羊角椒新品种寿研梦扬的选育

寿研梦扬是由母本CSVHPM1407001和父本CSVHPF1407002配制而成的羊角椒一代杂种。植株长势旺盛,连续坐果能力强;果实长羊角形,果长25～30 cm,果肩宽3～4 cm;青熟果黄绿色,老熟果红色;外表光亮,商品性好,耐贮运;单果质量100 g左右,辣味浓,宜鲜食;田间对病毒病、炭疽病和疫病的抗性强于对照喜洋洋。保护地栽培鲜椒产量可达12 840 kg·(667 m~2)~(-1)左右。适宜山东、河北等地区早春、秋延保护地种植。     

黑甜糯玉米新品种黑甜糯639的选育

黑甜糯639是以糯玉米自交系HNF为母本,以甜玉米自交系D91为父本配制而成的黑甜糯玉米一代杂种。生育期为91 d(天),株高263 cm,穗位151 cm,雄穗主轴与分枝角度中等,一级分枝18～23个,果穗筒型,籽粒黑紫色,甜糯籽粒比例为1∶3,籽粒可溶性糖含量为12.5%,支链淀粉占总淀粉含量的98.1%,口感佳。高抗丝黑穗病、茎腐病、大斑病,抗穗腐病和矮花叶病,平均每667 m~2鲜穗产量900 kg左右。适宜在山西省鲜食糯玉米主产区种植。     

早熟松散型花椰菜新品种优松58的选育

优松58是以细胞质雄性不育系HZ-28为母本,以自交系HL-94为父本配制而成的早熟松散型花椰菜一代杂种。华北地区秋露地从定植至收获60 d(天)左右。株型半直立,生长势强,叶片椭圆形,深绿色,叶缘多波浪;花球半球形,白色,球面光滑,花梗绿,口感脆嫩、甜,品质优,单球质量1.0 kg左右。常规栽培平均每667 m~2产量2 000 kg以上,可适当密植,田间对霜霉病、黑腐病的抗性强于对照津松62,适合北京、天津、河北、河南、山东、安徽等地秋季露地栽培。     

豇豆新品种之豇618的选育

之豇618是以从四川引进的麻子豇豆为母本,以从辽宁引进的ZH优选株系为父本进行杂交,采用系统选育结合分子标记辅助抗枯萎病鉴定育成的中熟豇豆新品种。植株蔓生,花紫色,主侧蔓均可结荚,平均单株结荚14.4条;商品荚油绿色,条荚顺直,喙绿色,鼠尾少,平均荚长63.7 cm,单荚质量26.6 g,豆荚肉厚,粗纤维含量低,口感糯、微甜,可溶性糖含量为24.0 mg · g~(-1);对日照长短不敏感,中抗枯萎病和病毒病,早期产量与之豇106相当,总产量2 000 kg · (667 m~2)~(-1)左右,适宜在全国各地(除高寒地区外)种植。     

辣椒新品种桂牛5号的选育

桂牛5号是以自交系Ca1-5-1为母本,以自交系Ca1-3-8为父本配制而成的牛角椒一代杂种。中早熟,植株生长势较强,连续坐果能力强;果实长牛角形,果长25～30 cm,果肩宽3.5～4.0 cm,单果质量125 g左右;青熟果黄绿色,老熟果鲜红色,商品性好,微辣,果实干物质含量7.88%,VC含量1?530 mg · kg~(-1),辣椒素含量0.023%,宜鲜食,耐贮运;田间对病毒病、炭疽病、疫病的抗性强于对照黄美龙,露地栽培鲜椒产量3?500 kg · (667 m~2)~(-1)左右,适宜广西、广东等地春、秋露地种植。     

叶用芥菜新品种甬雪5号的选育

甬雪5号是以胞质雄性不育系07-50A为母本,以自交系09-3-1为父本配制而成的晚熟叶用芥菜(雪里蕻)一代杂种。播种至采收约112 d(天)。株型开展,生长势强,叶浅绿色,倒卵形,叶缘浅锯齿,叶裂刻深裂,叶面微皱、有光泽。平均有效蘖数26个,单株质量约1.1 kg,一般每667 m~2产量5?000 kg左右。抗病毒病(TuMV),加工品质优良,适宜在长江流域种植。     

菜用豌豆尖专用品种云豌1号的选育

云豌1号是以食荚90-17(无须蔓生品种)为母本,以食荚大菜豌(矮生品种)为父本进行杂交,经系统选育而成的矮生无须菜用豌豆新品种。植株直立矮生,株高50～60 cm,复叶无须(即卷须退化),营养体发达,叶片肥厚,嫩梢纤维少,幼苗质地柔软,食用品质佳,VC含量34.9 mg · kg~(-1),总黄酮含量3?290 mg · kg~(-1)。一般每667 m~2可产嫩尖850～1?200 kg,适宜云南省海拔1?100～2?400 m的豌豆产区或南方生境相似的秋播豌豆产区种植。     

低聚半乳糖干预缓解肠道炎症的研究进展

肠道炎症已成为我国社会健康的难题和挑战，其发病率在我国迅速增长。肠道炎症发病原因复杂，目前尚缺乏有效的缓解药物，因此加强肠道炎症有效缓解物质的研发至关重要。低聚半乳糖（galactooligosaccharide，GOS）是一种食疗益生性较优的乳源功能性低聚糖，能够有效促进肠道内益生菌的增殖，改变肠道菌群结构，刺激免疫应答，进而改善肠黏膜屏障功能，缓解肠道炎症。本文综述近年来国内外有关肠道炎症及GOS干预缓解肠道炎症作用的研究进展，并对其应用前景进行展望，为此领域的研究提供科学依据。     

Ethanol extract from Cortex Albiziae attenuates mouse acute liver injury induced by carbon tetrachloride via modulation of NF-κB pathway

AIM:To investigate the protective effect of ethanol extract from Cortex Albiziae on acute liver injury, and to explore its possible mechanism. METHODS:Acute liver injury in mice was induced by single intraperitoneal injection of 25% carbon tetrachloride (olive oil solubilization). The effective parts of ethanol extract from Cortex Albizziae against acute liver injury were screened. The pathological changes of the liver tissues were examined by pathological sections with HE staining. The activity of total superoxide dismutase (T-SOD) and the content of malondialdehyde (MDA) of the liver tissues were detected, the serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were mea-sured by ELISA, and the protein expression levels of NF-κB p65, Bcl-2 and Bax in the liver cells of the mice in each group were determined by Western blot. RESULTS:Compared with model group, the serum levels of AST and ALT in low-dose n-butanol phase of ethanol extract from Cortex Albiziae (AB-L, 4 mg·kg^-1·d^-1) group and high-dose n-butanol phase of ethanol extract from Cortex Albiziae (AB-H, 8 mg·kg^-1·d^-1) group were significantly decreased. The necrosis extent and degree of the hepatocytes and infiltration of inflammatory cells were significantly lower than that in model group. Compared with model group, the serum levels of TNF-α and IL-6 in AB-H group and AB-L group were significantly decreased (P<0.05). The protein level of NF-κB p65 in the nuclei of mouse liver cells in AB-H group and AB-L group were also decreased significantly (P<0.05). Compared with model group, the protein expression of Bax was decreased, the protein expression of Bcl-2 was increased, and the Bcl-2/Bax ratio was increased in AB-L group and AB-H group. CONCLUSION:The n-butanol phase of ethanol extract from Cortex Albiziae may protect the liver by reducing the activation of NF-κB p65, inhibiting the excessive release of inflammatory cytokines IL-6 and TNF-α, and decreasing hepatocyte apoptosis via regulating Bcl-2 and Bax expression.