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Lung cancer is one of the deadliest cancers worldwide, including in Taiwan. The poor prognosis of the advanced lung cancer lies in delayed diagnosis and non-druggable targets. It is worth paying more attention to these ongoing issues. Public databases and an in-house cohort were used for validation. The KM plotter was utilized to discover the clinical significance. GSEA and GSVA were adopted for a functional pathway survey. Molecular biological methods, including proliferation, migration, and the EMT methods, were used for verification. Based on public databases, the increased expression of Ladinin 1 (LAD1) was presented in tumor and metastatic sites. Furthermore, an in-house cohort revealed a higher intensity of LAD1 in tumor rather than in normal parts. The greater the expression of LAD1 was, the shorter the duration of lung adenocarcinoma (LUAD) patient survival. Moreover, the association of B3GNT3 with LAD1 affected the survival of LUAD patients. Functional analyses using GSEA and GSVA revealed the associations with survival, migration, invasion, and EMT. Biologic functions supported the roles of LAD1 in proliferation via the cell cycle and migration in EMT. This study reveals that LAD1 plays a major role in regulating proliferation and migration in lung cancer and impacts survival in LUAD. It is worth investing in further studies and in the development of drugs targeting LAD1.

The establishment of a pre-metastatic niche (PMN) is critical for cancer metastasis. However, it remains unclear as to which phenotypes induce changes in the PMN. Single-cell transcriptomic profiling of all cells of the lung in cancer-bearing MMTV-PyVT mice revealed an increased infiltration of N2-type neutrophils and classical monocytes associated with chronic inflammation; notably, lung neutrophils isolated from mice with primary cancer exhibited similar N2-type phenotypes and expressed high levels of inflammatory and angiogenic factors. We also discovered a new cluster of Ki67-upregulated lymphatic endothelial cells (ECs) that activated several cell division-related pathways. Receptor–ligand interactions within the lung potentially mediated PMN formation; these were exemplified by the cross talk of lymphatic EC–N2-type neutrophil via S100A6. In vitro study revealed S100A6 impaired EC tight junction and increased the transendothelial migration of neutrophils. Our results highlight the molecular mechanisms that shape lung PMN and inspire preventive strategies for lung metastasis in breast cancer.

Lung cancer is well known for its high mortality worldwide. The treatment for advanced lung cancer needs more attention to improve its survival time. A disintegrin and metallopeptidase with thrombospondin motifs 8 (ADAMTS8) has been linked to several cancer types. However, its role in lung cancer is worthy of deep investigation to promote novel drug development. This study took advantage of RNA-seq and bioinformatics to verify the role that ADAMTS8 plays in lung cancer. The functional assays suggested that ADAMTS8 mediates invasion and metastasis when expressed at a low level, contributing to poor overall survival (OS). The expression of ADAMTS8 was under the regulation of GATA Binding Protein 1 (GATA1) and executed its pathologic role through Thrombospondin Type 1 Domain Containing 1 (THSD1) and ADAMTS Like 2 (ADAMTSL2). To define the impact of ADAMTS8 in the lung cancer treatment strategy, this study further grouped lung cancer patients in the TCGA database into mutated epidermal growth factor receptor (EGFR)/wild-type EGFR and programmed death ligand 1 (PD-L1) high/low groups. Importantly, the expression of ADAMTS8 was correlated positively with the recruitment of anticancer NKT cells and negatively with the infiltration of immunosuppressive Treg and exhausted T cells. The results indicated that lung cancer patients with higher ADAMTS8 levels among wild-type EGFR or low PD-L1 groups survive longer than those with lower levels do. This study indicates that ADAMTS8 might be a treatment option for patients with lung adenocarcinoma who lack efficient targeted or immunotherapies.

A novel positive-displacement multiphase pump named synchronal rotary multiphase pump (SRMP) was introduced. The two-phase leakage flows through the various leakage clearances in the SRMP were theoretically analyzed and formulated. Calculations on the leakage loss of a SRMP prototype were performed. The results show that the leakage loss is mainly produced by the leakage through the radical clearance between the rotor and cylinder. The SRMP presents a lower volumetric efficiency at a higher pressure difference. The leakage loss increases rapidly with the increase of the gas volume fraction of the two-phase working fluids.

This article presents design and measurement of a planar multiband (GSM850/900, DCS, PCS, and UMTS bands) antenna used in a laptop computer. The antenna can be identified by crossly connecting a meandered inverted-F configuration and a T-shaped monopole. The inverted-F part is mainly responsible for GSM-band operation. To cover the DCS, PCS, and UMTS bands, a T-shaped monopole is added. Although directly connecting them together, VSWR cannot meet the specification at the higher band. Therefore, an open-tub is added at bottom end of the T-shaped monopole. It is investigated that the stub serves as a capacitive match element. After tuning length of this stub, all properties of the pentaband antenna include the bandwidth, radiating pattern, and gain variation can satisfy practical applications. © 2011 Wiley Periodicals, Inc. Microwave Opt Technol Lett 53:857–861, 2011; View this article online at wileyonlinelibrary.com. DOI 10.1002/mop.25859

The effects of parasitic elements on the voltage standing wave ratios (VSWR's) of two antennas are investigated. First, a parasitic monopole is used for a normal-mode helical antenna. The VSWR investigation shows that dual-frequency operation is obtained by the parasitic element effects. The dual-frequency operation is revealed as a function of monopole position above a ground plane (monopole height). As the monopole height decreases, the separation of a higher resonance frequency f/sub H/ from a lower resonance frequency f/sub L/ increases. For a monopole length of L/sub MP//spl ap/0.4/spl lambda//sub HX/, where /spl lambda//sub HX/ is the resonance wavelength of the helix, the frequency bandwidth for a VSWR=2 criterion is 12.5% in the lower frequency f/sub L/ region and 5.2% in the higher frequency f/sub H/ region, with a frequency separation ratio of f/sub H//f/sub L/=2.14. Secondly, L-figured parasitic elements are used for an inverted-F antenna (IFA). The parasitic elements improve the VSWR performance. The frequency bandwidth for a VSWR=2 criterion is approximately two times as wide as that of the single IFA. It is also found that bending the horizontal sections of the IFA and parasitic elements contributes to reducing the antenna size while not significantly deteriorating the VSWR bandwidth. The radiation patterns are also presented and discussed.

The effects of timosaponin A-III (TA-III), from Rhizoma Anemarrhenae, on Ca(2+) mobilization in vascular endothelial cells and smooth muscle cells and on vascular tension have been explored. TA-III increased intracellular Ca(2+) concentrations ([Ca(2+)](i)) in endothelials cells at a concentration larger than 5 microM with an EC(50) of 15 microM, and increased [Ca(2+)](i) in smooth muscle cells at a concentration larger than 1 microM with an EC(50) of 8 microM. Within 5 min, the [Ca(2+)](i) signal was composed of a gradual rise, and the speed of rising depended on the concentration of TA-III. The [Ca(2+)](i) signal was abolished by removing extracellular Ca(2+) and was recovered after reintroduction of Ca(2+). The TA-III-induced [Ca(2+)](i) increases in smooth muscle cells were partly inhibited by 10 microM nifedipine or 50 microM La(3+), but was insensitive to 10 microM verapamil and diltiazem. TA-III (10-100 microM) inhibited 0.3 microM phenylephrine-induced vascular contraction, which was abolished by pretreatment with 100 microM N(omega)-nitro-L-arginine (L-NNA) or by denuding the aorta. TA-III also increased [Ca(2+)](i) in renal tubular cells with an EC(50) of 8 microM. Collectively, the results show for the first time that TA-III causes [Ca(2+)](i) increases in the vascular system. TA-III acted by causing Ca(2+) influx without releasing intracellular Ca(2+). TA-III induced relaxation of phenylephrine-induced vascular contraction via inducing release of nitric oxide from endothelial cells.

The purpose of the present study was to examine the mechanisms underlying the putative hypotensive actions of iso-S-petasin, a sesquiterpene extract of Petasites formosanus through both in vivo and in vitro experiments. Intravenous administration of iso-S-petasin elicited dose-dependent (0.1-1.5 mg/kg) hypotensive and bradycardiac responses in anesthetized rats. Isometric tension recording in isolated thoracic aorta revealed that iso-S-petasin (0.01-100 microM) inhibited KCl- or Bay K 8644 (1,4-dihydro-2,6-dimethyl-5-nitro-4-[2'-(trifluoromethyl)phenyl]-3-pyridinecarboxylic acid methyl ester)-induced vasoconstriction independent of endothelium. Iso-S-Petasin also attenuated Ca(2+)-induced vasoconstriction in a concentration-dependent manner in Ca(2+)-depleted/high K(+)-depolarized ring segments, indicating that iso-S-petasin inhibited Ca(2+) influx into vascular smooth muscle cells. This was confirmed by whole-cell patch-clamp recording in cultured vascular smooth muscle cells where iso-S-petasin (10-100 microM) appeared to directly inhibit the L-type voltage-dependent Ca(2+) channel (VDCC) activity. Intracellular Ca(2+) concentration ([Ca(2+)](i)) measurements using the fluorescent probe fura-2/AM (1-[2-(5-carboxyoxazol-2-yl)-6-aminobenzofuran-5-oxy]-2-(2'-amino-5'-methylphenoxy)-ethane-N,N,N',N'-tetraacetic acid pentaacetoxymethyl ester) showed suppression of the KCl-stimulated increase in [Ca(2+)](i) by iso-S-petasin (10, 100 microM). In conclusion, these results suggest that Ca(2+) antagonism of the L-type VDCC in vascular smooth muscle cells might largely account for the hypotensive action of iso-S-petasin.

A 1.95-kg fetus delivered at 33 weeks' gestational age survived less than 1 hour. Physical examination and autopsy disclosed an enormous, protuberant primary malignant melanoma of the skin, enveloping most of the back. A rim of surrounding hyperpigmented skin proved to be a giant congenital melanocytic nevus (GCMN), from which the cutaneous melanoma had arisen. Autopsy demonstrated metastatic melanoma in the lungs, liver, spinal cord, leptomeninges, and placenta. Radiography and dissection confirmed that the melanoma had minimal connection to spinal or neural structures. The mother was clinically free of tumor 8 months after she was delivered of the infant. Pathologic, radiographic, histologic, immunohistochemical, and ultrastructural investigations of this unique case are presented.