A case report of acute renal failure associated with bee pollen contained in nutritional supplements.

We report a case of renal failure associated with the ingestion of bee pollen containing nutritional supplement. A 49-year-old male patient who had been ingesting a nutritional supplement for more than five months had breathing difficulties, anuria, exceptional weight gain (20 kg) due to systemic edema, and loss of appetite. A renal biopsy confirmed interstitial nephritis with the presence of eosinophils, which is suggestive of drug-induced acute renal failure.

Early morphological changes leading to central polydactyly, syndactyly, and central deficiencies: an experimental study in rats.

Purpose: Various combinations of central polydactyly, syndactyly, and cleft hand have been frequently observed in the individual hands and feet in the same patients. Little is known, however, about the early changes of abnormal induction of digital rays during limb development. To determine the early changes and process of formation of central polydactyly, syndactyly, and cleft hand, we experimentally induced these anomalies in the hind limbs of rat embryos and discussed the relationship among these abnormalities.

Busulfan-induced central polydactyly, syndactyly and cleft hand or foot: a common mechanism of disruption leads to divergent phenotypes.

The prevalence of clinical phenotypes that exhibit combinations of central polydactyly, syndactyly, or cleft hand or foot is higher than would be expected for random independent mutations. We have previously demonstrated that maternal ingestion of a chemotherapeutic agent, busulfan, at embryonic day 11 (E11) induces these defects in various combinations in rat embryo limbs. In an effort to determine the mechanism by which busulfan disrupts digital development, we examined cell death by Nile Blue staining and TdT-mediated dUTP nick end labeling (TUNEL) assays; we also carried out whole mount in situ hybridization for fibroblast growth factor-8 (Fgf8), bone morphogenetic protein-4 (Bmp4), and sonic hedgehog (Shh) to examine developmental pathways linked to these defects.

Developmental abnormalities in rat embryos leading to tibial ray deficiencies induced by busulfan.

Background: Little is known about the developmental changes associated with tibial ray deficiencies. The aim of this study was to detect cell death, proliferation, and gene expression that result in tibial ray deficiencies.

Methods: We induced tibial ray deficiencies in rat embryos using a teratogenic agent (busulfan) and observed the developmental changes in 1126 hindlimbs.

Developmental failure of phalanges in the absence of growth/differentiation factor 5.

Growth/differentiation factor 5 (GDF5) is a member of the bone morphogenetic protein (BMP) family, which has been implicated in several skeletogenic events including cartilage and bone formation. To study the role of GDF5, we analyzed digit development in brachypodism (bp) mice, which carry functional null mutations of the Gdf5 gene and exhibit a reduction in the length of digit bones and loss of the middle phalanges. In situ detection of apoptosis and whole-mount detection of cell death showed abnormal apoptosis in the developing phalanges of bp mice.

Matrix metalloproteinase-9 expression, tartrate-resistant acid phosphatase activity, and DNA fragmentation in vascular and cellular invasion into cartilage preceding primary endochondral ossification in long bones.

Vascular and cellular invasion into cartilage are essential for endochondral ossification. Recently it has been shown that matrix metalloproteinase-9 (MMP-9)/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes. To study vascular and cellular invasion into cartilage preceding primary endochondral ossification in long bones, precursor femurs from 13- to 16-day-old murine embryos were sectioned.

Lmx1b expression during joint and tendon formation: localization and evaluation of potential downstream targets.

The tetrapod limb exhibits distinct dorsoventral joint, tendon, and muscle asymmetry. The LIM-homeodomain transcription factor, Lmx1b, is required to achieve the dorsal character of these structures, but the mechanism by which Lmx1b orchestrates this asymmetrical development is unknown. To identify target tissues and genes regulated by Lmx1b, we examined Lmx1b expression during joint, tendon and muscle formation (9.

Involvement of the activin-follistatin system in tubular regeneration after renal ischemia in rats.

This study was conducted to investigate the involvement of the activin-follistatin system in renal regeneration after ischemic injury. Expression of mRNA for the activin beta(A) subunit was not detected in normal kidneys but increased markedly after renal ischemia. Immunoreactive beta(A) subunit was detected in tubular cells of the outer medulla in ischemic but not normal kidneys.

Elevated levels of serum sulfite in patients with chronic renal failure.

Sulfite, a well known air pollutant, is toxic for humans, especially those with sulfite hypersensitivity. Sulfite is also generated endogenously, during normal metabolism of sulfur-containing amino acids. Mammalian tissues contain the enzyme sulfite oxidase, which detoxifies both endogenous and exogenous sulfite by oxidation to sulfate.