15.11: Additional Links - Biology

15.11: Additional Links - Biology

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15.11: Additional Links

15.11: Additional Links - Biology

New International Version
It went to the northern slope of Ekron, turned toward Shikkeron, passed along to Mount Baalah and reached Jabneel. The boundary ended at the sea.

New Living Translation
The boundary then proceeded to the slope of the hill north of Ekron, where it turned toward Shikkeron and Mount Baalah. It passed Jabneel and ended at the Mediterranean Sea.

English Standard Version
The boundary goes out to the shoulder of the hill north of Ekron, then the boundary bends around to Shikkeron and passes along to Mount Baalah and goes out to Jabneel. Then the boundary comes to an end at the sea.

Berean Study Bible
Then it went out to the northern slope of Ekron, curved toward Shikkeron, proceeded to Mount Baalah, went on to Jabneel, and ended at the Sea.

King James Bible
And the border went out unto the side of Ekron northward: and the border was drawn to Shicron, and passed along to mount Baalah, and went out unto Jabneel and the goings out of the border were at the sea.

New King James Version
And the border went out to the side of Ekron northward. Then the border went around to Shicron, passed along to Mount Baalah, and extended to Jabneel and the border ended at the sea.

New American Standard Bible
Then the border proceeded to the side of Ekron northward. And the border turned to Shikkeron and continued to Mount Baalah and proceeded to Jabneel, and the border ended at the sea.

NASB 1995
The border proceeded to the side of Ekron northward. Then the border curved to Shikkeron and continued to Mount Baalah and proceeded to Jabneel, and the border ended at the sea.

NASB 1977
And the border proceeded to the side of Ekron northward. Then the border curved to Shikkeron and continued to Mount Baalah and proceeded to Jabneel, and the border ended at the sea.

Amplified Bible
The border proceeded to the slope [of the hill] of Ekron northward, then curved to Shikkeron and continued to Mount Baalah and proceeded to Jabneel. Then the border ended at the [Mediterranean] sea.

Christian Standard Bible
Then the border reached to the slope north of Ekron, curved to Shikkeron, proceeded to Mount Baalah, went to Jabneel, and ended at the Mediterranean Sea.

Holman Christian Standard Bible
Then the border reached to the slope north of Ekron, curved to Shikkeron, proceeded to Mount Baalah, went to Jabneel, and ended at the Mediterranean Sea.

American Standard Version
and the border went out unto the side of Ekron northward and the border extended to Shikkeron, and passed along to mount Baalah, and went out at Jabneel and the goings out of the border were at the sea.

Aramaic Bible in Plain English
And the border went out to the side of Aqroon from the North and faced the border toward Shekrun and it passed to the Mountain of Baala and it went out to Yahbayel and the limits of the borders were on the west

Brenton Septuagint Translation
And the border terminates behind Accaron northward, and the borders will terminate at Socchoth, and the borders will go on to the south, and will terminate at Lebna, and the issue of the borders will be at the sea and their borders shall be toward the sea, the great sea shall be the boundary.

Contemporary English Version
It continued along to the hillside north of Ekron, curved around to Shikkeron, and then went to Mount Baalah. After going to Jabneel, the border finally ended at the Mediterranean Sea,

Douay-Rheims Bible
And it reacheth northward to a part of Accaron at the side: and bendeth to Sechrona, and passeth mount Baala: and cometh into Jebneel, and is bounded westward with the great sea.

English Revised Version
and the border went out unto the side of Ekron northward: and the border was drawn to Shikkeron, and passed along to mount Baalah, and went out at Jabneel and the goings out of the border were at the sea.

Good News Translation
The border then went out to the hill north of Ekron, turned toward Shikkeron, past Mount Baalah, and on to Jamnia. It ended at the Mediterranean Sea,

GOD'S WORD® Translation
From there the border goes on the north side of Ekron and turns to Shikkeron, on to Mount Baalah, and comes out at Jabneel. The border ends at the Mediterranean Sea.

International Standard Version
The border proceeded north to the edge of Ekron, then curved to Shikkeron and on to Mount Baalah, proceeding then to Jabneel, where the boundary ended at the sea.

JPS Tanakh 1917
And the border went out unto the side of Ekron northward and the border was drawn to Shikkeron, and passed along to mount Baalah, and went out at Jabneel and the goings out of the border were at the sea.

Literal Standard Version
and the border has gone out to the side of Ekron northward, and the border has been marked out [to] Shicron, and has passed over to Mount Ba‘alah, and gone out [to] Jabneel and the outgoings of the border have been at the sea.

NET Bible
It then extended to the slope of Ekron to the north, went toward Shikkeron, crossed to Mount Baalah, extended to Jabneel, and ended at the sea.

New Heart English Bible
and the border went out to the side of Ekron northward and the border extended to Shikkeron, and passed along to Mount Baalah, and went out at Jabneel and the goings out of the border were at the sea.

World English Bible
and the border went out to the side of Ekron northward and the border extended to Shikkeron, and passed along to Mount Baalah, and went out at Jabneel and the goings out of the border were at the sea.

Young's Literal Translation
and the border hath gone out unto the side of Ekron northward, and the border hath been marked out to Shicron, and hath passed over to mount Baalah, and gone out to Jabneel and the outgoings of the border have been at the sea.

Joshua 15:9
From the hilltop the border curved to the spring of the Waters of Nephtoah, proceeded to the cities of Mount Ephron, and then bent around toward Baalah (that is, Kiriath-jearim).

Joshua 15:10
The border curled westward from Baalah to Mount Seir, ran along the northern slope of Mount Jearim (that is, Chesalon), went down to Beth-shemesh, and crossed to Timnah.

Joshua 15:12
And the western border was the coastline of the Great Sea. These are the boundaries around the clans of the descendants of Judah.

1 Samuel 17:52
Then the men of Israel and Judah charged forward with a shout and pursued the Philistines to the entrance of Gath and to the gates of Ekron. And the bodies of the Philistines were strewn along the Shaaraim road to Gath and Ekron.

And the border went out to the side of Ekron northward: and the border was drawn to Shicron, and passed along to mount Baalah, and went out to Jabneel and the goings out of the border were at the sea.

Joshua 15:45 Ekron, with her towns and her villages:

Joshua 19:43 And Elon, and Thimnathah, and Ekron,

1 Samuel 5:10 Therefore they sent the ark of God to Ekron. And it came to pass, as the ark of God came to Ekron, that the Ekronites cried out, saying, They have brought about the ark of the God of Israel to us, to slay us and our people.

Malignant glioma: genetics and biology of a grave matter

This extract was created in the absence of an abstract.

Malignant brain tumors strike deep into the psyche of those receiving and those delivering the diagnosis. Malignant gliomas, the most common subtype of primary brain tumors, are aggressive, highly invasive, and neurologically destructive tumors considered to be among the deadliest of human cancers. In its most aggressive manifestation, glioblastoma (GBM), median survival ranges from 9 to 12 months, despite maximum treatment efforts—a statistical fact that has changed little over several decades of technological advances in neurosurgery, radiation therapy, and clinical trials of conventional and novel therapeutics. Over the same time period, there has been an explosion of knowledge in cancer biology and basic science discovery that has fueled meaningful progress in the treatment of many common human cancers, including those of the breast, lung, and prostate. It is perplexing that therapies used effectively in the treatment of these solid tumors are overwhelmingly ineffective in the treatment of GBM, perhaps reflecting the eccentric biology and cellular origin of this neoplasm. To date, only one new agent has been documented to have modest activity against intermediate-grade gliomas, whereas no effective agents have emerged for the treatment of GBM, despite 20 years of enrolling patients in clinical trials. It is ironic that although a comprehensive view of the genetic lesions encountered in malignant gliomas has been compiled, substantive conceptual and practical barriers remain in assigning functional significance to these genetic changes and in harnessing this basic information into the development of drugs that make a difference in patient care.

The history of treating malignant gliomas dates back to the middle of the 19th century and parallels landmark advances in modern surgical technique and the clinical discipline of neurology. The first brain tumor surgery of the modern era was performed in 1884 by Rickman Godlee ( Kaye and Laws 1995 ). By 1900, the initial enthusiasm …

Results and discussion

In order to investigate how the EBOV genome changes with increasing pathogenicity, a forced evolution model was used in which EBOV was sequentially passaged in vivo using a guinea pig model of infection. EBOV is initially non-pathogenic in guinea pigs, but becomes more virulent and adapted to replicating in this host [16],[17].

Adaptation of EBOV to guinea pigs

Guinea pigs were infected with EBOV (ME718 strain) and the virus was serially passaged to develop uniform lethality in guinea pigs (Figure 1). There were 10 guinea pigs per passage. Four animals were used for the preparation of spleen homogenate for subsequent virus infection (culled 7 days post challenge) and six were taken forward for measuring survival rates and clinical parameters (for up to 14 days post challenge). Adaptation of EBOV to growth in the guinea pigs was achieved with serial passage involving a subcutaneous injection of 10 4 TCID50 EBOV, with spleens harvested 7 days post infection (as a source of progeny virus). Virus titre was determined and a new inoculum prepared before administering 10 4 TCID50 EBOV to a new group of guinea pigs. This was repeated until there was clinical and virological evidence that the virus adapted to the guinea pig host. Animals were observed for 2 weeks post infection. Weight data indicated that guinea pigs showed a minimal response to the initial challenge, whereas with subsequent passages weight loss exceeding 10% was observed (Figure 2A). Similarly, with temperatures the same responses were observed, where only after initial passage in the guinea pigs were temperature increases of between 1°C and 2.5°C observed (Figure 2B). At passage two several animals that met humane clinical endpoints displayed symptoms of hypothermia prior to being euthanized. Hypothermia has been previously observed in Rhesus macaques experimentally infected with EBOV via the aerosol route [18]. Six animals from each passage study that were scheduled to last 14 days post infection were used to assess mortality. By five passages, 75% mortality was observed with a challenge dose of 10 4 TCID50. There was also no increase in viral titre in the spleen collected from animals culled at day 7 (Table 1) compared with the previous passage, indicating that the viral burden had peaked. The minimum lethal dose of the passaged virus was determined to be 10 3 TCID50 (Figure 3).

Passaging of virus in vivo . In order to give a reproducible model of infection EBOV was passaged five times in guinea pigs in a forced evolution model. There were 10 animals per group, where four animals were used for harvesting spleens for virus preparation and the remaining six animals used to measure clinical parameters.

Clinical data in the form of weight gain/loss and departure difference from EBOV-infected guinea pigs using virus that had been passaged from spleens harvested 7 days post infection: (A) weight and (B) temperature changes compared to day of challenge, compared to control uninfected animals. Data points represent mean values from 10 animals up to day 7, and six animals up to day 14, with error bars denoting standard error.

Kaplan-Meier survival plot of EBOV-infected guinea pigs when different virus concentrations were used for challenge. Survival studies lasted for 14 days.

This method of adapting EBOV has been used by others and mortality was first shown to occur during passages three to four [19]–[21]. Complete lethality was then detected soon after, but ranged from passage four to seven [16],[17],[20],[21]. While 50% lethality was seen in the second passage in the current study, this was most likely due to the low titres in the passage one material requiring a higher concentration of spleen homogenate to be delivered to the guinea pigs in order to achieve challenge with 10 4 TCID50. This amount of material would have had adverse impacts due to lipid peroxidation, and protein oxidation and pro-apoptotic factors through cellular damage during preparation of the homogenate.

Analysis of EBOV genome sequence with passage

Viral RNA was purified from spleens isolated from four guinea pigs from passage one through to five using a Qiagen Viral isolation kit. This allowed the safe transfer of nucleic acid from CL4 to CL2 and CL1 for further analysis. RNA was pooled from each passage and sequenced using MiSeq to avoid potential problems (associated with HiSeq) with the polyA carrier in the viral isolation kit. Sequence analysis indicated an increased proportion of sequence reads mapping to the EBOV genome with passage (Table 1). By our low stringency mapping approach, there were 4,298 reads in RNA sequenced from passage one material compared to 12,060 reads in RNA sequenced from passage five material. The decrease in percentage reads mapping to the Ebola genome in passage five compared to passage four may in part be due to the greater proportion of total reads mapped in passage five compared to passage four. Alternatively, these represent pooled samples and there was likely to be variation among individual clinical samples. Similarly, using a high stringency analysis of the alignments (see methods) we found 478 reads and 7,142 reads at passages one and five, respectively. This correlated well with the increase in viral titres observed with each passage. Nevertheless we regard viral titre as the definitive measure of viral load.

Increased editing in the GP gene with passage

Sequence analysis identified editing in the mRNA encoding GP1,2, suggesting that viral mRNA might be co-purified or that there is editing of the genome itself during viral replication. Previous work has shown that approximately 20% of GP mRNA analysed from Ebola virus infected cells can be edited [8]. When we used TopHat [22] to align the sequencing reads to the viral genome and then searched the aligned reads for evidence of insertions within sequence reads mapping to the appropriate area on the viral genome. Analysis of the sequence data from each of the passages revealed that at passage one there were no insertions (0/23 sequence reads mapped to that region), at passage two approximately 15% of sequence reads had insertions (3/22 reads), similarly at passage three approximately 15% of reads had insertions (10/68 reads) but by passage four there was an increase to approximately 30% (36/124) and by passage five there were insertions in approximately 25% of the sequence reads mapping to that region (25/99 reads). Although the numbers of sequence reads were low, the data suggested that the proportion of full length mRNA encoding GP1,2 increased with sequential passage and this may be associated with the gain of virulence observed with sequential passage in the guinea pig model. One interpretation of this data is that the amount of GP1,2 was limiting in early passages. As the proportion of edited mRNA increased so more GP1,2 was available for virus assembly and on virus particles and this contributed to the increase in progeny virus observed in the later passages. However, a more stringent analysis of sequence reads that mapped to the relevant region of the glycoprotein gene showed additional A residues at the following rates: 0 out of 2 mapped reads for passage one, 2 out of 3 (66%) mapped reads at passage two, 17 out of 45 (37.8%) reads at passage three, 45 out of 115 (39.1%) mapped reads for passage four and 37 out of 91 (40.7%) mapped reads for passage 5. Thus, an analysis of those reads mapped at a higher stringency indicated an increased rate of editing both overall and increasing with passage. However, the low number of reads overall means these observations must be treated with caution.

Nucleotide substitutions become established with passage

EBOV sequence at each passage was analysed for coverage and variants using QuasiRecom [23], allowing us to determine consensus nucleotide at each position, map the frequency of minor variants. Thus we determine a consensus sequence for the virus at each passage and compare these consensus sequences to the published EBOV sequence at each particular passage. Examining the minor variants allowed us to determine if changes became established. For example, a minor variant at passage three that is not present at passage four indicates the sequence change did not become established. Thus we could distinguish whether a coding change became established with passage or not. There were two major types of substitutions those that appeared in passages two to four and were selected against by passage five (Table 2) or alternatively substitutions that became established by passage five (Table 3). Some of these correlated with previous point mutational analysis, thus placing confidence in the approach.

Some viral proteins accumulated substitutions whereas other did not. No substitutions were observed in either VP40 or VP30 by passage five. VP40 is a viral matrix protein with multiple roles in the virus life cycle, associating with both cellular and other viral proteins including the ribonucleoprotein complex. It is also involved in virus assembly and release (for example, [24],[25]), and thus may be evolutionary constrained. Likewise VP30 is a transcription factor and modulates interaction with NP and VP35 (for example, [26]) and may operate independently of the host cell for function.

Some substitutions were present in early passages but were lost by passage five. For example in VP35 at passages one and two, the predominant amino acid at position 84 was a Gly rather than the Glu found in the input sequence. By passages three, four and five this was again a Glu. In VP40 at passages two and three the predominant amino acid at position 16 was a Pro rather than the Ala found at passages one and two and the input sequence. By passages four and five, this had become an Ala again. Some of these changes have been previously associated with virulence. For example, in VP24, the predominant amino acid at position 163 changes from a Lys to Arg in passage three (and then Lys becomes dominant again in passages four and five), which is a conserved substitution. This substitution was described previously by Kugelman et al., who postulated that this amino acid change in VP24 might modulate interaction with other proteins instead of having an effect on structural stability [27].

A number of amino acid substitutions became established during adaptation and were present in passage five (Table 3). For example, the predominant amino acid at position 26 in VP24 becomes a Phe in place of a Leu. This substitution has previously been identified as being responsible for an increase in virulence in the guinea pig model using reverse genetics [28], and thus places confidence in the analysis of consensus sequence to detect biologically relevant variations. Using data from the stringent analysis, the frequency of amino acid substitution (amino acid changes/number of amino acid in the ORF) appeared to be of the same order of magnitude for each of the proteins that had an amino acid substitution(s) by passage five (Table 3). For NP this was 0.001, VP35 was 0.003, sGP was 0.006, VP24 was 0.004 and L was 0.005. However, there were no coding mutations in VP40 and VP30. While we observed 11 coding changes by passage five in the L protein, a study investigating adaptions of EBOV to a mouse model highlighted two coding changes and one silent change. This may reflect a difference in adaption of the virus to the two hosts.

As noted by Ebihara et al., additional mutations in the L protein are likely to contribute to virulence by affecting viral RNA synthesis [29]. These may also mediate both viral and host cell interactions. A similar situation has been described for influenza A virus where a cellular protein is critical for polymerase activity and transmission between different species and interaction of this protein with the polymerase is determined by a single amino acid substitution [30],[31]. However, with that said, data indicates that VP24 associates with a number of different cellular proteins that may be critical for its function inside virus infected cells (for example, [32]–[35]). It is interesting to speculate that the adaptation of the L protein to the new host may be correlated with the increase in RNA editing activity to transcribe the GP1,2 mRNA. This editing activity of the polymerase complex maybe associated with and mediated by a host cell factor, although both cis-acting factors on the EBOV genome and VP30 have been implicated in this process [36].

In this study, a virus (EBOV) that was not initially virulent in guinea pigs was serially passaged and became more pathogenic in its new host. Several alterations in the amino acid coding sequence were associated with this increase in virulence. A reverse genetics approach would precisely characterise these changes and their linkage with pathogenicity and virulence. Interestingly, this approach was used in a mouse model study of EBOV to investigate the molecular determinants of virulence [29]. There are several implications of our research for the biology of EBOV and associated outbreaks. EBOV causes a zoonotic infection [1],[37] and humans have been considered a dead end host, with the long-term survival of EBOV in nature likely being dependent on its ability to persist in its natural host. Our data suggest that the selection pressures at the initial stages of replication in a new host are different from those when the virus becomes established, and this may be dependent on population size, density and route of transmission. Therefore, as EBOV is so pathogenic in humans, one possibility for a sustained human-to-human transmission scenario might be selection of variants that are less pathogenic and that could lead to a more long-term infection of the population, thus allowing EBOV to persist. However, balanced with this are the social aspects of infection. For example, where humans tend to gather to grieve, suggesting that a reduction in pathogenicity is not the only way the virus can be marinated long term in the human population. Our study can be considered a model for the initial jump of EBOV from a reservoir into a new host, where selection pressure may be at its highest. The data presented in this study, using a forced evolutionary and transmission model, would suggest that the initial evolutionary trajectory of EBOV in a new host leads to a gain in virulence. Given the circumstances of the sustained transmission of EBOV in the current outbreak in West Africa, increases in virulence maybe associated with prolonged and uncontrolled epidemics of EBOV.

Teaching schedule: 3rd and 7th period

We will meet in room 203 at the Boys and Girls club. If we use another room, such as a computer lab, we will meet in our classroom and walk there together.

Course Standards (Next Generation Science Standards):

HS-LS1 From Molecules to Organisms: Structures and Processes

HS-LS2 Ecosystems: Interactions, Energy, and Dynamics

HS-LS3 Heredity: Inheritance and Variation of Traits

HS-LS4 Biological Evolution: Unity and Diversity

HS-ESS1 Earth's Place in the Universe

HS-ESS3 Earth and Human Activity

Course Description:

CLHS Biology is a class with many components, including a focus on reading, writing, lab practices and biology content. Students will learn about biological phenomenon while developing science and engineering skills. We do not use a textbook for this course, but there will be frequent online readings required print copies are available by request.

Course Objectives:

Understand the major biological concepts

Understand the role, place, and interactions of humans in the biosphere

Appreciate the diversity of living systems

Demonstrate mastery of the process of scientific inquiry

Use cognitive skills such as critical thinking, problem solving, and ethical analysis

Understand that science is a way of knowing and technology is a way of adapting

Understand the personal, social, and ethical implications of biology and biotechnology

Use educational technology as tools for learning

Materials needed daily:

3 Ring Binder (You can bring one of your own, or Mr. Sidarous will sell you a binder for $1)

Loose leaf paper (You can bring your own, or Mr. Sidarous will sell you paper for $1)


Students will be required to use the school’s website ( ) during the class. Through the website, each student will receive an account, which gives them an email address, a personal calendar, a space to work on documents online, a space to create a personal website, and other functionality. Additionally, the course calendar and assignments will also be available on the website on the Biology page. Mr. Sidarous will train students in computer use as well as use of the website in class, but some work must be done outside of class, including online lessons and assessments. If a student does not have access to the Internet at home, they may use the school’s computer laboratory before or after school. Additionally, the Chicago Public Library has free computer access.


Homework assignments are intended to reinforce the concepts learned in class and prepare students for examinations. Assignments may be turned in one day late, but 50% will be deducted for turning in the homework late. After one day, no late work will be accepted. Late homework will always result in an after school detention to be served that day. Students with unexcused absences will receive a zero for any assignments due that day. Students will do their homework in a binder which must be brought to class every day. Some assignments will be done in groups of 2 or 4 however each student is responsible for completing his/her own homework, in his/her own words. Any two laboratory entries with identical (word for word) entries will not receive credit for the assignment.


The units we will be studying are as follows:

Structure & Function in Organisms

Energy & Matter in Organisms


The quarter grade will be determined using the following percentage breakdown:

The quarter grade is determined by totaling all the points in each grade category and dividing by the total points possible. Keep in mind that each category is weighted using the percentage breakdowns given. For the participation grade, each student will be evaluated as to their attendance and their involvement in the class. If a student comes to class each day with no unexcused absences or tardies and participates in class discussions, they will receive all of the participation points. Students will lose points if they do not have their homework, disrupt the class, are tardy, or cut. Unexcused absences will result in an automatic zero for the day as well as for any homework due that day. Students may earn extra participation points through exemplary work and effort.


Mastery grades are a system of grading students based on their demonstrated level of mastery of concepts (“Essential Skills”), rather than just calculating an average based on the total number of “points” they earn in a semester. It measures demonstrated student learning, not speed of learning. At the beginning of every unit, the teacher will break down the standards for the unit into smaller objectives and criteria using a detailed rubric. During the unit, the student is assessed to see if they truly know the material using a variety of assessments, such as traditional pencil-and-paper tests, projects, discussions, or reports. The class grade will be based on all of the evidence the teacher collects demonstrating mastery of the essential standards. The goal of this approach is to provide the teacher, student, and parent as accurate a picture as possible of the student’s learning and to encourage a dialogue about how the student can master the material for the class. In particular, because learning is a process that takes place over time, each assessment will provide feedback for the student about what to focus on next, and the student will be allowed to retake assessments. If the new assessments shows a higher level of mastery, that new score replaces the old one.


The honors option is intended to provide students with extended learning opportunities within a course of study. These opportunities are independent study tasks that provide additional depth of content, advanced concepts and a chance for more authentic applications of skills and knowledge. The honors option is also an opportunity for students to begin thinking and working on their college interests. If student does not meet the requirements established at the beginning of the semester, students will not be given the honors credit and the honors course designation will not appear on their transcripts. In addition, students must maintain at least a C average in their assigned class to stay within the honors tract . Successful completion of the honors option in a course is designated on the student’s transcript. Also, keep in mind that the honors option designated grades carry different values for calculating grade point averages.

WHO lists additional COVID-19 vaccine for emergency use and issues interim policy recommendations

WHO today listed the Sinopharm COVID-19 vaccine for emergency use, giving the green light for this vaccine to be rolled out globally. The Sinopharm vaccine is produced by Beijing Bio-Institute of Biological Products Co Ltd, subsidiary of China National Biotec Group (CNBG).

&ldquoThe addition of this vaccine has the potential to rapidly accelerate COVID-19 vaccine access for countries seeking to protect health workers and populations at risk,&rdquo said Dr Mariângela Simão, WHO Assistant-Director General for Access to Health Products. &ldquoWe urge the manufacturer to participate in the COVAX Facility and contribute to the goal of more equitable vaccine distribution.&rdquo

WHO&rsquos Emergency Use Listing (EUL) is a prerequisite for COVAX Facility vaccine supply. It also allows countries to expedite their own regulatory approval to import and administer COVID-19 vaccines.

The EUL assesses the quality, safety and efficacy of COVID-19 vaccines, as well as risk management plans and programmatic suitability, such as cold chain requirements. The assessment is performed by the product evaluation group, composed by regulatory experts from around the world and a Technical Advisory Group (TAG), in charge of performing the risk-benefit assessment for an independent recommendation on whether a vaccine can be listed for emergency use and, if so, under which conditions.

In the case of the Sinopharm vaccine, the WHO assessment included on-site inspections of the production facility.

The Sinopharm product is an inactivated vaccine called SARS-CoV-2 Vaccine (Vero Cell). Its easy storage requirements make it highly suitable for low-resource settings. It is the also first vaccine that will carry a vaccine vial monitor, a small sticker on the vaccine vials that change color as the vaccine is exposed to heat, letting health workers know whether the vaccine can be safely used.

WHO&rsquos Strategic Advisory Group of Experts on Immunization (SAGE) has also completed its review of the vaccine. On the basis of all available evidence, WHO recommends the vaccine for adults 18 years and older, in a two-dose schedule with a spacing of three to four weeks. Vaccine efficacy for symptomatic and hospitalized disease was estimated to be 79%, all age groups combined.

Few older adults (over 60 years) were enrolled in clinical trials, so efficacy could not be estimated in this age group. Nevertheless, WHO is not recommending an upper age limit for the vaccine because preliminary data and supportive immunogenicity data suggest the vaccine is likely to have a protective effect in older persons. There is no theoretical reason to believe that the vaccine has a different safety profile in older and younger populations. WHO therefore recommends that countries using the vaccine in older age groups conduct safety and effectiveness monitoring to make the recommendation more robust.

WHO emergency use listing

The emergency use listing (EUL) procedure assesses the suitability of novel health products during public health emergencies. The objective is to make medicines, vaccines and diagnostics available as rapidly as possible to address the emergency, while adhering to stringent criteria of safety, efficacy and quality. The assessment weighs the threat posed by the emergency as well as the benefit that would accrue from the use of the product against any potential risks.

The EUL pathway involves a rigorous assessment of late phase II and phase III clinical trial data as well as substantial additional data on safety, efficacy, quality and a risk management plan. These data are reviewed by independent experts and WHO teams who consider the current body of evidence on the vaccine under consideration, the plans for monitoring its use, and plans for further studies.

As part of the EUL process, the company producing the vaccine must commit to continue to generate data to enable full licensure and WHO prequalification of the vaccine. The WHO prequalification process will assess additional clinical data generated from vaccine trials and deployment on a rolling basis to ensure the vaccine meets the necessary standards of quality, safety and efficacy for broader availability.

WHO also listed the Pfizer/BioNTech vaccine for emergency use on 31 December 2020 two AstraZeneca/Oxford COVID-19 vaccines on 15 February 2021, produced by AstraZeneca-SKBio (Republic of Korea) and the Serum Institute of India and COVID-19 vaccine Ad26.COV2.S developed by Janssen (Johnson & Johnson) on 12 March 2021.

SAGE is the principal advisory group to WHO for vaccines and immunization. It is charged with advising WHO on overall global policies and strategies, ranging from vaccines and technology, research and development, to delivery of immunization and its linkages with other health interventions. SAGE is concerned not just with childhood vaccines and immunization, but all vaccine-preventable diseases.

SAGE has issued recommendations on Pfizer (8 January 2021), Moderna (25 January 2021), AstraZeneca (21 April 2021), and Janssen COVID (17 March 2021) vaccines, as well as issued a framework for access and population prioritization roadmap.

SAGE and EUL are complementary but independent processes. The EUL process is centered on determining if a manufactured product is quality-assured, safe and effective. SAGE is policy oriented. Policy recommendations for a vaccine are only of value to a vaccination campaign when the product has been listed or authorized for use.

In the context of COVID-19 and due the pressing need for vaccines, the Secretariat of SAGE and the EUL team have been working in parallel to allow WHO EUL and policy recommendations, based on the available evidence, to be issued in a synchronized manner.


The two species of bed bugs (Insecta: Hemiptera: Cimicidae) usually implicated in human infestations are Cimex lectularius and C. hemipterus. Although rare, humans may become incidental hosts of Cimex species of bats and birds.

Life Cycle:

Adults and all nymphal stages of Cimex spp. need to take blood meals from warm-blooded hosts, which are typically humans for C. lectularius and C. hemipterus, although other mammals and birds can be utilized in the absence of a human host. Female bed bugs lay about five eggs daily throughout their adult lives in a sheltered location (mattress seams, crevices in box springs, spaces under baseboards, etc). Eggs hatch in about 4-12 days into first instar nymphs which must take a blood meal before molting to the next stage. The bugs will undergo five nymphal stages ( , , , , ), each one requiring a blood meal before molting to the next stage, with the fifth stage molting into an adult . Nymphs, although lacking wing buds, resemble smaller versions of the adults. Nymphs and adults take about 5-10 minutes to obtain a full blood meal. The adults may take several blood meals over several weeks, assuming a warm-blooded host is available. Mating occurs off the host and involves a unique form of copulation called &lsquotraumatic insemination&rsquo whereby the male penetrates the female&rsquos abdominal wall with his external genitalia and inseminates into her body cavity. Adults live 6-12 months and may survive for long periods of time without feeding.

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Valuable data often go unpublished when they could be helping to progress science. Hence, the BMC Series introduced Data notes, a short article type allowing you to describe your data and publish them to make your data easier to find, cite and share.

You can publish your data in BMC Genomic Data (genomic, transcriptomic and high-throughput genotype data) or in BMC Research Notes (data from across all natural and clinical sciences).

More information about our unique article type can be found on the BMC Genomic Data and BMC Research Notes journal websites.


The field of dentistry is undergoing substantial changes that are relevant to the range of services that general dentists (GDs) provide. These include the changing picture of dental economics and dental care utilization, demography of patient populations, the scope of practice, changing delivery models, access to care, and an increased interest in the relationship between oral health and general health [1, 2]. One vision for the future of general dentistry is that it serves as a segue into the health care system at large, offering an opportunity to monitor, refer, or treat both oral health and general medical conditions [3]. In that vision, GDs function in a primary care role, and the comprehensiveness of the procedures that GDs provide takes on additional significance.

GDs assume a dual role as providers of primary oral health care and as gatekeepers who refer patients to specialists [4]. In 1996, about 81% of all dental visits in the United States were provided by GDs [5]. Nonetheless, a study of Michigan children’s Medicaid claims data found that about 20% of dentists only provided diagnostic and preventive services for their Medicaid patients, meaning that for these children Medicaid coverage was not a segue into comprehensive primary dental care that included restorative care [6]. Most dental extractions are provided by GDs, especially among lower-income patients [7]. Most non-surgical periodontal care is provided in GDs’ offices, and increases in demand for periodontal services are being met mainly by GDs, not periodontists [5, 8]. As long as they are capable of providing the service to the standard of care, GDs substitute for a specialist’s care, instead of complementing it, which has economic and delivery system implications [5].

Decisions made to treat or refer may be a means for GDs to adapt to changing economic demand and the needs of their patient population. It is known that characteristics of the patient population that the GD serves can substantially influence the specific types of services provided [9]. An Australian study led to the conclusion that dental service rates are influenced by a large number of small effects from a wide range of dentist, practice, and patient factors [10]. A few studies have identified certain dentist characteristics as being associated with provision of endodontic, periodontal, and oral surgical services [11–14]. However, little is known about how commonly GDs provide directly a comprehensive range of procedures, or about factors associated with this provision. Therefore, our objectives were to: (1) determine whether and how often GDs provide specific dental procedures and (2) test the hypothesis that provision is significantly associated with key dentist, practice, and patient population characteristics.

Financial Analyst

Financial analysts evaluate stocks, bonds, mutual funds, and other investments for clients and businesses. Biology majors can use their advanced mathematical skills to help assess the success of various investments.  

Most analysts focus on specific industries, and biology majors are particularly well suited for working as analysts in biotechnology, pharmaceuticals, medical products, health services, and environmental companies.

Financial analysts, like biology majors, use computer-based resources to gather and analyze data to draw conclusions.

They must have the writing skills to generate reports summarizing their findings. A bachelor’s degree is often enough to get started in a career as a financial analyst.

Salary and Job Outlook: The Bureau of Labor Statistics (BLS) estimates that financial analysts earned a median annual salary of $81,590 in May 2019. The top 10% earned $156,150 or more while the bottom 10% earned $47,230 or less.

The BLS projected that employment in this field will grow by 5% between 2019 and 2029, faster than average for all occupations.  

Watch the video: Action 11 Module 1. Timeline of Biology (May 2022).