bluuebunny/crossref_metadata_2025 huggingface dataset:
Changes in Central Arterial Pressure Waveforms during the Normal Menstrual Cycle
Authors: Ounis-Skali Nadia , Mitchell Gary F. , Solomon Caren G. , Solomon Scott D. , Seely Ellen W.
Published: August 2007

Background

Changes in estradiol and progesterone during the human menstrual cycle may impact vascular and cardiac function. Renin-angiotensin-aldosterone system (RAAS) hormones increase during the luteal phase of the menstrual cycle and may antagonize the vascular effects of estradiol. This study was designed to investigate central arterial changes, cardiac function, and RAAS activity in response to gonadal steroid variations during the menstrual cycle.

Methods

We studied 15 women during the follicular and midluteal phases with determination of estradiol, progesterone, hormones of the RAAS, and spot urine sodium and creatinine levels. Central pulsatile hemodynamics was evaluated using calibrated carotid tonometry and central aortic Doppler flow. Systolic ejection period (SEP) and systolic pressure time integral (SPTI) were computed from carotid pressure waveforms.

Results

Levels of estradiol, progesterone, and RAAS hormones were higher in the luteal phase. SEP and SPTI were lower during the luteal phase, whereas central and peripheral blood pressures and measures of arterial stiffness were unchanged between the two phases. The urine sodium-to-creatinine ratio was similar at both phases.

Conclusion

Central arterial stiffness does not differ between the follicular and midluteal phases of the menstrual cycle in healthy women, despite significant changes in estradiol and progesterone levels. Systole was shortened during the midluteal phase. RAAS activation during the luteal phase may be responsible for a lack of the expected estradiol-mediated reduction in arterial stiffness between the two phases of the menstrual cycle. Because load was unchanged, the decrease in SEP and SPTI may represent a direct effect of estrogen, progesterone, or RAAS activation on ventricular function.
Effects of Antenatal Betamethasone on Maternal and Fetoplacental Matrix Metalloproteinases 2 and 9 Activities in Human Singleton Pregnancies
Authors: Gharraee Zahra , Beharry Kay D.A. , Valencia Arwin M. , Cho Steve , Guajardo Leonel , Nageotte Michael P. , Modanlou Houchang D.
Published: August 2007

Background

A single course of antenatal betamethasone is administered to women at risk of preterm labor to advance fetal lung maturation. Matrix metalloproteinases (MMPs) are collagen-degrading enzymes that remodel extracellular matrix components during lung development. We tested the hypothesis that the effects of betamethasone on fetal lung maturation involve changes in MMP activity.

Methods

We conducted a prospective, observational pilot study of three groups of singleton pregnancies. Group 1 ( n = 21) was composed of women who were antenatally treated with a single course of betamethasone and who delivered < 37 weeks of gestation, group 2 ( n = 7) was composed of matched untreated women who delivered < 37 weeks of gestation, and group 3 ( n = 15) was composed of untreated women who delivered > 37 weeks of gestation. Maternal blood, mixed cord blood, and placental samples were collected at the time of delivery for MMP-2 and MMP-9 activity and tissue inhibitor of metalloproteinases (TIMP)-1 and -2 levels.

Results

MMP-2 activity was significantly higher in the maternal, placental, and fetal compartments in group 1 compared with group 2 ( p < .05). TIMP-2 levels were lower in groups 1 and 2 compared with group 3. Maternal TIMP-2 levels were higher ( p < 0.003), whereas fetal TIMP-1 ( p < .01) and MMP-9 to TIMP-1 ratios ( p < .05) were lower when delivery was delayed more than 2 weeks following betamethasone treatment.

Conclusion

We conclude that elevated MMP-2 activity in the maternal and fetoplacental compartments may suggest a mechanism, in part, for betamethasone-induced fetal lung maturation.
Feasibility Assessment of Cerebrospinal Fluid from HIV-1-Infected Children for HIV Proviral DNA and Monocyte Chemoattractant Protein 1 Alleles
Authors: Shiramizu Bruce , Lau Emily , Tamamoto Alyson , Uniatowski Justin , Troelstrup David
Published: August 2007

The objective of the study was to assess the feasibility of measuring human immunodeficiency virus 1 (HIV-1) proviral deoxyribonucleic acid (DNA) and associated single-nucleotide polymorphism (SNP) of monocyte chemoattractant protein 1 (MCP1) in pediatric cerebrospinal fluid (CSF). The importance of HIV DNA and MCP1 SNP has been suggested to be independently important in progression to acquired immune deficiency syndrome (AIDS) and neurocognitive impairment in adults. In children, measuring both factors in the CSF may help us understand the neuropathogenic process leading to HIV-1-associated encephalopathy (HAE). Repository specimens from 27 perinatally HIV-1-infected children with HAE were assessed for HIV DNA copy by real-time polymerase chain reaction and compared with MCP1 2578G SNP mutations measured by digesting amplified 361 bp fragments. When compared with MCP1 2578G SNP, a significant number with the mutation had high HIV DNA compared with those with wild type ( p < .01), with no levels detected in HIV-1-seronegative control specimens. There were six CSF specimens with enough supernatant to measure MCP1 levels by enzyme-linked immunosorbent assay, which showed high levels in those with the MCP1 2578G mutation. This study demonstrates, for the first time, that CSF HIV DNA and MCP1 SNP can be measured and could be potential tools in future clinical studies to understand the pathogenesis of pediatric HAE.
Abnormal Levels of Serum Antielastin Antibodies in Children with Diabetes Mellitus Type 1
Authors: Nicoloff George , Weiss Antony S. , Iotova Violeta , Tzaneva Valentina , Petrova Chayka , Domuschieva Nadja , Nikolov Asparuh , Tzvetanov Plamen , Christova Petkana
Published: August 2007

Antibodies to α-elastin (elastin breakdown product) and elastin sequences devoid of cross-linked regions (linear elastin) are found in the serum of all human subjects and correlate with their respective serum peptide levels. The aim of this study was to determine if the serum level of antielastin antibodies (AEAbs) differs between type 1 diabetic children and nondiabetic children. Enzyme-linked immunosorbent assay was used to measure the levels of immunoglobulin (Ig)G and IgM AEAbs in the sera of 45 diabetic children (mean age 12.8 ± 3.2 years, diabetes duration 5.3 ± 3.6 years). Twenty-two children presented with vascular complications (group 1), whereas 23 displayed no vascular complications (group 2). The controls were 18 healthy children (mean age 11.9 ± 2.3 years). Diabetic patients showed statistically significant higher levels of IgM α-AEAbs (0.82 ± 0.26 vs 0.61 ± 0.14, p = .0013) than the control group. In group 1, α-AEAbs showed statistically significant higher level than controls: IgG (0.86 ± 0.42 vs 0.59 ± 0.12; p = .0109) and IgM (0.88 ± 0.24 vs 0.61 ± 0.14; p = .0001). IgM antilinear elastin antibodies (ALEAbs) in group 1 were significantly lower than in controls (0.462 ± 0.191 vs 0.652 ± 0.127; p= .0009). IgG α-AEAbs showed correlation with microalbuminuria ( r = −.26; p = .05) and IgM ALEAbs correlated with microalbuminuria ( r = −.32; p = .035). IgG α-AEAbs correlated with neuropathy ( r = −.32; p = .035). Group 1 patients displayed a correlation between IgG ALEAbs and retinopathy ( r = −.48; p = .023) and IgM ALEAbs and microalbuminuria ( r = .52; p = .014). Levels of AEAbs and ALEAbs can serve as immunologic markers of the extent of elastin degradation. These markers may provide a tool to study elastin metabolism and a potential clinical role for AEAbs in the pathogenesis and development of vascular complications in diabetic children.