The nucleation and growth of Pt atomic layer deposition (ALD) on Al 2 O 3 substrates was studied using (methylcyclopentadienyl)-trimethyl platinum (MeCpPtMe 3 ) and O 2 plasma as the reactants. The nucleation of Pt ALD was examined on Al 2 O 3 ALD substrates at 300 C using a variety of techniques including spectroscopic ellipsometry, x-ray reflectivity, x-ray photoelectron spectroscopy, and scanning electron microscopy. These techniques revealed that Pt ALD does not nucleate and grow immediately on the Al 2 O 3 ALD substrates. There was negligible Pt ALD during the first 38 ALD cycles. The Pt ALD growth rate then increased substantially during the next 12 ALD cycles. Subsequently, the Pt ALD growth rate reached a steady state linear growth regime for >50 ALD cycles. These measurements suggest that the Pt ALD first forms a number of nanoclusters that grow slowly during the first 38 ALD cycles. These islands then merge during the next 12 cycles and yield a steady state Pt ALD growth rate of $0.05 nm/cycle for >50 ALD cycles. The Pt ALD film at the onset of the steady state linear growth regime was approximately 2-3 nm in thickness. However, the SEM images of these Pt ALD films appeared corrugated and wormlike. These films also had a density that was only 50-70% of bulk Pt. Film densities that were consistent with bulk Pt were not observed until after >100 ALD cycles when the Pt ALD films appeared much smoother and were 4-5 nm in thickness. The Pt ALD nucleation rate could be enhanced somewhat using different O 2 plasma parameters.

It has been suggested that adenosine monophosphateactivated protein kinase (AMPK) and 12 AMPK-related kinases (ARK), including novel (nua) kinase family 1 (NUAK1), are activated by master kinase LKB1, a major tumor suppressor. Apart from evidence to suggest that NUAK1 participates in induction of tumor survival, invasion and p53-independent cellular senescence, its detailed biological functions remain unclear. Here we showed that in the presence of wild-type LKB1, NUAK1 directly interacts with and phosphorylates p53 in vitro and in vivo. The phosphorylation of p53 induced by LKB1 required the kinase activity of NUAK1 and phosphorylation of NUAK1 at Thr211 by LKB1 was essential for its kinase activity, which leads to the conclusion that LKB1 activates NUAK1 and regulates phosphorylation of p53 through the NUAK1 kinase, at least partially. LKB1/ NUAK1 activation leads to cell cycle arrest at the G 1 /S border by inducing expression of p21/WAF1. Under the regulation of LKB1, NUAK1 interacts with p53 in the nucleus and binds to the p53-responsive element of p21/WAF1 promoter. These findings have highlighted a novel role for NUAK1 in LKB1-related signaling pathways; NUAK1 can regulate cell proliferation and exert tumor suppression through direct interaction with p53.

The aim of this study was to assess a specific protocol for the treatment of patients with a parosteal osteosarcoma of the distal femur with limb salvage involving hemicortical resection and reconstruction using recycled pasteurised autograft and internal fixation. Between January 2000 and January 2010, 13 patients with a mean age of 26.5 years (17 to 39) underwent this procedure. All the tumours were staged according to Enneking's criteria: there were eight stage IA tumours and five stage IB tumours. The mean follow-up was 101.6 months (58 to 142), and mean post-operative Musculoskeletal Tumour Society functional score was 88.6% (80% to 100%) at the final follow-up. All the patients had achieved bony union; the mean time to union was 11.2 months (6 to 18). Local recurrence occurred in one patient 27 months post-operatively. No patient had a pulmonary metastasis. A hemicortical procedure for the treatment of a parosteal osteosarcoma is safe and effective. Precise pre-operative planning using MRI is essential in order to define the margins of resection. Although it is a technically demanding procedure, gratifying results make it worthwhile for selected patients.

Solitary intracranial plasmacytoma (SIP) is very rare. This case report presents serial findings of SIP located in the spheno-clival region in a 54-year old female who presented with an inferior hemianopia in the right eye and an enlarged physiological blind spot in both eyes. Based on the initial diagnosis of a spheno-clival region chordoma, the tumour was partially resected by the nasal-sphenoidal sinus approach. Subsequently, the correct diagnosis of SIP was made based on the pathology and immunohistochemical staining of the tumour. The patient was treated using a whole skull-base radiation therapy protocol with 45 Gy and she was in good physical condition during the subsequent 22 months. The findings of a series of similar case reports documenting SIP in 20 cases published from 1976 to 2008 are also reviewed. Based on these case reports, the key features of SIP, including their clinical manifestations, clinical imaging characteristics, treatment and prognosis, are described.