesized that CSP-I inhibits ANG II-mediated increases in intracellular Ca2+ concentrations by interfering with intracellular signaling including the P13K/Akt pathway. We also hypothesize that AT2 receptors associate with Cay-I. Our results show that there is a close association of AT1, AT2, and ERa with Cay-I in human arterial smooth muscle cells in culture. CSP-I inhibits ANG II-induced intracellular signaling. [ABSTRACT FROM AUTHOR]

Several studies have emphasized the importance, of dystrophin-associated protein complex (DAPC) to maintain the vascular function in development of dilated cardiomyopathy in dystrophyc patients has been shown. Previously we postulated the presence of an utrophin associated protein complex (UAPC) in endothelium from umbilical cord vessels. In this work, we demonstrate that utrophin indeed forms a complex, with beta-dystroglycan, epsilon sarcoglycan, caveolin-1, and endothelial nitric oxide synthase (eNOS) in human umbilical vein endothelial cells, by co-immunoprecipitation and Western blot analysis. Additionally, we observed an increment in the levels of all proteins of complex after mechanical stretching. Interestingly, this stimulus also induced eNOS up-regulation, activation and release from the UAPC and led to a significant increase in nitric oxide production. Finally, we propose that UAPC in HUVECs may play an important role in the regulation of vascular tone during mechanical stress. CONACyT 39542-Q, 144593 [ABSTRACT FROM AUTHOR]

During Chronic Obstructive Pulmonary Disease (COPD) progression, the intracellular antioxidant defence in RBCs must preserve the integrity of the plasmalemma through NADPH+ generation to obtain a sufficient number of reduced non-protein SH-groups. Here, we studied the activities of enzymes in RBCs that are related to glutathione metabolism under conditions of increasing oxidative stress, which are associated with COPD progression, by increasing cellular damage in vitro with PM2.5, a ROS generator. The study included 43 patients, who were separated according to their GOLD classification into moderate and severe groups, along with 11 healthy volunteers (HV). Blood samples were analysed for G6PD, GAPDH, GPx, and GR. The results showed significant decreases in the oxidation of the G6PD, GR and GPx proteins, resulting in decreased enzymatic activity. By contrast, an increase (p<0.05) in GAPDH was observed, suggesting a pool of ATP on the membrane. However, it is evident that RBCs are damaged during the progression of COPD, although their integrity is preserved, and they retain limited function, thus allowing patient survival without haemolysis.

The cochlear outer hair cells serve a tuning function, and any dysfunction of their electromotile response can be reflected in language disorders. Otoacoustic emissions can be used to determine any dysfunction of these cells. A set of clinical records was established to register the neurological and auditory functioning in 42 children, followed by assessment with the Wechsler Intelligence Scale for Children (WISC), the Initial Language Test (ILT), the Auditory and Phonetic Discrimination Evaluation (APDE), tests for measuring Brainstem Auditory Evoked Potential (BAEP) and Transient Otoacoustic Emissions (TOAE). Subjects were classified into 3 groups in this study: Control (C; n = 20), Syntactic Phonological Disorder (SPD; n = 17), and those with Phonological Disability (PD; n = 5). BAEP studies showed a clear response when all children were stimulated to 20 dB. TOAE responses displayed clear and significant differences with half-octave band reproducibility for both ears, the largest effect being observed in the right ear. The results that were compared using ANOVA tests, showed that cochlear processing affects the brain language function, playing a critical role in the language phonetic process.

Glutamate dehydrogenase (GDH, E.C. 1.4.1.3.) is a key enzyme for the biosynthesis and modulation of glutamate (GLU) metabolism and an indirect γ-aminobutyric acid (GABA) source, here we studied the effect of anticonvulsants such as pyridoxal phosphate (PPAL), aminooxyacetic acid (AAOA), and hydroxylamine (OHAMINE) on GDH activity in mouse brain. Moreover, since GLU is a glucogenic molecule and anoxia is a primary cause of convulsions, we explore the effect of these drugs on oxygen consumption. Experiments were performed in vitro as well as in vivo for both oxidative deamination of GLU and reductive amination of α-ketoglutarate (αK). Results in vitro showed that PPAL decreased oxidative deamination of GLU and oxygen consumption, whereas AAOA and OHAMINE inhibited GDH activity competitively and also inhibited oxygen consumption when αK reductive amination was carried out. In contrast, results showed that in vivo, all anticonvulsants enhanced GLU utilization by GDH and also decreased oxygen consumption. Together, results suggest that GDH activity has repercussions on oxygen consumption, which may indicate that the enzyme activity is highly regulated by energy requirements for metabolic activity. Besides, GDH may participate in regulation of GLU and, indirectly GABA levels, hence in neuronal excitability, becoming a key enzyme in seizures mechanism.

Aromatase CYP19 catalyzes the synthesis of estrogen from androgens in a tissue-specific manner. This enzyme is present in several tissues, including gonads, brain and fatty tissue. More recently, its presence has been described in vessels. Here, we describe the expression of aromatase in human uterine artery and compare its expression with that found in arteries of estrogen-dependent uterine leiomyomata from women. To do this, we employed immunohystochemical and in situ hybridization techniques. We used, a polyclonal antibody raised against the carboxyl terminus of aromatase (ARO) and RNAm probes, of the exon 1 of ARO. We found an increased immunoreactivity of ARO in uterine arteries of patients with leiomyoma as compared with control group. Probe showing positive signal in skin fibroblasts (1b), showed positive hybridization signal in normal artery, while probes with positive signal in placenta (1a), ovary (1c) and testis (1d) were over-expressed in arteries of leiomyomas.