Restoring the Fact/Law Distinction in Patent Claim Construction

Two decades ago, the Supreme Court sought to promote more effective, transparent patent litigation in Markman v. Westview Instruments by ruling that “the construction of a patent, including terms of art within its claim, is exclusively within the province of the court.” In so doing, the Court removed interpretation of patent claims from the black box of jury deliberations by holding that the Seventh Amendment right to a jury trial did not extend to patent claim construction. Failing to find clear historical evidence of how claim construction was handled in 1791, the Court turned to “the relative interpretive skills of judges and juries and the statutory policies that ought to be furthered by the allocation.” It concluded that federal district court judges were better equipped than juries to resolve the mixed fact/law controversies inherent in construing disputed patent claim terms, thereby leading to more effective and transparent patent litigation. Fully achieving the Court’s goal of more effective and transparent patent litigation, however, depends on district judges having the flexibility to learn pertinent facts, build a reviewable record, and explain the basis for their claim constructions

Hyperactivation of protein kinase B and ERK have discrete effects on survival, proliferation, and cytokine expression in Nf1-deficient myeloid cells

AbstractThe Nf1 tumor suppressor encodes a GTPase-activating protein for Ras. Previous work has implicated hyperactive Ras in the aberrant growth of Nf1-deficient cells; however, there are limited data on which effectors modulate specific phenotypes. To address this, we generated myeloid cell lines by infecting fetal liver cells with a retrovirus encoding a truncated allele of c-Myb. Granulocyte-macrophage colony stimulating factor (GM-CSF) promoted the survival of wild-type Myb cells in a dose-dependent manner. By contrast, Nf1-deficient myeloid cells deprived of growth factors, were resistant to apoptosis due to hyperactivation of the phosphoinositide-3-OH kinase/protein kinase B cascade. Nf1−/− cells also demonstrated growth factor-independent proliferation and upregulation of GM-CSF mRNA production that were dependent upon Raf/MEK/ERK signaling. These data link specific Ras effectors with discrete cellular phenotypes in Nf1-deficient cells