Rhizobacteria Communities of Phytoremediation Plant Species in Petroleum Hydrocarbon Contaminated Soil of the Sudd Ecosystem, South Sudan.

The Sudd wetland is one of the oil-rich regions of South Sudan where environmental pollution resulting from oil extraction activities has been unprecedented. Although phytoremediation is the most feasible technique, its efficacy reduces at high TPH concentration in soil. This has made rhizoremediation the most preferred approach. Rhizoremediation involves use of a combination of phytoremediation and biostimulation. The process is catalyzed by the action of rhizobacteria. Therefore, the objective of this study is to characterize rhizobacteria communities prevalent in phytoremediation species growing in hydrocarbon-contaminated soils biostimulated with cattle manure. The treatments studied were plant species only (T1), plant species and hydrocarbons (T2), plant species and manure (T3), and plant species, manure, and hydrocarbons (T4). The rhizobacteria communities were determined using pyrosequencing of 16S rRNA. In the treatment with phytoremediation species, hydrocarbons 75 g · kg-1soil, and cattle manure 5 g · kg-1soil (T4), there was a significant increase (p < 0.05) in rhizobacteria abundance with the highest ASV observed in H. rufa (4980) and the lowest in S. arundinaceum (3955). In the same treatment, bacteria community diversity was high in H. rufa (Chao1, 10310) and the least in S. arundinaceum (Chao 1, 8260) with Proteobacteria, Firmicutes, and Actinobacteria as the dominant phyla. Similarly, in contaminated soil treated with cattle manure, there was a significant increase (p < 0.05) in abundance of rhizobacteria genera with Pseudomonas dominating across phytoremediation species. H. rufa was dominated by Bacillus, Fusibacter, and Rhodococcus; G. barbadense was mainly associated with Luteimonas and Mycobacterium, and T. diversifolia was inhabited by Bacillus and Luteimonas. The rhizosphere of O. longistaminata was dominated by Bacillus, Fusibacter, and Luteimonas, while S. arundinaceum was largely inhabited by Sphingomonas. These rhizobacteria genera ought to be applied in the Sudd region for bioremediation.

The Uromodulin C744G mutation causes MCKD2 and FJHN in children and adults and may be due to a possible founder effect.

Autosomal dominant medullary cystic kidney disease type 2 (MCKD2) is a tubulo-in terstitial nephropathy that causes renal salt wasting, hyperuricemia, gout, and end-stage renal failure in the fifth decade of life. This disorder was described to have an age of onset between the age of 20-30 years or even later. Mutations in the Uromodulin (UMOD) gene were published in patients with familial juvenile hyperuricemic nephropathy (FJHN) and MCKD2. Clinical data and blood samples of 16 affected individuals from 11 different kindreds were collected. Mutational analysis of the UMOD gene was performed by exon polymerase chain reaction (PCR) and direct sequencing. We found the heterozygous C744G (Cys248Trp) mutation, which was originally published by our group, in an additional four kindreds from Europe and Turkey. Age of onset ranged from 3 years to 39 years. The phenotype showed a variety of symptoms such as urinary concentration defect, vesicoureteral reflux, urinary tract infections, hyperuricemia, hypertension, proteinuria, and renal hypoplasia. Haplotype analysis showed cosegragation with the phenotype in all eight affected individuals indicating that the C744G mutation may be due to a founder effect. Moreover, we describe a novel T229G (Cys77Gly) mutation in two affecteds of one kindred. Three of the affected individuals were younger than 10 years at the onset of MCKD2/FJHN. Symptoms include recurrent urinary tract infections compatible with the published phenotype of the Umod knockout mouse model. This emphasizes that MCKD2 is not just a disease of the young adult but is also relevant for children.

Oral versus initial intravenous therapy for urinary tract infections in young febrile children.

BACKGROUND: The standard recommendation for treatment of young, febrile children with urinary tract infection has been hospitalization for intravenous antimicrobials. The availability of potent, oral, third-generation cephalosporins as well as interest in cost containment and avoidance of nosocomial risks prompted evaluation of the safety and efficacy of outpatient therapy. METHODS: In a multicenter, randomized clinical trial, we evaluated the efficacy of oral versus initial intravenous therapy in 306 children 1 to 24 months old with fever and urinary tract infection, in terms of short-term clinical outcomes (sterilization of the urine and defervescence) and long-term morbidity (incidence of reinfection and incidence and extent of renal scarring documented at 6 months by 99mTc-dimercaptosuccinic acid renal scans). Children received either oral cefixime for 14 days (double dose on day 1) or initial intravenous cefotaxime for 3 days followed by oral cefixime for 11 days. RESULTS: Treatment groups were comparable regarding demographic, clinical, and laboratory characteristics. Bacteremia was present in 3.4% of children treated orally and 5.3% of children treated intravenously. Of the short-term outcomes, 1) repeat urine cultures were sterile within 24 hours in all children, and 2) mean time to defervescence was 25 and 24 hours for children treated orally and intravenously, respectively. Of the long-term outcomes, 1) symptomatic reinfections occurred in 4.6% of children treated orally and 7.2% of children treated intravenously, 2) renal scarring at 6 months was noted in 9.8% children treated orally versus 7.2% of children treated intravenously, and 3) mean extent of scarring was approximately 8% in both treatment groups. Mean costs were at least twofold higher for children treated intravenously ($3577 vs $1473) compared with those treated orally. CONCLUSIONS: Oral cefixime can be recommended as a safe and effective treatment for children with fever and urinary tract infection. Use of cefixime will result in substantial reductions of health care expenditures.

Current status of pediatric home peritoneal dialysis training in the United States.

There are little aggregate data that examine attributes of peritoneal dialysis (PD) training programs for children. We determined characteristics of pediatric home PD training programs in a sample of 54 centers in the NAPRTCS PD registry by telephone interview. Sixty-seven percent of the programs trained pediatric patients only (P-only); 33% were combined pediatric/adult (P/A) programs; 33 programs had dedicated training rooms. Most programs trained 5 to 8 patients/year; only 2 trained more than 12 patients/year. Forty-eight of 54 programs (89%) taught both automated and manual PD techniques; the preferred type of PD varied. All units preferred to train 2 people. The patient was often one of the trainees, but the minimal eligible age varied greatly. The patients were trained as inpatients (IP) in 38 units (70%) and as outpatients (OP) in 16 units (30%). P-only programs were less likely to train as OP (20%) than P/A programs (50%) (p < 0.01). There was no difference in the mean training time for P-only versus P/A programs. However, training that took more than 6 days occurred more often when done as an IP (79%) than as an OP (56%) (p = 0.057). Furthermore, only 25% of IP units that took more than 6 days to train offered training on the weekend; none of the IP units that took more than 10 days offered weekend training. In conclusion, the structure of PD training programs for children in the United States varies tremendously. OP training is usually shorter in duration and potentially more cost-effective.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of systemic glucose concentration on brain metabolism following repeated brain ischemia.

Since systemic glucose concentration is an important determinant of ischemic brain metabolism in neonates, we sought to determine if the systemic glucose concentration influences brain metabolic alterations following repeated partial ischemia. A group of hyperglycemic piglets (n = 12) were compared to a group of modestly hypoglycemic piglets (n = 12) using in vivo 2H and 31P magnetic resonance spectroscopy to simultaneously measure cerebral blood flow and phosphorylated metabolites before, during and 30 min after two 10-min episodes of ischemia (i.e. Recovery 1 and 2). For both groups, beta-ATP levels at Recovery 1 and 2 were lower than Control (91 +/- 11 and 83 +/- 15% of Control, respectively for both groups combined, P = 0.002 vs Control). Inorganic phosphorus was elevated in hyperglycemic piglets at Recovery 1 and 2 (117 +/- 15 and 118 +/- 10% of Control). In contrast, in modestly hypoglycemic piglets inorganic phosphorus progressively rose from Recovery 1 (131 +/- 24% of Control) to Recovery 2 (149 +/- 37% of Control), and differed from the hyperglycemic group (P = 0.02). These changes did not correlate with post-ischemic cerebral blood flow, cerebral O2 delivery or cerebral glucose delivery. In both groups phosphocreatine and intracellular pH returned to Control values during Recovery 1 and 2. The progressive increase in inorganic phosphorus post-ischemia in hypoglycemic piglets suggests that modest hypoglycemia during and following repeated partial ischemia adversely affects immediate brain metabolic recovery.

Serum and urine soluble interleukin-2 receptor in idiopathic nephrotic syndrome.

Although a cellular immune pathogenesis is suspected in idiopathic nephrotic syndrome of childhood (INS), there is scant direct evidence of in vivo immune activation. In order to investigate cytokine cascade activation in INS, soluble interleukin-2 receptor (sIL-2R) in plasma and urine was characterized and its levels measured in INS patients during relapse. Immunochemically detectable sIL-2R had a molecular mass of 35-46 kDa in both serum and urine and the molecule appears to be excreted intact; the pI was 5.05. INS patients had elevated serum sIL-2R levels compared with adult normal controls (845 +/- 97 vs. 373 +/- 47 U/ml, P = 0.001) and were significantly higher than previously published age-matched controls. Urinary excretion of sIL-2R was 47.2 +/- 13 U/mg creatinine in patients. Both the sIL-2R excretion rate and the fractional excretion of sIL-2R were positively correlated with the excretion of albumin (P = 0.02 and 0.002, respectively). These increased serum and urine levels occurred whether relapse was or was not associated with an intercurrent illness. We conclude that: (1) despite increased sIL-2R excretion during INS relapse, serum levels are significantly elevated; (2) while the elevated urinary levels could result from enhanced intrarenal production, they more likely reflect the increased serum levels; (3) the elevated sIL-2R levels support an immune pathogenesis in INS.

Energy reserves and utilization rates in developing brain measured in vivo by 31P and 1H nuclear magnetic resonance spectroscopy.

Age-related changes in cerebral energy utilization were examined in swine, a species whose maximal rate of development is known to occur in the perinatal period. Interleaved in vivo 31P and 1H nuclear magnetic resonance spectroscopy was used to measure the rates of change in cerebral concentrations of phosphocreatine (PCr), nucleoside triphosphates, and lactate following complete ischemia, induced via cardiac arrest, in a total of 19 newborn, 10-day-old, and 1-month-old piglets. Preischemic concentrations of these three metabolites plus glucose and glycogen were determined in a separate experiment on 12 piglets whose brains were funnel-frozen in situ. The rate constants for the PCr and ATP decline and lactate increase were determined by nonlinear regression fits to the experimental data, assuming first-order kinetics. The rate constants and preischemic metabolite concentrations were used to calculate the initial flux of high-energy phosphate equivalents (approximately P), which was used as an estimate of cerebral energy utilization at the point when ischemia was initiated. Cerebral energy utilization equaled 6.5 +/- 1.9, 9.5 +/- 3.2, and 15.1 +/- 3.2 mumol approximately P/g/min in newborn, 10-day-old, and 1-month-old piglets, respectively. Within each age group the energy utilization rate was not altered by hyperglycemia-induced increases in cerebral energy reserves, but during hypoglycemia cerebral energy utilization rates decrease. The slope of approximately P versus time decreased with the duration of ischemia, indicating that cerebral energy utilization rates decrease after the first few minutes of ischemia. Newborn piglets had higher cerebral energy utilization rates compared with literature values for newborn rats and mice. This is consistent with the concept that newborns from a species with a perinatal stage of maximal growth and development will have higher cerebral energy demands compared with newborns from a species such as rodents, whose maximal growth occurs postnatally. However, this conclusion remains tentative because literature cerebral utilization rates estimated from the initial slope of approximately P-versus-time plots tend to underestimate the true rate, since the assumption of continued linearity may not be valid for the interval chosen.

Glucose-associated alterations in ischemic brain metabolism of neonatal piglets.

BACKGROUND AND PURPOSE: During global brain ischemia or hypoxia-ischemia in adults, hyperglycemia is deleterious to the brain. In contrast, similar adverse effects have not been found in neonatal animals. This investigation examined neonatal piglets to determine if there were specific alterations of ischemic brain metabolism associated with different systemic glucose concentrations and to potentially clarify the effects of hyperglycemia during ischemia in neonates. METHODS: Two groups of animals (n = 12 in each group) were studied during partial ischemia to compare the effects of hyperglycemia (plasma glucose concentration, 258 +/- 97 mg% [mean +/- SD]) with modest hypoglycemia (plasma glucose concentration, 62 +/- 23 mg%). A broad spectrum of cerebral blood flow reduction was achieved by combining inflation of a cervical pressure cuff with varying degrees of hemorrhagic hypotension. High-energy phosphorylated metabolites, intracellular pH, and cerebral blood flow were simultaneously measured using a magnetic resonance spectroscopic technique. Brain metabolic variables (beta-ATP, inorganic phosphorus, phosphocreatine, intracellular pH) were plotted as a function of blood flow reduction during partial ischemia for each group. RESULTS: During ischemia values of cerebral blood flow were comparably distributed between groups and ranged from 15% to 110% of those of control. At a given reduction of cerebral blood flow, hyperglycemic piglets maintained a higher concentration of beta-ATP (p = 0.011) and had a smaller increase in inorganic phosphorus (p less than 0.001). At cerebral blood flow less than 50% of control, the intracellular pH of piglets with modest hypoglycemia during partial ischemia was never reduced to less than 6.46, whereas intracellular pH fell as low as 5.97 for hyperglycemic animals. CONCLUSIONS: ATP preservation may account for the differing effects of glucose during ischemia in neonates compared with adults, provided that the accentuated brain acidosis is not deleterious to neonatal brain tissue.

Cerebral acid buffering capacity at different ages measured in vivo by 31P and 1H nuclear magnetic resonance spectroscopy.

Cerebral acidosis occurring during ischemia has been proposed as one determinant of tissue damage. Newborn animals appear to be less susceptible to ischemic tissue damage than adults. One possible component of ischemic tolerance could derive from maturational differences in the extent of acid production and buffering in newborns compared to adults. The purpose of this study was to measure the dependency of acid production on the blood plasma glucose concentrations and acid buffering capacity of piglets at different stages of development. Complete ischemia was induced in 29 piglets ranging in postconceptual age from 111 to 156 days (normal term conception, 115 days). Brain buffering capacity during the first 30 min of ischemia was quantified in vivo, via 31P and 1H nuclear magnetic resonance (NMR) spectroscopy, by measuring the change in intracellular brain pH for a given change in the concentration of compounds that contribute to the production of hydrogen ions. Animals from all four age groups showed a similar linear correlation between preischemia blood glucose concentration and intracellular pH after 30 min of ischemia. For each animal the slope of the plot of intracellular pH versus cerebral buffer base deficit was used to calculate the buffer capacity. Using data obtained over the entire 30 min of ischemia, there was no difference in the mean buffer capacity of the different age groups, nor was there a significant correlation between buffer capacity and age. However, there was a significant increase in buffer capacity for the intracellular pH range 6.6-6.0, compared to 7.0-6.6, for all age groups. No significant differences in buffer capacity for these two pH ranges were observed between any of the age groups. Acid buffering capacity was also measured by performing pH titrations on brain tissue homogenized in the presence of inhibitors of glycolysis and creatine kinase. Plots of homogenate pH versus buffer base deficit showed a nonlinear trend similar to that seen in vivo, indicating an increase in buffer capacity as intracellular pH decreases. A comparison of newborn and 1-month-old brain tissue frozen under control conditions or after 45 min of ischemia revealed no differences that could be attributed to age and a slight decrease in buffer capacity of ischemic brain compared to control brain tissue homogenates. There was no difference between the brain buffering capacity measured in vivo using 31P and 1H NMR and that measured in vitro using brain homogenates.

Blood flow and metabolism during and after repeated partial brain ischemia in neonatal piglets.

BACKGROUND AND PURPOSE: Our investigation sought to determine whether neonatal brain ischemic vascular and metabolic effects were altered by repeated episodes of ischemia. METHODS: We studied twelve piglets using in vivo magnetic resonance spectroscopy to obtain multiple, simultaneous measurements of cerebral blood flow and phosphorylated metabolites from the same tissue volume. The relationship between cerebral blood flow and energy metabolism was examined over a range of reduced cerebral blood flow (90-10% of control). Three episodes of partial ischemia were studied, each lasting 10 minutes and separated by 45 minutes. RESULTS: During each interval of ischemia, plots of the percent reduction in cerebral blood flow versus the percent change in phosphorylated metabolites (phosphocreatine, inorganic phosphorus) or unit change in intracellular pH did not differ in slope and intercept. The relationship between beta-ATP and cerebral blood flow during repeated ischemia revealed similar slopes, but a lower intercept during the third interval of ischemia (p = 0.029). After ischemia, cerebral blood flow was reduced as a function of the severity of the preceding ischemia. After each interval of ischemia, phosphocreatine and intracellular pH were unchanged from preischemic values. Inorganic phosphorus remained elevated after ischemia (117 +/- 16 and 118 +/- 11% of control, p less than 0.005, following the first and second intervals of ischemia), and beta-ATP was restored to progressively lower values (92 +/- 10 and 83 +/- 11% of control, p less than 0.025). Calculated free ADP decreased after ischemia and correlated with the postischemic level of beta-ATP (r = 0.63, p = 0.001). CONCLUSIONS: These results demonstrate that the relationship between cerebral blood flow and metabolism was reasonably preserved during repeated partial ischemia. However, following ischemia, alterations occurred in both cerebral blood flow and metabolism. These alterations may reflect a relative inhibition of ATP production by metabolic regulators such as ADP on either glycolysis or oxidative phosphorylation or both.

The effect of age on glucose-modulated cerebral agonal glycolytic rates measured in vivo by 1H NMR spectroscopy.

The purpose of this study was to investigate the effect of plasma glucose concentration on cerebral agonal glycolytic rates in piglets of different ages. Twenty-four piglets were divided into four different age groups corresponding to 113, 121, 128, and 145 d postconception (normal gestation = 115 d). For each group the agonal glycolytic rate was measured by monitoring the rate of cerebral lactate accumulation after total ischemia. Ischemia was induced by cardiac arrest, and the rate of lactate formation was measured in vivo using proton nuclear magnetic resonance spectroscopy. Before cardiac arrest, the blood plasma glucose concentration for individual piglets was adjusted to a specific value in the range 1-30 mM. The dependence of agonal glycolytic rate upon blood glucose concentration was analyzed for each age group, using the Michaelis-Menten equation to evaluate Vmax, the maximal rate of glucose utilization, and Km the concentration of plasma glucose at which the half maximal rate of utilization occurs. Vmax for the two youngest age groups of piglets had significantly different (p less than 0.05) values compared with each other (1.38 +/- 0.17 and 1.92 +/- 0.64 mumol.g-1.min-1, respectively) and with the two older groups of animals (2.99 +/- 0.52 and 3.42 +/- 0.65 mumol.g-1.min-1, respectively). The Km values determined for the two youngest age groups (0.79 +/- 0.70 and 1.79 +/- 0.33 mM, respectively) also were significantly lower than for the two older age groups (4.96 +/- 2.90 and 4.82 +/- 2.96 mM, respectively). We conclude that throughout the first 2 wk of life there are marked increases in the cerebral glycolytic capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Disturbances of brain maturation and neurodevelopment during chronic renal failure in infancy.

Fifteen infants with moderate to severe congenital renal disease were prospectively studied by serial renal, neurodevelopmental, neurophysiologic, and anthropometric assessments. The observation period ranged from 3 to 25 months (mean = 10.9). Eight patients maintained a Mental Development Index (MDI) above the 16th percentile (greater than -1 SD) and comprised group 1. Of the remaining seven patients (group 2), three had an MDI less than 16th percentile when first studied and four had serial decreases of the MDI to less than 16th percentile. Although motor development was more delayed in group 2 at study entry, there were no significant changes of motor performance levels for either group during the study period. Group 2 patients had smaller length (p less than 0.05) and head circumference (p less than 0.05) standard deviation scores in comparison with group 1, and they had higher serum creatinine values (mean = 3.8 vs 1.3 mg/dl, respectively; p less than 0.01). By spectral electroencephalography, the expected progressive increase of the frequency of cerebral cortical background activity with age was demonstrated in group 1 but was not seen in group 2 (multivariate analysis of variance p less than 0.03). This increase of faster-frequency activity was primarily manifested in the left cerebral hemisphere of group 1 patients (p less than 0.01), a finding that was also absent in group 2. The frequent occurrence of neurodevelopmental abnormalities in infants with renal failure is possibly a consequence of impaired dominant hemispheric maturation in the first several years of life, which is clinically manifested as deterioration of cognitive function.