Draft Genome Sequence of Streptomyces sp. Strain C8S0, Isolated from a Highly Oligotrophic Sediment.

Streptomyces spp. are prolific bacteria producing bioactive metabolites. We present the draft genome sequence of Streptomyces sp. strain C8S0, which was isolated from a highly oligotrophic sediment from the Cuatro Cienegas Basin (Mexico). The whole-genome assembly comprised 6,898,902 bp, with 18 biosynthetic gene clusters, including those for nonconventional terpenes, nonribosomal peptides, and polyketides.

Assessing Human Health Risks Associated with Consumption of Metal Content in Shrimp from NW Mexico.

Shrimp of Farfantepenaeus californiensis (78 groups) and Litopenaeus stylirostris (14 groups) were caught in the northwestern fishing zones in Mexico during the 2014-2015 fishing season (September-February); both shrimp species have high commercial value. Muscle, hepatopancreas and exoskeleton were analyzed to determine their metal contents. For F. californiensis, the highest Cd, Pb and Zn contents were determined in specimens caught off the State of Baja California Sur (BCS) with 22.4 ± 8.9 (hepatopancreas), 2.83 ± 4.63 (muscle), and 748.5 ± 1567 (muscle) µg/g, in the regions off Mulegé, Los Cabos and Los Cabos, respectively. For L. stylirostris, the fishing zone of Comundú (BCS) showed higher Cd (12.3 ± 11.5 µg/g), Cu (569.1 ± 646.5 µg/g) and Zn (549.7 ± 400.7 µg/g) contents; all values were determined in the hepatopancreas. Regarding the hazard quotient and total hazard quotient calculated in this study, the consumption of marine shrimp caught off NW Mexico does not represent a risk to human health (both < 1).

Low bone mineral density and associated factors in patients with haemophilia in Colombia.

INTRODUCTION: Patients with haemophilia may have lower levels of bone mineral density (BMD) compared with the general population. Moreover, haemophilic patients have increased risk factors for low bone mineral density (LBMD) such as arthropathy and resulting immobility, increasing their risk for osteoporosis and fractures. AIM: To assess the prevalence of LBMD and associated risk factors among a group of Colombian haemophilic patients. METHODS: In this case-control study, 90 patients with haemophilia A and B, over the age of five, were recruited. Controls were healthy participants matched by age, gender, body mass index (BMI), socioeconomic status, and race. All participants underwent dual energy X-ray absorptiometry (DXA) and the Global Physical Activity Questionnaire. Blood tests were collected to evaluate LBMD determinants in cases. RESULTS: BMD was lower in cases than in the control group. BMD of femoral necks was 0.907 g/cm2 in cases vs. 1.020 g/cm2 in controls (P = .019), and BMD of hips 0.930 g/cm2 in cases vs. 1030 g/cm2 in controls (P = .019). The greater the severity of haemophilia, the lower BMD in spine, femoral neck, and hips. Elevated C-protein levels were found in 44.1% of patients with LBMD and 14.8% with normal BMD (P = .003). The study found an adjusted prevalence ratio of 2.11, indicating that haemophilic patients are two times more likely to have LBMD (CI95% = 1.43-3.11 P < .001). CONCLUSION: Results from the present study showed that haemophilia was associated with a higher frequency of LBMD. Severity of haemophilia, haemophilic arthropathy, and elevated C-reactive protein levels was directly associated with LBMD.

DNA is hypomethylated in circadian manifestations of bruxism.

OBJECTIVE: The aim of this study was to compare the global DNA methylation levels in patients under bruxism treatment and a control group. METHODS: Subjects undergoing bruxism treatment were classified in awake bruxism (42 patients), sleep bruxism (32 patients) and both conditions (42 patients). The control group included 42 individuals. A colorimetric assay (MethylFlash Methylated DNA 5-mC Quantification Kit, Epigenetic Group Inc., NY, USA) was used to determine the global DNA methylation levels. RESULTS: Statistically significant differences were found in amounts of methylated DNA in all circadian manifestations of bruxism compared with a control group (sleep bruxism = 0.95% ± 2.02%; awake bruxism = 0.87% ± 2.1%; sleep and awake bruxism = 0.17% ± 0.25%; Control = 1.69% ± 1.6%; Kruskal-Wallis test [p = .0001] followed by Dunn's test [p < .05]). CONCLUSION: Patients undergoing bruxism treatment exhibited hypomethylated DNA levels when compared to control group. Our results suggest that DNA hypomethylation might be a novel aetiologic factor in bruxism aetiology. Further researches must be performed exploring the role of epigenetics modifications in circadian manifestations of bruxism.

Transporter genes ABCG2 rs2231142 and ABCB1 rs1128503 polymorphisms and atorvastatin response in Chilean subjects.

WHAT IS KNOWN AND OBJECTIVE: Statins are first-line therapy for reducing high cholesterol levels. However, response to these drugs shows high interindividual variability. We aimed to investigate the influence of two single nucleotide polymorphisms (SNP) (ABCB1 rs1128503 and ABCG2 rs2231142) in the ABC transporter genes on response to short-term low-dose atorvastatin in Chilean hypercholesterolaemic patients. METHODS: We studied 127 Chilean hypercholesterolaemic patients treated with 10 mg/d atorvastatin for 4 weeks. The lipid profile was determined before and after drug administration. Genotyping of the rs1128503 and rs2231142 variants was performed using TaqMan® Drug Metabolism Genotyping Assays. RESULTS AND DISCUSSION: Genotype distribution for all polymorphisms investigated was consistent with the Hardy-Weinberg equilibrium. Atorvastatin reduced TC, LDL-C and TG concentrations (P<.05), whereas HDL-C levels were found to be increased (P<.05). Minor allele frequencies for rs1128503 and rs2231142 variants were 0.453 and 0.075, respectively. In this study, patients prescribed with short-term low-dose atorvastatin and carrying ABCB1 (rs1128503) or ABCG2 (rs2231142) SNPs did not show differences in LDL-C response (P>.05). WHAT IS NEW AND CONCLUSION: The ABCB1 SNP was not associated with response to atorvastatin in Chilean subjects. The few ABCG2 421A homozygotes did not allow meaningful inferences to be made for this polymorphism.

Genetic polymorphisms in the serotonergic system are associated with circadian manifestations of bruxism.

Bruxism (BRX) is a condition of great interest for researchers and clinicians in dental and medical areas. BRX has two circadian manifestations; it can occur during sleep (sleep bruxism, SB) or during wakefulness (awake bruxism, WB). However, it can be suffered together. Recent investigations suggest that central nervous system neurotransmitters and their genes could be involved in the genesis of BRX. Serotonin is responsible for the circadian rhythm, maintaining arousal, regulating stress response, muscle tone and breathing. Thus, serotonin could be associated with BRX pathogenesis. The aim of this work was to evaluate the frequency of genetic polymorphisms in the genes HTR1A (rs6295), HTR2A (rs1923884, rs4941573, rs6313, rs2770304), HTR2C (rs17260565) and SLC6A4 (rs63749047) in subjects undergoing BRX treatment. Patients included were classified according to their diagnosis in awake bruxism (61 patients), sleep bruxism (26 patients) and both (43 patients). The control group included 59 healthy patients with no signs of BRX. Data showed significant differences in allelic frequencies for the HTR2A rs2770304 polymorphism, where the C allele was associated with increased risk of SB (odds ratio = 2·13, 95% confidence interval: 1·08-4·21, P = 0·03). Our results suggest that polymorphisms in serotonergic pathways are involved in sleep bruxism. Further research is needed to clarify and increase the current understanding of BRX physiopathology.

Clinical, imaging and genetic analysis of double bilateral radix entomolaris.

BACKGROUND: Anatomy describes that first mandibular molars have two roots: 1 mesial, with 2 root canals, and 1 distal, with 1 root canal. The presence of three roots in these teeth is uncommon. Root anatomical variations have an impact, especially in endodontic, where the highest rates of nonsurgical treatment failures are due to the inability to identify and access roots and/or accessory canals. The aim of this research is to report a case of double three-rooted mandibular first molar through clinical, imaging and genetic analysis. MATERIALS AND METHODS: Using a panoramic radiography, the presence of three roots in teeth 36 and 46 was diagnosed in a female patient. Additionally, it was indicated a cone beam computed tomography. Moreover, leukocyte genomic DNA was obtained from a blood sample of the patient to determine her ethnicity through analysis of mitochondrial DNA haplogroups using polymerase chain reaction-length restriction fragment polymorphism (PCR-RFLP). RESULTS: Both molars had three roots, 1 mesial (M), 1 distolingual (DL), also known as radix entomolaris (RE), and a distovestibular (DV). For both teeth, M root had 2 canals, and DV and DL roots presented just 1 canal. Mitochondrial DNA analysis determined presence of haplogroup C, corresponding to Amerindian ethnicity. CONCLUSIONS: The presence of RE is uncommon. This case report contributes to describe this rare anatomical variation. To our knowledge, this is the first molecular-genetic study applied to dental anatomy and gives basis to develop future research in the area.

Toluene increases acute thermonociception in mice.

Toluene is an abused solvent widely used in several commercial products. Recent evidence indicates that this solvent is a non-competitive inhibitor of NMDA receptors. Since NMDA receptors have been implicated in pain, this paper describes studies of the effects of increasing concentrations of inhaled toluene on nociception. Swiss Webster mice were exposed to toluene (500-8000 ppm) in static exposure chambers for 30 min. After completing the exposure period, animals were tested for nociception using the hot plate test. Toluene dose-dependently increased nociception as reflected by shorter latencies for the reflex, paw-lick and escape responses in toluene-treated mice with respect to their controls (animals exposed to air). In order to determine the possible role of opioids in this response, morphine (1-10 mg/kg) was injected before toluene inhalation. Toluene was not able to block morphine-induced antinocieption, however, it produced a shift of the morphine dose-response curve to lower effects, suggesting a physiological antagonism. No potentiation was seen when toluene was administered in combination with naloxone. Present results suggest that toluene increases nociception via neurotransmitter systems others than the glutamatergic.

Apolipoprotein B gene polymorphisms: prevalence and impact on serum lipid concentrations in hypercholesterolemic individuals from Brazil.

Genetic polymorphisms at the apolipoprotein B (apo B) have been associated with elevated plasma concentrations of low-density lipoprotein (LDL) cholesterol, atherosclerosis and increased risk for coronary artery disease (CAD). In the present study, four apo B gene polymorphisms (MspI, XbaI, Ins/Del and 3'HVR) have been investigated to determine their frequencies and influence on the lipid profile of 177 hypercholesterolemic white Brazilian subjects (HG) and 100 control individuals (CG). The genotype distribution and allele frequency of MspI, XbaI and Ins/Del polymorphisms of apo B gene were similar between HG and CG groups. The frequency of the alleles smaller than 43 repeats (< or =43) of 3'HVR polymorphism in the HG group was higher when compared to controls (16.4 vs. 8.5%, P<0.05). Moreover, these alleles were associated with higher total cholesterol concentrations in serum of hypercholesterolemic individuals (P<0.05). In addition, an association between Ins/Del and 3'HVR polymorphism was observed. The alleles < or =43 and Del were more frequent in the HG when compared to the CG individuals (P<0.05). We concluded that 3'HVR polymorphism at the apo B gene may be an important genetic marker to evaluate atherosclerotic disease risk.

Polymorphisms of the low-density lipoprotein receptor gene in Brazilian individuals with heterozygous familial hypercholesterolemia

Familial hypercholesterolemia (FH) is a metabolic disorder inherited as an autosomal dominant trait characterized by an increased plasma low-density lipoprotein (LDL) level. The disease is caused by several different mutations in the LDL receptor gene. Although early identification of individuals carrying the defective gene could be useful in reducing the risk of atherosclerosis and myocardial infarction, the techniques available for determining the number of the functional LDL receptor molecules are difficult to carry out and expensive. Polymorphisms associated with this gene may be used for unequivocal diagnosis of FH in several populations. The aim of our study was to evaluate the genotype distribution and relative allele frequencies of three polymorphisms of the LDL receptor gene, HincII1773 (exon 12), AvaII (exon 13) and PvuII (intron 15), in 50 unrelated Brazilian individuals with a diagnosis of heterozygous FH and in 130 normolipidemic controls. Genomic DNA was extracted from blood leukocytes by a modified salting-out method. The polymorphisms were detected by PCR-RFLP. The FH subjects showed a higher frequency of A+A+ (AvaII), H+H+ (HincII1773) and P1P1 (PvuII) homozygous genotypes when compared to the control group (P<0.05). In addition, FH probands presented a high frequency of A+ (0.58), H+ (0.61) and P1 (0.78) alleles when compared to normolipidemic individuals (0.45, 0.45 and 0.64, respectively). The strong association observed between these alleles and FH suggests that AvaII, HincII1773 and PvuII polymorphisms could be useful to monitor the inheritance of FH in Brazilian families

Polymorphisms of the low-density lipoprotein receptor gene in Brazilian individuals with heterozygous familial hypercholesterolemia.

Familial hypercholesterolemia (FH) is a metabolic disorder inherited as an autosomal dominant trait characterized by an increased plasma low-density lipoprotein (LDL) level. The disease is caused by several different mutations in the LDL receptor gene. Although early identification of individuals carrying the defective gene could be useful in reducing the risk of atherosclerosis and myocardial infarction, the techniques available for determining the number of the functional LDL receptor molecules are difficult to carry out and expensive. Polymorphisms associated with this gene may be used for unequivocal diagnosis of FH in several populations. The aim of our study was to evaluate the genotype distribution and relative allele frequencies of three polymorphisms of the LDL receptor gene, HincII(1773) (exon 12), AvaII (exon 13) and PvuII (intron 15), in 50 unrelated Brazilian individuals with a diagnosis of heterozygous FH and in 130 normolipidemic controls. Genomic DNA was extracted from blood leukocytes by a modified salting-out method. The polymorphisms were detected by PCR-RFLP. The FH subjects showed a higher frequency of A+A+ (AvaII), H+H+ (HincII(1773)) and P1P1 (PvuII) homozygous genotypes when compared to the control group (P<0.05). In addition, FH probands presented a high frequency of A+ (0.58), H+ (0.61) and P1 (0.78) alleles when compared to normolipidemic individuals (0.45, 0.45 and 0.64, respectively). The strong association observed between these alleles and FH suggests that AvaII, HincII(1773) and PvuII polymorphisms could be useful to monitor the inheritance of FH in Brazilian families.

Seven DNA polymorphisms at the candidate genes of atherosclerosis in Brazilian women with angiographically documented coronary artery disease.

The possible association of genetic markers at the apolipoprotein E (HhaI polymorphism), apolipoprotein B (XbaI, EcoRI and Ins/Del polymorphisms), and low-density lipoprotein receptor (LDLR) (AvaII, HincII and PvuII polymorphisms) with coronary artery disease (CAD) was evaluated in 50 Brazilian women with CAD diagnosed by angiography and in 100 healthy women (controls). The frequency of E3/E4 genotype for HhaI polymorphism at the Apo E gene was significantly higher in CAD patients than in controls (40% vs. 14%, respectively, P<0.001). Similarly, the X-X- genotype for XbaI polymorphism was more frequent in CAD individuals than controls (42% vs. 12%, P<0.0001). The A+A+ and P1P1 genotypes for AvaII and PvuII polymorphisms at the LDLR locus were also higher in CAD subjects than controls (44% vs. 16%, P<0.001 and 64% vs. 39%, P<0.05, respectively). The estimated relative risks for CAD in women carrying the E3/E4, X-X-, A+A+ and P1P1 genotypes were 4.1 [95% confidence interval (CI), 3.0-5.6], 5.3 (95% CI, 3.8-7.5), 4.1 (95% CI, 3.0-5.5), and 2.8 (95% CI, 2.2-3.6), respectively. This study demonstrates that Apo E, Apo B and LDLR gene polymorphisms are associated with CAD in Brazilian Caucasian women.

Lipid-lowering response of the HMG-CoA reductase inhibitor fluvastatin is influenced by polymorphisms in the low-density lipoprotein receptor gene in Brazilian patients with primary hypercholesterolemia.

Although the efficacy of fluvastatin (HMG-CoA reductase inhibitor) in the treatment of primary hypercholesterolemia is well documented, a wide interindividual variation treatment response has been observed. We have studied the possible role of the AvaII (exon 13), HincII (exon 12), and PvuII (intron 15) polymorphisms at the low-density lipoprotein receptor (LDLR) gene on lipid-lowering response in 55 patients (36 to 70 years old) with primary hypercholesterolemia treated with fluvastatin for 16 weeks. LDLR genotypes were determined by PCR-RFLP. The results indicate that the AvaII and PvuII polymorphisms influence the cholesterol-lowering response of the HMG-CoA reductase inhibitor Fluvastatin. Patients carrying A+A+ (AvaII) or P1P1 (PvuII) homozygous genotypes presented lower reduction in total cholesterol, LDL-C and apolipoprotein B levels after 16 weeks of treatment with fluvastatin, when compared to other genotypes (P<0.05). Our data also support the previous assumption that the AvaII, HincII, and PvuII polymorphisms of the LDLR gene are associated with variation of serum cholesterol levels. Therefore, the identification of the LDLR genetic profile may provide better prediction of a patient's clinical response to fluvastatin.

Uso indiscriminado de antimicrobianos en el servicio de Medicina Interna del Centro Médico Nacional Adolfo Ruiz Cortines / Indiscriminate use of antimicrobial agents in the internal medicine service of Centro Médico Nacional Adolfo Ruiz Cortines

Antecedentes: de un tiempo a la fecha se ha perpetrado un uso indiscriminado de antimicrobianos en los servicios de medicina interna de la mayor parte de los hospitales. Objetivo: determinar si esta práctica tiene lugar también en el servicio de medicina interna del Centro Médico Nacional Adolfo Ruiz Cortines de Veracruz. Material y métodos: estudio descriptivo, prospectivo y observacional donde se incluyeron 67 pacientes hospitalizados en el servicio de medicina interna, a quienes se les impuso un tratamiento antimicrobiano debido a enfermedades infecciosas. Para conseguir el objetivo se analizaron los expedientes clínicos de los pacientes, así como su estado físico, los registros de enfermería, los reportes de laboratorio, el número de antibióticos administrados a cada paciente, la duración del tratamiento y la congruencia entre el diagnóstico y la medicación. También se realizó una descripción estadística. Resultados: se evaluaron 25 hombres y 42 mujeres de entre 21 y 93 años de edad, a quienes se les administraron 148 antibióticos divididos en 130 esquemas de tratamiento, con un rango de 1 a 6 antibióticos por paciente. En 39 esquemas (30 por ciento) la duración fue menor de cinco días y en 35 esquemas (26.9 por ciento) menor de 10. Sólo el 10 por ciento de los cultivos se reportaron como positivos (50 por ciento de los cuales fueron obra de Candida albicans). Conclusiones: el número de antibióticos por individuo fue grande, como lo refleja el esquema de tres o más, dado en 40 por ciento de los casos, al igual que el resultado de cultivos negativos, por lo cual se concluye que sí existe uso indiscriminado de antimicrobianos en el servicio de medicina interna del nosocomio en estudio.

Pvu II intron 15 polymorphism at the LDL receptor gene is associated with differences in serum lipid concentrations in subjects with low and high risk for coronary artery disease from Brazil.

Coronary artery disease (CAD) has a high prevalence in the Brazilian population. Nevertheless, studies of genetic risk factors for CAD in this country have not been sufficiently conducted. We used the Pvu II polymorphism (intron 15) at the low-density lipoprotein receptor (LDLR) gene to study the effect of variation at this locus in determining plasma lipid concentrations in 128 white subjects presenting a lipid profile suggesting high risk for CAD (HRG) and 100 white normolipidemic individuals (controls, CG). The Pvu II polymorphism was detected by PCR-RFLP. The P1P1 genotype for Pvu II polymorphism (homozygous for absence of restriction site) was greater in HRG individuals than in CG subjects (57% vs. 38%, P<0.05). Moreover, the P1P1 genotype was strongly associated with high concentrations of total cholesterol (P=0.0001), triglycerides (P=0. 0295), LDL-C (P=0.0001), and VLDL-C concentrations (P=0.0280) and lower HDL-C concentrations (P=0.0051) in HRG subjects. Similarly, the CG individuals with P1P1 genotype presented high concentrations of total cholesterol and LDL-C compared to other genotypes (P=0. 0001). This study demonstrates the influence of Pvu II polymorphism of the LDLR on serum lipid concentrations of individuals with low and high risk for CAD from Brazil.

Early changes in nitric oxide synthase activity in atrial intramural arteries following experimental spinal cord injury in rats.

Previously, we have shown that immediately after an experimental spinal cord injury (SCI) in anaesthetized rats, there is a large fall in mean arterial pressure (MAP) and heart rate (HR), followed by an abrupt increase in MAP. To evaluate the participation of nitric oxide (NO), we evaluated the activity of nitric oxide synthase (NOS) using Nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemistry in sections of atria at several post-injury time-intervals. Staining increased at 3 min, reached a maximum at 9 min and diminished 30 min after injury. Pretreatment with atropine prevented changes in MAP, HR and NADPH-d staining suggesting that such modifications result from an increased vagal stimulation. In conclusion, the NOS activity is transiently elevated in the atrial intramural arteries of rats subjected to an SCI.

Effects of Ava II and Hinc II polymorphisms at the LDL receptor gene on serum lipid levels of Brazilian individuals with high risk for coronary heart disease.

Coronary heart disease (CHD) has presented high prevalence in the Brazilian population. Nevertheless, studies of genetic risk factors for CHD in our country are insufficiently carried out. We have investigated the effects of Ava II (exon 13) and Hinc II (exon 12) polymorphisms at the low-density lipoprotein receptor (LDLR) gene on circulating lipids of 170 white unrelated individuals presenting a lipid profile with high risk for CHD (HRG) and 130 controls (CG) from São Paulo City, Brazil. Ava II and Hinc II polymorphic regions at the LDLR gene were amplified by PCR and analyzed by enzymatic isotyping. The frequency of the genotypes A+A+ (Ava II) and H+H+ (Hinc II) was greater in HRG group compared to that of the controls (32 vs. 16% and 32 vs. 18%, respectively). Moreover, in the HRG group, A+A+ and H+H+ genotypes were associated with high concentrations of total cholesterol and LDL-C in serum (P = 0.0001). Our results indicate that Ava II and Hinc II polymorphisms at the LDLR locus contribute to the variability of total cholesterol and LDL-C levels in HRG individuals. These data suggest that the LDLR polymorphism remains a useful genetic marker for predicting CHD risk.

Differences in basal nocturnal, meal-stimulated, and pentagastrin-stimulated gastric secretion values in a sample of healthy volunteers in basal conditions and under ranitidine influence.

The gastric secretion values from 16 healthy male volunteers are reported. A nasogastric tube was positioned in the gastric antrum and 10-min gastric secretion samples were obtained hourly by continuous suction. Basal nocturnal, meal-stimulated, and pentagastrin-stimulated gastric acid secretion were measured. Experimental sessions were carried out in control conditions and repeated after a 7-day treatment with placebo and ranitidine (150 mg b.i.d.) in a double-blind procedure. We found six subjects (group I) with basal nocturnal, meal-stimulated, and pentagastrin-stimulated gastric secretion values statistically lower than then rest of the group (group II). Basal nocturnal secretion mean values were 3.99 +/- 6.6 mmol/L (group I) and 59.2 +/- 22.1 mmol/L (group II) (p < 0.01). Meal-stimulated gastric acidity mean values were 33.1 + 17.3 mmol/L (group I) and 65.6 +/- 30.6 mmol/L (group II) (p < 0.05). Pentagastrin-stimulated gastric secretion mean values were 8 +/- 2 mmol/h (group I) and 19.2 +/- 2.7 mmol/h (group II) (p < 0.01). Ranitidine significantly inhibited basal nocturnal, meal-stimulated, and pentagastrin-stimulated gastric acidity values mostly in group II. These results suggest that there are two different patterns of gastric secretion in the healthy male population.