Understanding and Measurement for the Binding Energy of Hydrogen bonds of Biomass-Derived Hydroxyl Compounds

Experimental measurement for the binding energy of hydrogen-bonds (HBs) has long been an attractive and challenging topic in chemistry and biochemistry. In the present study, the binding energy of OH···O HBs can be determined by ¹H NMR technique using a set of model biomass-derived hydroxyl compounds, including furfuryl alcohol, isosorbide, tetrahydrofurfuryl alcohol, and (<i>S</i>)-3-hydroxytetrahydrofuran. By performing concentration- and temperature-variation experiments, we put forward a modified Arrhenius-type equation, in which the compensated natural logarithm of the chemical shift (ln δ + Δ_δ) is linearly correlated with 1/<i>T</i>. HBs energies can be directly determined by the slope of the plot, and are substantiated by density functional theory (DFT) theoretical calculations. This study provides a reliable method to measure the binding energy of OH···O HBs in hydroxyl-containing biomass-derived feedstocks

Enhanced autophagy induced by Tat–Beclin-1 abolishes the neuroprotective effects of GM1.

<p>(A) Representative images of TTC stained sections and quantification of infarct size in sham, MCAO+saline, MCAO+Tat–Beclin-1, MCAO+GM1, and MCAO+Tat–Beclin-1+GM1 groups. n = 6 per group. (B) Neurological scores for the modified Garcia test. n = 6–12 per group. (C) Representative Western blotting images of LC3-I, LC3-II, P62, Beclin-1 and β-Actin in MCAO+saline, MCAO+GM1, MCAO+Tat–Beclin-1, and MCAO+Tat–Beclin-1+GM1 groups. n = 6 per group. (D) Quantification of LC3-II/LC3-I in the ipsilateral hemisphere. (E) Quantification of P62 in the ipsilateral hemisphere. (F) Quantification of Beclin-1 in the ipsilateral hemisphere.*<i>p</i> < 0.05 vs sham; #<i>p</i> < 0.05 vs MCAO+saline; @<i>p</i> < 0.05 vs MCAO+Tat–Beclin-1; & <i>p</i> < 0.05 vs MCAO+GM1.</p

GM1 (50 mg/kg) treatment improves neurological scores and reduces infarct volume at 72 hours after MCAO.

<p>GM1 was administrated soon after reperfusion and then once daily for 2 days at three doses (25, 50, and 100 mg/kg) by intraperitoneal injection. MCAO rats were injected with the same volume of saline as a control. (A) Experimental design and animal treatment. (B) Neurological scores for the modified Garcia test in sham, MCAO+saline and GM1 (25, 50, 100 mg/kg) treatment groups. n = 10–12 rats per group. (C) Representative images of TTC stained sections and infarct volume in sham, MCAO+saline and GM1 treatment groups. n = 6 per group. *<i>p</i> < 0.05 vs sham; #<i>p</i> < 0.05 vs MCAO+saline.</p

Immunofluorescence staining for LC3-II and Beclin-1 expression in sham, MCAO+saline and GM1 (50 mg/kg) treatment groups 72 hours following MCAO injury.

<p>(A) Representative images of LC3-II (red) and Beclin-1 (green) staining in the perihematomal area. Bar = 50μm. (B) Schematic diagram showing examples of the areas (black squares) that were selected for counting of LC3-II and Beclin-1 positive cells in the perihematomal region. (C) Quantification of LC3-II positive cells in the perihematomal region (10 fields/brain). (D) Quantification of Beclin-1 positive cells in the perihematomal region (10 fields/brain). The data show that GM1 treatment significantly reduced the number of LC3-II and Beclin-1 positive cells after MCAO insult. n = 5 per group. *<i>p</i> < 0.05 vs sham; #<i>p</i> < 0.05 vs MCAO.</p

GM1 inhibits neuronal autophagic activity following MCAO injury.

<p>(A) Representative Western blotting images of LC3-I, LC3-II, P62, and Beclin-1 in the ipsilateral hemisphere at 72 hours after MCAO injury. β-Actin is shown as a loading control. (B) Quantification of the LC3-II/LC3-I ratio in the ipsilateral hemisphere at 72 hours after MCAO injury. (C) Quantification of P62 in the ipsilateral hemisphere at 72 hours after MCAO injury. (D) Quantification of Beclin-1 in the ipsilateral hemisphere at 72 hours after MCAO injury. n = 6 per group. *<i>p</i> < 0.05 vs sham; #<i>p</i> < 0.05 vs MCAO+saline.</p

sj-docx-1-wso-10.1177_17474930241228956 – Supplemental material for Type of anesthesia for endovascular therapy in acute ischemic stroke: A literature review and meta-analysis

Supplemental material, sj-docx-1-wso-10.1177_17474930241228956 for Type of anesthesia for endovascular therapy in acute ischemic stroke: A literature review and meta-analysis by Yitong Jia, Yao Feng, Yanhui Ma, Guang Feng, Na Xu, Meng Li, Miao Liu, Zhen Fan and Tianlong Wang in International Journal of Stroke</p

Patient Demographics and Anesthesia/Surgery Data, Beijing, China (N = 830).

<p>¹ Magnitude of surgery as below: minor surgery: excision of lesion of skin; drainage of breast abscess, etc. Intermediate surgery: primary repair of inguinal hernia; excision of varicose vein(s) of leg; tonsillectomy/adenotonsillectomy; knee arthroscopy, etc. major surgery: total abdominal hysterectomy; endoscopic resection of prostate; lumbar discectomy; thyroidectomy, etc. major surgery plus: total joint replacement; lung operations; colonic resection; radical neck dissection; neurosurgery; cardiac surgery)</p><p>² Arthroscopic, laparoscopic, etc</p><p>³ Time from incision to closure</p><p>⁴ Time from induction to discontinuation of anesthetic agents</p><p>Patient Demographics and Anesthesia/Surgery Data, Beijing, China (N = 830).</p

Incidence of intraoperative hypothermia, patient warming and clinical outcome (N = 830).

<p>¹ passive warming includes comforter, blanket etc</p><p>² active warming includes electric heated blanket, space heater etc</p><p>Incidence of intraoperative hypothermia, patient warming and clinical outcome (N = 830).</p

Risk factors associated with intraoperative hypothermia, Beijing, China (N = 830).

<p>OR, Odds Ratio, Significant level indicates as P<0.05.</p><p>¹ adjusted OR were presented after adjusting all the variables in above table.</p><p>² patients receiving unwarmed IV fluid only</p><p>Risk factors associated with intraoperative hypothermia, Beijing, China (N = 830).</p

Change of intraoperative core temperature during operations.

<p>Patients’ core temperature was measured at the tympanic membrane beginning every 15 minutes after the induction of anesthesia and until the end of the operation. A total of 830 subjects were enrolled in the study; 89 (10.7%) received active warming, and 741(89.3%) received no warming.</p