341) Pathological lesions together with molecular genetics and serological results |
342) ion of sleep homeostasis and describe the molecular genetics techniques that are use |
343) Traditional anticoagulants, such as low-molecular-weight heparin and vitamin K ant |
344) ies, taurocholic acid (TA)-conjugated low-molecular-weight heparin derivative (LHT7) |
345) lcium channel-mediated Ca(2+) influx, the molecular identification of the calcium ch |
346) h between these species do not complement molecular identification through DNA barco |
347) Molecular knowledge has deeply affected th |
348) te recent advances in the biochemical and molecular knowledge of these diseases, no |
349) It displayed a molecular mass of 29-kDa in both gel filtr |
350) The molecular mass was estimated to be 58 kD b |
351) was to evaluate the midgut damage and its molecular mechanisms, and the protective r |
352) therapy of TBI and explore its potential molecular mechanisms, therefore providing |
353) ke other variants of liposarcoma, lacks a molecular or genetic signature. |
354) Notably, molecular or pharmacologic inhibition of t |
355) upon exposing the dehydrated substance to molecular oxygen. |
356) cted to dry conditions in the presence of molecular oxygen. |
357) ata for reconstructing and addressing new molecular perspectives for balitorid phylo |
358) ata for reconstructing and addressing new molecular perspectives for balitorid phylo |
359) ith previous findings, support the use of molecular phenotypic over morphologic pre- |
360) Calcium and vitamin D modify the molecular phenotypic profiles of colon cry |
361) ly studied with the availability of large molecular phylogenies and comparative data |
362) ion as to how well anatomical data mirror molecular phylogenies and how best to deal |
363) ploited near-infrared fluorescence (NIRF) molecular probes injected locally at the i |
364) Taken together, these NIRF molecular probes represent a useful tool t |
365) oglia, and inflammatory microglia and the molecular profiles that are associated wit |
366) that cause their distinct functional and molecular profiles. |
367) determined virulence-associated genes and molecular subtype changes of the surviving |
368) mimicked that found in basal/claudin-low molecular subtype within the triple negati |
369) However, recent progress in CRC molecular therapies may provide new insigh |
370) inical development of small molecules and molecular therapies. |
371) cribes facets of this phenomenon, but its molecular underpinnings are incompletely c |
372) and transcriptomic studies argue that the molecular underpinnings of the disease are |
373) effect of various polymer concentrations, molecular weights (Mws) and drug loads on |
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