Composition of the adult digestive tract bacterial microbiome based on seven mouth surfaces, tonsils, throat and stool samples

Background

To understand the relationship between our bacterial microbiome and health, it is essential to define the microbiome in the absence of disease. The digestive tract includes diverse habitats and hosts the human body's greatest bacterial density. We describe the bacterial community composition of ten digestive tract sites from more than 200 normal adults enrolled in the Human Microbiome Project, and metagenomically determined metabolic potentials of four representative sites.

Results

The microbiota of these diverse habitats formed four groups based on similar community compositions: buccal mucosa, keratinized gingiva, hard palate; saliva, tongue, tonsils, throat; sub- and supra-gingival plaques; and stool. Phyla initially identified from environmental samples were detected throughout this population, primarily TM7, SR1, and Synergistetes. Genera with pathogenic members were well-represented among this disease-free cohort. Tooth-associated communities were distinct, but not entirely dissimilar, from other oral surfaces. The Porphyromonadaceae, Veillonellaceae and Lachnospiraceae families were common to all sites, but the distributions of their genera varied significantly. Most metabolic processes were distributed widely throughout the digestive tract microbiota, with variations in metagenomic abundance between body habitats. These included shifts in sugar transporter types between the supragingival plaque, other oral surfaces, and stool; hydrogen and hydrogen sulfide production were also differentially distributed.

Conclusions

The microbiomes of ten digestive tract sites separated into four types based on composition. A core set of metabolic pathways was present across these diverse digestive tract habitats. These data provide a critical baseline for future studies investigating local and systemic diseases affecting human health.     

Luteinizing hormone secretion and corpus luteum function in cows receiving two levels of progesterone

The objectives of this experiment were to determine if subnormal levels of progesterone (P4) indicative of luteal insufficiency influence (1) pulsatile release of luteinizing hormone (LH), (2) the interval to the preovulatory surge of LH after removal of P4, and (3) the secretion of P4 during the estrous cycle subsequent to administration of subnormal levels of P4. On Day 5 (Day = 0 day of estrus) of the estrous cycle, cows received P4-releasing intravaginal devices (PRID) to produce normal (2 PRIDs; n = 7) or subnormal (0.5 PRID; n = 6) concentrations of P4. Five cows served as controls. On Day 10, serial blood samples were collected from all cows. Collection of blood samples was again initiated on Day 17 in cows receiving PRIDs. The PRIDs were removed and blood collection continued for 78 h. Daily blood samples were collected from all animals for 42 days subsequent to estrus (estrous cycles 1 and 2, respectively). During estrous cycle 1, mean concentration of P4 was lower (p less than 0.05) and frequency of pulses of LH was higher (p less than 0.05) in cows receiving subnormal P4 than in cows receiving normal P4 and control cows. Plasma concentrations of estradiol (E2) were higher (p less than 0.05) on Days 9-16 of estrous cycle 1 in cows receiving subnormal P4 than in cows receiving normal P4 or in control cows. Concentrations of E2 were greater (p less than 0.05) at 6, 18, and 30 h following removal of PRIDs in cows receiving subnormal P4 than in cows receiving normal P4.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship between serum luteinizing hormone and estradiol in prepubertal boars

Effects of estradiol on serum luteinizing hormone (LH) were studied in prepubertal boars. In Exp. 1, 15-wk-old boars were given (iv) 50 mug estradiol, 1 mg testosterone or 1.5 ml ethanol. Estradiol (P<0.05) decreased LH over a 2.5-hr period, but testosterone did not. In Exp. 2, an estradiol implant reduced LH sample variance (P<0.01) while LH (547 +/- 96 vs 655 +/- 43 pg/ml) and estradiol (14.2 +/- 3.3 vs 18.4 +/- 1.0 pg/ml; control vs implant) were unchanged in 12-wk-old boars. Pulsatile LH releases (4.3 +/- 1.1 vs 3.0 +/- 0.4 pulses/pig/8 hr; control vs treated) and pulse amplitude (272 +/- 34 vs 305 +/- 40 pg/ml) were not affected. The implant tended to decrease serum testosterone (4.86 +/- 0.75 vs 7.66 +/- 1.51 ng/ml; P<0.10). In Exp. 3, LH was higher after zero implants than after four implants (279 +/- 7 vs 227 +/- 9 pg/ml; P<0.01), and LH after two implants was also higher than after four implants (263 +/- 7 pg/ml; P<0.01) in 14-wk-old boars in a Latin square design. Peak LH after 40 mug gonadotropin releasing hormone (GnRH) was less after two and four implants (1,100 +/- 126 and 960 +/- 167 pg/ml, respectively; P<0.01) than after zero implants (1,742 +/- 126 pg/ml). Slope of the first 20 min of LH response to GnRH was greater after zero implants (45.3 pg/min; P<0.05) than after either two or four implants (20.6 and 16.9 pg/min, respectively). Implant treatment decreased serum testosterone (P<0.025) but increased estradiol (P<0.10). Small changes in serum estradiol resulted in changes in LH. These changes in sample variance and mean LH were recognized by boars as different from normal because serum testosterone decreased. Changes in LH may result from estradiol's negative effect on pituitary responsiveness to endogenous GnRH because response to exogenous GnRH was depressed by estradiol.     

Effect of 17beta-estradiol on the preovulatory surge of LH in the bovine female

The hypothesis tested was that increasing concentration of 17beta-estradiol (E(2)) subsequent to luteolysis stimulates the preovulatory surge of LH and that a decline in E(2) after the initial rise is not necessary to trigger the preovulatory surge of LH in the bovine female. Beef cows were synchronized to Day 16 of the estrous cycle. At Hour 0, all cows were ovariectomized and received one of four E(2) treatments: 1) luteal phase E(2) (LE; n=5), 2) increasing then decreasing E(2) (DE; n=5), 3) increasing and subsequent maintenance of high E(2) (IE; n=4), and 4) no E(2) (NE; n=3). Cows in the LE group received one E(2) implant at Hour 0 which provided low concentrations of E(2). Cows in the DE group received one E(2) implant at 0, 8, 16, 24, 32 and 40 hours; implants were subsequently removed at 8-hour intervals, thus mimicking the preovulatory rise and fall of E(2). Cows in the IE group were treated with the same regimen of E(2) implants as cows of the DE group, except that no E(2) implants were removed. Blood samples were collected at Hour 0 and at hourly intervals from Hour 2 through 80, for serum LH and E(2) quantification. The number of cows responding with a surge of LH was 0/3, 0/5, 4/5 and 3/4 for the NE, LE, DE and IE treatments, respectively. The proportion of cows responding with an LH surge was different (P<0.01) when data for cows in the NE and LE groups were pooled and compared with the pooled data of cows in the DE and IE groups. The mean time of the LH surge was not different (P>0.80) for cows responding with an LH surge (DE and IE treatments). Thus, increased levels of E(2) greater than luteal phase concentrations are needed to initiate preovulatory surges of LH, and it appears that concentrations of E(2) need to reach a certain level but do not need to decrease after this initial rise to stimulate a surge release of LH.     

Electrical and adaptive properties of rod photoreceptors in bufo marinus. I. Effects of altered extracellular Ca(2+) levels

The effects of altering extracellular Ca(2+) levels on the electrical and adaptive properties of toad rods have been examined. The retina was continually superfused in control (1.6 mM Ca(2+)) or test ringer’s solutions, and rod electrical activity was recorded intracellularly. Low-calcium ringer’s (10(-9)M Ca(2+)) superfused for up to 6 min caused a substantial depolarization of the resting membrane potential, an increase in light-evoked response amplitudes, and a change in the waveform of the light-evoked responses. High Ca(2+) ringer’s (3.2 mM) hyperpolarized the cell membrane and decreased response amplitudes. However, under conditions of either low or high Ca(2+) superfusion for up to 6 min, in both dark-adapted and partially light-adapted states, receptor sensitivity was virtually unaffected; i.e., the V-log I curve for the receptor potential was always located on the intensity scale at a position predicted by the prevailing light level, not by Ca(2+) concentration. Thus, we speculate that cytosol Ca(2+) concentration is capable of regulating membrane potential levels and light-evoked response amplitudes, but not the major component of rod sensitivity. Low Ca(2+) ringer’s also shortened the period of receptor response saturation after a bright but nonbleaching light flash, hence accelerating the onset of both membrane potential and sensitivity recovery during dark adaptation.

Exposure of the retina to low Ca(2+) (10(-9)M) ringer’s for long periods (7-15 min) caused dark-adapted rods to lose responsiveness. Response amplitudes gradually decreased, and the rods became desensitized. These severe conditions of low Ca(2+) caused changes in the dark-adapted rod that mimic those observed in rods during light adaptation. We suggest that loss of receptor sensitivity during prolonged exposure to low Ca(2+) ringer’s results from a decrease of intracellular (intradisk) stores of Ca(2+); i.e., less Ca(2+) is thereby released per quantum catch.

     

Genetic islands of <Emphasis Type="Italic">Streptococcus agalactiae</Emphasis> strains NEM316 and 2603VR and their presence in other Group B Streptococcal strains

Background  

Streptococcus agalactiae (Group B Streptococcus; GBS) is a major contributor to obstetric and neonatal bacterial sepsis. Serotype III strains cause the majority of late-onset sepsis and meningitis in babies, and thus appear to have an enhanced invasive capacity compared with the other serotypes that cause disease predominantly in immunocompromised pregnant women. We compared the serotype III and V whole genome sequences, strains NEM316 and 2603VR respectively, in an attempt to identify genetic attributes of strain NEM316 that might explain the propensity of strain NEM316 to cause late-onset disease in babies. Fourteen putative pathogenicity islands were described in the strain NEM316 whole genome sequence. Using PCR- and targeted microarray- strategies, the presence of these islands were assessed in a diverse strain collection including 18 colonizing isolates from healthy pregnant women, and 13 and 8 invasive isolates from infants with early- and late-onset sepsis, respectively.     

Concentrations and ecological risks of metals in surface sediments of some coastal creeks in the Niger Delta,Nigeria

The concentrations of nine metals were measured by atomic absorption spectrophotometry in surface sediments of three coastal creeks, namely, the Ifie, Egbokodo and Ubeji creeks, in the Niger Delta of Nigeria, from August 2012 to January 2013. The aim of the study was to provide information on the spatial and seasonal distribution patterns, degree of contamination, and ecological risks of metals in these sediments. The mean concentrations of the nine metals in these creek sediments ranged from 0.30 to 3.20?mg kg^?1 Cd; 10.7 to 24.7?mg kg^?1 Pb, 125 to 466?mg kg^?1 Cr; 3.1.10 to 14.9?mg kg^?1 Cu; 4.7 to 14.3?mg kg^?1 Co; 61.1 to 115?mg kg^?1 Ni; 106 to 183?mg kg^?1 Mn; 52.0 to 170?mg kg^?1 Zn and 5 469 to 20 639?mg kg^?1 Fe. In general, the metal concentrations were higher in the dry season than the wet season, except for Cr. The concentrations of Cd, Cr, Ni and Zn were above their regulatory control limits in sediment as specified by the Nigerian Regulatory Authority and Cd was identified as the main ecological risk factor. The enrichment factors for the studied metals followed the order: Cd > Cr > Ni > Zn > Pb > Co > Mn > Cu. The average multiple pollution index values indicated that these sediments were severely polluted with significant inputs from Cd, Ni and Cr.