Conjunto residencial en la ex fábrica Lanificio, distrito de Jose Luis Bustamante y Rivero – Arequipa

TesisEl déficit de vivienda por el crecimiento vegetativo y las constantes migraciones han generado una ocupación del suelo con densidades bajas, depredación de zonas de cultivo y desequilibrio ambiental, que se traducen en “desorden urbano” con una demanda social insatisfecha. La ocupación del suelo por el déficit cuantitativo, está directamente relacionado al déficit cualitativo de la misma, haber, si entendemos esta paradoja sabremos que la horizontalidad cada vez más extensa asegura menor calidad de vida para unos y para todos dentro de la ciudad. Arequipa fue y es la ciudad destino de las migraciones en el sur del Perú fenómeno que ha generado una transformación violenta y traumática en la estructura monocéntrica e imagen horizontal de la ciudad. La migración primero y el aumento vegetativo de la población como segunda causa, aseguran mayor demanda de viviendas, la invasión de terrenos eriazos y hasta zonas de riesgo en el primero y la habilitación de terrenos agrícolas en el segundo son estilos recurrentes que en conjunto sobrevaloran el costo del suelo por la especulación. No menos importante en este escenario real es la actuación ausente de los gobiernos regional y local, en los últimos quince años y durante la gestión del expresidente regional Juan Manuel Guillen Benavides se llegó a los límites del desborde del casco urbano y la periferia. De acuerdo a estudios de mercado el déficit de vivienda en la provincia de Arequipa proyectado al 2014 es de 31,627 viviendas. En el distrito de J. L. Bustamante y Rivero que tiene una extensión 1,083 has. y una población 81,359 Hab. (Tercera en la provincia) no tiene áreas de expansión por ser mediterráneo, Esto hace necesario la adopción de políticas de densificación para no depredar terrenos agrícolas en atención del déficit actual que según el Plan Urbano Distrital se requiere 3,624 viviendas al presente año. (Plan, 2005)

Low grade urothelial carcinoma mimicking basal cell hyperplasia and transitional metaplasia in needle prostate biopsy

ABSTRACT Purpose The vast majority of urothelial carcinomas infiltrating the bladder are consistent with high-grade tumors that can be easily recognized as malignant in needle prostatic biopsies. In contrast, the histological changes of low-grade urothelial carcinomas in this kind of biopsy have not been studied. Materials and Methods We describe the clinicopathologic features of two patients with low-grade bladder carcinomas infiltrating the prostate. They reported dysuria and hematuria. Both had a slight elevation of the prostate specific antigen and induration of the prostatic lobes. Needle biopsies were performed. At endoscopy bladder tumors were found in both cases. Results Both biopsies showed nests of basophilic cells and cells with perinuclear clearing and slight atypia infiltrating acini and small prostatic ducts. The stroma exhibited extensive desmoplasia and chronic inflammation. The original diagnosis was basal cell hyperplasia and transitional metaplasia. The bladder tumors also showed low-grade urothelial carcinoma. In one case, the neoplasm infiltrated the lamina propria, and in another, the muscle layer. In both, a transurethral resection was performed for obstructive urinary symptoms. The neoplasms were positive for high molecular weight keratin (34BetaE12) and thrombomodulin. No metastases were found in either of the patients, and one of them has survived for five years. Conclusions The diagnosis of low-grade urothelial carcinoma in prostate needle biopsies is difficult and may simulate benign prostate lesions including basal cell hyperplasia and urothelial metaplasia. It is crucial to recognize low-grade urothelial carcinoma in needle biopsies because only an early diagnosis and aggressive treatment can improve the prognosis for these patients

Nerve spectroscopy: understanding peripheral nerve autofluorescence through photodynamics

Background: Being able to accurately identify sensory and motor nerves is crucial during surgical procedures to prevent nerve injury. We aimed to (1) evaluate the feasibility of performing peripheral human nerve visualization utilizing nerves’ own autofluorescence in an ex-vivo model; (2) compare the effect of three different nerve fiber fixation methods on the intensity of fluorescence, indicated as the intensity ratio; and (3) similarly compare three different excitation ranges. Methods: Samples from various human peripheral nerves were selected postoperatively. Nerve fibers were divided into three groups: Group A nerve fibers were washed with a physiologic solution; Group B nerve fibers were fixated with formaldehyde for 6 h first, and then washed with a physiologic solution; Group C nerve fibers were fixated with formaldehyde for six hours, but not washed afterwards. An Olympus IX83 inverted microscope was used for close-up image evaluation. Nerve fibers were exposed to white-light wavelength spectrums for a specific time frame prior to visualization under three different filters—Filter 1—LF405-B-OMF Semrock; Filter 2—U-MGFP; Filter 3—U-MRFPHQ Olympus, with excitation ranges of 390–440, 460–480, and 535–555, respectively. The fluorescence intensity of all images was subsequently analyzed using Image-J Software, and results compared by analysis of variance (ANOVA). Results: The intensity ratios observed with Filter 1 failed to distinguish the different nerve fiber groups (p = 0.39). Conversely, the intensity ratios seen under Filters 2 and 3 varied significantly between the three nerve-fiber groups (p = 0.021, p = 0.030, respectively). The overall intensity of measurements was greater with Filter 1 than Filter 3 (p < 0.05); however, all nerves were well visualized by all filters. Conclusion: The current results on ex vivo peripheral nerve fiber autofluorescence suggest that peripheral nerve fiber autofluorescence intensity does not greatly depend upon the excitation wavelength or fixation methods used in an ex vivo setting. Implications for future nerve-sparing surgery are discussed.Fil: Dip, Fernando. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; ArgentinaFil: Aleman, Rene. Cleveland Clinic Florida; Estados UnidosFil: Socolovsky, Mariano. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; ArgentinaFil: Villalba, Nerina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; ArgentinaFil: Falcone, Jorge. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; ArgentinaFil: Lo Menzo, Emanuele. Cleveland Clinic Florida; Estados UnidosFil: White, Kevin P.. Scienceright Research Consulting; CanadáFil: Rosenthal, Raul J.. Cleveland Clinic Florida; Estados Unido

A Subpopulation of the K562 Cells Are Killed by Curcumin Treatment after G2/M Arrest and Mitotic Catastrophe.

Curcumin is extensively investigated as a good chemo-preventive agent in the development of many cancers and particularly in leukemia, including treatment of chronic myelogenous leukemia and it has been proposed as an adjuvant for leukemia therapies. Human chronic myeloid leukemia cells (K562), were treated with 20 μM of curcumin, and we found that a subpopulation of these cells were arrested and accumulate in the G2/M phase of the cell cycle. Characterization of this cell subpopulation showed that the arrested cells presented nuclear morphology changes resembling those described for mitotic catastrophe. Mitotic cells displayed abnormal chromatin organization, collapse of the mitotic spindle and abnormal chromosome segregation. Then, these cells died in an apoptosis dependent manner and showed diminution in the protein levels of BCL-2 and XIAP. Moreover, our results shown that a transient activation of the nuclear factor κB (NFκB) occurred early in these cells, but decreased after 6 h of the treatment, explaining in part the diminution of the anti-apoptotic proteins. Additionally, P73 was translocated to the cell nuclei, because the expression of the C/EBPα, a cognate repressor of the P73 gene, was decreased, suggesting that apoptosis is trigger by elevation of P73 protein levels acting in concert with the diminution of the two anti-apoptotic molecules. In summary, curcumin treatment might produce a P73-dependent apoptotic cell death in chronic myelogenous leukemia cells (K562), which was triggered by mitotic catastrophe, due to sustained BAX and survivin expression and impairment of the anti-apoptotic proteins BCL-2 and XIAP