Familial hypokalemic periodic paralysis. Clinical, diagnostic and therapeutic aspects

A model of induced lactation was modified to examine the effects of bovine prolactin (bPRL) and bovine placental lactogen (bPL) on mammary growth and differentiation. Thirty-two peripubertal, non-pregnant Holstein heifers were given daily s.c. injections of oestradiol (0.05 mg/kg) and progesterone (0.25 mg/kg) for 7 days to initiate mammary growth. Treatment with bromocriptine (40 mg/3 days) reduced serum PRL concentrations to approximately 25% of pretreatment levels, for the duration of the study. On the day following the last steroid injection, groups of eight heifers were given twice daily s.c. injections of either saline (negative control), recombinant bPRL (rbPRL; 80 mg/day) or recombinant bPL (rbPL; 80 and 160 mg/day) for 7 days. At the end of this period (day 15), growth and differentiation of the mammary glands were assessed. Treatment with rbPL increased total mammary DNA above control value by 50 and 60% for the 80 and 160 mg/day doses respectively. However, total DNA was not different for the control and rbPRL-treated groups. The blood serum concentration of alpha-lactalbumin was measured daily throughout the study and used as an index of mammary differentiation. Both rbPRL and rbPL stimulated mammary differentiation (i.e. induction of milk synthesis), although rbPRL appeared to be more potent than rbPL. These results indicate that rbPL is lactogenic in vivo and strongly suggest that bPL is a mammary mitogen.     

Prostanoid biosynthesis by blood monocytes of children with hyperprostaglandin E syndrome

Hyperprostaglandin E syndrome (HPS), the prenatal variant of Bartter's syndrome, is characterized by a marked and selective stimulation of prostaglandin E (PGE2) synthesis. In the study group HPS patients showed increased urinary levels of PGE2, an index of renal, and of 11 alpha-hydroxy-9,15-dioxo-2,3,4,5,20-pentanor-19-carboxyprostano ic acid (PGE-M), an index of systemic PGE2 synthesis of 470% and of 570%, respectively. In addition, plasma concentration of PGE-M was also elevated 6.3-fold when compared with a control group. The urinary levels of other prostanoids were unaltered. During indomethacin treatment in both groups prostanoid excretion rates were suppressed to similar levels. To investigate the origin of stimulated prostanoid biosynthesis in HPS patients CD14+ monocytes were isolated from plasma samples, and the prostanoid synthesis was analyzed. The pattern and amounts of metabolites synthesized from endogenous arachidonic acid pools did not vary significantly between monocytes of the HPS and the control group. Thromboxane A2 (TXA2) was formed as the major prostanoid product. Using PGH2 as an exogenous substrate, again no difference in PGE2 biosynthesis was observed, indicating no difference in PGE-synthetic activity between both groups. Additionally, mRNA expression analysis of CD14+ monocytes via RT-PCR delineated the constitutive expression of cyclooxygenase-1, cyclooxygenase-2, and thromboxane synthase mRNA in cells from HPS patients and controls without statistical differences between these two groups. In conclusion, our data show that monocytes are not the source for the increased PGE2 biosynthesis in children with HPS, and a genetic defect in PGE synthesis can be excluded as the primary event in the pathogenesis in HPS.     

Spectrophotometric determination of some antioxidants with potassium permanganate and metol

New spectrophotometric methods for the assay of some antioxidants have been developed using potassium permanganate and metol (p-N-methyl amino phenol). Metol is oxidised at pH 3.0 with potassium permanganate and coupled with antioxidants to give λ_max at 560 nm for propyl gallate and gallic acid and 510nm for butylated hydroxy anisole. The method is simple, sensitive, reproducible and accurate within ±1% and applicable to the assay of antioxidants (gallic acid, propyl gallate and butylated hydroxy anisole) in oils and fats.     

Analysis of interfacial failure in a composite microbundle pull-out experiment

Modeling of the failure of polymer-matrix composites requires substantial information about the mechanisms of failure at the interface, and load redistribution around fiber breaks in the composite. Current interface experiments involving the use of ‘microcomposites’ of single embedded fibers in a matrix generally do not include all the key geometric features of the real composite; in particular, they do not include the effects of fiber volume fraction and the higher matrix shear resulting from closely neighboring fibers. A new experiment was recently devised to assess some of these effects: it is referred to as the single-fiber pull-out from microbundle (SFPOM) experiment. It consists of a hexagonal arrat of seven fibers in a matrix where the outer six fibers are restrained and the center fiber is pulled out. Recent experimental data from tests with this geometry are analyzed here using three mechanical models of the failure process, and parametric studies of the data are performed to assess the appropriateness of each model. Two of the models, based on fracture energy considerations as applied earlier to single embedded fibers in a matrix and adapted to our geometry, were found to model data from the SFPOM experiments poorly. The third model assumes the existence of three zones near a fiber break, including elastic, plastic and frictional debond zones, and was found to provide reasonable fit to the data under realistic assumptions.