380 research outputs found
Measurement of serum total and free prostate-specific antigen in women with colorectal carcinoma
We investigated the diagnostic value and the relationship with clinicopathological features of total and free prostate-specific antigen by measuring the concentrations of these markers in the sera of 75 women with colorectal carcinoma and in 30 healthy women. Measurements were performed by immunoradiometric assay which utilizes monoclonal and polyclonal anti-prostate-specific antigen antibodies; the lowest detection level for both markers was 0.01βngβmlβ1. Free prostate-specific antigen levels were significantly higher in women with colorectal carcinoma than healthy women (P=0.006). The percentage of free prostate-specific antigen predominant (free prostate-specific antigen/total prostate-specific antigen >50%) subjects was 20% in colorectal carcinoma patients and 3.3% in healthy women (P=0.035). Cut-off values were 0.34βngβmlβ1 for total prostate-specific antigen and 0.01βngβmlβ1 for free prostate-specific antigen. In women with colorectal carcinoma, total prostate-specific antigen positivity was 20% and free prostate-specific antigen positivity was 34.6%. When compared to negatives, total prostate-specific antigen positive patients had a lower percentage of well-differentiated (P=0.056) and early stage (stages I and II) tumours (P=0.070). However, patients with predominant free prostate-specific antigen, had a higher percentage of well-differentiated (P=0.014) and early stage tumours (P=0.090) than patients with predominant bound prostate-specific antigen. In conclusion, although the sensitivity of free prostate-specific antigen predominancy is low (20%), in distinguishing women with colorectal carcinoma than healthy women, its specificity is high (96.7%). Free prostate-specific antigen predominancy tends to be present in less aggressive tumours. These findings may indicate clinical significance of preoperative measurement of serum total and free prostate-specific antigen in women with colorectal carcinoma
Extended Hemi-Hepatectomy with Portal Vein Reconstruction in a Patient with Situs Ambiguous
We report a case of far-advanced hepatocellular carcinoma (HCC) with situs ambiguous, complex visceral and vascular anomalies, who was successfully managed by extended hemi-hepatectomy. A 67-year-old man was referred to our hospital with a large liver mass. Abdominal ultrasonography, computed tomography and angiography revealed HCC with a diameter of 10 cm, with tumor thrombus in the main and first branch of the portal vein. Multiple complex anomalies in the abdomen were determined preoperatively. He had right-sided spleens-stomach-duodenum, liver at midline, inferior vena cava interruption with azygous continuation, and hepatic arterial anomaly. Extended left lobectomy of the liver with reconstruction of the portal vein was performed. Postoperatively, the patient recovered without major complications, and he was discharged on postoperative day 21. We report the first successful extended hepatectomy with portal vein reconstruction for HCC in a patient with rare situs anomalies
No association for Chinese HBV-related hepatocellular carcinoma susceptibility SNP in other East Asian populations.
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New susceptibility and resistance HLA-DP alleles to HBV-related diseases identified by a trans-ethnic association study in Asia
Previous studies have revealed the association between SNPs located on human leukocyte antigen (HLA) class II genes, including HLA-DP and HLA-DQ, and chronic hepatitis B virus (HBV) infection, mainly in Asian populations. HLA-DP alleles or haplotypes associated with chronic HBV infection or disease progression have not been fully identified in Asian populations. We performed trans-ethnic association analyses of HLA-DPA1, HLA-DPB1 alleles and haplotypes with hepatitis B virus infection and disease progression among Asian populations comprising Japanese, Korean, Hong Kong, and Thai subjects. To assess the association between HLA-DP and chronic HBV infection and disease progression, we conducted high-resolution (4-digit) HLA-DPA1 and HLA-DPB1 genotyping in a total of 3,167 samples, including HBV patients, HBV-resolved individuals and healthy controls. Trans-ethnic association analyses among Asian populations identified a new risk allele HLA-DPB1*09 ratio 01 (P = 1.36 x 10(-6); OR= 1.97; 95% CI, 1.50-2.59) and a new protective allele DPB1*02 ratio 01 (P = 5.22 x 10(-6); OR = 0.68; 95% CI, 0.58-0.81) to chronic HBV infection, in addition to the previously reported alleles. Moreover, DPB1*02 ratio 01 was also associated with a decreased risk of disease progression in chronic HBV patients among Asian populations (P = 1.55 x 10(-7); OR = 0.50; 95% CI, 0.39-0.65). Trans-ethnic association analyses identified Asian-specific associations of HLA-DP alleles and haplotypes with HBV infection or disease progression. The present findings will serve as a base for future functional studies of HLA-DP molecules in order to understand the pathogenesis of HBV infection and the development of hepatocellular carcinoma.published_or_final_versio
Thermal-elastic stresses and the criticality of the continental crust
Heating or cooling can lead to high stresses in rocks due to the different thermal-elastic properties of minerals. In the upper 4 km of the crust, such internal stresses might cause fracturing. Yet it is unclear if thermal elasticity contributes significantly to critical stresses and failure deeper in Earth's continental crust, where ductile creep causes stress relaxation. We combined a heating experiment conducted in a Synchrotron microtomograph (Advanced Photon Source, USA) with numerical simulations to calculate the grain-scale stress field in granite generated by slow burial. We find that deviatoric stresses >100 MPa can be stored during burial, with relaxation times from 100's to 1000's ka, even in the ductile crust. Hence, grain-scale thermal-elastic stresses may serve as nuclei for instabilities, thus rendering the continental crust close to criticality
Galactic Effects on Habitability
The galactic environment has been suspected to influence planetary
habitability in many ways. Very metal-poor regions of the Galaxy, or those
largely devoid of atoms more massive than H and He, are thought to be unable to
form habitable planets. Moreover, if such planets do form, the young system is
subjected to close stellar passages while it resides in its stellar birth
cluster. Various potential hazards remain after clusters disperse. For
instance, central galactic regions may present risks to habitability via nearby
supernovae, gamma ray bursts (GRBs), and frequent comet showers. In addition,
planets residing within very wide binary star systems are affected by the
Galaxy, as local gravitational perturbations from the Galaxy can increase the
binary's eccentricity until it destabilizes the planets it hosts. Here we
review the most recent work on the main galactic influences over planetary
habitability. Although there must be some metallicity limit below which rocky
planets cannot form, recent exoplanet surveys show that they form around stars
with a very large range of metallicities. Once formed, the probability of star
clusters destabilizing planetary systems only becomes high for rare, extremely
long-lived clusters. Regarding threats to habitability from supernovae, GRBs,
and comet showers, many recent studies suggest that their hazards are more
limited than originally thought. Finally, denser regions of the Galaxy enhance
the threat that very wide binary companions pose to planetary habitability, but
the probability that a very wide binary star disrupts habitability will always
be substantially below 100% for any environment. While some Milky Way regions
must be more hospitable to habitable planets than others, it is difficult to
state that habitable planets are confined to any well-defined region of the
Galaxy or that any other particular region of the Galaxy is uninhabitable.Comment: Invited review chapter, accepted for publication in the "Handbook of
Exoplanets"; 19 pages; 2 figure
Flow-Dependent Mass Transfer May Trigger Endothelial Signaling Cascades
It is well known that fluid mechanical forces directly impact endothelial signaling pathways. But while this general observation is clear, less apparent are the underlying mechanisms that initiate these critical signaling processes. This is because fluid mechanical forces can offer a direct mechanical input to possible mechanotransducers as well as alter critical mass transport characteristics (i.e., concentration gradients) of a host of chemical stimuli present in the blood stream. However, it has recently been accepted that mechanotransduction (direct mechanical force input), and not mass transfer, is the fundamental mechanism for many hemodynamic force-modulated endothelial signaling pathways and their downstream gene products. This conclusion has been largely based, indirectly, on accepted criteria that correlate signaling behavior and shear rate and shear stress, relative to changes in viscosity. However, in this work, we investigate the negative control for these criteria. Here we computationally and experimentally subject mass-transfer limited systems, independent of mechanotransduction, to the purported criteria. The results showed that the negative control (mass-transfer limited system) produced the same trends that have been used to identify mechanotransduction-dominant systems. Thus, the widely used viscosity-related shear stress and shear rate criteria are insufficient in determining mechanotransduction-dominant systems. Thus, research should continue to consider the importance of mass transfer in triggering signaling cascades
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