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In Mexico strawberry production has great economic importance for the local and export markets as the country is the main strawberry supplier to the United States (SIAP, 2020). In 2022, strawberry plants with yellowing and wilting leaves, root rot and wilting, necrosis of vascular bundles and small fruits symptoms were observed in different commercial fields in the north-central Mexican state of Sinaloa, causing yield losses of about 10%. Typical Fusarium spp. colonies were recovered from all samples. They produced abundant white aerial mycelium with cream to orange pigment and branched septate hyphae (Fig. 1) (Leslie and Summerell, 2006). A total of 18 monosporic isolates were obtained by serial dilutions. The 18 isolates grown for 10 days on carnation leaf agar (CLA) produced hyaline microconidia with 0-2 septa, measuring 9.2 - 15.4 by 4.5 - 6.5 µm (n = 40) and hyaline macroconidia with three septa that measured 28.4 - 53.5 by 4.5 - 9 µm (n = 40). Chlamydospores were not observed. A fragment of the translation elongation factor 1-alpha (EF1-alpha) gene was amplified by polymerase chain reaction (PCR) using the primer pair EF-1/EF-2 (O'Donnell et al. 1998) from two monosporic isolates. The sequences were registered in the NCBI GenBank under accession numbers OR878541 and OR878543 (FRESIN178 and FRESIN194). BLASTn queries of NCBI GenBank identified the sequences as F. falciforme with 98% and 100% similarity to accession numbers OQ262968 and DQ246941 respectively. Fusarium ID database also identified the sequences as F. falciforme, is a member of the F. solani species complex (FSSC). Phylogenetic analysis revealed the partial EF1 sequences grouped with F. falciforme (Fig. 2). A pathogenicity test was performed on thirty strawberry plants (cv. Cabrillo) grown in sterile vermiculite. The plants were inoculated by immersing roots in 20 mL of a conidial suspension (1 × 105 conidia/mL) of isolate FRESIN194. Twelve uninoculated plants served as the control. All plants were grown for 60 days under greenhouse conditions (28 to 35°C). The assay was repeated twice. After 50 days, symptoms of root rot and wilting leaves like those observed in the field were observed. Uninoculated control plants did not develop symptoms. The fungus was reisolated from necrotic tissues of the inoculated plants and identified as F. falciforme by sequencing the EF1-alpha gene and morphological characteristics, completing Koch's postulates. Fusarium falciforme has been reported as the causal agent of root rot, stem rot, and wilt of tomato, papaya, chickpea, onion, common bean, and maize in Mexico (Díaz-Najera et al. 2021, Douriet-Angulo et al. 2021, Felix et al 2022, Tirado-Ramírez et al 2018, Vega-Gutiérrez et al. 2019a, Vega-Gutiérrez et al. 2019b). To our knowledge this is the first report of F. falciforme causing root rot and wilt on strawberry in Sinaloa, Mexico. This result provides useful information for the development and implementation of disease control strategies to mitigate damage caused by F. falciforme.
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Safflower cultivation is of great socioeconomic importance worldwide. Production is intended for the extraction of oil from the seeds. In 2021 Mexico ranked fifth in world production with approximately 52,553.28 tons (SIAP, 2021). In April 2022, in the north-central zone of Sinaloa, Mexico, diseased plants were reported in fields planted with safflower. Symptoms included chlorotic plants, necrosis and rot in vascular bundles, dwarfed plants and reflexed plants bent towards the ground. The disease caused estimated losses of 15% of seed production, with respect to the production obtained from the previous year in the safflower fields surveyed. Twenty-five plants with symptoms were sampled to isolate the pathogen. Plants were cut at the base of the stem near the roots and roots cut into 5 mm2 pieces. Tissue samples were superficially disinfected by immersing in 70% alcohol for 10 sec, 2% sodium hypochlorite for 1 min, washed in sterile water, and placed on potato dextrose agar (PDA) at 28 ºC for 7 days in the dark. Twelve monosporic isolates derived from the PDA culture were morphologically characterized. Abundant white aerial mycelium and small pink to dark violet pigments in the center of the culture were observed. From 10-day-old cultures grown on carnation leaf agar medium microconidia and macroconidia were produced. Microconidia were hyaline, had zero to two septa, and were oval or ellipsoidal, 4.6 to 14 x 1.8 to 4.2 µm (n = 40). The macroconidia were hyaline, were slightly curved with three to five septa, and measured from 26 to 69 x 3 to 6.1 µm (n = 40). No chlamydospores were observed. According to the morphological characteristics, the isolates were identified as Fusarium verticillioides (Leslie and Summerell, 2006). DNA was extracted from one isolate and the Translation Elongation Factor 1-α (EF1) gene was amplified and sequenced (O'Donnell et al. 2010). The sequence obtained from isolate FV3CARCULSIN with 645 base pairs was submitted to NCBI GenBank with accession number OQ262963. The BLAST search revealed 100% similarity with F. verticillioides isolate 13 (KM598773) (Lizárraga et al. 2015). Identification in FUSARIUM ID resulted in a 99.85% similarity with isolate F. verticillioides CBS 131389 (MN534047) (Yilmaz et al. 2021). A phylogenetic tree, made with sequences of the EF1 gene, revealed that FV3CARCULSIN was most closely related to F. verticillioides (100% bootstrap). Pathogenicity tests were carried out on safflower plants (cv. Oleico) grown in sterile vermiculite. Plants were inoculated with a conidial suspension (1 × 105 conidia/ml) obtained from FV3CARCULSIN grown on PDA for 7 days. A total of 45 plants were inoculated by drenching the roots with 20 ml of inoculum when the plants were 20 days old. Fifteen plants served as negative controls without inoculation. Plants were kept for 60 days in greenhouse conditions; however, after 45 days the plants began to die. The assay was conducted twice. Rotting and necrosis was observed in the roots of the plants. The pathogen was reisolated from the tissue of all the plants with symptoms and identified as F. verticillioides using morphological characteristics and EF1 sequences, completing Koch's postulates. No symptoms were observed in control plants after 60 days. This is the first report of root rot in safflower caused by F. verticillioides in Mexico. The fungus has been reported in maize (Figueroa et al. 2010), but it is unknown if it could be the same pathogen of safflower. Identification of the pathogen is important for implementing management methods to reduce yield losses and for additional studies on the impact of the disease on oil quality extracted from safflower seeds.
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Mexico is the fifth largest producer of papaya in the world with an estimated production of 1, 134, 753 metric tons per year (FAOSTAT 2022). In February 2022, in the center zone of Sinaloa State (Mexico), in a seedling-producing greenhouse, papaya seedlings were observed with an incidence (20%) of root and stem rot and necrotic tissue. Symptomatic tissues were collected from 10 papaya plants, which were cut into small pieces and surface sterilized sequentially with 70% alcohol for 20 s and 1% sodium hypochlorite for 2 min, dried, placed on potato dextrose agar (PDA), and incubated at 26°C in darkness for 5 days. Typical Fusarium spp. colonies were obtained from all root samples. Ten pure cultures were obtained by single-spore culturing and morphologically characterized on PDA and carnation leaf agar (CLA) media. On PDA, the colonies produced abundant white aerial mycelium, and the center of old cultures was yellow pigmentation (Leslie and Summerell 2006). From 10-day-old cultures grown on CLA medium, macroconidia were slightly curved, which showed zero to three septa, with some slightly sharp apices, and basal cells with notches, the measurements were from 22.53 to 48.94 x 6.9 to 13.73 µm (n= 50). The microconidia were presented in abundant chains of microconidia. The microconidia presented thin walls, oval and hyaline in shape, forming long chains, measuring 10.4 to 14.25 x 2.4 to 6.8 µm (n= 50). Chlamydospores were not observed. The translation elongation factor 1 alpha (EF1-α) gene (O'Donnell et al. 1998) was amplified by polymerase chain reaction and sequenced from isolate FVTPPYCULSIN (GenBank accession no. OM966892). Maximum likelihood analysis was carried out using the EF1-α sequence (OM966892) and other species from the genus Fusarium. Phylogenetic analysis revealed that the isolate was Fusarium verticillioides (100% bootstrap). Furthermore, the isolate FVTPPYCULSIN was 100 % similar with other reported Fusarium verticillioides sequence (GenBank accession nos. MN657268) (Dharanendra et al. 2019). Pathogenicity tests were performed on 60-day-old papaya plants (cultivar Maradol) grown on autoclaved sandy loam soil mix. Ten plants per isolate (n = 10) were inoculated by drenching with 20 ml of a conidial suspension (1 × 105 CFU/ml) of each isolate per plant. The suspension was obtained by collecting the spores of each isolate grown on PDA with 10 ml of an isotonic saline solution. Ten noninoculated plants served as controls. Plants were maintained for 60 days under greenhouse conditions (25 to 30°C). The assay was conducted twice. Root and stem rot similar to that observed on the infected plants in the greenhouse was observed on the papaya plants. No symptoms were observed on noninoculated control plants after 60 days. The pathogen was reisolated from the necrotic tissue from all inoculated plants and was identified again as Fusarium verticillioides by sequencing the partial EF1-α gene again and based on its morphological characteristics, genetic analysis, and pathogenicity test, fulfilling Koch's postulates. The molecular identification was confirmed via BLAST on the Fusarium ID and Fusarium MLST databases. The isolate FVTPPYCULSIN was deposited in the fungal collection of the Faculty of Agronomy of the Autonomous University of Sinaloa. To our knowledge, this is the first report of root and stem rot of papaya caused by F. verticillioides. Papaya is an important fruit crop in Mexico, and the occurrence of this disease needs to be taken into account in papaya production.
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In this study, the antifungal, biosurfactant and bioemulsifying activity of the lipopeptides produced by the marine bacterium Bacillus subtilis subsp. spizizenii MC6B-22 is presented. The kinetics showed that at 84 h, the highest yield of lipopeptides (556 mg/mL) with antifungal, biosurfactant, bioemulsifying and hemolytic activity was detected, finding a relationship with the sporulation of the bacteria. Based on the hemolytic activity, bio-guided purification methods were used to obtain the lipopeptide. By TLC, HPLC and MALDI-TOF, the mycosubtilin was identified as the main lipopeptide, and it was further confirmed by NRPS gene clusters prediction based on the strain's genome sequence, in addition to other genes related to antimicrobial activity. The lipopeptide showed a broad-spectrum activity against ten phytopathogens of tropical crops at a minimum inhibitory concentration of 400 to 25 µg/mL and with a fungicidal mode of action. In addition, it exhibited that biosurfactant and bioemulsifying activities remain stable over a wide range of salinity and pH and it can emulsify different hydrophobic substrates. These results demonstrate the potential of the MC6B-22 strain as a biocontrol agent for agriculture and its application in bioremediation and other biotechnological fields.
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Strawberry (Fragaria × ananassa) is a fruit of economic importance for Mexico, occupying the third place in world production, with an approximate production of 861, 337 t (SIAP, 2021). In January 2021, in Culiacan, Sinaloa, Mexico (24°46'46â³N; 107°27'04â³ W), wilting symptoms (stunted growth, leaf yellowing and wilting, necrosis in vascular bundles, root rot and wilting) were observed on commercial strawberry crops, with an incidence of 5 to 10 %. Tissue samples from symptomatic roots were cut and disinfected with alcohol, sodium hypochlorite and sterile water, to later be plated on potato dextrose agar (PDA). Fifteen monosporic isolates were obtained by single-spore culturing (Hansen and Smith, 1932). Typical Fusarium spp. colonies were obtained from all root samples. On PDA the colonies were abundant with white aerial mycelium, hyphae were branched and septate, and light-yellow pigmentation was observed in the center of old cultures (Leslie and Summerell 2006). From 10-day-old cultures grown on carnation leaf agar medium, macroconidia were slightly curved, showing three marked septa, broad central cells, slightly tapered apices, foot-shaped basal cells and measured 59.6 - 73.4 (xÌ = 68.7) x 10.4 - 14.9 µm (xÌ = 13.6) (n = 40). The microconidia (n = 40) were thin-walled, hyaline, ovoid unicellular that measured 19.7 - 32.2 (xÌ = 26.6) x 8.8 - 11.8 µm (xÌ = 10.2). The translation elongation factor 1 alpha (EF1-α) gene (O'Donnell et al. 1998) was amplified by polymerase chain reaction and sequenced. Maximum likelihood analysis was carried out using the EF1-α sequence from the isolate FKTFRESCULSIN (GenBank accession no. OK491929) and other Neocosmospora and Fusarium species. Phylogenetic analysis revealed the isolate was Fusarium keratoplasticum (currently named Neocosmospora keratoplastica) belonging to the Fusarium solani species complex (FSSC). Pathogenicity tests were performed on strawberry plants (cultivar Camarosa) grown on autoclaved sandy loam soil mix. Twenty plants were inoculated by drenching with 20 ml of a conidial suspension (1 × 105 CFU/ml) in an isotonic saline solution of FKTFRESCULSIN grown on PDA. Ten uninoculated plants served as controls. Plants were maintained for 60 days under greenhouse conditions (25 to 30°C). The assay was conducted twice. Root and stem rot similar to that observed on the infected plants in the field was observed. No symptoms were observed on uninoculated control plants after 60 days. The pathogen was reisolated from necrotic tissue from all inoculated plants and identified as F. keratoplasticum by sequencing the partial EF1-α gene and based on its morphological characteristics, thus fulfilling Koch's postulates. To our knowledge, this is the first report of root rot and wilt of strawberry caused by F. keratoplasticum in Mexico; it also contributes knowledge to the scientific community, since there is little information about this pathogen causing damage to plants in the world. Strawberry is an important crop in Mexico, and the occurrence of this disease could threaten strawberry production.
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Mango (Mangifera indica L.) is the most economically important fruit in the tropical and subtropical regions of the world. Mexico is ranked the fourth largest mango producer worldwide with an approximate production of 2 396 675 t in 2019 (FAO 2020). Sinaloa is the principal mango production state in Mexico with 410,147 t in 2020 (SIAP 2021). Mango malformation disease (MMD) is one of the main limitations in the production of this crop worldwide, causing serious losses in yield. During December 2017 to April 2018, symptoms of MMD were observed in commercial mango in the municipality of El Rosario (Sinaloa, Mexico). These symptoms included malformed and compacted inflorescences, abnormal development of vegetative shoots with shortened internodes at an incidence of 25 %. Tissue from 15 symptomatic trees were superficially disinfested with 2% sodium hypochlorite and transferred to potato dextrose agar (PDA). Typical Fusarium spp. colonies were obtained from all samples. Fifteen pure cultures were obtained by single spore culturing. White to cream-colored aerial mycelia of typical Fusarium colonies were observed from all samples on PDA (Leslie and Summerell 2006). From 10-day-old cultures grown on carnation leaf agar medium, macroconidia (n = 50) were hyaline, relatively slender with a curve, 4 to 5 septate, and measured 39.5 to 76.8 x 5.7 to 9.5 µm. The microconidia (n = 50) were hyaline and pyriform, without septa, and measured 8.1 to 10.6 x 5.1 to 6.9 µm. Chlamydospores were observed. The EF1-α gene (O'Donnell et al. 1998) was amplified by PCR and sequenced from the isolates. The EF1-α sequence from one representative isolate (128FRSIN) was deposited in GenBank with the accession number MK932806. Maximum likelihood analysis was carried out using the representative EF1-α sequence for F. proliferatum (MK932806) and other Fusarium species. Phylogenetic analysis revealed the isolate most closely related was F. proliferatum (100% bootstrap). The molecular identification was also confirmed via BLAST on the Fusarium ID and Fusarium MLST databases. The pathogenicity tests were carried out on healthy three-month-old mango plants. Twenty plants and five shoots per plant were inoculated with 20 µl of the conidial suspension (1 x 106 conidia/ml) (Freeman et al. 1999). Twenty plants served as noninoculated controls. Plants were maintained for 365 days under greenhouse conditions (25 to 30°C). The assay was conducted twice. Symptoms of multiple vegetative shoots and shortened internodes were observed four months after inoculation on the infected plants with an average disease of 4.5 in the first trial and 4.4 in the second assay according to the disease severity scale outlined by Iqbal et al., (2006). No symptoms were observed on non inoculated control plants after 365 days. One isolate per plant was isolated again from the plants with malformation symptoms (n=20), and identified again as F. proliferatum, by morphological and molecular characteristics. F. proliferatum was identified as the causal agent of MMD in China by Zhan et al. (2010). To our knowledge, this is the first report of F. proliferatum causing MMD in Mexico. The development of management strategies to prevent crop loss is required in this important mango production area.
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Bean (Phaseolus vulgaris) is the second most important crop in Mexico after corn due to high consumption in all regions of the country. Sinaloa state is ranked second in Mexico, producing 140,830 tons in 2020 (SIAP, 2021). In October 2020, wilting symptoms (stunted growth, withered leaves, root rot and wilt) were observed on commercial bean crops in three fields in Culiacan, Sinaloa with an incidence of 3 to 5%. Tissue samples from symptomatic roots were plated on potato dextrose agar (PDA). Typical Fusarium spp. colonies were obtained from all root samples. Three pure cultures were obtained by single-spore culturing. On PDA, the colonies produced abundant white aerial mycelium, and the center of old cultures was light pink with yellow pigmentation (Leslie and Summerell 2006). Macroconidia, from 10-day-old cultures grown on carnation leaf agar, were slightly curved, with three septa, wide central cells, slightly sharp apices, basal foot-shaped cells, measuring 38.5 ï± 2.5 × 5.5 ï± 1.0 µm (n = 40). Microconidia were hyaline, ovoid, unicellular and measured 12.0 ï± 1.5 x 4.8 ï± 0.95 µm (n= 40). Chlamydospores were not observed. The translation elongation factor 1 alpha (EF1-α) gene (O'Donnell et al. 1998) was amplified by polymerase chain reaction and sequenced from isolate FNTL6P7CULSIN (GenBank accession no. OK491917). Maximum likelihood analysis was carried out using the EF1-α sequence (OK491917) and other species from the genus Fusarium. Phylogenetic analysis revealed the isolate was F. nygamai (100% bootstrap). Moreover, isolate FNTL6P7CULSIN was 99.7% (648 bp/649bp), and 99.9 % (648bp/650bp) similar, respectively, with other reported F. nygamai sequences (GenBank accession no. OL415419 and KR612341). Pathogenicity tests were performed on 20-day-old bean plants (cultivar Mayocoba) grown on autoclaved sandy loam soil mix. Twenty plants were inoculated by drenching with 20 ml of a conidial suspension (1 × 105 CFU/ml) in an isotonic saline solution of FNTL6P7CULSIN grown on PDA. Ten uninoculated plants served as controls. Plants were maintained for 60 days under greenhouse conditions (25 to 30°C). The assay was conducted twice. Root and stem rot similar to that observed on the infected plants in the field was observed. No symptoms were observed on uninoculated control plants after 60 days. The pathogen was reisolated from necrotic tissue from all inoculated plants and identified as F. nygamai by sequencing the partial EF1-α gene and based on its morphological characteristics, thus fulfilling Koch's postulates. Fusarium nygamai was associated with Fusarium foot rot of rice in Sardinia by Balmas et al., (2000). Also, this pathogen was reported by Leyva (2015) causing root rot in Maize in Sinaloa, Mexico. To our knowledge, this is the first report of root rot and wilt of bean caused by F. nygamai in Mexico. Bean is an important crop in Mexico, and the occurrence of this disease could threaten bean production.
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Fusarium wilt is one of the main limiting factors for tomato production in Mexico. One thousand and fifty isolates were obtained from vascular tissues tomato plants showing wilt and yellowing symptoms in Sinaloa, Mexico. The pathogenic isolates were evaluated through phylogenetic analysis of the TEF-1α gene and ITS region, morphological markers and pathogenicity tests. Within the 15 pathogenic Fusarium isolates, 7 were identified as F. oxysporum and 8 as F. falciforme. Phylogenetic analysis of Fusarium oxysporum f. sp. lycopersici and Fusarium falciforme isolates confirmed that both populations are constituted by distinct phylogenetic lineages. The isolates showed differences in aggressiveness; F. falciforme was the most aggressive. Isolates of both complexes triggered similar aerial symptoms of yellowing and darkening of the vascular tissues in tomato plants. But only F. falciforme isolates triggered necrosis in the plant crowns. Morphological markers allowed differentiating isolates from distinct complexes but not differentiating between lineages.
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BACKGROUND: Cardiac hypertrophy is characterized by alterations in both cardiac bioenergetics and insulin sensitivity. Insulin promotes glucose uptake by cardiomyocytes and its use as a substrate for glycolysis and mitochondrial oxidation in order to maintain the high cardiac energy demands. Insulin stimulates Ca(2+) release from the endoplasmic reticulum, however, how this translates to changes in mitochondrial metabolism in either healthy or hypertrophic cardiomyocytes is not fully understood. RESULTS: In the present study we investigated insulin-dependent mitochondrial Ca(2+) signaling in normal and norepinephrine or insulin like growth factor-1-induced hypertrophic cardiomyocytes. Using mitochondrion-selective Ca(2+)-fluorescent probes we showed that insulin increases mitochondrial Ca(2+) levels. This signal was inhibited by the pharmacological blockade of either the inositol 1,4,5-triphosphate receptor or the mitochondrial Ca(2+) uniporter, as well as by siRNA-dependent mitochondrial Ca(2+) uniporter knockdown. Norepinephrine-stimulated cardiomyocytes showed a significant decrease in endoplasmic reticulum-mitochondrial contacts compared to either control or insulin like growth factor-1-stimulated cells. This resulted in a reduction in mitochondrial Ca(2+) uptake, Akt activation, glucose uptake and oxygen consumption in response to insulin. Blocking mitochondrial Ca(2+) uptake was sufficient to mimic the effect of norepinephrine-induced cardiomyocyte hypertrophy on insulin signaling. CONCLUSIONS: Mitochondrial Ca(2+) uptake is a key event in insulin signaling and metabolism in cardiomyocytes.
Assuntos
Cálcio/metabolismo , Cardiomegalia/metabolismo , Insulina/metabolismo , Mitocôndrias Cardíacas/metabolismo , Miócitos Cardíacos/metabolismo , Animais , Animais Recém-Nascidos , Sinalização do Cálcio , Retículo Endoplasmático/metabolismo , Glucose/metabolismo , Receptores de Inositol 1,4,5-Trifosfato/metabolismo , Consumo de Oxigênio , Ratos Sprague-Dawley , Transdução de SinaisRESUMO
Cardiomyocyte hypertrophy has been associated with diminished mitochondrial metabolism. Mitochondria are crucial organelles for the production of ATP, and their morphology and function are regulated by the dynamic processes of fusion and fission. The relationship between mitochondrial dynamics and cardiomyocyte hypertrophy is still poorly understood. Here, we show that treatment of cultured neonatal rat cardiomyocytes with the hypertrophic agonist norepinephrine promotes mitochondrial fission (characterized by a decrease in mitochondrial mean volume and an increase in the relative number of mitochondria per cell) and a decrease in mitochondrial function. We demonstrate that norepinephrine acts through α1-adrenergic receptors to increase cytoplasmic Ca(2+), activating calcineurin and promoting migration of the fission protein Drp1 (encoded by Dnml1) to mitochondria. Dominant-negative Drp1 (K38A) not only prevented mitochondrial fission, it also blocked hypertrophic growth of cardiomyocytes in response to norepinephrine. Remarkably, an antisense adenovirus against the fusion protein Mfn2 (AsMfn2) was sufficient to increase mitochondrial fission and stimulate a hypertrophic response without agonist treatment. Collectively, these results demonstrate the importance of mitochondrial dynamics in the development of cardiomyocyte hypertrophy and metabolic remodeling.
Assuntos
Calcineurina/metabolismo , Mitocôndrias Cardíacas/fisiologia , Dinâmica Mitocondrial , Miócitos Cardíacos/fisiologia , Agonistas alfa-Adrenérgicos/farmacologia , Animais , Cálcio/metabolismo , Sinalização do Cálcio , Cardiomegalia/metabolismo , Células Cultivadas , Dinaminas/genética , Dinaminas/metabolismo , GTP Fosfo-Hidrolases , Hipertrofia/metabolismo , Proteínas de Membrana/metabolismo , Proteínas Mitocondriais/metabolismo , Norepinefrina/farmacologia , Transporte Proteico , Ratos Sprague-Dawley , Receptores Adrenérgicos alfa 1/metabolismoRESUMO
El feocromocitoma es un tumor que produce catecolaminas,mayor responsable de la hipertensión arterial en jóvenes,con mayor frecuencia se localiza en la medula suprarrenal, unilateral.Generalmente asociado con neoplasia endócrina múltiple.Los pacientes presentan una serie de síntomas, entre ellosla hipertensión arterial.Se presenta el caso de una paciente de 31 años, con doloren hipocondrio derecho de un año de evolución, tipo pesadezy pérdida de peso de 3 kg. Al examen físico se constató tumoraciónen hipocondrio derecho que llega a epigastrio, de 12cm de diámetro. Con el diagnóstico de tumor retroperitonealobtenido por imágenes se decide una laparotomía exploradoradonde se visualizó un tumor de 18cm. de diámetro, sólido, enpolo superior del riñón derecho, adherido a vena cava. Se realizóuna exéresis tumoral y el informe de anatomía patológicaconfirmó feocromocitoma
Assuntos
Catecolaminas , Medula Suprarrenal , Neoplasia Endócrina MúltiplaRESUMO
Differentiation of vascular smooth muscle cells (VSMC) is an essential process of vascular development. VSMC have biosynthetic, proliferative, and contractile roles in the vessel wall. Alterations in the differentiated state of the VSMC play a critical role in the pathogenesis of atherosclerosis and intimal hyperplasia, as well as in a variety of other human diseases, including hypertension, asthma, atherosclerosis and vascular aneurysm. This review provides an overview of the current state of knowledge of molecular mechanisms involved in controlling VSMC proliferation, with particular focus on glucose metabolism and its relationship with mitochondrial bioenergetics. Increased levels of glucose transporter 1 (GLUT1) are observed in VSMC after endothelial injury, suggesting a relationship between glucose uptake and VSMC proliferation. Mitochondrial dysfunction is a common feature in VSMC during atherosclerosis. Alterations in mitochondrial function can be produced by dysregulation of mitofusin-2, a small GTPase associated with mitochondrial fusion. Moreover, exacerbated proliferation was observed in VSMC from pulmonary arteries with hyperpolarized mitochondria and enhanced glycolysis/glucose oxidation ratio. Several lines of evidence highlight the relevance of glucose metabolism in the control of VSMC proliferation, indicating a new area to be explored in the control of vascular pathogenesis.
Assuntos
Aterosclerose/metabolismo , Proliferação de Células , Glucose/metabolismo , Mitocôndrias Musculares/metabolismo , Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso/metabolismo , Proteínas Quinases Ativadas por AMP/metabolismo , Animais , Aterosclerose/patologia , Metabolismo Energético , Humanos , Hiperplasia , Insulina/metabolismo , Fator de Crescimento Insulin-Like I/metabolismo , Músculo Liso Vascular/patologia , Miócitos de Músculo Liso/patologia , Estresse Oxidativo , Transdução de Sinais , Serina-Treonina Quinases TOR/metabolismoRESUMO
Introducción: El tumor sólido pseudopapilar del páncreases un tumor epitelial de baja malignidad que afecta a mujeresjóvenes y corresponde de 1 a 2 % de todas las neoplasias delpáncreas. Se reporta el caso de una mujer, 20 años, con 1 año deevolución de dolor en hipocondrio izquierdo con anemia leve.La ecografía abdominal mostró una tumoración en hemiabdomenizquierdo correspondiente a una masa mixta en páncreas. Serealizó pancreatectomía distal y esplenectomía. La anatomía patológicareportó neoplasia epitelial sólida y pseudopapilar de 13cm del cuerpo y cola del páncreas, sin compromiso esplénico.Conclusión: El tumor sólido pseudopapilar del páncreas esuna neoplasia de etiología desconocida más frecuente en mujeresjóvenes, que debe formar parte de los diagnósticos diferencialesante un tumor en páncreas. La cirugía por sí sola tiene unnivel de curación excelente
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Carcinoma , Esplenectomia , PancreatectomiaRESUMO
La ingestión de cuerpos extraños es un problema frecuenteen la infancia pero puede presentarse a otras edades; 80-90% delos mismos progresan espontáneamente y son expulsados y sólo1% requiere de intervención quirúrgica para su extracción. Sepresenta el caso de un paciente con un cuadro de abdomen agudoquirúrgico por perforación del colon sigmoides, secundaria ala ingestión involuntaria de hueso de pollo, se realizó laparotomía,extracción del hueso, sigmoidectomia y colostomía iliaca
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Abdome Agudo , Cirurgia Geral , Dor AbdominalRESUMO
The process of muscle remodeling lies at the core of most cardiovascular diseases. Cardiac adaptation to pressure or volume overload is associated with a complex molecular change in cardiomyocytes which leads to anatomic remodeling of the heart muscle. Although adaptive at its beginnings, the sustained cardiac hypertrophic remodeling almost unavoidably ends in progressive muscle dysfunction, heart failure and ultimately death. One of the features of cardiac remodeling is a progressive impairment in mitochondrial function. The heart has the highest oxygen uptake in the human body and accordingly it has a large number of mitochondria, which form a complex network under constant remodeling in order to sustain the high metabolic rate of cardiac cells and serve as Ca(2+) buffers acting together with the endoplasmic reticulum (ER). However, this high dependence on mitochondrial metabolism has its costs: when oxygen supply is threatened, high leak of electrons from the electron transport chain leads to oxidative stress and mitochondrial failure. These three aspects of mitochondrial function (Reactive oxygen species signaling, Ca(2+) handling and mitochondrial dynamics) are critical for normal muscle homeostasis. In this article, we will review the latest evidence linking mitochondrial morphology and function with the process of myocardial remodeling and cardiovascular disease.
Assuntos
Doenças Cardiovasculares/metabolismo , Mitocôndrias Cardíacas/metabolismo , Remodelação Ventricular , Cálcio/metabolismo , Humanos , Estresse OxidativoRESUMO
Endoplasmic reticulum (ER) stress activates an adaptive unfolded protein response (UPR) that facilitates cellular repair, however, under prolonged ER stress, the UPR can ultimately trigger apoptosis thereby terminating damaged cells. The molecular mechanisms responsible for execution of the cell death program are relatively well characterized, but the metabolic events taking place during the adaptive phase of ER stress remain largely undefined. Here we discuss emerging evidence regarding the metabolic changes that occur during the onset of ER stress and how ER influences mitochondrial function through mechanisms involving calcium transfer, thereby facilitating cellular adaptation. Finally, we highlight how dysregulation of ER-mitochondrial calcium homeostasis during prolonged ER stress is emerging as a novel mechanism implicated in the onset of metabolic disorders.