Effect of collisions with a second fluid on the temporal development of nonlinear, single-mode, Rayleigh-Taylor instability.

Goncharov's [Phys. Rev. Lett. 88, 134502 (2002)0031-900710.1103/PhysRevLett.88.134502] nonlinear model of a single-mode Rayleigh-Taylor instability (RTI) is investigated for a partially ionized plasma in a predominantly neutral background. Terminal bubble and spike velocities are derived from the nonlinear equations in the case where the RTI dynamics is dominated by collisions between neutrals and ions. Direct numerical simulations are used to justify the use of Goncharov's model in this regime and observe its limitations.

Cardiac arrhythmia and late-onset muscle weakness caused by a myofibrillar myopathy with unusual histopathological features due to a novel missense mutation in FLNC.

Myofibrillar myopathies (MFM) are mostly adult-onset diseases characterized by progressive morphological alterations of the muscle fibers beginning in the Z-disk and the presence of protein aggregates in the sarcoplasm. They are mostly caused by mutations in different genes that encode Z-disk proteins, including DES, CRYAB, LDB3, MYOT, FLNC and BAG3. A large family of French origin, presenting an autosomal dominant pattern, characterized by cardiac arrhythmia associated to late-onset muscle weakness, was evaluated to clarify clinical, morphological and genetic diagnosis. Muscle weakness began during adult life (over 30 years of age), and had a proximal distribution. Histology showed clear signs of a myofibrillar myopathy, but with unusual, large inclusions. Subsequently, genetic testing was performed in MFM genes available for screening at the time of clinical/histological diagnosis, and desmin (DES), αB-crystallin (CRYAB), myotilin (MYOT) and ZASP (LDB3), were excluded. LMNA gene screening found the p.R296C variant which did not co-segregate with the disease. Genome wide scan revealed linkage to 7q.32, containing the FLNC gene. FLNC direct sequencing revealed a heterozygous c.3646T>A p.Tyr1216Asn change, co-segregating with the disease, in a highly conserved amino acid of the protein. Normal filamin C levels were detected by Western-blot analysis in patient muscle biopsies and expression of the mutant protein in NIH3T3 showed filamin C aggregates. This is an original FLNC mutation in a MFM family with an atypical clinical and histopathological presentation, given the presence of significantly focal lesions and prominent sarcoplasmic masses in muscle biopsies and the constant heart involvement preceding significantly the onset of the myopathy. Though a rare etiology, FLNC gene should not be excluded in early-onset arrhythmia, even in the absence of myopathy, which occurs later in the disease course.

Can we simulate an action that we temporarily cannot perform?

AIMS OF THE STUDY: The scope of individuals' motor repertoire and expertise influences the way they perceive the actions of others. When observing skilled actions, experts recruit the cortical network subserving action perception (action observation network, AON) to a greater extent than non-experts. However, it remains unknown whether and how a temporary motor injury affects activation within the AON. MATERIALS AND METHODS: To investigate this issue, brain hemodynamic activity was recorded twice in thirteen national female gymnasts suffering from a lower extremity injury at the onset of the experiment. The gymnasts were scanned one month after the injury and were shown gymnastics routines they were able and temporarily unable to perform. Six months later, after complete recovery, they were scanned again and shown the same routines they were now able to practice. RESULTS: Results showed: first, that the level of activity within the inferior parietal lobule and MT/V5/EBA (extrastriate body area), areas constitutive of the AON, was independent of the gymnasts' physical condition. Second, when gymnasts were hurt (vs. when recovered), higher activity in the cerebellum was detected. CONCLUSION: The equal contribution of MT/V5/EBA and inferior parietal lobule during the observation of movements the gymnasts were able or unable to practice suggests respectively that physical provisional incapacity does not interfere with the perceptual processing of body shape and motion information, and that motor expertise may prevent the decay of sensorimotor representations. Higher activations in the cerebellum may suggest that this structure plays a role in dissociating perceived physically feasible movements from those that are provisionally unfeasible.

Self-regulation of inter-hemispheric visual cortex balance through real-time fMRI neurofeedback training.

Recent advances in neurofeedback based on real-time functional magnetic resonance imaging (fMRI) allow for learning to control spatially localized brain activity in the range of millimeters across the entire brain. Real-time fMRI neurofeedback studies have demonstrated the feasibility of self-regulating activation in specific areas that are involved in a variety of functions, such as perception, motor control, language, and emotional processing. In most of these previous studies, participants trained to control activity within one region of interest (ROI). In the present study, we extended the neurofeedback approach by now training healthy participants to control the interhemispheric balance between their left and right visual cortices. This was accomplished by providing feedback based on the difference in activity between a target visual ROI and the corresponding homologue region in the opposite hemisphere. Eight out of 14 participants learned to control the differential feedback signal over the course of 3 neurofeedback training sessions spread over 3 days, i.e., they produced consistent increases in the visual target ROI relative to the opposite visual cortex. Those who learned to control the differential feedback signal were subsequently also able to exert that control in the absence of neurofeedback. Such learning to voluntarily control the balance between cortical areas of the two hemispheres might offer promising rehabilitation approaches for neurological or psychiatric conditions associated with pathological asymmetries in brain activity patterns, such as hemispatial neglect, dyslexia, or mood disorders.

Cyclic stretch reveals a mechanical role for intermediate filaments in a desminopathic cell model.

Mechanics is now recognized as crucial in cell function. To date, the mechanical properties of cells have been inferred from experiments which investigate the roles of actin and microtubules ignoring the intermediate filaments (IFs) contribution. Here, we analyse myoblasts behaviour in the context of myofibrillar myopathy resulting from p.D399Y desmin mutation which disorganizes the desmin IF network in muscle cells. We compare the response of myoblasts expressing either mutated or wild-type desmin to cyclic stretch. Cells are cultivated on supports submitted to periodic uniaxial stretch of 20% elongation amplitude and 0.3 Hz frequency. We show that during stretching cycles, cells expressing mutated desmin reduce their mean amplitude both for the elongation and spreading area compared to those expressing wild-type desmin. Even more unexpected, the reorientation angles are altered in the presence of p.D399Y desmin. Yet, at rest, the whole set of those parameters are similar for the two cell populations. Thus, we demonstrate that IFs affect the mechanical properties and the dynamics of cell reorientation. Since these processes are known due to actin cytoskeleton, these results suggest the IFs implication in mechanics signal transduction. Further studies may lead to better understanding of their contribution to this process.

Similarities and differences in perceiving threat from dynamic faces and bodies. An fMRI study.

Neuroscientific research on the perception of emotional signals has mainly focused on how the brain processes threat signals from photographs of facial expressions. Much less is known about body postures or about the processing of dynamic images. We undertook a systematic comparison of the neurofunctional network dedicated to processing facial and bodily expressions. Two functional magnetic resonance imaging (fMRI) experiments investigated whether areas involved in processing social signals are activated differently by threatening signals (fear and anger) from facial or bodily expressions. The amygdala (AMG) was more active for facial than for bodily expressions. Body stimuli triggered higher activation than face stimuli in a number of areas. These were the cuneus, fusiform gyrus (FG), extrastriate body area (EBA), temporoparietal junction (TPJ), superior parietal lobule (SPL), primary somatosensory cortex (SI), as well as the thalamus. Emotion-specific effects were found in TPJ and FG for bodies and faces alike. EBA and superior temporal sulcus (STS) were more activated by threatening bodies.

Perceiving fear in dynamic body expressions.

Characteristic fear behaviour like putting the hands in front of the face and running for cover provides strong fear signals to observers who may not themselves be aware of any danger. Using event-related functional magnetic resonance imaging (fMRI) in humans, we investigated how such dynamic fear signals from the whole body are perceived. A factorial design allowed us to investigate brain activity induced by viewing bodies, bodily expressions of fear and the role of dynamic information in viewing them. Our critical findings are threefold. We find that viewing neutral and fearful body expressions enhances amygdala activity; moreover actions expressing fear activate the temporal pole and lateral orbital cortex more than neutral actions; and finally differences in activations between static and dynamic bodily expressions were larger for actions expressing fear in the STS and premotor cortex compared to neutral actions.

The serpin protease nexin-1 regulates vascular smooth muscle cell adhesion, spreading, migration and response to thrombin.

BACKGROUND: Protease nexin-1 (PN-1) is an important physiological regulator of thrombin in the brain. PN-1 is also present in aortic smooth muscle cells and may thus participate in vascular biology. However, little is known about its function in the vessel wall. OBJECTIVES: In this study, we investigated the effect of PN-1 overexpression in smooth muscle cells (SMCs), on their sensitivity to thrombin, and their capacity for adhesion, spreading and migration. RESULTS: Two clones exhibiting a two- to threefold increase in PN-1 expression were selected and compared with untransfected and mock-transfected cells. Overexpression of PN-1 was observed to inhibit thrombin-induced cell responses as indicated by a twofold decrease in induction of PAI-1 expression, a decreased calcium mobilization in response to low thrombin concentrations and a twofold increase in the capacity to inhibit thrombin catalytic activity. Overexpression of PN-1 did not modify adhesion, spreading, and migration of SMCs on type I collagen. In contrast, SMCs overexpressing PN-1 exhibited a 40% reduction in adhesion, a 50% reduction in spreading and a complete absence of migration on vitronectin when compared with control SMCs. CONCLUSIONS: Our studies thus reveal that PN-1 is likely to play a critical role in regulating essential cell functions such as (i) thrombin-induced responses, which are dependent on its antiprotease activity, and (ii) adhesion, spreading, and migration, which are independent of its antiprotease activity and may be related to its interaction with other partners, such as vitronectin in the present case.

[Post-radiotherapy cutaneous neuro-endocrine carcinoma]. / Carcinome neuro-endocrine cutané en zone irradiée.

INTRODUCTION: Merkel cell carcinoma or cutaneous neuroendocrine carcinoma is an uncommon severe disease. The carcinogenic effect of ionizing radiations has been suspected in exceptional observations. We report the sixth case of Merkel cell neuroendocrine carcinoma in a patient with prior radiotherapy. CASE REPORT: An 86-year-old man underwent radiotherapy for a basal cell carcinoma of the tip of the nose and developed a highly aggressive Merkel cell carcinoma at the same location 6 years later. DISCUSSION: The development of Merkel cell carcinoma on irradiated tissue accounts for 2.6 p. 100 of the 227 publications where dermatological history was reported. This percentage may be underestimated. The similar localizations of the irradiated zone and the site of cancer development 5 years later suggest that the Merkell cell carcinoma may be a radio-induced tumor. The delay may vary from 5 to 47 years. The similarity of the carcinogenic factors involved in Merkel cell carcinoma and squamous cell or basal cell carcinomas (ultraviolet, ionizing irradiation) and the frequent association of different types favor an epidermal origin for Merkel cell carcinoma. In clinical practice, past history of radiotherapy in an area where Merkell cell carcinoma develops indicates that therapeutic management must exclude post-operative radiotherapy.