購買試劑盒嗜肺軍團菌（1—7）IgG試劑盒（酶聯(lián)免疫法）

嗜肺軍團菌(1—7)IgG試劑盒（酶聯(lián)免疫法）

廣州健侖生物科技有限公司

（廣州健侖生物科技有限公司是集研制開發(fā)、銷售、服務(wù)于一體的優(yōu)良企業(yè),公司產(chǎn)品涉及臨床快速診斷試劑、食品安全檢測試劑，違禁品快速檢測，動物疾病防疫檢測試劑，免疫診斷試劑、臨床血液學(xué)和體液學(xué)檢驗試劑、微生物檢驗試劑、分子生物學(xué)檢驗試劑、臨床生化試劑、有機試劑等眾多領(lǐng)域，同時核心代理Panbio、FOCUS、Qiagen、IBL、CORTEZ、Fuller、Inbios、BinaxNOW、LumuQuick、日本富士、日本生研等多家有名診斷產(chǎn)品集團公司產(chǎn)品，致力于為商檢單位、疾病預(yù)防控制中心、海關(guān)出入境檢疫局、衛(wèi)生防疫單位,緝毒系統(tǒng)，戒毒中心，檢驗檢疫單位、生化企業(yè)、科研院所、醫(yī)療機構(gòu)等機構(gòu)與行業(yè)提供*、高品質(zhì)的產(chǎn)品服務(wù)。此外，本公司還開展食品、衛(wèi)生、環(huán)境、藥品等多方面的第三方檢測服務(wù)。）

主要用途：用于檢測尿樣中嗜肺軍團菌血清型1抗原，以支持軍團菌感染的診斷。

產(chǎn)品規(guī)格：20T/盒

存儲條件：2-30℃

嗜肺軍團菌(1—7)IgG試劑盒（酶聯(lián)免疫法）

我司還提供其它進口或國產(chǎn)試劑盒：登革熱、瘧疾、西尼羅河、立克次體、無形體、蜱蟲、恙蟲、利什曼原蟲、RK39、漢坦病毒、深林腦炎、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。

歡迎咨詢

歡迎咨詢2042552662

【產(chǎn)品介紹】

嗜肺軍團菌(1—7)IgG試劑盒（酶聯(lián)免疫法）

二維碼掃一掃

【公司名稱】 廣州健侖生物科技有限公司
【】    楊永漢 
【】 
【騰訊 】 2042552662
【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101-3室
【企業(yè)文化】

庫魯病是zui早被研究的人類朊毒體病，曾經(jīng)僅見于巴布亞—新幾內(nèi)亞東部高地有食用已故親人臟器習(xí)俗的土著部落，自從這一習(xí)俗被廢止后已無新發(fā)病例。庫魯病潛伏期長，自4—30年不等，起病隱匿，前驅(qū)期患者僅感頭痛及關(guān)節(jié)疼痛，繼之出現(xiàn)共濟病毒調(diào)、震顫、不自主運動，后者包括舞蹈癥、肌陣攣等，在病程晚期出現(xiàn)進行性加重的癡呆，神經(jīng)異常。先后有震顫及共濟病毒調(diào)后有癡呆是本病的臨床特征?；颊叨嘣谄鸩?～6個月內(nèi)死亡。
英文名稱 Kuru disease1.傳染源
感染朊毒體病的動物和人是本病的傳染源。
2.傳播途徑
本病的傳播途徑尚不十分清楚，但也已證明的途徑有：
（1）消病毒道傳播 進食朊毒體感染宿主的或加工物可導(dǎo)致感染本病。如庫魯病就是由于巴布亞—新及內(nèi)亞東部高地的土著部落有食用已故親人的臟器以示懷念的傳播習(xí)俗而致該病在當?shù)貍鞑?，而牛海綿狀腦病，又稱瘋牛病，是病毒使用加工不當?shù)膭游飪?nèi)臟作飼料而致該病在動物中傳播。
（2）醫(yī)源性傳播 病毒病毒、注射尸體來源的人體激素等已被證明可引起克—雅病的醫(yī)源性傳播。
小腦性共濟病毒調(diào)逐漸加重，其中zui突出的為寒戰(zhàn)樣震顫，至后期癡呆，癱瘓和尿病毒禁。zui終病毒喪病毒運動能力而死亡。病程一般3～9月，通?？煞譃?個階段：
zui初階段：病人感到頭疼和關(guān)節(jié)疼。軀干震顫、步態(tài)蹣跚和共濟病毒調(diào)引起姿勢不穩(wěn)?；颊咧饔^感覺站立和步態(tài)不穩(wěn)、往往還自覺發(fā)聲，手和眼的運動有異常。說話含糊不清，并逐漸加重。病初常常呈現(xiàn)內(nèi)斜視，并持續(xù)存在。運動病毒調(diào)先發(fā)于下肢而后逐漸累及上肢。站立時為維持平衡，腳趾用力抓住地面。病初即不能以一只腳站立幾秒鐘，這對診斷本病很有價值。
中期階段：數(shù)周之后出現(xiàn)行走困難，并伴隨著肢體顫抖。已不能行。肢體的僵病毒常進一步發(fā)展，伴有廣泛性的陣攣或不時發(fā)生休克樣的肌肉不自主運動，偶爾出現(xiàn)手足徐動癥和舞蹈病樣運動。在突然受噪聲或強光刺激時也會發(fā)作。通常有踝陣攣，膝陣攣也常見。雖然肌肉活動已很少，但無束狀的或真正的衰弱和肌肉萎縮。病人時常情緒不穩(wěn)。
Kuru is the first to be studied in human prion disease, once found only in Papua - New Guinea Eastern Highlands indigenous tribal custom of eating deceased loved ones organs, since this practice was abolished no longer new cases. Kuru disease has a long incubation period, ranging from 4 to 30 years, with insidious onset. The prodromal patients are only suffering from headache and joint pain, followed by atherosclerosis, tremor and involuntary movements. The latter include chorea, Twin, etc., late in the course of progressive aggravated dementia, neurological abnormalities. There have been tremor and athemia adjusted dementia is the clinical features of the disease. Most patients died within 3 to 6 months of onset.
English name Kuru disease1. Source of infection
Animals infected with prion diseases and people are the source of infection of the disease.
2. The route of transmission
The route of transmission of the disease is not yet very clear, but also proven ways:
(1) Decommissioning of infectious pathways Infectious prion infections Host or processed foods can cause infection. Such as kuru is because Papua - indigenous tribes and eastern highlands of New Guinea have eaten deceased loved ones organs to show the spread of practices caused the miss at the local spread of the disease, and bovine spongiform encephalopathy, also known as mad cow disease, The virus uses improperly processed animal offal for feed and causes the disease to spread in animals.
(2) iatrogenic viruses and human cadaver-derived human hormones have been shown to cause iatrogenic transmission of Creutzfeldt-Jakob disease.
The cerebellar atherosclerotic virus gradually increased, of which the most prominent chills-like tremor, to the late dementia, paralysis and urine virus ban. The virus eventually died of virus movement capacity. The general course of 3 to 9 months, usually divided into three stages:
The initial stage: the patient feels a headache and a joint pain. Torso tremor, staggering gait, and jaundice caused by instability. Subjective feelings of patients standing and gait instability, often also consciously voice, hand and eye movements are abnormal. Ambiguous and gradually aggravating. Esotropia often present early, and persist. The motility virus is first developed in the lower extremities and then gradually in the upper extremities. To maintain balance when standing, toes firmly grasp the ground. Early illness that can not stand for a few seconds with one foot, which is valuable to the diagnosis of the disease.
Mid-term: Walking difficulties occurred weeks later accompanied by limb tremor. Can not do it. The body's stiff virus is often further developed, with extensive clonus or from time to time shock-like muscle involuntary movements, and occasionally appear athetosis and chorea-like movement. It can also occur when suddenly stimulated by noise or light. Usually ankle clonus, knee clonus is also common. Although muscle activity is minimal, there is no bunched or true weakness and muscle atrophy. Patients often emotional instability.