Biomedical subjects

Jiang Xu

Publications and source records attributed to Jiang Xu.

At least 19 recordsLinked to original sources

PubMed2006

Interplay of bonding and geometry of the adsorption complexes of light alkanes within cationic faujasites. Combined spectroscopic and computational study.

A FT-IR spectroscopic study of methane, ethane, and propane adsorption on magnesium and calcium forms of zeolite Y reveals different vibrational properties of the adsorbed molecules depending on the exchanged cation. This is attributed to different adsorption conformations of the hydrocarbons. Two-fold eta(2) coordination of light alkanes is realized for MgY, whereas in case of CaY zeolite quite different adsorption modes are found, involving more C-H bonds in the interaction with the cation. The topological analysis of the electron density distribution function of the adsorption complexes shows that when a hydrocarbon coordinates to the exchanged Mg(2+) ions, van der Waals bonds between H atoms of the alkane and basic zeolitic oxygens significantly contribute to the overall adsorption energy, whereas in case of CaY zeolite such interactions play only an indirect role. It is found that, due to the much smaller ionic radius of the Mg(2+) ion as compared to that of Ca(2+), the former ions are significantly shielded with the surrounding oxygens of the zeolitic cation site. This results in a small electrostatic contribution to the stabilization of the adsorbed molecules. In contrast, for CaY zeolite the stabilization of alkanes in the electrostatic field of the partially shielded Ca(2+) cation significantly contributes to the adsorption energy. This is in agreement with the experimentally observed lower overall absorption of C-H stretching vibrations of alkanes loaded to MgY as compared to those for CaY zeolite. The preferred conformation of the adsorbed alkanes is controlled by the bonding within the adsorption complexes that, in turn, strongly depends on the size and location of the cations in the zeolite cavity.

Journal Article↗

PubMed2006

A protein kinase, interacting with two calcineurin B-like proteins, regulates K+ transporter AKT1 in Arabidopsis.

Potassium is an essential mineral element for plant growth and development. Although it is known that plants absorb and transport K+ through membrane transporters, it remains unclear how these transporters are regulated. Here we show that the protein kinase CIPK23, encoded by the LKS1 gene, regulates K+ uptake under low-K+ conditions. Lesion of LKS1 significantly reduced K+ uptake and caused leaf chlorosis and growth inhibition, whereas overexpression of LKS1 significantly enhanced K+ uptake and tolerance to low K+. We demonstrate that CIPK23 directly phosphorylates the K+ transporter AKT1 and further find that CIPK23 is activated by the binding of two calcineurin B-like proteins, CBL1 and CBL9. We propose a model in which the CBL1/9-CIPK23 pathway ensures activation of AKT1 and enhanced K+ uptake under low-K+ conditions.

Animals↗

PubMed2006

[Clinical experience of treatment of 275 mandible fractures].

OBJECTIVE: To evaluate the treatment effect of mandible fractures. METHODS: Clinical data of 275 mandibular fracture patients of Tongchuan people's hospital were analysed. RESULTS: (1) The systemic health of 27 non-surgery cases were influenced during the intermaxillary ligation and 3 cases of them had deformity of maxillofacial region. (2) In the surgery group, 5 of 73 cases fixed by steel wire had disorder of occlusion, 6 of 169 cases fixed by titanium mini plate accepted secondary operation of removing the plates, and 6 cases fixed by bioabsorbable mini plate had better effect. CONCLUSION: The internal rigid fixation is an appropriate and effective method for the mandible fractures.

Bone Plates↗

PubMed2005

Lack of inducible NO synthase reduces oxidative stress and enhances cardiac response to isoproterenol in mice with deoxycorticosterone acetate-salt hypertension.

Although NO derived from endothelial NO synthase (eNOS) is thought to be cardioprotective, the role of inducible NO synthase (iNOS) remains controversial. Using mice lacking iNOS (iNOS-/-), we studied (1) whether development of hypertension, cardiac hypertrophy, and dysfunction after deoxycorticosterone acetate (DOCA)-salt would be less severe compared with wild-type controls (WT; C57BL/6J), and (2) whether the cardioprotection attributable to lack of iNOS is mediated by reduced oxidative stress. Mice were uninephrectomized and received either DOCA-salt (30 mg/mouse SC and 1% NaCl+0.2% KCl in drinking water) or vehicle (tap water) for 12 weeks. Systolic blood pressure (SBP) was measured weekly. Left ventricular (LV) ejection fraction (EF) by echocardiography and cardiac response to isoproterenol (50 ng/mouse IV) were studied at the end of the experiment. Expression of eNOS and iNOS as well as the oxidative stress markers 4-hydroxy-2-nonenal (4-HNE, a marker of lipid peroxidation) and nitrotyrosine (a marker for peroxynitrite) were determined by Western blot and immunohistochemical staining, respectively. DOCA-salt increased SBP and LV weight similarly in both strains and decreased EF in WT but not in iNOS-/-. Cardiac contractile and relaxation responses to isoproterenol were greater, 4-HNE and nitrotyrosine levels were lower, and eNOS expression tended to be higher in iNOS-/-. We conclude that lack of iNOS leads to better preservation of cardiac function, which may be mediated by reduced oxidative stress and increased eNOS; however, it does not seem to play a significant role in preventing DOCA-salt-induced hypertension and hypertrophy.

Aldehydes↗

PubMed2005

Formation of M2+(O2)(C3H8) species in alkaline-earth-exchanged Y zeolite during propane selective oxidation.

The adsorption of oxygen and d2-propane (CH3CD2CH3) on a series of alkaline-earth-exchanged Y zeolite at room temperature was studied with in situ infrared spectroscopy. Surprisingly at room temperature, oxygen adsorption led to the formation of supercage M2+(O2) species. Further, at low propane coverage, propane was found to adsorb linearly on Mg2+ cations, but a ring-adsorption structure was observed for propane adsorbing on Ca2+, Sr2+, and Ba2+ cations. It is demonstrated that O2 and propane can simultaneously attach to one active center (M2+) to form a M2+(O2)(C3H8) species, which is proposed to be the precursor in thermal propane selective oxidation. Selectivity to acetone in the propane oxidation reaction decreases with increasing temperature and cation size due to the formation of 2-propanol and carboxylate ions. An extended reaction scheme for the selective oxidation of propane over alkaline earth exchanged Y zeolites is proposed.

Journal Article↗

PubMed2005

Role of inducible nitric oxide synthase in cardiac function and remodeling in mice with heart failure due to myocardial infarction.

Using inducible nitric oxide (NO) synthase (iNOS) knockout mice (iNOS-/-), we tested the hypotheses that 1) lack of iNOS attenuates cardiac remodeling and dysfunction and improves cardiac reserve postmyocardial infarction (MI), an effect that is partially mediated by reduction of oxidative stress due to reduced interaction between NO and reactive oxygen species (ROS); and 2) the cardioprotection afforded by iNOS deletion is eliminated by Nomega-nitro-L-arginine methyl ester (L-NAME) due to inhibition of endothelial NOS (eNOS) and neuronal NOS (nNOS). MI was induced by ligating the left anterior descending coronary artery. Male iNOS-/- mice and wild-type controls (WT, C57BL/6J) were divided into sham MI, MI+vehicle, and MI+l-NAME (100 mg.kg(-1).day(-1) in drinking water for 8 wk). Cardiac function was evaluated by echocardiography. Left ventricular (LV) maximum rate of rise of ventricular pressure divided by pressure at the moment such maximum occurs (dP/dt/instant pressure) in response to isoproterenol (100 ng.kg(-1).min(-1) iv) was measured with a Millar catheter. Collagen deposition, myocyte cross-sectional area, and expression of nitrotyrosine and 4-hydroxy-2-nonenal (4-HNE), markers for ROS, were determined by histopathological and immunohistochemical staining. We found that the MI-induced increase in LV chamber dimension and the decrease in ejection fraction, an index of systolic function, were less severe in iNOS-/- compared with WT mice. L-NAME worsened LV remodeling and dysfunction further, and these detrimental effects were also attenuated in iNOS-/- mice, associated with better preservation of cardiac function. Lack of iNOS also reduced nitrotyrosine and 4-HNE expression after MI, indicating reduced oxidative stress. We conclude that iNOS does not seem to be a pathological mediator of heart failure; however, the lack of iNOS improves cardiac reserve post-MI, particularly when constitutive NOS isoforms are blocked. Decreased oxidative stress and other adaptive mechanisms independent of NOS may be partially responsible for such an effect, which needs to be studied further.

Animals↗

PubMed2005

Temporal dissociation of early lexical access and articulation using a delayed naming task--an FMRI study.

Neuroimaging studies of overt speech hold an important practical advantage allowing monitoring of subject performance, particularly valuable in disorders like aphasia. However, speech production is not a monotonic process but a complex sequence of stages. Levelt and colleagues have described these as roughly corresponding to two originally independent systems--conceptual and sensorimotor--that are linked in the formulation and expression of spoken language. In the initial stages a word is chosen to match a concept (lexical selection); in the later stages the sound and motor patterns are encoded and the word is uttered (articulation). It has been difficult to discriminate these stages using conventional neuroimaging techniques. We designed a functional magnetic resonance imaging study in an attempt to do this, by introducing a latency into a conventional naming paradigm, delaying the articulated response. Our results showed that left hemisphere perisylvian areas were active throughout, interacting with visual and heteromodal areas during early lexical access and with motor and auditory areas during overt articulation. These results are consistent with the broadest version of the Levelt model and with that derived from Chomsky's minimalist program in which a core language system interacts with conceptual-intentional systems and articulatory-perceptual systems during the early and late stages of lexical access respectively.

Adult↗

PubMed2005

Language in context: emergent features of word, sentence, and narrative comprehension.

Context exerts a powerful effect on cognitive performance and is clearly important for language processing, where lexical, sentential, and narrative contexts should differentially engage neural systems that support lexical, compositional, and discourse level semantics. Equally important, but thus far unexplored, is the role of context within narrative, as cognitive demands evolve and brain activity changes dynamically as subjects process different narrative segments. In this study, we used fMRI to examine the impact of context, comparing responses to a single, linguistically matched set of texts when these were differentially presented as random word lists, unconnected sentences and coherent narratives. We found emergent, context-dependent patterns of brain activity in each condition. Perisylvian language areas were always active, consistent with their supporting core linguistic computations. Sentence processing was associated with expanded activation of the frontal operculum and temporal poles. The same stimuli presented as narrative evoked robust responses in extrasylvian areas within both hemispheres, including precuneus, medial prefrontal, and dorsal temporo-parieto-occipital cortices. The right hemisphere was increasingly active as contextual complexity increased, maximal at the narrative level. Furthermore, brain activity was dynamically modulated as subjects processed different narrative segments: left hemisphere activity was more prominent at the onset, and right hemisphere more prominent at the resolution of a story, at which point, it may support a coherent representation of the narrative as a whole. These results underscore the importance of studying language in an ecologically valid context, suggesting a neural model for the processing of discourse.

Adult↗

PubMed2005

Role of the B1 kinin receptor in the regulation of cardiac function and remodeling after myocardial infarction.

Kinins exert cardioprotective effects via 2 G-protein-coupled receptors, B1 and B2. Using B1 kinin receptor gene knockout mice (B1-/-), we tested the hypotheses that the B1 receptor plays an important role in preservation of cardiac function, whereas lack of B1 may accelerate cardiac remodeling and dysfunction after myocardial infarction, and that B2 receptors may compensate for lack of B1, whereas blockade of B2 receptors in B1-/- mice may cause further deterioration of cardiac function and remodeling. Female B1-/- mice and wild-type controls (C57BL/6J, B1+/+) underwent sham surgery or myocardial infarction and were treated with either vehicle or B2-antagonist (icatibant, 500 microg/kg per day, subcutaneous) for 8 weeks. We found that in sham myocardial infarction, B1-/- mice had a larger left ventricular diastolic chamber dimension both initially and at 4 to 8 weeks compared with B1+/+. Left ventricular mass and myocyte size were also larger in B1-/- with sham operation than in B1+/+, although cardiac function did not differ between strains. After myocardial infarction, cardiac remodeling and function were similar in both strains, although B1-/- mice tended to have lower blood pressure. Blockade of B2 receptors tended to worsen cardiac remodeling and dysfunction in B1-/- but not in B1+/+. These results may suggest that B2 receptors play an important role in compensating for lack of B1 receptors in mice with myocardial infarction. Dual blockade of both B1 and B2 eliminates this compensation, leading to further deterioration of cardiac dysfunction and remodeling after myocardial infarction.

Animals↗

PubMed2005

Inhibition of p38 mitogen-activated protein kinase protects the heart against cardiac remodeling in mice with heart failure resulting from myocardial infarction.

BACKGROUND: Mitogen-activated protein kinases (MAPKs) have emerged as an important pathophysiologic regulator during the development of heart failure (HF). p38 MAPK activity is elevated in cardiac hypertrophy and HF. We used a mouse model of myocardial infarction (MI) to test the hypotheses that (1) inhibition of p38 MAPK activity may improve cardiac function and remodeling after myocardial infarction (MI) and (2) coadministration of a p38 inhibitor (p38i) and an angiotensin-converting enzyme inhibitor (ACEI) may provide only limited further cardioprotection in this model. METHODS AND RESULTS: MI was induced in C57BL/6J mice by ligating the left anterior descending coronary artery and then either left untreated or treated with a p38i (SC-409, 30 mg/kg/day in chow), ACEI (enalapril, 20 mg/kg in drinking water), or p38i plus ACEI for 12 weeks. Echocardiography was performed and systolic blood pressure measured before MI and weekly thereafter. At the end of the study, interstitial collagen fraction (ICF) and myocyte cross-sectional area (MCSA) were examined histologically. We found that p38i significantly increased left ventricular ejection fraction and cardiac output and decreased left ventricular area at diastole, ICF, and MCSA. ACEi and p38i each had similar beneficial effects in this mouse model of HF produced by a large MI. Coadministration of p38i and ACEi did not provide any additional benefit. CONCLUSION: Our data suggest that inhibition of p38 MAPK provides significant cardioprotection in mice with HF post-MI.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2004

Electrophysiological-anatomic correlates of ATP-triggered vagal reflex in the dog. V. Role of purinergic receptors.

The mechanism of extracellular ATP-triggered vagal depressor reflex was further studied in a closed-chest canine model. Adenosine and ATP were administered individually in equimolar doses (0.01-1.0 mumol/kg) into the right coronary artery (RCA) and left circumflex coronary artery (LCA). When administered into the RCA, adenosine and ATP exerted an identical and relatively small negative chronotropic effect on sinus node automaticity; the time to peak negative chronotropic effect was >/=7 s. When administered into the LCA, adenosine had no effect on sinus node automaticity, whereas ATP markedly suppressed sinus node automaticity. This effect of ATP 1) reached its peak in <2 s after its administration, 2) was short lasting, and 3) was completely abolished by either intravenous administration of the muscarinic cholinergic blocker atropine (0.2 mg/kg) or intra-LCA administration of 2',3'-O-(2,4,6-trinitrophenyl)-ATP (TNP-ATP), a potent P2X(2/3) purinergic receptor (P2X(2/3)R) antagonist, but not by diinosine pentaphosphate (Ip(5)I), a potent inhibitor of P2X(1)R and P2X(3)R. Repetitive administrations of ATP were not associated with reduced effects, indicative of receptor desensitization, thereby excluding the involvement of the rapidly desensitized P2X(1)R in the action of ATP. It was concluded that ATP triggers a cardio-cardiac vagal depressor reflex by activating P2X(2/3)R located on vagal sensory nerve terminals localized in the left ventricle. Because these terminals mediate vasovagal syncope, these data could suggest a mechanistic role of extracellular ATP in this syndrome and, in addition, give further support to the hypothesis that endogenous ATP released from ischemic myocytes is a mediator of atropine-sensitive bradyarrhythmias associated with left ventricular myocardial infarction.

Adenosine↗

PubMed2004

Role of a selective aldosterone blocker in mice with chronic heart failure.

BACKGROUND: Spironolactone, a nonselective aldosterone blocker, has a cardioprotective effect; however, significant endocrine side effects limit its use. Eplerenone is a new selective aldosterone blocker. We investigated whether eplerenone attenuates cardiac remodeling and improves function in a mouse model of heart failure and whether coadministration of eplerenone and an angiotensin-converting enzyme inhibitor (ACEi) provides better cardioprotection than either agent alone. METHODS AND RESULTS: C57BL/6J mice were subjected to myocardial infarction (MI) by ligating the left anterior descending coronary artery. Two weeks later, the mice were either left untreated or treated with (1) eplerenone, (2) ACEi, or (3) eplerenone plus ACEi for 12 weeks. Systolic blood pressure (SBP) was measured and echocardiography performed before MI and weekly thereafter. At the end of the study, interstitial collagen fraction (ICF) and myocyte cross-sectional area (MCSA) were examined histologically. We found that (1) eplerenone significantly improved ejection fraction and cardiac output and decreased left ventricular (LV) systolic area, LV weight, ICF, and MCSA independently of changes in SBP compared with untreated animals; (2) ACEi had similar beneficial effects, accompanied by a significant reduction in SBP; and (3) combined treatment offered limited additional benefit beyond monotherapy. CONCLUSIONS: In mice with MI, eplerenone attenuates progression of heart failure comparably to ACEi, and its effect is independent of BP lowering.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2004

Dual inhibition of ACE and NEP provides greater cardioprotection in mice with heart failure.

BACKGROUND: Vasopeptidase inhibitors (VPi) may provide a new means of treating hypertension and congestive heart failure, because they simultaneously block angiotensin-converting enzyme (ACE) and neutral endopeptidase-24.11 (NEP-24.11), thereby inhibiting the renin-angiotensin system and enhancing vasodilator and natriuretic substances such as kinins and natriuretic peptides. METHODS: Using B(2) kinin receptor gene knockout mice (B(2)-/-), we tested the hypotheses that (1) VPi may provide better cardioprotection than ACE or NEP inhibitors alone (ACEi and NEPi) and (2) the effects of these inhibitors are partially mediated by kinins. Four weeks after myocardial infarction, B(2)-/- mice and B(2)+/+ mice were started on vehicle, ACEi (ramipril, 2.5 mg/kg/d), NEPi (candoxatril, 20 mg/kg/d) or VPi (omapatrilat, 50 mg/kg/d), which was continued for 20 weeks. Systolic blood pressure was measured weekly and cardiac function evaluated monthly by echocardiography. Myocyte cross-sectional area and interstitial collagen fraction were measured histopathologically. RESULTS: We found that ACEi or NEPi improved cardiac function and remodeling and that these effects were more obvious in mice receiving VPi. Furthermore, the beneficial cardiac effects of ACEi, NEPi, and VPi were significantly attenuated in B(2)-/- mice. We concluded that dual inhibition of ACE and NEP with VPi provides better cardioprotection than ACEi or NEPi alone in mice with congestive heart failure induced by myocardial infarction, and these effects are mediated at least in part via kinins.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2004

[Study on preparation of beta-cyclodextrin inclusion volatile oil from Rhizoma Curcumae].

OBJECTIVE: To study optimum inclusion process conditions for volatile oil from Rhizoma Curcumae. METHOD: The study was carried out with orthogonal design. The process conditions were studied by determining the utilazision ratio of volatile oil from Rhizoma Curcumae, the oil-bearing rate and extract ratio of inclusion compound. RESULTS: The optimum preparation conditions for inclusion were established as: volatile oil:beta-CD was 1:8, the inclusion temperature was at 80 degrees C and inclusion time for 3 h, ultilizasion rate of volatile oil was 86%. CONCLUSION: The method can be used for mass production.

Curcuma↗

PubMed2003

Ac-SDKP reverses inflammation and fibrosis in rats with heart failure after myocardial infarction.

Inflammation may play an important role in the pathogenesis of cardiac fibrosis in heart failure (HF) after myocardial infarction (MI). N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring antifibrotic peptide whose plasma concentration is increased 4- to 5-fold by angiotensin-converting enzyme inhibitors. We tested the hypothesis that in rats with HF after MI, Ac-SDKP acts as an anti-inflammatory cytokine, preventing and also reversing cardiac fibrosis in the noninfarcted area (reactive fibrosis), and thus affording functional improvement. We found that Ac-SDKP significantly decreased total collagen content in the prevention group from 23.7+/-0.9 to 15.0+/-0.7 microg/mg and in the reversal group from 22.6+/-2.2 to 14.4+/-1.6 (P<0.01). Interstitial collagen volume fraction and perivascular collagen were likewise significantly reduced. We also found that infiltrating macrophages were reduced from 264.7+/-8.1 to 170.2+/-9.2/mm2, P<0.001 (prevention), and from 257.5+/-9.1 to 153.1+/-8.5 mm2, P<0.001 (reversal), while transforming growth factor (TGF)-beta-positive cells were decreased from 195.6+/-8.4 to 129.6+/-5.7/mm2, P<0.01 (prevention), and from 195.6+/-8.4 to 130.7+/-10.8/mm2, P<0.01 (reversal). Ac-SDKP did not alter either blood pressure or left ventricular hypertrophy (LVH); however, it depressed systolic cardiac function in the prevention study while having no significant effect in the reversal group. We concluded that Ac-SDKP has an anti-inflammatory effect in HF that may contribute to its antifibrotic effect; however, this decrease in fibrosis without changes in LVH was not accompanied by an improvement in cardiac function.

Animals↗

PubMed2002

Electroencephalographic activity in a flanker interference task using Japanese orthography.

The neural activities for color word interference effects were investigated using event-related brain potentials (ERPs) recorded in a flanker-type interference task. Kanji words (Japanese morphograms) and kana words (Japanese phonograms) were used as the flanker stimuli to obtain insights about hemispheric specialization for processing two types of Japanese orthographies. Interference effects in reaction time were larger when kanji words were presented in the left visual field and when kana words were in the right visual field. ERPs were modulated by the incongruent flankers, which generated a negative ERP component with the different onset and offset depending on flanker attributes. Consistent with the behavioral data, the interference-related negativity was observed for kanji words presented in the left visual field and for kana words in the right visual field. The negativity distributed maximally over the fronto-central site. The early part of the negativity distributed strongly over the frontal midline area, whereas it extended bilaterally over the frontal area in the late phase. The present results support the view of preferential processing of kanji in the right hemisphere and that of kana in the left hemisphere. The temporal profile of scalp topographies for the interference-related neural activity suggests that the medial and dorsolateral prefrontal regions may be involved in maintaining attentional set and conflict resolution.

Adult↗

PubMed2002

Age-dependent atrial remodeling induced by recombinant human interleukin-11: implications for atrial flutter/fibrillation.

Recombinant human interleukin-11 (rhIL-11) has been used to alleviate side effects caused by chemotherapy in patients with neoplastic diseases and as an experimental anti-inflammatory agent. Its use in elderly patients has been associated with increased frequency of atrial flutter/fibrillation (AF). The mechanism of the latter phenomenon was studied in a rat model in vivo. Adult and old Fischer 344 rats fed with either normal diet or sodium-restricted diets were treated with rhIL-11 or vehicle (control) (1 mg/kg/day, i.p., 7 days); cardiac electrophysiologic parameters and atrial dimensions were determined. In adult rats, rhIL-11 was without effect, and atrial pacing did not induce AF. In contrast, in old rats, rhIL-11 shortened atrial refractoriness and increased atrial dimensions. Also, atrial pacing induced AF in old rats treated with rhIL-11 more than in controls. These effects of rhIL-11 in old rats were reversed by sodium-restricted diet. It was concluded that rhIL-11 induces age-dependent atrial remodeling manifested by atrial stretch and reduced atrial refractoriness, which favor AF. Na retention is the most likely mechanism underlying this effect of rhIL-11.

Age Factors↗

PubMed2002

Myocardial infarction and cardiac remodelling in mice.

We established a mouse model of cardiac dysfunction due to myocardial infarction (MI). For this we ligated the left anterior descending coronary artery in male C57BL/6J mice and assessed healing and left ventricular (LV) remodelling at 1, 2 and 4 days and 1, 2 and 4 weeks after MI. Echocardiography was performed at 1 and 2 weeks and 1, 2, 4 and 6 months after MI. We found that neutrophil infiltration of the infarct border was noticeable at 1-2 days. Marked macrophage infiltration occurred at day 4, while lymphocyte infiltration was apparent at 7-14 days. Massive proliferation of fibroblasts and collagen accumulation began by day 7-14, and scar formation was completed by day 21. LV diastolic dimension increased markedly at 2 weeks and remained at the same level thereafter. LV shortening fraction decreased significantly at 2 weeks and then slowly decreased. In non-infarcted areas of the LV, myocyte cross-sectional area and interstitial collagen fraction increased progressively, reaching a maximum at 4 months. This study provides important qualitative and quantitative information about the natural history of cardiac remodelling after MI in mice.

Animals↗