Litter decomposition by soil fauna: effect of land use in agroecosystems.

Soil fauna plays a key role in organic matter decomposition. Litter decomposition depends on the relationships of soil fauna and microorganisms as well as climate and litter quality. The decomposer community is sensitive to land use. Thus, physical-chemical disturbances, like soil tillage, can exercise important control on the soil fauna. In order to study the effect of land use and its impact on litter decomposition by soil fauna, a litter-bag experiment was conducted in the Pampa Serrana region, Azul district, Argentina. Litter-bags were made in three different mesh-sizes, allowing the access of micro, micro + meso and micro + meso + macrofauna. Four different treatments were defined: naturalized grassland and three agricultural agroecosystems under different tillage systems, i.e., conservation tillage, conventional-conservation tillage and conventional tillage. Decomposition rate and remaining litter were measured across three different seasons. We found that naturalized grassland obtained the highest decomposition rates and the least remaining litter compared to conservation and conventional tillage systems. No difference in litter decomposition was identified among agricultural agroecosystems. Micro + meso + macrofauna presented the highest decomposition rate and the lowest remaining litter of soil fauna groups, in all agroecosystems. In contrast, microfauna decomposition rate was the lowest and produced the highest remaining litter. Micro + mesofauna presented values of decomposition rate and remaining litter that differed significantly from the rest of the groups in some seasons. These results highlight the importance of soil fauna in litter decomposition and the negative effects of different land use systems on litter decomposition by soil fauna.

Heart and lungs in COPD. Close friends in real life--separate in daily medical practice?

Chronic obstructive pulmonary disease (COPD) is associated with a 2-3 times higher rate of cardiovascular disorders (CVD) which is independent of other risk factors. A low FEV1 is a specific predictor of mortality as a result of cardiac causes, even stronger than increased cholesterol: for each 10% reduction of FEV1, cardiovascular mortality increases by 28%. The main causes of death among COPD patients are of cardiovascular origin. COPD and CVD have two major risk factors in common - advanced age and tobacco smoking. The search for a pathogenetic link between the two conditions focuses mainly on systemic extension of pulmonary inflammation. Despite such a frequent association, pulmonologists and cardiologists in both the clinical and the research settings often underestimate the importance of a correct diagnosis and severity stratification of the two combined conditions. Spirometry, in particular, is largely underprescribed. Missed diagnosis and severity stratification, incomplete knowledge of adverse drug events and lack of resources lead to undertreatment of patients combining COPD and CVD, and in particular, the underuse of beta-blockers, inhaled bronchodilators and rehabilitation. Clinical studies focusing on this group of patients should be promoted in the future to test therapies and manage options. Furthermore, efforts must be made to improve the present standards of care, which falls short of recommended levels, starting from the often-neglected use of spirometry to confirm a diagnosis of COPD.

[Leptin as a possible marker of augmented metabolic risk during pregnancy]. / La leptina come possibile marker di aumentato rischio metabolico in gravidanza.

AIM: Leptin is a proteic hormone, isolated in 1994, mainly synthetized in the white adipose tissue. Aim of this study was to compare leptin concentrations in normal pregnancies with those measured in pregnancies complicated by gestational diabetes or gestational hypertension or pre-eclampsia. METHODS: We enrolled 48 pregnant women: 18 with uncomplicated pregnancy, 11 with gestational diabetes, 19 with gestational hypertension or pre-eclampsia. Leptin concentrations were measured in maternal serum at enrollment, together with insulin and cortisol, at delivery and in the immediate postpartum. At delivery serum leptin was calculated in the cord blood too. RESULTS: Fasting plasma leptin and insulin were higher in the group of patients with gestational hypertension, than in the other groups. Third-trimester maternal leptin concentrations correlated significantly with insulin levels in the group of women with gestational diabetes and in the group with gestational hypertension or pre-eclampsia, but not in the women with an uncomplicated pregnancy. CONCLUSIONS: Leptin concentrations in pregnancies complicated by hypertensive disorders are significantly higher than in normal pregnancies. The increased leptin concentrations are independent of associated proteinuria, as women with simple gestational hypertension and preeclampsia showed comparable third-trimester leptin concentrations. In both women with gestational diabetes and women with hypertensive disorders, serum leptin correlated closely with serum insulin, suggesting that the association between leptin and insulin resistance is preserved in pregnancy. Whatever the reasons for an increased maternal leptin production in pregnancies complicated by hypertension, maternal leptin homeostasis does not seem to influence foetal serum leptin concentrations, which seems to be mainly related to birth weight.

Quantitative expression of the human kallikrein gene 9 (KLK9) in ovarian cancer: a new independent and favorable prognostic marker.

Many members of the human kallikrein gene family were found to be differentially expressed in various malignancies and some are useful cancer diagnostic/prognostic markers. KLK9 is a newly discovered human kallikrein gene that is expressed in several tissues including thymus, testis, spinal cord, salivary gland, ovary, and skin. Like other kallikreins, the KLK9 gene was found to be regulated by steroid hormones in cancer cell lines. Our purpose is to examine whether quantitative analysis of KLK9 expression has prognostic value in ovarian cancer. We studied the expression of KLK9 by quantitative reverse transcription-PCR in 168 consecutive ovarian tumors of different stages, grades, and histological types, and correlated the expression with clinicopathological parameters, response to chemotherapy, and patients' survival. We found that KLK9 expression was significantly higher in patients with early disease stages (I or II; P = 0.044) and in patients with optimal debulking (P = 0.019). Kaplan-Meier survival curves demonstrated that patients with KLK9-positive tumors have substantially longer progression-free and overall survival (P < 0.001 and P = 0.016, respectively). When the Cox proportional hazard regression analysis was applied to subgroups of patients, KLK9 expression was found to be a significant predictor of progression-free survival in the subgroup of patients with low-grade tumors [hazard ratio (HR), 0.13; P = 0.0015], early stage (HR, 0.099; P = 0.031); and those with optimal debulking (HR, 0.26; P = 0.012). After adjusting for other known prognostic variables, KLK9 retained its independent prognostic value in all of these subgroups of patients. A negative correlation was found between the expression levels of CA125 and KLK9 (rs, 0.350; P = 0.002). Our results indicate that KLK9 is under steroid hormone regulation in ovarian and breast cancer cell lines. Immmunohistochemically, human kallikrein protein (hK9) was localized in the cytoplasm, but not in the nuclei, of the epithelial cells of ovarian cancer tissues. We conclude that KLK9 is a potential new independent favorable prognostic marker for early stage, low-grade, optimally debulked ovarian cancer patients.

Preserved insulin sensitivity and {beta}-cell activity, but decreased glucose effectiveness in normal-weight women with the polycystic ovary syndrome.

Insulin resistance and hyperinsulinemia are often considered intrinsic features of the polycystic ovary syndrome (PCOS). Nevertheless, conflicting results of insulin sensitivity and secretion have been obtained in the subgroup of normal-weight women with PCOS. Differences in body composition, ethnicity, and diet composition and a family history of metabolic diseases may act as confounding variables in women with PCOS. In the present study, insulin sensitivity and secretion were estimated by an iv glucose tolerance test (IVGTT), analyzed by minimal models, in 20 normal-weight healthy women with PCOS and no family history of type 2 diabetes mellitus and in 20 normally ovulating women, matched for age and body mass index. Insulin sensitivity [mean (95% confidence intervals); PCOS 4.0 (2.8-5.1) vs. controls 4.5 (3.5-5.4) 10(-4) min(-1)/microU.ml], and insulin secretion, expressed as the acute insulin response to glucose [PCOS 3.7 (3.3-4.2) vs. controls 3.7 (3.4-4.0) microU/ml] were similar in the two groups. The women with PCOS showed an increased proportion of total body fat (PCOS 29% vs. controls 27.2%; P < 0.01). They also showed decreased glucose effectiveness, i.e. the proportion of glucose uptake independent from insulin activity [PCOS 2.6 (2.1-3.0) vs. controls 3.8 (3.0-4.6) mg x 100 min(-1); P = 0.01]. The levels of insulin sensitivity and of glucose effectiveness did not correlate in either group. Whether the isolated finding of decreased glucose effectiveness could reflect an early stage in the development of the metabolic aberrations often associated with the syndrome remains to be clarified.

Nongenomic effects of 1alpha,25-dihydroxyvitamin D(3).

The hormonally active form of vitamin D, 1alpha,25-dihydroxyvitamin D(3), is the key molecule of the vitamin D endocrine system, which produces biological effects in about 30 target cell systems. Growing experimental evidence supports the hypothesis that these biological effects can be generated both by a signal transduction mechanism involving a nuclear receptor (nVDR) that modulates gene transcription, and via a nongenomic receptor located in the plasma membrane (mVDR), which modulates a complex signaling system involving the rapid opening of Ca(2+) channels. Some data reviewed herein also indicate that crosstalk between genomic and nongenomic pathways operates in several cell types, and suggest that the physiological role of the rapid, nongenomic actions might involve the regulation of hormone-mediated gene activation.

Evidence for a dose-response effect between p53 (but not p21WAF1/Cip1) protein concentrations, survival, and responsiveness in patients with epithelial ovarian cancer treated with platinum-based chemotherapy.

The prognostic values of p53 and of its downstream mediator p21WAF1/Cip1 in patients receiving adjuvant chemotherapy for epithelial ovarian cancer have not been clearly established. Tumor extracts from a series of 120 patients treated postsurgically with cisplatin or carboplatin alone or together with other chemotherapeutics for primary ovarian carcinoma were assayed both for p53 protein by an immunofluorometric assay developed by us and for p21 protein by a commercially available immunoassay. Relative risks (RRs) for cancer relapse and death after 24 months of follow-up were determined by multivariate Cox regression analysis. Disease-free (DFS) and overall survival (OS) probabilities were also examined by the Kaplan-Meier method and log-rank tests. All other procedures were similarly nonparametric and based on two-sided tests of significance. Concentrations of p53 were elevated in patients with advanced stage disease (P = 0.02) or poorly differentiated (P = 0.03), suboptimally debulked tumors (P = 0.02), as well as in patients who failed to respond to chemotherapy (P = 0.03), as assessed by computed tomography scanning, serum CA125 determination, and second-look laparotomy. Statistically significant associations between concentrations of p53 and p21 were not found, nor were relationships demonstrated between concentrations of p21 and other clinicopathological variables or treatment response. Univariate analysis showed that p53 concentrations above the median indicated significantly higher risks for relapse (P = 0.04) and death (P < 0.01) and showed trends for increasing risks for relapse (P = 0.04) and death (P < 0.01) when p53 was considered as a four-level categorical variable. Multivariate analyses adjusted for age, stage, grade, and residual tumor size confirmed these observations (RR = 1.50; P = 0.05 for DFS and RR = 1.92; P = 0.03 for OS) for median-dichotomized p53, but the trends were of borderline significance (P = 0.09 for DFS and P = 0.07 for OS). In contrast, p21 positivity was not a significant predictor of favorable outcome in univariate survival analysis, and use of a three-level variable combining positivity or negativity status for both p53 and p21 did not yield greater separation of patients into risk groups (P = 0.07 for DFS and P = 0.06 for OS) than the use of p53 alone. Assessment of p53 expression may be an independent indicator of poor prognosis in ovarian cancer patients treated with adjuvant chemotherapy. The prognostic value of p21 expression, however, could not be demonstrated in our series of ovarian cancer patients.

Higher human kallikrein gene 4 (KLK4) expression indicates poor prognosis of ovarian cancer patients.

PURPOSE: Kallikrein gene 4 (KLK4, also known as prostase/KLK-L1), located on chromosome 19q13.4, is one of the newly discovered members of the human KLK-like gene family. This gene is up-regulated by androgens in the LNCaP prostatic carcinoma cell line and by androgens and progestins in the BT-474 breast cancer cell line. On the basis of its apparent association with hormonally regulated tissues, we have undertaken to examine the prognostic value of KLK4 expression in 147 malignant ovarian tissues. EXPERIMENTAL DESIGN: Tumors were pulverized, total RNA was extracted, and cDNA was prepared by reverse transcription. KLK4 was amplified by PCR using gene-specific primers, and its identity was verified by sequencing. Ovarian tissues were then classified as KLK4-positive or -negative, based on ethidium bromide visualization of the PCR product on agarose gels. RESULTS: KLK4 was found to be expressed in 69 (55%) of 147 of ovarian cancer samples. We found a strong positive association between KLK4 expression and tumor grade (P = 0.02) and clinical stage (P < 0.001). Univariate survival analysis revealed that patients with ovarian tumors positive for KLK4 expression had an increased risk for relapse and death (P = 0.003 and 0.001, respectively). Whereas knowledge of KLK4 status did not significantly increase the prognostic power of the multivariate models, additional analyses did determine that KLK4 was an independent unfavorable prognostic factor in patients with grade 1 and 2 tumors. CONCLUSIONS: Our findings indicate that KLK4 expression is associated with more aggressive forms of ovarian cancer.

The human KLK8 (neuropsin/ovasin) gene: identification of two novel splice variants and its prognostic value in ovarian cancer.

UNLABELLED: KLK8 (neuropsin/ovasin) is a new member of the human kallikrein gene family, which consists of enzymes with serine protease enzymatic activity. Recent reports have implicated KLK8 in ovarian cancer. KLK8 may have potential clinical value for disease diagnosis or prognosis and it may also be a useful therapeutic target. PURPOSE: We undertook this study to evaluate the prognostic value of KLK8 in ovarian carcinoma by examining its expression in ovarian tumors. EXPERIMENTAL DESIGN: The KLK8 gene was analyzed by reverse transcription-PCR and direct sequencing in several human normal tissues. Subsequently, its expression was studied in a set of ovarian tumors, and statistical analysis was performed. RESULTS: We have identified two novel mRNA splice variants of the KLK8 gene, which are abundantly expressed in many tissues. These new variants were named KLK8 type 3 and type 4. Study of the expression of the KLK8 gene and its spliced variants in ovarian tumors indicated that the new variants were expressed very frequently and that full-length KLK8 expression is an independent and favorable prognostic marker for ovarian cancer. Patients with higher KLK8 expression in the tumor have lower grade disease, lower residual tumor left after surgery, live longer, and relapse less frequently. In multivariate analysis, higher KLK8 expression was significantly associated with longer disease-free survival. CONCLUSIONS: These results suggest that KLK8 is a novel, favorable prognostic marker in ovarian cancer. Because KLK8 encodes for a predicted secreted protein, its detection in serum may aid in ovarian cancer diagnosis.

Drug resistance-associated markers P-glycoprotein, multidrug resistance-associated protein 1, multidrug resistance-associated protein 2, and lung resistance protein as prognostic factors in ovarian carcinoma.

Intrinsic and/or acquired resistance to chemotherapy is the major obstacle to overcome in the treatment of patients with ovarian carcinoma. The aim of the present study was to investigate the prognostic value of drug resistance-associated proteins P-glycoprotein (P-gp), multidrug resistance-associated protein 1 (MRP1), canalicular multispecific organic anion transporter (c-MOAT/MRP2), and lung resistance protein (LRP) in ovarian carcinoma. Expression of P-gp, MRP1, MRP2, and LRP was determined by immunohistochemistry of frozen tissue sections of 115 ovarian carcinoma patients and related to clinicopathological factors, response to chemotherapy, and progression-free survival. P-gp expression was observed in 20 of 115 (17%), MRP1 in 51 (44%), MRP2 in 19 (16%), and LRP in 85 (74%) tumors. Expression of MRP1 was related to MRP2 (P<0.0001) and P-gp (P<0.001) expression, whereas LRP expression was more frequently observed in patients with early stage (P<0.01), lower grade (P<0.05), and smaller residual tumor (P<0.05). Early stage (P<0.001), smaller residual tumor (P<0.001), and lower differentiation grade (P<0.05) were related to longer (progression-free) survival. P-gp, MRP1, MRP2, and LRP expression were neither related to response to first-line chemotherapy in 59 evaluable patients nor to progression-free survival in all patients. On multivariate analysis, only stage and residual tumor were independent prognostic factors for survival. In conclusion, in ovarian carcinoma, MRP1 expression is associated with MRP2 and P-gp expression, whereas LRP expression is associated with favorable clinicopathological characteristics. Assessment of P-gp, MRP1, MRP2, or LRP does not allow prediction of response to chemotherapy or survival in ovarian carcinoma.

Response of the pituitary-adrenal axis to hypoglycemic stress in women with the polycystic ovary syndrome.

The role of the adrenals in the polycystic ovary syndrome (PCOS) is debated. Both single steroid-converting enzyme abnormalities and increased adrenal activity have received support. The conventional Synacthen test using pharmacological doses of ACTH results in unphysiological levels of ACTH. Therefore, we used insulin-induced hypoglycemia (0.15 IU/kg BW) to asses the responses of ACTH, cortisol, pregnenolone, 17-hydroxypregnenolone, dehydroepiandrosterone, progesterone, 17-hydroxyprogesterone, and androstenedione in 18 women with PCOS and in 17 normal women of similar age and body mass index. The blood glucose concentration at 30 min was 2 mmol/L or less in all women, i.e. well below the threshold of the hormonal counterregulatory response. The women with PCOS showed a lower ACTH response, expressed as the maximum increment above basal [mean (95% confidence interval): PCOS, 11.1 (6.9-15.3); controls, 19.9 (13.8-26) pmol/L; P < 0.05], but a quantitatively comparable [PCOS, 207.2 (148.5-266.5); controls, 167.1 (100.6-233.2) nmol/L; P = NS] and more prompt cortisol response than the controls (by chi2 test, P < 0.05), resulting in a higher molar ratio between the maximum increments of cortisol and ACTH [PCOS, 13.9 (8.7-19); controls, 8.8 (5.7-12); P < 0.05]. The women with PCOS did, however, show a more rapid decline in cortisol levels than the controls (P < 0.05 at 120 and 180 min). The responses of the androgens and intermediate adrenal steroids were similar in women with PCOS and controls. The findings suggest an adaptation to increased adrenal reactivity to endogenous ACTH in women with PCOS. Exposure to hypoglycemia as a model of stress was not followed by hypersecretion of adrenal androgens and revealed no signs of steroid enzyme disturbances in women with PCOS.

IGFBP-3 in epithelial ovarian carcinoma and its association with clinico-pathological features and patient survival.

Insulin-like growth factor binding protein-3 (IGFBP-3) regulates the mitogenic and anti-apoptotic actions of insulin-like growth factors (IGFs). To study the role of IGFBP-3 in ovarian cancer progression, we measured IGFBP-3 concentrations in tumour tissues from 147 patients with epithelial ovarian carcinoma and examined its associations with clinicopathological features of disease and patient survival. The average age of the patients was 54.6 years (range 25-88 years) and the median follow-up time was 37 months. IGFBP-3 levels were measured with a commercial immunoassay kit. Low IGFBP-3 levels were significantly associated with unfavourable prognostic features of the disease, including advanced stage (P=0.048), large size of residual tumour (P=0.007), and suboptimal debulking outcome (P=0.007). Low IGFBP-3 levels were also associated with a significantly increased risk for disease progression (RR=1.92; 95% confidence interval (CI) 1.05-3.45; P=0.034), but the association was not sustained when other clinical and pathological variables were adjusted for in the analysis. No significant associations were observed between the IGFBP-3 level and patients' overall survival and response to chemotherapy. Findings of the study indicate that IGFBP-3 may play a role in the progression of epithelial ovarian cancer, but that it has no independent value in predicting either disease prognosis or the response of patients to chemotherapy.

The effect of menopause on blood lipid and lipoprotein levels. The Icarus Study Group.

There is increasing evidence from epidemiological studies that exogenous estrogen (hormone replacement therapy) protects against the elevated risk of cardiovascular disease in women after the menopause. However, it is still uncertain whether the postmenopausal decrease in endogenous estrogen in itself contributes significantly to this increase in risk. Most of the studies that have provided evidence linking cardiovascular disease with menopause have involved North American women, who may differ significantly from Europeans in terms of lifestyle and diet. ICARUS (Italian Climacteric Research Group Study) is an observational study that involves Italian Menopause Clinics, with the objective of collecting observational data on menopause and its management. The results of a cross-sectional analysis of 9309 women, free from any hormonal treatment and enrolled up to March 1997, are reported here. Data show that the menopause has a marked effect on the circulating levels of lipids and lipoproteins. From pre- to post-menopause there are significant increases in total cholesterol (6.9% before and 4.4% after adjustment for covariates including chronological age, educational level, center, BMI, smoking habits, hypertension and diabetes, previous contraceptive use, and time since menopause), LDL (7.5% before, 4.0% after), and triglycerides (9.0% before, 3.2% (ns) after). However, there is no significant change in HDL. Among postmenopausal women, no effect on lipid profile of time since menopause was observed.

Binding of sex steroid binding protein to plasma membranes of human testis.

The existence of a specific binding site for sex steroid binding protein (SBP or SHBG) was detected on plasma membranes prepared from the testis of a patient affected by a variant form of testicular feminization. A binding technique using [125I]SBP as a tracer allowed us to identify a single set of binding sites, characterized by a Kd of 1.917 x 10(-11) M. The maximum number of binding sites was 5.2 fmol/mg membrane protein. Membranes were also prepared from a sample of genital skin from the same patient, but no binding for [125I]SBP was detectable. The evidence of the SBP membrane receptor in the testis of a patient affected by Morris syndrome extends our knowledge about the tissue distribution of the SBP receptor and suggests the possible implication of SBP and its recognition system in a disorder related to peripheral androgen insensitivity.

Steroid gradients across the cancerous breast: an index of altered steroid metabolism in breast cancer?

The concentrations of 17 beta-estradiol, estrone, testosterone (T), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate, androstenedione (A), cortisol and prolactin (PRL) were determined in the peripheral venous blood and in the lateral thoracic vein of 14 premenopausal and 34 postmenopausal women who underwent surgery for a breast carcinoma. The difference between the two blood samples, defined as concentration gradient across the cancerous breast, was calculated for all hormones. A significant peripheral-local concentration gradient was found for DHEA and A both in pre- and postmenopausal patients, whereas for T it was observed only in postmenopausal subjects. Furthermore, DHEA and A gradients were correlated to the presence of estrogen receptors as determined by a radioligand binding assay. An inverse relationship between DHEA gradient and the expression of estrogen receptors was observed in premenopausal women, whereas in postmenopausal patients an opposite, although not significant, trend was found. These results suggest that in the cancerous breast: (1) DHEA, A and T (the latter only in postmenopause) could be taken up from plasma, and thus there could be a storage of these steroids inside the breast tissue and/or perhaps some alterations in their local metabolism; (2) androgens could play a different role in breast carcinogenesis in relation to the estrogen circulating levels and to the expression of estrogen receptors.

A two-stage screening test for pregnancy-induced hypertension and preeclampsia.

OBJECTIVE: To assess the benefit of uterine artery Doppler ultrasound examination with ambulatory 24-hour blood pressure (BP) monitoring as a two-stage screening test for women at risk for pregnancy-induced hypertension, preeclampsia, or fetal growth restriction (FGR). METHODS: Uterine artery Doppler ultrasound was performed at 20-22 weeks' gestation on women at risk for pregnancy-induced hypertension, preeclampsia or FGR who were referred to our antenatal clinics. Abnormal findings were rechecked at 24 weeks' gestation. We selected 180 subjects (90 with abnormal uterine Doppler and 90 with normal uterine Doppler) for 24-hour BP monitoring with a portable automated device, immediately after recruitment, and the midline estimating statistics of rhythm of systolic and diastolic BPs were calculated. RESULTS: The highest incidence of pregnancy-induced hypertension and preeclampsia, with or without FGR, occurred in patients with abnormal uterine Doppler and a systolic midline estimating statistic of rhythm of at least 111 mmHg or a diastolic midline estimating statistic of rhythm of at least 68 mmHg. The specificity and positive predictive value of abnormal uterine Doppler ultrasound alone were low (55 and 27%, respectively), whereas the association of abnormal Doppler ultrasound with both systolic and diastolic midline estimating statistics of rhythm equal or above the selected cutoff values increased the specificity and positive predictive value to 93 and 63%, respectively. CONCLUSION: In clinical practice, a first-stage test with uterine artery Doppler ultrasound at 20-24 weeks' gestation, followed by a second-stage test with ambulatory 24-hour BP monitoring in patients with abnormal uterine Doppler, might indicate women at risk of developing pregnancy-induced hypertension or preeclampsia.

Blood pressure patterns in normal pregnancy and in pregnancy-induced hypertension, preeclampsia, and chronic hypertension.

OBJECTIVE: To compare the 24-hour blood pressure (BP) pattern in physiologic pregnancy, pregnancy-induced hypertension, preeclampsia, and chronic hypertension. METHODS: We investigated four groups of women with singleton pregnancy: 73 controls, 48 patients with pregnancy-induced hypertension, 38 with preeclampsia, and 53 with mild to moderate chronic hypertension. The 24-hour BP monitoring was performed longitudinally in controls and in patients with chronic hypertension, and at the time of diagnosis in those with pregnancy-induced hypertension or preeclampsia. RESULTS: Nineteen thousand eight hundred seventy-two BP measurements were analyzed. In controls, the mean values of BP indices were lower than those first reported in nonpregnant women, and the acrophase was always localized in the first part of the afternoon. In pregnancy-induced hypertension and especially in preeclampsia, besides the obvious quantitative increase in BP, circadian BP oscillations were less pronounced than in controls, and the severity of hypertension seemed to favor the loss of diurnal rhythm. Conversely, in chronic hypertension, circadian oscillations were the same as in controls. CONCLUSION: Standardized 24-hour BP monitoring during pregnancy allows quantitative and qualitative evaluations of the hypertensive status. However, if such a technique is used routinely in every clinical setting, we should establish specific thresholds of normality for pregnancy.

Microinjection of mitochondria into zygotes creates a model for studying the inheritance of mitochondrial DNA during preimplantation development.

OBJECTIVE: To determine the effect of mutant mitochondria on preimplantation embryo development and of preimplantation embryo development on the survival of mutant mitochondrial DNA. DESIGN: Laboratory research. SETTING: Academic research laboratory. PATIENT(S): None. INTERVENTION(S): Mutant and wild-type mitochondria, fractionated from tissue obtained from a patient with MELAS syndrome, a mitochondrial disease, were microinjected into mouse zygotes. Control zygotes received either no injection or sham injection. MAIN OUTCOME MEASURE(S): Preimplantation embryo development and survival of mutant mitochondrial DNA as determined by polymerase chain reaction analysis. RESULT(S): After microinjection into zygotes, the MELAS mutation could be identified by polymerase chain reaction until the hatched blastocyst stage of embryo development. The survival of MELAS-injected zygotes, observed for 4 days after injection, did not differ from the survival of zygotes injected with wild-type mitochondria or from the survival of uninjected or sham-injected controls. CONCLUSION(S): It appears that preimplantation embryo development does not screen out mitochondrial DNA mutations introduced into fertilized oocytes, and low levels of mutant mitochondrial DNA do not disrupt early embryo development.

Effect of volumetric mixtures of peritoneal and follicular fluid from the same woman on sperm motility and acrosomal reactivity in vitro.

OBJECTIVE: To study the effect of peritoneal (PF) and follicular fluids (FF from the same woman) as well as of given volumetric combinations thereof on sperm motility and acrosomal reactivity. DESIGN: Prospective. Peritoneal fluid and FF were incubated separately or in given volumetric combinations (PF/FF = 100/0, 75/25, 50/50, 25/75, 0/100; vol/vol) with swim-up sperm suspensions. SETTING: In vitro fertilization and general infertility clinic and laboratories. PATIENTS, PARTICIPANTS: Women participants of the gamete intrafallopian transfer program (motility study, n = 20; acrosomal reaction study, n = 14). Sperm donors of the artificial insemination program and men with given sperm parameters. INTERVENTIONS: Hormonal stimulation. Laparoscopy. MAIN OUTCOME MEASURES: Progressive velocity and percentage of motile gametes measured with multiple-exposure photography. Acrosomal reactivity measured by an immunofluorescent technique. RESULTS: Follicular fluid always influenced progressive motility and also sustained the number of motile gametes, as function of time, better than PF or the PF/FF mixtures (P less than 0.05). The acrosomal reactivity of sperm incubated in the various PF/FF combinations was low; after 5 hours only the FF-sperm suspensions showed a significant enhancement of acrosomally reacted gametes. CONCLUSION: At ovulation, FF transmit positive (motility- and acrosomal reactivity-enhancing) signals to sperm, whereas PF may transmit positive, neutral, or negative signals (noise signals). The volumetric combination of FF and PF in the tubal environment, which may differ from cycle to cycle and from woman to woman, could therefore result in synergic (or antagonistic) effects on the sperm fertility potential.

The concentration of nitrite in seminal plasma does not correlate with sperm concentration, sperm motility, leukocytospermia, or sperm culture.

OBJECTIVE: To correlate the concentration of nitrite (the stable metabolite of nitric oxide) in seminal plasma with sperm number and motility, leukocytospermia, and sperm culture. DESIGN: Prospective study. SETTING: Academic research institution. PATIENT(S): Seventy normozoospermic or dyspermic men enrolled in an artificial insemination/in vitro fertilization program. INTERVENTION(S): Semen samples (n = 70) were checked for sperm concentration, total sperm count, sperm motility, seminal leukocyte concentration, and sperm culture; similarly, the concentration of nitrite in seminal plasma was measured by Griess reaction. MAIN OUTCOME MEASURE(S): Measurement of nitrite concentration in seminal plasma and its correlation with sperm concentration, total sperm count, sperm motility, leukocytospermia, and sperm culture. RESULT(S): The concentration of nitrite in seminal plasma does not correlate with sperm concentration, total sperm count, or with the proportion of immotile or rapid-forward motile spermatozoa. Moreover, the concentration of nitrite in seminal plasma is not significantly increased when sperm culture is positive, nor does it correlate with leukocyte concentration in semen. CONCLUSION(S): Our results do not support the hypothesis that in vivo nitric oxide synthesis affects sperm function; alternatively, our results could suggest that nitrite in the seminal plasma is not a sensitive marker of in vivo nitric oxide synthesis.