How to write anabstract

KavitaDhanwada

What is an abstract?

A summary of your research, usually in oneparagraph, that states the major aspects of the work that was done.

It helps readers decide whether they want to read the rest of the poster or paper – so make it clear,concise and articulate.

Has to have enough key information to make ituseful to someone who may want to referenceyour work.

What are the components of anabstract?1. Context

2. Question(s) being asked

3. Methods (very abbreviated)

4. Results

5. Conclusion/Significance

All of this needs to be said in about 200-300 words –needs to be exact and concise as well as inclusive.

How do I start? Wait until you are done with the rest of the

poster/paper

Start by writing a summary that includes whatever you think is important, and then make edits by removing unnecessary words, while stillretaining the necessary concepts.

Include key phrases from different sections ofposter as you start.

Don’t be too technical in this section.

Suggested format for abstractUsually have a specific sequence that is followed:1. Why is this work being done – give 1-2 sentence background

2. What is the question(s) you asked - (or purpose or work).

State the purpose very clearly in the third sentence. (Should be clear from the first 2 sentences.)

3. What were the methods used?

Name or briefly describe the basic methodology used without going into excessivedetail-be sure to indicate the key techniques used.

4. What were the major findings including key quantitative results, or trends.

Report those results which answer the questions you were asking

Identify trends, relative change or differences, etc.

5. End with interpretations and conclusions.

Clearly state the implications of the answers your results gave you.

What you should NOT put in anabstract Lengthy background information

Reference citations

Long, incomplete sentences

Abbreviations or terms that may be confusing toreaders (if used, spell it out the first time used)

Any sort of illustration, figure, or table, or references to them.

Sample abstract (200 words)Metolachlor is one of the most commonly used herbicides in the United

States. Protein synthesis is inhibited when roots and shoots of susceptible plants absorb this synthetic herbicide. While quite effective in killing weeds, several studies have shown that exposure to metolachlor results in decreased cell proliferation, growth and reproductive ability of non-target organisms. However, the mode of metolachlor action in non-target organisms has not yet been elucidated. The current study assessed effects of metolachlor exposure on immortalized human liver (HepG2) cells. Results from cell proliferation assays showed that a 72-hour exposure to 50 parts per billion (ppb) metolachlor significantly inhibited growth of these cells compared to untreated controls while a decrease in the cell division rate required exposure to 500 ppb metolachlor for 48 hours. Flow cytometry analysis of cell cycle distribution revealed that 500 ppb metolachlor treatment resulted in fewer HepG2 cells in G2/M phase after 72 hours. Real-time PCR analysis showed a significant decrease in the abundance of the cyclin A transcripts after 12 hours in cells exposed to 300 ppb metolachlor.These results suggest metolachlor may affect progression through the S phase of the cell cycle and entrance into the G2 phase.

Sample abstract (274 words)Metolachlor, a commonly used herbicide in the United States, is especially prevalent in

the Midwest and can contaminate ground and surface waters. Metolachlor exposure hasbeen shown to induce genotoxic effects in tadpoles and lymphocytes as well as cytotoxiceffects in lymphocytes and has also been shown to slow or inhibit cell growth in a varietyof cell types. Research from our laboratory has shown that growth is inhibited in normal human fibroblasts and human liver cells (HepG2) after metolachlor exposure.

In the current study, the level of phosphorylated Retinoblastoma (Rb) protein is being studied to determine a mechanism for decreased cell growth. To determine if metolachlor exposure leads to lower levels of phosphorylated Rb, HepG2 cells were treated with various concentrations of metolachlor (0 to 1000 ppb) for 48 and 72 hours. ELISA assayswere used to quantify total Rb protein, as well as phosphorylated Rb protein (at Ser780), as phosphorylation of this consensus sites has been shown to be involved in disruption of E2F binding.

ELISA results showed that HepG2 cells exposed to 100, 300 and 1000 ppb metolachlor for72 hrs had lower levels of phosphorylated Ser780 Rb compared to control cells while nosignificant difference was seen in levels of total Rb protein in any herbicide treated samplecompared to control. In contrast, only HepG2 cells exposed to 100 ppb metolachlor for 48 hrs had lower levels of Ser780 Rb but also had lower levels of total Rb at 100, 500 and 1000ppb. These results suggest that metolachlor exposure to non-target human cells can leadto changes in the levels of phosphorylated Rb and possible cell cycle arrest.

Which sentence (s) include background, context?Metolachlor, a commonly used herbicide in the United States, is especially

prevalent in the Midwest and can contaminate ground and surface waters.Metolachlor exposure has been shown to induce genotoxic effects in tadpoles and lymphocytes as well as cytotoxic effects in lymphocytes and has also been shown to slow or inhibit cell growth in a variety of cell types. Research from our laboratory has shown that growth is inhibited in normal human fibroblasts and human liver cells (HepG2) after metolachlor exposure.

In the current study, the level of phosphorylated Retinoblastoma (Rb) protein is being studied to determine a mechanism for decreased cell growth. To determine if metolachlor exposure leads to lower levels of phosphorylated Rb, HepG2 cells were treated with various concentrations of metolachlor (0 to 1000 ppb) for 48 and 72 hours. ELISA assays were used to quantify total Rb protein, as well as phosphorylated Rb protein (at Ser780), as phosphorylation of this consensus sites has been shown to be involved in disruption of E2F binding.

ELISA results showed that HepG2 cells exposed to 100, 300 and 1000 ppb metolachlor for 72 hrs had lower levels of phosphorylated Ser780 Rb compared to control cells while no significant difference was seen in levels of total Rb proteinin any herbicide treated sample compared to control. In contrast, only HepG2 cells exposed to 100 ppb metolachlor for 48 hrs had lower levels of Ser780 Rb but also had lower levels of total Rb at 100, 500 and 1000 ppb. These results suggest that metolachlor exposure to non-target human cells can lead to changes in the levels of phosphorylated Rb and possible cell cycle arrest.

Which sentence (s) include background, context?Metolachlor, a commonly used herbicide in the United States, is especially

prevalent in the Midwest and can contaminate ground and surface waters. Metolachlor exposure has been shown to induce genotoxic effects in tadpoles and lymphocytes as well as cytotoxic effects in lymphocytes and has also been shown to slow or inhibit cell growth in a variety of cell types. Research from our laboratory has shown that growth is inhibited in normal human fibroblasts and human liver cells (HepG2) after metolachlor exposure.

In the current study, the level of phosphorylated Retinoblastoma (Rb) protein is being studied to determine a mechanism for decreased cell growth. To determine if metolachlor exposure leads to lower levels of phosphorylated Rb, HepG2 cells were treated with various concentrations of metolachlor (0 to 1000 ppb) for 48 and 72 hours. ELISA assays were used to quantify total Rb protein, as well as phosphorylated Rb protein (at Ser780), as phosphorylation of this consensus sites has been shown to be involved in disruption of E2F binding.

ELISA results showed that HepG2 cells exposed to 100, 300 and 1000 ppb metolachlor for 72 hrs had lower levels of phosphorylated Ser780 Rb compared to control cells while no significant difference was seen in levels of total Rb protein in any herbicide treated sample compared to control. In contrast, only HepG2 cells exposed to 100 ppb metolachlor for 48 hrs had lower levels of Ser780 Rb but also had lower levels of total Rb at 100, 500 and 1000 ppb. These results suggest that metolachlor exposure to non-target human cells can lead to changes in the levels of phosphorylated Rb and possible cell cycle arrest.

What is the question (s) being addressed?Metolachlor, a commonly used herbicide in the United States, is especially

prevalent in the Midwest and can contaminate ground and surface waters.Metolachlor exposure has been shown to induce genotoxic effects in tadpoles and lymphocytes as well as cytotoxic effects in lymphocytes and has also been shown to slow or inhibit cell growth in a variety of cell types. Research from our laboratory has shown that growth is inhibited in normal human fibroblasts and human liver cells (HepG2) after metolachlor exposure.

In the current study, the level of phosphorylated Retinoblastoma (Rb) protein is being studied to determine a mechanism for decreased cell growth. To determine if metolachlor exposure leads to lower levels of phosphorylated Rb, HepG2 cells were treated with various concentrations of metolachlor (0 to 1000 ppb) for 48 and 72 hours. ELISA assays were used to quantify total Rb protein, as well as phosphorylated Rb protein (at Ser780), as phosphorylation of this consensus sites has been shown to be involved in disruption of E2F binding.

ELISA results showed that HepG2 cells exposed to 100, 300 and 1000 ppb metolachlor for 72 hrs had lower levels of phosphorylated Ser780 Rb compared to control cells while no significant difference was seen in levels of total Rb proteinin any herbicide treated sample compared to control. In contrast, only HepG2 cells exposed to 100 ppb metolachlor for 48 hrs had lower levels of Ser780 Rb but also had lower levels of total Rb at 100, 500 and 1000 ppb. These results suggest that metolachlor exposure to non-target human cells can lead to changes in the levels of phosphorylated Rb and possible cell cycle arrest.

What is the question (s) being addressed?Metolachlor, a commonly used herbicide in the United States, is especially

prevalent in the Midwest and can contaminate ground and surface waters. Metolachlor exposure has been shown to induce genotoxic effects in tadpoles and lymphocytes as well as cytotoxic effects in lymphocytes and has also been shown to slow or inhibit cell growth in a variety of cell types. Research from our laboratory has shown that growth is inhibited in normal human fibroblasts and human liver cells (HepG2) after metolachlor exposure.

In the current study, the level of phosphorylated Retinoblastoma (Rb) protein is being studied to determine a mechanism for decreased cell growth. To determine if metolachlor exposure leads to lower levels of phosphorylated Rb, HepG2 cells were treated with various concentrations of metolachlor (0 to 1000 ppb) for 48 and 72 hours. ELISA assays were used to quantify total Rb protein, as well as phosphorylated Rb protein (at Ser780), as phosphorylation of this consensus sites has been shown to be involved in disruption of E2F binding.

ELISA results showed that HepG2 cells exposed to 100, 300 and 1000 ppb metolachlor for 72 hrs had lower levels of phosphorylated Ser780 Rb compared to control cells while no significant difference was seen in levels of total Rb protein in any herbicide treated sample compared to control. In contrast, only HepG2 cells exposed to 100 ppb metolachlor for 48 hrs had lower levels of Ser780 Rb but also had lower levels of total Rb at 100, 500 and 1000 ppb. These results suggest that metolachlor exposure to non-target human cells can lead to changes in the levels of phosphorylated Rb and possible cell cycle arrest.

What methods are being used?Metolachlor, a commonly used herbicide in the United States, is especially

prevalent in the Midwest and can contaminate ground and surface waters.Metolachlor exposure has been shown to induce genotoxic effects in tadpoles and lymphocytes as well as cytotoxic effects in lymphocytes and has also been shown to slow or inhibit cell growth in a variety of cell types. Research from our laboratory has shown that growth is inhibited in normal human fibroblasts and human liver cells (HepG2) after metolachlor exposure.

In the current study, the level of phosphorylated Retinoblastoma (Rb) protein is being studied to determine a mechanism for decreased cell growth. To determine if metolachlor exposure leads to lower levels of phosphorylated Rb, HepG2 cells were treated with various concentrations of metolachlor (0 to 1000 ppb) for 48 and 72 hours. ELISA assays were used to quantify total Rb protein, as well as phosphorylated Rb protein (at Ser780), as phosphorylation of this consensus sites has been shown to be involved in disruption of E2F binding.

ELISA results showed that HepG2 cells exposed to 100, 300 and 1000 ppb metolachlor for 72 hrs had lower levels of phosphorylated Ser780 Rb compared to control cells while no significant difference was seen in levels of total Rb proteinin any herbicide treated sample compared to control. In contrast, only HepG2 cells exposed to 100 ppb metolachlor for 48 hrs had lower levels of Ser780 Rb but also had lower levels of total Rb at 100, 500 and 1000 ppb. These results suggest that metolachlor exposure to non-target human cells can lead to changes in the levels of phosphorylated Rb and possible cell cycle arrest.

What methods are being used?Metolachlor, a commonly used herbicide in the United States, is especially prevalent in the

Midwest and can contaminate ground and surface waters. Metolachlor exposure has been shown to induce genotoxic effects in tadpoles and lymphocytes as well as cytotoxic effectsin lymphocytes and has also been shown to slow or inhibit cell growth in a variety of cell types. Research from our laboratory has shown that growth is inhibited in normal humanfibroblasts and human liver cells (HepG2) after metolachlor exposure.

In the current study, the level of phosphorylated Retinoblastoma (Rb) protein is being studied to determine a mechanism for decreased cell growth. To determine if metolachlor exposure leads to lower levels of phosphorylated Rb, HepG2 cells were treated with various concentrations of metolachlor (0 to 1000 ppb) for 48 and 72 hours. ELISA assayswere used to quantify total Rb protein, as well as phosphorylated Rb protein (at Ser780), as phosphorylation of this consensus sites has been shown to be involved in disruption of E2F binding.

ELISA results showed that HepG2 cells exposed to 100, 300 and 1000 ppb metolachlor for72 hrs had lower levels of phosphorylated Ser780 Rb compared to control cells while nosignificant difference was seen in levels of total Rb protein in any herbicide treated samplecompared to control. In contrast, only HepG2 cells exposed to 100 ppb metolachlor for 48 hrs had lower levels of Ser780 Rb but also had lower levels of total Rb at 100, 500 and 1000ppb. These results suggest that metolachlor exposure to non-target human cells can leadto changes in the levels of phosphorylated Rb and possible cell cycle arrest.

ResultsMetolachlor, a commonly used herbicide in the United States, is especially

prevalent in the Midwest and can contaminate ground and surface waters.Metolachlor exposure has been shown to induce genotoxic effects in tadpoles and lymphocytes as well as cytotoxic effects in lymphocytes and has also been shown to slow or inhibit cell growth in a variety of cell types. Research from our laboratory has shown that growth is inhibited in normal human fibroblasts and human liver cells (HepG2) after metolachlor exposure.

In the current study, the level of phosphorylated Retinoblastoma (Rb) protein is being studied to determine a mechanism for decreased cell growth. To determine if metolachlor exposure leads to lower levels of phosphorylated Rb, HepG2 cells were treated with various concentrations of metolachlor (0 to 1000 ppb) for 48 and 72 hours. ELISA assays were used to quantify total Rb protein, as well as phosphorylated Rb protein (at Ser780), as phosphorylation of this consensus sites has been shown to be involved in disruption of E2F binding.

ELISA results showed that HepG2 cells exposed to 100, 300 and 1000 ppb metolachlor for 72 hrs had lower levels of phosphorylated Ser780 Rb compared to control cells while no significant difference was seen in levels of total Rb proteinin any herbicide treated sample compared to control. In contrast, only HepG2 cells exposed to 100 ppb metolachlor for 48 hrs had lower levels of Ser780 Rb but also had lower levels of total Rb at 100, 500 and 1000 ppb. These results suggest that metolachlor exposure to non-target human cells can lead to changes in the levels of phosphorylated Rb and possible cell cycle arrest.

ResultsMetolachlor, a commonly used herbicide in the United States, is especially prevalent in

the Midwest and can contaminate ground and surface waters. Metolachlor exposure hasbeen shown to induce genotoxic effects in tadpoles and lymphocytes as well as cytotoxiceffects in lymphocytes and has also been shown to slow or inhibit cell growth in a varietyof cell types. Research from our laboratory has shown that growth is inhibited in normal human fibroblasts and human liver cells (HepG2) after metolachlor exposure.

In the current study, the level of phosphorylated Retinoblastoma (Rb) protein is being studied to determine a mechanism for decreased cell growth. To determine if metolachlor exposure leads to lower levels of phosphorylated Rb, HepG2 cells were treated with various concentrations of metolachlor (0 to 1000 ppb) for 48 and 72 hours. ELISA assayswere used to quantify total Rb protein, as well as phosphorylated Rb protein (at Ser780), as phosphorylation of this consensus sites has been shown to be involved in disruption of E2F binding.

ELISA results showed that HepG2 cells exposed to 100, 300 and 1000 ppb metolachlor for72 hrs had lower levels of phosphorylated Ser780 Rb compared to control cells while nosignificant difference was seen in levels of total Rb protein in any herbicide treated samplecompared to control. In contrast, only HepG2 cells exposed to 100 ppb metolachlor for 48 hrs had lower levels of Ser780 Rb but also had lower levels of total Rb at 100, 500 and 1000ppb. These results suggest that metolachlor exposure to non-target human cells can leadto changes in the levels of phosphorylated Rb and possible cell cycle arrest.

Conclustions/summary?Metolachlor, a commonly used herbicide in the United States, is especially

prevalent in the Midwest and can contaminate ground and surface waters.Metolachlor exposure has been shown to induce genotoxic effects in tadpoles and lymphocytes as well as cytotoxic effects in lymphocytes and has also been shown to slow or inhibit cell growth in a variety of cell types. Research from our laboratory has shown that growth is inhibited in normal human fibroblasts and human liver cells (HepG2) after metolachlor exposure.

In the current study, the level of phosphorylated Retinoblastoma (Rb) protein is being studied to determine a mechanism for decreased cell growth. To determine if metolachlor exposure leads to lower levels of phosphorylated Rb, HepG2 cells were treated with various concentrations of metolachlor (0 to 1000 ppb) for 48 and 72 hours. ELISA assays were used to quantify total Rb protein, as well as phosphorylated Rb protein (at Ser780), as phosphorylation of this consensus sites has been shown to be involved in disruption of E2F binding.

ELISA results showed that HepG2 cells exposed to 100, 300 and 1000 ppb metolachlor for 72 hrs had lower levels of phosphorylated Ser780 Rb compared to control cells while no significant difference was seen in levels of total Rb proteinin any herbicide treated sample compared to control. In contrast, only HepG2 cells exposed to 100 ppb metolachlor for 48 hrs had lower levels of Ser780 Rb but also had lower levels of total Rb at 100, 500 and 1000 ppb. These results suggest that metolachlor exposure to non-target human cells can lead to changes in the levels of phosphorylated Rb and possible cell cycle arrest.

Conclusion/summaryMetolachlor, a commonly used herbicide in the United States, is especially

prevalent in the Midwest and can contaminate ground and surface waters. Metolachlor exposure has been shown to induce genotoxic effects in tadpoles and lymphocytes as well as cytotoxic effects in lymphocytes and has also been shown to slow or inhibit cell growth in a variety of cell types. Research from our laboratory has shown that growth is inhibited in normal human fibroblasts and human liver cells (HepG2) after metolachlor exposure.

In the current study, the level of phosphorylated Retinoblastoma (Rb) protein is being studied to determine a mechanism for decreased cell growth. To determine if metolachlor exposure leads to lower levels of phosphorylated Rb, HepG2 cells were treated with various concentrations of metolachlor (0 to 1000 ppb) for 48 and 72 hours. ELISA assays were used to quantify total Rb protein, as well as phosphorylated Rb protein (at Ser780), as phosphorylation of this consensus sites has been shown to be involved in disruption of E2F binding.

ELISA results showed that HepG2 cells exposed to 100, 300 and 1000 ppb metolachlor for 72 hrs had lower levels of phosphorylated Ser780 Rb compared to control cells while no significant difference was seen in levels of total Rb protein in any herbicide treated sample compared to control. In contrast, only HepG2 cells exposed to 100 ppb metolachlor for 48 hrs had lower levels of Ser780 Rb but also had lower levels of total Rb at 100, 500 and 1000 ppb. These results suggest that metolachlor exposure to non-target human cells can lead to changes in the levels of phosphorylated Rb and possible cell cycle arrest.

Sample abstract (200 words)Metolachlor is one of the most commonly used herbicides in the United States. Protein

synthesis is inhibited when roots and shoots of susceptible plants absorb this syntheticherbicide. While quite effective in killing weeds, several studies have shown that exposureto metolachlor results in decreased cell proliferation, growth and reproductive ability ofnon-target organisms. However, the mode of metolachlor action in non-target organisms hasnot yet been elucidated. The current study assessed effects of metolachlor exposure onimmortalized human liver (HepG2) cells. Results from cell proliferation assays showed thata 72-hour exposure to 50 parts per billion (ppb) metolachlor significantly inhibited growthof these cells compared to untreated controls while a decrease in the cell division raterequired exposure to 500 ppb metolachlor for 48 hours. Flow cytometry analysis of cellcycle distribution revealed that 500 ppb metolachlor treatment resulted in fewer HepG2 cells in G2/M phase after 72 hours. Real-time PCR analysis showed a significant decrease inthe abundance of the cyclin A transcripts after 12 hours in cells exposed to 300 ppb metolachlor. These results suggest metolachlor may affect progression through the S phaseof the cell cycle and entrance into the G2 phase.

Sample abstract (200 words) Metolachlor is one of the most commonly used herbicides in the United States. Protein

synthesis is inhibited when roots and shoots of susceptible plants absorb this syntheticherbicide. While quite effective in killing weeds, several studies have shown thatexposure to metolachlor results in decreased cell proliferation, growth and reproductiveability of non-target organisms. However, the mode of metolachlor actionin non-target organisms has not yet been elucidated. The current study assessed effectsof metolachlor exposure on immortalized human liver (HepG2) cells. Results from cell proliferation assays showed that a 72-hour exposure to 50 parts per billion (ppb) metolachlor significantly inhibited growth of these cells compared to untreated controlswhile a decrease in the cell division rate required exposure to 500 ppb metolachlor for48 hours. Flow cytometry analysis of cell cycle distribution revealed that 500 ppbmetolachlor treatment resulted in fewer HepG2 cells in G2/M phase after 72 hours.Real-time PCR analysis showed a significant decrease in the abundance of the cyclin Atranscripts after 12 hours in cells exposed to 300 ppb metolachlor. These resultssuggest metolachlor may affect progression through the S phase of the cell cycle andentrance into the G2 phase.

When you are done

CHECK YOUR WORK!

Make sure that the information you have in the abstract “matches” what you have in the rest ofthe poster. You want to have the SAMEinformation in both places.

Go over it with your mentor.