干旱胁迫下喷施黄腐酸对燕麦光合及其抗氧化酶活性的影响

为了揭示黄腐酸对干旱胁迫下燕麦光合及其抗氧化酶活性的影响机理,该研究选用燕麦品种‘燕科2号’为材料,采用盆栽试验,以正常供水(田间持水量的75%)为对照(CK),设干旱胁迫处理(田间持水量的45%,D0)、D0 + 喷施不同浓度黄腐酸(0、200、400、600、800、1 000 mg/L)处理(D1~D5),测定各处理燕麦干鲜重、光合性能及其抗氧化酶活性。结果表明:(1)与CK相比,干旱胁迫下燕麦幼苗地上部鲜重和干重、叶片光合色素含量、净光合速率(P_n)、蒸腾速率(T_r)、气孔导度(G_s)均显著降低,并导致叶片F_v/F_m、qP、ETR和Φ_PSⅡ显著下降,使叶片抗氧化酶 SOD、POD、CAT活性分别显著提高25.68%、19.98%和7.29%。(2)与D0相比,D0 +喷施600 mg/L黄腐酸后,燕麦幼苗地上部鲜重和干重分别显著提高了28.59%和39.13%,叶片叶绿素a、叶绿素a+b、类胡萝卜素和P_n、G_s、T_r及F_v/F_m、Φ_PSⅡ、ETR分别显著增加了25.17%、21.03%、47.37%和74.38%、26.47%、43.34%及6.49%、69.57%、70.71%,C_i和F_o、NPQ分别显著降低了19.52%和13.32%、43.75%。(3)干旱胁迫下喷施不同浓度的黄腐酸均使幼苗叶片中SOD、POD、CAT活性较D0处理显著增加,其中喷施600 mg/L黄腐酸的叶片SOD、POD、CAT活性最高,分别较D0处理显著增加了12.19%、76.57%和55.26%。研究认为,叶面喷施适宜浓度黄腐酸能够显著提高干旱胁迫下燕麦幼苗的光合作用及其抗氧化能力,缓解干旱对燕麦幼苗的伤害,进而促进燕麦幼苗的生长,且以叶面喷施600 mg/L黄腐酸效果最佳。     

重度干旱胁迫下燕麦叶片活性氧清除系统对喷施腐植酸水溶肥的响应

以燕麦品种‘燕科2号’为试验材料,采用盆栽方式,设置正常供水(CK)、正常供水下喷施腐植酸水溶肥(CKH)、重度干旱胁迫(SS)和重度干旱胁迫下喷施腐植酸水溶肥(SSH)４个处理,对燕麦叶片中活性氧水平、抗氧化酶活性、总抗氧化剂含量及产量等进行测定,以明确腐植酸水溶肥(HA)对重度干旱胁迫下燕麦叶片活性氧清除系统的调控效应,并探讨HA对燕麦耐旱性的影响及其作用机制。结果表明：(1)与CK相比,燕麦叶片超氧阴离子( O₂^-·)、羟自由基(·OH)、过氧化氢(H₂O₂)和丙二醛(MDA)含量、以及超氧化物歧化酶(SOD)和过氧化物酶(POD)活性在重度干旱胁迫下显著提高,且均在喷施HA后比重度干旱胁迫处理显著降低,但此时活性氧的水平仍显著高于CK。(2)与CK相比,燕麦叶片过氧化氢酶(CAT)、抗坏血酸过氧化物酶(APX)、谷胱氨肽还原酶(GR)和谷胱氨肽过氧化物酶(GPX)活性在重度干旱胁迫下显著降低,而其总抗氧化能力(T AOC)显著提高,它们在喷施HA后均比重度干旱胁迫处理显著提高,但各酶活性仍不同程度低于CK。(3)与CK相比,燕麦籽粒产量和生物产量在重度干旱胁迫下显著下降,喷施HA后又比重度干旱胁迫显著升高,但仍显著低于CK。研究认为,喷施HA可有效提高重度干旱胁迫下燕麦叶片抗氧化酶活性,促进抗氧化物质再生,增强叶片的总抗氧化能力,从而有效清除重度干旱胁迫引起的活性氧积累,降低重度干旱胁迫对植物细胞膜的氧化损伤,最终缓解重度干旱胁迫对燕麦造成的伤害,一定程度上能够减少籽粒产量的损失。     

盐与碱胁迫对燕麦离子平衡和有机酸含量的影响

以燕麦品种‘白燕2号’为材料,试验分别设置0、50、100、150、200 mmol/L盐胁迫(NaCl∶Na₂SO₄=5∶1)和碱胁迫(NaHCO₃∶Na₂CO₃=5∶1)处理的温室内盆栽试验,观测燕麦植株生长速率、植株含水率、叶片离子含量及叶片各类有机酸含量,分析不同盐胁迫、碱胁迫对燕麦离子平衡的影响,并比较燕麦对两类胁迫的适应性差异。结果显示：(1)燕麦植株生长速率和植株含水率在低浓度(50和100 mmol/L)盐胁迫下均升高,而高浓度(150和200 mmol/L)盐胁迫下则降低;燕麦植株生长速率和植株含水率均随碱胁迫浓度增加而降低;在相同胁迫浓度下,碱胁迫对植株生长率、植株含水率的影响大于盐胁迫。(2)燕麦叶片K⁺、Ca²⁺、Mg²⁺、H₃PO^-₄、NO^-₃ 含量均随盐、碱浓度升高而降低,而Na⁺、Cl^-、SO^2-₄含量在盐、碱胁迫下均大幅上升;200 mmol/L盐、碱胁迫下,Na⁺ 含量分别较对照增加367.15%和518.41%,Cl^- 含量分别较对照增加785.07%和52.59%,SO^2-₄ 分别较对照增加142.01%和52.86%。(3)200 mmol/L盐、碱胁迫下,有机酸分别较对照增加74.52%和1 232.34%;碱胁迫及高浓度盐胁迫下燕麦叶片的柠檬酸、乌头酸、琥珀酸和苹果酸含量均高于对照,且乌头酸是燕麦响应盐胁迫、碱胁迫的主要有机酸成分,柠檬酸和琥珀酸略有变化,而甲酸、乙酸、乳酸、苹果酸、草酸含量均相对较低。研究表明,碱胁迫对燕麦植株生长速率、植株含水率、叶片离子含量及叶片各类有机酸含量的影响大于盐胁迫;盐胁迫与碱胁迫均引起燕麦叶片阳离子(Na⁺)大量积累,而K⁺、Ca²⁺、Mg²⁺、H₃PO^-₄及NO^-₃吸收受阻;燕麦叶片在盐胁迫下主要通过积累Cl^-调节叶片离子平衡,而碱胁迫下主要通过积累有机酸来调节离子平衡;有机酸是燕麦叶片响应碱胁迫的特异代谢物,其中乌头酸是其有机酸的主要成分。     

干旱胁迫对燕麦生长及叶片光系统Ⅱ活性的影响

以‘燕科2号’燕麦品种为试验材料,采用盆栽控水的方式分别设置正常供水(75%田间持水量)、中度干旱胁迫(60%田间持水量)、重度干旱胁迫(45%田间持水量)3个水分处理,利用叶绿素荧光技术研究了不同水分梯度下燕麦生长和叶片光反应系统Ⅱ(PSⅡ)功能的变化,探讨干旱胁迫对燕麦叶片光合性能的影响。结果表明：(1)干旱胁迫导致燕麦株高变矮,叶片数、主茎数、穗数减少,叶片失绿发黄及籽粒产量显著下降。(2)与正常供水相比,重度干旱胁迫下燕麦叶片最大光化学效率(F_v/F_m)和光合性能指数(PI_ABS)显著降低。(3)重度干旱胁迫导致燕麦叶片单位反应中心吸收的光能(ABS/RC)和单位反应中心耗散掉的能量(DI₀/RC)明显下降,单位反应中心用于电子传递的能量(ET₀/RC)和单位反应中心捕获的光能(TR₀/RC)明显升高;有活性反应中心的开放程度(Ψ₀)和电子传递链的量子产额(φ_E0)明显下降、非光化学淬灭最大量子产额(φ_D0)明显升高,V_J、V_K、V_L 3个位点的相对荧光强度明显升高,OJIP曲线初始斜率M_o明显升高。研究发现,燕麦叶片PSⅡ对中度干旱胁迫具有较强的适应能力,而重度干旱胁迫严重伤害其叶片PSⅡ反应中心,导致其反应中心能流分配失衡,电子传递受阻和PSⅡ稳固性减弱,进而影响燕麦光合作用,最终导致燕麦生长受到抑制。     

Application of Lake-model based indices from chlorophyll fluorescence on sugarcane seedling Application of Lake-model based indices from chlorophyll fluorescence on sugarcane seedling

 为从能量平衡及分配的角度研究干旱胁迫下甘蔗(Saccharum officinarum)苗期光系统的运转状况, 进而为丰富不同甘蔗品种的抗旱性评价指标及实现对季节性干旱胁迫的快速诊断提供理论依据, 该研究通过对基于Lake模型的叶绿素荧光参数在不同入射光强下变化的动态分析, 研究光合电子传递链中能量平衡状态对不同水分梯度(40%、25%、10%、8%)的响应。结果表明: 两个供试品种(耐旱品种‘ROC22’和非耐旱品种‘ROC16’)的最大光能利用效率(F_v/F_m)、相对电子传递速率(rETR)、光系统II(PSII)量子效率(Φ_II)和光化学猝灭(q_L)均随着干旱胁迫程度的增加而下降, 可调节性能量耗散(Φ_NPQ)和非调节性能量耗散(Φ_NO)则随着干旱胁迫程度的增加而上升。除Φ_NO之外的叶绿素荧光参数的变化幅度均随着光合有效辐射(PAR)的增加而增大。在干旱胁迫的前中期, 相对于‘ROC22’, ‘ROC16’的PSII反应中心能够维持较高的开放程度; 但‘ROC22’调节能量耗散的能力和对干旱胁迫的敏感程度均高于‘ROC16’, 说明较强的光保护能力是‘ROC22’的抗旱性高于‘ROC16’的主要原因之一。对干旱胁迫敏感且在不同PAR下较为稳定的Φ_NO可作为甘蔗苗期抗旱性的快速诊断和评价指标。rETR对递增的PAR的响应表现为随着干旱胁迫程度的增加而提前出现峰值或下降趋势, 但是不同水分梯度下的rETR在PAR较低时并无显著差异, 表明干旱胁迫下光抑制现象的提早出现是造成光系统损伤的首要因素, 高光强对干旱胁迫信号起放大作用。     

外源SNP对干旱胁迫下不同马铃薯品种叶片抗氧化酶活性的影响

以正常水分状态、轻度干旱胁迫、中度干旱胁迫和重度干旱胁迫下的马铃薯抗旱品种‘底西瑞’和干旱敏感品种‘大西洋’ 植株为材料,于现蕾期采用0（对照）和0.01 mmol·L^-1 SNP分别喷施各处理植株,对不同处理下2个品种的植株形态、叶片超氧阴离子和H₂O₂含量以及抗氧化酶活性进行比较分析,探讨外源SNP对干旱状态下马铃薯的生理应答机制,为马铃薯的抗旱栽培提供新的技术理论支持。结果显示：（1）SNP喷施对重度水分胁迫下马铃薯植株的正常生长具有一定的保护作用。（2）在干旱胁迫条件下,马铃薯叶片POD活性在品种‘底西瑞’中增加而在品种‘大西洋’中降低,超氧阴离子含量和H₂O₂含量以及CAT和APX活性在各品种中均增加,但超氧阴离子含量和H₂O₂含量增加程度与胁迫程度无关。（3）抗旱品种‘底西瑞’在干旱胁迫下的超氧阴离子含量低于干旱敏感品种‘大西洋’,而其POD、CAT和APX活性则高于‘大西洋’; 0.01 mmol·L^-1SNP处理未改变马铃薯叶片中超氧阴离子和H₂O₂含量随土壤水分的变化趋势,但改变了‘大西洋’叶片中SOD、POD、CAT活性以及‘底西瑞’叶片中APX活性的变化趋势。（4）外源喷施0.01 mmol·L^-1SNP降低了‘底西瑞’在中度和重度胁迫下以及‘大西洋’在轻度和中度胁迫下超氧阴离子含量,提高了干旱胁迫下‘底西瑞’和‘大西洋’的POD和APX活性。研究表明,POD、CAT和APX可作为马铃薯水分胁迫下的应答以及品种抗旱性的筛选指标,外源SNP可通过诱导增强干旱胁迫下马铃薯的抗氧化酶活性来提高其抗旱性。     

干旱及复水条件下外源褪黑素对玉米叶片光合作用的影响

为探究干旱胁迫及复水后外源褪黑素对玉米叶片光合作用的影响和调控机制。以玉米陕单609盆栽苗为试验材料,叶面喷施褪黑素100 μmol/L在重度干旱和复水后分别测定了生物量、净光合速率（P_n）以及光合电子传递速率等指标。结果显示：外源褪黑激素可减轻干旱胁迫引起的生长抑制;外源褪黑激素处理的植株表现出比未处理植株更高的P_n、气孔导度（G_s）以及更低的胞间CO₂浓度（C_i）;外源褪黑素增加了干旱胁迫下OJIP曲线的荧光参数φ_P0、φ_E0、ψ₀以及光合性能指数PI_abs;外源褪黑素也提高了干旱胁迫下叶片PSⅡ和PSI有效量子产量[Y（Ⅱ）,Y（I）];也增加了干旱胁迫下叶片的PSⅡ和PSI电子传递速率（ETRⅡ,ETRI）,但降低了干旱胁迫下叶片PSI受体侧限制[Y（NA）]和供体侧限制[Y（ND）]。表明外源褪黑素对干旱胁迫下光抑制具有一定的缓解作用。复水后,干旱胁迫下褪黑素处理玉米叶片各参数都恢复到对照水平;而干旱胁迫处理玉米叶片各参数复水后不能完全恢复。可见,喷施褪黑素不仅缓解干旱胁迫对玉米PSⅡ和PSI结构和功能的损伤,而且能加速复水后光合机构功能的恢复,促进玉米植株恢复性生长。因此喷施褪黑素加强玉米叶片光合作用适应干旱环境是一种重要的调控方式。     

水分和腐植酸对燕麦果聚糖代谢的影响

探讨水分和腐植酸(HA)对燕麦不同器官非结构性碳水化合物(NSC)积累与分配的影响,进一步明确水分和HA对燕麦糖代谢和粒重形成的作用机制,可为旱作地区燕麦的推广种植提供理论指导和技术支撑。试验以‘蒙农大燕1号'和‘内燕5号'两个燕麦品种为材料,分别在旱作(无灌溉)和有限灌溉(拔节期和抽穗期每次灌水60 mm)两个水分条件下喷施HA与清水(CK),研究燕麦开花后不同时期NSC组分在茎、叶、穗中的动态变化以及叶片中碳代谢相关酶活性的变化。结果表明: 两个燕麦品种茎、叶、穗中的NSC组分含量均随开花后时间的延长先升高后降低,且两品种各器官中的NSC组分含量大致相同;与CK相比,在灌水条件下喷施HA后蒙农大燕1号穗部的果聚糖含量提升幅度明显大于旱作条件;喷施HA后蒙农大燕1号叶片中果聚糖外水解酶和转化酶活性分别显著提高了27.1%和30.6%,单穗粒重显著提高了55.9%,且与旱作条件下相比提高幅度更大;蒙农大燕1号籽粒千粒重和单穗粒重与叶片果聚糖含量呈显著正相关关系。综上,水分和腐植酸协同作用可以有效调节燕麦果聚糖的积累及主要代谢酶活性,从而提高千粒重和单穗粒重,促进产量形成。     

干旱胁迫对2种光合类型C4荒漠植物叶片光合特征酶和抗氧化酶活性的影响

以荒漠C₄草本植物蔷薇猪毛菜(NADP苹果酸酶型,NADP-ME）和粗枝猪毛菜（NAD苹果酸酶型,NAD-ME）为研究对象,采用盆栽控水试验设置正常供水和轻度、中度、重度干旱处理（土壤含水量分别为田间持水量80%、60%、45%和35%）,通过测定不同程度干旱胁迫下叶片含水量、C₄光合特征酶和抗氧化酶活性等指标,探讨不同类型C₄荒漠植物光合特征酶和抗氧化系统对干旱逆境的适应机制。结果显示：（1）2种植物叶片含水量均随干旱胁迫的加剧不同程度降低。（2）叶片磷酸烯醇式丙酮酸羧化酶（PEPC）活性在中度干旱胁迫下显著增加而在重度干旱胁迫下急剧下降;蔷薇猪毛菜NAD-ME活性和粗枝猪毛菜NADP-ME活性都很低,且它们基本不受干旱胁迫的影响;随干旱胁迫的加剧,蔷薇猪毛菜NADP-ME活性呈下降趋势,而粗枝猪毛菜NAD-ME活性先显著增加而在重度干旱胁迫下显著降低。（3）随着干旱胁迫的加剧,叶片超氧化物歧化酶（SOD）活性呈下降趋势,过氧化物酶（POD）活性在不同程度干旱胁迫下均有不同程度增加;过氧化氢酶（CAT）活性在中度干旱胁迫下均有不同程度的增加,但在重度干旱胁迫下蔷薇猪毛菜CAT活性降低,而粗枝猪毛菜CAT活性显著增加;丙二醛（MDA）含量随干旱胁迫的加剧均有不同程度的增加。研究认为,一定程度干旱胁迫下,2种荒漠植物的PEPC活性均有增加;不同光合类型C₄植物叶片脱羧酶（NADP-ME和NAD-ME）对干旱胁迫的响应有明显的差异。POD和CAT是这两种C₄植物适应干旱胁迫的主要抗氧化酶,但蔷薇猪毛菜CAT在重度干旱胁迫下没有起到积极保护作用。     

水分胁迫对燕麦穗颖渗透调节和抗氧化能力的影响

以抗旱性不同的燕麦品种‘蒙燕1号’(抗旱性强)和‘坝莜3号’(水分敏感)为试验材料,采用盆栽方式研究了抽穗期和灌浆期水分胁迫对燕麦穗颖渗透调节和抗氧化能力的影响。结果表明:(1)水分胁迫处理均显著促进了不同抗旱性品种穗颖渗透调节物质(游离脯氨酸和可溶性蛋白)含量增加,并以抗旱品种累积水平高于水敏感品种,且两种渗透调节物质对抽穗期胁迫的反应比灌浆期胁迫更敏感。(2)两时期的水分胁迫处理均能降低不同抗旱性品种穗颖SOD和POD活性,抗旱品种的保护酶活性要高于水敏感品种,抗旱品种的SOD活性降低幅度明显低于水敏感品种,而POD活性降低幅度在两品种间差异不明显。(3)水分胁迫导致2个品种穗颖丙二醛(MDA)含量和相对电导率显著增加,细胞膜结构受到严重伤害,且水敏感品种受害程度大于抗旱品种。(4)水分胁迫使2个品种单株籽粒产量下降,且在中度胁迫和重度胁迫下,抗旱品种的减产幅度要低于同期水敏感品种;水分胁迫下,水敏感品种‘坝莜3号’减产4.54%~30.29%,抗旱品种‘蒙燕1号’减产6.69%~23.54%。可见,抗旱性强的燕麦品种在受到水分胁迫的条件下能通过增强穗颖渗透调节和抗膜质过氧化能力、减弱穗颖细胞质膜损伤程度来适应干旱胁迫,最大限度减少水分胁迫对穗颖的伤害,有利于稳产。     

The pathogenesis of thyroid autoimmune diseases: New T lymphocytes – Cytokines circuits beyond the Th1−Th2 paradigm

Autoimmune thyroid disease (AITD) is one of the most common organ-specific autoimmune disorders. It mainly manifests as Hashimoto's thyroiditis (HT) and Graves’ disease (GD). HT is characteristic of hypothyroidism resulting from the destruction of the thyroid while GD is characteristic of hyperthyroidism due to excessive production of thyroid hormone induced by thyrotropin receptor-specific stimulatory autoantibodies. T lymphocytes and their secretory cytokines play indispensable roles in modulating immune responses, but their roles are often complex and full of interactions among distinct components of the immune system. Dysfunction of these T cells or aberrant expressions of these cytokines can cause the breakdown of immune tolerance and result in aberrant immune responses during the development of AITDs. This review summarizes recently identified T subsets and related cytokines and their roles in the pathogenesis of AITDs with the hope to provide a better understanding of the precise roles of notably identified T subsets in AITDs and facilitate the discovery of functional molecules or novel immune therapeutic targets for AITDs.     

水稻叶绿素a氧化酶基因突变体的鉴定及其对氮营养的响应

对从日本获得的水稻Tos17插入突变基因进行了鉴定,并通过PCR技术对其插入位点和纯合体进行了分析和筛选。结果表明,Tos17插入在序列号为DP000086的基因,在此基因反向互补序列的1579bp处,在mRNA序列的第5个外显子区域,是水稻的一个叶绿素a氧化酶基因,而且此基因在单一的铵营养下表达减弱,氮饥饿条件下表达增强。利用Tos17未端和插入位点上下游设计引物进行PCR反应,鉴定到3株纯合突变体株,为进一步研究其功能奠定了基础。     

17-allylamino-17-demethoxygeldanamycin impeded chemotherapy through antioxidant activation via reducing reactive oxygen species-induced cell death

Hyperthermia enhances the anticancer effects of thymidylate synthase (TYMS) inhibitors (raltitrexed, RTX) and improves the precise biochemical mechanisms partially through enhancement of intracellular drug absorption. Recent research focuses on the potential anticancer drug target Heat Shock Protein 90 (HSP90), which could increase the sensitivity of cancer cells to TYMS inhibitors; however, with different HSP90 inhibitors, several research studies finally showed a poor efficacy in preclinical or clinical research. Here, we showed that 17-allylamino-17-demethoxygeldanamycin (17-AAG, HSP90 inhibitor) affects the efficacy of chemotherapy through antioxidant activation–induced resistance. In this study, we found that RTX, alone or in combination with hyperthermia, triggers reactive oxygen species (ROS) exposure and thus induces cell death. Also, the addition of hyperthermia showed more ROS exposure and function. The pharmacologic inhibition of HSP90 reversed the effects of chemotherapeutical treatments, while the overexpression of HSP90 showed no relation with these effects, which demonstrated that dysregulation of HSP90 might have a significant impact on chemotherapeutic treatments. The addition of 17-AAG increased the activation of antioxidant with increased antioxidant enzymes, thus affecting the RTX efficacy.     

Quantitation of deoxycorticosterone and its relationship to progesterone in the prepartum bovine.

A method and its validation is described for the radioimmunological measurement of deoxycorticosterone (DOC) in bovine serum. Levels of DOC and progesterone were determined in six pregnant heifers from one to three weeks before and during parturition. Levels of these steroids fluctuated widely from day to day and tended to be inversely related (r = -0.24). High levels of DOC in conjunction with low levels of progesterone at or near parturition are suggestive that DOC is involved in the parturition process.     

miR-17-5p promotes proliferation and epithelial-mesenchymal transition in human osteosarcoma cells by targeting SRC kinase signaling inhibitor 1

MicroRNA-17-5p (miR-17-5p) and epithelial-mesenchymal transition (EMT) have been reported to participate in the development and progression of multiple cancers. However, the relationship between the miR-17-5p and EMT in osteosarcoma (OS) is still poorly understood. This study was to investigate the effects of the miR-17-5p and its potential mechanism in regulating proliferation, apoptosis, and EMT of human OS. Quantitative real-time PCR was used to detect the miR-17-5p and SRC kinase signaling inhibitor 1 (SRCIN1) messenger RNA expression in OS specimens and cell lines. After transfection with miR-17-5p inhibitors, proliferation, apoptosis, migration, and invasion of OS cells were assessed by using the Cell Counting Kit-8, the annexin V-FITC apoptosis, wound-healing, and transwell assays. The SRCIN1 was validated as a target of the miR-17-5p through bioinformatics algorithms and luciferase reporter assay. Moreover, the expression of EMT markers, E-cadherin, N-cadherin, and Snail was identified by the Western blot analysis. MiR-17-5p was significantly upregulated in OS tumor samples and cell lines. It inhibited proliferation and EMT, and promoted apoptosis in OS. The SRCIN1 was identified as a direct target of the miR-17-5p. Silenced miR-17-5p could change the expression of EMT markers, such as upregulating the expression of E-cadherin, and downregulating the expression of N-cadherin and Snail through targeting the antioncogenic SRCIN1. These findings suggest that the miR-17-5p promotes cell proliferation, and EMT in human OS by directly targeting the SRCIN1, and reveal a branch of the miR-17-5p/SRCIN1/EMT signaling pathway involved in the progression of OS.     

In vitro metabolism of 4-androstene-3,17-dione and testosterone by rat submaxillary gland.

Tritiated 4-androstene-3,17-dione and testosterone were incubated with submaxillary gland homogenates of male and female rats. The metabolism was predominately reductive. In 15 and 180 min incubations submaxillary tissue converted 4-androstene-3,17-dione chiefly to androsterone. Less testosterone, 17 beta-hydroxy-5 alpha-androstan-3-one, 5 alpha-androstane-3,17-dione, 5 alpha-androstane-3 alpha, 17 beta-diol, and 4-androstene-3 alpha, 17 beta-diol were also identified. Testosterone was converted to the same products plus 4-androstene-3,17-dione. 5 alpha-Androstane-3 alpha, 17 beta-diol was the major testosterone metabolite. Qualitatively the metabolism by male and female submaxillary gland was similar.     

Calcium-independent and dependent steps in action of Clostridium perfringens enterotoxin on HeLa and Vero cells.

Purified enterotoxin (20–200 ng/ml) of $\text{Clostridium}$$\text{perfringens}$ rapidly induced bled and balloon formation on HeLa and Vero cells in the presence, but not the absence, of Ca²⁺. The action of the toxin involved two, sequential, temperature-dependent steps: The first was Ca²⁺-independent and included binding of toxin and the bound toxin after 30–60 sec could no longer be removed by washing. The second step was Ca²⁺-dependent and eventually led to bled and balloon formation. On adding Ca²⁺ to cells pretreated with toxin in Ca²⁺-free medium, bled and balloon formation started immediately. The ionophore A23187 mimicked the action of toxin. The effects of sucrose (0.2 M), trypsin-treatment of the cells and various pretreatments of the toxin on the action of enterotoxin were studied.     

Aged regulatory T cells protect from autoimmune inflammation despite reduced STAT3 activation and decreased constraint of IL-17 producing T cells

Regulatory T cells (Tregs) are specialized CD4⁺ T lymphocytes helping defend against autoimmunity and inflammation. Although age is associated with increased inflammation and autoimmunity, few reports address age effects of immune regulation or auto‐aggressive T cells. We show here that young and aged naïve CD4⁺ T cells are equivalently auto‐aggressive in vivo in T cell‐driven autoimmune colitis. Young and aged CD4⁺ Tregs equally suppressed age‐matched T cell proliferation in vitro and controlled clinical and pathologic T cell‐driven autoimmune colitis, suggesting equivalent regulatory function. However, whereas young and aged CD4⁺ Tregs suppressed interferon (IFN)‐γ⁺ T cells equivalently in this model, aged CD4⁺ Tregs unexpectedly failed to restrain interleukin (IL)‐17⁺ T cells. Nonetheless, young and aged CD4⁺ Tregs equally restrained IL‐17⁺ T cells in vivo during acute inflammation, suggesting a chronic inflammation‐related defect in aged CD4⁺ Tregs. In support, aged Tregs expressed reduced STAT3 activation, a defect associated with poor IL‐17‐producing T cell restraint. Aged naïve mice had markedly increased programmed death (PD)‐1⁺ T cells, but these exhibited no significant auto‐aggressive or regulatory functions in T cell‐driven colitis. Young CD8⁺ CD122^? T cells induce autoimmune bone marrow failure, but we show that aged CD8⁺ CD122^? T cells do not. These data demonstrate no apparent age‐related increase in auto‐aggressive T cell behavior, but disclose previously unrecognized functional defects in aged CD4⁺ Tregs during chronic inflammation. IL‐17 can be inflammatory and contributes to certain autoimmune disorders. Reduced aged Treg function during chronic inflammation and reduced IL‐17 restraint could contribute to age‐related inflammation or autoimmunity.