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BACKGROUND: Bullous pilomatricoma is a rare variant of pilomatricoma. As it has been published in sporadic case reports, a limited understanding of its clinicopathological characteristics restricts its effective diagnosis and treatment. OBJECTIVES: This study aimed to analyze the clinicopathological and immunohistochemical characteristics of bullous pilomatricoma to better understand the bullous transformation of pilomatricoma. METHODS: The authors conducted a retrospective study of 12 patients with bullous pilomatricoma and compared their clinical, histopathological, and immunohistochemical data with those of patients with ordinary pilomatricoma. RESULTS: Bullous pilomatricoma showed no sex preference, with a mean onset age of 31.2 years. The common sites were the upper extremities and trunk. Bullous pilomatricoma had a shorter disease duration, a larger diameter, and a greater tendency to increase in size than those of ordinary pilomatricoma. Histopathologically, bullous pilomatricoma had a shorter duration, lesser calcification, more mitotic figures, and distinct dermal features from those of ordinary pilomatricoma. Immunohistochemically, the expression of Matrix Metalloprotease (MMP)-2, MMP-9, vascular endothelial growth factor receptor-3 (VEGFR-3), and VEGF-C was elevated. STUDY LIMITATIONS: The study was retrospective, and the sample size was small. CONCLUSION: The distinctive features of bullous pilomatricoma potentially result from dermal changes associated with the release of angiogenic factors and proteolytic enzymes. This comprehensive analysis provides novel insights into the clinical features and pathogenesis of bullous pilomatricoma.

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ABSTRACT Objective: This study aimed to compare the levels of HIF1-α, VEGF, TNF-α, and IL-10 in the peri-implant crevicular fluid of patients with and without peri-implantitis. Methods: Forty patients, comprising 16 with and 24 without peri-implantitis were selected. Results: Patients with peri-implantitis exhibited significantly higher HIF-1α levels than those without peri-implantitis (p=0.0005). TNF-α revealed significant positive correlations with IL-10 (p=0.0008) and VEGF (p=0.0246), whereas HIF-1α and IL-10 levels (p=0.0041) demonstrated a negative and significative correlation in the peri-implantitis group. Conclusion: This study, for the first time demonstrates the balance of HIF-1α, TNFα, IL-10, and VEGF in peri-implantitis. It shows an elevated HIF-1α levels in patients with peri-implantitis, which could have stemmed from persistent inflammation- triggered hypoxia. Furthermore, the positive correlation between TNF-α and VEGF suggests intensified proinflammatory activity in peri-implantitis. Nevertheless, further studies are essential to understand these immune dynamics in peri-implantitis.

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Abstract Background Bullous pilomatricoma is a rare variant of pilomatricoma. As it has been published in sporadic case reports, a limited understanding of its clinicopathological characteristics restricts its effective diagnosis and treatment. Objectives This study aimed to analyze the clinicopathological and immunohistochemical characteristics of bullous pilomatricoma to better understand the bullous transformation of pilomatricoma. Methods The authors conducted a retrospective study of 12 patients with bullous pilomatricoma and compared their clinical, histopathological, and immunohistochemical data with those of patients with ordinary pilomatricoma. Results Bullous pilomatricoma showed no sex preference, with a mean onset age of 31.2 years. The common sites were the upper extremities and trunk. Bullous pilomatricoma had a shorter disease duration, a larger diameter, and a greater tendency to increase in size than those of ordinary pilomatricoma. Histopathologically, bullous pilomatricoma had a shorter duration, lesser calcification, more mitotic figures, and distinct dermal features from those of ordinary pilomatricoma. Immunohistochemically, the expression of Matrix Metalloprotease (MMP)-2, MMP-9, vascular endothelial growth factor receptor-3 (VEGFR-3), and VEGF-C was elevated. Study limitations The study was retrospective, and the sample size was small. Conclusion The distinctive features of bullous pilomatricoma potentially result from dermal changes associated with the release of angiogenic factors and proteolytic enzymes. This comprehensive analysis provides novel insights into the clinical features and pathogenesis of bullous pilomatricoma.

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SUMMARY OBJECTIVE: Coronavirus disease 2019 emerges as a disease caused by severe acute respiratory syndrome coronavirus 2. It is a systemic disease associated with vascular inflammation and endothelial damage. In this study, we aimed to investigate whether vascular endothelial growth factor gene insertion/deletion polymorphism is associated with coronavirus disease 2019 in the Turkish population. METHODS: The study included 179 participants (79 patients with coronavirus disease 2019 and 100 controls). DNA isolation was made from peripheral blood, and then the polymerase chain reaction analysis was performed. RESULTS: When we analyze vascular endothelial growth factor gene insertion/deletion polymorphism in the study group, we found that the DD genotype and D allele were found to be statistically significantly different when compared to coronavirus disease 2019 patients with high vitamin D value (p=0.005 for DD genotype and p=0.006 for D allele) in the control group. In this high-level control group, when we analyze II+ID genotype versus DD, a statistically significant difference was also detected (p=0.007). CONCLUSION: As a result of the study, we found that DD genotype and D allele were associated with vitamin D level in Turkish patients with coronavirus disease 2019.

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SUMMARY OBJECTIVE: In this study, we aimed to determine the impact of the antiangiogenic medications, namely, aflibercept and cabergoline in the prevention and treatment of ovarian hyperstimulation syndrome in a rat model. METHODS: A total of 36 female Wistar rats were randomly allocated to one of the five groups, including disease-free and ovarian hyperstimulation syndrome controls: Group no OHSS (control, n=6) received saline only intraperitoneally (i.p.); group just OHSS (ovarian hyperstimulation syndrome only, n=6) received 10 IU pregnant mare serum gonadotropin and 30 IU human chorionic gonadotropin subcutaneously to produce ovarian hyperstimulation syndrome; group cabergoline+OHSS (cabergoline+ovarian hyperstimulation syndrome, n=8) received 100 μg/kg oral cabergoline; group aflibercept (12.5 mg/kg)+OHSS (aflibercept+ovarian hyperstimulation syndrome, n=8) received 12.5 mg/kg i.p. aflibercept; and group aflibercept (25 mg/kg)+OHSS (aflibercept+ovarian hyperstimulation syndrome, n=8) received 25 mg/kg i.p. aflibercept. The groups were compared for ovarian weight, immunohistochemical vascular endothelial growth factor expression, spectrophotometric vascular permeability evaluated with methylene blue solution in peritoneal lavage, and body weight growth. RESULTS: Vascular endothelial growth factor immunoexpression was substantially greater in the just OHSS group (22.00±10.20%) than in the aflibercept (12.5 mg/kg)+OHSS (7.87±6.13%) and aflibercept (25 mg/kg)+OHSS (5.63±4.53%) groups (p=0.008 and p=0.005, respectively). Post-hoc tests indicated that cabergoline, 12.5 mg/kg aflibercept, and 25 mg/kg aflibercept decreased vascular permeability compared to the untreated ovarian hyperstimulation syndrome group (p=0.003, p=0.003, and p=0.001, respectively). JOH group had the heaviest ovaries, whereas aflibercept (25 mg/kg)+OHSS group had the lightest. In terms of body weight gain, cabergoline+OHSS group was substantially greater than the aflibercept (12.5 mg/kg)+OHSS and aflibercept (25 mg/kg)+OHSS groups (p=0.006 and p=0.007, respectively). CONCLUSION: Aflibercept, an antiangiogenic medication, decreased ovarian hyperstimulation syndrome by lowering the vascular permeability and vascular endothelial growth factor expression.

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Vascular endothelial growth factor (VEGF) is a key regulator of angiogenesis, a physiological process characterized by the formation of new vessels from a preexisting endothelium. VEGF has also been implicated in pathologic states, such as neoplasias, intraocular neovascular disorders, among other conditions. VEGFs are distributed in seven different families: VEGF-A, B, C, D, and PIGF (placental growth factor), which are identified in mammals; VEGF-E, which are encountered in viruses; and VEGF-F or svVEGF (snake venom VEGF) described in snake venoms. This is the pioneer review of svVEGF family, exploring its distribution among the snake venoms, molecular structure, main functions, and potential applications.

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ABSTRACT Objective: To evaluate the effects of photobiomodulation therapy in redox status, angiogenesis marker - vascular endothelial growth factor - and in the functional recovery in denervated muscle. Methods: A total of 32 female Wistar rats underwent a crush injury and were randomly divided into four groups: Light Emitting Diode Group 2 and Control Group 2 (muscle collected 2 days after injury), and Light Emitting Diode Group 21 and Control Group 21 (muscle collected 21 days afterinjury). Light Emitting Diode Group 2 and Light Emitting Diode Group 21 received two and ten light emitting diode applications (630±20nm, 9J/cm2, 300mW), respectively, and the Control Group 2 and Control Group 21 did not receive any treatment. The function was evaluated by grasping test at four moments (pre-injury, 2, 10 and 21 post-injury days). The flexor digitorum muscle was collected for analysis of immunolocalization of vascular endothelial growth factor and redox parameters. Results: Functional improvement was observed at the second and tenth post-injury day in treated groups compared to control (p<0.005). The muscle tissue of treated groups presented higher immunohistochemical expression of vascular endothelial growth factor. Photobiomodulation therapy decreased the oxidative damage to lipid in Light Emitting Diode Group 2 compared to Control Group 2 (p=0.023) in the denervated muscle. Conclusion: Photobiomodulation therapy accelerated the functional recovery, increased angiogenesis and reduced lipid peroxidation in the denervated muscle at 2 days after injury.

RESUMO Objetivo: Avaliar os efeitos da terapia de fotobiomodulação no estado redox, no marcador de angiogênese - fator de crescimento endotelial vascular - e na recuperação funcional do músculo desnervado. Métodos: Um total de 32 ratas Wistar foi submetido a uma lesão por esmagamento e dividido aleatoriamente em quatro grupos: Grupo Diodo Emissor de Luz 2 e Grupo Controle 2 (músculo coletado 2 dias após a lesão), além do Grupo Diodo Emissor de Luz 21 e do Grupo Controle 21 (músculo coletado 21 dias após a lesão). Grupo Diodo Emissor de Luz 2 e Grupo Diodo Emissor de Luz 21 receberam duas e dez aplicações de diodo emissor de luz (630±20nm, 9J/cm2e 300mW), respectivamente, e Grupo Controle 2 e Grupo Controle 21 não receberam tratamento. A função foi avaliada pelo teste de preensão em quatro momentos (pré-lesão, 2, 10 e 21 dias após a lesão). O músculo flexor dos dedos foi coletado para análise dos parâmetros redox e da imunolocalização do fator de crescimento endotelial vascular. Resultados: Houve melhora funcional no segundo e décimo dia pós-lesão nos grupos tratados em comparação aos controles (p<0,005). O tecido muscular dos grupos tratados apresentou maior expressão imuno-histoquímica do fator de crescimento endotelial vascular. A terapia de fotobiomodulação diminuiu o dano oxidativo aos lipídeos no Grupo Diodo Emissor de Luz 2 comparado ao Grupo Controle 2 (p=0,023) no músculo desnervado. Conclusão: A terapia de fotobiomodulação acelerou a recuperação funcional, aumentou a angiogênese e reduziu a peroxidação lipídica no músculo desnervado 2 dias após a lesão.

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OBJECTIVE: To verify the photobiomodulation effect on angiogenic proteins produced and released by dental human pulpal fibroblasts (HPFs). MATERIAL AND METHODS: HPFs were irradiated with 660-nm low-level laser at fluences of 2.5 J/cm2 and 3.7 J/cm2. The control group was not irradiated. MTT, crystal violet, and ELISA assays respectively verified viability, proliferation, and angiogenic protein (supernatant/lysate) at 6 h, 12 h, and 24 h after photobiomodulation. Capillary-like structure formation assay verified functional role. Two-way ANOVA/Tukey's test and ANOVA/Bonferroni's multiple comparisons test respectively verified cell viability/proliferation and intragroup and intergroup comparisons of protein synthesis (p < 0.05). RESULTS: Irradiated and non-irradiated HPFs showed statistically similar cell viability and proliferation pattern. Intragroup comparisons showed similar patterns of protein synthesis for all groups: VEGF-A, VEGF-C, and vascular endothelial growth factor receptor 1 (VEGFR1) increased significantly in the supernatant, while FGF-2 and VEGF-A increased significantly in the lysate. The lower fluence significantly increased BMP-9 (6 h) in the supernatant and VEGFR1 (6 h and 12 h) and VEGF-D (24 h) in the lysate, while the higher fluence significantly increased BMP-9 (6 h) in the supernatant and VEGFR1 (12 h) in the lysate. Regardless of the time, both fluences statistically downregulated placental growth factor (PLGF) and PDGF secretion. Both fluences statistically decreased VEGF-A secretion (24 h) and PLGF production (6 h). CONCLUSION: Photobiomodulation produced stimulatory effects on angiogenic protein secretion by pulp fibroblasts. In terms of photobiomodulation, over time, both fluences significantly increased the secretion of VEGF-A, VEGF-C, and VEGFR1 and significantly upregulated BMP-9 (6 h) in the supernatant; for capillary-like structure formation, the fluence of 2.5 J/cm2 was better than the fluence of 3.7 J/cm2. CLINICAL RELEVANCE: This study results addressed effective photobiomodulation parameters tailored for pulp angiogenesis.

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This study aimed to compare the synthesis and secretion of VEGF-A, VEGF-C, VEGF-D, VEGFR1, VEGFR2, and FGF-2 between pulp fibroblasts from human primary teeth (HPF) and stem cell from human deciduous teeth (SHED) before and after photobiomodulation. HPF were obtained from explant technique and characterized by immunohistochemistry, while SHED were obtained from digestion technique and characterized by flow cytometry. HPF (control group) and SHED were plated, let to adhere, and put on serum starvation to synchronize the cell cycles prior to photobiomodulation. Then, both cell lineages were irradiated with 660-nm laser according to the following groups: 2.5 and 3.7 J/cm2. MTT and crystal violet assays respectively verified viability and proliferation. ELISA Multiplex Assay assessed the following proteins: VEGF-A, VEGF-C, VEGF-D, VEGFR1, VEGFR2, FGF-2, at 6, 12, and 24 h after photobiomodulation, in supernatant and lysate. Two-way ANOVA/Tukey test evaluated cell viability and proliferation, while angiogenic production and secretion values were analyzed by one-way ANOVA (P < .05). Statistically similar HPF and SHED viability and proliferation patterns occurred before and after photobiomodulation (P > .05). HPF exhibited statistically greater values of all angiogenic proteins than did SHED, at all study periods, except for FGF-2 (supernatant; 12 h); VEGFR1 (lysate; non-irradiated; 12 h); and VEGFR1 (lysate; non-irradiated; 24 h). Photobiomodulation changed the synthesis and secretion of angiogenic proteins by HPF. HPF produced and secreted greater values of all tested angiogenic proteins than did SHED before and after irradiation with both energy densities of 2.5 and 3.7 J/cm2.

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This study evaluated the association of polymorphisms of VEGF (endothelial vascular growth factor) gene + 936C/T (rs3025039), 1154 G/A (rs 1570360) and -2578 C/A (rs 699947) in patients with polycystic ovary syndrome (PCOS) and to perform the haplotypes formed by the alleles in the Brazilian population. A total of 110 women without PCOS and 112 women with PCOS were included in the study. Genotyping analyses were performed using the PCR-RFLP assays (rs 3025039 and rs 699947) and by allelic discrimination using the real-time PCR technique (rs 1570360). In the univariate analysis, we observed a significant difference between the groups for the polymorphism rs 1570360 and this polymorphism presented statistical differences between the groups for the recessive model (p = .04). The frequency of the T-G-C haplotype showed a statistically significant difference between women with PCOS and controls (p = .05). The -2578 A/C polymorphism was more frequent in the control group, which may be associated with a protective characteristic for the PCOS manifestation. In the sample analysis, polymorphism rs 1570360 is associated with PCOS and the T-G-C haplotype could be associated with protective factors.

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ABSTRACT BACKGROUND: Increased angiogenetic activity in inflammatory bowel disease (IBD) has been shown in previous studies. The aim of this study was to evaluate the relationship of serum vascular endothelial growth factor (VEGF) and endostatin levels with clinical features and mucosal expression in patients with ulcerative colitis (UC). DESIGN AND SETTING: Cross-sectional analytical study conducted in a tertiary-level public hospital. METHODS: Serum VEGF and endostatin levels were determined in 82 individuals: 39 with UC, 28 with irritable bowel syndrome (IBS) and 15 healthy controls (HCs), using enzyme-linked immunosorbent assays (ELISA). VEGF and endostatin expressions were studied using immunohistochemistry (IHC). RESULTS: Mean serum VEGF and endostatin levels were significantly higher in patients with UC than in patients with IBS and in HCs (511.9 ± 377.5 pg/ml, 305.0 ± 121.42 pg/ml and 36.1 ± 40.6 pg/ml; P = 0.001 for VEGF; and 155.50 ± 59.8 ng/ml, 116.9 ± 23.8 ng/ml and 102.2 ± 22.4 ng/ml; P < 0.001 for endostatin, respectively). There was a positive correlation between serum VEGF and endostatin levels (r = 0.422; P < 0.01). Mean H-scores for VEGF expression were higher in the active UC group than in the inactive UC and IBS groups, in the stroma, endothelium and epithelium. Mean H-scores for endostatin expression were higher in the active UC group than in the inactive UC and IBS groups, in the stroma and endothelium. There was no endostatin expression in the epithelium. CONCLUSION: Increased endostatin appears to be a defensive reaction to increased VEGF in patients with UC.

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Resumo: Introdução: endometriose é uma doença benigna, capaz de progredir extensamente e gerar clones atípicos. Considerada precursora dos carcinomas de células claras (CCOC) e endometrióide (EOC) de ovário, atualmente chamados carcinomas de ovário associados à endometriose (EAOC). Objetivos: comparar o perfil epidemiológico, a associação com endometriose e a expressão de marcadores imuno-histoquímicos para ARID1A, VEGF, PD-L1 e PARP-1 em mulheres com CCOC e EOC, e sua correlação com a sobrevida livre de progressão (SLP) e sobrevida global (SG). Métodos: estudo de coorte reconstituída, com 50 casos incluídos de CCOC e EOC tratados no CAISM-UNICAMP entre 1995 até 2016, acompanhados até 02/2017. Microarranjos de tecido com amostras de CCOC, EOC e endometriose foram corados com anticorpos monoclonais contra ARID1A, e para os biomarcadores proteicos VEGF, PD-L1, PARP-1 através de imuno-histoquímica. A expressão de ARID1A foi classificada (0 a 100) conforme a porcentagem de células não coradas. A expressão de VEGF, PD-L1 e PARP-1 foi classificada (0 a 300) conforme a multiplicação da porcentagem de células coradas por um fator da intensidade de expressão (ausente=0; fraco=1; moderado=2; forte=3). Idade ao diagnóstico; menopausa; índice de massa corpórea (IMC); CA-125; diagnóstico de endometriose; datas do diagnóstico, da progressão, do óbito e da última consulta foram recuperados dos prontuários. Comparação entre grupos foi realizada através de testes T e de ?2. A SLP (diferença de tempo entre o diagnóstico e a data de progressão) e a SG (diferença de tempo entre o diagnóstico e o óbito ou data da última data de consulta) foi avaliada através de curvas de Kaplan-Meyer e teste de Log-Rank ou regressão de COX. Resultados: 23 mulheres com CCOC (46%), e 27 com EOC (54%) foram incluídas; 80% tinham endometriose associada, 42% eram nulíparas, 42% eram pré-menopausa e CA125 foi elevado em todos estádios (FIGO I-II= média 614.7Ui/mL; FIGO III-IV= media 2361.2Ui/mL). A média de idade ao diagnóstico foi 7 anos menor em mulheres com EOC do que naquelas com CCOC. O CCOC foi mais diagnosticado em estágios iniciais quando associado à endometriose (p=0,03). O prognóstico dos EOC e CCOC em estádios iniciais foi semelhante (p=0,96). Os CCOC não associado à endometriose tiveram menor SG (p=0,04). A expressão de todos os biomarcadores esteve presente nos EAOC e na endometriose. O aumento da expressão de VEGF entre endometriose e câncer foi significativo (p=0,0002). A hiperexpressão de PARP-1 correlacionou-se negativamente com a SLP (p=0,03) e SG (p=0,01) em estádios iniciais. Conclusão: Os CCOC e EOC são comumente diagnosticados em estádios iniciais (FIGO I-II= 68%) e estão frequentemente associados à endometriose (80% dos casos). Quando associados à endometriose, os CCOC foram mais diagnosticados em estádios iniciais e tiveram SG maior. Houve elevada porcentagem de células com ARID1A mutado nos EAOC (>40%). VEGF se expressou mais intensamente nos CCOC e EOC que na endometriose, já a expressão de PD-L1 e de PARP-1 foi similar. Apenas a hiperexpressão de PARP-1 reduziu significativamente a SLP e a SG nos CCOC e EOC nos estádios iniciais(AU)

Abstract: Introduction: Endometriosis is a benign disease, able to progress widely and generate atypical clones. It is a precursor of clear cell ovarian carcinomas (CCOC) and endometrioid ovarian carcinomas (EOCs), now called endometriosis-associated ovarian carcinomas (EAOC). Objectives: To compare the epidemiological profile, association with endometriosis and the expression of immunohistochemical markers for ARID1A, VEGF, PD-L1 and PARP-1 in women with CCOC and EOC, and its correlation with progression-free survival (PFS) and overall survival (OS). Methods: A reconstituted cohort study with 50 cases of CCOC and EOC included. Cases were treated at CAISM-UNICAMP between 1995 and 2016, followed up until 02/2017. Tissue microarrays with CCOC, EOC and endometriosis samples were stained with monoclonal antibodies against ARID1A, and for VEGF, PD-L1, PARP-1 biomarkers by immunohistochemistry. The expression of ARID1A was classified (0 to 100) according to the percentage of unstained cells. The expression of VEGF, PD-L1 and PARP-1 was classified (0 to 300) multiplying the percentage of stained cells by an intensity of expression factor (absent=0, weak=1, moderate=2, strong=3). Age at diagnosis; menopause; BMI (body mass index); CA-125 levels; diagnosis of endometriosis; date of diagnosis, date of progression, date of death and date of last consultation were retrieved from the medical records. Comparison between groups was performed through T and ?2 tests. The PFS (difference in time between diagnosis and progression date) and OS (difference in time between diagnosis and death or the last date of consultation) was assessed using Kaplan-Meyer curves and Log-Rank test or COX multivariate models. Results: twenty-three women with CCOC (46%), and 27 with EOC (54%) were included; 80% had associated endometriosis, 42% were nulliparous, 42% were premenopausal, and CA125 was elevated at all stages (FIGO I-II = mean 614.7Ui / mL; FIGO III-IV = mean 2361.2Ui / mL). The mean age at diagnosis was 7 years lower in women with EOC than in those with CCOC. CCOC when associated with endometriosis were more diagnosed at early stages (p=0.03). The prognosis of EOC and CCOC at early stages was similar (p=0.96). CCOCs not associated with endometriosis had shorter OS (p=0.04). Expression of all biomarkers was present in the EAOC and endometriosis. The increase in VEGF expression between endometriosis and cancer was significant (p=0.0002). The overexpression of PARP-1 correlated negatively with PFS (p=0.03) and OS (p=0.01) at FIGO I-II stages. Conclusion: The diagnosis of women with EOC was made earlier than in those with CCOC. CCOC and EOC are commonly diagnosed in early stages (FIGO I-II - 68%) and were associated with endometriosis (80% of cases). When associated with endometriosis, clear cell carcinomas are more likely diagnosed at early stages, and the association of endometriosis with CCOC improves OS. There was a high percentage of cells with mutated ARID1A gene in EAOC (> 40%). VEGF was expressed more intensely in CCOC and EOC than in endometriosis, whereas expression of PD-L1 and PARP-1 was similar. Only the overexpression of PARP-1 significantly reduced PFS and OS in CCOC and EOC at early stages(AU)

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POEMS syndrome is characterized by Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal protein and Skin changes. We report a woman with the syndrome, who had peripheral polyneuropathy, osteosclerotic myeloma, monoclonal IgA elevation, hypothyroidism, hypogonadotrophic hypogonadism, hyperprolactinemia, adrenal insufficiency, hepatosplenomegaly, lymphadenopathy, thyroid and parotid enlargement, Castleman’s disease, papilledema, stiff and hyperpigmented skin, white nails, clubbing, ascites and chronic diarrhea. She had also a nephropathy characterized by microscopic hematuria, proteinuria, renal insufficiency and a unilateral kidney retraction. She was treated with melphalan and prednisone, achieving remission of the disease and nephropathy. She survived twelve years and died due to a myocardial infarction 20 years after POEMS diagnosis.

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Retinal vein occlusion (RVO) is a common retinal vascular disease classified according to the anatomical location of the occlusion in central (CRVO) or branch (BRVO) retinal vein occlusion. RVO is an important cause of visual loss worldwide and frequently results in visual impairment and ocular complications. Major causes of vision loss in BRVO and CRVO include macular edema (ME), capillary non-perfusion, and neovascularization, causing glaucoma, vitreous hemorrhage and/or tractional retinal detachment.[1-4] Macular edema is the leading cause of decreased central visual acuity in RVO.[5] Recently, there was a paradigm shift in the treatment of ME due to RVO with the advent of new pharmacotherapy treatment strategies and combination therapies. This paper reviews the current thinking and discusses the evidence behind the emerging treatment options for ME following RVO, including laser photocoagulation, intravitreal anti-vascular endothelial growth factor (VEGF), intravitreal corticosteroid-based pharmacotherapies, and surgical management.

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ABSTRACT The worldwide incidence of kidney cancer is estimated at 337,860 new cases per year in the International Agency for Research on Cancer's GLOBOCAN 2012 update, with an estimated 143,369 deaths annually. Over the past 10 years, there have been significant advances in the treatment of advanced/metastatic renal cell carcinoma, including the development of targeted therapies. Currently recommended first-line treatments include sunitinib, temsirolimus, bevacizumab plus interferon, and pazopanib, or high-dose interleukin-2 or sorafenib for selected patients. Recommended second-line treatments include all of the above agents, as well as everolimus and axitinib. Unfortunately, combination therapies have generally resulted in increased toxicity and little improvement in efficacy. Recent studies focused on identification of predictive biomarkers for responses to specific targeted therapies and have not been successful to date. Despite recent advances in targeted treatment for metastatic renal cell carcinoma, important questions regarding biomarkers of efficacy, and optimal combination and sequencing of agents remain to be answered. This paper reviews literature concerned with first-and second-line treatment of metastatic renal cell carcinoma and will discuss key issues in Latin America.

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Macular cystoid edema is one of the major causes of decreased vision after cataract surgery. The inflammatory process appears to be the main causal factor of the edema. The major risk factors are: surgical complications, previous retinal diseases, diabetes, uveitis and use of prostaglandins drops. The diagnosis is clinically, but fluorescein angiography and optical coherence tomography are also important to detect swelling and assist in differential diagnosis. Although pre-operative prophylaxis do not have scientific evidence, it is recommended especially in cases with risk factors. The initial treatment includes a combination of both topic corticosteroid and nonsteroidal anti-inflammatory. Chronic and refractory cases can be managed with alternatives treatment, such as intravitreal triamcinolone and anti-angiogenic. This article aims to discuss various aspects of pseudophakic macular cystoid edema.

O edema macular cistoide é uma das principais causas de baixa de visão após cirurgia de catarata. O processo inflamatório parece ser o principal fator causal do edema. São considerados fatores de risco complicações cirúrgicas, doenças retinianas prévias, diabetes, uveítes e uso de colírios de prostaglandinas. O diagnóstico é feito clinicamente, mas a angiografia fluoresceínica e a tomografia de coerência óptica também são ferramentas importantes para detectar o edema e auxiliar no diagnóstico diferencial. Apesar da profilaxia pré-operatória não ter evidência científica, ela é preconizada especialmente nos casos com fatores de risco. O tratamento inicial é realizado com associação de corticoide e anti-inflamatório não hormonais tópicos. Os casos crônicos e refratários têm diversas alternativas de tratamento, sendo o uso de triancinolona e antiangiogênicos intravítreos as mais utilizadas. Este artigo se propõe a discutir diversos aspectos do edema macular cistoide pseudofácico.

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Objective Evaluate the effects of VEGF165 gene transfer in the process of remodeling of the extracellular matrix after an acute myocardial infarct. Methods Wistar rats were submitted to myocardial infarction, after the ligation of the left descending artery, and the left ventricle ejection fraction was used to classify the infarcts into large and small. The animals were divided into groups of ten, according to the size of infarcted area (large or small), and received or not VEGF165 treatment. Evaluation of different markers was performed using immunohistochemistry and digital quantification. The primary antibodies used in the analysis were anti-fibronectin, anti-vimentin, anti-CD44, anti-E-cadherin, anti-CD24, anti-alpha-1-actin, and anti-PCNA. The results were expressed as mean and standard error, and analyzed by ANOVA, considering statistically significant if p≤0.05. Results There was a significant increase in the expression of undifferentiated cell markers, such as fibronectin (protein present in the extracellular matrix) and CD44 (glycoprotein present in the endothelial cells). However, there was decreased expression of vimentin and PCNA, indicating a possible decrease in the process of cell proliferation after treatment with VEGF165. Markers of differentiated cells, E-cadherin (adhesion protein between myocardial cells), CD24 (protein present in the blood vessels), and alpha-1-actin (specific myocyte marker), showed higher expression in the groups submitted to gene therapy, compared to non-treated group. The value obtained by the relation between alpha-1-actin and vimentin was approximately three times higher in the groups treated with VEGF165, suggesting greater tissue differentiation. Conclusion The results demonstrated the important role of myocytes in the process of tissue remodeling, confirming that VEGF165 seems to provide a protective effect in the treatment of acute myocardial infarct. .

Objetivo Avaliar os efeitos da transferência gênica do VEGF165 no processo de remodelamento da matriz extracelular após infarto agudo do miocárdio. Métodos Ratos Wistar foram submetidos ao infarto do miocárdio por ligação da artéria coronária descendente esquerda, e a fração de ejeção de ventrículo esquerdo foi utilizada para classificar os infartos em grandes e pequenos. Os animais foram divididos em grupos de dez animais, de acordo com o tamanho do infarto (grande ou pequeno), e receberam ou não tratamento com o VEGF165. A avaliação dos diferentes marcadores foi realizada por imuno-histoquímica e quantificação digital. Os anticorpos primários utilizados foram antifibronectina, antivimentina, anti- CD44, anti-E-caderina, anti-CD24, anti-alfa-1-actina e anti-PCNA. Os resultados foram representados como média e erro padrão, e analisados por ANOVA, sendo considerado estatisticamente significativo se p≤0,05. Resultados Houve aumento significativo da expressão de marcadores de células indiferenciadas, como fibronectina (proteína presente na matriz extracelular) e CD44 (glicoproteína presente nas células endoteliais). Entretanto, houve diminuição da expressão de vimentina e PCNA, indicando possível diminuição do processo de proliferação celular após o tratamento com VEGF165. Os marcadores de células diferenciadas, E-caderina (proteína de adesão entre as células do miocárdio), CD24 (proteína presente nos vasos sanguíneos) e alfa-1-actina (marcador especifico de miócitos) também apresentaram maior expressão nos grupos submetidos à terapia gênica, comparativamente com o grupo não tratado. O valor obtido pela relação entre alfa-1-actina e vimentina foi aproximadamente três vezes maior nos grupos tratados com VEGF165, indicando maior diferenciação tecidual. Conclusão O papel dos miócitos se mostrou importante no processo de remodelamento tecidual, confirmando que o VEGF165 parece conferir um efeito protetor no tratamento do infarto agudo do miocárdio. .

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INTRODUCTION: Vascular endothelial growth factor is thought to be an important angiogenic factor involved in tumor growth, progression, and metastasis. OBJECTIVE: The present study evaluated the relation between tissue expression, serum and salivary levels of vascular endothelial growth factor in head and neck squamous cell carcinomas, and their correlation with clinicopathologic features. METHODS: Samples were collected from 30 patients with head and neck squamous cell carcinomas and 24 healthy volunteers. Immunohistochemical analysis was used for tissue expression and enzyme-linked immunosorbent assay was employed to measure serum and salivary levels. RESULTS: No vascular endothelial growth factor staining was observed in normal tissues, whereas vascular endothelial growth factor expression was seen in 6 patients (20%). Mean serum level of VEGF was 83.7±104.47 in patients and 50.04±32.94 in controls. Mean salivary level of vascular endothelial growth factor was 174.41±115.07 in patients and 149.58±101.88 in controls. No significant difference was found by Mann-Whitney test between controls and patients (p=0.411, p=0.944, respectively). No correlation was found between vascular endothelial growth factor tissue expression and its serum and salivary level. CONCLUSION: Overexpression of vascular endothelial growth factor was found in head and neck squamous cell carcinoma patients, suggesting its role in the pathogenesis of head and neck squamous cell carcinoma, but no relation was found between tissue expression, serum levels, and salivary levels of this marker.

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Introduction: Vascular endothelial growth factor is thought to be an important angiogenic factor involved in tumor growth, progression, and metastasis. Objective: The present study evaluated the relation between tissue expression, serum and salivary levels of vascular endothelial growth factor in head and neck squamous cell carcinomas, and their correlation with clinicopathologic features. Methods: Samples were collected from 30 patients with head and neck squamous cell carcinomas and 24 healthy volunteers. Immunohistochemical analysis was used for tissue expression and enzyme-linked immunosorbent assay was employed to measure serum and salivary levels. Results: No vascular endothelial growth factor staining was observed in normal tissues, whereas vascular endothelial growth factor expression was seen in 6 patients (20%). Mean serum level of VEGF was 83.7 ± 104.47 in patients and 50.04 ± 32.94 in controls. Mean salivary level of vascular endothelial growth factor was 174.41 ± 115.07 in patients and 149.58 ± 101.88 in controls. No significant difference was found by Mann-Whitney test between controls and patients (p = 0.411, p = 0.944, respectively). No correlation was found between vascular endothelial growth factor tissue expression and its serum and salivary level. Conclusion: Overexpression of vascular endothelial growth factor was found in head and neck squamous cell carcinoma patients, suggesting its role in the pathogenesis of head and neck squamous cell carcinoma, but no relation was found between tissue expression, serum levels, and salivary levels of this marker. .

Introdução: Acredita-se que o fator de crescimento vascular endotelial (FCEV) seja um importante fator angiogênico envolvido no crescimento, na progressão e na metástase tumoral. Objetivo: O presente estudo avalia a relacão entre a expressão tecidual e os níveis séricos e salivares do FCEV em carcinomas de células escamosas da cabeca e pescoco (CCECPs) e sua correlacão com aspectos clinicopatológicos. Método: Foram coletadas amostras de 30 pacientes com CCECP e de 24 voluntários saudáveis. Utilizamos análise imuno-histoquímica para a expressão tecidual e ELISA para determinação dos níveis séricos e salivares. Resultados: Não foi observada coloração para FCEV nos tecidos normais, enquanto que foi observada expressão de FCEV em seis pacientes (20%). O nível sérico médio de FCEV foi 83,7 ± 104,47 em pacientes e 50,04 ± 32,94 em controles. O nível salivar médio de FCEV foi de 174,41 ± 115,07 em pacientes e 149,58 ± 101,88 em controles. Não foi observada diferenca significativa pelo teste de Mann-Whitney entre controles e pacientes (respectivamente, p = 0,411, p = 0,944). Não foi observada relacão entre a expressão tecidual de FCEV e seus níveis séricos e salivares. Conclusão: A expressão elevada de FCEV foi observada em pacientes com CCECP, e isso sugere seu papel na patogênese de CCECP, mas não foi observada relacão entre a expressão tecidual e os níveis séricos e salivares desse marcador. .

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Background: Prostate cancer (PC) is the second cause of death by cancer in men in Chile. Its behavior is so variable that it is necessary to search reliable prognostic markers. Vascular Endothelial Growth Factor (VEGF) is one of the most powerful pro-angiogenic factors. There is no agreement on its validity as a diagnostic or prognostic factor. Aim: To search for VEFG in prostatic tissue. Material and Methods: This study was performed in prostatectomy tissue coming from 41 patients with PC and 39 patients with benign prostatic hyperplasia (BPH). Specimens were studied using immunohistochemical staining for VEGF. The percentage of stained glandular cells per patient was calculated and associated with pathological diagnosis in cancer patients. Results: PC biopsies had a mean of 82% of VEGF (+) stained cells, while BPH had only 1.6% (p < 0.01). No relationship was found between the percentage of staining and recurrence at one year of follow-up in the case of PC. Conclusions: These results would rule out VEGF as a prognostic factor in this series of patients.

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