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In this study, the near-field (up to three chord lengths) development of a wing-tip vortex is numerically investigated at two angles of attack (five and ten degrees). The application of a vorticity confinement model to an Unsteady Reynolds averaged Navier–Stokes (URANS) model and Large Eddy Simulation (LES) is examined with the focus of preventing the rapid dissipation of vorticity in a wing-tip vortex. Vortex core size and trajectory were predicted well by the LES model, whereas the URANS model predicted a large vortex core, which remained constant with downstream distance. The LES model correctly predicted the jet-like axial velocity for an angle of attack of ten degrees and the LES and experimental axial velocity excess had the same value of 111% of free-stream velocity at two chord lengths downstream. The LES model predicted the turbulence in the vortex reasonably well as the maximum turbulent root mean square (rms) velocities were within 15% and 35% of experimental values at two and three chord lengths downstream for angles of attack of ten and five degrees respectively. The URANS model predicted the mean flow for an angle of attack of five degrees reasonably well but greatly under-predicted the mean flow for an angle of attack of ten degrees and the turbulence levels at all downstream locations.

The near-field (up to three chord lengths) development of a wing-tip vortex is investigated both numerically and experimentally. The research was conducted in a medium speed wind tunnel on a NACA 0012 square tip half-wing at a Reynolds number of 3.2 × 105. A full Reynolds stress turbulence model with a hybrid unstructured grid was used to compute the wing-tip vortex in the near field while an x-wire anemometer and five-hole probe recorded the experimental results. The mean flow of the computed vortex was in good agreement with experiment as the circulation parameter was within 6% of the experimental value at x/ c = 0 for α = 10° and the crossflow velocity magnitude was within 1% of the experimental value at x/ c = 1 for α = 5°. The trajectory of the computed vortex was also in good agreement as it had moved inboard by the same amount (10% chord) as the experimental vortex at the last measurement location. The axial velocity excess is under predicted for α = 10°, whereas the velocity deficit is in relatively good agreement for α = 5°. The computed Reynolds shear stress component 〈 u′v′〉 is in good agreement with experiment at x/ c = 0 for α = 5°, but is greatly under predicted further downstream and at all locations for α = 10°. It is thought that a lack of local grid refinement in the vortex core and deficiencies in the Reynolds stress turbulence model may have led to errors in the mean flow and turbulence results respectively.

Saccharomyces cerevisiae strains lacking a functional Pho85 cyclin-dependent kinase (cdk) exhibit a complex phenotype, including deregulation of phosphatase genes controlled by the transcription factor Pho4, slow growth on rich media, failure to grow using galactose, lactate or glycerol as a carbon source and hyperaccumulation of glycogen. The ability of Pho85 to regulate the transcription factor Pho4 is mediated by its association the Pho80 cyclin. Some other regulatory functions of the Pho85 cdk have been shown to be mediated via its interaction with a recently identified family of Pho80-related cyclins (Pcls). Here, we show that the poorly characterized Pho80-like protein Pcl7 forms a functional kinase complex with the Pho85 cdk, and that the activity of this complex is inhibited in response to phosphate starvation. Additionally, we show that Pcl7 interacts with the phosphate-regulated cyclin-cdk inhibitor Pho81, and that the regulation of the Pcl7-Pho85 complex in response to changes in phosphate levels is dependent on Pho81. Thus, we demonstrate for the first time that the Pho81 regulator is not dedicated to regulating Pho80, but may act to co-ordinate the activity of both the Pho80-Pho85 and Pcl7-Pho85 cyclin-cdk complexes in response to phosphate levels. We also demonstrate that expression of Pcl7 is cell cycle regulated, with maximal activity occurring in mid to late S-phase, perhaps suggesting a role for Pcl7 in cell cycle progression. Finally, we describe the phenotype of pcl7Delta and pcl6Delta yeast strains that have defects in carbon source utilization.

(1995). Crime Commissions and the Criminal Trial—The Criminal Justice Commission. Current Issues in Criminal Justice: Vol. 6, No. 3, pp. 371-377.

turbulence intensity of 9% just after the trailing edge. Maximum turbulence intensity after x/c = 0 is observed in the vortex core which decays with downstream distance. Five-hole probe mean velocity measurements revealed jet like and wake like axial velocity profiles depending on wing angle of attack, with values of 1.33U∞ and 0.83U∞ being measured for 10° and 5°. Axial vorticity is also observed to increase gradually with downstream distance. A full Reynolds stress turbulence model with a second order upwind differencing scheme is used to compute the vortex in the near-field. Vortex structure and trajectory correlate well with experiment. It is thought that the dissipative nature of the second order convection scheme led to discrepancies between numerical and experimental results.

This paper is about actuarial methods of funding pension schemes and follows on from the report of the Working Party of the Pensions Standards Joint Committee on Terminology of Pension Funding Methods (The Terminology Report) published in 1984. It looks at the basic structure of the main methods and at how they behave. We then discuss the question of the suitability of the methods under various conditions. The reader may find it useful to have a copy of the Terminology Report to hand.The paper is written against a background of uncertainty, as regards the State Earnings-Related Pension Scheme, and of great debate and legislative activity as regards Occupational Pension Schemes. This activity and debate makes it more important than ever before that the actuarial profession explains its methods and approaches to those in the pensions industry who are not actuaries, but who nevertheless rely on actuarial advice.

Importance Ischaemic heart disease is the leading cause of death worldwide. Percutaneous coronary Intervention (PCI) and coronary artery bypass graft surgery (CABG) represent the primary treatment options for coronary revascularisation in patients with significant coronary artery disease. Significant left main coronary artery disease is increasingly being treated with PCI. This is despite the CABG remaining the gold standard of treatment in left main disease – and holding class 1A indication from both US and European Societies. However, as interventional techniques have become more refined coupled with the advent of drug eluting stents and – the outcomes of patients with left main disease treated with PCI have improved. This serves to threaten the long-standing position of CABG as the primary treatment of left main disease. Objective Since July 2013 PCI for unprotected LMCA stenosis has been performed in the cardiology department of the University Hospital Limerick (UHL). The primary aim of this study is to assess the outcomes of patients with unprotected significant LMCA stenosis (> 50%) who underwent PCI in the cardiology department of UHL in 2013 and 2014. The performance of this cohort will then be compared to those underwent CABG for unprotected left main disease within the same time frame. Methods Patients with significant ULMCA disease who attended UHL between January 2013 and July 2014, and subsequently underwent PCI or CABG, were identified from the clinical registry. Baseline demographic and cardiac risk factor data was collected for each patient. The SYNTAX 5 and the European System for Cardiac Operative Risk Evaluation (euroSCORE) were calculated for each subject. This determined their severity of coronary artery disease and surgical risk. The primary end points of this study were in-hospital major adverse cardiac and cerebrovascular events (MACCE) and length of hospital stay. MACCE were defined as death, Q wave myocardial infarction, CVA, the requirement for repeat revascularisation, and re-admission within 30 days. Finally, in October 2014, 50 of 57 participants were followed up by telephone questionnaire where; angina severity (CCS score), heart failure status (NYHA classification), and quality of life (EQD5L) were also determined. Analysis was performed using SPSS for Windows Version 22. Categorical variables were compared across both groups using Fischer’s exact test or the Chi-Square test where appropriate. Continuous variables were compared using the Independent Samples Median Testing. A p value of Results 57 patients with significant LMCAD attending UHL were identified from the clinical registry. 27 patients underwent PCI (median age 67.71) and 30 CABG (median age 68.59). A high volume of emergency index admissions was common to both the PCI and CABG arms of the study (PCI 70.4 vs CABG 75.9, p = 0.765). Male patients dominated both the PCI and CABG groups, at 85.2% and 82.8% respectively. Diabetes was present in under 20% of both groups (PCI 18.5 vs. 17.2, p = 1). A history of myocardial infarction (inclusive of the index admission) was also common to both cohorts (PCI 51.9 vs 41.4), p = 0.592. Angina was seen in 81.5% of the PCI-treated patients and 75.9% of the CABG grip, p = 0.748. Renal impairment as determined by creatinine clearance was significantly associated with allocation to CABG surgery (PCI 80.8 vs CABG 56.3, p = 0.004). While the PCI patients had a higher surgical risk as measured by the euroSCORE, this difference was not of statistical significance (PCI 19.2 vs, 6.9, p = 0.236). The PCI group had a shorter length of stay (6.6 vs. 37.6 days, p = 0.06). What is more, those who were treated with CABG had to wait significantly longer for their revascularisation (PCI 3.4 vs CABG 8 days, p = 0.04). PCI is the treatment of choice in 90.5% of patients presenting to UHL with mild to intermediate left main disease. On the contrary however, when disease burden is severe the Heart team in UHL refer 77% of patients for CABG. Both of these differences were of statistical significance (p Conclusions This study has provided baseline and outcome data on patients at UHL with left main disease and subsequently treated with PCI or CABG. At UHL, patients with mild to moderate coronary artery disease (SYNTAX 0–32) are most often treated with PCI. However, in the presence of severe disease (SYNTAX > 33) tend to be referred to a tertiary centre for CABG. The average follow up for all patients was 293 days. At the time, there was no significant differences in the occurrence of all MACCE, death, myocardial infarction, stroke or target vessel revascularisation. Patients treated with CABG had a longer hospital stay but this was not of statistical significance. The EuroQoL questionnaire provides an interesting insight into the subjective experience of the patient after PCI or CABG. Both PCI and CABG can be viewed as reasonable options for treating left main coronary artery disease, as they share similiar short term outcome. More data is need on the durability of PCI in the long term.

We show here that the choline transporter-like (CTL) family is more extensive than initially described with five genes in humans and complex alternative splicing. In adult rat tissues, CTL2-4 mRNAs are mainly detected in peripheral tissues, while CTL1 is widely expressed throughout the nervous system. During rat post-natal development, CTL1 is expressed in several subpopulations of neurones and in the white matter, where its spatio-temporal distribution profile recalls that of myelin basic protein, an oligodendrocyte marker. We identified two major rat splice variants of CTL1 (CTL1a and CTL1b) differing in their carboxy-terminal tails with both able to increase choline transport after transfection in neuroblastoma cells. In the developing brain, CTL1a is expressed in both neurones and oligodendroglial cells, whereas CTL1b is restricted to oligodendroglial cells. These findings suggest specific roles for CTL1 splice variants in both neuronal and oligodendrocyte physiology.

Bedrock-controlled channel systems exhibit considerable morphological variation. Both bedrock-influenced and al- luvial morphological units coexist to form a system of changing channel patterns in response to changes in the relative influence of the controlling process variables. This article investigates the morphological composition of the bedrock- influenced Sabie River, Mpumalanga Province, South Africa, mapping 25 km of river channel at the scale of individual morphological units. Cluster and discriminant analyses define objective reach–scale “channel type” assemblages based on morphological unit composition. A number of robust clusters emerged that could be broadly classified into five channel types, namely, bedrock anastomosed, mixed anastomosed, pool-rapid, braided, and alluvial single-thread. The cluster analysis revealed that these channel types fit on a continuum from bedrock-dominated channels to fully alluvial systems. Each channel type could also be characterized by a certain set of “dominant” morphological units, which changed from bedrock-influenced at one end of the continuum (bedrock anastomosed, pool-rapid) to alluvial deposits at the other (braided, alluvial single-thread). An investigation of the role of controlling process variables in defining these channel types revealed a broad link between the degree of bedrock influence and the amount of available energy within the system as defined by indices such as the flow regime and water-surface slope variation. It is clear that the bedrock-dominated channel types are characterized by energy levels in excess of those accepted for alluvial systems, and an extended river classification is presented for the Sabie River that includes these bedrock channels. The mixed anastomosing channel type on the Sabie River is characterized by higher available energy levels than braided or alluvial single-thread reaches. As such, it appears to be a higher-energy example of an anabranched system, probably formed as a result of sediment accumulation on top of a high-energy bedrock anastomosed channel template.

Eleven pediatric patients with nephrosis and focal segmental glomerulosclerosis were treated with long-term (8-38 months) ciclosporin A in combination with steroids. All had abnormal height-velocity curves and multiple hospitalizations for complications of nephrosis. Eight patients attained remission with a dramatic improvement in growth and decrease in necessity for hospitalization for therapy of nephrosis complications, while maintaining adequate renal function. Three nonresponders developed end-stage renal disease. Long-term ciclosporin A therapy may be of benefit in steroid-resistant nephrosis in childhood.

Formation of posterior subcapsular cataracts is a known complication of systemic corticosteroid therapy. However, the relation between steroid dosage, cumulative dose and type of steroid on one hand and the subsequent formation of cataract on the other is unclear. We carried out a study to determine the incidence of posterior subcapsular cataracts in 64 children who had undergone renal transplantation and to attempt to determine what factors were associated with cataract formation. Cataracts were detected in 17 (26%) of the patients. The steroid dosage, cumulative dose and duration of therapy were not associated with cataract formation. There was a significant difference in the distribution of HLA-CW3 antigen between the patients with cataracts and those without cataracts. The reason for the link between corticosteroid therapy and formation of posterior subcapsular cataracts remains unclear.

High dose loop diuretic therapy was administered at time of admission to hospital or at time of diagnosis to 54 patients with childhood hemolytic uremic syndrome. Forty-one patients maintained a diuresis sufficient to avoid the necessity for dialysis. When compared to an earlier time period the dialysis rate fell from 82% to 24% with furosemide therapy. Though a change in disease severity may explain the decrease in necessity for dialysis, a salutary effect of furosemide therapy may also be responsible.

Experience with percutaneous gastrojejunostomy is described in children on chronic cycler peritoneal dialysis. We recommend this mode of enteral alimentation for children requiring caloric supplementation.

A wide spectrum of renal diseases ranging from glomerulopathic lesions to tumors may be associated with HIV infection. This infection may also complicate the course of dialysis and renal transplantation. We review the renal complications of HIV infection.

Peritoneal dialysis catheters are at risk for exit-site contamination when swimming or bathing. Also in pre-toilet trained children fecal and urine contamination can occur. The use of Tegaderm dressings prevents contamination and thus minimizes restriction of activity in children.

The experiments described in this paper were designed to test whether increasing choline availability over normal physiological levels increases acetylcholine synthesis in the cat's superior cervical ganglion. When ganglia were perfused with Krebs solution, an increase in the medium's choline concentration over physiological (10(-5)M) levels increased tissue choline but did not increase tissue acetylcholine or the release of acetylcholine from stimulated ganglia. However, increasing plasma choline in the whole animal increased ganglionic acetylcholine levels. The basis for this difference in the effects of in vivo and in vitro exposure to elevated choline levels on the tissue acetylcholine content was found to involve plasma factor(s), rather than indirect actions of choline, and the acetylcholine content of isolated ganglia was increased when the tissue was perfused with plasma, instead of Krebs solution, containing 10(-3)M-choline. The extra acetylcholine generated by this procedure was associated with a subsequent transient increase in transmitter release during short intervals of stimulation, but most of the extra acetylcholine was not readily available for release from stimulated ganglia. It is concluded that increasing choline available to sympathetic ganglia over physiological concentration does not have a sustained effect on the turnover of releasable transmitter under the conditions of these experiments.

It has been shown previously that the accumulation of the choline analogues, homocholine and triethylcholine, by the cat superior cervical ganglion is enhanced during preganglionic nerve stimulation. In the present experiments, this enhanced accumulation was measured under various conditions in order to compare this phenomenon to the high affinity choline transport mechanism described for synaptosomes. Similar conditions were then used to determine the relationship between acetylcholine synthesis and the activation of choline transport in ganglia, the latter being inferred from the preceeding experiments. The enhanced accumulation of choline analogues by stimulated ganglia was found to be Na + -dependent, Cl − -independent, would accept Ba 2+ and Sr 2+ as substitutes for Ca 2+ , but was not apparent during chemical depolarization. Choline transport activity was increased without a proportional increase in acetylcholine synthesis when ganglia were stimulated during perfusion with a medium in which BaCl 2 replaced CaCl 2 ; hence, choline uptake and acetylcholine synthesis can be dissociated during stimulation. Acetylcholine synthesis was not impaired, although choline transport did not appear to be activated during exposure of ganglia to high [K + ] or veratridine; however, extracellular choline was utilized for the synthesis of acetylcholine during exposure of ganglia to high [K + ]. Accumulation of choline analogues was also enhanced during a period of rest that followed a period of conditioning stimulation; this phenomenon was found to be Na + -dependent, Cl − -independent and Ca 2+ -independent. The post-stimulation increase in choline transport activity was associated with a rebound increase in acetylcholine content and this was also eliminated by the substitution of Li + for Na + . The results of this study suggest that the relationship between choline uptake and acetylcholine synthesis might change following an alteration in functional state.

Based on the histologic aspects of the lesions, primary nephrosis with focal glomerular sclerosis has been classified into focal segmental glomerulosclerosis (FSG) and focal global glomerulosclerosis (FGG). Several reports [1–14] define its clinical presentation and attempt to identify the initial signs that indicate a poor prognosis. The criteria indicating poor prognosis were reported to be age of onset [15, 16], the presence of a nephrotic syndrome [10, 15, 17], mesangial proliferation [14], the presence of focal segmental glomerulosclerosis on early biopsies [17], the association of glomerulotubular imbalance [18], the severity of the lesions on an early biopsy [1–3, 5, 6, 8, 10, 12, 13, 17], and especially the resistance of these patients to corticosteroid and immunosuppressive therapy [1–3, 6, 8, 9, 11–13, 16, 17]. The long-term followup of children with focal glomerular sclerosis has been analyzed in detail, however, only in a few articles [2, 3, 17], and these reports have concluded that the prognosis is generally poor. The purpose of our study is to report the outcome of observing 32 children with primary nephrosis and focal glomerular sclerosis over a period of several years. We observed that the long-term prognosis in our series is more favorable than that described by other reports. We believe that this discrepancy is due to the referral profile of our institution and that our population of patients more accurately reflects the full spectrum of the natural history of the disease.

Summary Arachidonic acid infusion in rabbits is highly lethal, death occuring in greater than 90% of animals and most within 1 to 2 minutes. This effect may be inhibited by prior administration of vitamin E. Pathologic examination of renal tissue from animals killed in this manner demonstrated immunoglobulin and fibrin deposition in the glomeruli and interstitium of the kidney. No pathologic alterations were detected by light microscopy. Electromicroscopy revealed some endothelial cell swelling with no evidence of electron dense deposits, indicating the absence of immune complexes. Pathologic examination of the kidneys suggest the deposition of immunoglobulin in a non complexed form.

A 23-year-old girl with a ventriculo-atrial shunt presented with hematuria, proteinuria and severe oedema. Diphtheroid organisms were cultured from blood, cerebrospinal fluid and the shung valve. Immunoglobulin, complement components and diphtheroid antigenic material were demonstrated in the glomeruli by immunofluorescence microscopy. Treatment of her shunt infection by shunt replacement and antibiotic therapy resulted in slow resolution of her nephritis. The slow resolution of her nephritis suggests that prompt resolution of immune complex disease due to prolonged bacterial injection cannot always be anticipated, even after successful eradication of infection.

Little is known about the specificity of the mechanisms involved in the synthesis and release of acetylcholine for the acetyl moiety. To test this, blocks of tissue from the electric organ of Torpedo were incubated with either [1-14C]acetate or [1-14C]propionate, and the synthesis, storage, and release of [1-14C]acetylcholine and [14C]propionylcholine were compared. To obtain equivalent amounts of the two labeled choline esters, a 50-fold higher concentration of propionate than of acetate was needed. Following subcellular fractionation, similar proportions of [14C]acetylcholine and [14C]propionylcholine were recovered with synaptosomes and with synaptic vesicles. Furthermore, both labeled choline esters were protected to a similar extent from degradation during homogenization of tissue in physiological medium, indicating that the two choline esters were equally well incorporated into synaptic vesicles. Yet depolarization of tissue blocks by 50 mM KCI released much less [14C]propionylcholinc than [14C]acetylcholine. During field stimulation of the tissue blocks, the difference between the releasibility of the two choline esters was less marked, but acetylcholine was still released in preference to propionylcholine. Evidence for specificity of the release mechanism was also obtained when the release of the two choline esters in response to field stimulation was compared in tissue blocks preincubated with both [3H]choline and [14C]propionate.

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.

Sodium-dependent binding of [3H]hemicholinium-3 was observed to be 10-fold higher with presynaptic membranes from the electric organ than with electroplaque membranes and this binding site copurified with synaptosomal membranes. The KD for specific [3H]hemicholinium-3 binding was found to be 31 +/- 4 nM and the Bmax, 5.0 +/- 0.2 pmol/mg protein; a Ki of 16 nM was estimated for hemicholinium-3 as a competitive inhibitor of high-affinity choline transport in electric organ synaptosomes. Choline and choline analogues were equally potent as inhibitors of [3H]choline uptake and [3H]hemicholinium-3 binding. Tubocurarine and oxotremorine also inhibited uptake and binding, but carbachol was without effect in both tests. These findings suggest that [3H]hemicholinium binds to the high-affinity choline transporter present at the cholinergic nerve terminal membrane. A comparison of maximal velocities for choline transport and the maximal number of hemicholinium-3 binding sites indicated that the high-affinity choline transporter has an apparent turnover number of about 3s-1 at 20 degrees C under resting conditions. The high transport rates observed in electric organ synaptosomes are likely due to the high density of high-affinity choline transporters in this tissue, estimated on the basis of [3H]hemicholinium-3 binding to be of the order of 100/micron2 of synaptosomal membrane.

An 11-year-old girl who presented with pneumonia, pleural effusion, hematuria, and red blood cell casts is described. Mycoplasma pneumoniae complement fixation titers were elevated. The pneumonia resolved following therapy with tetracycline. Light microscopy of renal biopsy tissue revealed an acute glomerulonephritis; immunofluorescent studies showed deposits of IgG, C3 and mycoplasma antigen along the glomerular capillary walls and in the mesangium; subendothelial and subepithelial deposits were seen by electron microscopy. This is the first report of acute glomerulonephritis associated with M. pneumoniae infection with evidence of mycoplasma-induced immune complex nephritis.

Pre-formed immune complexes solubilized in antigen excess were infused into rats with nephrotoxic serum nephritis and normal control animals. Complex localization was evident in seven of ten nephrotoxic animals suggesting that the presence of immune mediated glomerular injury makes the kidney susceptibility to further immune injury.

Proteoliposomes made by a butanol-sonication technique from electric organ presynaptic membranes showed choline transport activity. In contrast to intact nerve terminals, the uptake of choline was dissociated from its conversion to acetylcholine in this preparation. The kinetics of choline uptake by proteoliposomes was best described by two Michaelis-Menten components. At a low concentration of choline, uptake was inhibited by hemicholinium-3 and required external Na+ and, thus, closely resembled high-affinity choline uptake by intact cholinergic nerve terminals. Choline transport could be driven by the Na+ gradient and by the transmembrane potential (inside negative) but did not directly require ATP. External Cl-, but not a Cl- gradient, was needed for choline transport activity. It is suggested that internal K+ plays a role in the retention of choline inside the proteoliposome. Proteoliposomes should prove a useful tool for both biochemical and functional studies of the high-affinity choline carrier.

Based on recent evidence of a genetic influence on prognosis (1) and the existence of red cell membrane phospholipid depletion with low or absent serum α-tocopherol (2) levels in three children with the Hemolytic Uremic Syndrome (H.U.S.), we wish to suggest the existence of an inborn error of antioxident capacity as the basic pathogenetic mechanism in the development of the hemolytic uremic syndrome (H.U.S.).

Seventeen children with acute renal failure due to the hemolytic-uremic syndrome were examined with duplex Doppler ultrasound. Serial measurements of intrarenal arterial pulsatility were obtained by means of the Pourcelot index. These were compared with daily urine volume, both during the phase of renal failure (during which most of the children were undergoing peritoneal dialysis) and during recovery of renal function. During oliguria or anuria there was either no intrarenal arterial flow (ie, absent Doppler shifts), or absent, reversed, or markedly reduced diastolic flow. Within 24-48 hours after diastolic Doppler shifts returned to normal, diuresis occurred. The Doppler examination enabled prediction of recovery and allowed dialysis treatment to be abbreviated or, in some cases, canceled.

Subacute sclerosing panencephalitis (SSPE) is a progressive neurologic disease associated with chronic measles infection. We have assessed renal function parameters and renal biopsy details in 14 patients with SSPE. All had normal renal function. However, 9 had microscopic hematuria. 9 patients had focal segmental mesangial proliferation and 5 had capillary wall thickening with deposits visible by light microscopy. 13 patients had glomerular C3 deposition and 4 had IgG deposits. SSPE is a disease caused by chronic viral infection, in which nephritogenic complex formation may occur.

ENGLISH law is the foundation of the legal system in the Territory of Papua and New Guinea and the common law of England remains a very important component of the basic law.1 English precedents are frequently cited in the courts of the Territory. However no English court is a member of the local curial hierarchy and it therefore follows that no English precedent ever binds a Territory court by virtue of the doctrine of stare decisis. This article explores the possibility that certain English decisions may be binding for another reason-by virtue of the reception of the common law.

Seventeen children who had vesicoureteral reflux underwent urodynamic and rectal manometric studies. All had uninhibited bladder contractions. All had rectal dilatation confirming the presence of constipation by rectal balloon manometry. The recurrent association of constipation with ureteral reflux suggests the possibility of a nonfortuitous association.

10 children underwent cadaveric renal transplantation between the ages of 8.0 and 12.5 years for uremia secondary to infantile cystinosis. 6 children are doing well 6-62 months after-transplantation. 3 of the 4 other recipients required a second graft and eventually died of uremia or fulminant viral encephalitis, the other lost her first graft due to accelerated acute rejection and is now on maintenance hemodialysis. No further systemic complications of cystinosis have been observed in the patients with functioning grafts. Our experience confirms that kidney transplantation is the treatment of choice for uremic children with infantile cystinosis.