<?xml version="1.0" encoding="utf-8"?>
<export-example>
  <doc>
    <id>1814</id>
    <completedYear/>
    <publishedYear>2023</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst/>
    <pageLast/>
    <pageNumber>99</pageNumber>
    <edition/>
    <issue/>
    <volume/>
    <type>bachelorthesis</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2023-10-03</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>2023-09-15</thesisDateAccepted>
    <title language="eng">The use of biocatalysis in the diagnosis and treatment of colorectal cancer (CRC)</title>
    <abstract language="eng">Colorectal cancer is a significant global health burden. Early-stage colorectal cancer is asymptomatic, which, coupled with the fact that later stages of CRC have a very low prognosis, and that current methods of diagnosis and treatment significantly impact the patient, exploring alternate ways to diagnose and treat CRC is vital.&#13;
Biocatalysis is the use of naturally found catalysts such as nanozymes and enzymes in order to catalyze reactions. Due to their characteristics and uses, biocatalysts are seen as promising alternatives to current methods of CRC diagnosis and therapy.&#13;
This research-based bachelor thesis aims to summarize and analyze current traditional and biocatalytic methods that exist to diagnose and treat CRC, in order to seek the potential of biocatalysis in this field, as well as discuss its current state and its future in comparison to currently implemented methods. It provides an extensive overview of traditional and biocatalytic approaches to diagnosis and therapy, considering important factors such as efficacy, sensitivity, selectivity, cost, and safety.&#13;
The thesis also delves into the use of biocatalysis for important points such as the early diagnosis of CRC, and the challenges faced during development, regulation, and monetary concerns. Through careful analysis of the strengths and limitations of techniques in the field, as well as personal opinions on the future of research, conclusions on given hypotheses regarding biocatalysis in CRC diagnosis and therapies were presented and included strong support for the unquestionable potential of biocatalysis use in cancer healthcare, while highlighting possibilities to tap into that potential by scrutinizing their equally as unquestionable current limitations.&#13;
Overall, this thesis aspires to contribute, on however minuscule a scale, towards the advancement of CRC diagnosis and therapy approaches, with the ambition of improving patient care and prognosis, as well as quality of life for those struggling or who will struggle in the future with the disease, together with their kin who are profoundly affected as well.</abstract>
    <identifier type="urn">urn:nbn:de:hbz:1383-opus4-18147</identifier>
    <enrichment key="opus.source">publish</enrichment>
    <enrichment key="opus.doi.autoCreate">false</enrichment>
    <enrichment key="opus.urn.autoCreate">true</enrichment>
    <licence>CC BY-NC-ND 4.0 International - Namensnennung-Nicht kommerziell-Keine Bearbeitungen</licence>
    <author>Basil Mazen Hammoudeh</author>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Colorectal cancer</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Cancer</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Biocatalysis</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Enzymes</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Diagnosis</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Therapy</value>
    </subject>
    <collection role="institutes" number="">Fakultät Life Sciences</collection>
    <thesisPublisher>Hochschule Rhein-Waal</thesisPublisher>
    <thesisGrantor>Hochschule Rhein-Waal</thesisGrantor>
    <file>https://opus4.kobv.de/opus4-rhein-waal/files/1814/BasilHammoudeh_Thesis_FINAL_SIGNED.pdf</file>
  </doc>
  <doc>
    <id>2166</id>
    <completedYear>2025</completedYear>
    <publishedYear>2025</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst/>
    <pageLast/>
    <pageNumber>92</pageNumber>
    <edition/>
    <issue/>
    <volume/>
    <type>bachelorthesis</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>--</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">The effects of cannabinoids CBD and WIN 55 212-2 against oxidative stress in BR1 Astrocytes from a proteomic viewpoint</title>
    <abstract language="eng">Oxidative stress is a common hallmark observed in neurodegenerative diseases, acting either as a triggering factor or as a consequence of the neurodegenerative process. Astrocytes play a crucial role in mediating oxidative stress caused by physiological processes, such as the byproducts of mitochondrial function during cellular respiration. Given the critical role of oxidative stress in the progression of many neurodegenerative diseases, identifying molecules capable of modulating this response and mitigating oxidative damage is of considerable interest. &#13;
Cannabinoids such as cannabidiol (CBD) and WIN 55.212-2, known for their &#13;
capability of influencing the endocannabinoid system through their interaction &#13;
with cannabinoid receptors (namely, CB1R and CB2R), and therefore the Central Nervous System, are promising candidates for such modulation. This work aimed to explore, through proteomics, the potential effect that the mentioned cannabinoids might have against oxidative stress induced by hydrogen peroxide in astrocytes, possibly mitigating some of the oxidative damage.</abstract>
    <identifier type="urn">urn:nbn:de:hbz:1383-opus4-21665</identifier>
    <enrichment key="opus.import.date">2025-03-17T08:49:42+00:00</enrichment>
    <enrichment key="opus.source">sword</enrichment>
    <enrichment key="opus.import.user">swordtest</enrichment>
    <enrichment key="opus.doi.autoCreate">false</enrichment>
    <enrichment key="opus.urn.autoCreate">true</enrichment>
    <licence>CC BY 4.0 International - Namensnennung</licence>
    <author>Leonardo Henrique Dos Santos</author>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Cannabis</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>WIN 55.212-2</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>CBD</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Astrocytes</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Proteomics</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Neurodegeneration</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Neurodegenerative Diseases</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>OmicScope</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Oxidative Stress</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Hydrogen Peroxide</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>BR1 Astrocytes</value>
    </subject>
    <collection role="institutes" number="">Fakultät Life Sciences</collection>
    <collection role="Import" number="import">Import</collection>
    <thesisPublisher>Hochschule Rhein-Waal</thesisPublisher>
    <thesisGrantor>Hochschule Rhein-Waal</thesisGrantor>
    <file>https://opus4.kobv.de/opus4-rhein-waal/files/2166/8597_20251201223822_Signed Final Version Thesis Leonardo Henrique Dos Santos 25061.pdf</file>
  </doc>
  <doc>
    <id>2115</id>
    <completedYear/>
    <publishedYear>2024</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst/>
    <pageLast/>
    <pageNumber>55</pageNumber>
    <edition/>
    <issue/>
    <volume/>
    <type>bachelorthesis</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2024-11-27</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">A Systematic Review of Rapamycin- Mediated Fetal Hemoglobin Induction via the mTOR Pathway</title>
    <abstract language="eng">mTOR inhibitor rapamycin has been observed to induce fetal hemoglobin in patients of β-hemoglobinopathies, a group of disorders in which mutations in the gene responsible β-globin chains results in reduced or malformed RBC production, leading to anemia. The induction of fetal hemoglobin bypasses these mutations, as they are found on the gene responsible for adult hemoglobin. Following birth, the fetal hemoglobin gene is silenced, and the adult gene is activated through a process known as the hemoglobin switch. Rapamycin treatment reverses this hemoglobin switch but the mechanism by which it does so is currently unknown. Rapamycin functions through its inhibition of mTORC1, a protein complex responsible for nutrient- and growth factor-dependent cell growth and proliferation. This literature review seeks to collate existing information on the mTORC1 signalling pathway and the hemoglobin switch, allowing for a specific mechanism by which rapamycin induces fetal hemoglobin through its inhibition of mTORC1 to be hypothesized. Following the literature search, 55 studies on the mTORC1 pathway and 31 studies on the hemoglobin switch were summarized. Using the information gained from this, three hypotheses were put forward for the possible induction mechanism, out of which the primary hypothesis is based on the hemoglobin switching factor KLF1. This was based on the observation that the knockdown of Raptor, a crucial component of mTORC1, in mice caused a decreased expression of KLF1. As KLF1 is an essential component of the hemoglobin switch, this provides a direct link between the inhibition of mTORC1 and the reversal of the hemoglobin switch. Additionally, the efficiency of rapamycin in comparison to other methods of fetal hemoglobin was discussed, including newer generations of mTOR inhibitors developed using rapamycin as a foundation. Finally, possible avenues of research to confirm the validity of the proposed hypotheses and to address points of ignorance within each topic were discussed.</abstract>
    <identifier type="urn">urn:nbn:de:hbz:1383-opus4-21155</identifier>
    <enrichment key="opus.source">publish</enrichment>
    <enrichment key="opus.doi.autoCreate">false</enrichment>
    <enrichment key="opus.urn.autoCreate">true</enrichment>
    <licence>CC BY 4.0 International - Namensnennung</licence>
    <author>Hasiru Ratnayake</author>
    <collection role="institutes" number="">Fakultät Life Sciences</collection>
    <thesisPublisher>Hochschule Rhein-Waal</thesisPublisher>
    <thesisGrantor>Hochschule Rhein-Waal</thesisGrantor>
    <file>https://opus4.kobv.de/opus4-rhein-waal/files/2115/ratnayakerapamycin.pdf</file>
  </doc>
</export-example>
