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™ Recombinant Viral Technology. AccuPlex™ rEbola GP/NP ... Library. AccuType™ Viral Isolates. Aneuploidy Reference ... Recombinant DNA/RNA Custom Development Services ... SeraCare Life Sciences. Login MY CART. MY PROFILE. Products. AccuPlex™ Recombinant Viral Technology. AccuPlex™ rEbola GP/NP Reference Material. ACCURUN® Controls for Research. ACCURUN® Controls for Clinical Lab. ACCURUN® EPIC Package Insert Library. AccuType™ Viral Isolates. Aneuploidy Reference Materials. Custom Control, Assay and Panel Development. Disease State Materials. Disease State Panels. HIV Drug Resistance Reference Materials. HSA, BSA, HGG Male AB. KPL Antibodies, Reagents, and Kits. SeraCon™ Basematrix Processed Plasma. Seraseq™ Solid Tumor Mutation Mix-I AF20. Company. Who We Are. Best-in-Class Quality Standards. Our Facilities. News Center. Trade Shows and Events. Contact Us. Who We Serve. Diagnostics Research. IVD Manufacturing. Clinical Laboratories. Career Opportunities. Overview. Our Work Environment. Our Culture. Ou...
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*  'Junk DNA' can sense viral infection
Junk DNA' can sense viral infection. Home. Medical research. ... 24, 2012 'Junk DNA' can sense viral infection April 24, ... unimportant "junk DNA," scientists have learned that non-...
*  Erythropoietin alpha Human | ProSpec
Enzymes. Viral Antigens. Recombinant Proteins. ... Services. DNA Cloning. Protein Expression. ... Enzymes. Viral Antigens. Recombinant Proteins. ... Erythropoietin alpha Human. Growth Factors. Chemokines. CD Antigens. Neurotrophins. Hormones. Enzymes. Viral Antigens. Recombinant Proteins. Natural Proteins. Monoclonal Antibodies. Monoclonal Antibody. Growth Factors. Chemokines. CD Antigens. Neurotrophins. Hormones. Enzymes. Viral Antigens. Recombinant Proteins. Natural Proteins. Monoclonal Antibodies. Protein Catalog >> Growth Factors >> EPO a Human. EPO a Human. Erythropoietin-Alpha Human Recombinant. Synonyms Erythropoietin-Alpha, EPO-a, EPO-alpha, Epoetin, EP, MGC138142. Description Erythropoietin-alpha Human Recombinant is produced in Chinese hamster ovary CHO cells by recombinant DNA technology is a single, polypeptide chain containing 166 amino acids and having a predicted molecular mass of 21,000 Dalton and apparent glycosylated molecular mass of 36-40kDa. Source Chinese Hamster Ovary Ce...
B Virus HBV DNA Test: Hepatitis B Virus HBV DNA test ... the presence of viral DNA and measure the amount of DNA viral ... either detects the viral antigens e.g. HBsAg, HBeAg or HBcAg or...
*  Cancers | Free Full-Text | Possible DNA Viral Factors of Human Breast Cancer | HTML
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, Genes, Ap-1, DNA, Gene, Methylation, Epigenetic, ... Guanosine, Viral DNA , Viral Genes , Transcription Factor , ... virus requires a viral genome with 5-methylcytosine residues... W
*  What two different DNA viral infections can be identified with | Solution Inn
What two different DNA viral infections can be identified with ... What two different DNA viral infections can be identified with ... some ways that DNA viruses can become oncogenic. b Why is...
*  Hepatitis B Surface Antigen(HBsAg) Loss in Chronic Hepatitis B Patients With Low Viral Load - Full T
with low HBV DNA viral load will induce a high rate of HBsAg ... patients with high viral load after treatment with ADF and Peg- ... B Patients With Low Viral Load. MedlinePlus related topics:..."Hepatitis B"&rank=5

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(1/26780) Marker effects on reversion of T4rII mutants.

The frequencies of 2-aminopurine- and 5-bromouracil-induced A:T leads to G:C transitions were compared at nonsense sites throughout the rII region of bacteriophage T4. These frequencies are influenced both by adjacent base pairs within the nonsense codons and by extracodonic factors. Following 2AP treatment, they are high in amber (UAG) and lower in opal (UGA) codons than in allelic ochre (UAA) codons. In general, 5BU-induced transitions are more frequent in both amber and opal codons than in the allelic ochre codons. 2AP- and 5BU-induced transition frequencies in the first and third positions of opal codons are correlated with those in the corresponding positions of the allelic ochre codons. Similarly, the frequencies of 2AP-induced transition in the first and second positions of amber codons and their ochre alleles are correlated. However, there is little correlation between the frequencies of 5BU-induced transitions in the first and second positions of allelic amber and ochre codons.  (+info)

(2/26780) Four dimers of lambda repressor bound to two suitably spaced pairs of lambda operators form octamers and DNA loops over large distances.

Transcription factors that are bound specifically to DNA often interact with each other over thousands of base pairs [1] [2]. Large DNA loops resulting from such interactions have been observed in Escherichia coli with the transcription factors deoR [3] and NtrC [4], but such interactions are not, as yet, well understood. We propose that unique protein complexes, that are not present in solution, may form specifically on DNA. Their uniqueness would make it possible for them to interact tightly and specifically with each other. We used the repressor and operators of coliphage lambda to construct a model system in which to test our proposition. lambda repressor is a dimer at physiological concentrations, but forms tetramers and octamers at a hundredfold higher concentration. We predict that two lambda repressor dimers form a tetramer in vitro when bound to two lambda operators spaced 24 bp apart and that two such tetramers interact to form an octamer. We examined, in vitro, relaxed circular plasmid DNA in which such operator pairs were separated by 2,850 bp and 2,470 bp. Of these molecules, 29% formed loops as seen by electron microscopy (EM). The loop increased the tightness of binding of lambda repressor to lambda operator. Consequently, repression of the lambda PR promoter in vivo was increased fourfold by the presence of a second pair of lambda operators, separated by a distance of 3,600 bp.  (+info)

(3/26780) Human topoisomerase I promotes initiation of simian virus 40 DNA replication in vitro.

Addition of purified human topoisomerase I (topo I) to simian virus 40 T antigen-driven in vitro DNA replication reactions performed with topo I-deficient extracts results in a greater than 10-fold stimulation of completed molecules as well as a more than 3-fold enhancement of overall DNA replication. To further characterize this stimulation, we first demonstrate that bovine topo I but not Escherichia coli topo I can also enhance DNA replication. By using several human topo I mutants, we show that a catalytically active form of topo I is required. To delineate whether topo I influences the initiation or the elongation step of replication, we performed delayed pulse, pulse-chase, and delayed pulse-chase experiments. The results illustrate that topo I cannot promote the completion of partially replicated molecules but is needed from the beginning of the reaction to initiate replication. Competitive inhibition experiments with the topo I binding T antigen fragment 1-246T and a catalytically inactive topo I mutant suggest that part of topo I's stimulation of replication is mediated through a direct interaction with T antigen. Collectively, our data indicate that topo I enhances the synthesis of fully replicated DNA molecules by forming essential interactions with T antigen and stimulating initiation.  (+info)

(4/26780) Induction of AT-specific DNA-interstrand crosslinks by bizelesin in genomic and simian virus 40 DNA.

Bizelesin is a bifunctional AT-specific DNA alkylating drug. Our study characterized the ability of bizelesin to induce interstrand crosslinks, a potential lethal lesion. In genomic DNA of BSC-1 cells, bizelesin formed from approx. 0.3 to 6.03+/-0.85 interstrand crosslinks per 106 base pairs, at 5-100 nM drug concentration, respectively, comparable to the number of total adducts previously determined in the same system (J.M. Woynarowski, M.M. McHugh, L.S. Gawron, T.A. Beerman, Biochemistry 34 (1995) 13042-13050). Bizelesin did not induce DNA-protein crosslinks or strand breaks. A model defined target, intracellular simian virus 40 (SV40) DNA, was employed to map at the nucleotide level sites of bizelesin adducts, including potential interstrand crosslinks. Preferential adduct formation was observed at AT tracts which are abundant in the SV40 matrix associated region and the origin of replication. Many sites, including each occurrence of 5'-T(A/T)4A-3', co-mapped on both DNA strands suggesting interstrand crosslinks, although monoadducts were also formed. Bizelesin adducts in naked SV40 DNA were found at similar sites. The localization of bizelesin-induced crosslinks in AT-rich tracts of replication-related regions is consistent with the potent anti-replicative properties of bizelesin. Given the apparent lack of other types of lesions in genomic DNA, interstrand crosslinks localized in AT-rich tracts, and to some extent perhaps also monoadducts, are likely to be lethal effects of bizelesin.  (+info)

(5/26780) Hybrid capture II, a new sensitive test for human papillomavirus detection. Comparison with hybrid capture I and PCR results in cervical lesions.

AIM: To test a new assay for the detection of human papillomavirus (HPV) DNA, hybrid capture II (HC II), compared with the previous commercialized hybrid capture I (HC I) and polymerase chain reaction (PCR) results on cervical scrapes from fresh cone excision biopsy samples. METHODS: The three methods were used on cervical scrapes from 42 fresh cone excision biopsy samples. There were nine metaplastic and inflammatory lesions, five low grade lesions, and 28 high grade lesions. PCR was performed using the general primers GP5+/GP6+. The viral load of high risk HPV DNA was estimated by the ratio of relative light units to positive control values in the samples. RESULTS: The sensitivity of HC I for the detection of high grade lesions was 71.4%, while it was 92.8% for HC II and 96.4% for the PCR. Considering only the absence of detectable cervical in situ neoplasia, the specificity was 88.9% for HC I, 66.7% for HC II, and 66.7% for PCR. With HC II, for a ratio of cervical sample to normal control of > 200, the sensitivity for the detection of high grade lesion was only 34.6% with a specificity of 66.7%. CONCLUSIONS: HPV detection with the HC II assay is more sensitive than the previous HC I and represents a more convenient and easier test than PCR for routine use. Nevertheless the viral load estimated with this test cannot be a reliable predictive indicator of high grade lesions.  (+info)

(6/26780) Human papillomavirus DNA in adenosquamous carcinoma of the lung.

AIM: To investigate the presence of human papillomavirus (HPV) DNA in adenosquamous carcinoma of the lung--which is relatively common in Okinawa but not in mainland Japan--and examine its histological features. METHODS: Of 207 cases where primary lung cancers were surgically removed between January 1995 and June 1997 in Okinawa, 23 were adenosquamous carcinoma. HPV was detected by non-isotopic in situ hybridisation (NISH) and polymerase chain reaction (PCR) amplification with primers specific for E6 and E7 regions of the HPV genome. PCR products were analysed by Southern blotting. Immunohistochemical determination of high molecular weight cytokeratin (HMC) and involucrin was also carried out. RESULTS: 18 cases were positive for HPV DNA by PCR and NISH. HPV types 6, 11, 16, and 18 were found. Seven cases were dual positive for different types of HPV. Using NISH, HPV was also found in the squamous cell components and in neighbouring enlarged adenocarcinoma cells. The HMC and involucrin were demonstrated immunohistochemically in the same areas. CONCLUSIONS: HPV DNA was found in a high proportion (78.3%) of adenosquamous carcinomas in Okinawa, a region where HPV has previously been shown to be prevalent in squamous cell carcinoma of the lung. The adenocarcinoma cells adjacent to the squamous cell carcinoma component were enlarged and positive for HPV, HMC, and involucrin. This is thought to indicate the transition from adenocarcinoma to squamous cell carcinoma.  (+info)

(7/26780) A review of statistical methods for estimating the risk of vertical human immunodeficiency virus transmission.

BACKGROUND: Estimation of the risk of vertical transmission of human immunodeficiency virus (HIV) has been complicated by the lack of a reliable diagnostic test for paediatric HIV infection. METHODS: A literature search was conducted to identify all statistical methods that have been used to estimate HIV vertical transmission risk. Although the focus of this article is the analysis of birth cohort studies, ad hoc studies are also reviewed. CONCLUSIONS: The standard method for estimating HIV vertical transmission risk is biased and inefficient. Various alternative analytical approaches have been proposed but all involve simplifying assumptions and some are difficult to implement. However, early diagnosis/exclusion of infection is now possible because of improvements in polymerase chain reaction technology and complex estimation methods should no longer be required. The best way to analyse studies conducted in breastfeeding populations is still unclear and deserves attention in view of the many intervention studies being planned or conducted in developing countries.  (+info)

(8/26780) Novel endotheliotropic herpesviruses fatal for Asian and African elephants.

A highly fatal hemorrhagic disease has been identified in 10 young Asian and African elephants at North American zoos. In the affected animals there was ultrastructural evidence for herpesvirus-like particles in endothelial cells of the heart, liver, and tongue. Consensus primer polymerase chain reaction combined with sequencing yielded molecular evidence that confirmed the presence of two novel but related herpesviruses associated with the disease, one in Asian elephants and another in African elephants. Otherwise healthy African elephants with external herpetic lesions yielded herpesvirus sequences identical to that found in Asian elephants with endothelial disease. This finding suggests that the Asian elephant deaths were caused by cross-species infection with a herpesvirus that is naturally latent in, but normally not lethal to, African elephants. A reciprocal relationship may exist for the African elephant disease.  (+info)

How does a Protease inhibitor work to treat HIV infection?

A) It prevents the release of new viral particles.
B) It prevents the cleavage of host DNA preventing viral DNA from being inserted into host DNA.
C) It cleaves Reverse transcriptase preventing the generation of viral DNA.
D) It prevents the binding of gp120 to the CD4 protein.
E) It cleaves viral proteins interfering with their function.


Protease allows the cutting of the strands for the virus to replicate itself,.. protease INHIBITORS stop this process of cutting.

How can you tell the difference between bacterial meningitis and viral meningitis?

I've been diagnosed with viral meningitis but I'm not sure the doctor was right since I've never gotten a spinal tap to check the fluids. I need to know if I can distinguish between the two kinds of meningitis. The faster and more informative the response, the better.

When did you first become ill if it was 3 days or more ago then it is viral otherwise you would be dead. If it has been less then 3 days go to you local ER asap and tell them what your dr told you. Your dr is an idiot for saying that the only way to see if it is meningitis is to do an LP or grow blood cultures. I think what you have is viral because if it was bacterial you would not be able to be sitting on the computer.

For all you know you don't have Meningitis at all.
Good luck and i hope your feeling better soon

What viral infections can you get in the throat?

I have a viral infection in my throught and they didn't tell me what kind. So I want to know what my possibilities are.

There are so many viruses that can cause a sore throat.

How long does it take to get over viral meningitis?

My daughter, aged 20 is still feeling ill one week after being diagnosed with viral meningitis. She is nauseous and wants to know if it is normal and how long it takes to go away. She is not eating, feels completely helpless and just wants to sleep all the time. Has anyone been through this and what advice can you give. All advice will be appreciated. Thank you.

Viral Meningitis can take month's to recover from, as sufferer's can develop a post-viral syndrome that causes severe fatigue, and associated symptoms such as headaches. It is a syndrome like chronic fatigue. The general period of disease of viral meningitis can typically last up to one week, with symptoms gradually lessening. If you believe recovery is not moving fast enough, I would check in with your doctor.

What is the difference between a viral infection and a bacterial infection?

Or just viral and bacterial; I am interested in biology. Unfortunately, I don't know everything =P


viral infection is caused by a virus and bacterial is caused by bacteria.

When looking at the symptoms of a disease, how can a doctor determine whether it is bacterial or viral?

In other words, what is the difference between how viral infections and bacterial infections affect the body?  How are the symptoms between the two types of diseases different?  After a doctor learns what symptoms a patient has, what further tests or examinations would he/she run to determine whether the disease is bacterial or viral?

In some cases it can be tough.  But there are several ways to try & sort it out.  First, what is going around?  If a virus is spreading through the area, epidemiology suggests it is a virus.  Furthermore, viral infections tend to cause a wide range of symptoms due to the way the virus attacks the body--fever, muscle aches, headache, rash, joint aches, etc all at once highly suggest a virus.  Bacterial infections tend to be more localized--pneumonia causes respiratory symptoms primarily--not joint pain too.  A bacterial infection that has spread so much to cause a lot of symptoms (called "sepsis") has the person very very ill.  Viruses are also much more common than bacterial infections.  Often time its a educated guess (that's why MDs spend so much time in school--you have to know alot about everything to discard causative agents to make an educated guess).  They can do more tests (a Complete blood count, or CBC, will show more lymphs in a viral infection & more ploys in a bacterial).  There are also antibody tests to specific causes.  However, many times, its too expensive & not worth all the time & effort to make a definitive diagnosis.  If you are going to get better anyway in 5-7 days, most people would not want to spend $500 or more to find out EXACTLY what they had.  That's why you are told to return if not better in x days or suddenly get worse.  Then the testing can be better utilized to find a source.  Some tests would be xrays (chest etc); a spinal fluid exam, blood tests like the CBC or antibody tests, blood, urine, sputum cultures for bacteria, viral cultures, bronchial washings of the airways for tests, TB testing, there are many tests and as they become negative, more exotic & rare things are tested for.  You always start with the most obvious & proceed to the rare.

How long before my viral infection will clear up?

Today i found out that I have a viral infection.
I'm going camping with scouts on Friday until Sunday and can't miss it. Will my viral infection be cleared up by then.
Also I am on paracetamol (flu tablets) and Betnesol (Nose drops).
And I am a 14 year old girl.

Speak to your doctor, if you...
 "go to work or school in this condition not only risk spreading the virus to their colleagues but also run a higher risk of catching a bacterial infection"

It will last as long as your body takes to deal with it.
eg a cold (viral infection) lasts around a week.

How high does the viral count have to be for Hepatitis B to be concerned?

I have a friend who's viral count for hepatitis that's about 40 million. Is this dangerous?

yes, viral loads above 2000 are worrisome.  The higher the viral load, the more likely you are to get liver cancer, for example.  Also, viral load can correlate with liver damage.  This is in contrast to hepatitis C where it does not correlate.  This person needs evaluation by a hepatologist (liver specialist).  I would start by looking at