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There are many reported benefits to plants of arbuscular mycorrhizal fungi (AMF), including positive plant biomass responses; however, AMF can also induce biomass depressions in plants, and this response receives little attention in the literature. High-throughput phenotyping (HTP) technology permits repeated measures of an individual plant's aboveground biomass. We examined the effect on AMF inoculation on the shoot biomass of three contrasting plant species: a vegetable crop (tomato), a cereal crop (barley), and a pasture legume (Medicago). We also considered the interaction of mycorrhizal growth responses with plant-available soil zinc (Zn) and phosphorus (P) concentrations. The appearance of a depression in shoot biomass due to inoculation with AMF occurred at different times for each plant species; depressions appeared earliest in tomato, then Medicago, and then barley. The usually positive-responding Medicago plants were not responsive at the high level of soil available P used. Mycorrhizal growth responsiveness in all three species was also highly interactive with soil Zn supply; tomato growth responded negatively to AMF inoculation in all soil Zn treatments except the toxic soil Zn treatment, where it responded positively. Our results illustrate how context-dependent mycorrhizal growth responses are and the value of HTP approaches to exploring the complexity of mycorrhizal responses.

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The regulation of host-mediated apoptosis by the E6 and E7 oncoproteins has garnered attention because it is believed to be an important strategy employed by high-risk (HR)-human papillomaviruses (HPVs) to evade immune surveillance. Additionally, the revelation that E5 can protect cells from tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis suggests that it may also play a role in undermining host defense mechanisms. Cellular transformation is an unintended consequence of persistent infection by HR-HPVs, and it is therefore likely that the primary function of E5, E6 and E7 is to regulate cell survival throughout the normal viral life cycle in order to ensure viral replication and promote the spread of progeny. The purpose of this article is to review the literature on the regulation of host-mediated apoptosis by E5, E6 and E7 that describes the mechanisms employed by HR-HPVs to persist in the host and create the conditions necessary for cellular transformation.

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Viruses have developed sophisticated strategies to evade host defenses and facilitate the production and spread of progeny. In this study, we show that transfection of the human papillomavirus (HPV) 16 E6 oncogene into HCT116 cells provides protection from tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-mediated apoptosis. Additionally, we demonstrate that the protection provided by E6 is dose-dependent because higher levels of E6 provide greater protection. The mechanism underlying this protection involves a rapid reduction in the protein levels of both Fas-associated death domain (FADD) and procaspase 8, which results in suppression of the activation of caspases 8, 3 and 2. Interestingly, E6 does not interfere with the mitochondrial apoptotic pathway even though HCT116 cells have been classified as type II cells with regard to TRAIL signaling. These findings demonstrate that E6 has a more generalized effect on signaling by death ligands than was previously thought and support the notion that E6 can utilize p53-independent mechanisms to modulate cell survival.

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OBJECTIVE: To examine the long-term effects of hysterectomy with conservation of the ovaries on bone density of the lumbar spine and proximal femur. METHODS: A cross-sectional study of the bone density of 40 postmenopausal women who had undergone hysterectomy with ovarian conservation before menopause compared with a matched group of 40 women who had not had hysterectomy. The 40 women who had undergone hysterectomy were also compared with a control population, using multiple linear regression analysis. Bone density of the femoral neck and lumbar spine was measured by quantitative digital radiography. RESULTS: Bone density in the hysterectomy group was significantly reduced at the spine (P < .05) and at the femoral neck (P < .05) compared with the matched group. Comparisons of the hysterectomy group with the reference group demonstrated that in addition to significant reductions in bone density at the spine (P < .05) and hip (P < .05), bone density at the femoral neck (P < .05), trochanter (P < .05), Ward's triangle (P < .05), and the second (P < .05) and fourth (P < .05) lumbar vertebrae was also significantly less in the hysterectomy group. CONCLUSION: Premenopausal women who have hysterectomy will have significantly lower bone density than controls, despite conservation of both ovaries at the time of surgery.

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OBJECTIVE: To determine the effect on the bone density of the skeleton after changing from oral oestrogen to subcutaneous oestradiol and testosterone replacement. DESIGN: Prospective non-randomized single centre study. SUBJECTS: Twenty women who were receiving long-term oral oestrogen replacement. Ten changed to oestradiol and testosterone implants; the remaining ten continued with oral oestrogens. MAIN OUTCOME MEASURES: Bone density was measured using dual photon absorptiometry at the lumbar spine and neck of femur at the start of the study and after one year. RESULTS: The bone density increased significantly by 5.7% at the spine and by 5.2% at the neck of femur in those women who changed to implant therapy but remained unchanged in those women who continued with oral therapy. CONCLUSION: Subcutaneous oestradiol and testosterone implants will result in an increase in bone mass even after many years of oral oestrogen replacement therapy.

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Percutaneous estradiol (E2) implants effectively preserve bone density in postmenopausal women. However, these implants are often given with testosterone, which may itself have an anabolic effect on bone. To determine whether testosterone confers any additional bone-sparing effect, we studied 50 postmenopausal women randomly allocated to receive E2 (75 mg) alone or with testosterone (100 mg) every 6 months for 1 year. Women with an intact uterus received cyclic norethindrone (5 mg) for 10 days of each calendar month. Twenty-five untreated women were recruited to act as a reference group. Bone density was measured at the lumbar spine and proximal femur by dual x-ray densitometry. By 1 year, bone density at the lumbar spine had fallen by 1.8% in the reference group. In the women treated with E2 alone, it increased significantly by 7.8% (P less than .0001) and in those receiving E2 with testosterone, it increased by 6.3% (P less than .0001). At the femoral neck, bone density decreased by 3% in the controls and increased by approximately 4% in both treated groups (P less than .0001). The increase in bone density at these sites was unrelated to the woman's chronological age, menopausal age, or initial bone density. However, it correlated significantly with the serum E2 levels attained after 1 year of therapy. In no treated patients did bone density decrease significantly. These data show that testosterone confers no additional bone-sparing effect in postmenopausal women.

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The effect of hormone implants on the bone density of postmenopausal women was studied in 110 patients (mean age 54.7 years; mean menopausal age 8.6 years, range 2-30) who had received hormone replacement in the form of estradiol (50-75 mg) and testosterone (100 mg) pellets at 6-month intervals for 2-24 years (mean 5.2). They were compared with 254 untreated women (mean age 55.0 years; mean menopausal age 6.8 years, range 1-37). The bone density at the spine, measured by quantitative digital radiography, was 1.123 grams hydroxyapatite (gHa)/cm2 in the treated group and 0.951 gHa/cm2 in the controls (P less than .0001). The total bone density at the proximal femur was 1.002 gHa/cm2 in the treated group, compared with 0.914 gHa/cm2 in the controls (P less than .0001). There were significant differences in the density of the trochanteric, intertrochanteric, and neck areas of the proximal femur as well as the Ward triangle (all P less than .0001). These differences became significant from the age of 55 at the neck of the femur, Ward triangle, and lumbar spine, and from age 60 for all other values. Subcutaneous estradiol and testosterone prevent postmenopausal osteoporosis and maintain normal bone density for as long as treatment is continued.

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One hundred and fifty new patients attending the Menopause Clinic at Dulwich Hospital were questioned on their attitudes and fears about hormone replacement therapy and the perceived attitudes of their general practitioner. The majority of patients attending the clinic had initiated referral themselves and many had travelled from outside the health authority area in order to be seen. The waiting list for an appointment was often unacceptable. We conclude that specialist menopause clinics in teaching hospitals are unable to cope with the demand for information about the menopause and hormone replacement from post-menopausal women and suggest alternative means for providing this service.

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Twenty-three postmenopausal women with a median of 2 years past menopause (range, 1 to 12 years) and a median age of 52 years (range, 39 to 62 years) were recruited to participate in a longitudinal study designed to investigate the factors that influence the increase in bone density with subcutaneous estradiol and testosterone implants. All women received 75 mg of estradiol with 100 mg testosterone subcutaneously. Bone density was measured at the spine and hip by dual-photon absorptiometry before therapy and after 1 year of subcutaneous hormonal therapy. The mean pretreatment bone density at the lumber vertebrae and neck of the femur was 0.84 grams of hydroxyapatite per square centimeter (SD, 0.11) and 0.73 grams of hydroxyapatite per square centimeter (SD, 0.10), respectively. The bone density at both sites increased with values of 0.91 grams of hydroxyapatite per square centimeter (SD, 0.11) and 0.75 grams of hydroxyapatite per square centimeter (SD, 0.11), respectively. These values represent an increase of 8.3% (p less than 0.0001) at the spine and 2.8% (p less than 0.01) at the neck of the femur. The plasma estradiol level increased from a median of 80.5 pmol/L to 453 pmol/L (p less than 0.001). The percentage increase of vertebral bone density was not related to age, number of years past the menopause, pretreatment bone density, or serum testosterone levels, but a significant correlation was found between the percentage increase in bone density at the spine and the serum estradiol level (p less than 0.02, r = 0.45).

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The serum oestradiol levels of 1388 women treated with hormone implants at a menopause clinic were reviewed in 1988. Thirty-eight (3%) were found to be above 1750 pmol/l. Of these 38 women with supraphysiological oestradiol levels 23 had started therapy for menopausal symptoms and 15 for the premenstrual syndrome (PMS). Of the 23 women treated for menopausal symptoms 11 had a history of psychiatric referral for depression and nine had undergone a surgical menopause. Nine of the 15 women with PMS had a history of psychiatric referral for depressive symptoms. We conclude that the women who attain supraphysiological levels of oestradiol on implant therapy have a high frequency of psychopathology or surgical menopause and may require higher oestradiol levels for adequate control of symptoms.

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40 patients with premenstrual symptoms were randomly allocated to receive placebo patches or active treatment with transdermal oestradiol patches (2 x 100 micrograms) to suppress ovulation. Norethisterone 5 mg was given in each group from day 19-26 of the cycle to ensure a regular withdrawal bleed. Treatment was for 6 months with crossover at 3 months. Patients completed the Moos menstrual distress questionnaire (MDQ) and the premenstrual distress questionnaire (PDQ) daily throughout the study. 5 patients withdrew, 4 because of skin reactions and 1 because of considerable improvement with initial (active) treatment. After 3 months, both groups showed improvement in MDQ and PDQ scores. In general, between 3 and 6 months, patients who switched from active treatment to placebo had deteriorating scores while patients who switched from placebo to active treatment maintained or improved upon their initial gains. Significant improvements occurred after changing to active treatment in five of six negative MDQ symptom clusters and in six of ten PDQ symptoms.

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