Absence of Stress-Induced Anisotropy During Brittle Deformation in Antigorite Serpentinite

Knowledge of the seismological signature of serpentinites during deformation is fundamental for interpreting seismic observations in subduction zones, but this has yet to be experimentally constrained. We measured compressional and shear wave velocities during brittle deformation in polycrystalline antigorite, at room temperature and varying confining pressures up to 150 MPa. Ultrasonic velocity measurements, at varying directions to the compression axis, were combined with mechanical measurements of axial and volumetric strain, during direct loading and cyclic loading triaxial deformation tests. An additional deformation experiment was conducted on a specimen of Westerly granite for comparison. At all confining pressures, brittle deformation in antigorite is associated with a spectacular absence of stress‐induced anisotropy and with no noticeable dependence of wave velocities on axial compressive stress, prior to rock failure. The strength of antigorite samples is comparable to that of granite, but the mechanical behavior is elastic up to high stress ( urn:x-wiley:jgrb:media:jgrb53171:jgrb53171-math-0001 of rock strength) and nondilatant. Microcracking is only observed in antigorite specimens taken to failure and not in those loaded even at 90–95% of their compressive strength. Microcrack damage is extremely localized near the fault and consists of shear microcracks that form exclusively along the cleavage plane of antigorite crystals. Our observations demonstrate that brittle deformation in antigorite occurs entirely by “mode II” shear microcracking. This is all the more remarkable than the preexisting microcrack population in antigorite, is comparable to that in granite. The mechanical behavior and seismic signature of antigorite brittle deformation thus appears to be unique within crystalline rocks

Envenomation by Micrurus coral snakes in the Brazilian Amazon region: report of two cases

Two cases of proven coral snake bites were reported in Belém, Pará State, Brazil. The first case was a severe one caused by Micrurus surinamensis. The patient required mechanical ventilation due to acute respiratory failure. The second case showed just mild signs of envenomation caused by Micrurus filiformis. Both patients received specific Micrurus antivenom and were discharged without further complications. Coral snake bites are scarcely reported in the Amazon region and there is a broad spectrum of clinical manifestations, varying from extremely mild to those which may rapidly lead to death if the patient is not treated as soon as possible

Forelimb posture in dinosaurs and the evolution of the avian flapping flight-stroke

Ontogenetic and behavioral studies using birds currently do not document the early evolution of flight because birds (including juveniles) used in such studies employ forelimb oscillation frequencies over 10 Hz, forelimb stroke-angles in excess of 130°, and possess uniquely avian flight musculatures. Living birds are an advanced morphological stage in the development of flapping flight. To gain insight into the early stages of flight evolution (i.e., prebird), in the absence of a living analogue, a new approach using Strouhal number inline image was used. Strouhal number is a nondimensional number that describes the relationship between wing-stroke amplitude (A), wing-beat frequency (f), and flight speed (U). Calculations indicated that even moderate wing movements are enough to generate rudimentary thrust and that a propulsive flapping flight-stroke could have evolved via gradual incremental changes in wing movement and wing morphology. More fundamental to the origin of the avian flapping flight-stroke is the question of how a symmetrical forelimb posture—required for gliding and flapping flight—evolved from an alternating forelimb motion, evident in all extant bipeds when running except birds

Mutations in myosin heavy chain 11 cause a syndrome associating thoracic aortic aneurysm/aortic dissection and patent ductus arteriosus.

We have recently described two kindreds presenting thoracic aortic aneurysm and/or aortic dissection (TAAD) and patent ductus arteriosus (PDA)1, 2 and mapped the disease locus to 16p12.2-p13.13 (ref. 3). We now demonstrate that the disease is caused by mutations in the MYH11 gene affecting the C-terminal coiled-coil region of the smooth muscle myosin heavy chain, a specific contractile protein of smooth muscle cells (SMC). All individuals bearing the heterozygous mutations, even if asymptomatic, showed marked aortic stiffness. Examination of pathological aortas showed large areas of medial degeneration with very low SMC content. Abnormal immunological recognition of SM-MHC and the colocalization of wild-type and mutant rod proteins in SMC, in conjunction with differences in their coimmunoprecipitation capacities, strongly suggest a dominant-negative effect. Human MYH11 gene mutations provide the first example of a direct change in a specific SMC protein leading to an inherited arterial disease