The roles of neutrophils linking periodontitis and atherosclerotic cardiovascular diseases

Inflammation plays a crucial role in the onset and development of atherosclerosis. Periodontitis is a common chronic disease linked to other chronic inflammatory diseases such as atherosclerotic cardiovascular diseases (ASCVD). The mechanistic pathways underlying this association are yet to be fully understood. This critical review aimed at discussing the role of neutrophils in mediating the relationship between periodontitis and ASCVD. Systemic inflammation triggered by periodontitis could lead to adaptations in hematopoietic stem and progenitor cells (HSPCs) resulting in trained granulopoiesis in the bone marrow, thereby increasing the production of neutrophils and driving the hyper-responsiveness of these abundant innate-immune cells. These alterations may contribute to the onset, progression, and complication of atherosclerosis. Despite the emerging evidence suggesting that the treatment of periodontitis improves surrogate markers of cardiovascular disease, the resolution of periodontitis may not necessarily reverse neutrophil hyper-responsiveness since the hyper-inflammatory re-programming of granulopoiesis can persist long after the inflammatory inducers are removed. Novel and targeted approaches to manipulate neutrophil numbers and functions are warranted within the context of the treatment of periodontitis also to mitigate its potential impact on ASCVD

Otkrivanje delecije kromosoma 1 pomoću tehnike FISH na otiscima ependimoma ukazuje na regiju izvan kromosoma 22 važnu za recidiv tumora

Ependymomas are glial tumors. They constitute approximately 5%-10% of intracranial tumors. Ependymomas are tumors which can recur. Predictive factors of outcome in ependymomas are not well established. Karyotypic studies are relatively scarce and loss of chromosome 22 has been described to correlate with recurrence. We are unaware of any reports involving chromosome 1 aberrations in the malignant progression of ependymomas. Cytogenetic analysis of 4 ependymomas was performed using double-target fluorescent in situ hybridization (FISH) and focusing on chromosomes 1 and 22. One patient had recurrent tumor. FISH was performed on 500 nuclei/tumors. All four cases showed a loss of chromosome 22q, while only one showed an additional loss of chromosome 1p, and it was the one with tumor relapse. We support the presence of tumor suppressor gene on 1p associated with relapse in ependymomas and suggest that the chromosome 1p status by FISH may identify a high risk group of patients harboring this tumor. Additional studies in this direction are needed, as our results refer to a minimal number of individuals analyzed.Ependimomi su glialni tumori. Oni čine otprilike 5%-10% intrakranijskih tumora. Ependimomi su tumori koji se mogu ponavljati. Čimbenici koji bi ukazivali na ishod ependimoma nisu dobro utvrđeni. Kariotipska ispitivanja su relativno rijetka, a opisano je kako gubitak kromosoma 22 korelira s ponovnom pojavom tumora. Nisu nam poznata izvješća o upletenosti aberacija kromosoma 1 u malignoj progresiji ependimoma. U ovoj studiji je citogenetska analiza 4 ependimoma provedena pomoću dvociljne fluorescentne in situ hibridizacije (FISH) i fokusiranja na kromosomima 1 i 22. U jednog se bolesnika radilo o ponovnoj pojavi tumora. FISH je izvedena na 500 jezgara/tumora. Sva četiri slučaja pokazala su gubitak kromosoma 22q, dok je samo jedan, i to onaj s ponovnim razvojem tumora, pokazao dodatni gubitak kromosoma 1p. Priklanjamo se mišljenju kako je prisutnost gena tumorske supresije na 1p udru žena s recidivom kod ependimoma i ukazujemo na to da bi status kromosoma 1p utvrđen pomoću FISH mogao identificirati visoko rizičnu skupinu bolesnika koji nose ovaj tumor. Potrebne su daljnje studije u ovom smjeru, jer se naši rezultati odnose na mali broj analiziranih osoba

Author Correction: Scalable and robust SARS-CoV-2 testing in an academic center.

An amendment to this paper has been published and can be accessed via a link at the top of the paper

Age effect on bone mineral density changes in breast cancer patients receiving anastrozole: results from the ARBI prospective clinical trial

PURPOSE: We investigated whether age at anastrozole (A) initiation influences the effect of treatment on bone mineral density (BMD). We conducted a post hoc analysis of the dataset of Arimidex Bone Mass Index Oral Bisphosphonates prospective trial, studying the effect of risedronate (R) on BMD of postmenopausal, early breast cancer patients receiving A. METHODS: Patients were stratified into those with normal BMD or mild osteopenia (T > −2) receiving A-only and patients with mild or severe osteopenia (T ≤ −2) or osteoporosis (T < −2.5) receiving A and per os R (A + R). Depending on age on treatment initiation, patients were grouped into two age cohorts, above and below 65 years. BMD change in lumbar spine (LS) and hip (HP) was evaluated at 12 months. An analysis of patients with normal BMD at baseline was additionally performed. RESULTS: Among patients receiving A-only, women ≤65 years were more likely to have a decrease in LS-BMD than older (p = 0.034). HP-BMD decrease at 12 months was not related to age (p = 0.182). In patients with mild or severe osteopenia or osteoporosis, treated with A + R, no age effect was observed for LS or HP (p = 0.099 and p = 0.939, respectively). Among patients with normal BMD at baseline, the age effect on LS-BMD change was more profound (p = 0.026). CONCLUSIONS: Our study suggests that younger postmenopausal women with normal BMD or mild osteopenia receiving A-only face an increased risk of bone loss in LS. Among patients with mild or severe osteopenia or osteoporosis treated with A + R, 12 months LS or HP BMD variations were configured regardless of age group