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Vasodilation in hypertensive patients, patients with hypercholesterolaemia and patients with diabetes mellitus is rapidly restored after treatment with dihydropyridines comparative analyses between different anti-hypertensive drugs have shown that nifedipine most potently enhances these effects.5, 7 Other studies have shown that nifedipine has an effect on endothelial permeability and can reduce the increased flux of water and protein into the intima and the vessel wall. This protective effect diminishes intima oedema and reduces the growth and hypertrophy of vascular smooth muscle cells.8 The results of these experimental studies provide evidence of the cellular mechanisms of nifedipine in the pathogenesis of atherosclerosis and served as a basis for designing several clinical trials, which are discussed in this article.

Two molecular markers will be studied as possible indicators for lung cancer risk in the labs of Jeff Ross, MD and Jill Kolesar, PharmD. "We are looking for markers to identify individuals at an increased risk of lung cancer, before they get the cancer, " said Kolesar, Associate Professor at the UW School of Pharmacy. "Finding these markers would allow us to target individuals for increased screening, earlier intervention and lung cancer prevention. Examined a few hours later, which indicates asynchronous pronucleus formation Staessen et al., 1993 ; . As it became routine clinical practice in IVF to re-evaluate 1PN oocytes, in order to dispel confusion with asynchronous pronucleus formation, the incidence of diploid embryos fell from 80 to 50% Staessen et al., 1993 ; . After ICSI, diploid embryos developing from 1PN oocytes were also observed: 27.9% were diploid, with equal proportions showing XX or XY signals. These results indicate, however, that some of the 1PN oocytes observed 1618 h after injection do indeed result from a normal fertilization process. At 810 h after injection, the asynchronous appearance of pronuclei has been observed Nagy et al., 1994 however 1618 h after injection it was not observed. The systematic introduction of a second observation of 1PN oocytes could also be considered in the ICSI programme. Of particular interest is the observation of an 8-cell embryo after ICSI with two Y- and two 18-specific signals and, probably, a 46, YY chromosome status. This `embryo' originated from the development of an oocyte involving only the male genome, which was initially diploid or underwent subsequent diploidization. The female genome was completely extruded or inactivated. After ICSI and after IVF, 2- to 8-cell embryos developing from monopronucleated oocytes are all found to be uniformly haploid; the incidence of this, however, was significantly higher after ICSI 31.2% ; than after IVF 13.1% ; . For both groups of embryos, 2- to 8-cell embryos with all blastomeres containing only one Y- and one 18-specific signal or, probably, with a 23, Y chromosome status were observed. This again indicates an androgenetic origin: the sperm nucleus had been activated and was involved in the monopronucleus formation while the female genome was completely excluded. Some of the 23, X embryos may be paternal in origin; however, proportionally more 23, X were found, indicative of a higher proportion of activation of the oocyte genome. Monopronuclear oocytes obtained after ICSI n 21 ; and after IVF n 21 ; and cleaving into embryos were analysed by Sultan et al. 1995 ; using the FISH technique, giving the following results: after IVF, 14.3% were found to be haploid and 61.9% were diploid, of which about half were XY. After ICSI, the majority 66.7% ; of the embryos were found to be haploid and only 9.5% were diploid. Also, one haploid and one diploid embryo contained a Y chromosome. Our results for IVF are quite similar to those of Sultan et al. 1995 ; , although for ICSI Sultan et al. reported a higher proportion of haploid cases in their small sample. The presence of 23, X 46, XX mosaics can be explained by activation of the oocyte followed by spontaneous diploidization after the first cleavage. This may also lead to the other observed mosaicisms, i.e. X18 XXX181818 and X18 XXX181818 XXXX18181818. Complex mosaic embryos, with and without the presence of a Y chromosome, have been observed. After normal fertilization, irregular chromosome segregations leading to mosaicisms have also been reported, although at lower incidences and seldom from the first division onwards Munne et al., 1994 ; , indicating that 1PN-derived embryos are more unstable.

Increased glucose production 238 ; . Excessive rhIGF-I has been reported to induce features of acromegaly in a girl with Laron's syndrome 239 ; . These findings are similar to those observed after GH replacement in adult GH deficiency GHD ; 240 ; and suggest circulating IGF-I, as opposed to auto- or paracrine, is important in mediating many of the actions of GH. This supports the appropriateness of serum IGF-I as a marker of disease activity in pegvisomant-treated patients with acromegaly. In our experience, with sufficiently high doses of pegvisomant, it is possible to reduce serum IGF-I below the agerelated lower limit of normal in patients with acromegaly, raising the question of overtreatment and its diagnosis. Even when serum IGF-I is reduced to the normal age-related reference range, the potential for overtreatment remains, as many patients with adult GHD, diagnosed using provocative tests of GH secretion, have normal serum IGF-I values. Serum IGF-I is of diagnostic value in patients with childhood onset GHD, but in patients with GHD of adult onset, the value of serum IGF-I in predicting the response to provocative tests of GH secretion declines with increasing age 241, 242 ; . In elderly patients with GHD, although serum IGF-I is significantly lower than that observed in normal agematched subjects, values below the lower limit of the normal reference range are observed in only 17% of patients 243 ; . GHD may account for the increased mortality observed in patients with hypopituitarism on full replacement therapy except GH 244 247 ; . Thus, although a reduction in mortality is anticipated after serum IGF-I normalization in acromegaly when pegvisomant is used, the reliance on serum IGF-I data in the absence of meaningful serum GH data represents a formidable task. The diagnosis of overtreatment represents a further challenge, as standard provocative tests cannot be employed due to high circulating GH levels. Long-term prospective studies are thus required to define the optimal treatment target for serum IGF-I in patients receiving this therapy, as morbidity and mortality may increase with overtreatment.

Treatment group. Although the IGF-II assay used in these experiments was not species-specific, this profound decrease in IGF-II production almost certainly reflects tumor production as the serum IGF-II concentrations were not significantly different between the animals that received MZ-4 71 and those that did not. The precise mechanism of the downregulation of tumor autocrine IGF-II production by the GHRH antagonists is unknown, but it has been observed in both in vitro and in vivo experiments, indicating that it is at least partially mediated by direct actions at the cellular level. Although less extensively studied, the GH receptor antagonist pegvisomant has been demonstrated to also reduce intratumor IGF production 99 ; . The ability to down-regulate endogenous IGF production is likely to be a critical component, if not the most critical component, in mediating the antitumor effects of the GH and GHRH antagonist compounds. In addition to blocking an autocrine growth loop, decreasing endogenous IGF production may also make tumors more responsive to traditional agents such as cytotoxic chemotherapy or radiation. Modifying the IGFBP environment, whether through agents that modify tumor IGFBP production or simply by the exogenous administration of recombinant proteins, offers significant therapeutic opportunities. The antiestrogens, tamoxifen and ICI 182, 780, are excellent examples of agents that modify tumor IGFBP production. For instance, both have been demonstrated to increase IGFBP-3 production in MCF-7 cells, an estrogen-responsive breast cancer cell line. This alteration in IGFBP-3, at least in certain instances, appears to be able to inhibit IGF-I-stimulated cell proliferation. Many examples of the ability of exogenous IGFBP administration to inhibit tumor growth were detailed in the preceding text. Because IGF-II also circulates in complex with the IGFBPs, changes in the binding protein milieu should influence both IGF-I and IGF-II actions. It is important to remember, however, that the effects of all binding proteins are not always uniformly inhibitory. Additionally, at least some of their actions appear to be mediated in a manner that is independent of their actions on IGF bioavailability. Nevertheless, the IGFPBs are an important component of the natural physiological regulation of IGF actions and, as such, are promising candidates for therapeutic intervention. Agents that block IGF action at the receptor level are also excellent therapeutic candidates. For instance, IGF-I receptor blocking antibodies, such as IR3, should be capable of inhibiting the stimulatory actions of all IGF-I, not just the 75 80% that is regulated by GH. Additionally, because most of the growth-promoting actions of IGF-II appear to be mediated by the IGF-I receptor, therapeutic strategies that block the IGF-I receptor would also inhibit the actions of IGF-II. Any direct actions of GH, however, would not be attenuated with this approach. However, as the IGFs are important to many normal physiological activities in virtually every tissue, there has to be some concern about the ramifications of blocking the actions with systemic agents such as an IGF-I receptor antibody. Therefore, this type of approach may be most useful for those tumors that clearly overexpress IGF-I receptor and are therefore disproportionately susceptible to receptor blockade. The use of gene therapy approaches, such as antisense IGF-I receptor vectors that are targeted to the and penicillamine.

Housewives who have vegetable ffarSsn are mil? tiW t h | FRANKFURTER-CHEESE RIB ye&fi picklaf anfl tjaniilng vegeKABOB CAN REPLACE tables * Some et the will be plekied, others just eoafced and c * nsdt but' THE USUAL SANDWICH ePty shelves will sbon be leaded with imrs of ftsSpFUd ruite and vegFdR SUMMER etables for nest wlnteF's Use, Now * the hflysgwlfe who aoesn t Though the children are more than have a' garden ean keep eSoee watch on market prices and when some pleased that School is over for the certain thing she particularly likes suromer niany housewives are be * reaches lew, ean purchase In large ginning to worry about the neontime fflg&i, There used to" be only quantities and go to work * Flekled vegetables are really good breakfast and dinner to worry about; * nd nmko a tasty addition to bland but now, out of a alear sky, there comes a hungry pack at nbh * tlEftS meals as welL Of ceursei thefg are always PICKLED C A U iandwiches but we all tire of them If too many are served and require 4 heads cauliflower a change sueh a change as this, l sup salt that is so simple to prepare, yet fill * 3 quarts vinegar ing and ever so tasty * 2 cups sugar FRANKFURTER - CHEESE H sup mixed plekls spice's s KABOB SepAFste nsWerett s sf cauliflower, 2 large frankfurters add the salt and let stand overnight. % pound American cheese Plaee In csllaBder, EIBSB with cold water and let drain. Tie spices is a Cook the frankfurters in boiling .thin hag and boil with the vinegar water, Split the frankfurters; then and, sugar, throw ih the cauliflower, cut slices of American cheesg the hell a few minutes and pour to ovsr- iza of the frankfurters and place on flewlag in wide-msuthed sterilised two skewers in the following orders J a r air-tight, i & frankfurter, i slice cheese, % frankfurter, ete. Broil en both sides PlOKt D E l only for a moment and serve piping 1 peck string beans hit. Makes as many of these as de A quart vinegar sired and serve on skewers on a 1 quart water round platter placed lengthwise 1 pound sugar around dfeh. Fill the center apace % tablespoon cloves with relishes or whatever the chil * 1 stick eiBnamen, broken dren like * 'Wash and pick over the beans, string and eut. Ball in salt water i teaspoon to I quart of boiling water ; , EGGS IN BAKED POTATOES until tender. Drain and spread out to dry I then pack Into air-tight jars. There are some people Whose Boil the rest until a alee syrup is ob- breakfast consists of a cup of coffee tained. Let cool, then pour into jars, and a piece of toast * This may be and seal all right for the person who Is required to eat an early breakfast, beP I C K CAHHOTI fore they are quite awake. 2 pounds prepared garrets Here Is a little different way J of ' teaspoons salt to 1 quart water having potatoes and eggs: 4 cup mhied plees E.TCS IN SAKBD POTATOES i pint vinegar 1 prni carrot water 5 potatoes 4 cups sugar % 8 eggs - ' * . Wash, medium sUed earretg, cut !n 6 tablespoons grated chiese hali lengthwise, then crosswise in tablespoons butter 3-lnch pieces. Cook la boiling salted Bake the potatoes, cut off the top water until tender but net Broken, and remove half of the inside of the brain, aabi 1 pint liquid from carrots potato, in its place drop a raw egg, with the vinegar * sug&r and spiels salt, cayenne pepper, i tablespoon and bstt to syrUp, Add boiled ear- cheese in each and i teaspoon but * rots- l * et simmer slowly for several tet put back into a hot oven and hours, ntU Clear * -Bottle while hot, bake for 4 niihuies. and se&L and pennyroyal.

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