{"id":3068,"date":"2024-01-02T13:13:41","date_gmt":"2024-01-02T13:13:41","guid":{"rendered":"https:\/\/kleontas.com\/?page_id=3068"},"modified":"2024-02-19T09:53:25","modified_gmt":"2024-02-19T09:53:25","slug":"%ce%b5%ce%bd%ce%b4%ce%bf%ce%b8%cf%89%cf%81%ce%b1%ce%ba%ce%b9%ce%ba%ce%ae-%cf%85%cf%80%ce%b5%cf%81%ce%b8%ce%b5%cf%81%ce%bc%ce%b9%ce%ba%ce%ae-%cf%87%ce%b7%ce%bc%ce%b5%ce%b9%ce%bf%ce%b8%ce%b5%cf%81%ce%b1","status":"publish","type":"page","link":"http:\/\/kleontas.com\/en\/iatros-thorakoxeirourgos-xeirourgos-thorakos-thorakoxeirourgiki\/%CE%B5%CE%BD%CE%B4%CE%BF%CE%B8%CF%89%CF%81%CE%B1%CE%BA%CE%B9%CE%BA%CE%AE-%CF%85%CF%80%CE%B5%CF%81%CE%B8%CE%B5%CF%81%CE%BC%CE%B9%CE%BA%CE%AE-%CF%87%CE%B7%CE%BC%CE%B5%CE%B9%CE%BF%CE%B8%CE%B5%CF%81%CE%B1\/","title":{"rendered":"Intrathoracic hyperthermic chemotherapy (HITHOC)"},"content":{"rendered":"
\n\t\t\t\t
\n\t\t
\n\t\t\t\t\t
\n\t\t\t\t
\n\t\t\t\t
\n\t\t\t\t\t

Intrathoracic hyperthermic chemotherapy (HITHOC)\n<\/h4>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t
\n\t\t\t\t
\n\t\t\t\t\t\t\t\t\t

\u00a0<\/p>

Pleurodesis with periodic hyperthermic chemotherapy<\/strong><\/span><\/p>

(The text is taken from the doctoral thesis of Dr Athanasios Kleontas)<\/p>

\u00a0<\/p>

The action of hyperthermia at the cellular level<\/strong><\/span><\/p>

Increase in cell temperature in the range of 39-45\u00a0o<\/sup>C, can cause inhibition of their proliferation and cell death. The intensity of the effects depends on the combination of the temperature level and the time of exposure of the cells to that temperature, which together are expressed as thermal dose (111). Many changes occur during exposure of cells to elevated temperature. Temperature changes the characteristics of the cell membrane, causing modification of the cell morphology, intracellular concentrations of potassium and sodium ions and membrane potential (112-113). Surprisingly, none of the aforementioned phenomena directly correlate with impending cell death and therefore none of them adequately explain the direct mechanism of thermally induced cytotoxicity (112-113). Beyond membranes, secondary protein structures appear to be more sensitive to heat and perhaps heat-induced protein denaturation may explain the effects of mild hyperthermia on cells (111). Although DNA is not destroyed at temperatures of 39-45\u00a0o<\/sup>C, however, de novo DNA synthesis and polymerization exhibit sensitivity to heat, due to induced denaturation and aggregation of synthetases and polymerases (114-115). This appears to contribute significantly to cell cycle and cell death functions. It also causes disruption of key enzymatic functions of the cell, such as the DNA repair process. Nuclei are sensitive to hyperthermia, as are other enzymes used in RNA synthesis. Furthermore, there is an inability of RNA to interact with proteins during hyperthermia (116). Finally, after a sufficient thermal dose, cells are driven to death either through necrosis, where the cell very rapidly loses the integrity of its cell membrane, or through apoptosis, where programmed cell death is hastily triggered. Each of these two processes is subject to different immunoregulatory activities (117). Figure 12 below highlights the main biological ways in which the effect of hyperthermia attempts to produce therapeutic effects through the following immunological effects (118):<\/span><\/p>