Enzymatic hydrolysis of low temperature alkali pretreated wheat straw using immobilized β-xylanase nanoparticles

A low temperature alkali (LTA) pretreatment method was used to treat wheat straw. In order to obtain good results, different factors like temperature, incubation time, NaOH concentration and solid to liquid ratio for the pretreatment process were optimized. Wheat straw is a potential biomass for the production of monomeric sugars. The objective of the current study was to observe the saccharification (%) of wheat straw with immobilized magnetic nanoparticles (MNPs). For this purpose, immobilized MNPs of purified β-xylanase enzyme was used for hydrolysis of pretreated wheat straw. Wheat straw was pretreated using the LTA method and analyzed by SEM analysis. After completion of the saccharification process, saccharification% was calculated by using a DNS method. Scanning electron micrographs revealed that the hemicellulose, cellulose and lignin were partially removed and changes in the cell wall structure of the wheat straw had caused it to become deformed, increasing the specific surface area, so more fibers of the wheat straw were exposed to the immobilized β-xylanase enzyme after alkali pretreatment. The maximum saccharification potential of wheat straw was about 20.61% obtained after pretreatment with optimized conditions of 6% NaOH, 1/10 S/L, 30 °C and 72 hours. Our results indicate the reusability of the β-xylanase enzyme immobilized magnetic nanoparticles and showed a 15% residual activity after the 11th cycle. HPLC analysis of the enzyme-hydrolyzed filtrate also revealed the presence of sugars like xylose, arabinose, xylobiose, xylotriose and xylotetrose. The time duration of the pretreatment has an important effect on thermal energy consumption for the low-temperature alkali method.

A low temperature alkali (LTA) pretreatment method was used to treat wheat straw.     

一例特大听神经瘤患者术后伴多种并发症的护理

目的通过对一例特大听神经瘤术后伴多种并发症的患者的护理体会,分析总结其有效的护理方法。方法我科在2016年至2018年期间采用微创技术通过在全麻下经迷路径路听神经瘤的方式,对听神经瘤患者进行了肿瘤切除术,均康复出院。其中一例听神经瘤大小为5CM的特大听神经瘤患者,肿瘤位于左侧内听道、桥小脑角区,术后出现了颅内感染,颅内积气、积血,颅内压增高;肺部感染;面瘫引起的暴露性角膜炎;肝功异常(药物性肝损伤)等多个并发症。本文通过回顾的方式针对这一病例术后治疗护理涉及的感染高热,皮肤,眼部,腰池等多个方面的护理过程予以分析总结。结果虽然患者术后并发症涉及多个方面,病情较重,但对其有针对性的,积极有效的护理使其恢复较好,住院30天后康复出院。结论听神经瘤经迷路径路手术切除后虽然创伤较小,但就其部位解剖结构的特殊性和大小差异,尤其特大听神经瘤情况,易引发较多并发症,在术后护理中实时关注病人病情变化,同步采取有效措施,可有效地预防和治疗并发症,提高手术的成功率和病人愈后的生活质量。     

负压吸引法在内镜下经十二指肠乳头保胆取石术中的应用研究

为探究采用内镜逆行胰胆管造影术（endoscopic retrograde cholangiopancreatography, ERCP）联合单人经口胆道镜（SpyGlass）行经十二指肠乳头保胆取石术的有效性和安全性,并观察负压吸引法在取净胆囊结石及防止结石复发中可行性,回顾性分析2022年8月至2023年8月于北京友谊医院内镜中心采用负压吸引法行内镜下经十二指肠乳头保胆取石术的4例胆囊结石患者的临床资料,记录手术成功率和结石清除率、胆囊管超选时间、胆囊取石时间、术后并发症发生率等指标。手术成功率和结石清除率均为100%。胆囊管超选时间为6~30 min,其中2例患者在X线引导下进行胆囊管超选,超选时间分别为20 min和30 min;另2例患者为单人经口胆道镜引导下胆囊管超选,超选时间为6 min和8 min。胆囊取石时间为8~20 min,其中1例患者胆囊结石最大径为1 cm,激光碎石后使用取石网篮将结石取出;4例患者术中均使用网篮取石及负压吸引法取净结石。无严重并发症发生。术后随访8.5~24.0个月,无结石复发。本研究初步认为,内镜下经十二指肠乳头保胆取石术由于其超级微创的优势,技术上相对安全有效,值得临床进一步开展应用。     

Effect of intensive lifestyle intervention on the association between weight variability and major adverse cardiovascular events in overweight or obese adults with type 2 diabetes mellitus

Aims/introductionWeight variability is associated with cardiovascular outcomes in diabetic patients. However, whether the guideline‐recommended intensive lifestyle intervention (ILI) will affect this association in overweight or obese adults with diabetes is not well established.Materials and MethodsIn 3,859 participants from the Action for Health in Diabetes (Look AHEAD) trial, the associations of 4 year weight variability measured by variability independent of the mean (VIM) with major adverse cardiovascular event (MACE) and secondary outcomes in ILI and diabetes support & education (DSE) arm were evaluated.ResultsDuring a median follow‐up of 9.6 years, 255 (12.9%) participants in the ILI arm and 247 (13.2%) participants in the DSE arm developed MACE. Participants with the highest quartile of weight variability (VIM Q4) experienced a 2.23‐fold higher risk of MACE compared with the lowest quartile (VIM Q1) in the DSE arm (hazard ratio [HR] 2.23; 95% CI 1.51–3.30). Compared with the lowest weight variability (VIM Q1), participants with the highest weight variability (VIM Q4) were associated with higher risks of secondary cardiovascular composite outcome (HR 1.88; 95% CI 1.20–2.95), all‐cause mortality (HR 3.19; 95% CI 1.75–5.82), and myocardial infarction (HR 1.95; 95% CI 1.12–3.37) in the DSE arm.ConclusionsAmong the overweight or obese individuals with type 2 diabetes mellitus, rising weight variability was independently associated with increased MACE risks in the DSE arm. Therefore, a guideline‐recommended ILI strategy for weight loss should be adopted to improve cardiovascular outcomes without worrying about the effect of weight fluctuations.     

Semisupervised white matter hyperintensities segmentation on MRI

This study proposed a semisupervised loss function named level‐set loss (LSLoss) for cerebral white matter hyperintensities (WMHs) segmentation on fluid‐attenuated inversion recovery images. The training procedure did not require manually labeled WMH masks. Our image preprocessing steps included biased field correction, skull stripping, and white matter segmentation. With the proposed LSLoss, we trained a V‐Net using the MRI images from both local and public databases. Local databases were the small vessel disease cohort (HKU‐SVD, n = 360) and the multiple sclerosis cohort (HKU‐MS, n = 20) from our institutional imaging center. Public databases were the Medical Image Computing Computer‐assisted Intervention (MICCAI) WMH challenge database (MICCAI‐WMH, n = 60) and the normal control cohort of the Alzheimer''s Disease Neuroimaging Initiative database (ADNI‐CN, n = 15). We achieved an overall dice similarity coefficient (DSC) of 0.81 on the HKU‐SVD testing set (n = 20), DSC = 0.77 on the HKU‐MS testing set (n = 5), and DSC = 0.78 on MICCAI‐WMH testing set (n = 30). The segmentation results obtained by our semisupervised V‐Net were comparable with the supervised methods and outperformed the unsupervised methods in the literature.     

Hippocampus‐prefrontal cortex inputs modulate spatial learning and memory in a mouse model of sepsis induced by cecal ligation puncture

AimsSepsis‐associated encephalopathy (SAE) often leads to cognitive impairments. However, the pathophysiology of SAE is complex and unclear. Here, we investigated the role of hippocampus (HPC)‐prefrontal cortex (PFC) in cognitive dysfunction in sepsis induced by cecal ligation puncture (CLP) in mice.MethodsThe neural projections from the HPC to PFC were first identified via retrograde tracing and viral expression. Chemogenetic activation of the HPC‐PFC pathway was shown via immunofluorescent staining of c‐Fos‐positive neurons in PFC. Morris Water Maze (MWM) and Barnes maze (BM) were used to evaluate cognitive function. Western blotting analysis was used to determine the expression of glutamate receptors and related molecules in PFC and HPC.ResultsChemogenetic activation of the HPC‐PFC pathway enhanced cognitive dysfunction in CLP‐induced septic mice. Glutamate receptors mediated the effects of HPC‐PFC pathway activation in CLP mice. The activation of the HPC‐PFC pathway resulted in significantly increased levels of NMDAR, AMPAR, and downstream signaling molecules including CaMKIIa, pCREB, and BDNF in PFC. However, inhibition of glutamate receptors using 2,3‐dihydroxy‐6‐nitro‐7‐sulphamoyl‐benzo (F)quinoxaline (NBQX), which is an α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor (AMPAR inhibitor), or D‐2‐amino‐5‐phosphonopentanoate (D‐AP5), which is an NMDA receptor antagonist abolished this increase.ConclusionOur study reveals the important role of the HPC‐PFC pathway in improving cognitive dysfunction in a mouse model of CLP sepsis and provides a novel pathogenetic mechanism for SAE.     

Endogenous HMGB1 regulates GSDME-mediated pyroptosis via ROS/ERK1/2/caspase-3/GSDME signaling in neuroblastoma

Pyroptosis, a newly discovered mode of programmed cell death (PCD), is important in the regulation of cancer development. High mobility group box 1 (HMGB1) is a non-histone nuclear protein that is closely related to tumor development and chemotherapy resistance. However, whether endogenous HMGB1 regulates pyroptosis in neuroblastoma remains unknown. Here, we showed that HMGB1 showed ubiquitous higher expression in SH-SY5Y cells and clinical tumors, and was positively correlated with the risk factors of patients with neuroblastoma. Knockdown of GSDME or pharmacological inhibition of caspase-3 blocked pyroptosis and cytosolic translocation of HMGB1. Moreover, knockdown of HMGB1 inhibited cisplatin (DDP) or etoposide (VP16)-induced pyroptosis by decreasing GSDME-NT and cleaved caspase-3 expression, resulting in cell blebbing and LDH release. Knockdown of HMGB1 expression increased the sensitivity of SH-SY5Y cells to chemotherapy and switched pyroptosis to apoptosis. Furthermore, the ROS/ERK1/2/caspase-3/GSDME pathway was found to be functionally connected with DDP or VP16-induced pyroptosis. Hydrogen peroxide (H₂O₂, a ROS agonist) and EGF (an ERK agonist) promoted the cleavage of GSDME and caspase-3 in DDP or VP16 treatment cells, both of which were inhibited by HMGB1 knockdown. Importantly, these data were further supported by the in vivo experiment. Our study suggests that HMGB1 is a novel regulator of pyroptosis via the ROS/ERK1/2/caspase-3/GSDME pathway and a potential drug target for therapeutic interventions in neuroblastoma.