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Jun Liao

Publications and source records attributed to Jun Liao.

At least 19 recordsLinked to original sources
PubMed2007

The relation between collagen fibril kinematics and mechanical properties in the mitral valve anterior leaflet.

We have recently demonstrated that the mitral valve anterior leaflet (MVAL) exhibited minimal hysteresis, no strain rate sensitivity, stress relaxation but not creep (Grashow et al., 2006, Ann Biomed Eng., 34(2), pp. 315-325; Grashow et al., 2006, Ann Biomed. Eng., 34(10), pp. 1509-1518). However, the underlying structural basis for this unique quasi-elastic mechanical behavior is presently unknown. As collagen is the major structural component of the MVAL, we investigated the relation between collagen fibril kinematics (rotation and stretch) and tissue-level mechanical properties in the MVAL under biaxial loading using small angle X-ray scattering. A novel device was developed and utilized to perform simultaneous measurements of tissue level forces and strain under a planar biaxial loading state. Collagen fibril D-period strain (epsilonD) and the fibrillar angular distribution were measured under equibiaxial tension, creep, and stress relaxation to a peak tension of 90 N/m. Results indicated that, under equibiaxial tension, collagen fibril straining did not initiate until the end of the nonlinear region of the tissue-level stress-strain curve. At higher tissue tension levels, epsilonD increased linearly with increasing tension. Changes in the angular distribution of the collagen fibrils mainly occurred in the tissue toe region. Using epsilonD, the tangent modulus of collagen fibrils was estimated to be 95.5+/-25.5 MPa, which was approximately 27 times higher than the tissue tensile tangent modulus of 3.58+/-1.83 MPa. In creep tests performed at 90 N/m equibiaxial tension for 60 min, both tissue strain and epsilonD remained constant with no observable changes over the test length. In contrast, in stress relaxation tests performed for 90 min epsilonD was found to rapidly decrease in the first 10 min followed by a slower decay rate for the remainder of the test. Using a single exponential model, the time constant for the reduction in collagen fibril strain was 8.3 min, which was smaller than the tissue-level stress relaxation time constants of 22.0 and 16.9 min in the circumferential and radial directions, respectively. Moreover, there was no change in the fibril angular distribution under both creep and stress relaxation over the test period. Our results suggest that (1) the MVAL collagen fibrils do not exhibit intrinsic viscoelastic behavior, (2) tissue relaxation results from the removal of stress from the fibrils, possibly by a slipping mechanism modulated by noncollagenous components (e.g. proteoglycans), and (3) the lack of creep but the occurrence of stress relaxation suggests a "load-locking" behavior under maintained loading conditions. These unique mechanical characteristics are likely necessary for normal valvular function.

Animals↗
PubMed2006

Planar biaxial creep and stress relaxation of the mitral valve anterior leaflet.

A fundamental assumption in mitral valve (MV) therapies is that a repaired or replaced valve should mimic the functionality of the native valve as closely as possible. Thus, improvements in valvular treatments are dependent on the establishment of a complete understanding of the function and mechanical properties of the native normal MV. In a recent study [Grashow et al. ABME 34(2), 2006] we demonstrated that the planar biaxial stress-strain relationship of the MV anterior leaflet (MVAL) exhibited minimal hysteresis and a stress-strain response independent of strain rate, suggesting that MVAL could be modeled as a "quasi-elastic" material. The objective of our current study was to expand these results to provide a more complete picture of the time-dependent mechanical properties of the MVAL. To accomplish this, biaxial stress-relaxation and creep studies were performed on porcine MVAL specimens. Our primary finding was that while the MVAL leaflet exhibited significant stress relaxation, it exhibited negligible creep over the 3-h test. These results furthered our assertion that the MVAL functionally behaves not as a linear or non-linear viscoelastic material, but as an anisotropic quasi-elastic material. These results appear to be unique in the soft tissue literature; suggesting that valvular tissues are unequalled in their ability to withstand significant loading without time-dependent material effects. Moreover, insight into these specialized characteristics can help guide and inform efforts directed toward surgical repair and engineered valvular tissue replacements.

Animals↗
PubMed2006

Dissection of Tbx1 and Fgf interactions in mouse models of 22q11DS suggests functional redundancy.

The 22q11 deletion syndrome (22q11DS) is characterized by abnormal development of the pharyngeal apparatus. Mouse genetic studies have identified Tbx1 as a key gene in the etiology of the syndrome, in part, via interaction with the fibroblast growth factor (Fgf) genes. Three murine Fgfs, Fgf3, Fgf8 and Fgf10 are coexpressed in different combinations with Tbx1. They are all strongly downregulated in Tbx1-/- embryos, implicating epistatic interactions. Supporting this, Tbx1 and Fgf8 have been shown to genetically interact in the development of the fourth pharyngeal arch artery (PAA) and Fgf10 was identified to be a direct downstream target of Tbx1. To dissect the epistatic relationships of these genes during embryonic development and the molecular pathogenesis of the Tbx1 mutant phenotype, we generated Fgf10+/-;Tbx1+/- and Fgf3-/-;Tbx1+/- mice. Despite strong hypotheses that Fgf10 is the key gene downstream of Tbx1 in the development of the anterior heart field, we do not find evidence for genetic interaction between Tbx1 and Fgf10. Also, the Fgf3-/-;Tbx1+/- mutant mice do not show an additive phenotype. Furthermore, more severe defects do not occur in Fgf8+/-;Tbx1+/- mutants by crossing in the Fgf3 null allele. There is a possible additive effect only in PAA remodeling in the Fgf10+/-;Tbx1+/-;Fgf8+/- embryos. Our findings underscore the importance of potential functional redundancy with additional Fgfs in the development of the pharyngeal apparatus and cardiovascular system via Tbx1. This redundancy should be considered when looking at individual FGF genes as modifiers of 22q11DS.

Animals↗
PubMed2006

Skewness angle of interfibrillar proteoglycans increases with applied load on mitral valve chordae tendineae.

In highly aligned connective tissues, such as tendon, collagen fibrils are linked together by proteoglycans (PGs). Recent mechanical and theoretical studies on tendon micromechanics have implied that PGs mediate mechanical interactions between adjacent collagen fibrils. We used transmission electron microscopy to observe the collagen fibril-PG interactions in porcine mitral valve chordae under variable loading conditions and found that PGs attached to collagen fibrils perpendicularly in the load-free situation, and became skewed when the chordae were loaded. The average skewness angle of PGs increased with the applied load, and hence the strain in the chordae. The observation of PG skewing with the application of load demonstrates that, in mitral valve chordae, interfibrillar slippage occurs and that PGs play a role in fibril-to-fibril interaction and likely transfer force. The results of this study provide new insights into the mechanical role of PGs and support some recent theoretical models.

Animals↗
PubMed2006

Inactivation of Tbx1 in the pharyngeal endoderm results in 22q11DS malformations.

The 22q11 deletion (22q11DS; velo-cardio-facial syndrome/DiGeorge syndrome) is characterized by defects in the derivatives of the pharyngeal apparatus. Mouse genetic studies have identified Tbx1, a member of the T-box family of transcription factors, as being responsible for the physical malformations of the syndrome. Mice heterozygous for a null mutation in Tbx1 have mild anomalies, whereas homozygous Tbx1 mutants die at birth with severe defects in the derivatives of the pharyngeal apparatus, including cleft palate, thymus gland aplasia and cardiac outflow tract malformations. Tbx1 is expressed in the splanchnic mesenchyme, the pharyngeal endoderm (PE) and in the core mesoderm of the pharyngeal apparatus. Tissue interactions between the epithelia and mesenchyme of the arches are required for development of the pharyngeal apparatus; the precise role of Tbx1 in each tissue is not known. To assess the role of Tbx1 in the PE, a conditional allele of Tbx1 was generated using the Cre/loxP system. Foxg1-Cre was used to drive PE-specific ablation of Tbx1. Conditional null mutants survived embryogenesis, but died in the neonatal period with malformations identical to the defects observed in Tbx1 homozygous null mutants. The abnormalities appear to be secondary to failed outgrowth of the pharyngeal pouches. These results show that Tbx1 in the PE is required for the patterning and development of the pharyngeal apparatus, thereby disrupting the formation of its derivative structures.

Animals↗
PubMed2006

Tbx1 affects asymmetric cardiac morphogenesis by regulating Pitx2 in the secondary heart field.

Individuals with 22q11 deletion syndrome (22q11DS; DiGeorge/velo-cardio-facial syndrome) have multiple congenital malformations, including cardiovascular defects. Most individuals with this syndrome possess 1.5-3.0 Mb hemizygous 22q11.2 deletions. The T-box transcription factor TBX1, lies within the nested 1.5 Mb interval and is a strong candidate for its etiology. Inactivation of Tbx1 in the mouse results in neonatal lethality owing to the presence of a single cardiac outflow tract. One important goal is to understand the molecular pathogenesis of cardiovascular defects in this syndrome. However, the molecular pathways of Tbx1 are still largely unexplored. Here, we show that Tbx1 is co-expressed with the bicoid-like homeodomain transcription factor Pitx2 in secondary heart field cells in the pharyngeal mesenchyme. In situ hybridization studies in Tbx1(-/-) mouse embryos revealed downregulation of Pitx2 in these cells. To test for a possible genetic interaction, we intercrossed Tbx1(+/-) and Pitx2(+/-) mice. Tbx1(+/-); Pitx2(+/-) mice died perinatally with cardiac defects, including double outlet right ventricle, and atrial and ventricular septal defects, all occurring with variable penetrance. An enhancer located between exons 4 and 5 in which a putative T-half site was identified near an Nkx2.5-binding site regulates asymmetric expression of Pitx2. We show using in vitro studies that Tbx1 binds to this site and activates the Pitx2 enhancer with the synergistic action of Nkx2.5. The results presented in this study unravel a novel Tbx1-Pitx2 pathway linking Tbx1 to asymmetric cardiac morphogenesis.

Animals↗
PubMed2005

Molecular orientation of collagen in intact planar connective tissues under biaxial stretch.

Understanding of the mechanical behavior of collagenous tissues at different size scales is necessary to understand their physiological function as well as to guide their use as heterograft biomaterials. We conducted a first investigation of the kinematics of collagen at the molecular and fiber levels under biaxial stretch in an intact planar collagenous tissue. A synchrotron small angle X-ray scattering (SAXS) technique combined with a custom biaxial stretching apparatus was used. Collagen fiber behavior under biaxial stretch was then studied with the same specimens using small angle light scattering (SALS) under identical biaxial stretch states. Both native and glutaraldehyde modified bovine pericardium were investigated to explore the effects of chemical modification to collagen. Results indicated that collagen fiber and molecular orientation did not change under equibiaxial strain, but were observed to profoundly change under uniaxial stretch. Interestingly, collagen molecular strain initiated only after approximately 15% global tissue strain, potentially due to fiber-level reorganization occurring prior to collagen molecule loading. Glutaraldehyde treatment also did not affect collagen molecular strain behavior, indicating that chemical fixation does not alter intrinsic collagen molecular stiffness. No detectable changes in the angular distribution and D-period strain were found after 80 min of stress relaxation. It can be speculated that other mechanisms may be responsible for the reduction in stress with time under biaxial stretch. The results of this first study suggest that collagen fiber/molecular kinematics under biaxial stretch are more complex than under uniaxial deformation, and warrant future studies.

Animals↗
PubMed2004

Full spectrum of malformations in velo-cardio-facial syndrome/DiGeorge syndrome mouse models by altering Tbx1 dosage.

Velo-cardio-facial syndrome/DiGeorge syndrome (VCFS/DGS) is associated with de novo hemizygous 22q11.2 deletions and is characterized by malformations attributed to abnormal development of the pharyngeal arches and pouches. The main physical findings include aortic arch and outflow tract heart defects, thymus gland hypoplasia or aplasia and craniofacial anomalies. The disorder varies greatly in expressivity; while some patients are mildly affected with learning disabilities and subtle craniofacial malformations, others die soon after birth with major cardiovascular defects and thymus gland aplasia. In addition to the main clinical features, many other findings are associated with the disorder such as chronic otitis media and hypocalcemia. Tbx1, a gene encoding a T-box transcription factor, which is hemizygously deleted on chromosome 22q11.2, was found to be a strong candidate for the equivalent of human VCFS/DGS in mice. Mice hemizygous for a null allele of Tbx1 had mild malformations, while homozygotes had severe malformations in the affected structures; neither precisely modeling the syndrome. Interestingly, bacterial artificial chromosome (BAC) transgenic mice overexpressing human TBX1 and three other transgenes, had similar malformations as VCFS/DGS patients. By employing genetic complementation studies, we demonstrate that altered TBX1 dosage and not overexpression of the other transgenes is responsible for most of the defects in the BAC transgenic mice. Furthermore, the full spectrum of VCFS/DGS malformations was elicited in a Tbx1 dose dependent manner, thus providing a molecular basis for the pathogenesis and varied expressivity of the syndrome.

Animals↗
PubMed2004

Suppression of neural fate and control of inner ear morphogenesis by Tbx1.

Inner ear sensory organs and VIIIth cranial ganglion neurons of the auditory/vestibular pathway derive from an ectodermal placode that invaginates to form an otocyst. We show that in the mouse otocyst epithelium, Tbx1 suppresses neurogenin 1-mediated neural fate determination and is required for induction or proper patterning of gene expression related to sensory organ morphogenesis (Otx1 and Bmp4, respectively). Tbx1 loss-of-function causes dysregulation of neural competence in otocyst regions linked to the formation of either mechanosensory or structural sensory organ epithelia. Subsequently, VIIIth ganglion rudiment form is duplicated posteriorly, while the inner ear is hypoplastic and shows neither a vestibular apparatus nor a coiled cochlear duct. We propose that Tbx1 acts in the manner of a selector gene to control neural and sensory organ fate specification in the otocyst.

Animals↗
PubMed2004

Removal of fulvic acid from water electrochemically using active carbon fiber electrode.

Humic acids (HA) are a group of widely existing natural organic compounds and potential contaminants to underground water reservoirs. Fulvic acid (FA) is a typical humic acid of relatively low molecular weight. Electrochemical removal of FA from water by active carbon fiber (ACF) electrodes was studied by using light scattering photometer (LSP), fluorescence spectroscopy and total organic carbon analyzer (TOC). The experiments showed that FA molecules aggregated and that the average particle diameter in FA solution increased from below 10 nm to hundreds of nanometers during the treatment process. When iron was added to the anode, the FA could be coagulated efficiently at the early stage of the treatment. The proposed mechanism of the removal process is: adsorption of FA on ACF surface --> aggregation of FA --> desorption of FA aggregates from ACF --> coagulation of FA aggregates by nFe(OH)(2).mFe(OH)(3) dissolved from anode. Experiments were also repeated using graphite and stainless-steel electrodes, and the results were compared with that of ACF electrodes. FA aggregation was not observed in these experiments and most FA was not removed from the solution. At the end of this paper, FA samples from Huai River sediment were successfully treated using the ACF electrode.

Adsorption↗
PubMed2004

Relationship between collagen fibrils, glycosaminoglycans, and stress relaxation in mitral valve chordae tendineae.

The tensile properties of mitral valve chordae tendineae derive from their structural make-up. The objectives of this study were to compare the stress relaxation properties of different types of chordae and relate their variation to structural features. Fifty chordae from eight hearts were subjected to stress relaxation tests. The percent stress relaxation and the relaxation rates were found to increase in the order of marginal. basal, and strut chordae. The water content of the three types of chordae was the same (marginal 77.1+/-5.9%, basal 77.0+/-3.4%, strut 78.0+/-2.3% wet weight). The collagen, elastin, and glycosaminoglycan (GAG) content in chordae were quantified using hydroxyproline assay, fastin elastin assay, and fluorophore-assisted carbohydrate electrophoresis, respectively. Collagen content of marginal chordae was only slightly less than that of basal and strut chordae (marginal 56.6+/-8.2%, basal 61.4+/-5.6%, strut 63.8+/-3.9% dry weight). There was also no significant difference in elastin content between the chordae (marginal 5.3+/-3.2%, basal 5.4+/-2.7%, strut 4.6+/-1.7% dry weight). However, the concentrations of unsulfated chondroitin/dermatan sulfate, 6-sulfated chondroitin sulfate, and 4-sulfate chondroitin sulfate significantly decreased in the order of marginal, basal, and strut. The total GAG-content also decreased in the order of marginal, basal, and strut (p = 0.06). The greater amount of GAGs in marginal versus strut chordae is consistent with our previous observations that marginal chordae have a greater collagen fibril density and thus more GAG-mediated, fibril-to-fibril linkages. The greater number of proteoglycan linkages may prevent the slippage of fibrils with respect to each other, and thus reduce stress relaxation. The different viscoelastic properties of mitral valve chordae can thus be explained morphologically.

Chordae Tendineae↗
PubMed2003

Highly efficient direct third-harmonic generation based on control of the electro-optic effect in quasi-periodic optical superlattices.

We present a method for controlling the efficiency of direct third-harmonic generation in quasi-periodic optical superlattices by means of the electro-optic effect. The calculated results manifest that this method is extremely efficient for achieving high efficiency of direct third-harmonic generation in predesigned quasi-phase-matched coupled parametric processes and is feasible at any given fundamental intensity. In addition, we demonstrate that the electro-optic control approach is significantly better than the temperature-control method.

Journal Article↗
PubMed2003

A structural basis for the size-related mechanical properties of mitral valve chordae tendineae.

It has been reported previously that the mechanical properties of mitral valve chordae tendineae vary with chordal size and type. The popularity of mitral valve repair and chordal transposition warrant a better understanding of this phenomenon. The objectives of this study were to characterize the size- and type-related variations in chordal mechanics and explain them from the ultra-structural viewpoint. A total of 52 porcine mitral valve chordae from eight hearts were mechanically tested. We found that thicker chordae were more extensible than thinner chordae (4.2+/-1.5%, 8.1+/-2.5%, 15.7+/-3.9% and 18.4+/-2.8% strain corresponding to chordae with cross-sectional areas of 0.1-0.5, 0.5-1.0, 1.0-2.0, and 2.0-3.0mm(2), respectively), and had lower moduli (90.1+/-22.3, 83.7+/-18.5, 66.3+/-13.5 and 61.7+/-13.3 MPa corresponding to the same chordae groups). Polarized light microscopy was used to measure collagen fibril crimp. Thicker chordae had smaller crimp period than thinner chordae (11.3+/-1.4 microm vs. 14.8+/-3.0 microm), and were thus more highly crimped. Thicker chordae could therefore extend to greater strain before lock-up. Transmission electron microscopy (TEM) was used to measure choral fibril ultra-structure. Thinner chordae had lower average fibril diameter than thicker chordae but greater average fibril density. The cross-sectional area occupied by fibrils, however, was found to be constant at 49+/-2% regardless of chordal size or type. The difference in moduli between thick and thin chordae can therefore be explained by differences in fibril packaging and hence fibril-to-fibril interactions. According to a simple fibril interaction model, chordae with smaller diameter fibrils will have a greater number of fibril-to-fibril interactions, and hence a greater modulus.

Anatomy, Cross-Sectional↗
PubMed2002

The role of neural crest during cardiac development in a mouse model of DiGeorge syndrome.

The velo-cardio-facial syndrome (VCFS)/DiGeorge syndrome (DGS) is a genetic disorder characterized by phenotypic abnormalities of the derivatives of the pharyngeal arches, including cardiac outflow tract defects. Neural crest cells play a major role in the development of the pharyngeal arches, and defects in these cells are likely responsible for the syndrome. Most patients are hemizygous for a 1.5- to 3.0-Mb region of 22q11, that is suspected to be critical for normal pharyngeal arch development. Mice hemizygous for a 1.5-Mb homologous region of chromosome 16 (Lgdel/+) exhibit conotruncal cardiac defects similar to those seen in affected VCFS/DGS patients. To investigate the role of Lgdel genes in neural crest development, we fate mapped neural crest cells in Lgdel/+ mice and we performed hemizygous neural crest-specific inactivation of Lgdel. Hemizygosity of the Lgdel region does not eliminate cardiac neural crest migration to the forming aortic arches. However, neural crest cells do not differentiate appropriately into smooth muscle in both fourth and sixth aortic arches and the affected aortic arch segments develop abnormally. Tissue-specific hemizygous inactivation of Lgdel genes in neural crest results in normal cardiovascular development. Based on our studies, we propose that Lgdel genes are required for the expression of soluble signals that regulate neural crest cell differentiation.

Animals↗
PubMed2002

Crystal structure studies on rubrerythrin: enzymatic activity in relation to the zinc movement.

Rubrerythrin (Rr) is a non-heme iron protein isolated from anaerobic sulfate-reducing bacteria. Rr is a dimeric molecule, each monomer contains a Fe(SCys)(4) center in the C-terminal domain and a binuclear metal center in the N-terminal domain. Rr structures with different protein sources and/or preparation procedures have been studied. Two Rr crystal structures have been solved with significant differences in their binuclear metal centers. The first structure, which was obtained from expressed protein under aerobic conditions, has a diiron-oxo center. The second structure, which was obtained from native protein of Desulfovibrio vulgaris under aerobic conditions, has an Fe-Zn center with the zinc position differing from the corresponding iron position in the former structure by approximately 2 A. The crystal structures of Rr isolated from D. vulgaris (Hildenborough, NCIB 8303), the same as the second structured but prepared under anaerobic conditions, are reported in this paper. The binuclear metal center in these structures is an Fe-Zn center. When the crystal was exposed to air, the zinc atom moved gradually, approximately 2 A, accompanied by the entrance of a water molecule (or hydroxyl group) and changes in the binuclear metal center microenvironment. This finding can explain the differences between the two different structures. The results suggest that the zinc movement may be related to the enzymatic activity of Rr.

Bacterial Proteins↗
PubMed2002

Crystallization and preliminary crystallographic analysis of manganese superoxide dismutase from Bacillus halodenitrificans.

Manganese superoxide dismutase (GP-MnSOD), a component of the so-called 'green protein' (green protein complex) from the facultative anaerobic halodenitrifier Bacillus halodenitrificans, has been crystallized using the hanging-drop vapor diffusion method. Crystals have unit-cell parameters a=b=93.4 A, c=65.0 A, and belong to the space group P4(3)2(1)2. Preliminary analysis indicates there is one monomer in each asymmetric unit. The structural information from this enzyme will enrich our knowledge on its high catalytic activity and its possible role in green protein complex.

Bacillus↗
PubMed2002

[Relation between insulin-like growth factor-1 and insulin resistance in patients with acute stroke].

OBJECTIVE: To study the changes of plasma insulin-like growth factor -1 (IGF-1) and IGF binding protein 3 (IGFBP3) in patients with acute cerebral infarct (ACI) and acute cerebral hemorrhage (ACH) and the correlation of IGF-1 and IGFBP3 with plasma fasting insulin (FINS) related to insulin resistance (IR) and with insulin sensitive index (ISI). METHODS: The plasma IGF-1, IGFBP3 and FINS of 34 patients with ACI and 40 patients with ACH (within 2 days after onset) were measured by radioimmunoassay. Meanwhile, the fasting blood glucose (GS) of these patients was measured. 30 patients with ACH during convalescence (3 approximately 6 months after stroke) and 30 age-matched healthy individuals served as control groups. RESULTS: (1) The plasma IGF-1 and IGFBP3 and ISI were 17.3 +/- 7.0 mmol/L, 72.9 +/- 11.4 mmol/L and -4.2 +/- 0.3 respectively in the ACI group, 14.4 +/- 5.8 mmol/L, 57.8 +/- 17.2 mmol/L and -4.7 +/- 0.6 in the ACH group; 28.8 +/- 13.6 mmol/L, 87.4 +/- 18.3 mmol/L and -3.9 +/- 0.4 in the convalescence group; and 31.5 +/- 18.9 mmol/L, 93.1 +/- 28.0 mmol/L and -3.6 +/- 0.3 in the healthy control group. The values in the former two groups were significantly lower than those in the two control groups (F = 18.3, 20.2 and 17.2 respectively, P < 0.01). The plasma glucose was 6.1 +/- 1.0 mmol/L in ACI group, 6.4 +/- 2.1 mmol/L in ACH group, and 4.8 +/- 0.5 mmol/L in healthy control group (F = 8.5, P < 0.01). The plasma FINS was 15.7 +/- 3.1 mIU/L in ACI group, 19.7 +/- 9.6 mIU/L in ACH group, and 10.6 +/- 3.2 mIU/L in healthy control group (F = 10.6, P < 0.01). (2) In patients with ACI and ACH, there was a significant positive correlation between plasma IGF-1 and IGFBP3 (P < 0.01), between plasma IGF-1 and ISI (P < 0.01), and between IGFBP3 and ISI (P < 0.05); and there was a significant negative correlation between plasma IGF-1 and FINS and between IGFBP3 and FINS (P < 0.01). CONCLUSION: The plasma IGF-1 and IGFBP3 participates in the pathophysiologic course of ACI and ACH in the early stage. Insulin resistance exists in ACI and ACH. Plasma IGF-1 may play an important role in IR in ACI and ACH.

Aged↗