Serotonin has a multifunctional role in many different organs serving either as a neurotransmitter in the central nervous system or a paracrine factor in the gastrointestinal tract. Over 90% of serotonin is synthesised in the enterochromaffin cells of the intestine and subsequently taken up by platelets. The involvement of platelet-derived serotonin in liver mass restoration after partial hepatectomy or toxic injury has been greatly investigated during the last decade. There is a growing body of evidence implicating serotonin in hepatic regeneration through altered expression of serotonin receptor subtypes in the liver. This review article provides a brief overview on the current knowledge about the actions of serotonin in liver regeneration.

This study aimed to investigate the effect of 3 different eccentric-only power training volumes on muscle fiber type composition and power performance. Twenty-nine females were assigned into 3 groups and performed 10 weeks of either 3 (low volume), 6 (moderate volume), or 9 (high volume) sets/session of 4 fast-velocity eccentric-only half-squats against 70% of concentric 1-repetition maximum (1RM), followed by 3 maximum countermovement jumps (CMJs) after each set. Half-squat 1RM, CMJ height/power, maximum isometric force, rate of force development (RFD) and muscle fiber cross-sectional area (CSA) were increased in all groups (p = 0.001). Low-volume training induced higher increases in CMJ height/power and early RFD, compared with the moderate- and high-volume training programs (p < 0.001). Significant reductions in type IIx muscle fiber percentages and %CSAs were found after moderate- and high-volume training, with concomitant increases in type IIa fibers (p = 0.001). Significant correlations were found between the changes in type IIa and type IIx percentages, fiber CSA, %CSA, and the changes in performance (r: –0.787 to 0.792; p < 0.05). These results suggest that relatively large eccentric power training volumes may result in detrimental neuromuscular adaptations, minimal changes in early RFD, and a reduction of type IIx muscle fiber percentage. Novelty Low but not high volume of power training maintains type IIx muscle fibers. Early rate of force development increases after a low- or moderate-power training volume, but not after a high-power training volume. Training-induced changes in type IIx muscle fiber percentage is related with changes in early rate of force development.

The aim of the study was to evaluate power performance and muscle morphology adaptations in response to 5 weeks of fast-eccentric squat training (FEST) performed twice per week, with three different training volumes. Twenty-five moderately trained females were assigned into three groups performing eight repetitions of FEST of either four sets (4 × 8 group; N = 9), 6 sets (6 × 8 group; N = 8) or eight sets (8 × 8 group, N = 8). Before and after the intervention, countermovement jumping height (CMJh) and power (CMJp), half squat maximal strength (1-RM), quadriceps cross-sectional area (QCSA) and vastus lateralis (VL) architecture and fiber type composition were evaluated. Significant increases (p < 0.05) were found for all groups, with no differences among them in 1-RM (4 × 8: 14.8 ± 8.2%, 6 × 8: 13.1 ± 9.2% and 8 × 8: 21.6 ± 7.0%), CMJh (4 × 8: 12.5 ± 8.5%, 6 × 8: 11.3 ± 9.3% and 8 × 8: 7.0 ± 6.2%), CMJp (4 × 8: 9.1 ± 6.0%, 6 × 8: 7.1 ± 5.2% and 8 × 8: 5.0 ± 3.9%) and QCSA (4 × 8: 7.7 ± 4.7%, 6 × 8: 9.0 ± 6.8% and 8 × 8: 8.2 ± 6.5%). Muscle fiber type distribution remained unaltered after training in all groups. VL fascicle length increased and fascicle angle decreased only in 6 × 8 and 8 × 8 groups. In conclusion, four sets of eight fast-eccentric squats/week increase lower body power and strength performance and maintain type IIX muscle fibers after 5 weeks, at least in moderately trained females.

Congenital myopathies (CMs) constitute a group of heterogenous rare inherited muscle diseases with different incidences. They are traditionally grouped based on characteristic histopathological findings revealed on muscle biopsy. In recent decades, the ever-increasing application of modern genetic technologies has not just improved our understanding of their pathophysiology, but also expanded their phenotypic spectrum and contributed to a more genetically based approach for their classification. Later onset forms of CMs are increasingly recognised. They are often considered milder with slower progression, variable clinical presentations and different modes of inheritance. We reviewed the key features and genetic basis of late onset CMs with a special emphasis on those forms that may first manifest in adulthood.

Objective: Mutations in the prion‐like domain of RNA binding proteins cause dysfunctional stress responses and associated aggregate pathology in patients with neurogenic and myopathic phenotypes. Recently, mutations in ANXA11 have been reported in patients with amyotrophic lateral sclerosis and multisystem proteinopathy. Here we studied families with an autosomal dominant muscle disease caused by ANXA11:c.118G > T;p.D40Y.Methods: We performed deep phenotyping and exome sequencing of patients from four large Greek families, including seven affected individuals with progressive muscle disease but no family history of multi‐organ involvement or ALS.Results: In our study, all patients presented with an autosomal dominant muscular dystrophy without any Paget disease of bone nor signs of frontotemporal dementia or Parkinson's disease. Histopathological analysis showed rimmed vacuoles with annexin A11 accumulations. Electron microscopy analysis showed myofibrillar abnormalities with disorganization of the sarcomeric structure and Z‐disc dissolution, and subsarcolemmal autophagic material with myeloid formations. Molecular genetic analysis revealed ANXA11:c.118G > T;p.D40Y segregating with the phenotype.Interpretation: Although the pathogenic mechanisms associated with p.D40Y mutation in the prion‐like domain of Annexin A11 need to be further clarified, our study provides robust and clear genetic evidence to support the expansion of the phenotypic spectrum of ANXA11.