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Biology: The Unity and Diversity of Life (MindTap Course List)

15th Edition

ISBN:9781337408332

Author:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Publisher:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Chapter37: Immunity

Section: Chapter Questions

Problem 1DAA: Cervical Cancer Incidence in HPV-Positive Women A persistent infection with one of about 10 strains...

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Cervical Cancer Incidence In HPV-Positive Women In 2003, Michelle Khan and her coworkers published their findings on a 10-year study in which they followed cervical cancer incidence and HPV status in 20,514 women. All women who participated in the study were free of cervical cancer when the test began. Pap tests were taken at regular intervals, and the researchers used a DMA probe hybridization test (Section 15.3) to detect specific types of HPV in the women's cervical cells. The results are shown in FIGURE 37.26 as a graph of the incidence rate of cervical cancer by HPV type. HPV- positive women are often infected by more than one type, so the data were sorted into groups based on the women's HPV status ranked by type: either positive for HPV16; or negative for HPV16 and positive for HPV18; or negative for HPV16 and HPV18 and positive for any other cancer-causing HPV; or negative for all cancer-causing HPV. Follow-up time (months) FIGURE 37.26 Cumulative incidence rate of cervical cancer correlated with HPV status in, 20,514 women aged 16 years and cider. The data were grouped as follows: HPV16 positive HFV16 negative and HPV18 positive All other cancer-causing HPV Types combined No cancer-causing HPV type was detected. 2. In which group would women infected with both HPV16 and HPV18 fall?
Cervical Cancer Incidence In HPV-Positive Women In 2003, Michelle Khan and her coworkers published their findings on a 10-year study in which they followed cervical cancer incidence and HPV status in 20,514 women. All women who participated in the study were free of cervical cancer when the test began. Pap tests were taken at regular intervals, and the researchers used a DMA probe hybridization test (Section 15.3) to detect specific types of HPV in the women's cervical cells. The results are shown in FIGURE 37.26 as a graph of the incidence rate of cervical cancer by HPV type. HPV- positive women are often infected by more than one type, so the data were sorted into groups based on the women's HPV status ranked by type: either positive for HPV16; or negative for HPV16 and positive for HPV18; or negative for HPV16 and HPV18 and positive for any other cancer-causing HPV; or negative for all cancer-causing HPV. Follow-up time (months) FIGURE 37.26 Cumulative incidence rate of cervical cancer correlated with HPV status in, 20,514 women aged 16 years and cider. The data were grouped as follows: HPV16 positive HFV16 negative and HPV18 positive All other cancer-causing HPV Types combined No cancer-causing HPV type was detected. 3. Is it possible to estimate from this graph the overall risk of cervical cancer that is associated with infection of cancer-causing HPV of any type?
Cervical Cancer Incidence In HPV-Positive Women In 2003, Michelle Khan and her coworkers published their findings on a 10-year study in which they followed cervical cancer incidence and HPV status in 20,514 women. All women who participated in the study were free of cervical cancer when the test began. Pap tests were taken at regular intervals, and the researchers used a DMA probe hybridization test (Section 15.3) to detect specific types of HPV in the women's cervical cells. The results are shown in FIGURE 37.26 as a graph of the incidence rate of cervical cancer by HPV type. HPV- positive women are often infected by more than one type, so the data were sorted into groups based on the women's HPV status ranked by type: either positive for HPV16; or negative for HPV16 and positive for HPV18; or negative for HPV16 and HPV18 and positive for any other cancer-causing HPV; or negative for all cancer-causing HPV. Follow-up time (months) FIGURE 37.26 Cumulative incidence rate of cervical cancer correlated with HPV status in, 20,514 women aged 16 years and cider. The data were grouped as follows: HPV16 positive HFV16 negative and HPV18 positive All other cancer-causing HPV Types combined No cancer-causing HPV type was detected. 1. At 110 months into the study, what percentage of women who were not infected with any type of cancer-causing HPV had cervical cancer? What percentage of women who were infected with HPV16 also had cervical cancer?
Gerintic mutuations in thhe CDda gene uften reeult ir a CD4 T.cell desciency Which of the following scenarios would be most fikely to accur in e pallent with teveral hactri Oa This patent would be less abla to produce a humotal response against various pathogenic microorganisms O b. This patient would not ba able to giroduce memory calls OE This patient would be unable to taper of the immune response folowing pathogen clearance, leading to chronic infammating Od. This piatient wauld be unable to tespond ts certain vit al invaders such as Epstein Barr Vinus QUESTION 24 The adaptive imrmine system's ability to target a particular path ogen is know as: Ca specificity O b. opsonization O. variolation d memoly QUESTION 25 Which of the following is the site on the igG foe complement bindng in the classical pathway? O a. CH2 + CH2 Oh. CH3 + CH3 OG VL- VH O d. CL + CHT
At any given time, intestinal crypts of mice com-prise about 15 stem cells and 10 Paneth cells. After celldivision, which occurs about once a day, the daughtercells remain stem cells only if they maintain contact with aPaneth cell. This constant competition for Paneth-cell con-tact raises the possibility that crypts might become mono-clonal over time; that is, the crypt cells at one point in timemight derive from only 1 of the 15 stem cells that existedat some earlier time. To test this possibility, you use theso-called confetti marker that upon activation expressesany one of three fluorescent proteins in the stem cells ofthe crypt. You then examine crypts at various times todetermine whether they contain cells with multiple colorsor only one color (Figure Q22–1). Do the crypts becomemonoclonal over time or not? How can you tell?
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1696299405-SBI4U Test... & Preview File Edit View Go Tools Window Help 4 Apoft being educach pr er her s me Dining may waters and the day of the act of DCA I har ful 4 Part-Thinking and Ingairy (15) Camp Bukaryti gone uplates to Prakaryotic game regulation. What the 3. modderpoed for Deplication What they called How are they dont 5 P 5. Dedimxplain the process of transcription. Add 4 Frock point todemontherf of genc 6 P wwwwww V انادا در در درست 1696299405-SBI4U Test 3.pdf Page 6 of 10 days of this course. Please remember the Dropboxes will close 22 280 JAN 22 4. Outline the steps of Frederick Griffith's experiment on mice to demonstrate the transfer of genetic material using Streptococcus pneumoniae. tv V 2 U₁ Search 9 23 Page 5 of 10 80 ((( O Mon Jan 22 6:19 PM All Bookmarks A U
Effects of Kartagener Syndrome An abnormal form of the motor protein dynein causes Kartagener .syndrome, a genetic disorder characterized by chronic sinus and lung infections. Biofilms form in the thick mucus that collects in the airways, and the resulting bacterial activities and inflammation damage tissues. Men affected by Kartagener syndrome can produce sperm (FIGURE 4.20) but are typically infertile; some of them have become fathers after their sperm cells were injected directly into eggs. Review Figure 4.19, then explain these observations. FIGURE 4.20 An effect of Kartagener syndrome. Cross-section of a sperm flagellum an affected man (left) and an unaffected man (right).
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i in Course: 23SPCMP Anat & Phys... N The tissue type that is indicated by the black line in this image is Fill in the blank #3 Q E $ 4 R M Question 36-Lab Practical 1 -... F % 5 T G * 0 8 4+ 1949 9 The tissue type that is shown im ) 0 Help
Our government has finite funds to devote to cancer research.Discuss which of the following areas of research you think shouldreceive the most funding.A. Identifying and characterizing oncogenes and tumorsuppressorgenesB. Identifying agents in our environment that cause cancerC. Identifying viruses that cause cancer D. Devising methods aimed at killing cancer cells in the bodyE. Informing the public of the risks involved in exposure tocarcinogensIn the long run, in which of these areas would you expect successfulresearch to be the most effective in decreasing human mortalitydue to cancer?