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Parent teacher association

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Akbar Shashkov
Akbar Shashkov

FULL Maya 2017 Activation

Available for Maya 2018Viewport 2.0 fully supported in Maya 2018Fixes:-------* Fixed breaks upon impact doesnt behave correctly with impact massive objects* Fixed transition anim dynamics bodies doesnt adquire momentum sometimes* Fixed initial spin dependance on body/fbody mass* Fixed switching a fracture body static ON/OFF makes it to ignore its velocity parameters* Fixed switching a rigid body static ON/OFF in frame diferent than 0 reset its initial position* Fixed baking keys fails when cache mode is disabled and start frame diferent than 0* Fixed unbreakable activation at frame fractures moves in advance sometimes* Fixed Maya crash when trying to create a fracture body from jaggy fragments

FULL Maya 2017 Activation

08/05/2017This update features a number of fixes of previous version.Fixes:--------* rigid bodies are now deleted when deleting the fracture body they belong to* Fixed "activation at frame" option doesnt adquire momentum* Fixed Fracture bodies shows thick wires in VP2* Fixed shatter points doesnt match the object transform in frame diferent than 0 for animated objects* Fixed break treshold for relative to mass option was set incorrectly in Maya* Fixed selected pdi primitives arent displayed after scrubbing the time line in Maya legacy viewport* Fixed animated objects doesnt reshatter correctly in frame diferent than start frame* Fixed fracture body ability to spin is blocked if changing mass when the object is broken* Fixed shatterit crash for meshes made of diferent parts sometimes* Fixed plugin crash when displaying pdi primitives in directx mode* Fixed jagginess is badly applied to round geometry sometimes

The concept that antioxidants can protect cells and organs against oxidative stress has been established in numerous basic and clinical studies [1]. Nevertheless, nowadays, it has become evident that antioxidants of low molecular weight cannot protect the living organism against continuous stress and sometimes can even be deleterious [2]. Oxidants (electrophiles), on the other hand, were recently shown to be compounds capable of inducing cellular-protecting enzymes such as the phase II enzymes when provided in moderate concentrations. One of the basic factors activated when an electrophile is present is the transcription factor nuclear factor (erythroid-derived 2)-like 2, an NF-E2-related factor 2 (Nrf2), which is responsible for the induction of a variety of cytoprotective genes [3]. Regulated by the Keap1 metalloprotein, Nrf2 is capable of inducing a large number of genes encoding antioxidant enzymes and genes enabling homeostasis and controlling processes involved in the pathology of many diseases (e.g., immune and inflammatory responses, tissue remodeling and fibrosis, carcinogenesis, and metastasis) [4, 5]. Nrf2 plays a vital and crucial role in the maintenance of skin homeostasis and repair and regeneration in various disease states of the skin [6]. However, acute and chronic Nrf2 activation in a healthy epidermis resulted in a negative effect on skin integrity [6]. Endogenous Nrf2 has the ability to protect skin against UV irradiation [6]. Nrf2 is also capable of decreasing symptoms of skin photoaging (e.g., wrinkle formation, loss of skin flexibility) [6]. The pharmacological activation of Nrf2 was proven to provide protection against various toxic compounds responsible for a reduction in skin toxicity [6]. The role of Nrf2 in the prevention of skin carcinogenesis has been demonstrated in various research models [6]. Nrf2 is a key element in the prevention of chemically induced tumor formation and promotion [6]. Moreover, Nrf2 activation reduced solar-simulated UV radiation tumor formation in hairless mice [6]. Nrf2 also demonstrated its essentiality in the healing process of full-thickness wounds and in the recovery and repair of an epidermal barrier defect [6]. There are compelling evidences demonstrating Nrf2 activation as a promising strategy for the treatment of atopic dermatitis, psoriasis, and epidermal blistering diseases (e.g., Hailey-Hailey disease) [6]. Nrf2 activation in vitiligo vulgaris pigment disorder was investigated as a potential strategy to prevent the development of the disorder and treatment [6]. It was also suggested that activation of Nrf2 is important for the treatment of patients suffering from allergic skin inflammation (e.g., allergic contact dermatitis) [6].


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