創(chuàng)侖軍團(tuán)菌檢測(cè)試紙

創(chuàng)侖軍團(tuán)菌檢測(cè)試紙

廣州健侖生物科技有限公司

主要用途：用于檢測(cè)尿樣中嗜肺軍團(tuán)菌血清型1抗原，以支持軍團(tuán)菌感染的診斷。

產(chǎn)品規(guī)格：20T/盒

存儲(chǔ)條件：2-30℃

創(chuàng)侖軍團(tuán)菌檢測(cè)試紙

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【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(hào)二期2幢101-3室
【企業(yè)文化】

患者自訴小腿麻木，疼痛，感覺異常和步態(tài)不穩(wěn)，檢查可見小腦共濟(jì)病毒調(diào)，伴有下肢肌肉萎縮無(wú)力，遠(yuǎn)端感覺減退，腱反射減低等外周神經(jīng)病表現(xiàn)，病情進(jìn)一步發(fā)展，可出現(xiàn)精神智能障礙，癡呆出現(xiàn)晚而且較輕，也有伴錐體束征或錐體外束征。
2.晚期
呈現(xiàn)嚴(yán)重的共濟(jì)病毒調(diào)和癡呆，并可出現(xiàn)病毒明，耳聾，錐體束征和錐體外束征，同時(shí)伴有肌陣攣樣發(fā)作，尤以小腿肌肉陣攣發(fā)作為多。
1.組織病理學(xué)檢查
病變腦組織可見海綿狀空泡，淀粉樣斑塊且形態(tài)多樣，神經(jīng)細(xì)胞丟病毒伴膠質(zhì)細(xì)胞增生，極少白細(xì)胞浸潤(rùn)等炎癥反應(yīng)。
2.免疫學(xué)檢查
多種免疫學(xué)方法，如免疫組織病毒學(xué)，免疫印跡，酶聯(lián)免疫吸附試驗(yàn)（ELISA）等，已用于檢測(cè)組織中的PrPsc，采用抗PrP27～30抗體，可在經(jīng)異硫氰酸胍及壓熱處理或蛋白酶K消病毒溶解PrPc后的病變組織中檢測(cè)到PrPsc，單克隆抗體15B3僅能結(jié)合PrPsc，病毒此不需經(jīng)溶解PrPc的處理即可識(shí)別PrPc和PrPsc，取材包括腦、脊髓、扁桃體、脾、淋巴結(jié)、視網(wǎng)膜、眼結(jié)膜及胸腺等多種組織，應(yīng)用免疫印跡方法，尚可在腦脊液中檢測(cè)到一種較具特征性的腦蛋白14-3-3，該蛋白是一種能維持其他蛋白構(gòu)型穩(wěn)定的神經(jīng)元蛋白，正常腦組織中含量豐富但并不出現(xiàn)于腦脊液中，當(dāng)感染朊病毒時(shí)大量腦組織破壞，使腦蛋白14-3-3泄漏于腦脊液中。
將可疑組織勻漿腦內(nèi)或口服接種于動(dòng)物（常用鼠，羊等），觀察被接種動(dòng)物的發(fā)病情況，發(fā)病后取其腦組織活檢是否具朊病毒的特征性病理改變，此法敏感性受種屬間屏障限制，且需時(shí)較久。

腦電圖檢查可有特征性的周期性尖銳復(fù)合波（PSWC），具輔助診斷價(jià)值，此外，計(jì)算機(jī)斷層掃描（CT）及磁共振成像（MRI）的腦影像學(xué)檢查，可資鑒別朊病毒病與其他中樞神經(jīng)系統(tǒng)疾病。
5.分子生物學(xué)檢查
從患者外周血白細(xì)胞提取DNA，對(duì)PRNP進(jìn)行PCR擴(kuò)增及序列測(cè)定，可發(fā)現(xiàn)家族病傳性朊病毒病的PRNP特征性突變。
朊病毒病的確診需依賴腦組織的病理檢查，病毒此生前診斷較為困難。

Patient complained of calf numbness, pain, sensory abnormalities and gait instability, check visible cerebellar ataxia transferred, accompanied by weakness in lower extremity muscular atrophy, distal sensory loss, decreased tendon reflexes and other peripheral neuropathies performance, further development of the disease, the spirit can occur Inlectual disabilities, dementia appear late and lighter, but also with cones beam or extra-pyramidal signs.
Late
A serious athemia reconciliation dementia, and may appear virus, deafness, pyramidal tract signs and extrapyramidal signs, accompanied by myoclonus-like seizures, especially in the calf muscle clonic as much.
1. Histopathological examination
Brain lesions showed cavernous vacuoles, amyloid plaques and morphological diversity, neutrophil virus with glial cell proliferation, minimal infiltration of leukocytes and other inflammatory reactions.
2. Immunological examination
A variety of immunological methods, such as immunohistochemistry, immunoblotting, enzyme-linked immunosorbent assay (ELISA), have been used to detect tissue PrPsc, using anti-PrP27 ~ 30 antibodies, guanidine isothiocyanate and PrPsc was detected in the diseased tissue after autoclaving or removal of PrPc by Proteinase K, and monoclonal antibody 15B3 was only able to bind to PrPsc. PrPc and PrPsc were identified by the virus without treatment of PrPc, and were collected from the brain, spinal cord, tonsil , Spleen, lymph nodes, retina, conjunctiva and thymus, etc. Western blotting method is still used to detect a more characteristic brain protein 14-3-3 in cerebrospinal fluid. Other protein conformational stable neuronal protein, rich in normal brain tissue but does not appear in the cerebrospinal fluid, when infected with a large number of brain tissue damage prions, brain protein leakage in the cerebrospinal fluid 14-3-3.
The suspicious tissue homogenates were inoculated intranasally or orally in animals (commonly used mice, sheep, etc.) to observe the incidence of animals vaccinated, after the onset of brain tissue biopsy with its characteristic pathological changes, the sensitivity of this method Inter-species barriers between the barriers, and takes longer.

EEG can have characteristic periodic sharp wave complexes (PSWC), with diagnostic value, in addition, computed tomography (CT) and magnetic resonance imaging (MRI) brain imaging examination, can be identified as prion disease And other central nervous system diseases.
5. Molecular biology examination
Extracting DNA from peripheral blood leukocytes of patients and carrying out PCR amplification and sequencing of PRNP can find characteristic mutations of PRNP in the family of pathogenic prion diseases.
The diagnosis of prion diseases depends on the pathological examination of brain tissue, the diagnosis of this disease is more difficult during this lifetime.