碘对诱发易感和非易感小鼠自身免疫性甲状腺炎的实验研究

目的：研究典对实验性自身免疫性甲状腺炎（EAT）易和非易感小鼠诱发EAT的影响，进一步探讨自身免疫性甲状腺疾病（AITD）发病的机理。方法：采用EAT易感（TA－1）和非易感（BALB／c）小鼠经甲状腺球蛋白（Tg）免疫，诱发为EAT实验动物模型并给予不同水平的碘饮食，观察小鼠甲状腺组织的病理改变和炎细胞润程度，血清中Tg自身抗体的水平以及低磺和高碘Tg抗原性的不同。结果：（1）2种品系小鼠经Tg诱发，均出现不同水平的Tg自身抗性和甲状腺的炎症反应，血清中Tg自身抗体的出现早于甲状腺的病理改变。（2）TA－1小鼠的甲状腺炎症反应明显高于BALB／c小鼠，高碘组中的TA－1小鼠炎症较适碘组更明显，为弥漫性伴慢性炎症（＋＋＋）。（3）高碘Tg诱发的Tg抗体与高碘Tg抗原的反应明显高于与低碘Tg抗原的反应，低碘Tg诱发的Tg抗体反之，表明二者抗原性有所不同。结论：高碘摄入会使易感小鼠EAT的发病加重，其机理除了体内的遗传因素，可能与过度碘的Tg抗原性增强有关。     

碘对诱发实验性自身免疫性甲状腺炎形成的影响

目的建立诱发型实验性自身免疫性甲状腺炎(EAT)动物模型,研究碘对诱发EAT形成的影响,进一步探讨其可能的作用机制。方法:采用雌性Lewis大鼠诱发EAT并饲以不同碘含量的饮食,观察各组大鼠甲状腺病理改变、血清中Tg自身抗体水平、血清中甲状腺激素水平、脾细胞分泌TNF水平和甲状腺FasmRNA表达水平。结果1.诱发EAT的HI组大鼠炎症范围较广,为较重度炎症。NI组显示为轻度炎症,且为恢复期。LI组显示为滤泡内少量淋巴细胞浸润。2.诱发EAT的HI、NI和LI组大鼠血清中均出现较高水平的Tg自身抗体,3组间无显著性差异。3.诱发EAT的HI组大鼠脾细胞分泌TNE水平高于NI和LI组(P<0.05)。4.诱发EAT的HI、NI和LI组大鼠甲状腺FasmRNA的表达水平均较各自未诱发EAT的大鼠明显升高,其中HI组高于同组的NI和LI组,P<0.01。结论1.高碘饮食可使已诱发EAT的Lewis大鼠甲状腺组织炎症加重且炎症反应持续时间较长,考虑与脾细胞分泌的TNF水平和甲状腺FasmRNA的表达水平较高有关。2.未发现甲状腺组织炎症的程度与自身抗体水平相关。     

泌乳素对诱发自身免疫性甲状腺炎影响的实验研究

目的 观察和研究泌乳索在诱发实验性自身免疫性甲状腺炎形成中的影响。方法 采用SD大鼠在溴隐亭的干预条件下，诱发实验性自身免疫性甲状腺炎(EAT)，观察大鼠甲状腺组织的病理改变和血清中Tg自身抗体、泌乳露水平及脾脏中的IL—2／IL—2RmRNA的表达。结果 大鼠经溴隐亭干预，诱发的实验性自身免疫性甲状腺炎发病率和甲状腺组织中的炎细胞浸润程度、炎症反应均较未经溴隐亭干预直接诱发EAT组(HI—EAT组)明显减轻，血清中Tg自身抗体平均水平明显高于未诱发EAT大鼠。结论 大鼠经溴隐亭干预，血清中泌乳素水平低下，致IL—2／IL—2RmRNA的表达减少，降低IL—2／L—2R系统对免疫应答的激活作用，其EAT的发病率和甲状腺组织中炎症反应得到缓解，高泌乳素血症也是自身免疫性疾病发病机制中的重要因素。     

瘦素对实验性自身免疫性甲状腺炎影响的实验研究

目的研究瘦素在诱发实验性自身免疫性甲状腺炎（EAT）形成中的影响。方法采用C57BL／6J小鼠在外源性瘦素干预下诱发EAT，观察小鼠甲状腺组织病理改变、淋巴细胞增殖水平、脾细胞培养上清中IFN-γ和IL-4水平以及血清中甲状腺过氧化物酶抗体（TPO—Ab）、甲状腺球蛋白抗体（Tg—Ab）和瘦素水平。结果小鼠经外源性瘦素干预后，其血清中瘦素水平高于EAT组和对照组，实验性自身免疫性甲状腺炎的发病率和甲状腺组织中炎细胞浸润程度也较直接诱发EAT组明显增高。诱发EAT两实验组间比较，脾细胞增殖水平未见明显差异，但瘦素干预组脾细胞培养上清中IFN-γ水平较EAT组明显升高（P=0．000），而IL-4水平则低于EAT组（P=0．000）。两实验组小鼠血清中TPO—Ab和Tg—Ab水平均明显高于未诱发EAT对照组，但两组间比较均未见明显差异。结论瘦素的前炎症作用在实验性自身免疫性甲状腺炎的发生、发展中有重要免疫调节作用。     

碘对易感性不同大鼠诱发自身免疫性甲状腺炎的影响

目的研究碘对实验性自身免疫性甲状腺炎(EAT)易感性不同大鼠诱发EAT的影响,进一步探讨碘和易感性在自身免疫性甲状腺炎(AT)发病中的影响。方法采用猪甲状腺球蛋白(Tg)对不同碘摄入量的Lewis大鼠(EAT易感品系)和Wistar大鼠(EAT非易感品系)进行免疫,诱发EAT形成。观察大鼠甲状腺组织的病理改变和炎细胞浸润程度,用放射免疫分析法检测血清中Tg鄄Ab、TPO(甲状腺过氧化物酶)鄄Ab和甲状腺激素(TT3、TT4)水平。结果①诱发EAT的各组大鼠甲状腺组织均有不同程度的炎细胞浸润,不同碘水平的Lewis大鼠诱发EAT的甲状腺炎症反应均重于诱发EAT的Wistar大鼠,且甲状腺的炎症反应随碘摄入量的增加而加重。②诱发EAT的Lewis大鼠TPO鄄Ab水平明显高于Wistar大鼠各EAT组(P<0.01)。Tg鄄Ab和TPO鄄Ab水平随着碘摄入量的增加亦有升高的趋势。③100倍碘水平的各组T4水平下降(P<0.05),各组的血清T3水平比较差异无统计学意义。结论①EAT易感的Lewis大鼠诱发EAT的甲状腺炎症反应和血清中TPO鄄Ab水平均明显高于EAT非易感的Wistar大鼠。②碘摄入量的增加明显加重EAT的炎症反应,在EAT易感的Lewis大鼠中表现更为明显。③诱发EAT大鼠的甲状腺组织炎症程度和TPO鄄Ab水平相一致。因此,可认为TPO鄄Ab与EAT的发生、发展及甲状腺病变程度的关系更     

碘过量和甲状腺球蛋白免疫诱发NOD小鼠甲状腺炎的病变特征

目的 观察碘过量和甲状腺球蛋白(Tg)免疫诱发甲状腺炎的病变特点,进一步了解碘过量在自身免疫性甲状腺炎发病中的作用机制.方法 选用NOD小鼠,饮0.05%碘化钠(NaI)水和(或)Tg皮下免疫.观察甲状腺形态学改变和细胞凋亡情况;检测血清中TT4、TSH、甲状腺球蛋白抗体(TgAb)和甲状腺过氧化物酶抗体(TPOAb)水平;检测颈部淋巴结和脾脏淋巴细胞对Tg刺激的增殖反应和脾脏细胞培养上清中白细胞介素4(IL-4)和1γ-干扰素(IFN-γ)水平;实时荧光定量PCR法检测甲状腺绀织内IL-4、IFN-γ、趋化冈子配体10(CXCL10)、细胞间黏附因子1(ICAM-1)mRNA的表达.结果 碘过量组甲状腺滤泡扩张、胶质潴留;大昔淋巴细胞浸润和结构破坏;滤泡上皮细胞凋亡数量增加(34.66±2.78//vs 5.1 1±0.62,P<0.01);总T4下降、TSH升高,无自身抗体产生;淋巴结和脾脏细胞对Tg刺激增殖实验呈阳性反应.脾脏细胞上清中IL-4水平无升高,而IFN-升γ高[(1.272±0.049 vs 1.139±0.025)ng/L,P<0.01];甲状腺组织中除了IL4外,IFN-γ、CXCL10、ICAM-1 mRNA表达升高(均P<0.01).而Tg组甲状腺内有少量散在淋巴细胞浸润,产生了甲状腺自身抗体,脾脏细胞上清中IL-4水平升高[(18.508±0.113绑13.368±0.016)ng/L,P<0.01].碘和Tg联合作用炎症反应加重.结论 碘过量所致的NOD小鼠甲状腺炎主要是以Th1反应为主的器官特异性自身免疫性疾病.碘过量联合Tg免疫对诱发实验性自身免疫性甲状腺炎具有协同作用.     

肾上腺功能低下与自身免疫性甲状腺炎易感性的实验研究

目的研究肾上腺功能低下与自身免疫性甲状腺疾病(AITD)易感性的关系及外环境因素中的碘对易感和非易感个体诱发AITD的影响,并探讨其发病机理.方法选用Wistar大鼠,雌性,8周龄.大鼠随机分为6组①切除大鼠1+2/3侧肾上腺(ADX),模拟肾上腺功能低下或不全,高碘(HI)饮食喂养,诱发实验性自身免疫性甲状腺炎(experiment autoimmune thyroiditis,EAT),为去肾上腺高碘饮食EAT诱发组(ADX-HI-EAT组);②去肾上腺(ADX),适碘(NI)饮食喂养,诱发EAT为ADX-NI-EAT组;③适碘(NI)饮食喂养,诱发EAT为NI EAT组;④去肾上腺(ADX),高碘饮食对照组(ADX-HI组);⑤去肾上腺(ADX)适碘饮食对照组(ADX-NI组);⑥适碘饮食正常对照组(NI组).适碘饮食是用低碘饲料(碘含量≤35 μg/kg)加适碘水(含KI为0.3mg/L)喂养,高碘饮食用低碘饲料加高碘水(含KI为0.3mg/L)喂养,高碘饮食用低碘饲料加高碘水(含KI为30g/L)喂养.EAT的诱发采用同种属不同品系的SD大鼠Tg加完全福氏佐剂(freunds complete adjuvant)免疫Wistar大鼠(Tg每次2mg,每2周1次,共3次)诱发实验性甲状腺炎(EAT)的形成,末次免疫的4周后,处死全部大鼠.各组均观察其大鼠的发病率和甲状腺组织炎症反应,检测Tg自身抗体和Th1/Th2型主要细胞因子干扰素γ和白细胞介素-4(IFN-γ和IL-4)mRNA表达水平,同时还检测免疫应答协同刺激分子CD86mRNA的表达.结果 EAT非易感的Wistar大鼠切除大部分肾上腺后,促腺上腺皮质激素(ACTH)刺激实验证实肾上腺皮质储备功能较正常对照组明显低下(P＜0.01).切除肾上腺高碘饮食诱发EAT(ADX-HI-EAT)组的甲状腺组织炎细胞浸润明显和炎症反应较重,14例中2例为甲状腺组织炎细胞浸润为"+++",3例为"++",5例为"+",无炎细胞浸润者为4例.次之是去肾上腺适碘饮食诱发自身免疫性实验性甲状腺炎组(ADX-NI-EAT),10例中1例为"+++",2例为"++",2例为"+",无炎细胞浸润者为5例.适碘饮食诱发EAT(NI-EAT)组,8例中7例无炎细胞浸润,仅1例为"±".切除肾上腺高碘饮食对照组(ADX-HI)、切除肾上腺适碘饮食对照组(ADX-NI)和正常对照组(NI)大鼠甲状腺,均未发现明显的炎细胞浸润.大鼠切除肾上腺给予高碘饮食其EAT的发病率和甲状腺炎症反应较未切除肾上腺适碘组明显增加.ADX-HI-EAT和ADX-NI EAT组大鼠甲状腺组织中IFN-γmRNA表达水平分别为0.85±0.057和0.78±0.067(细胞因子/β-actin)明显高于NI-EAT、ADX HI、ADX-NI和NI组(P＜0.01).结论肾上腺功能低下或不全是构成EAT易感性的重要因素,高碘饮食会明显地增加易感大鼠(肾上腺切除)的发病率和甲状腺炎症反应.体内CD4+Th细胞向Th1细胞偏移,Th1/Th2型细胞群的失衡在EAT的发病机理中具有重要作用.     

泌乳素对诱发自身免疫性甲状腺炎影响的实验研究

目的临床上可观察到有时自身免疫性甲状腺炎常伴有高泌乳素血症,产后甲状腺炎也有较高的发病率(5%～10%).本实验研究泌乳素在诱发实验性自身免疫性甲状腺炎(experiment autoimmune thyroiditis,EAT)形成中的影响,进一步探讨泌乳素在自身免疫性甲状腺炎发病中的作用机理.方法选用SD大鼠,雌性,10周龄.大鼠随机分为4组,即SD大鼠在实验的全过程用溴隐亭(Br)灌胃(每只大鼠溴隐亭灌胃量为1mg·kg-1·d-1),诱发EAT,高碘(HI)饮食喂养为Br-HI-EAT组;SD大鼠高碘饮食喂养,诱发EAT为HI-EAT组;高碘饮食对照组(HI组);适碘(NI)饮食正常对照组(NI组).适碘饮食是用低碘饲料(碘含量≤3 5μg/kg)加适碘水(含KI为0.3mg/L)喂养,高碘饮食用低碘饲料加高碘水(含KI为30g/L)喂养.EAT的诱发采用同种属不同品系的Wistar大鼠甲状腺球蛋白(Tg)加完全福氏佐剂(completefreunds adijuvant)免疫SD大鼠(Tg每次1mg,每2周1次,共进行3次)诱发EAT的形成,末次免疫的4周后,处死全部大鼠.各组均观察其大鼠甲状腺组织的病理改变和血清中Tg自身抗体、泌乳素水平及脾脏中的白细胞介素-2/白细胞介素-2受体(IL2/IL-2R)mRNA的表达.结果大鼠经溴隐亭干预后,诱发EAT的高碘饮食(Br-HI-EAT)组,其血清中泌乳素水平为(2.32±0.096)μg/L低于诱发EAT的高碘饮食(HI-EAT)组(3.56±0.048)μg/L,P＜0.05.Br-HI-EAT组的发病率和甲状腺组织的炎细胞浸润(8例中有2例为"++",3例为"+",5例为"-")明显的轻于HI-EAT组(7例中2例为"+++",1例为"++",4例为"+");未诱发EAT的高碘饮食正常对照组(HI组)和正常对照组(NI组)的甲状腺组织中,未发现明显的炎细胞浸润;BR-HI-EAT组大鼠脾脏IL-2和IL-2RmRNA的表达分别为0.27±0.027和0.48±0.039(细胞因子/β-actin)也较HI-EAT组(0.60±0.013和0.75±0.018)明显降低(P＜0.01);诱发EAT两组大鼠血清中Tg自身抗体平均水平明显高于未诱发EAT大鼠(P＜0.01).结论大鼠经溴隐亭于预,致血清中泌乳素水平下降,其IL-2/IL-2RmRNA的表达也随之减少,降低IL-2/IL-2R系统对免疫应答的激活作用,其EAT的发病率和甲状腺组织中炎症反应得到缓解,可以认为泌乳素水平的变化也是影响自身免疫性疾病发病机制中的重要因素.     

硒对大鼠自身免疫性甲状腺炎的影响

目的研究硒对实验性自身免疫性甲状腺炎(EAT)大鼠甲状腺组织结构和自身抗体水平的影响。方法Wistar大鼠随机分为4组:对照组、EAT组、硒预防EAT组、硒治疗EAT组。除对照组外的各实验组均饮用0.05%的碘化钠水溶液,EAT组、硒预防EAT组和硒治疗EAT组在高碘的基础上皮下注射甲状腺球蛋白,建立自身EAT大鼠模型。硒预防EAT组和硒治疗EAT组在不同的时间灌胃给予亚硒酸钠,观察大鼠甲状腺组织变化和自身抗体水平。结果硒干预后甲状腺淋巴细胞浸润明显减少,滤泡破坏程度减轻。EAT组TGAb、TMAb为(62.07±10.01)、(51.50±5.91),硒预防EAT组的TGAb、TMAb为(40.28±6.91)、(35.02±3.67),低于EAT组(P<0.05),硒治疗EAT组的TGAb、TMAb为(42.80±13.90)、(35.00±5.64),低于EAT组(P<0.05),硒预防EAT组和硒治疗EAT组之间差异无统计学意义(P>0.05)。结论高碘的基础上免疫动物可造成大鼠甲状腺组织的破坏,而硒制剂使EAT大鼠病理改变明显减轻,并且在一定程度上预防和抑制其自身抗体水平的升高。     

雌激素对诱发自身免疫性甲状腺炎影响的实验研究

目的自身免疫性甲状腺疾病(autoimmune thyroid disease,AITD)的发病,女性多于男性,育龄期女性对AITD的易感性更高于男性,存在明显的性别差异.本文研究女性激素中的雌激素对诱发实验性自身免疫性甲状腺炎(experiment autoimmune thyroiditis,EAT)形成的影响,探讨雌激素在AITD发病机制中的作用.方法选用Wistar大鼠,雌性,10周龄.大鼠随机分为4组①切除大鼠的双侧全部卵巢(OVX),高碘(HI)饮食喂养,诱发EAT为OVX-HI-EAT组;③高碘饮食喂养,诱发EAT为HI-EAT组;③高碘饮食对照组(HI组);④适碘饮食正常对照组(NI组).适碘饮食是用低碘饲料(碘含量≤35μg/kg)加适碘水(含KI为0.3 mg/L)喂养,高碘饮食用低碘饲料加高碘水(含KI为15mg/l)喂养,EAT的诱发采用同种属不同品系的SD大鼠甲状腺球蛋白(Tg)加完全福氏佐剂(complete freund's adjuvant)免疫Wistar大鼠(Tg每次1 mg,每周2次,共3次),诱发EAT的形成,末次免疫的4周后,处死全部大鼠.各组均检测血清中雌二醇(Eα-17β)和泌乳素(PRL)水平,观察甲状腺组织炎细胞浸润程度和炎症反应,测定血清Tg抗体水平.并用逆转录-聚合酶链反应(RT-PCR)检测甲状腺组织中干扰素-γ(IFN-γ)和白细胞介素-10(IL-10)mRNA的表达水平.结果去卵巢高碘饮食诱发EAT(OVX-HI-EAT)组大鼠血清中E2-17β(17.60±1.03)pmol/L和PRL(2.45±0.15)μg/L水平均明显低于未切除卵巢的高碘饮食诱发EAT(HI-EAT)组、高碘饮食(HI)组和适碘饮食对照(NI)组,P＜0.01.OVX-HI EAT组诱发EAT的发病率和甲状腺的炎细胞浸润程度(10例中,甲状腺炎细胞浸润1例为"++",5例为"+")明显低于HIEAT组(8例中甲状腺炎细胞浸润5例为"++",2例为"+").甲状腺组织中Th1细胞因子IFN-γmRNA的表达水平,OVX-HI-EAT组为0.87±0.03(细胞因子/β-actin)低于HI-EAT组(0.99±0.002),P＜0.05.OVX-HI-EAT组Th2细胞因子与IL-10mRNA的表达水平为0.98±0.009(细胞因子/β-actin)高于HI-EAT组(0.83±0.05),P＜0.05.诱发EAT大鼠血清中Tg自身抗体的水平明显高于未诱发EAT组大鼠.结论雌激素水平低下可减少或缓解EAT的发病率和甲状腺的炎症反应,高水平雌激素是构成女性对AITD易感的重要因素,雌激素水平低下致Th1细胞偏于Th2细胞可能是EAT发病率和甲状腺炎症反应得以缓解的主要机制.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Changes in connexin43, the gap junction protein of astrocytes, during development of the rat pineal gland

Abstract: The abundance of gap junctions between rat pineal astrocytes formed by connexin43 (Cx43) was studied during development. Levels and distribution of Cx43 were measured by immunoblotting and indirect immunofluorescence, respectively. The amount of Cx43 in cells located within the gland was low until about the 7th postnatal day and increased to adult values between the 14th and 21st days postpartum. Although astrocytes, recognized by their vimentin immunoreactivity, were scarce before birth, they were abundant by the 7th postnatal day suggesting that the low levels of Cx43 found at this age corresponded to a low expression of this protein. Localization of the immunoreactivity to Cx43 and vimentin showed a close correlation, indicating that mature or immature pineal astrocytes form gap junctions made of Cx43. Since Cx43 levels attained their adult values at about the time the innervation and the functional state of the gland reached maturity (2–3 weeks after birth), it is proposed that astrocyte gap junctions are involved in the function of the adult rat pineal gland.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.     

Response of rat pineal melatonin to calcium, magnesium, and lithium is circadian stage dependent

Abstract: Herein we documented the response of pineal melatonin production to electrolytes known to be effective on pineal function in view of a possible circadian stage dependence. We studied the release of melatonin by perifused rat pineal glands at 2 different circadian stages corresponding to the middle of the light and dark periods, i.e., respectively, 7 and 19 HALO (Hours After Light Onset, L:D = 12:12). The initial efflux rates were, as expected, much higher in the perifusates of glands removed from rats sacrificed during the dark phase than of those removed during the light phase. After 3 hr of perifusion, melatonin release reached similar levels which were found constant up to the 8th hr of perifusion, whatever the circadian stage. Perifusion of the glands with physiological concentrations for the rat of calcium (5.2 mmol/1) and magnesium (1.34 mmol/1) resulted in a stimulatory effect on the pineal glands removed from rats sacrificed in the middle of the dark period (19 HALO), whereas no effects were observed on the pineal glands removed from rats sacrificed during the light (7 HALO). Lithium (0.28 and 0.55 mmol/1) was ineffective on melatonin release in pineal glands removed 7 and 19 HALO. Our results show differences in the initial efflux rates of melatonin and in the response of perifused pineal glands to calcium and magnesium according to the circadian stage.     

Presence of immunoreactive growth hormone and prolactin in the ovine pineal gland

Abstract: The use of antisera raised against bovine growth hormone (GH) and ovine prolactin (PRL) enabled the detection of related immunoreactive (ir) sequences of proteins in ovine pineal tissue. The isolation of PRL-like ir-material was accomplished using a 0.25 M ammonium sulphate (pH 5.5) extraction followed by ethanol precipitation, whereas the resulting 2.0 M ammonium sulphate (pH 7.0) precipitate contained a GH-like immunoreactivity. Gel chromatography of the GH-like immunoreactivity (Sephadex G-100) indicated the presence of several GH-like fragments ranging in the M_r range of 7,000 to 55,000. Analyses of the PRL-like ir-material found in pineal tissue on HPLC using a TSK 545-DEAE column led to the resolution into a single peak of immunoreactivity. A single peak of activity was also observed following chromatofocusing and hydrophobic interaction chromatography of the ir-peak from the TSK 545-DEAE column. The PRL-like ir-material inhibited the binding of [¹²⁵I]ovine PRL-S14 to anti-ovine PRL antibodies without showing an affinity for binding to anti-rat PRL or anti-bovine GH antibodies. Scatchard analysis of the binding of pineal PRL-like ir-material and pituitary ovine PRL-S14 to liver membranes from day-20 pregnant rats revealed similar affinity constants (K_a of 4.7 ± 0.2 × 10⁹ M^-1). In addition, the replication of Nb 2 Node rat lymphoma cells was stimulated by pineal PRL-like ir-material, an effect known to be specific for lactogenic hormones. The pineal PRL-like immunoreactivity appeared on sodium dodecyl sulfate polyacrylamide gels as a single major band of M_r 24,000. The functional status of PRL-and GH-like ir-material in the ovine pineal remains to be determined, but evidence is presented that the overall protein synthesis rate of the rat pineal responded to circulating concentrations of PRL.     

Microbiology of human immunodeficiency virus anorectal disease

PURPOSE: Individuals who are seropositive for the human immunodeficiency virus are at high risk for opportunistic infection and anorectal disorders. Little prospective information is available regarding anorectal pathogens in these patients. METHODS: One hundred sixty-three HIV-seropositive patients presented to the colorectal clinic between 1989 and 1992. Forty-seven (29 percent) patients were thought to have an infectious process and were prospectively studied using a standardized multiculture protocol. RESULTS: Mean age was 33 (range, 19–59) years. All were male; high-risk behavior accounted for 87 percent of HIV transmissions. Presenting complaints included anorectal pain (79 percent), pus per anum (28 percent), and blood per anum (26 percent). Examination revealed perianal tenderness (60 percent), condyloma (38 percent), perianal ulcers (38 percent), and anal fissures (34 percent). Sixty-six sets of cultures were performed; 28 patients had one set, 15 had two sets, and 4 had three sets. Thirty-two of these 47 patients (68 percent) had positive cultures including herpes (50 percent), cytomegalovirus (25 percent),Neisseria gonorrhoeae (16 percent), chlamydia (16 percent), acidfast bacilli (2 percent), and others (9 percent). Six of 32 patients with positive cultures had more than one organism cultured. Sixteen (50 percent) patients with positive cultures were treated medically, 8 (25 percent) were treated surgically and 8 (25 percent) were treated with both modalities. Sixty-one procedures were performed on 17 patients for condylomata. Eighteen patients had 20 procedures for abscesses, 50 percent of whom had positive cultures for other than common bowel flora; all improved. Fourteen patients underwent 33 procedures for perianal fistulas.Mycobacterium fortuitum was cultured from one patient who required 13 procedures for abscesses and fistulas. Forty-five (96 percent) patients were followed for an average of 12.5 months ±2.9 SEM (range, 1–94 months). Symptoms were improved or resolved in 22 of 32 (69 percent) patients with positive cultures and in 11 of 13 (84 percent) with negative cultures. CONCLUSIONS: Specific pathogens may often be identified in human immunodeficiency virus-seropositive patients with anorectal disorders if aggressively sought. Although patients without specific pathogens identified may be expected to improve with planned empiric treatment, positive identification allows more directed therapy.