Please help explain this figure ACell-to-cell transmission >(Relative, %)CInfection (RLU x10³)E1.51.00.5-0.0-Infection (RLU x10¹)G5-2 + 3 N4 Cell-free1.51 Cell-to-cell+Cell-free1.0-0.5-0HmTomato-Red20 0.2 0.5 1.5293T to H520 (SARS-CoV-2 (PV))→Cell-to-cell24 Day293T to PBMC (SARS-CoV-2 (PV))4 Day20 h5.24%ISARS-CoV (PV)SARS-CoV-2 (PV)4hACE20 0.2 0.5 1.5 (pg)B71.7%Cell-free infection(Relative, %)DInfection (RLU x10³)F373.2% 6.17%201Cell-to-cell(NCI-H520)15-14.7%12.3%1.18%9.32% 7.45%0.507% 1.31%10-0.713%5-Cell-free(NCI-H520)0.198.0%0.713%0.338% 97.3%SARS-CoV-2 N (FITC)Fig. 4. ACE2 enhances cell-to-cell transmission but is not absolutely required. (A and B) Cell-to-cell and cell-free infection were performed as describedfor Figs. 1 and 3 except that target cells were 293T transfected with different amounts of a plasmid encoding ACE2. Relative rates of cell-to-cell transmis-sion and cell-free infection were calculated by setting the values of 0.5 µg ACE2 to 1.0 (A and B, n = 3). (C-F) Experiments were carried out as describedfor Figs. 1 and 3 except that target cells were H520 and human PBMCs (n = 3 for each). (G) Vero-ACE2-TMPRSS2-mTomato (Red) cells were infected withMOI = 0.01 of authentic SARS-CoV-2 WT (USA-WA1/2020) for 18 h, followed by coculturing of the donor NCI-H520 cells for another 4 h or 20 h. Cellswere fixed and stained with an anti-SARS-CoV-2 N protein for flow cytometric analysis. The same number of NCI-H520 cells were infected with the WTSARS-CoV-2 harvested from the SARS-CoV-2-infected donor Vero-ACE2-TMPRSS2-mTomato cells for 4 h or 20 h for cell-free infection and analyzed byflow cytometry. (H) Results of Q3 quadrant analyses were plotted. ***P<0.001. PV, pseudotyped virus.2.512.0-1.5-1.0-0.5-0.0-SARS-CoV (PV)SARS-CoV-2 (PV)I푸ACE20 0.2 0.5 1.5 0 0.2 0.5 1.5 (ug)293T to H520 (SARS-CoV (PV))24Day293T to PBMC (SARS-CoV (PV))…‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒4 DaySARS-CoV-2 WA1 (authentic)Cell-free (co-culture)Cell-to-cell***Infection (RLU x104)801→Cell-to-cell60+Cell-free4020-5.0T2.5251 Cell-to-cell20 →→Cell-free1510- F5-2.01드 1.010-HInfection (Q3, %)220 h4h20 hMICROBIOLOGY

SARS-CoV-2 transmission mediates as cell to cell transmission. It has higher efficiency than…

A Cell-to-cell transmission > (Relative, %) C Infection (RLU x10³) E Infection (RLU x104) G 1.51 1.0 0.5- 0.0- 2 + 3 NO SARS-CoV (PV) SARS-CoV-2 (PV) 0 0.2 0.5 1.5 0 0.2 0.5 1.5 293T to H520 (SARS-CoV-2 (PV)) Day 293T to PBMC (SARS-CoV-2 (PV)) 4 Day 20 h →Cell-to-cell 4 Cell-free 1.51 Cell-to-cell +Cell-free 1.0- 0.5- mTomato-Red 2 5.24% 12.3% 1.18% 4h 3 73.2% 6.17% 9.32% 7.45% 0.507% 1.31% 71.7% 14.7% 0.713% ACE2 (ug) B Cell-free infection (Relative, %) D Infection (RLU x10³) F 85.0T Infection (RLU x104) 2.51 2.0- 1.5- 1.0- 0.5- 0.0- 801 60- Cell-to-cell (NCI-H520) Cell-free (NCI-H520) SARS-CoV (PV) SARS-CoV-2 (PV) 0 0.2 0.5 1.5 0 0.2 0.5 1.5 293T to H520 (SARS-CoV (PV)) →Cell-to-cell +Cell-free 4 Day 293T to PBMC (SARS-CoV (PV)) →-Cell-to-cell 4 Day SARS-CoV-2 WA1 (authentic) Cell-free (co-culture) Cell-to-cell www 20+Cell-free 0 H Infection (Q3, %) 201 15- 10- 0. ACE2 (ug)

A Cell-to-cell transmission > (Relative, %) C Infection (RLU x10³) E Infection (RLU x104) G 1.51 1.0 0.5- 0.0- 2 + 3 NO SARS-CoV (PV) SARS-CoV-2 (PV) 0 0.2 0.5 1.5 0 0.2 0.5 1.5 293T to H520 (SARS-CoV-2 (PV)) Day 293T to PBMC (SARS-CoV-2 (PV)) 4 Day 20 h →Cell-to-cell 4 Cell-free 1.51 Cell-to-cell +Cell-free 1.0- 0.5- mTomato-Red 2 5.24% 12.3% 1.18% 4h 3 73.2% 6.17% 9.32% 7.45% 0.507% 1.31% 71.7% 14.7% 0.713% ACE2 (ug) B Cell-free infection (Relative, %) D Infection (RLU x10³) F 85.0T Infection (RLU x104) 2.51 2.0- 1.5- 1.0- 0.5- 0.0- 801 60- Cell-to-cell (NCI-H520) Cell-free (NCI-H520) SARS-CoV (PV) SARS-CoV-2 (PV) 0 0.2 0.5 1.5 0 0.2 0.5 1.5 293T to H520 (SARS-CoV (PV)) →Cell-to-cell +Cell-free 4 Day 293T to PBMC (SARS-CoV (PV)) →-Cell-to-cell 4 Day SARS-CoV-2 WA1 (authentic) Cell-free (co-culture) Cell-to-cell www 20+Cell-free 0 H Infection (Q3, %) 201 15- 10- 0. ACE2 (ug)

Curren'S Math For Meds: Dosages & Sol

11th Edition

ISBN:9781305143531

Author:CURREN

Publisher:CURREN

Chapter16: Adult And Pediatric Dosages Based On Body Surface Area

Section: Chapter Questions

Problem 7.4P

See similar textbooks

Similar questions

A few years ago researchers identified another protein involved in cell invasion by P. falciparum, Rh5. PfRh5 is required in red blood cell invasion. It binds to a specific protein (basigin) in red blood cell membranes and it shows almost no variation among P. falciparum strains. What part(s) of this story is/are important relative to our discussion on malaria vaccines? Option C: PfRh1 appears to be invariant All three of these observations (A-C) are crucial Option A: PfRh1 is required for cell invasion, i.e. no alternative pathways Option B: PfRh1 binds to basigin Options A and C
Using the substrate Ac-Ser-Gln-Asn-Tyr*Pro-Val-Val-NH2 and 10 nM HIV-1 protease, an inhibitor showed competitive inhibition, and a family of lines of 1/v vs. 1/[substrate] at changing-fixed concentrations of this inhibitor were as below: Slope (apparent Km/Vmax) (sec): 17,241 21,072 24,904 28,735 32,567 [Inhibitor] (M): 0 10 20 30 40 The Ki value for this inhibitor is _________________
In 2013, there was an outbreak of methicillin-resistant Staphylococcusaureus (MRSA) at an NFL training facility. One player suffereda career-ending infection to his foot and sued the team owners for $20 million for unsanitary conditions that contributed to the bacterialinfection. A settlement with undisclosed terms was reached in2017. MRSA is highly contagious and is spread by direct skin contactor by airborne transmission and can result in amputation or death.In addition, MRSA is very difficult to treat because it is resistant tomany antibiotics. For example, b -lactam antibiotics, such as penicillin,function by binding to and inactivating bacterial penicillin-bindingproteins (PBPs), which synthesize the bacterial cell wall. However,MRSA expresses an alternative type of PBP, called PBP2a encodedby the mecA gene. b -lactam antibiotics only weakly bind PBP2a,and thus cell wall synthesis can continue in their presence. Moreover,in a system somewhat analogous to the regulation of the…
In 2013, there was an outbreak of methicillin-resistant Staphylococcusaureus (MRSA) at an NFL training facility. One player suffereda career-ending infection to his foot and sued the team owners for $20 million for unsanitary conditions that contributed to the bacterialinfection. A settlement with undisclosed terms was reached in2017. MRSA is highly contagious and is spread by direct skin contactor by airborne transmission and can result in amputation or death.In addition, MRSA is very difficult to treat because it is resistant tomany antibiotics. For example, b -lactam antibiotics, such as penicillin,function by binding to and inactivating bacterial penicillin-bindingproteins (PBPs), which synthesize the bacterial cell wall. However,MRSA expresses an alternative type of PBP, called PBP2a encodedby the mecA gene. b -lactam antibiotics only weakly bind PBP2a,and thus cell wall synthesis can continue in their presence. Moreover,in a system somewhat analogous to the regulation of the…
In 2013, there was an outbreak of methicillin-resistant Staphylococcusaureus (MRSA) at an NFL training facility. One player suffereda career-ending infection to his foot and sued the team owners for $20 million for unsanitary conditions that contributed to the bacterialinfection. A settlement with undisclosed terms was reached in2017. MRSA is highly contagious and is spread by direct skin contactor by airborne transmission and can result in amputation or death.In addition, MRSA is very difficult to treat because it is resistant tomany antibiotics. For example, b -lactam antibiotics, such as penicillin,function by binding to and inactivating bacterial penicillin-bindingproteins (PBPs), which synthesize the bacterial cell wall. However,MRSA expresses an alternative type of PBP, called PBP2a encodedby the mecA gene. b -lactam antibiotics only weakly bind PBP2a,and thus cell wall synthesis can continue in their presence. Moreover,in a system somewhat analogous to the regulation of the…
Based on your disc susceptibility results for E. coli R-, which ONE of the following is correct if considering treatment of an infection caused by this organism? Select one: A. All drugs evaluated could be considered for treatment in this case B. Zone sizes were too large so the results are inconclusive and should be repeated C. Ciprofloxacin is the most potent drug so this should be used preferentially over all others D. Nitrofurantoin and fosfomycin are the most potent so either drug should be used preferentially over all others E. High drug potency is associated with increased toxicity so the drug with the lowest potency should be considered preferentially
Penicillin was first used in the 1940s to treat gonorrhea infections produced by the bacterium Neisseria gonorrhoeae. In 1984, according to the CDC, fewer than 1% of gonorrhea infections were caused by penicillin-resistant N. gonorrhoeae. By 1990, more than 10% of cases were penicillin resistant and a few years later the level of resistance was 95%. Explain the various ways this resistance could be spread among the cells. Could this resistance pass to other infectious bacteria from N. gonorrhoeae?
A graduate student was assaying LD50 (lethal dose 50%) of two temperature-sensitive Francisella tularensis strains in HeLa cells (human cell line). Both strains can infect humans and cause fatal tularemia if untreated, but it is difficult to obtain LD50 values in human subjects. The data below shows LD50 (lethal dose 50%) values of the strains in human cell culture. Can you predict the more virulent strain of the two human pathogens? Francisella tularensis strain A: LD50 @ 20∘C= 100; LD50 @ 37∘C= 1000 Francisella tularensis strain B: LD50 @ 20∘C= 1000 LD50 @ 37∘C= 100 Group of answer choices It is not possible to determine the virulence of the two strains as human pathogens from the provided data Strain A and strain B are equally virulent as human pathogens, as they average out in virulence. Strain A is more virulent than strain A as a human pathogen. Strain B is more virulent than strain A as a human pathogen.
In a nutrient medium that lacks histidine, a thin layer of agar containing ~109 Salmonella typhimurium histidine auxotrophs (mutant cells that require histidine to survive) produces ~13 colonies over a two-day incubation period at 37 °C. How do these colonies arise in the absence of histidine? The experiment is repeated in the presence of 0.4 μg of 2-aminoanthracene. The number of colonies produced over two days exceeds 10,000.What does this indicate about 2-aminoanthracene? What can you surmise about its carcinogenicity?
MCQ --Rotarix is a vaccine indicated for the prevention of Rotavirus gastroenteritis caused by G1 and non-G1 types (G3, G4, and G9). Which of the following is NOT correct regards this vaccine? following immunisation, children may become irritable and experience diarrhoea ill infants or who born with SCID should not be immunized is live-attenuated vaccine derived from the G1P[8] rotavirus strain is prepared for IV administration is given in two doses None of the above
Several cell culture lines of epithelial cells, called “Cell Line A, B, or C,” are incubated with 104 infectious particles of influenza virus, and viral titers in the culture media are measured 2 days later. Looking at the results of this experiment, it is apparent that the three lines do not all show the same response to the virus. To investigate these differences, mixing experiments are performed, where cells from two different cell lines are mixed together at a 1:1 ratio before the Influenza infection. Based on the results shown in the figure below, propose an explanation for these data.
The growth of hybridoma cells, producing a monoclonal antibody, was monitored for 4 and a half days, and the results obtained are listed in the following table: time (days) nº cel/mL x 106 ln nº cel 0 0,45 -0,79851 0,2 0,52 -0,65393 0,5 0,65 -0,43078 1 0,81 -0,21072 1,5 1,22 0,198851 2 1,77 0,57098 2,5 2,13 0,756122 3 3,55 1,266948 3,5 4,02 1,391282 4 3,77 1,327075 4,5 2,2 0,788457 What is the maximum specific rate (µmax) of growth of these cells per day? what is the doubling time of these cells (in days)?