Purple urine bag syndrome (PUBS) is a unique disease entity characterized by an alarming purple discoloration of the urine secondary to recurrent urinary tract infections with indigo- and indirubin-producing bacteria. It is usually associated with prolonged urinary catheterization and chronic debilitated states. We hereby present a concise review of this rare phenomenon with historic perspectives, epidemiology, emphasizing on current concepts of etiology, pathogenesis, relevant clinical associations, treatment modalities, prognosis, and future directions in PUBS. In addition, we highlight an interesting occurrence of this intriguing phenomenon in a 39-year-old gentleman at our institution.
SummaryShwachman-Diamond syndrome (SDS) is an inherited bone marrow failure disorder with cytopenia and a high propensity for myelodysplastic syndrome (MDS) and leukaemia, particularly acute myeloid leukaemia. The mechanism of leukaemogenesis in SDS is unknown. In accordance to the multi-hit theory of carcinogenesis, it is likely that several molecular and cellular hits occur before MDS/leukaemia become apparent. This study used oligonucleotide microarray to identify gene expression patterns, which were shown to be associated with leukaemogenesis, in marrow mononuclear cells of nine SDS patients without overt transformation compared to healthy controls. Among 154 known leukaemia-related genes, several oncogenes were found to be upregulated, including LARG, TAL1 and MLL, and of several tumour suppressor genes were downregulated, including DLEU1, RUNX1, FANCD2 and DKC1. Real time polymerase chain reaction confirmed statistically higher expression of LARG and TAL1 in SDS marrows. We conclude that SDS marrow mononuclear cells exhibit abnormal gene expression patterns, which might result in continuous stimulation favouring evolution or progression of malignant clones. Additional molecular and cytogenetic events are probably necessary for the malignant process to be irreversible and complete.
The effects of the vortical wake shed by a finite span canard on a low Reynolds number airfoil were examined. Aerodynamic performance was evaluated through direct measurements of lift, drag, and 1/4-chord pitching moment. Spanwise static pressure and surface film visualization data were also acquired. A reduction in the downstream airfoil drag coefficient and an increase in its lift/drag were noted in the presence of the canard for a wide range of configurations. Static pressure and surface visualization data provided indication of some of the boundary-layer characteristics responsible for the drag behavior.
Nomenclaturewing chord length c c = canard chord length D =wing drag force L = wing lift force M =wing 1/4-chord pitching moment O c = canard offset, Z c /c P = static pressure q = dynamic pressure, -\/2(pU 1 ) R c = chord Reynolds number, -cU^/V S = nondimensional separation distance, =X c /c U^ -freestream velocity X c = stream wise distance between canard/wind 1/4-chord axes x = chordwise coordinate y -spanwise coordinate Z c = vertical displacement of canard 1/4-chord axis with respect to wing 1/4-chord axis a = wing incidence a c -canard incidence d c =declage, =(a c -a) e = down wash angle v = kinematic viscosity p = density
Cardiovascular diseases are the leading cause of death in patients with advanced renal disease. Although atherosclerosis is the major contributor, vascular calcification also plays an important role in progression of coronary as well as peripheral arterial disease in these patients. A large body of evidence suggests that hyperphosphatemia is the major contributor in progressive vascular calcification. We examine this large body of evidence with respect to the role of hyperphosphatemia in inducing vascular calcification and how, as a result, this possibly impacts an increase in adverse cardiovascular events. We also review various options as to how treating hyperphosphatemia might effect a decrease in cardiovascular morbidity and mortality.
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