詳細介紹
ACTH促腎上腺皮質(zhì)激素(兔多克隆抗體)
廣州健侖生物科技有限公司
ACTH 即促腎上腺皮質(zhì)激素(adreno-cortico-tropic-hormone)是維持腎上腺正常形態(tài)和功能的重要激素。它的合成和分泌是垂體前葉在下丘腦促皮質(zhì)素釋放激素(CRH)的作用下,在腺垂體嗜堿細胞內(nèi)進行的。此抗體與人的ACTH反應(yīng),同時與多種哺乳動物的ACTH有交叉反應(yīng),可用于垂體腺瘤的功能性分類,有助于區(qū)分原發(fā)性和轉(zhuǎn)移性垂體腫瘤。嗜鉻細胞瘤等部分神經(jīng)內(nèi)分泌腫瘤也可出現(xiàn)陽性反應(yīng)。
我司還提供其它進口或國產(chǎn)試劑盒:登革熱、瘧疾、流感、A鏈球菌、合胞病毒、腮病毒、乙腦、寨卡、黃熱病、基孔肯雅熱、克錐蟲病、違禁品濫用、肺炎球菌、軍團菌、化妝品檢測、食品安全檢測等試劑盒以及日本生研細菌分型診斷血清、德國SiFin診斷血清、丹麥SSI診斷血清等產(chǎn)品。
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【產(chǎn)品介紹】
細胞定位:細胞漿
適用組織:石蠟/冰凍
陽性對照:垂體
抗原修復(fù):熱修復(fù)(檸檬酸)
抗體孵育時間:30-60min
產(chǎn)品編號 | 產(chǎn)品名稱 | 克隆型別 |
OB001 | AACT(抗胰糜蛋白酶) | polyclonal |
OB002 | AAT(抗胰蛋白酶) | polyclonal |
OB003 | ACTH(促腎上腺皮質(zhì)激素) | polyclonal |
OB004 | Actin,Muscle Specific(肌肉特異性肌動蛋白) | HHF35 |
OB005 | Actin,Smooth Muscle(平滑肌肌動蛋白) | 1A4 |
OB006 | AFP(甲胎蛋白) | polyclonal |
ACTH促腎上腺皮質(zhì)激素(兔多克隆抗體)
1、傳染源:慢性病人、恢復(fù)期病人及健康的“排包囊者”為本病的傳染源。急性病人,當其糞便中僅排出滋養(yǎng)體時,不是傳染源。
2、傳播途徑:包囊在土壤中可以生存8天以上;在潮濕及涼爽環(huán)境內(nèi),如糞便中可以生存幾個星期。包囊可以通過污染飲水、食物、蔬菜等進入人體。在衛(wèi)生環(huán)境惡劣的地方,水源或食物易被糞便所污染。在以糞便作肥料的地區(qū),未洗凈、未煮熟的蔬菜是重要的傳播因素。 蠅類及蟑螂都可接觸糞便,體表攜帶和嘔吐排便,將包囊污染食物而成為重要傳播媒介。
3、流行特征:溶組織內(nèi)阿米巴病在熱帶、亞熱帶、溫帶地區(qū),發(fā)病較多,以秋季為多,夏季次之。發(fā)病率農(nóng)村高于城市,男子多于女子,成年多于兒童,幼兒患者很少,可能與吞食含包囊食物機會的多少有關(guān)。
病理改變
結(jié)腸病變以局限性粘膜下小膿腫開始,其孤立散在分布。組織破壞逐步向縱深發(fā)展,自粘膜下層直至肌層,形成口小底大的典型燒瓶樣潰瘍。早期病變僅可見粘膜小潰瘍,表面周圍略上翻,但邊緣不整齊,潰瘍表面可見深黃色或灰黑色壞死組織,在其深部可找到滋養(yǎng)體。潰瘍與潰瘍之間的粘膜一般正常,如無繼發(fā)細菌感染,則無炎癥反應(yīng)。病變主要屬于組織壞死、細胞溶化的性質(zhì),而非炎癥。
潰瘍底部的血管有血栓形成,但有時病變可破壞小動脈釀成嚴重甚至危及生命的出血。潰瘍亦可穿破肌層直至腸壁,使后者變得極薄,腸內(nèi)容可以滲漏至腹腔,或穿破腸壁,造成局限性腹腔膿腫或彌漫性腹膜炎。
在慢性病變中,息肉樣殘片可伸向腸腔。潰瘍愈合后仍可見到疤痕痕跡。由于滋養(yǎng)體反復(fù)侵入粘膜,加以細菌繼發(fā)感染,腸粘膜組織增生肥大,可出現(xiàn)大塊狀肉芽腫,成為阿米巴瘤(ameboma),其多見于抗原抗體、抗原抗體直腸交接處、橫結(jié)腸及盲腸。阿米巴瘤有時極為巨大、質(zhì)硬,難以同大腸癌腫鑒別。
阿米巴病變部位的分布依次為盲腸與升結(jié)腸、抗原抗體、直腸、闌尾和回腸下段。滋養(yǎng)體可進入門靜脈血流,在肝內(nèi)形成膿腫,且可以栓子形式流入肺、腦、脾等組織與抗原抗體,形成膿腫。
病變在顯微鏡下所見,組織壞死系其主要變化。輕度或中度淋巴細胞浸潤,并伴有少量中性粒細胞,此在有細菌繼發(fā)感染時更著。阿米巴滋養(yǎng)體滿布于整個病損中,尤其多見于病損擴展的邊緣,甚至在鄰近的正常組織中也有。
我司還提供其它進口或國產(chǎn)試劑盒:登革熱、瘧疾、流感、A鏈球菌、合胞病毒、腮病毒、乙腦、寨卡、黃熱病、基孔肯雅熱、克錐蟲病、違禁品濫用、肺炎球菌、軍團菌、化妝品檢測、食品安全檢測等試劑盒以及日本生研細菌分型診斷血清、德國SiFin診斷血清、丹麥SSI診斷血清等產(chǎn)品。
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【公司名稱】 廣州健侖生物科技有限公司
【市場部】 楊永漢
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【騰訊 】
【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號二期2幢101-103室
1, the source of infection: chronic patients, convalescent patients and healthy "platoon" as the source of infection. Acute patients are not the source of infection when only their trophozoites are excreted.
2, route of transmission: cysts in the soil can survive for more than 8 days; in humid and cool environment, such as the stool can survive for a few weeks. Encapsulation can enter the body by contaminating drinking water, food, vegetables and the like. In poor sanitary conditions, water or food is easily contaminated by faeces. In areas where manure is used as fertilizer, unwashed, uncooked vegetables are important sources of transmission. Flies and cockroaches can be exposed to excrement, body surface and vomiting, defecation, the capsule contaminated food has become an important media.
3, epidemiological characteristics: Entamoeba histolytica in tropical, subtropical, temperate regions, more incidence, with more fall, summer followed. Morbidity is higher in rural areas than in urban areas, with more males than females, more adulthood than children, and very few toddlers, which may be related to the chance of swallowed cysts containing food.
Pathological changes
Colon lesions start with localized submucosal small abscesses that are scattered in isolation. Tissue destruction gradually developed in depth, from the submucosa until the muscularis, the formation of large typical small mouth ulcers flask. Early lesions only visible mucosal ulceration, the surface slightly upside down, but the edge is not neat, the surface of the ulcer can be seen dark yellow or gray-black necrosis in the deep can find trophozoites. The mucosa between the ulcer and the ulcer is generally normal, without secondary bacterial infection, there is no inflammatory reaction. Lesions mainly belong to the nature of tissue necrosis, cytolysis, rather than inflammation.
The bottom of the ulcer blood vessels thrombosis, but sometimes the lesion can damage the small arteries causing serious and even life-threatening bleeding. Ulcers can also break through the muscular layer until the intestinal wall, making the latter extremely thin, intestinal contents can leak to the abdominal cavity, or wear broken bowel wall, resulting in localized abdominal abscess or diffuse peritonitis.
In chronic lesions, polypoid fragments can stretch to the intestine. Can still be seen after ulcer healing scar marks. As the trophozoites repeatedly invade the mucosa, bacterial secondary infection, intestinal mucosal hyperplasia hypertrophy, there may be massive granulomas, become ameboma (ameboma), which more common in antigen and antibody, antigen and antibody rectal junction, transverse colon and Cecum. Amoeba tumor is sometimes extremely large, hard, difficult to identify with colorectal cancer.
The distribution of the amoebic lesions was caecal and ascending colon, antigen antibody, rectum, appendix and lower ileum. Trophoblast can enter the portal vein blood flow, forming an abscess in the liver, and can flow into the lungs, brain, spleen and other tissue and antigen antibodies in the form of emboli to form abscesses.
Lesions seen under the microscope, tissue necrosis of its main changes. Mild or moderate lymphocytic infiltration, with a small amount of neutrophils, is more pronounced with bacterial secondary infection. Amoeba trophozoites are found throughout the entire lesion, most often at the margin of lesion expansion, even in adjacent normal tissues.