Production of conjugated linoleic acid by isolated Bifidobacterium strains

Two isolates from Korean faecal samples converted linoleic acid (LA) into conjugated linoleic acid (CLA), and were identified as Bifidobacterium breve and Bifidobacterium pseudocatenulatum by analysis of 16S rRNA sequences. In both cases, the major CLA was the cis-9, trans-11 isomer and CLA production paralleled the increase in cell biomass with both bacteria and was maximal at 30 h. The quantities of supernatant CLA produced by B. breve and B. pseudocatenulatum were 160 and 135 mg l^–1, from 500 mg LA l^–1, respectively. In the presence of 0.05% LA, the growth of B. breve was weakly inhibited but that of B. pseudocatenulatum was not affected over 6 days fermentation. During fermentation, the majority of CLA isomers were in the culture supernatant, but with washed cells obtained at the early stationary phase, 36 h, about 40% was detected in the cellular lipid. The optimal culture age with equal concentrations of washed cells for CLA production by the two bifidobacteria was determined to be 36 h. At this culture age, total CLA conversion of supernatant and cell pellets was 78% in B. breve and 69% in B. pseudocatenulatum from 0.01% LA.     

Anti-atopic dermatitis effects of Parasenecio auriculatus via simultaneous inhibition of multiple inflammatory pathways

The treatment of atopic dermatitis (AD) is challenging due to its complex etiology. From epidermal disruption to chronic inflammation, various cells and inflammatory pathways contribute to the progression of AD. As with immunosuppressants, general inhibition of inflammatory pathways can be effective, but this approach is not suitable for long-term treatment due to its side effects. This study aimed to identify a plant extract (PE) with anti-inflammatory effects on multiple cell types involved in AD development and provide relevant mechanistic evidence. Degranulation was measured in RBL-2H3 cells to screen 30 PEs native to South Korea. To investigate the anti-inflammatory effects of Parasenecio auriculatus var. matsumurana Nakai extract (PAE) in AD, production of cytokines and nitric oxide, activation status of FcεRI and TLR4 signaling, cell-cell junction, and cell viability were evaluated using qRT-PCR, western blotting, confocal microscopy, Griess system, and an MTT assay in RBL-2H3, HEK293, RAW264.7, and HaCaT cells. For in vivo experiments, a DNCB-induced AD mouse model was constructed, and hematoxylin and eosin, periodic acid-Schiff, toluidine blue, and F4/80-staining were performed. The chemical constituents of PAE were analyzed by HPLC-MS. By measuring the anti-degranulation effects of 30 PEs in RBL-2H3 cells, we found that Paeonia lactiflora Pall., PA, and Rehmannia glutinosa (Gaertn.) Libosch. ex Steud. show an inhibitory activity of more than 50%. Of these, PAE most dramatically and consistently suppressed cytokine expression, including IL-4, IL-9, IL-13, and TNF-α. PAE potently inhibited FcεRI signaling, which mechanistically supports its basophil-stabilizing effects, and PAE downregulated cytokines and NO production in macrophages via perturbation of toll-like receptor signaling. Moreover, PAE suppressed cytokine production in keratinocytes and upregulated the expression of tight junction molecules ZO-1 and occludin. In a DNCB-induced AD mouse model, the topical application of PAE significantly improved atopic index scores, immune cell infiltration, cytokine expression, abnormal activation of signaling molecules in FcεRI and TLR signaling, and damaged skin structure compared with dexamethasone. The anti-inflammatory effect of PAE was mainly due to integerrimine. Our findings suggest that PAE could potently inhibit multi-inflammatory cells involved in AD development, synergistically block the propagation of inflammatory responses, and thus alleviate AD symptoms.     

LncRNA‐AK137033 inhibits the osteogenic potential of adipose‐derived stem cells in diabetic osteoporosis by regulating Wnt signaling pathway via DNA methylation

ObjectivesBone tissue engineering based on adipose‐derived stem cells (ASCs) is expected to become a new treatment for diabetic osteoporosis (DOP) patients with bone defects. However, compared with control ASCs (CON‐ASCs), osteogenic potential of DOP‐ASCs is decreased, which increased the difficulty of bone reconstruction in DOP patients. Moreover, the cause of the poor osteogenesis of ASCs in a hyperglycemic microenvironment has not been elucidated. Therefore, this study explored the molecular mechanism of the decline in the osteogenic potential of DOP‐ASCs from the perspective of epigenetics to provide a possible therapeutic target for bone repair in DOP patients with bone defects.Materials and methodsAn animal model of DOP was established in mice. CON‐ASCs and DOP‐ASCs were isolated from CON and DOP mice, respectively. {"type":"entrez-nucleotide","attrs":{"text":"AK137033","term_id":"74205820","term_text":"AK137033"}}AK137033 small interfering RNA (SiRNA) and an {"type":"entrez-nucleotide","attrs":{"text":"AK137033","term_id":"74205820","term_text":"AK137033"}}AK137033 overexpression plasmid were used to regulate the expression of {"type":"entrez-nucleotide","attrs":{"text":"AK137033","term_id":"74205820","term_text":"AK137033"}}AK137033 in CON‐ASCs and DOP‐ASCs in vitro. Lentiviruses that carried shRNA‐{"type":"entrez-nucleotide","attrs":{"text":"AK137033","term_id":"74205820","term_text":"AK137033"}}AK137033 or {"type":"entrez-nucleotide","attrs":{"text":"AK137033","term_id":"74205820","term_text":"AK137033"}}AK137033 cDNA were used to knockdown or overexpress {"type":"entrez-nucleotide","attrs":{"text":"AK137033","term_id":"74205820","term_text":"AK137033"}}AK137033, respectively, in CON‐ASCs and DOP‐ASCs in vivo. Hematoxylin and eosin (H&E), Masson''s, alizarin red, and alkaline phosphatase (ALP) staining, micro‐computed tomography (Micro‐CT), flow cytometry, qPCR, western blotting, immunofluorescence, and bisulfite‐specific PCR (BSP) were used to analyze the functional changes of ASCs.ResultsThe DOP mouse model was established successfully. Compared with CON‐ASCs, {"type":"entrez-nucleotide","attrs":{"text":"AK137033","term_id":"74205820","term_text":"AK137033"}}AK137033 expression, the DNA methylation level of the sFrp2 promoter region, Wnt signaling pathway markers, and the osteogenic differentiation potential were decreased in DOP‐ASCs. In vitro experiments showed that {"type":"entrez-nucleotide","attrs":{"text":"AK137033","term_id":"74205820","term_text":"AK137033"}}AK137033 silencing inhibited the Wnt signaling pathway and osteogenic ability of CON‐ASCs by reducing the DNA methylation level in the sFrp2 promoter region. Additionally, overexpression of {"type":"entrez-nucleotide","attrs":{"text":"AK137033","term_id":"74205820","term_text":"AK137033"}}AK137033 in DOP‐ASCs rescued these changes caused by DOP. Moreover, the same results were obtained in vivo.ConclusionsLncRNA‐{"type":"entrez-nucleotide","attrs":{"text":"AK137033","term_id":"74205820","term_text":"AK137033"}}AK137033 inhibits the osteogenic potential of DOP‐ASCs by regulating the Wnt signaling pathway via modulating the DNA methylation level in the sFrp2 promoter region. This study provides an important reference to find new targets for the treatment of bone defects in DOP patients.     

植物细胞电融合技术在空间实验中的应用

细胞电融合是实用性很强的生物技术,然而在地面上由于重力沉降和热对流的影响,杂种细胞融合得率较低,使得这项技术在生产上的应用潜力难以发挥。大量的实验表明,空间微重力环境是实现细胞电融合的重要途径。今后有望利用空间微重力条件获得有价值的杂合细胞,培育作物新品种,为开展空间生物加工和空间制药提供良好基础。     

Finite element modelling of human auditory periphery including a feed-forward amplification of the cochlea

A three-dimensional finite element model is developed for the simulation of the sound transmission through the human auditory periphery consisting of the external ear canal, middle ear and cochlea. The cochlea is modelled as a straight duct divided into two fluid-filled scalae by the basilar membrane (BM) having an orthotropic material property with dimensional variation along its length. In particular, an active feed-forward mechanism is added into the passive cochlear model to represent the activity of the outer hair cells (OHCs). An iterative procedure is proposed for calculating the nonlinear response resulting from the active cochlea in the frequency domain. Results on the middle-ear transfer function, BM steady-state frequency response and intracochlear pressure are derived. A good match of the model predictions with experimental data from the literatures demonstrates the validity of the ear model for simulating sound pressure gain of middle ear, frequency to place map, cochlear sensitivity and compressive output for large intensity input. The current model featuring an active cochlea is able to correlate directly the sound stimulus in the ear canal with the vibration of BM and provides a tool to explore the mechanisms by which sound pressure in the ear canal is converted to a stimulus for the OHCs.     

20世纪90年代以来中国西南地区土地覆被变化

西南地区是我国重要的生态安全屏障区,也是气候敏感区和生态脆弱区。20世纪90年代以来,西南地区土地覆被发生了巨大变化,对生态环境和生态系统服务功能产生重大影响。基于全国30 m土地覆被数据集,分析了近20 a来西南地区土地覆被格局、变化及驱动因素。同时,基于MODIS-NDVI数据,利用像元二分模型估算了2000—2010年250 m分辨率年最大植被覆盖度,对森林、灌丛和草地的植被覆盖度变化进行分析。结果表明:1)2010年西南地区土地覆被以森林和草地为主,分别占总面积的29.08%和24.11%。2)1990—2010年西南地区森林、湿地和人工表面分别增加1.39%、5.86%和48.57%,灌丛、耕地和裸露地分别减少2.12%、2.88%和0.64%,变化的区域主要集中在生态建设重点区、城市圈、地震灾区、三峡库区、三江源区、青藏高原东南部和云南南部。3)2000—2010年西南地区森林、灌丛和草地植被覆盖度呈增加趋势的面积分别占26.54%、32.53%和28.87%,但汶川地震重灾区、横断山区、云南南部等地的森林及灌丛植被覆盖度下降,青藏高原东南部、川西高原草地退化。近20 a来,尽管气候变化对西南地区的土地覆被有一定影响,但人类活动仍然是导致其变化及时空差异的主要原因。     

刈割对外来入侵植物黄顶菊的生长、 气体交换和荧光的影响

为明确不同刈割处理对黄顶菊生长和生理特性的影响,本研究在田间条件下,对黄顶菊在生长季内不同时间进行刈割处理。结果表明,刈割降低了黄顶菊植株各部分的生物量积累,其中以刈割3次效果最为显著,使黄顶菊总生物量、根生物量、茎生物量、叶生物量分别较对照下降82.57%、44.53%、80.04%、91.76%;植株的高度和花序数随刈割次数的增加显著降低,其中刈割3次的花序数为0;刈割1次植株分枝数最大,出现超补偿现象,刈割3次分枝数显著低于其他处理;叶绿素含量除了刈割2次出现增高趋势外,随刈割次数的增加,叶绿素含量逐渐降低;刈割处理使黄顶菊净光合速率(Pn)、气孔导度(Cond)和蒸腾速率(Tr)均显著升高;刈割3次的PSⅡ的最大光化学效率(Fv/Fm)和PSⅡ的潜在活性(Fv/F0)显著低于其它各处理,而初始荧光(F0)则显著增加;生长指标的可塑性指数大于生理指标可塑性指数,表明前者在黄顶菊对刈割处理等物理措施适应方面起到了更为重要的作用。总之,刈割3次处理黄顶菊的各项生长和生理指标所受影响最大,对黄顶菊植株的再生和开花结实抑制效果最为理想。     

Doping‐Free Asymmetrical Silicon Heterocontact Achieved by Integrating Conjugated Molecules for High Efficient Solar Cell

Organic conjugated molecule/silicon (Si) heterojunction has been widely investigated to build up an asymmetrical heterocontact for efficient photovoltaics. However, it is still unclear how the organic molecular structures can affect their electronic coupling interaction with Si. Here, two widely explored electron acceptors of poly{[N,N′‐bis(2‐octyldodecyl)‐naphthalene‐1,4,5,8‐bis(dicarboximide)‐2,6‐diyl]‐alt‐5,5′‐(2,2′‐bithiophene)} (N2200) and [6,6]‐phenyl‐C₆₁‐butyric acid methyl ester (PCBM) are used to build up asymmetrical Si heterocontact to investigate their electronic coupling interaction. It is found that PCBM displays different electronic coupling with Si from N2200, which is ascribed to their various physical distance with Si based on a systematic and detailed density functional theory calculation. Organic layer incorporation not only suppresses the surface charge recombination velocity but also leads to an Ohmic contact between Si and Al. Therefore, a doping‐free organic/Si heterojunction photovoltaic with a power conversion efficiency of 14.9% is achieved with PCBM layer. This work discloses a key factor affecting organic/Si electronic coupling interaction, which helps build up high quality Si heterocontact for solar cells and other optoelectronic devices. Furthermore, the simplified heterocontact achieved by a low temperature, solution processed, and lithography‐free steps has a dramatic improvement on conventional diffusion doped‐silicon one at high temperature.     

Intravenous Mesenchymal Stem Cell Administration Modulates Monocytes/Macrophages and Ameliorates Asthmatic Airway Inflammation in a Murine Asthma Model

Although asthma is a common chronic airway disease that responds well to anti-inflammatory agents, some patients with asthma are unresponsive to conventional treatment. Mesenchymal stem cells (MSCs) have therapeutic potential for the treatment of inflammatory diseases owing to their immunomodulatory properties. However, the target cells of MSCs are not yet clearly known. This study aimed to determine the effect of human umbilical cord-derived MSCs (hUC-MSCs) on asthmatic lungs by modulating innate immune cells and effector T cells using a murine asthmatic model. Intravenously administered hUC-MSCs reduced airway resistance, mucus production, and inflammation in the murine asthma model. hUC-MSCs attenuated not only T helper (Th) 2 cells and Th17 cells but also augmented regulatory T cells (Tregs). As for innate lymphoid cells (ILC), hUC-MSCs effectively suppressed ILC2s by downregulating master regulators of ILC2s, such as Gata3 and Tcf7. Finally, regarding lung macrophages, hUC-MSCs reduced the total number of macrophages, particularly the proportion of the enhanced monocyte-derived macrophage population. In a closer examination of monocyte-derived macrophages, hUC-MSCs reduced the M2a and M2c populations. In conclusion, hUC-MSCs can be considered as a potential anti-asthmatic treatment given their therapeutic effect on the asthmatic airway inflammation in a murine asthma model by modulating innate immune cells, such as ILC2s, M2a, and M2c macrophages, as well as affecting Tregs and effector T cells.     

Host Genetics Predict Clinical Deterioration in HCV-Related Cirrhosis

Single nucleotide polymorphisms (SNPs) in the epidermal growth factor (EGF, rs4444903), patatin-like phospholipase domain-containing protein 3 (PNPLA3, rs738409) genes, and near the interleukin-28B (IL28B, rs12979860) gene are linked to treatment response, fibrosis, and hepatocellular carcinoma (HCC) in chronic hepatitis C. Whether these SNPs independently or in combination predict clinical deterioration in hepatitis C virus (HCV)-related cirrhosis is unknown. We genotyped SNPs in EGF, PNPLA3, and IL28B from liver tissue from 169 patients with biopsy-proven HCV cirrhosis. We estimated risk of clinical deterioration, defined as development of ascites, encephalopathy, variceal hemorrhage, HCC, or liver-related death using Cox proportional hazards modeling. During a median follow-up of 6.6 years, 66 of 169 patients experienced clinical deterioration. EGF non-AA, PNPLA3 non-CC, and IL28B non-CC genotypes were each associated with increased risk of clinical deterioration in age, sex, and race-adjusted analysis. Only EGF non-AA genotype was independently associated with increased risk of clinical deterioration (hazard ratio [HR] 2.87; 95% confidence interval [CI] 1.31–6.25) after additionally adjusting for bilirubin, albumin, and platelets. Compared to subjects who had 0–1 unfavorable genotypes, the HR for clinical deterioration was 1.79 (95%CI 0.96–3.35) for 2 unfavorable genotypes and 4.03 (95%CI 2.13–7.62) for unfavorable genotypes for all three loci (P_trend<0.0001). In conclusion, among HCV cirrhotics, EGF non-AA genotype is independently associated with increased risk for clinical deterioration. Specific PNPLA3 and IL28B genotypes also appear to be associated with clinical deterioration. These SNPs have potential to identify patients with HCV-related cirrhosis who require more intensive monitoring for decompensation or future therapies preventing disease progression.