666 research outputs found
Postmenopausal bone loss : prevention and replacement
Osteoporosis is a skeletal disorder predominantly affecting postmenopausal women. Combination therapy of Carbocalcitonin (Elcatonin) and oral conjugated oestrogens (Premarin) not only prevents postmenopausal bone loss but leads to an increase in bone mass in normal early postmenopausal women. The aims of the study was to investigate the effect of combination therapy. A combination of Elcatonin (Carbo calcitonin) and Premarin was compared to Premarin alone, and to Elcatonin (Carbocalcitonin) alone and all groups were then compared to a control group.peer-reviewe
Relationship of fetal alanine uptake and placental alanine metabolism to maternal plasma alanine concentration
Uterine and umbilical uptakes of alanine (Ala) were measured in 10 ewes
before (control) and during intravenous infusion of Ala, which increased
maternal arterial Ala concentration from 115 +/- 14 to 629 +/- 78 microM
(P < 0.001). In 8 of these ewes, placental Ala fluxes were traced by
constant intravenous infusion of L-[3,3,3-2H3]Ala in the mother and
L-[1-13C]Ala in the fetus. Rates are reported as micromoles per minute per
kilogram fetus. Ala infusion increased uterine uptake (2.5 +/- 0.6 to 15.6
+/- 3.1, P < 0.001), umbilical uptake (3.1 +/- 0.5 to 6.9 +/- 0.8, P <
0.001), and net uteroplacental utilization (-0.7 +/- 0.8 to 8.6 +/- 2.7, P
< 0.01) of Ala. Control Ala flux to fetus from mother (Rf,m) was much less
than the Ala flux to fetus from placenta (Rf,p) (0.17 +/- 0.04 vs. 5. 0
+/- 0.6). Two additional studies utilizing L-[U-13C]Ala as the maternal
tracer confirmed the small relative contribution of Rf,m to Rf,p. During
maternal Ala infusion, Rf,m increased significantly (P < 0.02) but
remained a small fraction of Rf,p (0.71 +/- 0.2 vs. 7.3 +/- 1.3). We
conclude that maternal Ala entering the placenta is metabolized and
exchanged for placental Ala, so that most of the Ala delivered to the
fetus is produced within the placenta. An increase in maternal Ala
concentration increases placental Ala utilization and the fetal uptake of
both maternal and placental Ala
Effect of dexamethasone on fetal hepatic glutamine-glutamate exchange
Intravenous infusion of dexamethasone (Dex) in the fetal lamb causes a
two- to threefold increase in plasma glutamine and other glucogenic amino
acids and a decrease of plasma glutamate to approximately one-third of
normal. To explore the underlying mechanisms, hepatic amino acid uptake
and conversion of L-[1-(13)C]glutamine to L-[1-(13)C]glutamate and
(13)CO(2) were measured in six sheep fetuses before and in the last 2 h of
a 26-h Dex infusion. Dex decreased hepatic glutamine and alanine uptakes
(P < 0.01) and hepatic glutamate output (P < 0.001). Hepatic outputs of
the glutamate (R(Glu,Gln)) and CO(2) formed from plasma glutamine
decreased to 21 (P < 0.001) and 53% (P = 0.009) of control, respectively.
R(Glu,Gln), expressed as a fraction of both outputs, decreased (P < 0.001)
from 0.36 +/- 0.02 to 0.18 +/- 0.04. Hepatic glucose output remained
virtually zero throughout the experiment. We conclude that Dex decreases
fetal hepatic glutamate output by increasing the routing of glutamate
carbon into the citric acid cycle and by decreasing the hepatic uptake of
glucogenic amino acids
Genomic Risk Profiling of Ischemic Stroke: Results of an International Genome-Wide Association Meta-Analysis
Introduction: Familial aggregation of ischemic stroke derives from shared genetic and environmental factors. We present a meta-analysis of genome-wide association scans (GWAS) from 3 cohorts to identify the contribution of common variants to ischemic stroke risk.Methods: This study involved 1464 ischemic stroke cases and 1932 controls. Cases were genotyped using the Illumina 610 or 660 genotyping arrays; controls, with Illumina HumanHap 550Kv1 or 550Kv3 genotyping arrays. Imputation was performed with the 1000 Genomes European ancestry haplotypes (August 2010 release) as a reference. A total of 5,156,597 single-nucleotide polymorphisms (SNPs) were incorporated into the fixed effects meta-analysis. All SNPs associated with ischemic stroke (P < 1 x 10(-5)) were incorporated into a multivariate risk profile model.Results: No SNP reached genome-wide significance for ischemic stroke (P < 5 x 10(-8)). Secondary analysis identified a significant cumulative effect for age at onset of stroke (first versus fifth quintile of cumulative profiles based on SNPs associated with late onset, beta = 14.77 [10.85, 18.68], P = 5.5 x 10(-12)), as well as a strong effect showing increased risk across samples with a high propensity for stroke among samples with enriched counts of suggestive risk alleles (P < 5 x 10(-6)). Risk profile scores based only on genomic information offered little incremental prediction.Discussion: There is little evidence of a common genetic variant contributing to moderate risk of ischemic stroke. Quintiles based on genetic loading of alleles associated with a younger age at onset of ischemic stroke revealed a significant difference in age at onset between those in the upper and lower quintiles. Using common variants from GWAS and imputation, genomic profiling remains inferior to family history of stroke for defining risk. Inclusion of genomic (rare variant) information may be required to improve clinical risk profiling
Association of Prediabetes and Diabetes With Stroke Symptoms The REasons for Geographic And Racial Differences in Stroke (REGARDS) Study
OBJECTIVE Stroke symptoms among individuals reporting no physician diagnosis of stroke are associated with an increased risk of future stroke. Few studies have assessed whether individuals with diabetes or prediabetes, but no physician diagnosis of stroke, have an increased prevalence of stroke symptoms.
RESEARCH DESIGN AND METHODS This study included 25,696 individuals aged â„45 years from the REasons for Geographic And Racial Differences in Stroke (REGARDS) study who reported no history of stroke or transient ischemic attack at baseline (2003â2007). Glucose measurements, medication use, and self-reported physician diagnosis were used to categorize participants into diabetes, prediabetes, or normal glycemia groups. The presence of six stroke symptoms was assessed using a validated questionnaire.
RESULTS The prevalence of any stroke symptom was higher among participants with diabetes (22.7%) compared with those with prediabetes (15.6%) or normal glycemia (14.9%). In multivariable models, diabetes was associated with any stroke symptom (prevalence odds ratio [POR] 1.28 [95% CI 1.18â1.39]) and two or more stroke symptoms (1.26 [1.12â1.43]) compared with normal glycemia. In analyses of individual stroke symptoms, diabetes was associated with numbness (1.15 [1.03â1.29]), vision loss (1.52 [1.31â1.76]), half-vision loss (1.54 [1.30â1.84]), and lost ability to understand people (1.34 [1.12â1.61]) after multivariable adjustment. No association was present between prediabetes and stroke symptoms.
CONCLUSIONS In this population-based study, almost one in four individuals with diabetes reported stroke symptoms, which suggests that screening for stroke symptoms in diabetes may be warranted
When love hurts : A systematic review on the effects of endometriosis surgical and pharmacological treatments on female sexual functioning
INTRODUCTION:
Endometriosis is associated with an increased risk of dyspareunia, therefore this chronic gynaecologic disease should be considered as a major cause of sexual dysfunctions. The aims of this study were to review the literature on the effects of endometriosis surgical and pharmacological treatments on female sexual functioning, and to provide suggestions for future treatment strategies.
MATERIAL AND METHODS:
We followed the PRISMA guidelines to conduct this systematic review, which involved an electronic database search of studies on the association between endometriosis and sexuality published between 2000 and 2016.
RESULTS:
As a result of the screening process, 22 studies were included in this systematic review. The 22 studies included were divided in 2 categories: 1) surgical intervention studies (n = 17), examining postoperative sexual outcomes of surgery for endometriosis; 2) pharmacological intervention studies (n = 5), evaluating the effects of pharmacological endometriosis treatments on sexual functioning. The studies considered showed that overall surgical and pharmacological interventions for endometriosis can lead to medium-/long-term improvement, but not necessarily to a definitive resolution of female sexual dysfunctions due to endometriosis.
CONCLUSIONS:
Sexual functioning is a multidimensional phenomenon and the ideal treatment for endometriosis related sexual dysfunctions should be conducted by a multidisciplinary team that involves not only gynaecologists, but also sexologists and psychologists/psychotherapists. Improving global sexual functioning, and not just reducing pain at intercourse, should be considered as a major clinical goal of endometriosis treatment
Stroke genetics: prospects for personalized medicine.
Epidemiologic evidence supports a genetic predisposition to stroke. Recent advances, primarily using the genome-wide association study approach, are transforming what we know about the genetics of multifactorial stroke, and are identifying novel stroke genes. The current findings are consistent with different stroke subtypes having different genetic architecture. These discoveries may identify novel pathways involved in stroke pathogenesis, and suggest new treatment approaches. However, the already identified genetic variants explain only a small proportion of overall stroke risk, and therefore are not currently useful in predicting risk for the individual patient. Such risk prediction may become a reality as identification of a greater number of stroke risk variants that explain the majority of genetic risk proceeds, and perhaps when information on rare variants, identified by whole-genome sequencing, is also incorporated into risk algorithms. Pharmacogenomics may offer the potential for earlier implementation of 'personalized genetic' medicine. Genetic variants affecting clopidogrel and warfarin metabolism may identify non-responders and reduce side-effects, but these approaches have not yet been widely adopted in clinical practice
The Ischemic Stroke Genetics Study (ISGS) Protocol
BACKGROUND: The molecular basis for the genetic risk of ischemic stroke is likely to be multigenic and influenced by environmental factors. Several small case-control studies have suggested associations between ischemic stroke and polymorphisms of genes that code for coagulation cascade proteins and platelet receptors. Our aim is to investigate potential associations between hemostatic gene polymorphisms and ischemic stroke, with particular emphasis on detailed characterization of the phenotype. METHODS/DESIGN: The Ischemic Stroke Genetic Study is a prospective, multicenter genetic association study in adults with recent first-ever ischemic stroke confirmed with computed tomography or magnetic resonance imaging. Patients are evaluated at academic medical centers in the United States and compared with sex- and age-matched controls. Stroke subtypes are determined by central blinded adjudication using standardized, validated mechanistic and syndromic classification systems. The panel of genes to be tested for polymorphisms includes ÎČ-fibrinogen and platelet glycoprotein Ia, Iba, and IIb/IIIa. Immortalized cell lines are created to allow for time- and cost-efficient testing of additional candidate genes in the future. DISCUSSION: The study is designed to minimize survival bias and to allow for exploring associations between specific polymorphisms and individual subtypes of ischemic stroke. The data set will also permit the study of genetic determinants of stroke outcome. Having cell lines will permit testing of future candidate risk factor genes
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