Anomalous muscle bundles are common in hypertrophic obstructive cardiomyopathy, and they may lead to middle-apical obstruction. Surgical myectomy provides excellent clinical outcomes with low risk for sufficient relief of obstruction and radical correction of intraventricular anomalies in patients with hypertrophic obstructive cardiomyopathy.

The effects of different lipids on tissue fatty acid profile and reproductive performance in female rice field eel were investigated in this study. Virgin female eels were fed with six diets containing different lipids (diets FO, LO, SO, PO and PL with fish oil, linseed oil, soybean oil, peanut oil and pork lard, respectively; diet APO with arachidonic acid and peanut oil). The results showed that there were positive correlations between the contents of 18:2n-6, 18:3n-3, arachidonic acid (ARA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in the tissues of eels and those of the corresponding fatty acids in their diets. The specific growth rate of eels fed with diet PO was the lowest and significantly lower than that of FO and SO. Gonad of eels fed with diets PO and PL showed hypogonadism. The long chain polyunsaturated fatty acids (LC-PUFA) can be synthesized by eels, but the quantity was not enough to meet their reproduction requirement completely. The fatty acid desaturation, rather than elongation probably was one of the limiting factors. Addition of proper amount of ARA in diet was favorable to the increase of the hatching rate of fertilized eggs, while EPA and DHA in diet were beneficial to the increase of the survival rate of larva. Both n-3PUFA and a suitable n-6/n-3PUFA ratio were necessary for growth and reproduction of eels.

Hypertrophic cardiomyopathy (HCM) represents one of the most common heritable heart diseases. However, the signalling pathways and regulatory networks underlying the pathogenesis of HCM remain largely unknown. Here, we present a strand-specific RNA-seq dataset for both coding and lncRNA profiling in myocardial tissues from 28 HCM patients and 9 healthy donors. This dataset constitutes a valuable resource for the community to examine the dysregulated coding and lncRNA genes in HCM versus normal conditions.

BackgroundFilamin C (FLNC) mutation was reported as a cause of HCM, with a high probability of sudden cardiac death. However, the mutation profile of FLNC, and its relationship with phenotypic expression in HCM, remains to be elucidated.MethodsIn this study, FLNC gene was sequenced in 540 HCM patients and 307 healthy controls.ResultsWe found that 39 (7.2%) patients carried FLNC mutations, with a similar frequency to that of controls (4.2%, p = 0.101). Pedigree analysis showed that mutations were not well segregated with HCM. The baseline characteristics between HCM patients, with and without mutations, were comparable. FLNC mutations did not increase the risk for either all‐cause mortality (HR 0.746, 95% CI 0.222–2.295, p = 0.575) or cardiac mortality (HR 0.615, 95% CI 0.153–1.947, p = 0.354) in HCM patients during a follow‐up of 4.7 ± 3.2 years. Moreover, there was no significant difference in survival free from sudden cardiac arrest (HR 0.721, 95% CI 0.128–3.667, p = 0.660) and heart failure (HR 0.757, 95% CI 0.318–1.642, p = 0.447).Conclusions FLNC mutations were common in both HCM patients and healthy population. The pathogenicity of FLNC mutations detected in HCM patients and its association with the clinical outcomes should be cautiously interpreted.