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Copyright of Question (1669-6581) is the property of Universidad Nacional de La Plata and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

I analyse the working conditions in the nursing sector in the city of Buenos Aires in order to show the relationship between feminization and the precarization of the workforce. First, neoliberal reforms undertaken in the health sector during the nineties decade are reviewed. In addition, I examine the category of work precarity, paying attention to the concept of a secondary workforce regarding females labor force participation. Finally, I consider the case of nursing workers to highlight the persistence of feminization and precariousness amongst them, despite the constant demand for professionals nationwide and the process of counter-reforms and union revitalization after 2003. I have chosen a qualitative methodology to examine official documents and also both local and foreigners' research data. I conclude that persisting representations of women and work are fundamental to understand the precarization of working conditions and the lack of socio-economic recognition in the nursing sector. [ABSTRACT FROM AUTHOR]

Copyright of Revista Colombiana de Ciencias Sociales is the property of Fondo Editorial Fundacion Universitaria Luis Amigo and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The influence of using TMOS or TEOS in the formation of CdS quantum dots in a silica matrix have been studied by X-ray absorption spectroscopy (XAS). The amount of Cd-S bonds have been monitored as a function of the nominal Cd concentration. The relative amount of CdS crystals depends on the precursor. The use of TEOS is not recommended because it gives a poor yield, especially for high Cd concentration. A discussion of the influence of CdS concentration in matrices from TMOS is carried out from structural models created from their pore volume distribution. The mean pore size becomes smaller and the size distribution more uniform when CdS concentration increases but the nanocrystals of low CdS nominal content present a more efficient quantum confinement. [ABSTRACT FROM AUTHOR]

Sarcoma with CIC-DUX4 gene fusion is emerging as the most prevalent subset of Ewing-like undifferentiated small round cell sarcomas with around 50 cases published. We report hereby the case of a 40-year-old male who presented a CIC-DUX4 sarcoma in deep soft tissues in his thigh. He had been diagnosed with neurofibromatosis type 1 at age 19 and over the years underwent resection of multiple neural neoplasms, including two malignant peripheral nerve sheath tumors with classical spindle-cell histopathology. The CIC-DUX4 sarcoma was treated with surgical resection, radiation and chemotherapy, but lung and brain metastases developed and the patient died from the disease 14 months after diagnosis. This is the first case of sarcoma with CIC-DUX4 gene fusion reported in a patient with NF1. Whether this association is coincidental or CIC-DUX4 sarcomas could be related to NF1 remains to be clarified. Study of alternative molecular alterations in EWSR1 -negative undifferentiated small round cell sarcomas is clinically relevant, since CIC-DUX4 sarcomas seem to be a very aggressive subset with poor response to the presently used therapeutic regimens. [ABSTRACT FROM AUTHOR]

The recent addition of novel immunotherapy drugs for the treatment of urothelial carcinoma makes it necessary the establishment of criteria to harmonize the immunohistochemical assessment of PD-L1, both as a prognostic factor and for the selection of patients to be treated. In this scenario, a group of uropathologists from the Spanish Society of Pathological Anatomy, together with a medical oncologist as an external collaborator subspecialized in uro-oncology, have prepared this document of recommendations based on the available evidence. During PD-L1 assessment it is especially relevant the selection of the sample, its processing, the immunohistochemical platform and antibody used, and the algorithm applied in the interpretation of results. All these aspects must be indicated in the results report, which should be easily interpretable in a context of rapid evolution of immunological therapies., (Copyright © 2023. Publicado por Elsevier España, S.L.U.)

Melanoma metastases are rare in the colon. Its diagnosis is difficult because they do not usually produce symptoms. They can present through the endoscopic image of a non-pigmented polyp. This is the case of a 56-year-old woman diagnosed with melanoma metastasis through polypectomy of an unusual-looking polyp.

These guidelines from the uropathology working group of the Spanish Society of Pathology (SEAP) are based on the European and ISUP 2015 recommendations and those of the College of American Pathologists, as well as the latest WHO 2016, TNM (AJCC) 2017 classifications. They include recommendations for specimen sampling, macro- and microscopic examination and immunohistochemistry. Gleason patterns are specified: Gleason pattern 3 includes hyperplastic, atrophic and microcystic glands, while pattern 4 includes all cribriform or glomeruloid glands. The Gleason score in prostatectomy specimens may change; if a tertiary pattern occurs in more than 5% of the tumour, it becomes a secondary pattern. In both biopsies and prostatectomy specimens, if the Gleason score is 7, the percentage of pattern 4 should be stated. Gleason scoring in tumor variants and special situations should also be specified. These recommendations should be adapted according to the resources available., (Copyright © 2019. Publicado por Elsevier España, S.L.U.)

Insulin Degrading Enzyme (IDE) is an endopeptidase that degrades insulin and glucagon. Ide gene has been associated with type-2 diabetes mellitus (DM2). However, the physiological role(s) of IDE in glucose homeostasis and its potential therapeutic benefit remain not completely known. To contribute in the understanding of IDE's role in glucose metabolism, we analyzed IDE protein level in pancreatic islets from two hyperinsulinemic mouse models, db/db and high-fat diet (HFD) mice, as well as in human islets from DM2 patients treated with oral hypoglycemic agents (OHAs) or insulin. IDE protein level was detected by staining and by western-blot. INS1E cells, rat and human islets were treated with insulin and IDE protein level was studied. We have shown for the first time IDE staining in rodent and human tissue, using the proper negative control, IDE null mouse tissue. Our staining indicates that IDE is expressed in both beta- and alpha-cells, with higher expression in alpha-cells. Db/db and HFD mice islets showed increased IDE protein level. Interestingly, human islets from DM2 patients treated with OHAs showed decreased IDE protein level in beta-cells. Meanwhile, islets from insulin-treated DM2 patients showed augmented IDE protein level compared to OHAs patients, pointing to an upregulation of IDE protein level stimulated by insulin. These data correlate nicely with insulin-stimulated upregulation of IDE in cultured INS1E cells, as well as in rat and human islets. In conclusion, our study shows that IDE is expressed in pancreatic beta- and alpha-cells of both rodents and humans, having higher expression in alpha-cells. Furthermore, insulin stimulates IDE protein level in pancreatic beta-cells. These results may have implications in how DM2 patient's treatment affects their beta-cell function.

Kidney cancer is the tenth most common cause of cancer death. There are a growing number of genes known to be associated with an increased risk of specific types of kidney cancer. People with Von Hippel-Lindau syndrome have about a 40% risk of developing multiple bilateral clear cell kidney cancers. They can also develop retinal and brain hemangioblastoma, kidneys or pancreas cysts, pheochromocytoma and endolymphatic sac tumor. Four phenotypes with different renal cancer and pheocromocitoma risk have been described depending on the germline mutation. Hereditary papillary renal cell carcinoma syndrome has type 1 papillary renal cell carcinomas associated with protooncogene c-MET germline mutations. Birt-Hogg-Dubé syndrome has FLCN gene mutations associated with fibrofolliculomas, lung cysts with a high risk for spontaneous pneumothorax, and a 15% to 30% risk of kidney cancer (most classified as chromophobe carcinoma, oncocytoma or oncocytic hybrid, but clear cell and papillary kidney cancers have also been reported). Histopathological findings such as oncocytosis and oncocytic hybrids are very unusual outside the syndrome. Hereditary leiomyomatosis and renal cell cancer syndrome shows mutations of Fumarate hydratase gene and cutaneous leiomyomata in 76% of affected individuals, uterine leiomyomata in 100% of females, and unilateral, solitary, and aggressive papillary renal cancer in 10 to 16% of patients. A specific histopathological change is eosinophilic prominent nucleoli with a perinucleolar halo. Tuberous sclerosis complex is one of the most prevalent (1/5.800) hereditary syndromes where renal disease is the second leading cause of death, associated with angiomyolipomas (70%), renal cysts, oncocytomas or clear cell cancer.