Search Results (59)

In this study, a rare 3.49-carat yellow diamond was analyzed to reconstruct the geological processes that led to its distinctive form. The diamond exhibits growth and dissolution features, indicating a complex history. To preserve the sample’s integrity, non-destructive analytical techniques—including VIS, UV–Vis–NIR, and IR spectroscopy—were employed. The yellow coloration of the diamond is attributed to the presence of N3 and N2 defects. Additionally, other defects such as N₃VH⁰ centers and platelets were detected; however, the latter do not contribute to the coloration. The observations of the etch pits and surface microreliefs suggest that the diamond underwent size reduction due to dissolution events, which also altered its crystal habit over time. The diamond’s initial mixed-habit morphology evolved into a more complex one through a series of growth and dissolution processes that began during mantle storage. Furthermore, the presence of brown surface stains indicates radiation damage, likely acquired during its residence in alluvial deposits at the Earth’s surface. Full article

Background: Medication-related osteonecrosis of the jaw (MRONJ) is drug-induced bone destruction that is exposed for a minimum of 6 to 8 weeks in patients who have not received head and neck radiotherapy and who have not been diagnosed with facial bone metastases. MRONJ treatment outcomes are unpredictable. Therefore, alternative treatment methods are being explored, such as blood-derived platelet-rich preparations enriched with growth factors, including advanced platelet-rich fibrin (A-PRF). The presence of growth factors may enhance healing and reduce post-procedure complications. There are no studies examining the effect of A-PRF on the healing of patients with MRONJ. The aim of this study was to retrospectively evaluate treatment outcomes of patients with MRONJ surgically treated without and with the use of A-PRF. Materials and methods: This retrospective study included 28 patients who suffered from osteomyelitis due to MRONJ and underwent surgical treatment between 2019 and 2024. The patients were divided into two groups: the first group received surgical treatment without A-PRF, and the second group received surgical treatment with the application of A-PRF. This study analyzed demographic and clinical data, as well as treatment outcomes. Results: The patients were aged from 43 to 82 years. The most common cause of MRONJ was the administration of zoledronic acid for oncological reasons (22 patients, 78.6%), given intravenously. In 20 patients (71.4%), the antiresorptive treatment lasted longer than three years. The obtained healing distribution was binomial (presence or absence of healing). Estimation of the probability of healing using the maximum likelihood method provided a result of approximately 64%. The probability of ten or more healed patients in the A-PRF group was 41%. A-PRF helps with a probability of 59%, and without A-PRF, it was lower. Concomitantly, the differences between the group with A-PRF and without A-PRF were not statistically significant. Conclusions: The patients with MRONJ should have regular check-ups with radiological examinations at least every six months to detect possible recurrence. Treatment for MRONJ is long and difficult. Treatment of non-advanced lesions, without additional risk factors (such as treatment with zoledronate intravenously for oncological purposes for 3 years), showed a better prognosis. Sometimes, in addition to surgery, it is necessary to consider alternative methods. A-PRF may enhance MRONJ healing. However, there is no evidence of a significant effect of A-PRF on the healing of MRONJ. Full article

Germline heterozygous variants in RUNX1 lead to Familial Platelet Disorder with Myeloid Leukemia Predisposition (FPD/AML). Cellular and/or animal models are helpful to uncovering the role of a variant in disease progression. Twenty-five mice per genotype (RUNX1^WT/WT, RUNX1^WT/L43S, RUNX1^L43S/L43S), previously generated by CRISPR/Cas9, and nine sub-lethally irradiated mice per genotype were investigated. Peripheral blood (PB), bone marrow (BM), and spleen samples were analyzed by flow cytometry and histopathology. Deregulated genes were analyzed by RNA-seq in BM. An aberrant myeloid Mac1⁺Sca1⁺ckit⁻ population in the PB, BM, and spleen of two homozygous and one heterozygous mouse was observed, as well as BM hypercellularity. No Mac1⁺Sca1⁺ckit⁻ cells were detected in any RUNX1^WT/WT mice. Moreover, the spleen of both homozygous mice showed destruction of the white/red pulp and the presence of apoptotic cells. The aberrant population was also detected in four irradiated mice, two heterozygous and two homozygous, in their PB, BM, and spleen. RNA-seq studies showed 698 genes significantly deregulated in the three non-irradiated Mac1⁺Sca1⁺ckit⁻ mice vs. six healthy mice, highlighting the alteration of genes involved in apoptosis and DNA repair. These results indicate that the homozygous form of the variant p.Leu43Ser may contribute to the pathogenesis of aberrant cells. Full article

Xenogenic collagen matrices are used in clinical practice for soft tissue augmentation around teeth and implants, either alone or biofunctionalized with injectable platelet-rich fibrin (iPRF). Their direct interaction with inflammatory cells may influence both healing and destructive inflammation processes. Therefore, expression of cyclooxygenases (COX-1 and COX-2) and prostanoids (PGE2 and TXB2) was studied in THP-1 monocyte/macrophage cultures exposed to porcine collagen matrices (a non-cross-linked monolayer scaffold composed of collagen type I, collagen type III, and elastin (MLCM), a bilayer scaffold made of collagen types I and III (BLCM), and a volume-stable cross-linked monolayer scaffold (VSCM)). The study showed that VSCM and MLCM significantly reduced PGE2 concentrations in THP-1 monocyte cultures. iPRF further reduced PGE2 concentrations when exposed to MLCM. In contrast, incubation of THP-1 monocytes with VSCM and BLCM resulted in a significant increase in TXB2 concentrations compared with control conditions. Incubation of macrophages with MLCM, VSCM, and BLCM increased PGE2 concentrations, with VSCM and BLCM additionally increasing TXB2 concentrations. iPRF in macrophage cultures with VSCM and BLCM also resulted in increased PGE2 and TXB2 concentrations compared with control conditions. Confocal microscopy revealed no visible differences in COX-1 immunoexpression in monocytes and macrophages cultured with collagen matrices, either with or without iPFR. Weak positive COX-2 immunofluorescence was observed in monocytes, while moderate positive immunofluorescence was detected in macrophages. In conclusion, it can be suggested that the studied collagen matrices interact with monocytes/macrophages, with MLCM exhibiting the highest compatibility. Full article

This study presents a novel approach to evaluate the galvanic corrosion risk of mild steel coated with graphene-embedded epoxy coatings. The potential for graphene platelets to promote anodic dissolution of the underlying steel substrate via galvanic corrosion mechanisms was systematically assessed through the accelerated alternating current-direct current-alternating current (AC-DC-AC) technique and cathodic disbondment testing. The possible risk of displacing cathodic reactions from the coating–steel interface to the dispersed graphene platelets within the epoxy matrix was investigated by evaluating the degradation trend of the graphene-containing coating under the AC-DC-AC test. The degradation behaviour of both pure epoxy and graphene-embedded epoxy coatings during accelerated aging was characterized using electrochemical impedance spectroscopy (EIS) measurements. The finding highlighted the negligible catalytic effect of incorporated graphene platelets on the anodic dissolution of steel substrate. On the other hand, as an inert filler, graphene platelets contributed to the enhancement of the structural integrity of the epoxy matrix during the AC-DC-AC test and natural immersion in NaCl 3.5 wt % solution by enhancing the barrier performance of the coating. Despite their spectacular barrier performance, damaged graphene-containing coatings performed inferiorly against corrosion-induced delamination compared to pure epoxy. Samples underwent the cathodic disbondment test to eliminate the effect of substrate anodic dissolution from corrosion-induced delamination. The accelerated delamination of graphene-embedded epoxy coatings was attributed to the destructive impact of graphene platelets on the interfacial adhesion of the epoxy matrix to the steel substrate. Full article

Atherosclerosis is caused by injury to the blood arteries and progressive oxidative stress. Blood cells play an important role in its development; thus, their protection is important. Naringenin (N) is documented to possess a protective action against atherosclerosis, and we hypothesize that its derivatives, naringin (Nr) and naringin dihydrochalcone (Nd), with slightly different structures, possess similar or better activity. Therefore, this research aimed to find the mechanism of protective action of N, Nr and Nd in relation to erythrocytes, peripheral blood mononuclear cells (PBMCs) and platelets in terms of their potential anti-atherosclerotic effect. Moreover, their physicochemical properties and the interaction of flavonoids with liposomes were studied. All flavonoids protected erythrocytes from AAPH- and H₂O₂-induced oxidation to varying degrees. None of them had a destructive effect on erythrocyte membrane, and they did not impact the metabolic activity of PBMC and platelets. Nr and Nd inhibited collagen-induced platelet aggregation better in tested concentrations than N. Studied compounds did not induce liposome aggregation, but N and Nd changed their dipole potential. Obtained results show that Nd possesses slightly better activity than N and may have a better potential health effect on blood cells, which is very important in the design of anti-atherosclerotic therapeutics. Full article

Thrombocytopenia frequently occurs in patients before, during, and after admission to Pediatric Intensive Care Units (PICUs). In critically ill children, it is often due to multifactorial causes and can be a sign of significant organ dysfunction. This review summarizes the potential causes/mechanisms of thrombocytopenia in acutely ill children, their identification, and treatments, with special attention paid to septic patients. The mechanisms of thrombocytopenia include decreased production and sequestration, but the most common reason is increased destruction or consumption. This review specifically reviews and compares the presentation, pathogenesis, and treatment of disseminated intravascular coagulation (DIC) and the thrombotic microangiopathic spectrum (TMA), including thrombocytopenia-associated multiorgan failure (TAMOF), hemolytic uremic syndrome, and other diagnoses. The other etiologies discussed include HLH/MAS, immune thrombocytopenia, and dilutional thrombocytopenia. Finally, this review analyzes platelet transfusions, the various thresholds, and complications. Full article

Background and Objectives: Immune thrombocytopenia (ITP) is an autoimmune disease characterized by the autoantibody-mediated destruction of platelets. The treatment of ITP aims to maintain a sufficient platelet count to prevent bleeding. First-line treatment options include corticosteroids and intravenous immunoglobulin (IVIg), while second-line treatments include splenectomy, rituximab and other immunosuppressive agents, and thrombopoietin (TPO) receptor agonists. This study aims to discuss the treatment methods and results from 100 patients with ITP at the Muğla Training and Research Hospital through a pharmacological approach. Materials and Methods: Demographic characteristics, clinical findings, bone marrow aspiration and biopsy results, and treatments and treatment responses at the time of diagnosis of the 100 patients with ITP who were treated and followed up in the period 2015–2023 were evaluated retrospectively. Results: In the third month after treatment, the overall response percentage was 100% in patients who received steroids only and 88% in patients who received IVIg treatment alone or in combination with steroids (p > 0.05). The most preferred second-line treatments were splenectomy (41%), eltrombopag (26%), and rituximab (10%). Bone marrow biopsy was performed in 54% of patients, where 35.1% showed increased megakaryocytes, 44.4% adequate megakaryocytes, and 14.8% decreased megakaryocytes. It is noted that eltrombopag and rituximab, in particular, yield higher complete remission rates than immunosuppressive drugs. Conclusions: Considering the side effects of immunosuppressive medications, IVIg, splenectomy, and steroid therapy, the use of new agents such as eltrombopag, which are easily tolerated and have a lower risk of side effects, is expected to increase. Full article

Background: Perinatal hypoxia may result in coagulation dysfunction. Diminished blood flow or oxygen to the fetus/neonate during the perinatal period can cause bone marrow and liver function impairment, leading to thrombocytopenia, impaired synthesis of clotting and fibrinolytic factors, and increased destruction of platelets in the small blood vessels. The goal of the present study was to evaluate the hemostatic status of newborns with perinatal hypoxia via the non-activated thromboelastometry (NATEM) assay in cord blood samples. Methods: 134 hypoxic neonates born in our maternity unit over a 1.5-year period were enrolled in this observational cohort study, and 189 healthy neonates served as the control group. Participation in the study was voluntary and parents signed informed consent prior to recruitment. Demographic and clinical data were recorded on admission, and the NATEM method was performed on cord blood samples. The following NATEM values were evaluated: clotting time (CT), alpha angle (α-angle), clot formation time (CFT), clot amplitude at 5 and 10 min. (A5, A10), maximum clot firmness (MCF), clot lysis index at 60 min. after CT (LI60), and maximum clot elasticity (MCE). Statistical analysis was conducted utilizing the SAS for Windows 9.4 software platform. Results: Neonates with perinatal hypoxia exhibited decreased fibrinolytic potential in comparison to healthy neonates, as indicated by increased LI60, and this difference was statistically significant (LΙ60: 94 (92–96) Vs 93 (91–95), p value = 0.0001). There were no statistically significant differences noted among the remaining NATEM variables. Conclusion: Our findings indicate decreased fibrinolytic potential in hypoxic neonates in comparison to healthy neonates, suggesting that NATEM could serve as an effective tool for promptly identifying hemostasis dysfunction in this group of neonates. Full article

Immune thrombocytopenia (ITP) is an autoimmune disease characterized by an isolated decrease in platelet count and an increased risk of bleeding. The pathogenesis is complex, affecting multiple components of the immune system and causing both peripheral destruction of platelets and inadequate production in the bone marrow. In this article, we review the treatment of ITP from a historical perspective, discussing first line and second line treatments, and management of refractory disease. Full article

Primary Immune Thrombocytopenia (ITP) is a rare autoimmune disease characterised by the immune-mediated destruction of peripheral blood platelets in patients leading to low platelet counts and bleeding. The diagnosis and effective management of ITP are challenging because there is no established test to confirm the disease and no biomarker with which one can predict the response to treatment and outcome. In this work, we conduct a feasibility study to check if machine learning can be applied effectively for the diagnosis of ITP using routine blood tests and demographic data in a non-acute outpatient setting. Various ML models, including Logistic Regression, Support Vector Machine, k-Nearest Neighbor, Decision Tree and Random Forest, were applied to data from the UK Adult ITP Registry and a general haematology clinic. Two different approaches were investigated: a demographic-unaware and a demographic-aware one. We conduct extensive experiments to evaluate the predictive performance of these models and approaches, as well as their bias. The results revealed that Decision Tree and Random Forest models were both superior and fair, achieving nearly perfect predictive and fairness scores, with platelet count identified as the most significant variable. Models not provided with demographic information performed better in terms of predictive accuracy but showed lower fairness scores, illustrating a trade-off between predictive performance and fairness. Full article

Immune thrombocytopenia (ITP) is an autoimmune disease characterized by an isolated decrease in the platelet count and an increased risk of bleeding. The pathogenesis is complex, affecting multiple components of the immune system and causing both peripheral destruction of platelets and impaired central megakaryopoiesis and platelet production in the bone marrow. Here, we intend to contextualize the current knowledge on the pathophysiology, terminology, epidemiology, clinical manifestations, diagnosis, and prognosis of ITP from a historical perspective and the first references to the never-stopping garnering of knowledge about this entity. We highlight the necessity to better understand ITP in order to be able to provide ITP patients with personalized treatment options, improving disease prognosis and reducing the incidence or frequency of refractoriness. Full article

Primary immune thrombocytopenia (ITP) is a complex autoimmune disease whose hallmark is a deregulation of cellular and humoral immunity leading to increased destruction and reduced production of platelets. The heterogeneity of presentation and clinical course hampers personalized approaches for diagnosis and management. In 2021, the Spanish ITP Group (GEPTI) of the Spanish Society of Hematology and Hemotherapy (SEHH) updated a consensus document that had been launched in 2011. The updated guidelines have been the reference for the diagnosis and management of primary ITP in Spain ever since. Nevertheless, the emergence of new tools and strategies makes it advisable to review them again. For this reason, we have updated the main recommendations appropriately. Our aim is to provide a practical tool to facilitate the integral management of all aspects of primary ITP management. Full article

The interactions between specific snake venom toxins and muscle constituents are the major cause of severe muscle damage that often result in amputations and subsequent socioeconomic ramifications for snakebite victims and/or their families. Therefore, improving our understanding of venom-induced muscle damage and determining the underlying mechanisms of muscle degeneration/regeneration following snakebites is critical to developing better strategies to tackle this issue. Here, we analysed intramuscular bleeding and thrombosis in muscle injuries induced by two different snake venom toxins (CAMP—Crotalus atrox metalloprotease (a PIII metalloprotease from the venom of this snake) and a three-finger toxin (CTX, a cardiotoxin from the venom of Naja pallida)). Classically, these toxins represent diverse scenarios characterised by persistent muscle damage (CAMP) and successful regeneration (CTX) following acute damage, as normally observed in envenomation by most vipers and some elapid snakes of Asian, Australasian, and African origin, respectively. Our immunohistochemical analysis confirmed that both CAMP and CTX induced extensive muscle destruction on day 5, although the effects of CTX were reversed over time. We identified the presence of fibrinogen and P-selectin exposure inside the damaged muscle sections, suggesting signs of bleeding and the formation of platelet aggregates/microthrombi in tissues, respectively. Intriguingly, CAMP causes integrin shedding but does not affect any blood clotting parameters, whereas CTX significantly extends the clotting time and has no impact on integrin shedding. The rates of fibrinogen clearance and reduction in microthrombi were greater in CTX-treated muscle compared to CAMP-treated muscle. Together, these findings reveal novel aspects of venom-induced muscle damage and highlight the relevance of haemostatic events such as bleeding and thrombosis for muscle regeneration and provide useful mechanistic insights for developing better therapeutic interventions. Full article

Primary immune thrombocytopenia (ITP) is an acquired blood disorder that causes a reduction in circulating platelets with the potential for bleeding. The incidence of ITP is slightly higher in adults and affects more women than men until 60 years, when males are more affected. Despite advances in basic science, primary ITP remains a diagnosis of exclusion. The disease is heterogeneous in its clinical behavior and response to treatment. This reflects the complex underlying pathophysiology, which remains ill-understood. Platelet destruction plays a role in thrombocytopenia, but underproduction is also a major contributing factor. Active ITP is a proinflammatory autoimmune disease involving abnormalities within the T and B regulatory cell compartments, along with several other immunological abnormalities. Over the last several years, there has been a shift from using immunosuppressive therapies for ITP towards approved treatments, such as thrombopoietin receptor agonists. The recent COVID-19 pandemic has hastened this management shift, with thrombopoietin receptor agonists becoming the predominant second-line treatment. A greater understanding of the underlying mechanisms has led to the development of several targeted therapies, some of which have been approved, with others still undergoing clinical development. Here we outline our view of the disease, including our opinion about the major diagnostic and therapeutic challenges. We also discuss our management of adult ITP and our placement of the various available therapies. Full article