Thermal Damage To Skin Research Articles

Experimental substantiation of the expediency of using hyperosmolar colloidal solutions for the correction of renal dysfunction in conditions of thermal skin damage

Experimental substantiation of the expediency of using hyperosmolar colloidal solutions for the correction of renal dysfunction in conditions of thermal skin damage

Inhibition of Let-7b-5p maturation by LIN28A promotes thermal skin damage repair after burn injury

Burn injuries, especially severe ones, result in direct and indirect thermal damage to skin tissues, with a complex and slow wound healing process. Improper treatment can induce sustained inflammatory responses, causing systemic damage. Lin28A, a highly conserved RNA binding protein, was found to exert a significant effect on cell proliferation and wound repair. Lin28A exerts the functions through inhibiting the maturation of the let-7 family miRNAs. Herein, the roles of Lin28A and let-7b in thermal injury repair were investigated using a mouse thermal injury model and a human skin fibroblast (HSF) model for thermal injuries. Lin28A could inhibit the maturation of let-7b, thus participating in skin repair after burns. In the animal model, Lin28A was highly expressed after thermal injury. In the HSF model for thermal injuries, downregulation of Lin28A inhibited the proliferation, migration, and extracellular matrix (ECM) generation of fibroblasts. When let-7b was knocked down in HSFs, the impacts on fibroblast functions caused by downregulation of Lin28A were partially reversed. Moreover, let-7b overexpression might significantly attenuate the promotive effects of Lin28A upon thermal injury repair. Finally, AKT2 and IGF1R were the let-7b target genes within cells. These findings reveal that Lin28A might promote thermal injury repair in burn-injured skin by inhibiting the maturation of let-7b and improving HSF viability and functions, thus illustrating the critical effect of let-7b on burn wound healing and providing new therapeutic targets and strategies for burn treatment.

Способ лечения радиационно-термических ожогов

The paper provides the procedure of preparation and application of the developed remedy for treatment of combined radiation-thermal skin injuries, caused by excessive heat and radiation. The developed medication, ointment, contains biologically active substances, such as streptoform, dimexide and a vaseline as the ointment base. Optimum ratio of ointment components was determined experimentally. The medication efficacy was studied in experiments on white rats of both sexes, with average mass of 180-200 grams. The animals were divided in groups according to the analogy principle. Radiation induced injury of skin were simulated with the use of the gamma ray unit “Puma” with absorbed dose of 7.0 Gy, exposure dose rate of 5.9 R/min (8.5х10-2 A/kg). The irradiated animals were subjected to a thermal skin damage (burn) by placing brass plate heated to 180oC immediately after the animals irradiation completion. The placed plate was hold to the hair-free skin area on the upper third of the thigh for several seconds. By degree of skin and subcutaneous tissues the thermal damage degree is identical to the degree of IIIB. Immediately after radiation exposure and introduction of thermal damages the experimental ointment samples were spread on the injury surface with the gauze sponge or plastic spreader once a day. The developed remedy was found to be effective. The mass fraction (wt%) of the burn-releaf ointment components are the following: dimexide 19-20 wt%; streptoform 30-35 wt%, vaseline 45-52 wt%.

Effect of the ointment based on benzosulfonate 1-ethyl-3-methyl-4,5-bis(N-methylcarbomoyl) imidazolium on wound healing in thermal skin damage in rats

AIM: Of the investigation was to assess the therapeutic efficacy of ointment based on benzosulfonate 1-ethyl-3-methyl-4,5-bis(N-methylcarbomoyl) imidazolium, an imidazol derivative, on healing of a thermal skin damage (burn wound) in rats.
 MATERIALS AND METHODS: In experiments on 150 male rats weighing 180200 g, the wound-healing effect of an ointment based on benzosulfonate 1-ethyl-3-methyl-4,5-bis(N-methylcarbomoyl) imidazolium (IEM-1181) after experimental thermal skin damage was studied. The ointment containing 10% of the compound IEM-1181 was prepared by the pharmacopoeial method based on lanolin. The control was the placebo effect (the basis of the ointment). For comparison, we used Solcoseril (ointment, Solco, Switzerland). Thermal damage to the skin of rats under ether anesthesia was carried out with a special device consisting of a metal plate and a temperature controller. The surface of the plate with a diameter of 1,5 cm was heated for 15 minutes to a temperature of 80С, and then applied to the pre-cut skin of the rats back (from the scapula caudally) for 15 seconds. After 24 hours, the skin of the animals developed damage to the epidermis and partially underlying dermis, corresponding to a grade II burn. The dynamics of changes in the burn wound was evaluated by 5, 10, 15, 20, 30, 40, 45, 50, 60, 70 days along the length of the contour bounding the affected area, using a curvimeter.
 RESULTS: It was found that 1-ethyl-3-methyl-4,5-bis(N-methylcarbomoyl) imidazolium benzosulfonate has a wound-healing effect in thermal skin damage in rats. With topical application of the ointment containing the test compound, the time of complete healing of the wound formed at the site of the burn defect was reduced by 30%, healing took place without signs of inflammation, with the formation of an elastic scar.
 CONCLUSIONS: Based on the conducted studies, it can be concluded that the ointment based on benzosulfonate 1-ethyl-3-methyl-4,5-bis(N-methylcarbomoyl) it has a wound-healing effect in thermal damage to the skin comparable in terms of the duration and degree of healing of burn defects with Solcoseril and can be the drug of choice for the treatment of grade II burns.

Indicators of the cell cycle in the thyroid gland in rats when using infusion of 0.9% NaCl solution on the background of thermal skin burns

Systemic damage of the organs, including the thyroid gland, is one of the key factors in the pathogenesis of burn disease due to thermal skin burns. The aim of this study was to investigate the indices of the cell cycle and DNA fragmentation of thyroid gland cells in rats with the use of infusion of 0.9% NaCl solution against the background of thermal skin burns. Experimental studies were conducted on 60 white male rats weighing 160-180 g, which was subjected to thermal burns of the skin of 2-3 degrees with a total area of 21-23% of the body surface. The first 7 days rats were infused with 0.9% NaCl solution into the inferior vena cava. Animals were removed from the experiment by decapitation (after 1, 3, 7, 14, 21, and 30 days). DNA content in the nuclei of the cells of the thyroid gland of rats was determined by flow cytometry. The statistical processing of the obtained results was carried out in the license package “STATISTICA 6.1” using nonparametric estimation methods. After 1 day after thermal skin damage and using 0.9% NaCl solution, lower (p<0.05) values of the S-phase index (0.234±0.094) were found compared to the control group without burn (0.652±0.134). The maximum decrease (p<0.01) of S-phase indicators (0.622±0.110 and 0.214±0.105, respectively) and a significant increase (p<0.01) of the SUB-G0G1 interval (5.288±0.840) compared to similar control group values (2.594±0.628) is observed after 3 days. The S-phase against the background of the introduction of 0.9% NaCl solution and thermal skin burn remained significantly lower than those of the similar control groups at 7 (p<0.01), 14 (p<0.05) and 21 days (p<0.05). At 14 days after thermal skin injury, the SUB-G0G1 interval (p<0.05) was lower than in the control group of rats. After 30 days, the G0G1 phase parameters were significantly lower (p<0.01), and the G2+M phase values were significantly (p<0.01) higher than those in the control group at the same time. Thus, it was found that 0.9% NaCl solution was not effective enough to correct cell division disorders during the entire observation period after skin burns.

Using Phase Change Materials and Air Gaps in Designing Fire Fighting Suits: A Mathematical Investigation

Firefighting is a hazardous occupation that requires the wearing of appropriate protective clothing which must be designed to be flame- and heat-resistant while also allowing for a firefighter’s ease of movement. To increase the thermal protection provided by a firefighting suit and decrease the likelihood of the firefighter receiving skin burns, we propose incorporating a layer of a phase-change material (PCM) as well as air gaps in its structure. We investigate the distribution of heat through the layers of a firefighting suit and skin to determine whether this approach will be successful when different suit configurations are exposed to a range of fire scenarios with external heat fluxes between $$5\,{\rm kWm}^{-2}$$ and $$84\,{\rm kWm}^{-2}$$ . We use a one-dimensional model of heat transfer which we solve numerically to determine the length of time each suit configuration allows a firefighter to be exposed to heated conditions before suffering irreversible thermal skin damage. Thermal damage to the skin is known to occur when the temperature in the basal layer exceeds $$44$$ °C. Our earlier research indicated that the combination of air gaps and a PCM layer reduces the likelihood of skin burns, and that the most effective position of a PCM in a suit is near the outer layer. This current work considers a number of different PCM compounds for providing additional thermal protection while ensuring that the extra weight required is feasible for a firefighting suit. We found that of the PCMs studied, $${\rm MgCl_2\cdot 6H_2O}$$ with an overall thickness of 0.17 mm gave the best improvement in the time until thermal skin damage (of between $$13\%$$ and $$19\%$$ ), depending on the fire scenario.

Lidocaine-induced potentiation of thermal damage in skin and carcinoma cells.

Lidocaine acts as a local anesthetic by blocking transmembrane sodium channel permeability, but also induces the synthesis of heat shock proteins and sensitizes cells to hyperthermia. A previous study reported two cases of deep focal skin ulceration at points corresponding to depot local lidocaine injection sites after treatment with non-ablative fractional resurfacing and it was hypothesized that lidocaine had focally sensitized keratinocytes to the thermal damage of laser treatment. The objective of this study was to investigate whether lidocaine potentiates hyperthermia damage to both normal and cancerous skin cells using an in vitro model. Normal skin cell lines (fibroblasts, keratinocytes), skin cancer cell lines (melanoma, basal cell carcinoma), and a mucosal cancer cell line (cervical carcinoma) were exposed to various concentrations of lidocaine (0-0.3%) with or without hyperthermia (37°C, 42°C). Compared to normal skin cells, we demonstrate that cancer cell lines show significantly increased cell toxicity when a moderate temperature (42°C) and low lidocaine concentrations (0.1-0.2%) are combined. The toxicity directly correlates with a higher percentage of cells in S-phase (28-57%) in the cancer cell lines compared to normal skin cell lines (13-19%; R-square 0.6752). These results suggest that lidocaine potentiates thermal sensitivity of cell cycle active skin cells. The direct correlation between cell toxicity and S-phase cells could be harnessed to selectively treat skin and mucosal cancer cells while sparing the surrounding normal tissue. Additional research pre-clinically and clinically using several different heat sources (e.g., lasers, ultrasound, etc.) and lidocaine concentrations is needed to confirm and optimize these results. Lidocaine-enhanced hyperthermia may provide a non-invasive, alterative treatment option for highly proliferating, superficial skin, and mucosal lesions such as cancer or warts. Lasers Surg. Med. 51:88-94, 2019. © 2018 Wiley Periodicals, Inc.

The effect of the new combined cream on the protein synthetic activity of cells on the model of the thermal skin damage in rats

Aim. To study the mechanisms of the reparative action of a new combined cream on the model of thermal burn injury in rats.Materials and methods. On the model of thermal burn in rats the reparative properties of the new combined cream under the conditional name “Dermalipoin” containing α-lipoic acid, urea, olive oil, tea tree oil, PEG-400 were studied. To determine the level of the protein synthetic activity of cells (epitheliocytes of the stratified squamous epithelium in the epidermis and cells of the fibroblast cell in the edges of healing of thermal damage) the content of ribonucleoproteins (RNP) in the cytoplasm and deoxyribonucleoproteins (DNP) in the nuclei of the cells was assessed by the cytometric method.Results and discussion. On the model of thermal burn in rats “Dermalipoin” cream showed a more active effect on reparative processes compared to the reference drugs – methyluracil ointment and “Titriol” gel. It indicates a significant increase in the protein synthetic function of epitheliocytes of the stratified squamous epithelium in the epidermis and cells of the fibroblastic series at the healing edges. The reparative activity of the cream was, first of all, provided by the presence of thiol (sulfhydryl) groups in the molecule of lipoic acid, giving it the properties of an antioxidant. The antioxidant effect of lipoic acid promotes more efficient DNA molecule reparation after damage as a result of the oxidative stress.Conclusions. “Dermalipoin” cream shows a marked reparative effect due to the increase of the protein synthetic activity and acceleration of reparation of DNA molecules of epithelial cells after damage; as a result, the process of healing burns accelerates.

Thermal Skin Damage During Reirradiation and Hyperthermia Is Time-Temperature Dependent

Toinvestigate the relationship of thermal skin damage (TSD) to time-temperature isoeffect levels for patients with breast cancer recurrence treated with reirradiation plus hyperthermia (reRT+HT), and to investigate whether the treatment history of previous treatments (scar tissue) is a risk factor for TSD. In this observational study, temperature characteristics of hyperthermia sessions were analyzed in 262 patients with recurrent breast cancer treated in the AMCbetween 2010 and 2014 with reirradiation and weekly hyperthermia for 1hour. Skin temperature was measured using a median of 42 (range, 29-82) measurement points per hyperthermia session. Sixty-eight patients (26%) developed 79 sites of TSD, after the first (n=26), second (n=17), third (n=27), and fourth (n=9) hyperthermia session. Seventy percent of TSD occurred on or near scar tissue. Scar tissue reached higher temperatures than other skin tissue (0.4°C, P<.001). A total of 102 measurement points corresponded to actual TSD sites in 35 of 79 sessions in which TSD developed. Thermal skin damage sites had much higher maximum temperatures than non-TSD sites (2.8°C, P<.001). Generalized linear mixed models showed that the probability of TSD is related to temperature and thermal dose values (P<.001) and that scar tissue is more at risk (odds ratio 0.4, P<.001). Limiting the maximum temperature of a measurement point to 43.7°C would mean that the probability of observing TSD was at most 5%. Thermal skin damage during reRT+HT for recurrent breast cancer was related to higher local temperatures and time-temperature isoeffect levels. Scar tissue reached higher temperatures than other skin tissue, and TSD occurred at lower temperatures and thermal dose values in scar tissue compared with other skin tissue. Indeed, TSD developed often on and around scar tissue from previous surgical procedures.

Skin and Subcutaneous Temperature Monitoring in Women during Laser-Assisted Liposculpture

Controlled subdermal dual wavelength energy (1064/1320) was applied in women treated for lipodysmorphia. Monitored surface and subdermal temperatures were analyzed and compared to desired thermal end points. A previously reported subdermal temperature monitor was used to measure subdermal temperature at the point of laser energy output. The treatment end point of ease of cannula insertion was used as an end point rather than fixed energy and temperature. Statistical analysis revealed significant skin and subdermal temperature differences at the completion of treatment. Subdermal temperature monitoring is recommended to minimize and avoid thermal skin damage. The empirical end point of tissue resistance and ease of cannula insertion used in this study (versus temperature elevation) may lead to a safer, more predictable laser-assisted lipolysis procedure.

Nociception and inflammatory hyperalgesia evaluated in rodents using infrared laser stimulation after Trpv1 gene knockout or resiniferatoxin lesion

TRPV1 is expressed in a subpopulation of myelinated Aδ and unmyelinated C-fibers. TRPV1+ fibers are essential for the transmission of nociceptive thermal stimuli and for the establishment and maintenance of inflammatory hyperalgesia. We have previously shown that high-power, short-duration pulses from an infrared diode laser are capable of predominantly activating cutaneous TRPV1+ Aδ-fibers. Here we show that stimulating either subtype of TRPV1+ fiber in the paw during carrageenan-induced inflammation or following hind-paw incision elicits pronounced hyperalgesic responses, including prolonged paw guarding. The ultrapotent TRPV1 agonist resiniferatoxin (RTX) dose-dependently deactivates TRPV1+ fibers and blocks thermal nociceptive responses in baseline or inflamed conditions. Injecting sufficient doses of RTX peripherally renders animals unresponsive to laser stimulation even at the point of acute thermal skin damage. In contrast, Trpv1−/− mice, which are generally unresponsive to noxious thermal stimuli at lower power settings, exhibit withdrawal responses and inflammation-induced sensitization using high-power, short duration Aδ stimuli. In rats, systemic morphine suppresses paw withdrawal, inflammatory guarding, and hyperalgesia in a dose-dependent fashion using the same Aδ stimuli. The qualitative intensity of Aδ responses, the leftward shift of the stimulus-response curve, the increased guarding behaviors during carrageenan inflammation or after incision, and the reduction of Aδ responses with morphine suggest multiple roles for TRPV1+ Aδ fibers in nociceptive processes and their modulation of pathological pain conditions.

Characterization of tissue ablation with a continuous wave holmium laser.

The pulsed holmium laser is a promising tool for tissue ablation but possesses some limitations. For example, it is capable of producing significant mechanical damage in certain tissues in the form of fissures and fractures. Because longer pulse durations should reduce mechanical damage, this study examined the tissue effects produced by a prototype continuous wave holmium laser. A prototype liquid nitrogen cooled holmium operating at 2.12 microns was used. The heat of ablation and ablation threshold were determined using a mass loss technique. Fresh pig skin was irradiated in air or under saline, and prepared for histologic analysis. Hemostasis was qualitatively assessed in vivo during incisions made in the skin, liver, and small intestine. Threshold radiant exposure and heat of ablation were calculated from the mass loss measurements to be 191 J/cm2 with a 95% confidence interval of -80-440 J/cm2. Residual thermal damage in skin ranged from 390 to 690 microns in saline and from 390 to 490 microns in air. Excellent hemostasis was achieved in all incisions. Using appropriate irradiation parameters, the continuous wave holmium laser produces tissue effects suitable for a general use surgical instrument. In addition, the laser source could become compact and inexpensive when diode-pumped and direct diode devices become available.

Effects of CO2 laser pulse duration in ablation and residual thermal damage: implications for skin resurfacing.

Resurfacing with the CO2 laser is rapidly gaining acceptance for skin rejuvenation. Advances in CO2 laser and scanning technology allow for precise tissue removal with minimal thermal damage. High energy CO2 laser pulses have been widely used effectively to smooth the surface of facial skin; however, pulse duration effects on ablation and thermal damage have not been systematically studied over the milli-second region (0.25-10 ms). This study characterizes the ablation threshold, heat of ablation, and residual thermal damage in skin resulting from CO2 laser pulses with a Gaussian beam profile. Mass loss from fresh pig skin was measured with an analytical balance, and residual thermal damage was determined through histology. Pulse durations > 1 ms were associated with higher ablation thresholds and localized increased thermal damage. Our results show that although pulse duration is an important determinant in ablation and thermal damage, irradiance is more critical as an independent parameter in predicting the effects of CO2 laser pulses.

Effect of mechanical tissue properties on thermal damage in skin after IR-laser ablation

The damage created instantaneously in dorsal skin and in the subjacent skeletal muscle layer after CO2 and Er3+ laser incisions is histologically and ultrastructurally investigated. Light microscopical examinations show an up to three times larger damage zone in the subcutaneous layer of skeletal muscle than in the connective tissue above. The extent of thermally altered muscle tissue is classified by different zones and characterized by comparison to long time heating injuries. The unexpectedly large damage is a result of the change of elastic properties occurring abruptly at the transition between different materials. This leads to a discontinuity of the cutting dynamics that reduces the ejection of tissue material. We show that the degree of thermal damage originates from the amount of hot material that is not ejected out of the crater acting as a secondary heat source.

The effect of CO/sub 2/ laser pulse repetition rate on tissue ablation rate and thermal damage

The ablation rate and thermal damage in skin produced by a superpulsed CO2 laser operating at pulse repetition rates between 1 and 900 Hz was measured. When delivering a fixed number of pulses (20 or 30) of equal energy, a 55-60% increase in the amount of tissue ablated was observed when the pulse repetition rate rose from 10 to 200 Hz. At pulse repetition rates greater than 200 Hz no further increase was seen. Under identical conditions, an 80% increase in the zone of thermal damage was observed when the pulse repetition rate was increased from 1 to 60 Hz. The large increases in tissue ablation and tissue damage may indicate the existence of a layer of mixed-phase (i.e., liquid and vapor) or metastable liquid which can store significant amounts of thermal energy between pulses. The data suggest that CO2 lasers should be operated at relatively low repetition rates for optimal performance.