86 research outputs found
Evaluation of the porcine ameroid constrictor model of chronic myocardial ischemia for therapeutic angiogenesis studies
Structured information during the ICU stay to reduce anxiety: study protocol of a multicenter randomized controlled trial
Functional Implications of LH/hCG Receptors in Pregnancy-Induced Cushing Syndrome
Context: Elevated human choriogonadotropin (hCG) may stimulate aberrantly
expressed luteinizing hormone (LH)/hCG receptor (LHCGR) in adrenal glands,
resulting in pregnancy-induced bilateral macronodular adrenal hyperplasia and
transient Cushing syndrome (CS). Objective: To determine the role of LHCGR in
transient, pregnancy-induced CS. Design, Setting, Patient, and Intervention:
We investigated the functional implications of LHCGRs in a patient presenting,
at a tertiary referral center, with repeated pregnancy-induced CS with
bilateral adrenal hyperplasia, resolving after parturition. Main Outcome
Measures and Results: Acute testing for aberrant hormone receptors was
negative except for arginine vasopressin (AVP)–increased cortisol secretion.
Long-term hCG stimulation induced hypercortisolism, which was unsuppressed by
dexamethasone. Postadrenalectomy histopathology demonstrated steroidogenically
active adrenocortical hyperplasia and ectopic cortical cell clusters in the
medulla. Quantitative polymerase chain reaction showed upregulated expression
of LHCGR, transcription factors GATA4, ZFPM2, and proopiomelanocortin (POMC),
AVP receptors (AVPRs) AVPR1A and AVPR2, and downregulated melanocortin 2
receptor (MC2R) vs control adrenals. LHCGR was localized in subcapsular, zona
glomerulosa, and hyperplastic cells. Single adrenocorticotropic
hormone–positive medullary cells were demonstrated in the zona reticularis.
The role of adrenal adrenocorticotropic hormone was considered negligible due
to downregulated MC2R. Coexpression of CYP11B1/CYP11B2 and AVPR1A/AVPR2 was
observed in ectopic cortical cells in the medulla. hCG stimulation of the
patient’s adrenal cell cultures significantly increased cyclic adenosine
monophosphate, corticosterone, 11-deoxycortisol, cortisol, and androstenedione
production. CTNNB1, PRKAR1A, ARMC5, and PRKACA gene mutational analyses were
negative. Conclusion: Nongenetic, transient, somatic mutation-independent,
pregnancy-induced CS was due to hCG-stimulated transformation of LHCGR-
positive undifferentiated subcapsular cells (presumably adrenocortical
progenitors) into LHCGR-positive hyperplastic cortical cells. These cells
respond to hCG stimulation with cortisol secretion. Without the ligand, they
persist with aberrant LHCGR expression and the ability to respond to the same
stimulus
Testing gravitational-wave searches with numerical relativity waveforms: Results from the first Numerical INJection Analysis (NINJA) project
The Numerical INJection Analysis (NINJA) project is a collaborative effort
between members of the numerical relativity and gravitational-wave data
analysis communities. The purpose of NINJA is to study the sensitivity of
existing gravitational-wave search algorithms using numerically generated
waveforms and to foster closer collaboration between the numerical relativity
and data analysis communities. We describe the results of the first NINJA
analysis which focused on gravitational waveforms from binary black hole
coalescence. Ten numerical relativity groups contributed numerical data which
were used to generate a set of gravitational-wave signals. These signals were
injected into a simulated data set, designed to mimic the response of the
Initial LIGO and Virgo gravitational-wave detectors. Nine groups analysed this
data using search and parameter-estimation pipelines. Matched filter
algorithms, un-modelled-burst searches and Bayesian parameter-estimation and
model-selection algorithms were applied to the data. We report the efficiency
of these search methods in detecting the numerical waveforms and measuring
their parameters. We describe preliminary comparisons between the different
search methods and suggest improvements for future NINJA analyses.Comment: 56 pages, 25 figures; various clarifications; accepted to CQ
Hydrothermal dolomitization of basinal deposits controlled by a synsedimentary fault system in Triassic extensional setting, Hungary
Dolomitization of relatively thick carbonate successions occurs via an effective fluid circulation mechanism, since the replacement process requires a large amount of Mg-rich fluid interacting with the CaCO3 precursor. In the western end of the Neotethys, fault-controlled extensional basins developed during the Late Triassic spreading stage. In the Buda Hills and Danube-East blocks, distinct parts of silica and organic matter-rich slope and basinal deposits are dolomitized. Petrographic, geochemical, and fluid inclusion data distinguished two dolomite types: (1) finely to medium crystalline and (2) medium to coarsely crystalline. They commonly co-occur and show a gradual transition. Both exhibit breccia fabric under microscope. Dolomite texture reveals that the breccia fabric is not inherited from the precursor carbonates but was formed during the dolomitization process and under the influence of repeated seismic shocks. Dolomitization within the slope and basinal succession as well as within the breccia zones of the underlying basement block is interpreted as being related to fluid originated from the detachment zone and channelled along synsedimentary normal faults. The proposed conceptual model of dolomitization suggests that pervasive dolomitization occurred not only within and near the fault zones. Permeable beds have channelled the fluid towards the basin centre where the fluid was capable of partial dolomitization. The fluid inclusion data, compared with vitrinite reflectance and maturation data of organic matter, suggest that the ascending fluid was likely hydrothermal which cooled down via mixing with marine-derived pore fluid. Thermal gradient is considered as a potential driving force for fluid flow
Pleiotropy among common genetic loci identified for cardiometabolic disorders and C-reactive protein.
Pleiotropic genetic variants have independent effects on different phenotypes. C-reactive protein (CRP) is associated with several cardiometabolic phenotypes. Shared genetic backgrounds may partially underlie these associations. We conducted a genome-wide analysis to identify the shared genetic background of inflammation and cardiometabolic phenotypes using published genome-wide association studies (GWAS). We also evaluated whether the pleiotropic effects of such loci were biological or mediated in nature. First, we examined whether 283 common variants identified for 10 cardiometabolic phenotypes in GWAS are associated with CRP level. Second, we tested whether 18 variants identified for serum CRP are associated with 10 cardiometabolic phenotypes. We used a Bonferroni corrected p-value of 1.1×10-04 (0.05/463) as a threshold of significance. We evaluated the independent pleiotropic effect on both phenotypes using individual level data from the Women Genome Health Study. Evaluating the genetic overlap between inflammation and cardiometabolic phenotypes, we found 13 pleiotropic regions. Additional analyses showed that 6 regions (APOC1, HNF1A, IL6R, PPP1R3B, HNF4A and IL1F10) appeared to have a pleiotropic effect on CRP independent of the effects on the cardiometabolic phenotypes. These included loci where individuals carrying the risk allele for CRP encounter higher lipid levels and risk of type 2 diabetes. In addition, 5 regions (GCKR, PABPC4, BCL7B, FTO and TMEM18) had an effect on CRP largely mediated through the cardiometabolic phenotypes. In conclusion, our results show genetic pleiotropy among inflammation and cardiometabolic phenotypes. In addition to reverse causation, our data suggests that pleiotropic genetic variants partially underlie the association between CRP and cardiometabolic phenotypes
Spontaneous breathing during general anesthesia prevents the ventral redistribution of ventilation as detected by electrical impedance tomography: a randomized trial.
Effect of Trigger Sensitivity on Redistribution of Ventilation During Pressure Support Ventilation Detected by Electrical Impedance Tomography.
In supine position, pressure support ventilation causes a redistribution of ventilation towards the ventral regions of the lung. Theoretically, a less sensitive support trigger would cause the patient to breathe more actively, potentially attenuating the
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Effect of Trigger Sensitivity on Redistribution of Ventilation During Pressure Support Ventilation Detected by Electrical Impedance Tomography.
In supine position, pressure support ventilation causes a redistribution of ventilation towards the ventral regions of the lung. Theoretically, a less sensitive support trigger would cause the patient to breathe more actively, potentially attenuating the
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