Search bioRxiv⌕ Search

Biology subjects

Hora, M.

Publications and source records attributed to Hora, M..

2 recordsLinked to original sources

Influence of upper limb training and analyzed muscles on estimate of physical activity during cereal grinding using saddle quern and rotary quern

Experimental grinding has been used to study the relationship between human humeral robusticity and cereal grinding in the early Holocene. However, such replication studies raise two questions regarding the robusticity of the results: whether female nonathletes used in previous research are sufficiently comparable to early agricultural females, and whether previous analysis of muscle activation of only four upper limb muscles is sufficient to capture the stress of cereal grinding on upper limb bones. We test the influence of both of these factors. Electromyographic activity of eight upper limb muscles was recorded during cereal grinding in an athletic sample of 10 female rowers and a nonathletic sample of 25 females and analyzed using both an eight- and four-muscle model. Athletes had lower activation than nonathletes in the majority of measured muscles, but most of these differences were non-significant. Furthermore, both athletes and nonathletes had lower muscle activation during saddle quern grinding than rotary quern grinding suggesting that the nonathletic sample can be used to model early agricultural females during saddle and rotary quern grinding. Similarly, in both eight- and four-muscle models, upper limb loading was lower during saddle quern grinding than during rotary quern grinding, suggesting that the upper limb muscles may be reduced to the previously used four-muscle model for evaluation of the upper limb loading during cereal grinding. Another implication of our measurements is to question the assumption that skeletal indicators of high involvement of the biceps brachii muscle can be interpreted as specifically indicative of saddle quern grinding.

physiology↗

Cysteine oxidation triggers amyloid fibril formation of the tumor suppressor p16INK4A

Accumulation of the CDK4/6 inhibitor p16INK4A in response to oncogenic transformation leads to cell cycle arrest and senescence and is therefore frequently lost in cancer. p16INK4A is also known to accumulate under conditions of oxidative stress and thus could potentially be regulated by the reversible oxidation of cysteines (redox signaling). Indeed, oxidation of the single cysteine in p16INK4A in human cells occurs under relatively mild oxidizing conditions and leads to disulfide-dependent dimerization. p16INK4A is an all alpha-helical protein, but here we report that upon cysteine-dependent dimerization, p16INK4A undergoes a dramatic structural rearrangement and forms aggregates that have the typical features of amyloid fibrils, including binding of diagnostic dyes, presence of cross-{beta} sheet structure, and typical dimensions found in electron microscopy. p16INK4A amyloid formation abolishes its function as a CDK4/6 inhibitor. Collectively, these observations mechanistically link the cellular redox state to the inactivation of p16INK4A through the formation of amyloid fibrils.

biochemistry↗