Objective: To investigate the influence of medical nutrition therapy (MNT) on borderline glucose intolerance (BGI) in pregnant Taiwanese women. Methods: A total of 5194 singleton pregnant women were enrolled in this prospective, non-randomized study. The participants were subjected to the 50 g 1-h glucose challenge test (GCT) and 100 g 3-h oral glucose tolerance test (OGTT) to screening gestational diabetes mellitus (GDM). BGI was defined as a positive GCT and normal OGTT results. GDM was defined as a positive GCT and abnormal OGTT results. The women were categorized into the following groups: (1) GCT-negative, n = 3881; (2) BGI with MNT, n = 273; (3) BGI without MNT, n = 712; and (4) GDM, n = 328. Multiple logistic analyses were used to estimate the risks of pregnancy outcomes. Results: The odds ratios (95% confidence interval) for total cesareans, third- or fourth-degree perineal lacerations, gestational hypertension or preeclampsia and macrosomia were 1.24 (1.04–1.49), 1.55 (1.06–1.28), 1.78 (1.21–2.61) and 2.50 (1.28–4.91) in the BGI without MNT group compared to the GCT-negative group. There was no difference between BGI with MNT and GCT-negative groups. Conclusions: Women with BGI who did not receive MNT had increased risks of adverse pregnancy outcomes, whereas who received MNT had no different risk with GCT-negative women.
When 2−1/Q<p≤2, we establish the Cloc0,1 and Cloc1,α-regularities of weak solutions to quasi-linear p-Laplacian type non-homogeneous equations in the Heisenberg group Hn, where Q=2n+2 is the homogeneous dimension of Hn.
In the Heisenberg group Hn, we obtain the local second-order HWloc2,2-regularity for the weak solution u to a class of degenerate parabolic quasi-linear equations ∂tu=∑i=12nXiAi(Xu) modeled on the parabolic p-Laplacian equation. Specifically, when 2≤p≤4, we demonstrate the integrability of (∂tu)2, namely, ∂tu∈Lloc2; when 2≤p<3, we demonstrate the HWloc2,2-regularity of u, namely, XXu∈Lloc2. For the HWloc2,2-regularity, when p≥2, the range of p is optimal compared to the Euclidean case.
The study of low-frequency density fluctuations in tokamak fusion plasmas is of great current interest. First, recent PLT results have demonstrated the significant potential of rf heating in the vicinity of the ion cyclotron frequency and its harmonics. Unfortunately, the physics associated with this form of heating is much more complicated than that of neutral beam injection due to the myriad of possible waves and absorption processes.
A low-frequency (<4 kHz), poloidally and toroidally symmetrical potential structure that peaks near zero frequency is observed in the edge plasma of the HL-2A tokamak. The axisymmetry structure exhibits a radial coherence length less than 1 cm. These characteristics are consistent with the theoretically predicted low-frequency zonal flows (LFZF). The radial wave-number frequency spectra of the LFZF show that the LFZF packets propagate both outwards and inwards. The geodesic acoustic mode (GAM) is found to coexist with the LFZF, and the LFZF is found to modulate the GAM and ambient turbulence with in-phase and antiphase relations, respectively, through an envelope analysis.
Abstract Background Lung cancer brain metastases (LC-BrMs) are frequently associated with dismal mortality rates in patients with lung cancer; however, standard of care therapies for LC-BrMs are still limited in their efficacy. A deep understanding of molecular mechanisms and tumor microenvironment of LC-BrMs will provide us with new insights into developing novel therapeutics for treating patients with LC-BrMs. Methods Here, we performed integrated analyses of genomic, transcriptomic, proteomic, metabolomic, and single-cell RNA sequencing data which were derived from a total number of 154 patients with paired and unpaired primary lung cancer and LC-BrM, spanning four published and two newly generated patient cohorts on both bulk and single cell levels. Results We uncovered that LC-BrMs exhibited a significantly greater intra-tumor heterogeneity. We also observed that mutations in a subset of genes were almost always shared by both primary lung cancers and LC-BrM lesions, including TTN , TP53 , MUC16 , LRP1B , RYR2 , and EGFR . In addition, the genome-wide landscape of somatic copy number alterations was similar between primary lung cancers and LC-BrM lesions. Nevertheless, several regions of focal amplification were significantly enriched in LC-BrMs, including 5p15.33 and 20q13.33. Intriguingly, integrated analyses of transcriptomic, proteomic, and metabolomic data revealed mitochondrial-specific metabolism was activated but tumor immune microenvironment was suppressed in LC-BrMs. Subsequently, we validated our results by conducting real-time quantitative reverse transcription PCR experiments, immunohistochemistry, and multiplexed immunofluorescence staining of patients’ paired tumor specimens. Therapeutically, targeting oxidative phosphorylation with gamitrinib in patient-derived organoids of LC-BrMs induced apoptosis and inhibited cell proliferation. The combination of gamitrinib plus anti-PD-1 immunotherapy significantly improved survival of mice bearing LC-BrMs. Patients with a higher expression of mitochondrial metabolism genes but a lower expression of immune genes in their LC-BrM lesions tended to have a worse survival outcome. Conclusions In conclusion, our findings not only provide comprehensive and integrated perspectives of molecular underpinnings of LC-BrMs but also contribute to the development of a potential, rationale-based combinatorial therapeutic strategy with the goal of translating it into clinical trials for patients with LC-BrMs.
Long-time precursors of order 5 times the global energy confinement time are observed for disrupting plasmas at the high-density limit on the Texas Experimental Tokamak. These precursors, occurring well in advance of any change in the plasma MHD activity, are reflected in the electron particle and heat transport along with the density fluctuation level. Enhanced microturbulence is proposed as the physical mechanism for the confinement degradation and subsequent disruption.
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