curl --location --request POST 'https://zylalabs.com/api/1915/papermill+text+comparison+api/1621/document+posting' --header 'Authorization: Bearer YOUR_API_KEY' 

--data-raw '{
    "id": "retracted_article_id2",
    "title": "Silencing circANKRD36 protects H9c2 cells against lipopolysaccharide-induced injury via up-regulating miR-138",
    "abstract": "Background: Myocarditis refers to the inflammatory process that affects the muscle tissue of the heart. Persistent myocardial inflammation promotes myocardial cell damage, which ultimately leads to heart failure or death. Therefore, we aimed to explore the functional impacts of circANKRD36 on myocarditis. Methods: H9c2 cells were pre-treated with lipopolysaccharide (LPS). Viability and apoptosis were evaluated utilizing CCK-8 assay and flow cytometry. Inflammatory cytokines mRNA expression and production were assessed by qRT-PCR and ELISA. Western blot was utilized to distinguish apoptosis and inflammatory related factors expression. Sequentially, the above mentioned parameters were reassessed when overexpressed miR-138. Results: LPS declined viability and as well as raised apoptosis and inflammatory injury in H9c2 cells. Silencing circular RNA ANKRD36 (si-circANKRD36) alleviated apoptosis and inflammatory injury induced by LPS. MiR-138 expression was suppressed by LPS and elevated by si-circANKRD36. Increase of viability and inflammatory injury induced by si-circANKRD36 was alleviated by down-regulation of miR-138. Eventually, si-circANKRD36 inhibited p38MAPK/NF-κB pathway which activated by LPS via up-regulating miR-138. Conclusion: Si-circANKRD36 exerted its anti-apoptosis and anti-inflammatory function under the condition of LPS in H9c2 cells through p38MAPK/NF-κB pathway and up-regulation of miR-138."
}'

    

import okhttp3.OkHttpClient;
import okhttp3.Request;
import okhttp3.Response;
import java.io.IOException;

public class Main {
    public static void main(String[] args) {
        OkHttpClient client = new OkHttpClient();

        // Build the GET request
        Request request = new Request.Builder()
            .url("https://zylalabs.com/api/1915/papermill+text+comparison+api/1621/document+posting")
            .get() // Use GET method without a body
            .addHeader("Authorization", "Bearer YOUR_API_KEY")
            .build();

        // Execute the request
        try (Response response = client.newCall(request).execute()) {
            if (response.isSuccessful()) {
                // Handle the response in case of a successful request
                String responseData = response.body().string();
                System.out.println(responseData);
            } else {
                // Handle errors
                System.out.println("Request error: " + response.code());
            }
        } catch (IOException e) {
            // Handle I/O exceptions
            e.printStackTrace();
        }
    }
}

var settings = {
  "url": "https://zylalabs.com/api/1915/papermill+text+comparison+api/1621/document+posting",
  "method": "POST",
  "timeout": 0,
  "headers": {
    "Authorization": "Bearer YOUR_API_KEY"
  },
};

$.ajax(settings).done(function (response) {
  console.log(response);
});

var data = "{\r\n    \"id\": \"retracted_article_id2\",\r\n    \"title\": \"Silencing circANKRD36 protects H9c2 cells against lipopolysaccharide-induced injury via up-regulating miR-138\",\r\n    \"abstract\": \"Background: Myocarditis refers to the inflammatory process that affects the muscle tissue of the heart. Persistent myocardial inflammation promotes myocardial cell damage, which ultimately leads to heart failure or death. Therefore, we aimed to explore the functional impacts of circANKRD36 on myocarditis. Methods: H9c2 cells were pre-treated with lipopolysaccharide (LPS). Viability and apoptosis were evaluated utilizing CCK-8 assay and flow cytometry. Inflammatory cytokines mRNA expression and production were assessed by qRT-PCR and ELISA. Western blot was utilized to distinguish apoptosis and inflammatory related factors expression. Sequentially, the above mentioned parameters were reassessed when overexpressed miR-138. Results: LPS declined viability and as well as raised apoptosis and inflammatory injury in H9c2 cells. Silencing circular RNA ANKRD36 (si-circANKRD36) alleviated apoptosis and inflammatory injury induced by LPS. MiR-138 expression was suppressed by LPS and elevated by si-circANKRD36. Increase of viability and inflammatory injury induced by si-circANKRD36 was alleviated by down-regulation of miR-138. Eventually, si-circANKRD36 inhibited p38MAPK\/NF-\u03baB pathway which activated by LPS via up-regulating miR-138. Conclusion: Si-circANKRD36 exerted its anti-apoptosis and anti-inflammatory function under the condition of LPS in H9c2 cells through p38MAPK\/NF-\u03baB pathway and up-regulation of miR-138.\"\r\n}";
var xhr = new XMLHttpRequest();
xhr.withCredentials = true;
    
xhr.addEventListener("readystatechange", function() {
if(this.readyState === 4) {
    console.log(this.responseText);
    }
});
    
xhr.open("POST", "https://zylalabs.com/api/1915/papermill+text+comparison+api/1621/document+posting");
xhr.setRequestHeader("Authorization", "Bearer YOUR_API_KEY");
xhr.send(data);

var axios = require('axios');
var data = "{\r\n    \"id\": \"retracted_article_id2\",\r\n    \"title\": \"Silencing circANKRD36 protects H9c2 cells against lipopolysaccharide-induced injury via up-regulating miR-138\",\r\n    \"abstract\": \"Background: Myocarditis refers to the inflammatory process that affects the muscle tissue of the heart. Persistent myocardial inflammation promotes myocardial cell damage, which ultimately leads to heart failure or death. Therefore, we aimed to explore the functional impacts of circANKRD36 on myocarditis. Methods: H9c2 cells were pre-treated with lipopolysaccharide (LPS). Viability and apoptosis were evaluated utilizing CCK-8 assay and flow cytometry. Inflammatory cytokines mRNA expression and production were assessed by qRT-PCR and ELISA. Western blot was utilized to distinguish apoptosis and inflammatory related factors expression. Sequentially, the above mentioned parameters were reassessed when overexpressed miR-138. Results: LPS declined viability and as well as raised apoptosis and inflammatory injury in H9c2 cells. Silencing circular RNA ANKRD36 (si-circANKRD36) alleviated apoptosis and inflammatory injury induced by LPS. MiR-138 expression was suppressed by LPS and elevated by si-circANKRD36. Increase of viability and inflammatory injury induced by si-circANKRD36 was alleviated by down-regulation of miR-138. Eventually, si-circANKRD36 inhibited p38MAPK\/NF-\u03baB pathway which activated by LPS via up-regulating miR-138. Conclusion: Si-circANKRD36 exerted its anti-apoptosis and anti-inflammatory function under the condition of LPS in H9c2 cells through p38MAPK\/NF-\u03baB pathway and up-regulation of miR-138.\"\r\n}";
var config = {
method: 'POST',
url: 'https://zylalabs.com/api/1915/papermill+text+comparison+api/1621/document+posting',
headers: { 
    'Authorization': 'Bearer YOUR_API_KEY'
    },
data : data
};
axios(config).then(function (response) {
console.log(JSON.stringify(response.data));
})
.catch(function (error) {
console.log(error);
});

$curl = curl_init();
    
curl_setopt_array($curl, array(
CURLOPT_URL => 'https://zylalabs.com/api/1915/papermill+text+comparison+api/1621/document+posting',
CURLOPT_RETURNTRANSFER => true,
CURLOPT_ENCODING => '',
CURLOPT_MAXREDIRS => 10,
CURLOPT_TIMEOUT => 0,
CURLOPT_FOLLOWLOCATION => true,
CURLOPT_HTTP_VERSION => CURL_HTTP_VERSION_1_1,
CURLOPT_CUSTOMREQUEST => 'POST',
CURLOPT_POSTFIELDS => '{
    "id": "retracted_article_id2",
    "title": "Silencing circANKRD36 protects H9c2 cells against lipopolysaccharide-induced injury via up-regulating miR-138",
    "abstract": "Background: Myocarditis refers to the inflammatory process that affects the muscle tissue of the heart. Persistent myocardial inflammation promotes myocardial cell damage, which ultimately leads to heart failure or death. Therefore, we aimed to explore the functional impacts of circANKRD36 on myocarditis. Methods: H9c2 cells were pre-treated with lipopolysaccharide (LPS). Viability and apoptosis were evaluated utilizing CCK-8 assay and flow cytometry. Inflammatory cytokines mRNA expression and production were assessed by qRT-PCR and ELISA. Western blot was utilized to distinguish apoptosis and inflammatory related factors expression. Sequentially, the above mentioned parameters were reassessed when overexpressed miR-138. Results: LPS declined viability and as well as raised apoptosis and inflammatory injury in H9c2 cells. Silencing circular RNA ANKRD36 (si-circANKRD36) alleviated apoptosis and inflammatory injury induced by LPS. MiR-138 expression was suppressed by LPS and elevated by si-circANKRD36. Increase of viability and inflammatory injury induced by si-circANKRD36 was alleviated by down-regulation of miR-138. Eventually, si-circANKRD36 inhibited p38MAPK/NF-κB pathway which activated by LPS via up-regulating miR-138. Conclusion: Si-circANKRD36 exerted its anti-apoptosis and anti-inflammatory function under the condition of LPS in H9c2 cells through p38MAPK/NF-κB pathway and up-regulation of miR-138."
}',
CURLOPT_HTTPHEADER => array(
    'Authorization: Bearer YOUR_API_KEY'
    ),
));
    
$response = curl_exec($curl);
    
curl_close($curl);
echo $response;

import requests
    
url = "https://zylalabs.com/api/1915/papermill+text+comparison+api/1621/document+posting"
    
payload = "{\r\n    \"id\": \"retracted_article_id2\",\r\n    \"title\": \"Silencing circANKRD36 protects H9c2 cells against lipopolysaccharide-induced injury via up-regulating miR-138\",\r\n    \"abstract\": \"Background: Myocarditis refers to the inflammatory process that affects the muscle tissue of the heart. Persistent myocardial inflammation promotes myocardial cell damage, which ultimately leads to heart failure or death. Therefore, we aimed to explore the functional impacts of circANKRD36 on myocarditis. Methods: H9c2 cells were pre-treated with lipopolysaccharide (LPS). Viability and apoptosis were evaluated utilizing CCK-8 assay and flow cytometry. Inflammatory cytokines mRNA expression and production were assessed by qRT-PCR and ELISA. Western blot was utilized to distinguish apoptosis and inflammatory related factors expression. Sequentially, the above mentioned parameters were reassessed when overexpressed miR-138. Results: LPS declined viability and as well as raised apoptosis and inflammatory injury in H9c2 cells. Silencing circular RNA ANKRD36 (si-circANKRD36) alleviated apoptosis and inflammatory injury induced by LPS. MiR-138 expression was suppressed by LPS and elevated by si-circANKRD36. Increase of viability and inflammatory injury induced by si-circANKRD36 was alleviated by down-regulation of miR-138. Eventually, si-circANKRD36 inhibited p38MAPK\/NF-\u03baB pathway which activated by LPS via up-regulating miR-138. Conclusion: Si-circANKRD36 exerted its anti-apoptosis and anti-inflammatory function under the condition of LPS in H9c2 cells through p38MAPK\/NF-\u03baB pathway and up-regulation of miR-138.\"\r\n}" 
headers = {
    'Authorization': 'Bearer YOUR_API_KEY'
}
    
response = requests.request("POST", url, headers=headers, data=payload)
    
print(response.text)
    

require "uri"
require "net/http"
    
url = URI("https://zylalabs.com/api/1915/papermill+text+comparison+api/1621/document+posting")
    
http = Net::HTTP.new(url.host, url.port);
request = Net::HTTP::POST.new(url)
request["Authorization"] = "Bearer YOUR_API_KEY"
request.body = "{\r\n    \"id\": \"retracted_article_id2\",\r\n    \"title\": \"Silencing circANKRD36 protects H9c2 cells against lipopolysaccharide-induced injury via up-regulating miR-138\",\r\n    \"abstract\": \"Background: Myocarditis refers to the inflammatory process that affects the muscle tissue of the heart. Persistent myocardial inflammation promotes myocardial cell damage, which ultimately leads to heart failure or death. Therefore, we aimed to explore the functional impacts of circANKRD36 on myocarditis. Methods: H9c2 cells were pre-treated with lipopolysaccharide (LPS). Viability and apoptosis were evaluated utilizing CCK-8 assay and flow cytometry. Inflammatory cytokines mRNA expression and production were assessed by qRT-PCR and ELISA. Western blot was utilized to distinguish apoptosis and inflammatory related factors expression. Sequentially, the above mentioned parameters were reassessed when overexpressed miR-138. Results: LPS declined viability and as well as raised apoptosis and inflammatory injury in H9c2 cells. Silencing circular RNA ANKRD36 (si-circANKRD36) alleviated apoptosis and inflammatory injury induced by LPS. MiR-138 expression was suppressed by LPS and elevated by si-circANKRD36. Increase of viability and inflammatory injury induced by si-circANKRD36 was alleviated by down-regulation of miR-138. Eventually, si-circANKRD36 inhibited p38MAPK\/NF-\u03baB pathway which activated by LPS via up-regulating miR-138. Conclusion: Si-circANKRD36 exerted its anti-apoptosis and anti-inflammatory function under the condition of LPS in H9c2 cells through p38MAPK\/NF-\u03baB pathway and up-regulation of miR-138.\"\r\n}"    
response = http.request(request)
puts response.read_body

printf '{
    "id": "retracted_article_id2",
    "title": "Silencing circANKRD36 protects H9c2 cells against lipopolysaccharide-induced injury via up-regulating miR-138",
    "abstract": "Background: Myocarditis refers to the inflammatory process that affects the muscle tissue of the heart. Persistent myocardial inflammation promotes myocardial cell damage, which ultimately leads to heart failure or death. Therefore, we aimed to explore the functional impacts of circANKRD36 on myocarditis. Methods: H9c2 cells were pre-treated with lipopolysaccharide (LPS). Viability and apoptosis were evaluated utilizing CCK-8 assay and flow cytometry. Inflammatory cytokines mRNA expression and production were assessed by qRT-PCR and ELISA. Western blot was utilized to distinguish apoptosis and inflammatory related factors expression. Sequentially, the above mentioned parameters were reassessed when overexpressed miR-138. Results: LPS declined viability and as well as raised apoptosis and inflammatory injury in H9c2 cells. Silencing circular RNA ANKRD36 (si-circANKRD36) alleviated apoptosis and inflammatory injury induced by LPS. MiR-138 expression was suppressed by LPS and elevated by si-circANKRD36. Increase of viability and inflammatory injury induced by si-circANKRD36 was alleviated by down-regulation of miR-138. Eventually, si-circANKRD36 inhibited p38MAPK/NF-κB pathway which activated by LPS via up-regulating miR-138. Conclusion: Si-circANKRD36 exerted its anti-apoptosis and anti-inflammatory function under the condition of LPS in H9c2 cells through p38MAPK/NF-κB pathway and up-regulation of miR-138."
}'| 
http --follow --timeout 3600 POST 'https://zylalabs.com/api/1915/papermill+text+comparison+api/1621/document+posting' \
Authorization:'Bearer YOUR_API_KEY'

var client = new RestClient("https://zylalabs.com/api/1915/papermill+text+comparison+api/1621/document+posting");
client.Timeout = -1;
var request = new RestRequest(Method.POST);
request.AddHeader("Authorization", "Bearer YOUR_API_KEY");
var body = "{\r\n    \"id\": \"retracted_article_id2\",\r\n    \"title\": \"Silencing circANKRD36 protects H9c2 cells against lipopolysaccharide-induced injury via up-regulating miR-138\",\r\n    \"abstract\": \"Background: Myocarditis refers to the inflammatory process that affects the muscle tissue of the heart. Persistent myocardial inflammation promotes myocardial cell damage, which ultimately leads to heart failure or death. Therefore, we aimed to explore the functional impacts of circANKRD36 on myocarditis. Methods: H9c2 cells were pre-treated with lipopolysaccharide (LPS). Viability and apoptosis were evaluated utilizing CCK-8 assay and flow cytometry. Inflammatory cytokines mRNA expression and production were assessed by qRT-PCR and ELISA. Western blot was utilized to distinguish apoptosis and inflammatory related factors expression. Sequentially, the above mentioned parameters were reassessed when overexpressed miR-138. Results: LPS declined viability and as well as raised apoptosis and inflammatory injury in H9c2 cells. Silencing circular RNA ANKRD36 (si-circANKRD36) alleviated apoptosis and inflammatory injury induced by LPS. MiR-138 expression was suppressed by LPS and elevated by si-circANKRD36. Increase of viability and inflammatory injury induced by si-circANKRD36 was alleviated by down-regulation of miR-138. Eventually, si-circANKRD36 inhibited p38MAPK\/NF-\u03baB pathway which activated by LPS via up-regulating miR-138. Conclusion: Si-circANKRD36 exerted its anti-apoptosis and anti-inflammatory function under the condition of LPS in H9c2 cells through p38MAPK\/NF-\u03baB pathway and up-regulation of miR-138.\"\r\n}";
request.AddParameter("text/plain", body, ParameterType.RequestBody);
IRestResponse response = client.Execute(request);
Console.WriteLine(response.Content);

package main
import (
    "fmt"
    "net/http"
    "io/ioutil"
)
func main() {
    url := "https://zylalabs.com/api/1915/papermill+text+comparison+api/1621/document+posting"
    method := "POST"
    payload := strings.NewReader("{
    "id": "retracted_article_id2",
    "title": "Silencing circANKRD36 protects H9c2 cells against lipopolysaccharide-induced injury via up-regulating miR-138",
    "abstract": "Background: Myocarditis refers to the inflammatory process that affects the muscle tissue of the heart. Persistent myocardial inflammation promotes myocardial cell damage, which ultimately leads to heart failure or death. Therefore, we aimed to explore the functional impacts of circANKRD36 on myocarditis. Methods: H9c2 cells were pre-treated with lipopolysaccharide (LPS). Viability and apoptosis were evaluated utilizing CCK-8 assay and flow cytometry. Inflammatory cytokines mRNA expression and production were assessed by qRT-PCR and ELISA. Western blot was utilized to distinguish apoptosis and inflammatory related factors expression. Sequentially, the above mentioned parameters were reassessed when overexpressed miR-138. Results: LPS declined viability and as well as raised apoptosis and inflammatory injury in H9c2 cells. Silencing circular RNA ANKRD36 (si-circANKRD36) alleviated apoptosis and inflammatory injury induced by LPS. MiR-138 expression was suppressed by LPS and elevated by si-circANKRD36. Increase of viability and inflammatory injury induced by si-circANKRD36 was alleviated by down-regulation of miR-138. Eventually, si-circANKRD36 inhibited p38MAPK/NF-κB pathway which activated by LPS via up-regulating miR-138. Conclusion: Si-circANKRD36 exerted its anti-apoptosis and anti-inflammatory function under the condition of LPS in H9c2 cells through p38MAPK/NF-κB pathway and up-regulation of miR-138."
}")
    client := &http.Client {
    }
    req, err := http.NewRequest(method, url, nil)
    if err != nil {
    fmt.Println(err)
    return
    }
    req.Header.Add("Authorization", "Bearer YOUR_API_KEY")
    res, err := client.Do(req)
    if err != nil {
    fmt.Println(err)
    return
    }
    defer res.Body.Close()

    body, err := ioutil.ReadAll(res.Body)
    if err != nil {
    fmt.Println(err)
    return
    }
    fmt.Println(string(body))
}