A Novel Mechanism of Skin Tumor Promotion Involving Interferon-gamma (IFNγ)/Signal Transducer and Activator of Transcription-1 (Stat1) Signaling in Epidermis

The JAK-STAT pathway is a major signaling pathway involved in many biological processes including proliferation, apoptosis, and differentiation. Aberrant expression of STATs has been reported in multiple human cancers and murine mouse models of tumorigenesis. Previous studies from our lab and others have established a critical role for Stat3 in epithelial tumorigenesis, but the role of Stat1 is largely unknown. The current study was designed to explore the role of Stat1 during multistage skin carcinogenesis. Topical treatment with both TPA and the anthrone derivative chrysarobin (CHRY) led to rapid phosphorylation of Stat1 on both tyrosine (Tyr701) and serine (Ser727) residues in epidermis. CHRY treatment also led to upregulation of unphosphorylated Stat1 (uStat1) at later time points. In addition, CHRY treatment also led to upregulation of IRF-1 mRNA and protein which was dependent on Stat1. Further analyses demonstrated that topical treatment with CHRY but not TPA upregulated interferon-gamma (IFNg) mRNA in the epidermis and that the induction of both IRF-1 and uStat1 was dependent on IFNg signaling. Stat1 deficient (Stat1-/-) mice were highly resistant to skin tumor promotion by CHRY. In contrast, the tumor response (in terms of both papillomas and squamous cell carcinomas) was similar in Stat1-/- mice and wild-type littermates with TPA as the promoter. Histological evaluation of the proliferative response confirmed the data obtained from the tumor study for both TPA and CHRY. In addition, maximal induction of both cyclooxygenase-2 and inducible nitric oxide synthase in epidermis following treatment with CHRY was also dependent on the presence of functional Stat1. Following CHRY treatment, Stat1-/- mice exhibited reduced macrophage infiltration and reduced production of many immune cell derived chemokines/cytokines. These studies define a novel mechanism associated with skin tumor promotion by the anthrone class of tumor promoters involving upregulation of IFNg signaling in the epidermis and downstream signaling through activated (phosphorylated) Stat1 and subsequent upregulation of IRF-1 and uStat1.

Retrospective analysis of Methicillin-Resistant Staphylococcus Aureus (MRSA) skin and Soft-Tissue Infections (SSTI) in a university hospital emergency department (ED)

Study Objective: Identify the most frequent risk factors of Community Acquired-MRSA (CA-MRSA) Skin and Soft-tissue Infections (SSTIs) using a case series of patients and characterize them by age, race/ethnicity, gender, abscess location, druguse and intravenous drug-user (IVDU), underlying medical conditions, homelessness, treatment resistance, sepsis, those whose last healthcare visit was within the last 12 months, and describe the susceptibility pattern from this central Texas population that have come into the University Medical Center Brackenridge (UMCB) Emergency Department (ED). ^ Methods: This study was a retrospective case-series medical record review involving a convenience sample of patients in 2007 from an urban public hospital's ED in Texas that had a SSTI that tested positive for MRSA. All positive MRSA cultures underwent susceptibility testing to determine antibiotic resistance. The demographic and clinical variables that were independently associated with MRSA were determined by univariate and multivariate analysis using logistic regression to calculate odds ratios (OR), 95% confidence intervals, and significance (p≤ 0.05). ^ Results: In 2007, there were 857 positive MRSA cultures. The demographics were: males 60% and females 40%, with the average age of 36.2 (std. dev. =13) the study population consisted of non-Hispanic white (42%), Hispanics (38%), and non-Hispanic black (18.8%). Possible risk factors addressed included using recreational drugs (not including IVDU) (27%) homelessness (13%), diabetes status (12.6%) or having an infectious disease, and IVDU (10%). The most frequent abscess location was the leg (26.6%), followed by the arm and torso (both 13.7%). Eighty-three percent of patients had one prominent susceptibility pattern that had a susceptibility rate for the following antibiotics: trimethoprim/sulfamethoxazole (TMP-SMX) and vancomycin had 100%, gentamicin 99%, clindamycin 96%, tetracycline 96%, and erythromycin 56%. ^ Conclusion: The ED is becoming an important area for disease transmission between the sterile hospital environment and the outside environment. As always, it is important to further research in the ED in an effort to better understand MRSA transmission and antibiotic resistance, as well as to keep surveillance for the introduction of new opportunistic pathogens into the population. ^

Investigation of the mechanism of increased melanoma incidence in UV -irradiated mouse skin

The availability of transplantable, syngeneic murine melanomas made it possible to study the potential effects of UV radiation on the growth and progression of melanomas in an animal model. The purpose of my study was to determine how UV-irradiation increases the incidence of melanoma out-growth, when syngeneic melanoma cells are transplanted into a UV-irradiated site. Short term intermittent UVB exposure produces a transitory change in the mice which allows the increased outgrowth of melanoma cells injected into the UV-irradiated site. One possible mechanism is an immunomodulatory effect of UVR on the host. An alternative mechanism to account for the increased tumor incidence in the UV-irradiated site, is the release of inflammatory mediators from UV-irradiated epidermal cells. A third possibility is that UVR could induce the production and/or release of melanoma-specific growth factors resulting in increased melanoma outgrowth.^ My first step in distinguishing among these different possible mechanisms was to characterize further the conditions leading to increased development of melanoma cells in UV-irradiated mouse skin. Next, I attempted to determine which of the 3 proposed mechanisms was most likely. To do this, I defined the specificity of the effect by examining the growth of additional C3H tumorigenic cell lines in UV-irradiated skin. Second, I determined the immunogenicity of these tumor cell lines. The tumor cell lines exhibiting increased tumor incidence are restricted to those tumor cell lines which are immunogenic in normal C3H mice. Third, I determined the effect of UVR on melanoma development did not occur in immunosuppressed mice.^ Because of results from these three lines of investigation suggested that the effect was immunologically mediated, I then investigated whether specific immune reactions were affected by local UV irradiation. To accomplish this, I investigated the effect of UVR on cutaneous immune cells and on induction of contact hypersensitivity (CHS), and I also determined the effect of UVR on the development and the expression of systemic immunity against the melanoma cells. There is no clear cut relationship between the number of Langerhans or Thy1+ cells and the UV effect on tumor incidence. Furthermore, there was no suppression of CHS in the UV-irradiated mice. While the development of systemic immunity is significantly reduced, it appears to be sufficient to provide in vivo immunity to tumor challenge. However the elicitation of tumor immunity in immunized mice can be abrogated if tumor challenge occurs in the site of UV irradiation. This investigation provides new information on an effect of UVR on the elicitation of tumor immunity. Furthermore, it indicates that UV radiation can play a role in the development of melanoma other than just in the transformation of melanocytes. ^

Alterations in the ras oncogene and the p53 tumor suppressor gene in ultraviolet radiation-induced skin carcinogenesis

A rapid increase of the ultraviolet radiation (UVR)-related skin cancer incidence has attracted more and more public attention during the last few decades. Prevention and treatment of UVR-related skin cancer has become an important public health issue in the United States. Recent studies indicate that mutations in ras and/or p53 genes may be involved in UVR-induced skin tumor development but the precise molecular mechanism remains unclear. In this study, alterations of H-ras and p53 genes were investigated in different stages of carcinogenesis in a chronic UVR (solar simulator) exposure-induced Sencar mouse skin carcinogenesis model in order to clarify the role of the alterations of these genes during the skin carcinogenesis process and to further understand the mechanisms by which UVR causes skin cancer.^ Positive ras-p21 staining in cell membranes and cytosol were detected in 18/33 (55%) of squamous cell carcinomas (SCCs), but were not detected in UV-exposed skin, papillomas, or spindle cell tumors (SCTs). Positive staining of the malignant progression marker K13 was found in 17/33 (52%) of SCCs only. A significant positive correlation was observed between the K13 and the ras-p21 expression. Polymerase chain reaction (PCR)-based single strand conformation polymorphism (SSCP) analysis and gene sequencing analysis revealed three point mutations, one (codon 56) in UV-exposed non-tumor bearing skin and the other two (codons 21 and 13) in SCCs. No UV-specific mutation patterns were found.^ Positive p53 nuclear staining was found in 10/37 (27%) of SCCs and 12/24 (50%) of SCTs, but was not detected in normal skin or papillomas. PCR-based SSCP and sequencing analysis revealed eight point mutations in exons 5 and 6 (four in SCTs, two in SCCs, and two in UV-exposed skin) including six C-T or C-A transitions. Four of the mutations occurred at a dipyrimidine (CC) sequence. The pattern of the mutations indicated that the mutagenic lesions were induced by UVR.^ These results indicate that overexpression of ras-p21 in conjunction with aberrant expression of K13 occurred frequently in UVR-induced SCCs in Sencar mouse skin. The point mutation in the H-ras gene appeared to be a rare event in UVR skin carcinogenesis and may not be responsible for overexpression of ras-p21. UVR-induced P53 gene alteration is a frequent event in UVR-induced SCCs and later stage SCT tumors in Sencar mice skin, suggesting the p53 gene mutation plays an important role in skin tumor malignant progression. ^

Modulation of cytochrome P450 enzyme activity and PAH -induced skin carcinogenesis by naturally occurring coumarins

The present study was designed to determine the potential anticarcinogenic activity of naturally occurring coumarins and their mechanism of action. The results indicated that several naturally occurring coumarins including bergamottin, coriandrin, imperatorin, isopimpinellin, and ostruthin, to which humans are routinely exposed in the diet, were effective inhibitors and/or inactivators of CYP1A1-mediated ethoxyresorufin-O-dealkylase (EROD) or CYP2B1-mediated pentoxyresorufin-O-dealkylase (PROD) in mouse liver microsomes. In addition, bergamottin and corandrin were also found to be inhibitors of purified human P450 1A1 in vitro. Further studies with coriandrin revealed that this compound was a mechanism-based inactivator of P450 1A1 and covalently bound to the P450 1A1 apoprotein. In cultured mouse keratinocytes, bergamottin and coriandrin effectively inhibited the B(a) P metabolism and significantly decreased covalent binding of B(a) P and DMBA to keratinocyte DNA and anti-diol-epoxide-DNA adducts derived from both B(a) P and DMBA in keratinocytes. The data from in vivo experiments showed that bergamottin and coriandrin were potent inhibitors of covalent binding of B (a) P to epidermal DNA and the formation of (+) anti BPDE-DNA adduct, whereas imperatorin and isopimpinellin were more potent inhibitors of covalent binding of DMBA to epidermal DNA. The ability of coumarins to inhibit covalent binding of B (a) P to DNA in mouse epidermis was positively correlated with their inhibitory effect P450 1A1 in vitro, while the inhibitory effect of coumarins on covalent binding of DMBA to epidermal DNA was positively correlated with their inhibitory effects on P450 2B1 and negatively to their inhibitory activity toward P450 1A1. The data from tumor experiments indicated that bergamottin, ostruthin, and coriandrin inhibited tumor initiation by B (a) P in a two-stage carcinogenesis protocol. Bergamottin was most effective in this regard and produced a dose dependent inhibition of papilloma formation in these experiments. In addition, imperatorin was an effective inhibitor of skin tumorigenesis induced by DMBA in SENCAR mouse skin using both a two-stage and a complete carcinogenesis protocol. At dose levels higher than those effective against DMBA, imperatorin also inhibited tumor initiation by B (a) P. The results to date demonstrate that several naturally occurring coumarins possess the ability to block tumor initiation and tumorigenesis by PAHs such as B (a) P and DMBA through inhibition of the P450s involved in the metabolic activation of these hydrocarbons. A working model for the involvement of specific P450s in the metabolic activation of these two PAHs was proposed. ^

Regulation of apoptosis during the pathogenesis of non -melanoma skin cancer

Previous studies from our lab have shown distinctive patterns of expression of bcl-2 gene family members in human nonmelanoma skin cancer (NMSC). To further evaluate the significance of these observations and to study the effects of cell death deregulation during skin carcinogenesis, we generated a transgenic mouse model (HK1.bcl-2) using the human keratin 1 promoter to target the expression of a human bcl-2 minigene to the epidermis. Transgenic protein expression was confirmed in all the layers of the epidermis except the stratum corneum using immunohistochemistry. Multifocal epidermal hyperplasia, without associated hyperkeratosis, was observed in newborn HK1.bcl-2 mice. Immunofluorescence staining using monoclonal antibodies specific for a variety of differentiation markers revealed aberrant expression of keratin 6 (K6) in the transgenic epidermis. Epidermal proliferative indexes, assessed by anti-BrdUrd immunofluorescence staining, were similar in control and transgenic newborn mice, but suprabasal proliferating cells were seen within the hyperplastic areas of the transgenic mouse skin. Spontaneous apoptotic indices of the epidermis were similar in both control and HK1.bcl-2 transgenic newborn mice, however, after UV-B irradiation, the number of "sunburn cells" was significantly higher in the control compared to the HK1.bcl-2 transgenic animals.^ Adult HK1.bcl-2 and control littermate mice were used in UV-B and chemical carcinogenesis protocols including DMBA + TPA. UV-B irradiated control and HK1.bcl-2 mice had comparable incidence of tumors than the controls, but the mean latency period was significantly shorter in the HK1.bcl-2 transgenic. Both control and transgenic animals included in chemical carcinogenesis protocols required application of both the initiating (DMBA) and promoting (TPA) agents to develop tumors. The frequency, number, and latency of tumor formation was similar in both groups of animals, however, HK1.bcl-2 mice exhibited a rate of conversion from benign papilloma to carcinoma 2.5 times greater than controls.^ Similar carcinogenesis experiments were performed using newborn mice. HK1.bcl-2 mice treated with UV-B plus TPA have a three fold greater incidence of tumor formation compared to controls littermates. HK1.bcl-2 transgenic animals also exhibited a shorter latency for papilloma formation when treated with DMBA plus TPA.^ HK1.bcl-2/v-Ha-ras double transgenic mice shared phenotypic features of both HK1.v-Ha-ras and HK1.bcl-2 transgenic mice, and exhibited focal areas of augmented hyperplasia. These double transgenic mice were susceptible to tumor formation by treatment with TPA alone.^ Cultures of primary keratinocytes were established from control, HK1.bcl-2, HK1.Ha-ras, and HK1.bcl-2/v-Ha-ras newborn mice. Cell viability was determined after exposure of the cells to UV-B irradiation, DMBA, TPA, or TGF-$\beta$1. Internucleosomal DNA fragmentation ("ladders") and morphological cellular changes compatible with apoptotic cell death were observed after the application of all these agents. HK1.bcl-2 keratinocytes were resistant to cell death induction by all of these agents except TGF-$\beta$1. HK1.Ha-ras cells had a higher spontaneous rate of cell death which could be compensated by co-expression of bcl-2.^ These findings suggest that bcl-2 dependent cell death suppression may be an important component of multistep skin carcinogenesis. ^

Involvement of {\it p53\/} in PUVA-induced skin cancers

A combination of psoralen and ultraviolet-A radiation, commonly referred to as "PUVA," is widely used in the treatment of psoriasis. However, PUVA treatment increases the risk of developing skin cancer in psoriasis patients and induces skin cancer in mice. It is, however unknown whether the increased incidence of skin cancer in PUVA treated psoriasis patients is due to the carcinogenic effects of PUVA therapy or due to an indirect effect such as immunosuppression, which can permit the growth of tumors induced by UVB radiation. In this study, we used the p53 tumor suppressor gene as a molecular marker to determine whether PUVA-induced mouse skin cancers contain unique mutations in p53 that are different from UV-induced mutations, and if so, determine whether skin cancers from PUVA treated patients have PUVA-type or UV-type p53 mutations. Since the DNA lesions induced by PUVA are quite different from those induced by UV, we hypothesize that p53 mutations induced by PUVA may also be different from those induced by UV.^ Analysis of PUVA-induced murine skin cancers for p53 mutations revealed that 14 of 15 (93%) missense mutations detected in these cancers were localized at 5$\sp\prime$-TA/5$\sp\prime$-TAT sites, potential sites of psoralen photoadditions. Mutations at these sequences are exceedingly rare in UV-induced murine skin cancers. In addition, PUVA-induced murine skin cancers did not contain UV signature (C $\to$ T or CC $\to$ TT transitions) mutations in p53. These results suggest that PUVA induces unique mutations in p53 that can be distinguished from those induced by UV.^ Next we determined whether SCCs arising in PUVA treated psoriasis patients have PUVA-type or UV-type p53 mutations. The results indicated that 16 of 25 (64%) missense p53 mutations detected in SCCs from PUVA treated patients were located at 5$\sp\prime$-TG, 5$\sp\prime$-TA and 5$\sp\prime$-TT sites, putative sites of psoralen photobinding. Interestingly, about 32% of p53 mutations detected in SCCs from PUVA treated patients had the UV signature. Taken together these results suggest that both PUVA and UVB play a role in the development of SCCs in psoriasis patients undergoing PUVA therapy. ^

The role of p53 in skin cancer induction by UV radiation and as a potential tumor antigen in UV-induced murine skin tumors

Carcinoma of the skin is the most common type of human cancer in the United States. Ultraviolet radiation (UVR) present in the sunlight is thought to be the major carcinogen responsible for induction of skin cancer. In UV-associated skin carcinogenesis, mutations in p53 are not only present with very high frequency, but occur early in the course of tumor development. In addition, UV-induced skin tumors in mice exhibit unique immunological characteristics. They are highly antigenic and express both individually-specific tumor transplantation antigens recognized by effector T cells and the UV-associated common antigen recognized by UV-induced suppressor T cells. ^ To examine the hypothesis that p53 plays a critical role in preventing skin cancer induction by UVR, mice constitutively lacking one or two functional p53 alleles were compared to wild-type mice for their susceptibility to UV carcinogenesis. Both p53 +/– and –/– mice showed greater susceptibility to skin cancer induction than wild-type mice, and –/– mice were the most susceptible, Accelerated tumor development in the p53 +/– mice was not associated with loss of the remaining wild-type allele of p53 , but in many cases was associated with UV-induced mutations in p53. Our studies clearly demonstrate the essential role of p53 in protection against UV carcinogenesis, particularly in the eye and epidermis. ^ The role of p53 in the antigenicity of UV-induced murine skin tumors was also addressed. Primary UV-induced tumors from p53 –/–, +/– and +/+ mice were transplanted into both normal and immunosuppressed mice, and rates of tumor rejection were compared. Tumors from mice with only one or no functional p53 alleles were less antigenic than those from mice with two functional p53 alleles. Moreover, tumors with no functional p53 also failed to grow well in chronically UV-irradiated mice. These results indicate that p53 contributes to the strong antigenicity of UV-induced murine skin tumors, and suggest that it may play a critical role in expression of the UV-associated common antigen recognized by suppressor T cells. ^ In this study we also monitored the effect of UVR on the development of lymphoid malignancies in p53 deficient mice. The incidence of lymphoid malignancies in UV-irradiated p53 +/– mice was drastically enhanced compared to that in unirradiated counterparts. The immune responses of the mice were identical and were suppressed to the same extent by UV irradiation regardless of the p53 genotype. These data provide the first experimental evidence that exposure to UVR can contribute to the development of lymphoid neoplasms in genetically susceptible hosts. ^

Participation of bcl -2 and bax in epidermal homeostasis and non-melanoma skin cancer

Non-melanoma skin cancer (NMSC) is the most frequently diagnosed form of cancer in United States. As in many other cancers, this slow growing malignancy manifests deregulated expression of apoptosis regulating proteins including bcl-2 family member proteins. To understand the role of apoptosis regulating protein in epidermal homeostasis and progression of NMSC, we investigated keratinocyte proliferation, differentiation and tumorigenesis in bcl-2 and bax null mice. The rate and the pattern of proliferation and spontaneous cell death were the same between the null and the control mice. Both bcl-2 and bax null epidermis showed decreased levels of cytokeratin 14 expression compared to the control littermates. Also, the gene knock out mice showed higher expression of cytokeratin 1 and loricrin in epidermis compared to the control mice. The apoptotic response to genotoxic agent, UV radiation (UVR), was assessed by counting sunburn cells. The bax null keratinocytes showed a resistance to apoptosis while bcl-2 null mice showed an increased susceptibility to cell death compared to the control mice. Moreover, we demonstrated an increase in tumor incidence in bax null mice compared to control littermates in the in vivo chemical carcinogenesis study. Next, we examined the tumor suppressor role of bax protein in NMSC by studying its participation in repair of UVR-mediated DNA lesions. In UVR treated primary keratinocytes from bax deficient mice, the level of CPD remaining was twice that of control cells at 48 hours. Similar results were obtained using embryonic fibroblasts from bax null and bax +/+ embryos, and also with a bax deficient prostate cancer cell line in which bax expression had been restored. However, the repair rate of 6-4 PP was unaffected by the absence of bax protein in all three of above mentioned cell types. In conclusion, bax protein may have a dual function in its role as tumor suppressor in NMSC. Bax may directly or indirectly facilitate DNA repair, or programmed cell death if DNA damage is too severe, thus, in either function, preserving genomic integrity following a genotoxic event. ^

Functional studies of *Ras and Bcl-2 oncoproteins in keratinocyte homeostasis and multistep skin carcinogenesis

To assess the effect of deregulated Ha-ras and bcl-2, individually and in combination on epidermal keratinocyte homeostasis and during multistep skin carcinogenesis, we generated skin-specific transgenic mice and keratinocyte transfectants constitutively expressing oncogenic Ha-ras and bcl-2 proteins. The deregulated Ha-ras and bcl-2 expression contributing to homeostatic imbalances in the skin had an additive effect on the probability of tumor development. They were also cooperative in incidence, growth, and latency of tumor formation, and they exhibited synergistic cooperation in malignant transformation of benign papillomas. To explain the homeostatic imbalances by Ha-ras and bcl-2 overexpression in the skin, we investigated the three major cellular processes of proliferation, cell death, and differentiation. Epidermal expression of Bcl-2 retarded keratinocyte proliferation in the epidermis of neonatal mice compared with results for control littermates. Constitutive expression of Ha-ras increased keratinocyte proliferation, and co-expression of bcl-2 modestly suppressed the ras-mediated abnormal proliferation of neonatal keratinocytes. Bcl-2 proteins in keratinocytes protected UV-treated cells from apoptotic cell death regardless of oncogenic ras expression in both non-neoplastic neonatal epidermis and human keratinocyte cell lines. The spontaneous apoptotic index (AI) was also lower in papillomas constitutively expressing bcl-2 compared with the ones that developed in control mice. Ras-overexpressing epidermis, including that in ras/bcl-2 double transgenic mice, had abnormal differentiation patterns compared with controls. The oncogenic ras protein had alterations in both epidermal distribution and the extent of cytokeratin 14 and involucrin expression. Abnormal expression of the hyperproliferation marker cytokeratin 6 and modest down regulation of cytokeratin 1 were also detected. Late appearance of filaggrin was another abnormal phenotype of the ras-expressing epidermis. Overexpression of bcl-2 had no effect on epidermal differentiation. Together, these findings suggest that constitutive expression of oncogenic Ha-ras and bcl-2 are important determinants of epidermal proliferation, viability and differentiation. In summary, our results demonstrated that the disruption of epidermal homeostasis by overexpressed ras and bcl-2 predisposes to hyperplastic growth of the epidermis and to papilloma development and that these proteins with distinct mechanisms for oncogenesis are functionally synergistic for malignant transformation of chemically induced skin carcinogenesis. ^

Histological structure of the facial skin in the bald uakari (Cacajao calvus), compared to other non-red Neotropical primates

In social species, such as primates, facial appearances transmit a variety of social signals. Although it is suggested that the intense red colour of the face of the bald uakari monkey might be an indicator of health, this hypothesis still has not been verified. This study describes the histological structure of the skin of the face in the bald uakari, compared with other non-red neotropical primates, to better understand the maintenance of its colour. The facial skin of the bald uakari monkey is characterized by a thinner epidermis, absence of melanin pigments and a high density of vascular capillaries that spread below the epidermis. These vascular capillaries are larger and more tortuous than in other neotropical primates. The skin of the face of the bald uakari monkey allows a direct external assessment of haematological status, suggesting that the colour of the face would be an honest indicator of health, but could also signal sexual or behavioural states.

Influence of body mass and skinfolds on skin temperature through infrared thermography

Thermal response of skin temperature (Tsk) has been studied during exercise and immediately after (Merla, 2010). However, more studies about the influence of exercise on Tsk through the time are required to understand the impact of physical activity on thermoregulatory system and metabolism

Effect of endurance, speed and strength training on skin temperature measured by infrared thermography = Efecto del entrenamiento de resistencia, velocidad y fuerza en la temperatura de la piel a través de la termografía infrarroja

La termografía infrarroja (TI) es una técnica no invasiva y de bajo coste que permite, con el simple acto de tomar una fotografía, el registro sin contacto de la energía que irradia el cuerpo humano (Akimov & Son’kin, 2011, Merla et al., 2005, Ng et al., 2009, Costello et al., 2012, Hildebrandt et al., 2010). Esta técnica comenzó a utilizarse en el ámbito médico en los años 60, pero debido a los malos resultados como herramienta diagnóstica y la falta de protocolos estandarizados (Head & Elliot, 2002), ésta se dejó de utilizar en detrimento de otras técnicas más precisas a nivel diagnóstico. No obstante, las mejoras tecnológicas de la TI en los últimos años han hecho posible un resurgimiento de la misma (Jiang et al., 2005, Vainer et al., 2005, Cheng et al., 2009, Spalding et al., 2011, Skala et al., 2012), abriendo el camino a nuevas aplicaciones no sólo centradas en el uso diagnóstico. Entre las nuevas aplicaciones, destacamos las que se desarrollan en el ámbito de la actividad física y el deporte, donde recientemente se ha demostrado que los nuevos avances con imágenes de alta resolución pueden proporcionar información muy interesante sobre el complejo sistema de termorregulación humana (Hildebrandt et al., 2010). Entre las nuevas aplicaciones destacan: la cuantificación de la asimilación de la carga de trabajo físico (Čoh & Širok, 2007), la valoración de la condición física (Chudecka et al., 2010, 2012, Akimov et al., 2009, 2011, Merla et al., 2010), la prevención y seguimiento de lesiones (Hildebrandt et al., 2010, 2012, Badža et al., 2012, Gómez Carmona, 2012) e incluso la detección de agujetas (Al-Nakhli et al., 2012). Bajo estas circunstancias, se acusa cada vez más la necesidad de ampliar el conocimiento sobre los factores que influyen en la aplicación de la TI en los seres humanos, así como la descripción de la respuesta de la temperatura de la piel (TP) en condiciones normales, y bajo la influencia de los diferentes tipos de ejercicio. Por consiguiente, este estudio presenta en una primera parte una revisión bibliográfica sobre los factores que afectan al uso de la TI en los seres humanos y una propuesta de clasificación de los mismos. Hemos analizado la fiabilidad del software Termotracker, así como su reproducibilidad de la temperatura de la piel en sujetos jóvenes, sanos y con normopeso. Finalmente, se analizó la respuesta térmica de la piel antes de un entrenamiento de resistencia, velocidad y fuerza, inmediatamente después y durante un período de recuperación de 8 horas. En cuanto a la revisión bibliográfica, hemos propuesto una clasificación para organizar los factores en tres grupos principales: los factores ambientales, individuales y técnicos. El análisis y descripción de estas influencias deben representar la base de nuevas investigaciones con el fin de utilizar la TI en las mejores condiciones. En cuanto a la reproducibilidad, los resultados mostraron valores excelentes para imágenes consecutivas, aunque la reproducibilidad de la TP disminuyó ligeramente con imágenes separadas por 24 horas, sobre todo en las zonas con valores más fríos (es decir, zonas distales y articulaciones). Las asimetrías térmicas (que normalmente se utilizan para seguir la evolución de zonas sobrecargadas o lesionadas) también mostraron excelentes resultados pero, en este caso, con mejores valores para las articulaciones y el zonas centrales (es decir, rodillas, tobillos, dorsales y pectorales) que las Zonas de Interés (ZDI) con valores medios más calientes (como los muslos e isquiotibiales). Los resultados de fiabilidad del software Termotracker fueron excelentes en todas las condiciones y parámetros. En el caso del estudio sobre los efectos de los entrenamientos de la velocidad resistencia y fuerza en la TP, los resultados muestran respuestas específicas según el tipo de entrenamiento, zona de interés, el momento de la evaluación y la función de las zonas analizadas. Los resultados mostraron que la mayoría de las ZDI musculares se mantuvieron significativamente más calientes 8 horas después del entrenamiento, lo que indica que el efecto del ejercicio sobre la TP perdura por lo menos 8 horas en la mayoría de zonas analizadas. La TI podría ser útil para cuantificar la asimilación y recuperación física después de una carga física de trabajo. Estos resultados podrían ser muy útiles para entender mejor el complejo sistema de termorregulación humano, y por lo tanto, para utilizar la TI de una manera más objetiva, precisa y profesional con visos a mejorar las nuevas aplicaciones termográficas en el sector de la actividad física y el deporte Infrared Thermography (IRT) is a safe, non-invasive and low-cost technique that allows the rapid and non-contact recording of the irradiated energy released from the body (Akimov & Son’kin, 2011; Merla et al., 2005; Ng et al., 2009; Costello et al., 2012; Hildebrandt et al., 2010). It has been used since the early 1960’s, but due to poor results as diagnostic tool and a lack of methodological standards and quality assurance (Head et al., 2002), it was rejected from the medical field. Nevertheless, the technological improvements of IRT in the last years have made possible a resurgence of this technique (Jiang et al., 2005; Vainer et al., 2005; Cheng et al., 2009; Spalding et al., 2011; Skala et al., 2012), paving the way to new applications not only focused on the diagnose usages. Among the new applications, we highlighted those in physical activity and sport fields, where it has been recently proven that a high resolution thermal images can provide us with interesting information about the complex thermoregulation system of the body (Hildebrandt et al., 2010), information than can be used as: training workload quantification (Čoh & Širok, 2007), fitness and performance conditions (Chudecka et al., 2010, 2012; Akimov et al., 2009, 2011; Merla et al., 2010; Arfaoui et al., 2012), prevention and monitoring of injuries (Hildebrandt et al., 2010, 2012; Badža et al., 2012, Gómez Carmona, 2012) and even detection of Delayed Onset Muscle Soreness – DOMS- (Al-Nakhli et al., 2012). Under this context, there is a relevant necessity to broaden the knowledge about factors influencing the application of IRT on humans, and to better explore and describe the thermal response of Skin Temperature (Tsk) in normal conditions, and under the influence of different types of exercise. Consequently, this study presents a literature review about factors affecting the application of IRT on human beings and a classification proposal about them. We analysed the reliability of the software Termotracker®, and also its reproducibility of Tsk on young, healthy and normal weight subjects. Finally, we examined the Tsk thermal response before an endurance, speed and strength training, immediately after and during an 8-hour recovery period. Concerning the literature review, we proposed a classification to organise the factors into three main groups: environmental, individual and technical factors. Thus, better exploring and describing these influence factors should represent the basis of further investigations in order to use IRT in the best and optimal conditions to improve its accuracy and results. Regarding the reproducibility results, the outcomes showed excellent values for consecutive images, but the reproducibility of Tsk slightly decreased with time, above all in the colder Regions of Interest (ROI) (i.e. distal and joint areas). The side-to-side differences (ΔT) (normally used to follow the evolution of some injured or overloaded ROI) also showed highly accurate results, but in this case with better values for joints and central ROI (i.e. Knee, Ankles, Dorsal and Pectoral) than the hottest muscle ROI (as Thigh or Hamstrings). The reliability results of the IRT software Termotracker® were excellent in all conditions and parameters. In the part of the study about the effects on Tsk of aerobic, speed and strength training, the results of Tsk demonstrated specific responses depending on the type of training, ROI, moment of the assessment and the function of the considered ROI. The results showed that most of muscular ROI maintained warmer significant Tsk 8 hours after the training, indicating that the effect of exercise on Tsk last at least 8 hours in most of ROI, as well as IRT could help to quantify the recovery status of the athlete as workload assimilation indicator. Those results could be very useful to better understand the complex skin thermoregulation behaviour, and therefore, to use IRT in a more objective, accurate and professional way to improve the new IRT applications for the physical activity and sport sector.

Effects of skin characteristics on impact response and bruising of apples and pears

Skin properties have an important influence on impact parameters and bruising. Skin deformation at puncture (a measure of the turgidity of the fruit skin) is negatively correlated with bruise volume in Golden apples after cold storage.

Relations between resistance of fruit and skin characteristics in tomato varieties.

Varietal differences in physical properties of processing tomato fruits related with resistance are determined. Mean values of skin resistance and firmness are highly correlated with rupture of the fruits by quasi-static compression and by impact. Skin resistance is dependent on the features of the epidermis, studied microscopically.