Thermal Therapy in Urologic Systems: A Comparison of Arrhenius and Thermal Isoeffective Dose Models in Predicting Hyperthermic Injury

2009 ◽  
Vol 131 (7) ◽  
Author(s):  
Xiaoming He ◽  
Sankha Bhowmick ◽  
John C. Bischof
Keyword(s):  
Kinetic Parameters ◽  
Thermal Injury ◽  
Tissue Injury ◽  
Kidney Tissue ◽  
Thermal Therapy ◽  
Tissue Type ◽  
Arrhenius Model ◽  
Traditional Use ◽  
Thermal Thresholds ◽  
Thermal Surgery

The Arrhenius and thermal isoeffective dose (TID) models are the two most commonly used models for predicting hyperthermic injury. The TID model is essentially derived from the Arrhenius model, but due to a variety of assumptions and simplifications now leads to different predictions, particularly at temperatures higher than 50°C. In the present study, the two models are compared and their appropriateness tested for predicting hyperthermic injury in both the traditional hyperthermia (usually, 43–50°C) and thermal surgery (or thermal therapy/thermal ablation, usually, >50°C) regime. The kinetic parameters of thermal injury in both models were obtained from the literature (or literature data), tabulated, and analyzed for various prostate and kidney systems. It was found that the kinetic parameters vary widely, and were particularly dependent on the cell or tissue type, injury assay used, and the time when the injury assessment was performed. In order to compare the capability of the two models for thermal injury prediction, thermal thresholds for complete killing (i.e., 99% cell or tissue injury) were predicted using the models in two important urologic systems, viz., the benign prostatic hyperplasia tissue and the normal porcine kidney tissue. The predictions of the two models matched well at temperatures below 50°C. At higher temperatures, however, the thermal thresholds predicted using the TID model with a constant R value of 0.5, the value commonly used in the traditional hyperthermia literature, are much lower than those predicted using the Arrhenius model. This suggests that traditional use of the TID model (i.e., R=0.5) is inappropriate for predicting hyperthermic injury in the thermal surgery regime (>50°C). Finally, the time-temperature relationships for complete killing (i.e., 99% injury) were calculated and analyzed using the Arrhenius model for the various prostate and kidney systems.

Supraphysiological Thermal Injury in Dunning AT-1 Prostate Tumor Cells

1999 ◽  
Vol 122 (1) ◽  
pp. 51-59 ◽  
Author(s):  
Sankha Bhowmick ◽  
David J. Swanlund ◽  
John C. Bischof
Keyword(s):  
Prostate Cancer ◽  
Survival Data ◽  
Process Model ◽  
Thermal Injury ◽  
Clonogenic Assay ◽  
Thermal Therapy ◽  
Experimental Results ◽  
Arrhenius Model ◽  
Membrane Injury ◽  
Thermal Transients

To investigate the potential application of thermal therapy in the treatment of prostate cancer, the effects of supraphysiological temperatures (40–70°C) for clinically relevant time periods (∼15 minutes) were experimentally studied on attached Dunning AT-1 rat prostate cancer cells using multiple assays. The membrane and reproductive machinery were the targets of injury selected for this study. In order to assess membrane injury, the leakage of calcein was measured dynamically, and the uptake of PI was measured post-heating (1–3 hours). Clonogenicity was used as a measure of injury to the reproductive machinery 7 days post-injury after comparable thermal insults. Experimental results from all three assays show a broad trend of increasing injury with an increase in temperature and time of insult. Membrane injury, as measured by the fluorescent dye assays, does not correlate with clonogenic survival for many of the thermal histories investigated. In particular, the calcein assay at temperatures of ⩽40°C led to measurable injury accumulation (dye leakage), which was considered sublethal, as shown by significant survival for comparable insult in the clonogenic assay. Additionally, the PI uptake assay used to measure injury post-thermal insult shows that membrane injury continues to accumulate after thermal insult at temperatures ⩾50°C and may not always correlate with clonogenicity at hyperthermic temperatures such as 45°C. Last, although the clonogenic assay yields the most accurate cell survival data, it is difficult to acquire these data at temperatures ⩾50°C because the thermal transients in the experimental setup are significant as compared to the time scale of the experiment. To improve prediction and understanding of thermal injury in this prostate cancer cell line, a first-order rate process model of injury accumulation (the Arrhenius model) was fit to the experimental results. The activation energy (E) obtained using the Arrhenius model for an injury criterion of 30 percent for all three assays revealed that the mechanism of thermal injury measured is likely different for each of the three assays: clonogenics (526.39 kJ/mole), PI (244.8 kJ/mole), and calcein (81.33 kJ/mole). Moreover, the sensitivity of the rate of injury accumulation dΩ/dt to temperature was highest for the clonogenic assay, lowest for calcein leakage, and intermediate for PI uptake, indicating the strong influence of E value on dΩ/dt. Since the clonogenic assay is linked to the ultimate survival of the cell and accounts for all lethal mechanisms of cellular injury, the E and A values obtained from clonogenic study are the best values to apply to predict thermal injury in cells. For higher temperatures (⩾50°C) indicative of thermal therapies, the results of PI uptake can be used as a conservative estimate of cell death (underprediction). This is useful until better experimental protocols are available to account for thermal transients at high temperature to assess clonogenic ability. These results provide further insights into the mechanisms of thermal injury in single cell systems and may be useful for designing optimal protocols for clinical thermal therapy. [S0148-0731(00)01301-7]

Structural Lesions on Kidney Biopsy in Youth-Onset and Adult-Onset Type 2 Diabetes

2022 ◽  
Author(s):  
Helen C. Looker ◽  
Laura Pyle ◽  
Tim Vigers ◽  
Cameron Severn ◽  
Pierre Saulnier ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Kidney Disease ◽  
Age Of Onset ◽  
Tissue Injury ◽  
Kidney Tissue ◽  
Glomerular Sclerosis ◽  
Oral Glucose ◽  
Adult Onset ◽  
Pima Indians

<b>Objective: </b>Type 2 diabetes (T2D) is a leading cause of end stage kidney disease (ESKD) worldwide. Recent studies suggest a more aggressive clinical course of diabetic kidney disease (DKD) in youth-onset than adult-onset T2D. We compared kidney structural lesions in youth- and adult-onset T2D to determine if youth-onset was associated with greater early tissue injury.<b></b> <p><b> </b></p> <p><b>Methods: </b>Quantitative microscopy was performed on kidney tissue obtained from research kidney biopsies in 161 Pima Indians (117 women, 44 men) with T2D. Onset of T2D was established by serial oral glucose tolerance testing and participants were stratified as youth-onset (<25 years) or adult-onset (≥25 years). Associations between clinical and morphometric parameters and age of onset were tested using linear models.<b></b></p> <p><b> </b></p> <p><b>Results: </b>At biopsy, the 52 participants with youth-onset T2D were younger than the 109 with adult-onset T2D (39.1±9.9 <i>vs.</i> 51.4±10.2 years, <i>p</i><0.0001), but their diabetes duration was similar (19.3±8.1 <i>vs.</i> 17.0±7.8 years, <i>p</i>=0.09). Median urine albumin-to-creatinine ratio was higher in the youth-onset group (58 [25<sup>th</sup>-75<sup>th</sup> percentile, 17-470] <i>vs.</i> 27 [13-73] mg/g, <i>p</i>=0.02). Youth-onset participants had greater glomerular basement membrane (GBM) width (552±128 nm <i>vs.</i> 490±114nm, <i>p</i>=0.002) and mesangial fractional volume (0.31±0.10 <i>vs</i>. 0.27±0.08, <i>p</i>=0.001) than adult-onset participants. Percentage glomerular sclerosis, glomerular volume, mesangial fractional volume, and GBM width were also inversely associated with age of diabetes onset as a continuous variable.<b></b></p> <p><b> </b></p> <p><b>Conclusion: </b>Younger age of T2D onset strongly associates with more severe kidney structural lesions. Studies are underway to elucidate the pathways underlying these associations.</p>

Does the Modified Arrhenius Model Reliably Predict Area of Tissue Ablation After Magnetic Resonance-Guided Laser Interstitial Thermal Therapy for Pediatric Lesional Epilepsy?

2021 ◽  
Author(s):  
Kelsey D Cobourn ◽  
Imazul Qadir ◽  
Islam Fayed ◽  
Hepzibha Alexander ◽  
Chima O Oluigbo
Keyword(s):  
Magnetic Resonance ◽  
Linear Regression ◽  
Magnetic Resonance Images ◽  
Thermal Therapy ◽  
Invasive Technique ◽  
Hypothalamic Hamartoma ◽  
Arrhenius Model ◽  
Laser Interstitial Thermal Therapy ◽  
Accuracy And Precision

Abstract BACKGROUND Commercial magnetic resonance-guided laser interstitial thermal therapy (MRgLITT) systems utilize a generalized Arrhenius model to estimate the area of tissue damage based on the power and time of ablation. However, the reliability of these estimates in Vivo remains unclear. OBJECTIVE To determine the accuracy and precision of the thermal damage estimate (TDE) calculated by commercially available MRgLITT systems using the generalized Arrhenius model. METHODS A single-center retrospective review of pediatric patients undergoing MRgLITT for lesional epilepsy was performed. The area of each lesion was measured on both TDE and intraoperative postablation, postcontrast T1 magnetic resonance images using ImageJ. Lesions requiring multiple ablations were excluded. The strength of the correlation between TDE and postlesioning measurements was assessed via linear regression. RESULTS A total of 32 lesions were identified in 19 patients. After exclusion, 13 pairs were available for analysis. Linear regression demonstrated a strong correlation between estimated and actual ablation areas (R2 = .97, P &lt; .00001). The TDE underestimated the area of ablation by an average of 3.92% overall (standard error (SE) = 4.57%), but this varied depending on the type of pathologic tissue involved. TDE accuracy and precision were highest in tubers (n = 3), with average underestimation of 2.33% (SE = 0.33%). TDE underestimated the lesioning of the single hypothalamic hamartoma in our series by 52%. In periventricular nodular heterotopias, TDE overestimated ablation areas by an average of 13% (n = 2). CONCLUSION TDE reliability is variably consistent across tissue types, particularly in smaller or periventricular lesions. Further investigation is needed to understand the accuracy of this emerging minimally invasive technique.

Temporal induction of clusterin in cisplatin nephrotoxicity.

1997 ◽  
Vol 8 (2) ◽  
pp. 302-305
Author(s):  
J R Silkensen ◽  
A Agarwal ◽  
K A Nath ◽  
J C Manivel ◽  
M E Rosenberg
Keyword(s):  
Serum Creatinine ◽  
Time Course ◽  
Tissue Injury ◽  
Kidney Tissue ◽  
Sprague Dawley ◽  
Outer Medulla ◽  
Creatinine Concentration ◽  
Cisplatin Nephrotoxicity ◽  
Tubular Necrosis ◽  
Outer Stripe

Clusterin is a ubiquitous glycoprotein induced in many organs, including the kidney, at times of tissue injury and/or remodeling. It is speculated in this study that clusterin preserves cell interactions that are otherwise perturbed by renal insults. The purpose of this study was to examine clusterin expression after cisplatin nephrotoxicity, a model characterized by a delayed time course of injury and a well-defined site of that injury (proximal tubule). Sprague-Dawley rats were treated with intravenous cisplatin (6 mg/kg) or vehicle. Serum creatinine concentrations were measured and kidneys harvested at 1, 2, and 5 days. Marked induction of clusterin mRNA was seen only at 5 days, a time when serum creatinine concentration was the highest. Histology of kidney tissue 5 days after cisplatin administration revealed marked tubular necrosis localized to the outer stripe of the outer medulla, a region rich in proximal tubules. Immunohistochemistry and in situ hybridization at 5 days demonstrated clusterin primarily in the inner stripe of the outer medulla. In conclusion, expression of clusterin follows renal injury with cisplatin at a time corresponding to the morphologic evidence of tubular necrosis and cell detachment; quite surprisingly, such expression occurs at a site distant from the primary injury.

In Vitro Assessment of the Efficacy of Thermal Therapy in Human Benign Prostatic Hyperplasia Tissue

2001 ◽  
Author(s):  
Sankha Bhowmick ◽  
Pragati Bhowmick ◽  
James E. Coad ◽  
John C. Bischof
Keyword(s):  
Tissue Injury ◽  
Lateral Lobe ◽  
Break Point ◽  
Thermal Therapy ◽  
Surgical Removal ◽  
Dye Uptake ◽  
Tissue Destruction ◽  
Uptake Study ◽  
Temperature Time

Abstract Correlation between thermal history and tissue destruction is of considerable importance for successful management of BPH using minimally invasive thermal therapies such as radiofrequency or microwave probes. In order to accomplish this goal, the present in vitro study assesses the cellular viability of BPH tissue subjected to different temperature-times in an experimental matrix. Hyperplastic prostatic tissue was obtained from 8 patients after the surgical removal of the glands for other reasons (typically cancer). A piece of tissue was taken from the lateral lobe of the gland and was then sectioned into multiple thin strips (1mm thick), placed on a coverslip and heated on a thermally controlled copper block to various temperatures (45°C-70°C) for various times (1 minute–60 minutes). After heat treatment, the tissue slices were cultured for 72 hours and viability data was obtained using two independent assays: histology and dye uptake. Results indicate that the hyperplastic prostate tissue showed a progressive histologic increase in irreversible stromal tissue injury with increasing temperature-time severity. A small amount (∼5% or less) of stromal apoptosis was found in the control and mildly treated tissue. Dye uptake studies for stromal viability paralleled the histologic findings for the temperature-time combinations explored in the present study. In vitro thermal injury thresholds for 90% destruction of human BPH tissue were identified at 45°C-60min, 55°C-20min, 60°C-5min and 70°C-2 min. The Arrhenius model of injury was fit to the viability data after controlled heating to obtain parameters that will allow the prediction of injury under variable heating conditions. Arrhenius analysis of both assays showed a break point at 60°C based on 90% normalized survival. The activation energy (E) values for temperatures below and above the break point were 199.05 and 66.04 kJ/mole for the dye uptake study and 162.6 and 62.99 kJ/mole for histology. The corresponding frequency factor (A) values below and above the break point were 1.81 × 1030 and 1.82 × 109 s−1 for dye uptake study and 2.84 × 1024 and 6.64 × 108 s−1 for histology. This study is the first to report Arrhenius parameters for human BPH tissue for supraphysiological thermal therapy and will be useful for prediction of tissue destruction during thermal therapy of BPH in the clinic.

Heterotopic Ossifications of the Forearm: A Cause of Post-Traumatic Loss of Pronation-Supination

2021 ◽  
Vol 8 (5) ◽  
Author(s):  
Hajar A ◽  
◽  
Khadija L ◽  
Jamal EF ◽  
Issam E-N ◽  
...  
Keyword(s):  
Open Fracture ◽  
Thermal Injury ◽  
Surgical Intervention ◽  
Tissue Injury ◽  
Early Stage ◽  
Soft Tissue Injury ◽  
Traumatic Loss ◽  
Ectopic Bone ◽  
Post Traumatic ◽  
Ossification Process

HO is defined by the development of ectopic mature bone within nonosseous tissues. It is a well-described phenomenon that complicates forearm fractures, especially when there is an open fracture, a significant soft tissue injury, and associated neural axis or thermal injury. HO mainly forms near metal hardware and may lead to the formation of radio-ulnar synostosis. CT is superior to plain radiographs, as it identifies the ectopic bone earlier, defines its exact localization, and helps planning the surgical intervention. Radiologic features are variable; in the early stage, CT shows a low-attenuation mass with indistinct surroundings. As the ossification process progresses, zones of mineralization are visible before leading to the formation of mature cortical bone at the periphery (Figure 1 and 2: arrows). Hastings classification describes 5 classes according to how HO affects the forearm range of motion.

The Course of Enzymatically Induced Lipid Peroxidation in Homogenized Porcine Kidney Tissue

1998 ◽  
Vol 53 (5-6) ◽  
pp. 431-438 ◽  
Author(s):  
Uwe Kießling ◽  
Gerhard Spiteller
Keyword(s):  
Lipid Peroxidation ◽  
Octadecadienoic Acid ◽  
Tissue Injury ◽  
Kidney Tissue ◽  
Oxidation Products ◽  
Mammalian Tissue ◽  
Porcine Kidney ◽  
Octadecanoic Acid ◽  
Biological Environment ◽  
Primary Oxidation

Homogenization of mammalian tissue - exemplified by porcine kidney - causes enzymatically induced lipid peroxidation (LPO) processes proven by measuring the amounts of the typical lipid peroxidation products 9- and 13-hydroxy-octadecadienoic acid (HODE) either after homogenization in aqueous (activation of enzymes) or an organic (inactivated enzymes) solvent. A kinetic study revealed that the level of the 9- and 13-isomer reached maximum values 6 hours after tissue injury. Within one day the amount of these primary oxidation products was reduced fast, indicating that they undergo degradation in their biological environment. In contrast, the level of 10-hydroxy-octadecanoic acid - obviously derived from LPO of oleic acid - increased continuously even after one day. These observations reflect that the generation and degradation of hydroperoxides occurs at different rates which might be of interest in pathological processes connected with tissue injury, e.g. myocardial infarction.

scholarly journals Blood-borne fragments of fibronectin after thermal injury

Blood ◽  
1991 ◽  
Vol 77 (9) ◽  
pp. 2037-2041 ◽  
Author(s):  
P La Celle ◽  
FA Blumenstock ◽  
TM Saba
Keyword(s):  
Thermal Injury ◽  
Proteolytic Enzymes ◽  
Tissue Injury ◽  
Plasma Concentrations ◽  
Vena Cava ◽  
Enzyme Linked Immunosorbent Assay ◽  
Plasma Fibronectin ◽  
Opsonic Activity ◽  
Macrophage Phagocytosis ◽  
Fibronectin Fragments

Abstract Fibronectin is an adhesive protein that can promote phagocytosis and endothelial cell adhesion. Plasma fibronectin declines following burn in animals and patients, potentially due to its complexing with circulating collagenous debris as well as its rapid binding to sites of tissue injury. Such depletion of fibronectin initiates an opsonic deficiency of the plasma. In view of the sensitivity of fibronectin to proteolytic enzymes, an additional factor that could contribute to the decrease of plasma opsonic activity after burn is the proteolytic fragmentation of fibronectin in the blood. In the current study, we determined if fibronectin fragments appear in the blood of anesthetized rats after a sublethal full-thickness skin burn of 15% to 16% of body surface. Plasma fibronectin concentration was quantified by enzyme- linked immunosorbent assay and the presence of fibronectin fragments in plasma was determined by immunoblot analysis. All blood was collected in an antiprotease mixture to yield final plasma concentrations of 0.15% EDTA, 3mmol/L phenylmethylsulfonyl fluoride, and 3 mmol/L iodoacetate to prevent degradation of fibronectin after sampling. Plasma fibronectin decreased 60% to 70% within 30 minutes post-burn, and this low level lasted for at least 4 hours. Within 30 minutes post- burn, two prominent fragments of fibronectin with a molecular weight of 110 +/- 2.2 kd and 122 +/- 3.3 Kd, respectively, were also detected in the plasma. Peak concentration of these fragments was detected at 60 minutes post-burn, but their level declined by 4 hours. By 4 hours, both bands appeared to resolve into doublets. To rule out the possibility that the fragments of fibronectin detected in the plasma were actually generated by coagulation enzymes activated at the site of peripheral blood sampling, rapid direct inferior vena cava sampling was performed, which also yield the presence of the fragments. Thus, fibronectin fragments exist in the plasma following thermal injury. Because fragments of fibronectin can compete with the intact fibronectin molecule with respect to its ability to stimulate macrophage phagocytosis, such fragments may contribute to altered systemic phagocytic host defense following thermal injury. Furthermore, because fibronectin peptides can compete with matrix fibronectin and impair adhesion of cultured endothelial cells, such circulating fragments may also influence the integrity of the vascular barrier.

A Medicolegal Analysis of Worker Appeals for Fibromyalgia as a Compensable Condition Following Workplace Soft-tissue Injury

2013 ◽  
Vol 40 (3) ◽  
pp. 323-328 ◽  
Author(s):  
MARY-ANN FITZCHARLES ◽  
PETER A. STE-MARIE ◽  
YORAM SHIR
Keyword(s):  
Health Status ◽  
Soft Tissue ◽  
Tissue Injury ◽  
Traumatic Event ◽  
Soft Tissue Injury ◽  
Tissue Type ◽  
Work Related ◽  
Physical Findings ◽  
Time From Injury ◽  
New Onset

Objective.Workplace injuries may be implicated in the causation of fibromyalgia (FM), hence linking FM to compensation. We examined the appeals by workers directed to an appeals tribunal for causation of FM following soft-tissue injury sustained in the workplace.Methods.One hundred fifty tribunal decisions relevant to FM were examined using a predetermined protocol. New-onset FM was appealed in 123, and aggravation of preexisting FM in 15.Results.All injuries were of a soft-tissue type, without persistent physical findings to explain continued symptoms. The tribunal accepted 67% of appeals for aggravation of FM, and 59% for new-onset FM. Time from injury to FM diagnosis was 4.3 ± 4.1 years, with 6.3 ± 2.8 physicians cited for each worker, and with previous health status not reported for 26%. Injuries were a single event in 68%, with location in low back for 44%, and shoulder/upper limb in 40%. The FM diagnosis was based on a rheumatologist report in 74%.Conclusion.Over half of appeals for aggravation or causation of FM following a work-related soft-tissue injury were accepted by the tribunal, with importance ascribed to a rheumatologist diagnosis. Concerns are raised regarding lengthy duration from injury to diagnosis, claimants’ high healthcare use, and neglect of mention of previous health status. The attribution of causation of FM to a soft-tissue workplace traumatic event is contentious and requires further examination.

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