Evidence for a novel neuronal mechanism driving Alzheimer's disease, upstream of amyloid.

This perspective offers an alternative to the amyloid hypothesis in the etiology of Alzheimer's disease (AD). We review evidence for a novel signaling mechanism based on a little-known peptide, T14. T14 could drive neurodegeneration as an aberrantly activated process of plasticity selective to interconnecting subcortical nuclei, the isodendritic core, where cell loss starts at the pre-symptomatic stages of the disease.

Catalytic activity of the Bin3/MEPCE methyltransferase domain is dispensable for 7SK snRNP function in .

Methylphosphate Capping Enzyme (MEPCE) monomethylates the gamma phosphate at the 5' end of the 7SK noncoding RNA, a modification thought to protect 7SK from degradation. 7SK serves as a scaffold for assembly of a snRNP complex that inhibits transcription by sequestering the positive elongation factor P-TEFb. While much is known about the biochemical activity of MEPCE , little is known about its functions , or what roles- if any-there are for regions outside the conserved methyltransferase domain.

Complete response to temozolomide in chronic lymphocytic leukemia.

We report a case of incidentally diagnosed chronic lymphocytic leukemia (CLL) in a patient with glioblastoma, which responded completely following standard treatment of the glioblastoma with temozolomide and cranial irradiation. The patient remained without an evidence of CLL until his death from recurrent glioblastoma. Further study of temozolomide for the treatment of CLL is indicated.

Zoledronic acid for neonatal subcutaneous fat necrosis.

Subcutaneous fat necrosis (SFN) in infants producing severe hypercalcemia is a life-threatening emergency. Pathophysiology may include enhanced gastrointestinal calcium absorption and bone resorption. We treated an infant with SFN and serum calcium of 15 mg/dL with prednisolone and low-dose zoledronic acid.

Biolayer interferometry of lipid nanodisc-reconstituted yeast vacuolar H -ATPase.

Vacuolar H -ATPase (V-ATPase) is a large, multisubunit membrane protein complex responsible for the acidification of subcellular compartments and the extracellular space. V-ATPase activity is regulated by reversible disassembly, resulting in cytosolic V -ATPase and membrane-integral V proton channel sectors. Reversible disassembly is accompanied by transient interaction with cellular factors and assembly chaperones.

Early endothelial damage detected by circulating particles in baboons fed a diet high in simple carbohydrates in conjunction with saturated or unsaturated fat.

Studies have shown that high-fat diets cause blood vessel damage, however, assessing pathological effects accurately and efficiently is difficult. In this study, we measured particle levels of static endothelium (CD31+ and CD105+) and activated endothelium (CD62E+, CD54+ and CD106+) in plasma. We determined individual responses to two dietary regimens in two groups of baboons.

Long descending cervical propriospinal neurons differ from thoracic propriospinal neurons in response to low thoracic spinal injury.

Background: Propriospinal neurons, with axonal projections intrinsic to the spinal cord, have shown a greater regenerative response than supraspinal neurons after axotomy due to spinal cord injury (SCI). Our previous work focused on the response of axotomized short thoracic propriospinal (TPS) neurons following a low thoracic SCI (T9 spinal transection or moderate spinal contusion injury) in the rat. The present investigation analyzes the intrinsic response of cervical propriospinal neurons having long descending axons which project into the lumbosacral enlargement, long descending propriospinal tract (LDPT) axons.