10 research outputs found
Translating Re (heat) in Traditional Chinese Medicine: A Comparative Study on Two English Translations of Huangdi Neijing Suwen (Yellow Emperor's Medical Classic - Basic Questions)
Discovery of a Potential Plasma Protein Biomarker Panel for Acute-on-Chronic Liver Failure Induced by Hepatitis B Virus
Hepatitis B virus (HBV)-associated acute-on-chronic liver failure (HBV-ACLF), characterized by an acute deterioration of liver function in the patients with chronic hepatitis B (CHB), is lack of predicting biomarkers for prognosis. Plasma is an ideal sample for biomarker discovery due to inexpensive and minimally invasive sampling and good reproducibility. In this study, immuno-depletion of high-abundance plasma proteins followed by iTRAQ-based quantitative proteomic approach was employed to analyze plasma samples from 20 healthy control people, 20 CHB patients and 20 HBV-ACLF patients, respectively. As a result, a total of 427 proteins were identified from these samples, and 42 proteins were differentially expressed in HBV-ACLF patients as compared to both CHB patients and healthy controls. According to bioinformatics analysis results, 6 proteins related to immune response (MMR), inflammatory response (OPN, HPX), blood coagulation (ATIII) and lipid metabolism (APO-CII, GP73) were selected as biomarker candidates. Further ELISA analysis confirmed the significant up-regulation of GP73, MMR, OPN and down-regulation of ATIII, HPX, APO-CII in HBV-ACLF plasma samples (p < 0.01). Moreover, receiver operating characteristic (ROC) curve analysis revealed high diagnostic value of these candidates in assessing HBV-ACLF. In conclusion, present quantitative proteomic study identified 6 novel HBV-ACLF biomarker candidates and might provide fundamental information for development of HBV-ACLF biomarker
Design and simulation of illuminator with micro scanning slit array for NA 0.75 lithography system
An illuminator with a micro scanning slit array for NA 0.75 lithography system has been proposed in this paper. In this illuminator, the beam is shaped by a diffractive optical element (DOE), a zoom and axicon lenses. The beam is homogenized by a micro intergrator rod array. The micro scanning slit array is used to substitute for the traditional internal rema. A micro lens array and a condenser image the micro scanning slit array onto the mask. This illuminator needs no illumination lens group and reduces the effect of the vibration introduced by the internal rema. The illuminator is designed and simulated. The result shows that the illuminating field on the mask has good uniformity and trapezoidal distribution along the scanning direction. The feasibility of the illuminator is verified
Preparation and characterisation of exfoliated muscovite/poly(2,3‐dimethylaniline) nanocomposites with an enhanced anticorrosive performance
Quantitative Proteomic Study Reveals Up-Regulation of cAMP Signaling Pathway-Related Proteins in Mild Traumatic Brain Injury
Traumatic brain injury (TBI), as
a neurological injury, becomes
a leading cause of disability and mortality due to lacking effective
therapy. About 75% of TBI is mild traumatic brain injury (mTBI). However,
the complex molecular mechanisms underlying mTBI pathophysiology remains
to be elucidated. In this study, iTRAQ-based quantitative proteomic
approach was employed to measure temporal-global proteome changes
of rat brain tissues from different time points (1 day, 7 day and
6 months) post single mTBI (smTBI) and repetitive mTBI (rmTBI). A
total of 5169 proteins were identified, of which, 237 proteins were
significantly changed between control rats and mTBI model rats. Fuzzy
c-means (FCM) clustering analysis classified these 237 proteins into
six clusters according to their temporal pattern of protein abundance.
Functional bioinformatics analysis and protein–protein interaction
(PPI) network mapping of these FCM clusters showed that phosphodiesterase
10A (Pde10a) and guanine nucleotide-binding protein G (olf) subunit
alpha (Gnal) were the node proteins in the cAMP signaling pathway.
Other biological processes, such as cell adhesion, autophagy, myelination,
microtubule depolymerization and brain development, were also over-represented
in FCM clusters. Further Western Blot experiments confirmed that Pde10a
and Gnal were acutely up-regulated in severity-dependent manner by
mTBI, but these two proteins could not be down-regulated to basal
level at the time point of 6 months post repetitive mTBI. Our study
demonstrated that different severity of mTBI cause significant temporal
profiling change at the proteomic level and pointed out the cAMP signaling
pathway-related proteins, Pde10a and Gnal, may play important roles
in the pathogenesis and recovery of mTBI
Quantitative Proteomic Study Reveals Up-Regulation of cAMP Signaling Pathway-Related Proteins in Mild Traumatic Brain Injury
Traumatic brain injury (TBI), as
a neurological injury, becomes
a leading cause of disability and mortality due to lacking effective
therapy. About 75% of TBI is mild traumatic brain injury (mTBI). However,
the complex molecular mechanisms underlying mTBI pathophysiology remains
to be elucidated. In this study, iTRAQ-based quantitative proteomic
approach was employed to measure temporal-global proteome changes
of rat brain tissues from different time points (1 day, 7 day and
6 months) post single mTBI (smTBI) and repetitive mTBI (rmTBI). A
total of 5169 proteins were identified, of which, 237 proteins were
significantly changed between control rats and mTBI model rats. Fuzzy
c-means (FCM) clustering analysis classified these 237 proteins into
six clusters according to their temporal pattern of protein abundance.
Functional bioinformatics analysis and protein–protein interaction
(PPI) network mapping of these FCM clusters showed that phosphodiesterase
10A (Pde10a) and guanine nucleotide-binding protein G (olf) subunit
alpha (Gnal) were the node proteins in the cAMP signaling pathway.
Other biological processes, such as cell adhesion, autophagy, myelination,
microtubule depolymerization and brain development, were also over-represented
in FCM clusters. Further Western Blot experiments confirmed that Pde10a
and Gnal were acutely up-regulated in severity-dependent manner by
mTBI, but these two proteins could not be down-regulated to basal
level at the time point of 6 months post repetitive mTBI. Our study
demonstrated that different severity of mTBI cause significant temporal
profiling change at the proteomic level and pointed out the cAMP signaling
pathway-related proteins, Pde10a and Gnal, may play important roles
in the pathogenesis and recovery of mTBI