Role of amyloid ß in the induction of lipolysis and secretion of adipokines from human adipose tissue.

Amyloid-ß (Aß) peptide, which is generated from proteolytic cleavage of amyloid precursor protein (APP), is a key molecule involved in the pathology of Alzheimer disease. Both APP and Aß peptides are expressed in adipose tissue, however it is currently unclear whether Aß can affect the key functions of adipose tissue. We aimed to explore whether Aß affected lipolysis and adipokine secretion in cultured human adipose tissue. We found that Aß25-35, which contains the main functional domain of the Aß, stimulated lipolysis via PKA and ERK1/2-dependent pathways and that Aß25-35 induced leptin and IL-6 secretion. It is concluded that Aß peptide exerts functional effects on adipose tissue that may lead to increased release of free fatty acids and pro-inflammatory adipokines.

Human adipose tissue conditioned media from lean subjects is protective against H2O2 induced neurotoxicity in human SH-SY5Y neuronal cells.

Adipose tissue secretes numerous hormone-like factors, which are known as adipokines. Adipokine receptors have been identified in the central nervous system but the potential role of adipokine signaling in neuroprotection is unclear. The aim of this study is to determine (1) Whether adipokines secreted from cultured adipose tissue of lean humans is protective against oxidative stress-induced neurotoxicity in human SH-SY5Y neuronal cells; and (2) To explore potential signaling pathways involved in these processes. Adipose tissue conditioned media (ATCM) from healthy lean subjects completely prevented H2O2 induced neurotoxicity, while this effect is lost after heating ATCM. ATCM activated the phosphorylation of ERK1/2, JNK and Akt at serine 308 in SH-SY5Y cells. PD98059 (25 µM), SP600125 (5 µM) and LY29400 (20 µM) partially blocked the protective effects of ATCM against H2O2 induced neurotoxicity. Findings demonstrate that heat-sensitive factors secreted from human adipose tissue of lean subjects are protective against H2O2 induced neurotoxicity and ERK1/2, JNK, and PI3K signaling pathways are involved in these processes. In conclusion, this study demonstrates preliminary but encouraging data to further support that adipose tissue secreted factors from lean human subjects might possess neuroprotective properties and unravel the specific roles of ERK1/2, JNK and PI3K in these processes.

Revisiting the "10% rule" in breast cancer sentinel lymph node biopsy: an approach to minimize the number of sentinel lymph nodes removed.

BACKGROUND: Sentinel lymph node (SLN) biopsy (SLNB) is an accurate and proven axillary staging procedure for early breast cancer. The aim of this study was to determine if the "10% rule" is applicable to the performance of SLNB at the investigators' institution and if the criteria used for SLNB at their institution could be refined to minimize the number of SLNs removed. METHODS: Retrospective analysis was conducted of a prospectively collected breast cancer SLNB database. Standard statistical methods were used for data analysis. RESULTS: Five hundred nine patients underwent a SLNB for breast cancer over a 5 year period. A mean of 2.5 SLNs were removed per patient. All patients with SLN metastasis were identified within the 1st 4 SLNs removed. CONCLUSIONS: The "10% rule" is best used as a guide at the investigators' institution. Strict adherence to this rule appears to result in the removal of an excessive number of lymph nodes, which may contribute to excessive health care costs and patient morbidity.