Prevalencia de lesiones por presión en pacientes del hospital Dr. José María Vargas 2021-2022. Estudio retrospectivo / Prevalence of pressure injuries in patients at Hospital Dr. Jose Maria Vargas 2021-2022. Retrospective study

Las lesiones por presión representan un problema de salud pública y de seguridad del paciente, debido a las elevadas tasas de prevalencia que condicionan y repercusiones en el ámbito sanitario y económico, tanto a nivel institucional como familiar y personal.Objetivo : analizar la prevalencia de las lesiones por presión en pacientes del Hospital Dr. José María Vargas, 2021-2022.Métodos : estudio retrospectivo, con enfoque cuantitativo, no experimental, descriptivo y de corte transversal, en el cual se efectuó revisión de historias clínicas. Con una población de 1838 pacientes que acudieron al Hospital José María Vargas de Cagua en el periodo de estudio, de los cuales se identificaron 25 casos con diagnóstico de lesión por presión; la muestra fue censal. Como instrumento de recolección de datos se empleó una ficha de registro. Resultados : las úlceras por presión tienen mayor prevalencia en pacientes con edad superior a 71 años, del sexo femenino, con antecedentes de diabetes mellitus, hipertensión arterial o accidente cerebrovascular. Con frecuencia se manifiesta clínicamente como una lesión única, grado II o III; mientras que las regiones anatómicas más afectadas son la región sacra, la región glútea y la cresta ilíaca. La prevalencia de la patología quedó asentada en 1,36%.Conclusión : las lesiones por presión tienen mayor prevalencia en pacientes de edad avanzada, sexo femenino y del entorno urbano, con antecedente de diabetes mellitus e hipertensión arterial. Se presentan como lesiones únicas, grado II-III, en la región sacra, habitualmente con evolución de hasta 7 días, y de origen comunitario(AU)

Pressure injuries represent a public health and patient safety problem, due to the high prevalence rates that condition and repercussions in the health and economic sphere, both at an institutional, family and personal level. Objective: to analyze the prevalence of pressure injuries in patients at the Dr. José María Vargas Hospital, 2021-2022. Methods: retrospective study, with a quantitative, non-experimental, descriptive and cross-sectional approach, in which medical records were reviewed. With a population of 1838 patients who attended the José María Vargas de Cagua Hospital in the study period, of which 25 cases diagnosed with pressure injury were identified; the sample was census. As a data collection instrument, a registration form was used. Results: pressure ulcers are more prevalent in patients older than 71 years, female, with a history of diabetes mellitus, arterial hypertension or stroke. It frequently manifests clinically as a single lesion, grade II or III; while the most affected anatomical regions are the sacral region, the gluteal region and the iliac crest. The prevalence of the pathology was established at 1.36%. Conclusion: pressure injuries are more prevalent in elderly, female and urban patients with a history of diabetes mellitus and arterial hypertension. They present as single lesions, grade II-III, in the sacral region, usually with evolution of up to 7 days, and of community origin(AU)

Estrogen disrupts chemokine-mediated chemokine release from mammary cells: implications for the interplay between estrogen and IP-10 in the regulation of mammary tumor formation.

Chemokines are pro-inflammatory cytokines that function to attract immune cells to the sites of tissue inflammation, injury or infection. We have formulated the hypothesis that release of one chemokine can serve, in a local paracrine or endocrine fashion, to induce the release of other chemokines from neighboring mammary cells. We set out to investigate whether specific chemokines could promote the release of other chemokine members from mammary cells, and whether estrogen could serve to disrupt the release of these chemokines from mammary cells. We found that treatment with the chemokine IP-10 resulted in significant increases in the amount of MIP-1alpha and MCP-1/JE released from murine mammary cells. Estrogen co-treatment significantly blocked the ability of IP-10 to trigger the release of MIP-1alpha and MCP-1/JE. Suppressive effects of estrogen were reversed upon co-treatment with 4-hydroxytamoxifen. Estrogen treatment significantly decreased expression of proteins corresponding to the chemokine receptors CXCR3 and CCR5 on mammary cells. Exposure of female mice to IP-10 in vivo significantly decreased the ability of estrogen to support the growth of CCL-51-based tumors in mammary tissue. Our results suggest that exposure of mammary tissue to estrogen may decrease the release of local chemokines from mammary cells, potentially increasing the risk of tumor growth through decreased immune surveillance. Ongoing studies are investigating the possible mechanisms through which IP-10 stimulates the release of chemokines from mammary cells, and how the action of IP-10 may serve to decrease mammary tumor formation.

[Polycystic hydatidosis: casual finding of calcified hydatid cyst simulating mesenteric neoplasm]. / Hidatidose policística: cisto hidático calcificado, simulando neoplasia mesentérica, descoberto acidentalmente.

A case of abdominal hydatidosis, without hepatic involvement, in a patient from the State of Acre is reported. The hydatid, already in degeneration and partially calcified, was discovered incidentally by a radiologic examination of the vertebral column, carried out for evaluating the state of an intervertebral disk prolapse. Although the images suggested a mesenteric tumor, attached to the intestinal wall, the finding of rostellar hooklets in the dense contents of the cyst, after surgical removal, revealed the parasitic nature of the lesion.

Hidatidose policística: cisto hidático calcificado, simulando neoplasia mesentérica, descoberto acidentalmente / Polycystic hydatidosis: casual finding of calcified hydatid cyst simulating mesenteric neoplasm

É descrito um caso de hidatidose abdominal, sem comprometimento hepático, em paciente do Estado do Acre. O cisto, já em degeneraçäo e parcialmente calcificado, foi descoberto, por acaso, mediante estudo radiológico da coluna vertebral feito para avaliaçäo de hérnia de disco, detectada algum tempo antes. Embora as imagens sugerissem uma neoplasia do mesentério, o achado de acúleos rostelares no conteúdo pastoso da hidátide, removida cirurgicamente, permitiu reconhecer-se a natureza parasitária da lesäo

Altered Bax expression and decreased apoptosis in bone marrow cells of lupus-susceptible NZB/W mice.

Estrogen is believed to contribute to the development of the autoimmune disorder systemic lupus erythematosus (SLE) (lupus) in women. We hypothesized that estrogen might promote the development of lupus by altering apoptosis of bone marrow cells, perhaps through regulation of the apoptotic proteins Bax and Bcl-2. We compared the effects of estrogen (E2) and thrombopoietin (TPO) on the expression of Bax or Bcl-2 in bone marrow cells isolated from female non-lupus (NZW or NZB parental strains) or lupus-prone (NZB and NZW cross; NZB/W) mice. We report that the basal level of Bax in parental bone marrow cells was significantly greater than that of cells from NZB/W animals. Treatment of NZB or NZW marrow cells with E2 resulted in a significant decrease in Bax expression, which was completely reversed upon co-treatment with TPO. Bax expression was not significantly altered by E2 and/or TPO in NZB/W cells. Bcl-2 levels did not differ between murine strains under basal or hormone-treated conditions. Lower basal expression of Bax protein was associated with significantly less apoptosis for NZB/W marrow cells. In addition, there were significantly greater numbers of cells in bone marrow of lupus-susceptible animals. Our results indicate that bone marrow cells of NZB/W animals differ physiologically from those of NZW or NZB mice, and suggest that decreased expression of Bax in bone marrow precursors may lead to decreased apoptosis of mature blood cells in lupus-susceptible mice.

Altered bone marrow cell sensitivity in the lupus-prone NZB/W mouse: regulation of CFU-GM colony formation by estrogen, tamoxifen and thrombopoietin.

Estrogen is thought to contribute to the onset of systemic lupus erythematosus (SLE) in women through mechanisms that are not completely understood. Although estrogen serves as a negative regulator in normal hematopoietic development, little research has been conducted examining alteration in hematopoietic development triggered by estrogen in lupus-susceptible individuals. We examined whether estrogen and other factors could influence colony formation of bone marrow cells obtained from normal and lupus-susceptible mice. Bone marrow cells isolated from New Zealand Black (NZB) and lupus-prone New Zealand Black and New Zealand White cross (NZB/W) mice were cultured in the presence of granulocyte-macrophage colony stimulating factor (GM-CSF) alone or in combination with estrogen, thrombopoietin (TPO), tamoxifen, estrogen and TPO. or estrogen and tamoxifen, and plated in methylcellulose culture medium. Plates were scored for the number of CFU-GM (colony forming unit granulocyte-macrophage) colonies after 6d in culture. For females of both mouse strains, estrogen significantly decreased (P < 0.05) the number of GM colonies. Co-treatment of NZB/W cells, but not NZB cells, with TPO or tamoxifen reversed the suppressive action of estrogen (P < 0.05). In contrast, while estrogen did suppress colony formation from cells of NZB/W males (P < 0.05), neither TPO nor tamoxifen reversed this effect. Our results indicate that the sensitivity of bone marrow cells isolated from both female and male NZB/W lupus-prone mice to hormones/growth factors is qualitatively different from cells of NZB mice, and suggest that hematopoietic alterations at the level of the bone marrow may be related to the pathogenesis of SLE.

Cell-surface sialoglycoconjugate structures in wild-type and mutant Crithidia fasciculata.

The cell-surface expression of sialoglycoconjugate structures in wild-type Crithidia fasciculata and its TFR(R1) drug-resistant mutant was analyzed with the aid of an influenza C virus strain, lectin, enzymatic treatment, and flow cytofluorimetry analysis probed with fluorescein isothiocyanate-labeled (FITC) lectins. 9-O-Acetyl-N-acetyl neuraminic acid (Neu5,9Ac2) structures mediate influenza C virus cell-binding. The SAalpha2,3Gal and SAalpha2,6Gal sequences are specifically recognized by Maackia amurensis (MAA) and Sambucus nigra (SNA) lectins, respectively. On the basis of these parameters the TFR(R1) mutant strain of C. fasciculata was found to contain exposed sialoglycoconjugates bearing Neu5,9Ac2 surface structures. After the removal of sialic acid residues by neuraminidase activity the marked increases in PNA (peanut agglutinin)-mediated agglutinating activity showed that those acidic units on C. fasciculata cells were glycosidically linked to D-galactose. The bond involves SAalpha2,6Gal and SAalpha2,3Gal linkages as suggested by the use of FITC-SNA and FITC-MAA lectins, respectively. Both SAalpha2,3Gal and SAalpha2,6Gal sequences were preferentially expressed by the TFR(R1) mutant. The SAalpha2,6 linkage markedly predominated. In the TFR(R1) mutant, but not in wild-type cells, two distinct populations of cells were distinguished by reactivity with FITC-SNA, one of which was enriched with surface SAalpha2,6Gal sequences. These diverse findings suggest that sialoglycoconjugate structures present on the flagellate surface may be associated with mutation and the cell growth cycle in C. fasciculata.

Immunogold labeling and cerium cytochemistry of the enzyme ecto-5'-nucleotidase in promastigote forms of Leishmania species.

We have applied both enzyme cytochemistry and immunological labeling techniques to characterize the enzyme 5'-nucleotidase (5'-Nase), at the ultrastructural level, in promastigote forms of four Leishmania species: Leishmania amazonensis, Leishmania mexicana, Leishmania donovani and Leishmania chagasi. The cerium phosphate staining was localized at the surface of the cell body, the flagellum and the flagellar pocket membranes of all the parasites studied. The immunogold labelling technique confirmed these results. In this report we localized 5'-Nase in L. chagasi and L. amazonensis which have been implicated respectively in visceral and cutaneous forms of leishmaniasis. In addition, we confirmed the localization of this phosphomonoesterase in the other two species studied. The superior quality of the images, obtained with both methodologies, confirms that these parasites possess mechanisms capable of hydrolyzing nucleotide monophosphates, and that the expression of 5'-Nase is associated with the outer surface of the plasma membrane.