Biomedical subjects

S K Liu

Publications and source records attributed to S K Liu.

At least 19 recordsLinked to original sources

PubMed2000

Association of Grb2, Gads, and phospholipase C-gamma 1 with phosphorylated LAT tyrosine residues. Effect of LAT tyrosine mutations on T cell angigen receptor-mediated signaling.

The linker for activation of T cells (LAT) is a critical adaptor molecule required for T cell antigen receptor (TCR)-mediated signaling and thymocyte development. Upon T cell activation, LAT becomes highly phosphorylated on tyrosine residues, and Grb2, Gads, and phospholipase C (PLC)-gamma1 bind LAT via Src homology-2 domains. In LAT-deficient mutant Jurkat cells, TCR engagement fails to induce ERK activation, Ca(2+) flux, and activation of AP-1 and NF-AT. We mapped the tyrosine residues in LAT responsible for interaction with these specific signaling molecules by expressing LAT mutants with tyrosine to phenylalanine mutations in LAT-deficient cells. Our results showed that three distal tyrosines, Tyr(171), Tyr(191), and Tyr(226), are responsible for Grb2-binding; Tyr(171), and Tyr(191), but not Tyr(226), are necessary for Gads binding. Mutation of Tyr(132) alone abolished PLC-gamma1 binding. Mutation of all three distal tyrosines also abolished PLC-gamma1 binding, suggesting there might be multiple binding sites for PLC-gamma1. Mutation of Tyr(132) affected calcium flux and blocked Erk and NF-AT activation. Since Grb2 binding is not affected by this mutation, these results strongly suggest that PLC-gamma activation regulates Ras activation in these cells. Mutation of individual Grb2 binding sites had no functional effect, but mutation of two or three of these sites, in combination, also affected Erk and NF-AT activation.

Adaptor Proteins, Signal Transducing↗

PubMed2000

Effects of atypical neuroleptics on sustained attention deficits in schizophrenia: a trial of risperidone versus haloperidol.

To help determine whether sustained attention deficits as measured with the Continuous Performance Test (CPT) are stable vulnerability indicators of schizophrenia, we compared the CPT performance of schizophrenic patients before and after treatment with risperidone or haloperidol. In this double blind trial, 56 schizophrenic patients were randomly assigned to a 12-week regimen of either risperidone or haloperidol, after a 1-week washout period. The patients undertook two sessions of the CPT (undegraded and 25% degraded) twice, one at the end of the washout period and the other at the end of the study. Thirty-eight patients completed the study, 19 in each group. Both groups experienced significant improvements in clinical symptoms, and the risperidone group showed no change in the severity of extrapyramidal symptoms. Despite those improvements, the CPT performance indexes did not change significantly from the beginning to the end of the study. These findings indicate that sustained attention deficits might be stable vulnerability indicators of schizophrenia.

Adult↗

PubMed1999

Familial hypertrophic cardiomyopathy in maine coon cats: an animal model of human disease.

BACKGROUND: A naturally occurring animal model of familial hypertrophic cardiomyopathy (FHCM) is lacking. We identified a family of Maine coon cats with HCM and developed a colony to determine mode of inheritance, phenotypic expression, and natural history of the disease. METHODS AND RESULTS: A proband was identified, and related cats were bred to produce a colony. Affected and unaffected cats were bred to determine the mode of inheritance. Echocardiography was used to identify affected offspring and determine phenotypic expression. Echocardiograms were repeated serially to determine the natural history of the disease. Of 22 offspring from breeding affected to unaffected cats, 12 (55%) were affected. When affected cats were bred to affected cats, 4 (45%) of the 9 were affected, 2 (22%) unaffected, and 3 (33%) stillborn. Findings were consistent with an autosomal dominant mode of inheritance with 100% penetrance, with the stillborns representing lethal homozygotes that died in utero. Affected cats usually did not have phenotypic evidence of HCM before 6 months of age, developed HCM during adolescence, and developed severe HCM during young adulthood. Papillary muscle hypertrophy that produced midcavitary obstruction and systolic anterior motion of the mitral valve was the most consistent manifestation of HCM. Cats died suddenly (n=5) or of heart failure (n=3). Histopathology of the myocardium revealed myocardial fiber disarray, intramural coronary arteriosclerosis, and interstitial fibrosis. CONCLUSIONS: HCM in this family of Maine coon cats closely resembles the human form of FHCM and should prove a valuable tool for studying the gross, cellular, and molecular pathophysiology of the disease.

Animals↗

PubMed1999

Cloning and characterization of mPAL, a novel Shc SH2 domain-binding protein expressed in proliferating cells.

Shc adaptor proteins play a role in linking activated cell surface receptors to the Ras signaling pathway in response to receptor mediated tyrosine kinase activation. While the function of Shc in the activation of the Ras pathway via binding to Grb2 has been well characterized, it is becoming increasingly apparent that Shc participates in additional signaling pathways through interactions with other cytoplasmic proteins. Using the yeast two-hybrid system, we have identified a unique Shc binding protein designated PAL (Protein expressed in Activated Lymphocytes) with no similarity to other known proteins. mPAL binds specifically to the Shc SH2 domain and unlike previously described Shc SH2 domain-protein interactions, the association of mPAL and Shc is phosphotyrosine-independent. Both mPAL RNA and protein expression are restricted to tissues containing actively dividing cells and proliferating cells in culture. mPAL expression is induced upon growth factor stimulation and is down-regulated upon growth inhibition. This pattern, and timing of mPAL expression and its association with the Shc adaptor molecule suggests a role for this protein in signaling pathways governing cell cycle progression.

3T3 Cells↗

PubMed1999

The hematopoietic-specific adaptor protein gads functions in T-cell signaling via interactions with the SLP-76 and LAT adaptors.

BACKGROUND: The adaptor protein Gads is a Grb2-related protein originally identified on the basis of its interaction with the tyrosine-phosphorylated form of the docking protein Shc. Gads protein expression is restricted to hematopoietic tissues and cell lines. Gads contains a Src homology 2 (SH2) domain, which has previously been shown to have a similar binding specificity to that of Grb2. Gads also possesses two SH3 domains, but these have a distinct binding specificity to those of Grb2, as Gads does not bind to known Grb2 SH3 domain targets. Here, we investigated whether Gads is involved in T-cell signaling. RESULTS: We found that Gads is highly expressed in T cells and that the SLP-76 adaptor protein is a major Gads-associated protein in vivo. The constitutive interaction between Gads and SLP-76 was mediated by the carboxy-terminal SH3 domain of Gads and a 20 amino-acid proline-rich region in SLP-76. Gads also coimmunoprecipitated the tyrosine-phosphorylated form of the linker for activated T cells (LAT) adaptor protein following cross-linking of the T-cell receptor; this interaction was mediated by the Gads SH2 domain. Overexpression of Gads and SLP-76 resulted in a synergistic augmentation of T-cell signaling, as measured by activation of nuclear factor of activated T cells (NFAT), and this cooperation required a functional Gads SH2 domain. CONCLUSIONS: These results demonstrate that Gads plays an important role in T-cell signaling via its association with SLP-76 and LAT. Gads may promote cross-talk between the LAT and SLP-76 signaling complexes, thereby coupling membrane-proximal events to downstream signaling pathways.

Adaptor Proteins, Signal Transducing↗

PubMed1999

Statistical method for characterization of hypertrophic cardiomyopathy by use of morphologic and pathologic measurements in pigs (Sus scrofa domestica).

BACKGROUND AND PURPOSE: Hypertrophic cardiomyopathy (HCM) is characterized by symmetric or asymmetric hypertrophy of the left and/or right ventricle. Morphologic and pathologic indices (MI and PI) of hearts were established for classification of HCM in pigs. METHODS: Fifty on-farm-performance-tested pigs (average body weight, 104.3 kg; age, 224.5 days) were randomly selected. Heart weight, length, width, heart-to-body weight ratio, and thickness of the cranial and middle portions of ventricular septum and left ventricular free wall were measured. Myocyte disorganization and necrosis, myocardial and endocardial fibrosis, and intramural coronary arterial occlusion were scored. Principal component analysis and stepwise regression analysis were used to establish MI and PI. RESULTS: MI was established by using the first principal component as the dependent variable and applying stepwise regression analysis. Hearts were classified as morphologically normal, suspicious, and hypertrophic according to the range of MI. The same statistical method was used to find PI. Hearts were classified as pathologically normal, moderately affected, or seriously affected according to the range of PI. Combining MI and PI, hearts could be classified into five groups: no hypertrophy with minor lesion (normal); hypertrophy but with rare lesion; no hypertrophy but seriously affected; suspicious; and hypertrophy and seriously affected (heart with HCM). Another 119 hearts were collected and classified. The variation of heart measurements was consistent with the original purpose of classification. CONCLUSIONS: Using fewer measurements for identification of HCM objectively in pigs seems to have practical application.

Animals↗

PubMed1999

Urinary catheter in laparoscopic cholecystectomy: is it necessary?

The aim of this prospective study was to evaluate the necessity or urinary catheterization in elective laparoscopic cholecystectomy. From April 1996 to April 1998, 261 patients undergoing elective laparoscopic cholecystectomy at a county hospital were randomized to either receive or not receive preoperative urinary bladder catheterization. Data analyzed included age and gender of patients, length of surgery, and intraoperative and perioperative complications such as visceral injury, urinary tract infection, and urinary retention. Our results showed, although not statistically significant, more urinary tract complications in the "with Foley" group than in the "without Foley" group (four vs one, respectively). There was no significant difference between the two groups with respect to length of operation and perioperative complications. There was no visceral injury or operative mortality in this study. We conclude that urinary catheterization can be omitted safely in elective laparoscopic cholecystectomy.

Adult↗

PubMed1998

Gads is a novel SH2 and SH3 domain-containing adaptor protein that binds to tyrosine-phosphorylated Shc.

Shc proteins are important substrates of receptor and cytoplasmic tyrosine kinases that couple activated receptors to downstream signaling enzymes. Phosphorylation of Shc tyrosine residues 239 and 317 leads to recruitment of the Grb2-Sos complex, thus linking Shc phosphorylation to Ras activation. We have used phosphorylated peptides corresponding to the regions spanning tyrosine 239/240 and 317 of Shc in an expression library screen to identify additional downstream targets of Shc. Here we report the identification of Gads, a novel adaptor protein most similar to Grb2 and Grap that contains amino and carboxy terminal SH3 domains flanking a central SH2 domain and a 120 amino acid unique region. Gads is most highly expressed in the thymus and spleen of adult animals and in human leukemic cell lines. The binding specificity of the Gads SH2 domain is similar to Grb2 and mediates the interaction of Gads with Shc, Bcr-Abl and c-kit. Gads does not interact with Sos, Cbl or Sam68, although the isolated carboxy terminal Gads SH3 domain is able to bind these molecules in vitro. Our results suggest that the unique structure of Gads regulates its interaction with downstream SH3 domain-binding proteins and that Gads may function to couple tyrosine-phosphorylated proteins such as Shc, Bcr-Abl and activated receptor tyrosine kinases to downstream effectors distinct from Sos and Ras.

3T3 Cells↗

PubMed1998

Myocardial collagen in cardiac hypertrophy resulting from chronic aortic regurgitation.

Myocardial fibrosis and abnormal myocardial collagen content are common in many forms of pathological cardiac hypertrophy, including that mediated by pressure overload. Recently, in an experimental animal model of chronic aortic regurgitation (AR), we found a strong relation between myocardial fibrosis and congestive heart failure development. To determine if these fibrotic lesions are composed of collagen, as they are in pressure overload, and to determine if potential preventive therapies should be developed similarly in both diseases, we assessed left ventricular collagen content at three time points after AR induction. Moderate to severe AR was induced in 19 New Zealand White rabbits by inserting a catheter through the carotid artery to perforate the aortic valve leaflets. Animals were killed (1) when they showed echocardiographically discernible systolic dysfunction or (2) if normal cardiac function continued, either early (1 month) or late (>3 years) after operation. Fourteen age-matched, sham-operated controls and seven normal unoperated rabbits also were studied. Collagen concentrations were determined biochemically by hydroxyproline measurement. Fibrosis was measured histologically using Mason's trichrome stain and the fibrous collagen-specific stain, Picro-Sirius Red. Our results show an age-related increase in left ventricular collagen concentration with no specific increase among animals with evidence of fibrosis. We conclude that, unlike pressure overload, volume overload produces fibrotic lesions not composed predominantly of excess collagen and that the therapy needed to prevent fibrosis may be different in these conditions. Further study is needed to define the chemical characteristics of the fibrous lesions and the pathophysiological importance of this finding.

Age Factors↗

PubMed1998

Fibrosis, myocyte degeneration and heart failure in chronic experimental aortic regurgitation.

Myocardial fibrosis and myocyte degeneration have been reported in patients with chronic aortic regurgitation (AR), and may be related to the pathophysiology of congestive heart failure (CHF) in this disease. To define the relationship between myocardial histopathologic variations and CHF in chronic AR, we performed gross and microscopic evaluations of postmortem tissue from a rabbit model of chronic AR manifesting left ventricular (LV) responses to AR similar to those in humans. Moderate-to-severe chronic AR (echocardiographic regurgitant fraction = 52 +/- 13%) was induced by closed-chest aortic valve perforation in 11 New Zealand White rabbits; 5 control rabbits were sham operated. Six of the 11 AR rabbits died 1.5 +/- 0.8 years (range 0.6-2.8 years) after AR induction; all 6 had gross and histologic anatomic evidence of CHF at necropsy. The remaining 5 AR rabbits survived until sacrifice at 2.9 +/- 0.1 years of AR; none had pathologic evidence of CHF. Cardiac hypertrophy and the extent of LV fibrosis and myocyte necrosis all were greatest among the 6 AR CHF rabbits. No inflammatory response was apparent in any animal. Moderate-to-severe chronic experimental AR frequently results in CHF which is strongly associated with myocardial fibrosis and necrosis, without evidence of inflammation. These histopathologic variations may be pathophysiologically related to CHF development.

Animals↗

PubMed1998

Sustained attention deficit and schizotypal personality features in nonpsychotic relatives of schizophrenic patients.

OBJECTIVE: The authors investigated whether nonpsychotic relatives of schizophrenic probands have an elevated risk of deficits in sustained attention as measured by the Continuous Performance Test (CPT), whether such deficits are associated with specific factors of schizotypy, and whether poor CPT performance by probands predicts poor performance by their relatives. In addition, the heritability of CPT performance in the families of schizophrenic probands was estimated. METHOD: The study subjects were 60 schizophrenic probands, 148 of their first-degree relatives, 20 normal comparison probands, and 42 of the comparison probands' first-degree relatives. Subjects completed undegraded and 25% degraded sessions of the CPT and were interviewed with use of the Chinese version of the Diagnostic Interview for Genetic Studies. Subjects' CPT sensitivity indexes, d', were standardized against those of a community sample of 345 subjects, with adjustment for age, sex, and level of education. RESULTS: On average, the d' values of the relatives of schizophrenic probands were lower than those of the relatives of comparison probands but higher than those of schizophrenic probands. Lower sensitivity indexes among the relatives of schizophrenic patients were associated with the interpersonal dysfunction and disorganization factors of schizotypy but not the cognitive/perceptual factor. When schizophrenic probands were divided into two subgroups by a cutoff of -3.0 for adjusted z score on the CPT, the d' values of relatives of probands with CPT deficits were lower than those of relatives of probands without deficits. The estimated heritability of performance on the CPT ranged from 0.48 to 0.62. CONCLUSIONS: Sustained attention deficit may be a genetic vulnerability marker for schizophrenia, and it may be more useful in linkage analysis than traditional phenotype definitions of schizophrenia.

Adult↗

PubMed1997

Clinical symptom dimensions and deficits on the Continuous Performance Test in schizophrenia.

We examined the relationships between symptom dimensions derived from factor analytic studies of schizophrenic symptoms and sustained attention deficits. Four factors, negative, delusion/hallucination, disorganization, and excitement, were yielded from factor analysis on 14 items of the Positive and Negative Syndrome Scale (PANSS) among 60 Chinese inpatients with acute schizophrenia. The negative dimension was associated with lower sensitivity index (d') while the excitement dimension was associated with higher d' on the Continuous Performance Test (CPT) after sex, age and education were adjusted for in multiple linear regressions. The positive dimension affected only response criterion (ln beta) and was not associated with the d' on the CPT. In contrast, the summed scores of PANSS Positive and Negative scales did not have significant correlations with d' on the CPT. Thus, the discriminant validity of these symptom dimensions of schizophrenia is supported by their correlations with CPT performance indices.

Acute Disease↗

PubMed1997

Operation in patients with incurable colon cancer--is it worthwhile?

PURPOSE: This study was designed to identify objective criteria that might help surgeons decide which patients with incurable colon cancer will benefit from palliative surgery and which will not. METHODS: Charts of 68 patients with incurable colon cancer were reviewed. Fifty-seven patients underwent resection, six had a bypass of a nonresectable cancer, and five had no surgery at all. Time to death was the major end point of the study. Minor end points were postoperative morbidity and mortality. Independent variables analyzed were comorbidity, preoperative carcinoembryonic antigen, liver function tests, extent of liver metastases, stage and site of tumor, and tumor cell differentiation. RESULTS: There were six postoperative deaths, and six patients had complications. Mean survival after palliative resection was 10.6 months, after bypass was 3.4 months, and after diagnosis in patients not operated on was 2 months. Patients with > 50 percent of their liver replaced by cancer had significantly worse survival than those with < 50 percent involvement (mean, 4.2 +/- 4 standard deviation (SD) vs. 14.4 +/- 10.6 SD; P < 0.003, Wilcoxon's rank-sum test). Tumor differentiation also influenced survival (poor, mean 8.4 +/- 8.2 SD; well/moderate, 12.5 +/- 9.2 SD; P < 0.02). No other variable had a significant effect on survival. CONCLUSION: Resection of primary colon cancer in patients with incurable disease has a relatively high postoperative mortality but is worthwhile as long as hepatic metastases occupy less than 50 percent of liver volume.

Aged↗

PubMed1997

Preferential mutagenesis of lacZ integrated at unique sites in the Escherichia coli chromosome.

To study the variation in spontaneous mutation frequencies in different chromosomal domains, a mini-Mu-kan-lacZ- transposable element was constructed to insert the lacZ-(Trp570 --> Opal) allele into many different loci in the Escherichia coli chromosome. Papillation on MacConkey lactose plates was used to screen for mini-Mu insertion mutants with elevated levels of spontaneous mutagenesis of lacZop --> LacZ+; candidates were then screened for normal mutation frequencies in other genes. Two different insertion mutants with this enhanced mutagenesis phenotype were isolated from 14000 colonies, and named plm-1 (preferential lacZ mutagenesis) and plm-2. The frequency of LacZ- --> LacZ+ mutations in these plm mutants was over 400-fold higher than that in isogenic strains containing mini-Mu-kan-lacZop insertions at other loci. Six Lac+ reversion (or suppression) mutations obtained from each of the two plm mutants were mapped by P1 transduction and all were found to be linked to the Kan(r) gene in the mini-Mu-kan-lacZop, suggesting that a localized mutagenic event is responsible for the preferential mutagenesis. Furthermore, both the LacZ+ --> LacZ- and Kan(r) --> Kan(s) mutant frequencies of these Lac+ revertants were in the range of 10(-3) to 10(-2), indicating that this putative localized mutagenesis is neither allele nor gene specific. To identify the plm loci, the chromosomal regions flanking the mini-Mu insertion sites were cloned and sequenced. A computer-assisted database search of homologous sequences revealed that the plm-1 locus is identical to the mutS gene; the mini-Mu insertion most probably results in the production of a truncated MutS protein. We suggest that the enhanced lacZ mutation frequency in plm-1 may be associated with an active process involving the putative truncated MutS protein. The DNA sequence of the plm-2 locus matched a putative malate oxidoreductase gene located at 55.5 min of the E. coli chromosome.

Alleles↗

PubMed1997

Intramural coronary artery disease in swine with naturally occurring hypertrophic cardiomyopathy.

Intramural coronary artery disease (ICAD) has been reported in myocardium affected with hypertrophic cardiomyopathy (HCM), but has never been studied in detail with respect to the cell type or lipid infiltration involved in the wall-thickening. The lack of heart samples may be one of the rationales to hamper the progress in investigating this disease. Recently, the discovery of naturally occurring HCM in swine has provided an excellent opportunity for the study of ICAD because of the high prevalence of ICAD in this animal. The present study provides a detailed structure feature in the thickened arterial wall of ICAD by both histologic and electron microscopic means. Morphologically, the feature of ICAD is due primarily to the neointimal thickening. Smooth muscle cells (SMC) and extracellular matrix (collagen and elastic fibers) are the major components responsible for the thickened neointima. Fragmentation of the internal elastic membrane is associated with the migration and proliferation of SMC from the media to the intima. Therefore, pigs with HCM may be a potential animal model not only for the study of the mechanism by which SMC migrate and proliferate into intima, but also for the future investigation of interventions in coronary artery occlusion.

Animals↗

PubMed1996

Rickets in a 6-month-old monkey.

A 6-month-old male monkey with rickets was found dead by its keeper. Radiographic studies showed osteopenia of the entire skeletal system, a cup-shaped concavity and poor mineralization of metaphyseal ends, and markedly widened and irregular epiphyseal growth plates of the long bones and ribs. Gross anatomic findings included bowing abnormalities and microfractures in the radius, ulna, tibia, and fibia, and enlarged and widened cartilage columns extending into the metaphyses in the long bones and ribs. Histologic features included deficient mineralization and irregular disordered columns of proliferating cartilage in growth plates extending into other zones, dilated vascular channels, and poor mineralization of chondroid and osteoid tissues.

Animals↗

PubMed1996

Substantial decrease of heat shock protein 90 in ventricular tissues of two sudden-death pigs with hypertrophic cardiomyopathy.

We recently developed a pig model with naturally occurring hypertrophic cardiomyopathy (HCM). To further characterize the biochemical features of high frequency of sudden death affected by this disease, the protein profiles of ventricular tissues were analyzed on normal, HCM, and HCM with sudden-death pigs. By sodium dodecylsulfate-polyacrylamide gel electrophoresis, a protein corresponding to an apparent molecular mass of 90 kDa (p90) was found to be markedly decreased in the HCM-affected tissues of sudden-death pigs, but not in HCM or normal pigs. Further study showed that the primary decrease of p90 in HCM pigs with sudden death was located mainly in the interventricular septum. As determined by the molecular mass and isoelectric point on 2-dimensional gels and Western immunoblot with a specific 90 kDa heat shock protein (HSP90) monoclonal antibody, the unknown protein was identified as HSP90. Our findings indicate for the first time that substantially decreased heart HSP90 is associated with HCM pigs with sudden death. Although the role that HSP90 may play in protecting pigs with HCM from sudden death is still nuclear, the model itself may provide further insight into understanding the role of heat shock proteins in cardiac sudden death.-Lee, W.-C., Lin, K.-Y., Chiu, Y.-T., Lin, J.-H., Cheng, H.-C., Huang, H.-C., Yang, P.-C., Liu, S.-K., Mao, S. J. T. Substantial decrease of heat shock protein 90 in ventricular tissues of two sudden-death pigs with hypertrophic cardiomyopathy.

Animals↗

PubMed1996

Heritability estimate of hypertrophic cardiomyopathy in pigs (Sus scrofa domestica).

The purpose of this study was to evaluate the heritability of hypertrophic cardiomyopathy (HCM) in pigs and the relation between HCM and heart measurements, pathologic features, and growth to provide references for HCM line development. A total of 353 on-farm tested gilts (females) and boars (males) from 74 sire families were randomly selected from a single breeding farm where HCM was prevalent. Hearts were collected after animals were slaughtered. Heart length, width, and weight, heart-to-body weight ratio, and thickness of the cranial, middle, and caudal portions of the ventricular septum, left and right ventricles, and apex were measured. Cardiac hypertrophy and myocyte disorganization, myocardial and endocardial fibrosis, and intramural coronary arterial occlusion were used as criteria for HCM. Growth traits were evaluated from average daily body weight gain, ultrasonically determined backfat thickness, loin-eye area, and performance selection index. Heritability of the disease was estimated by treating it as a threshold trait. The prevalence of HCM in three studied breeds was 5.26 in Duroc, 22.98 in Landrace, and 5.56% in Yorkshire pigs. The value in Landrace pigs was significantly (P < 0.001) higher than that in the other pigs. There was no significant difference between sexes. In general the heart of pigs with HCM was heavier, wider, longer, and thicker than that of clinically normal pigs. Backfat was the only growth trait with a difference (P < 0.05) among pig breeds. The HCM pigs were leaner than normal pigs. Leaner pigs may have a higher risk of HCM. Heritability of HCM was > 0.30 for all three breeds, but the standard errors of these estimates were high because of limited sample size, in particular for the Yorkshire and Duroc breeds. The preliminary results of this study indicate that HCM in pigs is moderately heritable; thus development of a high-HCM incidence line by selection is possible.

Animals↗