Modeling of the Flexible Needle Insertion into the Human Liver

The insertion of the needle is difficult because the deformation and displacement of the organs are the key elements in the surgical act. Liver and tumor modeling are essential in the development of the needle insertion model. The role of the needle is to deliver into the tumor an active chemotherapeutic agent. We describe in this chapter the deformation of the needle during its insertion into the human liver in the context of surgery simulation of the high- robotic-assisted intraoperative treatment of liver tumors based on the integrated imaging-molecular diagnosis. The needle is a bee barbed type modeled as a flexible thread within the framework of the Cosserat (micropolar) elasticity theory.

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On the flexible needle insertion into the human liver

Scientific Reports ◽

10.1038/s41598-021-89479-8 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Veturia Chiroiu ◽

Nicoleta Nedelcu ◽

Doina Pisla ◽

Ligia Munteanu ◽

Cristian Rugină

Keyword(s):

Elastic Properties ◽

Couple Stress ◽

Human Liver ◽

Liver Tumors ◽

Unit Area ◽

Needle Insertion ◽

Micropolar Elasticity ◽

Robotic Assisted ◽

Local Rotation

AbstractIn the present research, the navigation of a flexible needle into the human liver in the context of the robotic-assisted intraoperative treatment of the liver tumors, is reported. Cosserat (micropolar) elasticity is applied to describe the interaction between the needle and the human liver. The theory incorporates the local rotation of points and the couple stress (a torque per unit area) as well as the force stress (force per unit area) representing the chiral features of the human liver. To predict the deformation of the needle and the liver, the elastic properties of the human liver have been evaluated. Outcomes reveal that considering smaller deformations of the needle and the liver results in better needle navigation mechanism. The needle geometry can enhance the penetration.

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Emodin Enhances the Chemosensitivity of Endometrial Cancer by Inhibiting ROS-Mediated Cisplatin-resistance

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520618666171219113036 ◽

2018 ◽

Vol 18 (7) ◽

pp. 1054-1063 ◽

Cited By ~ 4

Author(s):

Ning Ding ◽

Hong Zhang ◽

Shan Su ◽

Yumei Ding ◽

Xiaohui Yu ◽

...

Keyword(s):

Drug Resistance ◽

Endometrial Cancer ◽

Cancer Cells ◽

Chemotherapeutic Agent ◽

Annexin V ◽

Chemotherapeutic Agents ◽

Endometrial Cancer Cell ◽

Animal Survival ◽

Apoptosis Level

Background: Endometrial cancer is a common cause of death in gynecological malignancies. Cisplatin is a clinically chemotherapeutic agent. However, drug-resistance is the primary cause of treatment failure. Objective: Emodin is commonly used clinically to increase the sensitivity of chemotherapeutic agents, yet whether Emodin promotes the role of Cisplatin in the treatment of endometrial cancer has not been studied. Method: CCK-8 kit was utilized to determine the growth of two endometrial cancer cell lines, Ishikawa and HEC-IB. The apoptosis level of Ishikawa and HEC-IB cells was detected by Annexin V / propidium iodide double-staining assay. ROS level was detected by DCFH-DA and NADPH oxidase expression. Expressions of drug-resistant genes were examined by real-time PCR and Western blotting. Results: Emodin combined with Cisplatin reduced cell growth and increased the apoptosis of endometrial cancer cells. Co-treatment of Emodin and Cisplatin increased chemosensitivity by inhibiting the expression of drugresistant genes through reducing the ROS levels in endometrial cancer cells. In an endometrial cancer xenograft murine model, the tumor size was reduced and animal survival time was increased by co-treatment of Emodin and Cisplatin. Conclusion: This study demonstrates that Emodin enhances the chemosensitivity of Cisplatin on endometrial cancer by inhibiting ROS-mediated expression of drug-resistance genes.

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The role of SIRT5 and p53 proteins in the sensitivity of colon cancer cells to chemotherapeutic agent 5-Fluorouracil

Molecular Biology Reports ◽

10.1007/s11033-021-06558-9 ◽

2021 ◽

Author(s):

Ozlem Ekremoglu ◽

Asli Koc

Keyword(s):

Colon Cancer ◽

Cancer Cells ◽

Chemotherapeutic Agent ◽

Colon Cancer Cells

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Glucuronidation of hyodeoxycholic acid in human liver. Evidence for a selective role of UDP-glucuronosyltransferase 2B4.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(19)74437-8 ◽

1993 ◽

Vol 268 (34) ◽

pp. 25636-25642

Author(s):

T Pillot ◽

M Ouzzine ◽

S Fournel-Gigleux ◽

C Lafaurie ◽

A Radominska ◽

...

Keyword(s):

Human Liver ◽

Hyodeoxycholic Acid ◽

Udp Glucuronosyltransferase

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Role of cytochrome P450IIIA4 in the metabolism of the pyrrolizidine alkaloid senecionine in human liver

Carcinogenesis ◽

10.1093/carcin/12.3.515 ◽

1991 ◽

Vol 12 (3) ◽

pp. 515-519 ◽

Cited By ~ 66

Author(s):

Cristobal L. Miranda ◽

Ralph L. Reed ◽

F. Peter Guengerich ◽

Donald R. Buhler

Keyword(s):

Human Liver ◽

Pyrrolizidine Alkaloid

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An incorrect inequality in micropolar elasticity theory

Zeitschrift für angewandte Mathematik und Physik ◽

10.1007/bf01627956 ◽

1970 ◽

Vol 21 (3) ◽

pp. 494-497 ◽

Cited By ~ 51

Author(s):

Stephen C. Cowin

Keyword(s):

Elasticity Theory ◽

Micropolar Elasticity

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Role of autophagy in the pathogenesis of liver diseases

Orvosi Hetilap ◽

10.1556/oh.2011.29269 ◽

2011 ◽

Vol 152 (49) ◽

pp. 1955-1961 ◽

Cited By ~ 4

Author(s):

Klára Werling

Keyword(s):

Endoplasmic Reticulum ◽

Liver Disease ◽

Liver Diseases ◽

Liver Tumors ◽

Liver Steatosis ◽

Prognostic Significance ◽

Adenosine Monophosphate ◽

Mutant Proteins ◽

Alpha 1 Antitrypsin Deficiency

Autophagy is a self-digestion process that plays an important role in the development, differentiation and homeostasis of cells, helping their survival during starvation and hypoxia. Accumulated mutant proteins in the endoplasmic reticulum can be degraded by autophagy in alpha-1 antitrypsin deficiency. Hepatitis C and B virus may exploit the autophagy pathway to escape the innate immune response and to promote their own replication. Autophagy is decreased in response to chronic alcohol consumption, likely due to a decrease in 5’-adenosine monophosphate-activated protein kinase, increase in mTOR activity and due to an alteration in vesicle transport in hepatocytes. In obesity and alcoholic liver disease the decreased function of autophagy causes formation of Mallory-Denk bodies and cell death. The deficient autophagy can contribute to liver steatosis, to endoplasmic reticulum stress, and to progression of liver disease. Autophagy defect in hepatocellular carcinoma suggests that it can serve a tumor-suppressor function. The autophagy protein Beclin-1 levels have prognostic significance in liver tumors. Understanding of the molecular mechanism and the role of autophagy may lead to more effective therapeutic strategies in liver diseases in the future. Orv. Hetil., 2011, 152, 1955–1961.

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