724 research outputs found
Thermopower modulation clarification of the intrinsic effective mass in a transparent oxide semiconductor, BaSnO3
Although there are so many reports on the carrier effective mass (m*) of a
transparent oxide semiconductor BaSnO3, it is almost impossible to know the
intrinsic m* value because the reported m* values are scattered from 0.06 to
3.7 m0. Here we successfully clarified the intrinsic m* of BaSnO3, m*=0.40 0.01
m0, by the thermopower modulation clarification method. We also found the
threshold of degenerate/non-degenerate semiconductor of BaSnO3; At the
threshold, the thermopower value of both La-doped BaSnO3 and BaSnO3 TFT
structure was 240 microvolt k-1, bulk carrier concentration was 1.4E19 cm-3,
and two-dimensional sheet carrier concentration was 1.8E12 cm-2. When the EF
locates above the parabolic shaped conduction band bottom, rather high mobility
was observed. On the contrary, very low carrier mobility was observed when the
EF lays below the threshold, most likely due to that the tail states suppress
the carrier mobility. The present results are useful for further development of
BaSnO3 based oxide electronics.Comment: 16 pages including 4 figure
Clinical features of neck and shoulder pain (Katakori) in Japanese hospital workers
Background: Non-specific pain or discomfort in the neck and shoulder girdle, called katakori in Japanese, is a common, chronic musculoskeletal condition worldwide. However, its various clinical features are incompletely characterized, even among medical professionals. We aimed to clarify factors affecting katakori and to investigate objectively the associated neck muscle stiffness and skeletal muscle volume. Methods: All staff members at our private hospital were surveyed about their lifestyle, physical and mental status, and katakori symptoms, using a self-administered questionnaire. Multiple logistic regression analysis was used to explore possible katakori risk factors. On secondary assessment, ultrasound elastography of the trapezius muscle as well as limb/trunk muscle mass were compared between subjects with severe symptoms and subjects without katakori, using propensity score matching. Results: Of 359 participants enrolled, nearly 75% had katakori to some degree. Spending time on a computer during work (adjusted odds ratio [aOR]:1.82 for 3-6 hours, aOR:2.48 for > 6 hours), being female (aOR:3.75), and having unsatisfactory sleep (aOR:2.92) were potential risk factors for katakori. Comparison of 13 matched pairs showed a significantly stiffer trapezius in subjects with severe katakori symptoms, but no apparent differences in limb/trunk muscle mass. Conclusions: Katakori was particularly prevalent in our hospital staff. Possible risk factors for disabling katakori were doing long-term computer work, being female, and having unsatisfactory sleep. Symptoms seem to be associated with elevated neck muscle stiffness. These findings could guide working condition improvements to mitigate katakori
EGFR T790M Mutation: A Double Role in Lung Cancer Cell Survival?
Abstract:Even though lung cancer patients harboring a mutation in the epidermal growth factor receptor (EGFR) gene exhibit an initial dramatic response to EGFR tyrosine kinase inhibitors (EGFR-TKIs), acquired resistance is almost inevitable after a progression-free period of approximately 10 months. A secondary point mutation that substitutes methionine for threonine at amino acid position 790 (T790M) is a molecular mechanism that produces a drug-resistant variant of the targeted kinase. The T790M mutation is present in about half of the lung cancer patients with acquired resistance, and reported to act by increasing the affinity of the receptor to adenosine triphosphate, relative to its affinity to TKIs. Nevertheless, several lines of evidence indicate that the T790M mutation confers growth advantage to cancer cells, and it was shown that mice expressing tetracycline-inducible EGFR transgenes harboring the T790M mutation develop lung tumors. Thus, T790M mutation seems to play a double role in the survival of lung cancer cells. Several second-generation EGFR-TKIs are currently being developed to overcome the acquired resistance caused by the T790M mutation. MET (met proto-oncogene) amplification or activation of IGF1R are reported as alternative mechanisms for acquired resistance to EGFR-TKIs. Clarification of the pathways leading to acquired resistance is essential to maximize the efficacy of EGFR-TKI therapy for patients with lung cancer
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