Table_1_Prognostic analysis of lung squamous cell carcinoma patients with second primary malignancies: a SEER database study.docx

BackgroundAs lung squamous cell carcinoma (LUSC) patients are at increased risk of developing a second primary cancer, this complicates the patient’s condition and thus makes prognostic assessment more difficult, posing a significant prognostic challenge for clinicians. Our goal was to assess the prognosis of LUSC patients with a second primary tumor, and provide insights into appropriate therapy and monitoring strategies.MethodsData was obtained for LUSC patients from the Surveillance, Epidemiology, and End Results (SEER) database. The LUSC patients were divided into three groups (LS-SPM, OT-LUSC and LUSC-only). Univariate and stratified analyses were performed for the baseline and clinical characteristics of the participants. Multiple regression and Kaplan-Meier survival analyses were also performed, followed by a final life table analysis.ResultsIn our sample of 101,626 patients, the HR for OS in the LS-SPM group was 0.40 in univariate analysis. Kaplan-Meier survival curves showed that LS-SPM patients had considerably longer lifespans compared to the other groups. The LS-SPM patients had median and mean survival times of 64 months and 89.11 months. Unadjusted and adjusted multiple regression analyses showed that LS-SPM patients had a superior survival compared to LUSC-only and OT-LUSC groups.ConclusionLS-SPM patients have a good prognosis with aggressive therapy and immune monitoring. The present study offers novel insights into the pathophysiological causes and treatments for LS-SPM.</p

The <i>wciN</i> Gene Encodes an α-1,3-Galactosyltransferase Involved in the Biosynthesis of the Capsule Repeating Unit of <i>Streptococcus pneumoniae</i> Serotype 6B

Almost all <i>Streptococcus pneumoniae</i> (pneumococcus) capsule serotypes employ the Wzy-dependent pathway for their capsular polysaccharide (CPS) biosynthesis. The assembly of the CPS repeating unit (RU) is the first committed step in this pathway. The <i>wciN</i> gene was predicted to encode a galactosyltransferase involved in the RU assembly of pneumococcus type 6B CPS. Herein, we provide the unambiguous <i>in vitro</i> biochemical evidence that <i>wciN</i> encodes an α-1,3-galactosyltransferase catalyzing the transfer of galactosyl from UDP-Gal onto the Glcα-pyrophosphate-lipid (Glcα-PP-lipid) acceptor to form Galα(1–3)­Glcα-PP-lipid. A chemically synthesized acceptor (Glcα-PP-O­(CH₂)₁₀CH₃) was used to characterize the WciN activity. The disaccharide product, i.e., Galα(1–3)­Glcα-PP-O­(CH₂)₁₀CH₃, was characterized by mass and NMR spectroscopy. Substrate specificity study indicated that the acceptor structural region composed of pyrophosphate and lipid moieties may play an important role in the enzyme-acceptor recognition. Furthermore, divalent metal cations were found indispensable to the WciN activity, suggesting that this glycosyltransferase (GT) belongs to the GT-A superfamily. By analyzing the activities of six WciN mutants, a DXD motif involved in the coordination of a divalent metal cation was identified. This work provides a chemical biology approach to characterize the activities of pneumococcal CPS GTs <i>in vitro</i> and will help to better understand the pneumococcal CPS biosynthetic pathway

Vasodilations in three various arteries.

<p>Vasodilatory effects of arotinolol and metoprolol in rats' aortas (A), renal (B) and mesenteric arteries (C). ^*<i>P</i><0.05 versus metoprolol. Data are expressed as percentage tension of phenylephrine-induced preconstruction. n = 8 in each group.</p

Glycosylation of MBP with <i>E. coli</i> O157:H7 O-Ag and analyzed by (A), coomassie blue staining and western blot with (B), anti-6×-His antibody; (C), anti-MBP antibody; (D), O157:H7 antiserum.

<p>Glycosylation of MBP with <i>E. coli</i> O157:H7 O-Ag and analyzed by (A), coomassie blue staining and western blot with (B), anti-6×-His antibody; (C), anti-MBP antibody; (D), O157:H7 antiserum.</p

Ser1177 phosphorylation of eNOS in thoracic aortas in SHRs.

<p>Effects of metoprolol or arotinolol on aortic p-eNOS level in SHR by western blotting assay. *<i>P</i><0.05 vs. SHR control, ^#<i>P</i><0.05 vs. metoprolol-treated group. n = 12 in each group.</p

Spleen lymphocyte subsets assay.

<p>Spleen lymphocytes were isolated and stained for FITC-CD3, PE-CD4 or PE-CD8 antibodies and then analyzed by flow cytometry. The percentage of (<b>A</b>), CD3⁺ CD4⁺ T cells; (<b>B</b>), CD3⁺ CD8⁺ were expressed as the arithmetic mean ±SD indicated by error bars. Exprements were repeated three times. Differences of two groups are indicated with symbols (*: P<0.05; **: P<0.01).</p

Serum bactericidal activity against <i>E. coli</i> O157:H7.

<p>The % killing of <i>E. coli</i> O157:H7 are expressed as the arithmetic mean ±SD indicated by error bars.</p

Cytokines determined by ELISPOT.

<p>(<b>A</b>), IFN-γ; (<b>B</b>), IL-4. The spots for cytokine-producing lymphocytes after stimulation with MBP or O-Ag-MBP were counted and expressed based on 1×10⁵ cells. Results are expressed as the arithmetic mean ±SD indicated by error bars. Differences of three groups stimulated at the same dose of MBP are indicated with symbols (*: P<0.05; **: P<0.001).</p

Involvement of potassium channels.

<p>(A) Cumulative concentration-response curves to arotinolol in the presence or absence of potassium channel inhibitor (TEA). ^*<i>P</i><0.05 for arotinolol vs. arotinolol + TEA. (B) Cumulative concentration-response curves to arotinolol in the presence or absence of 4-aminopyridine. ^*<i>P</i><0.05 for arotinolol vs. arotinolol + 4-aminopyridine. (C) Cumulative concentration-response curves to arotinolol in the presence or absence of glibenclamide. <i>P</i>>0.05 for arotinolol vs. arotinolol + glibenclamide. n = 8 in each group.</p

Tail SBP, CAP and PWV in SHRs treated with arotinolol and metoprolol.

<p>(A) Tail SBP before treatment and at week 8 in WKY, SHR control, or SHR treated with metoprolol or arotinolol. *<i>P</i><0.05 vs. those origins before treatment, ^#<i>P</i><0.05 vs. SHR control at week 8, <i>P</i>>0.05 for arotinolol vs. metoprolol groups at week 8. Central aortic pressure (B) and Pulse wave velocity (C) in WKY, SHR control, or SHR treated with metoprolol or arotinolol. *<i>P</i><0.05 vs. SHR control, ^#<i>P</i><0.05 vs. SHR treated with metoprolol. n = 12 in each group.</p