Elastic Anisotropy of Molecular Crystals Calculated by an Elastic Model Established on a Supramolecular Structural Unit

The crystal structure–elastic property relationship provides a foundation for the design of new materials. The supramolecular structural unit, i.e., the nearest neighbor coordination polyhedron, is proposed to describe the elastic deformation of molecular crystals. The elastic model established on the assumptions of bond-spring and spherical molecule demonstrates that the elastic modulus is intrinsically dependent on the coordination number (N), equilibrium centroid distance (Rij), intermolecular force constant (kij), and the angle (θij) between the intermolecular interactions and the normal to the crystal face. The supramolecular structural units are composed of 15, 13, 9, 7, 8, and 6 molecules, and the elastic moduli are in the ranges of 15.3–21.7, 14.3–19.5, 17.6–23.0, 6.2–9.1, 5.7–10.1, and 2.3–16.2 GPa for α-RDX, β-HMX, ε-CL-20, I-Aspirin, II-Aspirin, and IV-Aspirin, respectively. The predicted elastic moduli are consistent with previous theoretical and nanoindentation values, and the elastic anisotropy may be attributed to the change in the molecular conformation and arrangement of the intermolecular interactions. The supramolecular structural unit may fail to describe the long-range intermolecular interactions such as hydrogen bonds, halogen bonds, and π-packing. Therefore, The proposed method should be further optimized to apply to molecular crystals with planar molecules and graphite-like layered structures

Distribution of the 822 bp mtDNA deletion among cases and controls.

<p>Del, deletion. The median number of pack-years of combined cases and controls was utilized as the cut-point to stratify the cigarette smoking subjects. The single bar depicting the proportion of individuals who had the deletion or not. * indicating <i>p</i><0.001. (A) Distribution of the mtDNA deletion among subjects pooled from cases and controls and stratified by pack-years of cigarette smoking. Non-smokers who had no any history of cigarette smoking; Light-smokers who smoked 1–30 pack-years of smoking; Heavy-smokers who smoked >30 pack-years of smoking; <i>p</i> trend was calculated by the chi-square test for linear-by-linear association (both <i>p</i> value and <i>p</i> trend <0.001). (B) Distribution of the mtDNA deletion among light-cigarette and heavy-cigarette smoking subjects of combined cases and controls. Light-smokers who smoked 0–30 pack-years of smoking; Heavy-smokers who smoked >30 pack-years of smoking. ORs (95% CIs) and <i>p</i> value determined by multivariate logistic regression analysis, adjusted for age and gender (OR = 6.540, 95% CI = 3.247–13.174, adjusted <i>p</i> value<0.001). (C) Distribution of the mtDNA deletion among cases and controls. Compared with controls, the mtDNA deletion was significantly enriched in cases of lung cancer (<i>p</i><0.001). ORs (95% CIs) and <i>p</i> value determined by multivariate logistic regression analysis with adjustment for age, gender and smoking habits (OR = 3.776, 95% CI = 2.662–5.355, adjusted <i>p</i><0.001). (D) Distribution of the mtDNA deletion among non-cigarette smoking subjects pooled from cases and controls and stratified by gender. Non-smokers who had no any history of cigarette smoking. ORs (95% CIs) and <i>p</i> value determined by multivariate logistic regression analysis adjusted for age (OR = 5.814, 95% CI = 3.279–10.309, adjusted <i>p</i><0.001).</p

Distribution of the 822 bp deletion of mtDNA in major mtDNA haplogroups among male non-cigarette smoking subjects pooled from cases and controls^a.

<p>Del, deletion.</p><p>For multiple comparisons, <i>p</i> value was set <0.05/2×(n−1) (n = 8).</p>a<p>, non-cigarette smoking subjects who had no any history of cigarette smoking.</p>b<p>, ORs (95% CIs) and <i>p</i> value determined by multivariate logistic regression analysis adjusted for age.</p

Distribution of the 822 bp deletion of mtDNA in major mtDNA haplogroups among male cigarette smoking subjects pooled from cases and controls^a.

<p>Del, deletion.</p><p>For multiple comparisons, <i>P</i> value was set <0.05/2×(n−1) (n = 8).</p>a<p>, Cigarette smoking subjects who had any history of cigarette smoking.</p>b<p>, ORs (95% CIs) and <i>p</i> value determined by multivariate logistic regression analysis adjusted for age.</p

Characteristics of the study population.

a<p><i>χ</i>²-Test or Fisher's exact test.</p>b<p><i>t</i>-Test.</p>c<p>The median number of pack years of combined cases and controls were utilized as the cut-point.</p>d<p>restricted to males only.</p

Distribution of mtDNA haplogroups among cases and controls.

<p><i>χ</i>²-Test or Fisher's exact test. Bonferroni corrected <i>p</i><0.05/n (n = 17).</p>a<p>, ORs (95% CIs) and <i>p</i> value determined by multivariate logistic regression analysis, adjusted for age, gender, and pack-years of cigarette smoking.</p

Electrophoresis for the detection of the 822 bp mtDNA deletion and the 822 bp mtDNA deletion in the schematic representation of a linearized mitochondrial genome.

<p>(A) PCR products amplified with primers mtDNA-1 and mtDNA-2. The right lane is molecular marker DL 2000. W1, W2, and W3 showing PCR products with 1129 bp from wide type mtDNA, M1, M2, M3 and M4 indicating PCR products with 1129 bp and 307 bp from mutant mtDNA. (B) PCR products amplified with primers mtDNA-1 and mtDNA-3. The right lane is molecular marker DL 2000. W1 and W2 showing PCR products with 956 bp from wide type mtDNA, M1, M2, M3 and M4 indicating PCR products with 956 bp and 134 bp from mutant mtDNA. (C) The 822 bp mtDNA deletion in the schematic representation of a linearized mitochondrial genome. Mitochondrial nucleotides were numbered according to rCRS of mtDNA <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0031322#pone.0031322-Andrews1" target="_blank">[30]</a>. Nucleotide repeats at or near the sites of cleavage are bracketed. The placement of ▾ above the bracket indicates that the exact cleavage site within the nucleotide repeat was unknown. The deleted mtDNA fragment covered from 15587–15591 nps to 16408–16412 nps. CTCCG showed the 5 bp short direct repeats at both ends of the deletion regions. The deletion was formed by cleavage within the 5 bp direct repeats.</p

Additional file 1: of Association of APEX1 and OGG1 gene polymorphisms with breast cancer risk among Han women in the Gansu Province of China

A questionnaire survey of breast health. Questionnaire included participant's eating habits, living environment, lifestyle, smoking, physiological state, reproductive condition, past medical history and family history of cancer. (PDF 415 kb

Peripheral nerve injury associated with JEV infection in high endemic regions, 2016–2020: a multicenter retrospective study in China

Previously, we reported a cohort of Japanese encephalitis (JE) patients with Guillain–Barré syndrome. However, the evidence linking Japanese encephalitis virus (JEV) infection and peripheral nerve injury (PNI) remains limited, especially the epidemiology, clinical presentation, diagnosis, treatment, and outcome significantly differ from traditional JE. We performed a retrospective and multicenter study of 1626 patients with JE recorded in the surveillance system of the Chinese Center for Disease Control and Prevention, spanning the years 2016–2020. Cases were classified into type 1 and type 2 JE based on whether the JE was combined with PNI or not. A comparative analysis was conducted on demographic characteristics, clinical manifestations, imaging findings, electromyography data, laboratory results, and treatment outcomes. Among 1626 laboratory confirmed JE patients, 230 (14%) were type 2 mainly located along the Yellow River in northwest China. In addition to fever, headache, and disturbance of consciousness, type 2 patients experienced acute flaccid paralysis of the limbs, as well as severe respiratory muscle paralysis. These patients presented a greater mean length of stay in hospital (children, 22 years [range, 1–34]; adults, 25 years [range, 0–183]) and intensive care unit (children, 16 years [range, 1–30]; adults, 17 years [range, 0–102]). The mortality rate was higher in type 2 patients (36/230 [16%]) compared to type 1 (67/1396 [5%]). The clinical classification of the diagnosis of JE may play a crucial role in developing a rational treatment strategy, thereby mitigating the severity of the disease and potentially reducing disability and mortality rates among patients.</p