Effects of power training on neuromuscular performance and mechanical efficiency

Effects of power training with stretch-shortening cycle (SSC) exercises on mechanical efficiency (ME) were investigated with 9 young women who trained 3 times a week for 4 months. The training included various types of jumping exercises. Before and after the training as well as after the detraining (2 months) the subjects performed 6 different submaximal exercises with a special sledge apparatus. Each exercise involved 60 muscle actions lasting for a total of 3 min per testing condition. The work intensities were determined individually according to the recordings of distance obtained during the single maximal concentric exercises. The training caused the greatest changes of ME in conditions of higher prestretch intensities. The ME values changed from 49.3 ± 12.9% to 55.4 ± 12.1% in pure eccentric exercises and from 39.5 ± 4.6% to 46.1 ± 5.0% in SSC exercises during the training. After the training, the subjects preactivated their leg extensor muscles earlier before the impact, and the eccentric working phase was more powerful, because of higher tendomuscular stiffness. Higher preactivation of the measured muscles, higher flexion of knee and increased dorsiflexion of ankle joints in the beginning of contact caused the increased stiffness, possibly through more powerful reflex activation. At the same time the metabolic demands of muscles decreased, causing the increases of ME.     

The complex G protein-coupled receptor kinase 2 (GRK2) interactome unveils new physiopathological targets

GRK2 is a ubiquitous member of the G protein-coupled receptor kinase (GRK) family that appears to play a central, integrative role in signal transduction cascades. GRKs participate together with arrestins in the regulation of G protein-coupled receptors (GPCR), a family of hundreds of membrane proteins of key physiological and pharmacological importance, by triggering receptor desensitization from G proteins and GPCR internalization, and also by helping assemble macromolecular signalosomes in the receptor environment acting as agonist-regulated adaptor scaffolds, thus contributing to signal propagation. In addition, emerging evidence indicates that GRK2 can phosphorylate a growing number of non-GPCR substrates and associate with a variety of proteins related to signal transduction, thus suggesting that this kinase could also have diverse ‘effector’ functions. We discuss herein the increasing complexity of such GRK2 ‘interactome’, with emphasis on the recently reported roles of this kinase in cell migration and cell cycle progression and on the functional impact of the altered GRK2 levels observed in several relevant cardiovascular, inflammatory or tumour pathologies. Deciphering how the different networks of potential GRK2 functional interactions are orchestrated in a stimulus, cell type or context-specific way is critical to unveil the contribution of GRK2 to basic cellular processes, to understand how alterations in GRK2 levels or functionality may participate in the onset or development of several cardiovascular, tumour or inflammatory diseases, and to assess the feasibility of new therapeutic strategies based on the modulation of the activity, levels or specific interactions of GRK2.     

Molecular markers in oral epithelial dysplasia: review

The clinical and histologic features alone cannot accurately predict whether potentially malignant disorders of the oral mucosa remain stable, regress or progress to malignancy. Some of them, with or without epithelial dysplasia, may transform to invasive oral squamous cell carcinomas (OSCC). Identification of molecular markers which can predict disease progression is necessary to improve the management of these disorders. Many genes and signaling pathways have been shown to be involved in the development of OSCC. This review summarizes some molecular markers researched in the detection of pre-cancer. We highlight selected markers that are reported to be significantly associated with progression of potentially malignant disorders to OSCC. These include alterations in genes/pathways which control cellular signaling, cell cycle, apoptosis, genomic stability, cytoskeleton, angiogenesis, etc. However, these genetic tumor markers have so far not gained any use in routine diagnosis and their utility in the prediction of risk of malignant transformation remains unknown. It is, however, clear from the large number of studies, some described in this review, that multiple genes/pathways are involved in the progression from normal to metaplastic/dysplastic, and subsequently to cancer. It is therefore necessary to study those significant alterations in multiple genes simultaneously in biopsy samples from large cohorts of subjects.     

Glutathione Regeneration in Mammalian Erythrocytes

Glutathione (GSH) regeneration is a process in which cells reduce oxidised glutathione (GSSG) to GSH after exposure of cells to oxidants in the presence of suitable energy source such as glucose. This reaction consists of (1) membrane glucose transport, (2) phosphorylation of glucose by hexokinase (HK) utilising adenosine 5′-triphosphate (ATP), (3) reduction of nicotinamide–adenine dinucleotide phosphate (NADP) to its reduced form (NADPH) by glucose-6-phosphate dehydrogenase (G-6-PD) and 6-phosphogluconate dehydrogenase (6-PGD) and (4) reduction of GSSG to GSH by glutathione reductase (GR) using NADPH. The rate of GSH regeneration is thus dependent on the enzymatic activity and concentration of substrate. G-6-PD deficiency and enzyme inhibitory chemicals reduce GSH regeneration and concentration of substrate greatly influences the rate of GSH regeneration. Not only glucose but also mannose, fructose and galactose may also be used as energy source. Interspecies and intraspecies differences occur in the rate of GSH regeneration. These differences cannot be explained by variations in enzymatic activities. Although physiological relevance of GSH regeneration is still unclear, it is known that erythrocytes from G-6-PD-deficient patients have lowered erythrocyte deformability and shortened erythrocyte life-span. In-vitro experiments show lowered GSH regeneration enforces loss of deformability. These findings suggest that GSH regeneration plays an important role in erythrocyte biology.     

CYCLICAL ABSENTEEISM AMONG PRIVATE SECTOR,PUBLIC SECTOR AND SELF‐EMPLOYED WORKERS

This research note analyzes differences in the number of absent working days and doctor visits and in their cyclicality between private sector, public sector and self‐employed workers. For this purpose, I used large‐scale German survey data for the years 1995 to 2007 to estimate random effects negative binomial (count data) models. The main findings are as follows. (i) Public sector workers have on average more absent working days than private sector and self‐employed workers. Self‐employed workers have fewer absent working days and doctor visits than dependent employed workers. (ii) The regional unemployment rate is on average negatively correlated with the number of absent working days among private and public sector workers as well as among self‐employed men. The correlations between regional unemployment rate and doctor visits are only significantly negative among private sector workers. Copyright © 2012 John Wiley & Sons, Ltd.     

Pre- and postnatal exposure to ambient levels of urban particulate matter (PM2.5) affects mice spermatogenesis

This work characterizes the effects of ambient levels of urban particulate matter (PM_2.5) from the city of Sao Paulo on spermatogenesis using mice exposed during the embryo–fetal and/or postnatal phases of development. Parental generations (BALB/c mice) were exposed to air pollution in chambers with or without filtering PM_2.5 for 4 months. Animals were mated, and half of the 1-day-old offspring were moved between chambers, which yielded prenatal and postnatal groups. Remaining offspring comprised the non-exposed and pre+postnatal exposed groups. After 90 days, the animals were sacrificed for testis collection and weighing. Optical microscopy was used for the morphometric analyses of the cell counts, spermatogenic cycle, proliferation, and apoptosis. Prenatally exposed animals presented reduced body and testicular weight with an increased gonadosomatic index (GSI). Testicular volume also decreased, as well as the tubular diameter in testes of the same animals. Proliferation, apoptosis, and spermatogenic cycle analyses showed no significant differences among groups. However, the tubules at stage VII of pre- and postnatal animals presented a reduced number of elongated spermatids. Pre+postnatal group presented higher spermatid head retention at stages VIII–XII. These results show that ambient levels of PM_2.5 from Sao Paulo city affect spermatogenesis by damaging sperm production.     

Non-hepatic hyperammonaemia: an important,potentially reversible cause of encephalopathy

The clinical syndrome of encephalopathy is most often encountered in the context of decompensated liver disease and the diagnosis is usually clear cut. Non-hepatic causes of encephalopathy are rarer and tend to present to a wide range of medical specialties with variable and episodic symptoms. Delay can result in the development of potentially life threatening complications, such as seizures and coma.
Early recognition is vital. A history of similar episodes or clinical risk factors and early assessment of blood ammonia levels help establish the diagnosis. In addition to adequate supportive care, investigation of the underlying cause of the hyperammonaemia is essential and its reversal, where possible, will often result in complete recovery. Detection of an unborn error of metabolism should lead to the initiation of appropriate maintenance therapy and genetic counselling.


     

Disease severity and viral load are correlated in infants with primary respiratory syncytial virus infection in the community

Respiratory syncytial virus (RSV) is a major cause of respiratory tract infections in infants, with remarkable variability in disease severity. Factors determining severity of disease in previously healthy infants are still unclear. It was hypothesized that disease severity is correlated with viral load in primary RSV infection. Infants of a healthy birth cohort were included at signs of their first respiratory tract infection. Nasopharyngeal aspirate was obtained within 48–96 hr and disease severity was assessed with a previously published severity scoring model. PCR was applied to test the aspirates in a semi‐quantitative way for the presence of 10 respiratory pathogens. In case of multiple infection, the pathogen with the highest load was defined as the primary pathogen. The correlation between disease severity and viral load was analyzed. A total of 82 infants were included over a period of 2 years. Median age at first respiratory tract infection was 3 months. Pathogens were detected in 77 (94%) infants; more than one pathogen was detected in 35 (43%) infants. RSV was present in aspirates of 30 infants; in 16 aspirates RSV was the primary pathogen. A negative correlation between RSV CT‐value and disease severity was found in all RSV cases (ρ = ?0.52, P = 0.003) and in cases with RSV as the primary pathogen (ρ = ?0.54, P = 0.03). In conclusion, this is the first report on viral loads in previously healthy infants with RSV infection in the community. Disease severity correlated positively with viral load during primary RSV infection. J. Med. Virol. 82: 1266–1271, 2010. © 2010 Wiley‐Liss, Inc.