Systemically administered wound-homing peptide accelerates wound healing by modulating syndecan-4 function.

CAR (CARSKNKDC) is a wound-homing peptide that recognises angiogenic neovessels. Here we discover that systemically administered CAR peptide has inherent ability to promote wound healing: wounds close and re-epithelialise faster in CAR-treated male mice. CAR promotes keratinocyte migration in vitro. The heparan sulfate proteoglycan syndecan-4 regulates cell migration and is crucial for wound healing. We report that syndecan-4 expression is restricted to epidermis and blood vessels in mice skin wounds. Syndecan-4 regulates binding and internalisation of CAR peptide and CAR-mediated cytoskeletal remodelling. CAR induces syndecan-4-dependent activation of the small GTPase ARF6, via the guanine nucleotide exchange factor cytohesin-2, and promotes syndecan-4-, ARF6- and Cytohesin-2-mediated keratinocyte migration. Finally, we show that genetic ablation of syndecan-4 in male mice eliminates CAR-induced wound re-epithelialisation following systemic administration. We propose that CAR peptide activates syndecan-4 functions to selectively promote re-epithelialisation. Thus, CAR peptide provides a therapeutic approach to enhance wound healing in mice; systemic, yet target organ- and cell-specific.

CSK-mediated signalling by integrins in cancer.

Cancer progression and metastasis are processes heavily controlled by the integrin receptor family. Integrins are cell adhesion molecules that constitute the central components of mechanosensing complexes called focal adhesions, which connect the extracellular environment with the cell interior. Focal adhesions act as key players in cancer progression by regulating biological processes, such as cell migration, invasion, proliferation, and survival. Src family kinases (SFKs) can interplay with integrins and their downstream effectors. SFKs also integrate extracellular cues sensed by integrins and growth factor receptors (GFR), transducing them to coordinate metastasis and cell survival in cancer. The non-receptor tyrosine kinase CSK is a well-known SFK member that suppresses SFK activity by phosphorylating its specific negative regulatory loop (C-terminal Y527 residue). Consequently, CSK may play a pivotal role in tumour progression and suppression by inhibiting SFK oncogenic effects in several cancer types. Remarkably, CSK can localise near focal adhesions when SFKs are activated and even interact with focal adhesion components, such as phosphorylated FAK and Paxillin, among others, suggesting that CSK may regulate focal adhesion dynamics and structure. Even though SFK oncogenic signalling has been extensively described before, the specific role of CSK and its crosstalk with integrins in cancer progression, for example, in mechanosensing, remain veiled. Here, we review how CSK, by regulating SFKs, can regulate integrin signalling, and focus on recent discoveries of mechanotransduction. We additionally examine the cross talk of integrins and GFR as well as the membrane availability of these receptors in cancer. We also explore new pharmaceutical approaches to these signalling pathways and analyse them as future therapeutic targets.

Cooperative signaling between integrins and growth factor receptors in fibrosis.

Fibrosis is a pathological process characterized by accumulation of fibrous connective tissue in organs, leading to organ malfunction and failure. At the cellular level, tissue injury or cellular stress results in aberrant and/or sustained fibroblast "activation" leading to excessive extracellular matrix (ECM) accumulation and remodeling, as well as abnormal crosstalk with other cell types. Fibroblast functions within the fibrotic milieu are broad and complex, but among the most prominent are regulation of tissue architecture via modulation of ECM deposition and synthesis, and production of, activation of, and response to growth factors. Thus, both integrins and growth factor receptors (GFRs) play critical roles in fibroblast orchestration of tissue remodeling. However, the interplay between integrins and GFRs in this context is not fully understood. Their interaction has been described for other diseases, such as cancer. Here, we review the literature relevant to integrin/GFR interactions in the context of fibrosis, classify the known interactions into broad categories, and discuss research opportunities that may yield novel therapeutic targets for a broad range of debilitating chronic diseases.

Syndecan-4/PAR-3 signaling regulates focal adhesion dynamics in mesenchymal cells.

BACKGROUND: Syndecans regulate cell migration thus having key roles in scarring and wound healing processes. Our previous results have shown that Thy-1/CD90 can engage both αvß3 integrin and Syndecan-4 expressed on the surface of astrocytes to induce cell migration. Despite a well-described role of Syndecan-4 during cell movement, information is scarce regarding specific Syndecan-4 partners involved in Thy-1/CD90-stimulated cell migration. METHODS: Mass spectrometry (MS) analysis of complexes precipitated with the Syndecan-4 cytoplasmic tail peptide was used to identify potential Syndecan-4-binding partners. The interactions found by MS were validated by immunoprecipitation and proximity ligation assays. The conducted research employed an array of genetic, biochemical and pharmacological approaches, including: PAR-3, Syndecan-4 and Tiam1 silencing, active Rac1 GEFs affinity precipitation, and video microscopy. RESULTS: We identified PAR-3 as a Syndecan-4-binding protein. Its interaction depended on the carboxy-terminal EFYA sequence present on Syndecan-4. In astrocytes where PAR-3 expression was reduced, Thy-1-induced cell migration and focal adhesion disassembly was impaired. This effect was associated with a sustained Focal Adhesion Kinase activation in the siRNA-PAR-3 treated cells. Our data also show that Thy-1/CD90 activates Tiam1, a PAR-3 effector. Additionally, we found that after Syndecan-4 silencing, Tiam1 activation was decreased and it was no longer recruited to the membrane. Syndecan-4/PAR-3 interaction and the alteration in focal adhesion dynamics were validated in mouse embryonic fibroblast (MEF) cells, thereby identifying this novel Syndecan-4/PAR-3 signaling complex as a general mechanism for mesenchymal cell migration involved in Thy-1/CD90 stimulation. CONCLUSIONS: The newly identified Syndecan-4/PAR-3 signaling complex participates in Thy-1/CD90-induced focal adhesion disassembly in mesenchymal cells. The mechanism involves focal adhesion kinase dephosphorylation and Tiam1 activation downstream of Syndecan-4/PAR-3 signaling complex formation. Additionally, PAR-3 is defined here as a novel adhesome-associated component with an essential role in focal adhesion disassembly during polarized cell migration. These novel findings uncover signaling mechanisms regulating cell migration, thereby opening up new avenues for future research on Syndecan-4/PAR-3 signaling in processes such as wound healing and scarring.

Anti-neoplastic drugs increase caveolin-1-dependent migration, invasion and metastasis of cancer cells.

Expression of the scaffolding protein Caveolin-1 (CAV1) enhances migration and invasion of metastatic cancer cells. Yet, CAV1 also functions as a tumor suppressor in early stages of cancer, where expression is suppressed by epigenetic mechanisms. Thus, we sought to identify stimuli/mechanisms that revert epigenetic CAV1 silencing in cancer cells and evaluate how this affects their metastatic potential. We reasoned that restricted tissue availability of anti-neoplastic drugs during chemotherapy might expose cancer cells to sub-therapeutic concentrations, which activate signaling pathways and the expression of CAV1 to favor the acquisition of more aggressive traits. Here, we used in vitro [2D, invasion] and in vivo (metastasis) assays, as well as genetic and biochemical approaches to address this question. Colon and breast cancer cells were identified where CAV1 levels were low due to epigenetic suppression and could be reverted by treatment with the methyltransferase inhibitor 5'-azacytidine. Exposure of these cells to anti-neoplastic drugs for short periods of time (24-48 h) increased CAV1 expression through ROS production and MEK/ERK activation. In colon cancer cells, increased CAV1 expression enhanced migration and invasion in vitro via pathways requiring Src-family kinases, as well as Rac-1 activity. Finally, elevated CAV1 expression in colon cancer cells following exposure in vitro to sub-cytotoxic drug concentrations increased their metastatic potential in vivo. Therefore exposure of cancer cells to anti-neoplastic drugs at non-lethal drug concentrations induces signaling events and changes in transcription that favor CAV1-dependent migration, invasion and metastasis. Importantly, this may occur in the absence of selection for drug-resistance.

Common Bean Leaves as a Source of Dietary Iron: Functional Test in an Iron-Deficient Rat Model.

Recent findings made by our group indicate that the iron content in Phaseolus vulgaris leaves is at least four times greater than in grains therefore, we evaluated the effect of supplementation with bean leaf (iron content of 275 mg/kg on a dry basis) in iron-deficient rats. Anemia was induced by feeding rats with an iron-deficient diet (IDD) for 11 days and iron-recovery diets were subsequently tested for 14 days using a normal diet, a 10 % bean leaf-supplemented IDD (BLSD) or a ferrous sulfate-supplemented IDD. Decreased levels of leukocytes (64 %), erythrocytes (30 %), lymphocytes (62 %), granulocytes (72 %), hematocrit (34 %), hemoglobin (35 %), and ferritin (34 %) were observed in the iron-deficient rats compared to the control rats. BLSD supplementation showed the highest recovery values relative to those recorded for control rats: leukocytes (40 %), erythrocytes (24 %), lymphocytes (33 %), granulocytes (88 %), hematocrit (17 %), and hemoglobin (18 %), suggesting that common bean leaves could be a good source of bioavailable iron with possible immunomodulatory effects.

Cooked common beans (Phaseolus vulgaris L.) modulate renal genes in streptozotocin-induced diabetic rats.

Food consumption with different bioactive compounds could reduce the risk of diabetic complications. This study was designed to evaluate the effect of cooked common beans on differentially expressed genes in whole kidney homogenates of streptozotocin-induced diabetic rats. After 4weeks of treatment with a cooked bean supplemented (10%) diet, animals fed with Flor de Mayo bean (FMB) exerted the greatest protective effect, since they presented the lowest blood glucose levels, consistent with an increase in blood insulin levels, a decrease in urine albumin and urea levels and an increase in creatinine clearance (P≤.05). Regarding the gene expression of kidneys evaluated using expressed sequence tag, consumption of cooked beans improved the expression of Glu1, Cps1, Ipmk, Cacna1c, Camk1, Pdhb, Ptbp3 and Pim1, which are related to the elimination of ammonium groups, the regulation of inflammatory and oxidative response, as well as cell signaling and apoptosis. In addition, the beneficial effects observed were not related to their polyphenolic and saponin profile, suggesting the activity of other bioactive compounds or the synergistic interaction of these compounds. These results suggest that the consumption of cooked common beans (FMB) might be used as an alternative for the regulation of genes related to renal alterations.

Cooked common beans (Phaseolus vulgaris) protect against ß-cell damage in streptozotocin-induced diabetic rats.

Diabetes is a disease characterized by a hyperglycemic stage that leads to a chronic inflammatory state. We evaluated the in vivo effect of a diet supplemented with 25 % cooked black bean cultivar Negro 8025 (N8025) flour in streptozotocin-induced diabetic rats. The effect was assessed before (preventive-treatment) and after (treatment) the onset of diabetes. There is a significant decrease of total phenolic, tannins and anthocyanins content after cooking, and the concentration of most of the single phenols analyzed are only slightly decreased. The treatment group showed a significant reduction of glucose (22.8 %), triglycerides (21.9 %), total cholesterol (29.9 %) and LDL (56.1 %) that correlates with a protection of pancreatic ß-cells. The diet with N8025 flour before the induction of diabetes did not exert a protective effect (glucose levels are similar to the diabetic control) but they have low levels of total cholesterol (47.5 %) and LDL (56.1 %). The preventive-treatment group did not inhibit the increase of TNF-α and IL-1ß, whereas the treatment group did, compared to the diabetic control. Therefore, N8025 bean supplementation can be recommended to control diabetes.

Astrocytic αVß3 integrin inhibits neurite outgrowth and promotes retraction of neuronal processes by clustering Thy-1.

Thy-1 is a membrane glycoprotein suggested to stabilize or inhibit growth of neuronal processes. However, its precise function has remained obscure, because its endogenous ligand is unknown. We previously showed that Thy-1 binds directly to α(V)ß(3) integrin in trans eliciting responses in astrocytes. Nonetheless, whether α(V)ß(3) integrin might also serve as a Thy-1-ligand triggering a neuronal response has not been explored. Thus, utilizing primary neurons and a neuron-derived cell line CAD, Thy-1-mediated effects of α(V)ß(3) integrin on growth and retraction of neuronal processes were tested. In astrocyte-neuron co-cultures, endogenous α(V)ß(3) integrin restricted neurite outgrowth. Likewise, α(V)ß(3)-Fc was sufficient to suppress neurite extension in Thy-1(+), but not in Thy-1(-) CAD cells. In differentiating primary neurons exposed to α(V)ß(3)-Fc, fewer and shorter dendrites were detected. This effect was abolished by cleavage of Thy-1 from the neuronal surface using phosphoinositide-specific phospholipase C (PI-PLC). Moreover, α(V)ß(3)-Fc also induced retraction of already extended Thy-1(+)-axon-like neurites in differentiated CAD cells as well as of axonal terminals in differentiated primary neurons. Axonal retraction occurred when redistribution and clustering of Thy-1 molecules in the plasma membrane was induced by α(V)ß(3) integrin. Binding of α(V)ß(3)-Fc was detected in Thy-1 clusters during axon retraction of primary neurons. Moreover, α(V)ß(3)-Fc-induced Thy-1 clustering correlated in time and space with redistribution and inactivation of Src kinase. Thus, our data indicates that α(V)ß(3) integrin is a ligand for Thy-1 that upon binding not only restricts the growth of neurites, but also induces retraction of already existing processes by inducing Thy-1 clustering. We propose that these events participate in bi-directional astrocyte-neuron communication relevant to axonal repair after neuronal damage.

Chemical evaluation, antioxidant capacity, and consumer acceptance of several oak infusions.

As part of an ongoing screening on natural products, 4 oak leaves were analyzed as potential nutraceutical beverages. The phenolic composition, antioxidant capacity, and sensory preferences of leaves infusions from Quercus resinosa, Q. sideroxyla, Q. eduadii, and Q. durifolia in comparison with 2 commercial green teas were investigated. Herbal infusions from oak leaves and Green teas (1%, 80 °C, 10 min) were evaluated for total polyphenol content (TPC), total flavonoid content (TFC), HPLC analysis, trolox equivalent antioxidant capacity (TEAC), oxygen radical absorbance capacity (ORAC), soluble solids, pH, color, and consumer preference analysis. Q. resinosa leaves infusions have shown the highest TPC, TEAC, and ORAC values but they have attained the lowest preference score. Quercus leaves infusions with higher content of gallic acid and catechins showed best antioxidant capacity but lower consumer preference.

Inhibition of cyclin-dependent kinase 5 but not of glycogen synthase kinase 3-ß prevents neurite retraction and tau hyperphosphorylation caused by secretable products of human T-cell leukemia virus type I-infected lymphocytes.

Human T-cell leukemia virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a neurodegenerative disease characterized by selective loss of axons and myelin in the corticospinal tracts. This central axonopathy may originate from the impairment of anterograde axoplasmic transport. Previous work showed tau hyperphosphorylation at T(181) in cerebrospinal fluid of HAM/TSP patients. Similar hyperphosphorylation occurs in SH-SY5Y cells incubated with supernatant from MT-2 cells (HTLV-I-infected lymphocytes secreting viral proteins, including Tax) that produce neurite shortening. Tau phosphorylation at T(181) is attributable to glycogen synthase kinase 3-ß (GSK3-ß) and cyclin-dependent kinase 5 (CDK5) activation. Here we investigate whether neurite retraction in the SH-SY5Y model associates with concurrent changes in other tau hyperphosphorylable residues. Threonine 181 turned out to be the only tau hyperphosphorylated residue. We also evaluate the role of GSK3-ß and CDK5 in this process by using specific kinase inhibitors (LiCl, TDZD-8, and roscovitine). Changes in both GSK3-ß active and inactive forms were followed by measuring the regulatory phosphorylable sites (S(9) and Y(216) , inactivating and activating phosphorylation, respectively) together with changes in ß-catenin protein levels. Our results showed that LiCl and TDZD-8 were unable to prevent MT-2 supernatant-mediated neurite retraction and also that neither Y(216) nor S(9) phosphorylations were changed in GSK3-ß. Thus, GSK3-ß seems not to play a role in T(181) hyperphosphorylation. On the other hand, the CDK5 involvement in tau phosphorylation was confirmed by both the increase in its enzymatic activity and the absence of MT-2 neurite retraction in the presence of roscovitine or CDK5 siRNA transfection.

Non-digestible fraction of cooked bean (Phaseolus vulgaris L.) cultivar Bayo Madero suppresses colonic aberrant crypt foci in azoxymethane-induced rats.

The non-digestible fraction (NDF) of common bean (Phaseolus vulgaris L.) cultivar Bayo Madero was evaluated for its chemopreventive effect on azoxymethane (AOM) induced aberrant crypt foci (ACF) in rats. Diets containing cooked beans (CB) or its non-digestible fraction (NDF) were fed to 72 male rats after 2 azoxymethane injections (15 mg kg(-1) of body weight once a week for 2 weeks). ACF number, short chain fatty acids (SCFA) and ß-glucuronidase activity were measured in colon sections from rats sacrificed 7 weeks after the last AOM injection. Food intake and weight gain of rats were unaffected by CB and NDF. CB and NDF suppressed the AOM-induced formation of ACF (0.8 and 1.5 ACF/distal zone, respectively vs. 6.6 ACF/distal zone based on methylene blue stain) and lowered ß-glucuronidase activity in cecal, colonic and fecal content compared to AOM group. SCFA production was not significantly different among fecal, cecal and colonic content. These results indicate that CB and NDF from Bayo Madero provide direct chemoprotection against early stage of azoxymethane (AOM)-induced colon cancer in rats.

Comparative study of CSF neurofilaments in HTLV-1-associated myelopathy/tropical spastic paraparesis and other neurological disorders.

HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a progressive CNS disease leading to corticospinal tract degeneration. Various degenerative diseases have increased neurofilament subunit concentration in cerebrospinal fluid (CSF), frequently showing hyperphosphorylation in neurofilaments. The aim of this study was to determine if there were elevated concentrations of neurofilament light subunit (NFL) and phosphorylated forms of neurofilament heavy subunit (PNFH) in HAM/TSP CSF. NF concentrations were compared with those of controls and patients with neurodegenerative diseases associated with other retroviruses (HIV-associated dementia, HAD) and a form of prion disease (familiar Creutzfeldt-Jakob, FCJD). Western blotting of CSF with antibodies against NFL showed two immunoreactive bands of 66 and 59 kDa, the latter probably corresponding to a partially degraded NFL form. The concentration of the 59-kDa form was not different in HAM/TSP compared with controls, but it was significantly increased in HAD and FCJD groups. ELISA assay for PNFH did not show differences among HAM/TSP, HAD, and control groups, while PNFH concentration was significantly elevated in FCJD. Our results show that CSF NFL and PNFH are not molecular markers of axonal damage for HAM/TSP probably due to the slow progression of this disease. NFL phosphorylation studies required previous immunoprecipitation from CSF for mass spectrometric analysis. This preliminary analysis indicated phosphorylation at S472 and at some other residues.

Microtubule proteins and their post-translational forms in the cerebrospinal fluid of patients with paraparesis associated with HTLV-I infection and in SH-SY5Y cells: an in vitro model of HTLV-I-induced disease.

HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is characterized by axonal degeneration of the corticospinal tracts. The specific requirements for transport of proteins and organelles to the distal part of the long axon are crucial in the corticospinal tracts. Microtubule dysfunction could be involved in this disease, configuring an axonal transport disease. We measured tubulin and its post-translational modified forms (acetylated and tyrosinated) in CSF of patients and controls, as well as tau and its phosphorylated forms. There were no significant differences in the contents of tubulin and acetyl-tubulin between patients and controls; tyrosyl-tubulin was not detected. In HAM/TSP, tau levels were significantly reduced, while the ratio of pT181/total tau was higher in patients than in controls, this being completely different from what is reported in other neurodegenerative diseases. Phosphorylation at T181 was also confirmed by Mass Spectrometry analysis. Western Blotting with monospecific polyclonal antibodies against pS199, pT205, pT231, pS262, pS356, pS396, pS404 and pS422 did not show differences in phosphorylation in these residues between patients and controls. Treating human SH-SY5Y neuroblastoma cells, a well-known in vitro neurite retraction model, with culture supernatant of MT-2 cells (HTLV-I infected cell line that secretes the viral Tax protein) we observed neurite retraction and an increase in tau phosphorylation at T181. A disruption of normal phosphorylation of tau protein in T181 could result in its dysfunction, contributing to axonal damage.

Microtubule proteins and their post-translational forms in the cerebrospinal fluid of patients with paraparesis associated with HTLV-I infection and in SH-SY5Y cells: An in vitro model of HTLV-I-induced disease

HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is characterized by axonal degeneration of the corticospinal tracts. The specific requirements for transport of proteins and organelles to the distal part of the long axon are crucial in the corticospinal tracts. Microtubule dysfunction could beinvolved in this disease, configuring an axonal transport disease. We measured tubulin and its posttranslational modified forms (acetylated and tyrosinated) in CSF of patients and controls, as well as tau and its phosphorylated forms. There were no significant differences in the contents of tubulin and acetyl-tubulinbetween patients and controls; tyrosyl-tubulin was not detected. In HAM/TSP, tau levels were significantly reduced, while the ratio of pT181/total tau was higher in patients than in controls, this being completely different from what is reported in other neurodegenerative diseases. Phosphorylation at T181 was also confirmed by Mass Spectrometry analysis. Western Blotting with monospecific polyclonal antibodies against pS199, pT205, pT231, pS262, pS356, pS396, pS404 and pS422 did not show differences in phosphorylation in these residues between patients and controls. Treating human SH-SY5Y neuroblastoma cells, a well-known in vitro neurite retraction model, with culture supernatant of MT-2 cells (HTLV-I infected cell line that secretes theviral Tax protein) we observed neurite retraction and an increase in tau phosphorylation at T181. A disruptionof normal phosphorylation of tau protein in T181 could result in its dysfunction, contributing to axonal damage.

Enfermedad epitelial no neoplásica y carcinoma vulvar: experiencia en el Hospital Clínico de la Universidad de Chile / Non neoplastic epithelial disease and vulvar carcinoma: experience at Hospital Clínico Universidad de Chile

Se presenta la experiencia del autor, en la Enfermedad Epitelial No Neoplásica (EENN) y carcinoma vulvar. Se analizaron 18 pacientes operadas de patología vulvar tumoral en el período comprendido entre enero de 1987 y junio de 1998, en el Servicio de Ginecología, de estos 12 correspondieron a EENN y 6 a carcinoma vulvar. El 100 por ciento de pacientes con EENN consultaron por prurio vulvar, no asi en el carcinoma vulvar en el cual los síntomas fueron variados. El tiempo de evolución de la sintomatología fue en general prolongado, 4 años en promedio para la EENN y 5 años en promedio para carcinoma vulvar. El test de Collins fue positivo en 3 a 12 pacientes con EENN y en 3 de 6 con carcinoma vulvar. Todas las pacientes fueron sometidas a biopsias preporatorias, con una correlación con la postoperatoria de 83,4 por ciento. Resultado de las biopsias post operatorias fue el siguiente: Hiperplasia escamosa sin atipías 10 (55,6 por ciento), Liquen escleroso 2 (11,1 por ciento), Carcinoma microinvasor 1 (5,6 por ciento) y Carcinoma invasor 3 (16,7 por ciento). La evolución post operatoria fue adecuada en EENN, no presentando complicaciones y siendo dadas de alta en promedio de 1 día. En la neoplasia vulvar, 4 pacientes presentaron complicaciones que se manejaron médicamente y fueron dadas de alta en promedio de 8 días. En el caso de pacientes con EENN, 2 presentaron reaparición del prurito vulvar (al año y 8 años). Una paciente con carcinoma vulvar invasor y compromiso ganglionar falleció a los 5 años de un cuadro abdominal no precisado

Hábitos preferenciales de los consumidores de frijol común (Phaseolus vulgaris L) en México / Preferential habits of consumers of common bean (Phaseolus vulgaris L) in Mexico

El conocimiento de los hábitos preferenciales de los consumidores de frijol es fundamental para definir los objetos en los programas de mejoramiento genético y para diseñar las estrategias de mercadeo en una región o país determinados. El presente trabajo se basó en la aplicación de 1514 encuestas a consumidores de frijol de 14 entidades federativas de la República Mexicana. Para la interpretación de los resultados el país se dividió en cuatro regiones: Noroeste, Centro y Sur. En la región Noroeste el 98 por ciento de los encuestados consume frijol "Azufrado" (amarillo azufre); en el Noreste el 70 por ciento concume "Pinto" (beige con motas cafés) y "Bayo" (Beige); en la zona Sur el 90 por ciento consume frijol "Negro", mientras que en la zona Centro se consume todas las clases comerciales. Se detectó que dentro de cada clase comercial existen preferencias específicas en relación al tamaño y brillantez del grano; sin embargo, en la clase comercial Negro los consumidores prefieren el grano de testa opaca y tamaño de 18-22/100 semillas mientras que en la clase "Flor de Mayo" (beige con motas rosas) los consumidores prefieren grano de testa brillante y tamaño de 30-35/100 semillas. La principal característica que utilizan los consumidores para definir sus preferencias es el tiempo de cocción y el sabor. Se detectó que entre los consumidores de frijol los hábitos preferenciales están muy arraigadas pues el 70 por ciento declaró no estar dispuesto a cambiar el frijol de su preferencia aún cuando la clase alternativa fuese más barata. Por otro lado, los consumidores normalmente no remojan el grano en agua ni agregan sal al inicio del proceso de cocción para no afectar el sabor y apariencia del frijol. Estos resultados fueron confirmados con pruebas sensoriales. En el presente trabajo también se discuten aspectos relacionados con formas de procesamiento y consumo y algunos aspectos de mercadeo del grano de frijol

Hernioplástica ambulatoria en pacientes de la tercera edad / Ambulatory hernioplasty on third-age patients

Se intervinieron ambulatoriamente 52 pacientes de tercera edad en el lapso de mayo 1994, que presentaban hernias inguinales pequeñas o moderadas. Se incluyó sólo a pacientes con riesgo anestésicos I o II según clasificación ASA.Todos los casos se intervinieron con anestesia local. La morbilidad fue baja, con sólo 2 hematomas postoperatorio y una crisis hipertensivas durantela cirugía. El seguimiento no mostró ninguna infección de herida. No existe aún seguiento a largo plazo de la hernia en esta serie.

Efecto de la localidad de siembra sobre la aceptación sensorial y otras características nutricionales y de calidad del grano en frijol común (Phaseolus vulgaris L) / Effect of growing location on sensory properties and nutritional characteristics of black beans (Phaseolus vulgaris L)

Se llevó a cabo el análisis de la evaluación sensorial en función al sabor y aceptación general del frijol entero cocido, en cinco variedades de frijol sembrado en seis localidades de México. Se determinó el tiempo de cocción con cocedores tipo Mattson. Se cuantificó el contenido de taninos y la actividad específica de lectinas. Se observaron diferencias estadísticas significativas (p<0.05) en los estudios de evaluación sensorial de los materiales provenientes de Calera específicamente en las variedades que sufrieron heladas y bajas temperaturas. Características como el sabor, color, espesor de caldo e integridad del grano resultaron de interés a los jueces. Se encontraron diferencias significativas (p<0.05) en el tiempo de cocción entre genotipos y entre localidades, observándose un efecto importante en esta determinación causado por las heladas. No se encontró alguna correlación entre el contenido de Ca y Mg en el suelo y el tiempo de cocción de frijol. La concentración de taninos mostró diferencias significativas (p<0.05) para los genotipos y las localidades. La actividad específica de lectinas no mostró ninguna diferencia entre genotipos pero si entre localidades, sin efecto aparente por las bajas temperaturas