Neurological manifestations of COVID-19 in patients: from path physiology to therapy

Neurological Sciences - Coronavirus is a family of ARN positive single-stranded belonging to the family of Coronaviridae. There are several families of coronavirus that transmit more or less...     

Uncommon etiology of gastrointestinal bleeding: duodenal metastases from renal cell carcinoma

Because of its unpredictable behavior, renal cell carcinoma is one of the most controversial neoplasms. On the one hand, patients frequently show metastases at diagnosis because of its slight manifestations, while on the other, the neoplasm can remain stable after nephrectomy and can then metastasize many years later. When this happens, the metastases usually involve more than 2 organs. The most frequent sites of metastases are the lung and lymph nodes, followed by the bones and liver, while duodenal involvement is rare. Indeed, intestinal metastases are found in only 2% of autopsies and of these, renal cell carcinoma metastases account for 7.1%. We present a case of a solitary late recurrence presenting as upper gastrointestinal bleeding 19 years after nephrectomy for clear cell renal carcinoma.     

Late perforation of a thoracic aortic dacron graft by a metallic stent-graft component.

PURPOSE: To describe a case involving perforation of a previously placed aortic Dacron graft by the uncovered proximal stent of a thoracic stent-graft. CASE REPORT: A 76-year-old man with a surgically treated type A dissection presented with residual type B dissection. Thoracic stent-grafting of the entry site was performed successfully. After 2 years, the patient was admitted for evaluation of a non-pulsating parasternal mass. Computed tomography showed a large, hypodense liquid-like mass affecting the mediastinum up to the subcutaneous tissue. A false aneurysm at the proximal end of the stent-graft was observed arising from an aortic perforation by the uncovered stent. One week later, the mass had almost completely resolved, and the patient has been scheduled for close surveillance. CONCLUSION: This case illustrated the importance of thoroughly examining the long-term durability and compatibility of prosthetic materials.     

An anti-CD45RO immunotoxin kills latently infected human immunodeficiency virus (HIV) CD4 T cells in the blood of HIV-positive persons.

Highly active antiretroviral therapy has decreased the morbidity and mortality of human immunodeficiency virus (HIV) infection, but latently infected cells remain for prolonged periods. CD4(+) CD45RO(+) T cells are a major latent virus reservoir in HIV-infected persons. Replication-competent, latently HIV-infected T cells can be generated in vitro by infecting peripheral blood mononuclear cells with HIV and then eliminating the HIV-producing cells with an anti-CD25 immunotoxin (IT). The CD25(-) latently infected cells then can be eliminated with an anti-CD45RO IT. This study determined whether this IT also could kill latently infected CD4 T cells from HIV-infected persons with or without detectable plasma viremia. The results show that ex vivo treatment of cells from HIV-positive persons by anti-CD45RO IT reduces the frequency of both productively and latently infected cells. In contrast, CD4(+) CD45RA(+) naive T cells and a proportion of CD4(+) CD45RO(lo) memory T cells are spared.     

When Genetic Load Does Not Correlate with Phenotypic Spectrum: Lessons from the GnRH Receptor (GNRHR)

Context: A broad spectrum of GnRH-deficient phenotypes has been identified in individuals with both mono- and biallelic GNRHR mutations. Objective: The objective of the study was to determine the correlation between the severity of the reproductive phenotype(s) and the number and functional severity of rare sequence variants in GNRHR. Subjects: Eight hundred sixty-three probands with different forms of GnRH deficiency, 46 family members and 422 controls were screened for GNRHR mutations. The 70 subjects (32 patients and 38 family members) harboring mutations were divided into four groups (G1-G4) based on the functional severity of the mutations (complete or partial loss of function) and the number of affected alleles (monoallelic or biallelic) with mutations, and these classes were mapped on their clinical phenotypes. Results: The prevalence of heterozygous rare sequence variants in GNRHR was significantly higher in probands vs. controls (P < 0.01). Among the G1-G3 groups (homozygous subjects with successively decreasing severity and number of mutations), the hypogonadotropic phenotype related to their genetic load. In contrast, subjects in G4, with only monoallelic mutations, demonstrated a greater diversity of clinical phenotypes. Conclusions: In patients with GnRH deficiency and biallelic mutations in GNRHR, genetic burden defined by severity and dose is associated with clinical phenotype. In contrast, for patients with monoallelic GNRHR mutations this correlation does not hold. Taken together, these data indicate that as-yet-unidentified genetic and/or environmental factors may combine with singly mutated GNRHR alleles to produce reproductive phenotypes.