Discoveries (Craiova, Romania)最新文献

Ventricular tachycardia (VT) and ventricular fibrillation (VF) are the most frequent causes of death in the first 24 hours after myocardial infarction. Previous studies showed that depleting TRPV1 receptors with resiniferatoxin (RTX) led to a reduced risk of VT and VF post-myocardial infarction. Therefore, the question of resiniferatoxin as a cardioprotector against myocardial infarction (MI)-induced VT and VF was raised. The RNA sequence data from 3 groups of pigs, each having 4 animals (4 controls, 4 myocardial infarction - MI, and 4 RTX + MI) was analyzed through the lens of differentially expressed genes. The differential expression comparison was conducted in two ways: MI versus Control and RTX+MI versus MI. The results showed the downregulation of deleterious genes involved in inflammation and future plaque instability in the RTX group compared with the MI group. In the case of some of the genes, these findings were reinforced by obtaining the same trends in the MI versus Control group. All in all, we propose further investigation of RTX as a prophylactic method against cardiovascular complications of MI.

Metabolic syndrome X has been known to be a risk factor for the development of cardiovascular dysfunction. Insulin resistance, diabetes mellitus and serum lipid abnormalities, which are all seen in metabolic syndrome X, have been found to negatively impact heart function, leading to heart failure in particular. Heart failure is a condition resulting when the heart is unable to perform its function of providing sufficient blood flow to meet the body's requirements. The treatment of heart failure in metabolic syndrome X varies based on the various components of metabolic syndrome X, which include obesity, hyperglycemia, hypertension and dyslipidemia. Obesity is regarded as one of the derangements seen in patients with metabolic syndrome X. It is a significant risk factor in the development of cardiovascular disease, which may eventually lead to heart failure. However, the obesity paradox suggests that obesity provides a higher chance of survival in patients with metabolic syndrome and heart failure. This review article focuses on the pathophysiology of heart failure in patients who already have metabolic syndrome X, as well as the therapeutic management complexity of the two conditions taking into consideration the protective role provided by obesity.

We present a case of disseminated Pneumocystis jirovecii pneumonia in a patient with a medical history of glioblastoma multiforme associated with acute deep-vein thrombosis. The patient presented to the emergency department with clinical features of pulmonary infection, and the chest images showed pneumonia. Antibiotics were initiated (azithromycin, cefepime, and vancomycin) and the patient was transferred to the ward for further management, where the condition of the patient continued to worsen over the second day. The patient developed bilateral lower extremity swelling and the doppler ultrasound revealed bilateral lower extremity acute deep vein thrombosis. Laboratory results showed pancytopenia and transaminitis. However, a repeated chest X-ray showed ground-glass changes and interstitial infiltrates, suggestive of atypical infection. We indeed identified D-glucan which hints to a disseminated form of Pneumocystis jirovecii pneumonia infection in this patient. We further confirmed the Pneumocystis jirovecii pneumonia by polymerase chain reaction test from the fluid obtained via bronchoalveolar lavage. We, therefore, initiated intravenous trimethoprim/ sulfamethoxazole treatment with an anticoagulant, and the patient's condition improved. Our findings strongly suggest a possible link between Pneumocystis jirovecii pneumonia infection and thrombogenesis, with impact in medical practice.

Proximal myopathy presents as generalized muscle weakness commonly involving the muscles of upper and/or lower limbs. Toxins, long-term use of statins, corticosteroids, alcohol, SGLT2 inhibitors, COVID-19 vaccination, and antimalarials have been attributed to its development. In endocrine and metabolic disorders, adrenal dysfunction including both overproduction and insufficiency of the adrenal gland hormones has been reported to cause myopathy. Moreover, parathyroid and thyroid disorders along with pituitary gland disorders can also directly or indirectly contribute to this condition. In idiopathic inflammatory myopathies including polymyositis, dermatomyositis, inclusion body myositis (IBM), and Systemic Lupus Erythematosus (SLE), Sjögren's Syndrome, and overlap syndromes, moderate to severe muscle weakness has been observed. IBM has been reported to be the most prevalent acquired myopathy above the age of 50. Hereditary or congenital myopathies include limb girdle muscular dystrophies, facioscapulohumeral muscular dystrophy, Duchenne and Becker muscular dystrophy, and proximal myotonic myopathy. In addition to these, glycogen storage diseases such as the McArdle disease can also cause fast exhaustion, myalgia, and cramping in working muscles. It is pertinent to mention here that a class of hereditary metabolic myopathies, referred to as "lipid deposition myopathy" causes lipids to accumulate in skeletal muscle fibers, leading to lesions and degeneration. Among viral causes, HIV, dengue virus, influenza virus, hepatitis B virus, hepatitis C virus, SARS-CoV2 are also associated with muscle weakness. Sarcoidosis, an inflammatory disease, can also manifest as muscle weakness and myalgia. Owing to this complicated pathophysiology of proximal myopathy, this review aims to summarize the existing literature on conditions associated with this phenomenon and other recent developments that have been made regarding events leading to development of generalized muscle weakness. To the authors' knowledge this is the first narrative review that discusses causes and conditions associated with proximal myopathy in thorough detail.

Introduction and aims: Aplastic anemia is a rare, fatal bone marrow disorder that is presumed to be an autoimmune-mediated illness that actively destroys haematopoietic cells through a T helper type-1 cell response. Different cell types in the bone marrow and peripheral circulation produce chemokines, such as interleukin-6 (IL-6) and interleukin-8 (IL-8). The myelopoiesis that is profoundly impaired in aplastic anemia may be inhibited by these two, as critical and powerful inhibitors. Therefore, it is conceivable that their ongoing overproduction may contribute to aplastic anemia. We performed a quantitative enzyme-linked immunosorbent assay on the peripheral blood plasma to reveal the levels of IL-6 and IL-8 and their correlation to aplastic anaemia.

Materials and methods: A total of 80 cases of aplastic anemia were included in this study, diagnosed according to the criteria laid down by the International Agranulocytosis and Aplastic Anemia study group. A total of 10 healthy individuals served as controls in this study. With the help of a commercial ELISA kit and the instructions from the kit's maker, the levels of IL-6 and IL-8 were measured in a quantitative way.

Results: Mean serum IL-6 and IL-8 levels in cases were 283.28±220.27 and 122.56±97.79 pg/ml, respectively, as compared to 7.52±1.43 and 3.42±1.73 pg/ml levels in controls. Statistically, mean IL-6, as well as IL-8 levels, were significantly higher in aplastic anemia patients than in controls (p< 0.001). Levels of interleukins were also assessed in relation to the severity of the disease. Patients with very severe aplastic anaemia had significantly higher mean IL-6 and IL-8 levels (516.71±36.73 and 220.50±23.45 pg/ml, respectively), followed by severe aplastic anaemia (198.84±150.39 and 89.82±77.18 pg/ml, respectively) and non-severe aplastic anaemia (26.71±33.40 and 10.29±2.63 pg/ml, respectively) (p<0.001).

Conclusion: Blood serum levels of IL-6 and IL-8 were increased in aplastic anemia and showed a correlation with the severity of the disease. Hence, IL-6 and IL-8 may play an important role in the immune-mediated pathophysiology of aplastic anemia and their increasing levels are giving alarming signals for timely implementation of the appropriate treatment regimen to stop further progression of the disease. Additional studies are required in order to further investigate the exact involvement and role of IL-6 and IL-8 in aplastic anemia.

Objective: Energy drinks are becoming more popular every year, particularly among young adults such as college students, despite evidence that they have harmful health effects. The effect of energy drink consumption on plasma glucose, serum apolipoproteins, and triglyceride levels in students was investigated.

Methods: In order to test this, we chose two representative types of energy drinks in Nigeria, namely fearless and predator. These energy drinks are brand names of non-alcoholic beverages aimed to provide energy. 30 students, apparently healthy male human subjects aged 18 to 30 years who gave informed consent to the research work were randomly selected and divided into two groups: Group A (fearless energy drink consumers, n=15) and Group B (predator energy drink consumers, n=15).   RESULTS: The results demonstrated significant reductions in pulse rate (86.00±41.32 vs. 78.87±27.72; p=0.03) and BMI (21.41±1.93 vs. 21.7±12.02; p=0.00) as compared to baseline values after one month of "fearless energy drink" consumption. Plasma glucose levels were significantly higher (97.53±10.62 vs. 88.80±11.33; p=0.01) and Apo B levels were significantly lower (21.41±1.93 vs. 21.71±2.02; p=0.00) following two weeks of fearless energy drink consumption than in baseline. In addition, BMI and Apo B levels were significantly lower after two weeks of predator energy drink consumption, but plasma glucose levels were significantly higher after two weeks and one month of predator energy drink consumption, respectively (p<0.05). SBP, DBP, TG and Apo A levels did not differ significantly in both fearless and predator energy drink consumers at baseline and after the study period respectively (p>0.05).

Conclusion: This study has shown that the consumption of energy drinks causes significant alterations in BMI, pulse rate, plasma glucose and apolipoprotein B levels which may have important clinical consequences for energy drink consumers.

Background: Treatment of severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) remains a significant challenge in the face of increased worldwide morbidity and mortality. The acute illness caused by SARS-CoV-2 is initiated by a viral phase, followed by an inflammatory phase. Numerous anti-inflammatory and anti-viral therapies, with a relatively minor clinical effect, have been applied. Developing a safe and efficient direct anti-viral treatment is essential as it can block disease progression before significant complications ensue and potentially prevent transmission.

Aim: The present phase 1 study aimed to determine the safety of Codivir, a newly developed anti-viral agent, and to preliminarily assess its anti-viral activity in patients infected by COVID-19.

Methods: In vitro studies were conducted to determine the direct anti-viral effect of Codivir using an immunofluorescence-based assay and to assess its cytotoxic effect by tetrazolium assay (MTT). In a phase I clinical trial, Codivir was administered for ten days in 12 patients who were followed for its safety. Patients were followed for clinical manifestations during administration. Sequential nasal viral PCR titers (Cycle Threshold, CT) were determined preceding and during treatment.

Results: In vitro, Codivir showed activity against SARS-CoV-2 with 90% viral replication suppression and minimal cytotoxicity. The anti-viral activity was demonstrated at the early stages of infection, post-entry of the virus in the cell. Codivir was safe in all 12 patients in phase I clinical trial and significantly suppressed viral replication in 5/7 fully assessed patients, with an anti-viral effect noted as early as three days.

Summary: The present study's data support the safety of Codivir administration in humans and suggest its significant anti-COVID-19 effect. These results support the testing of the drug in more extensive controlled trials in patients with SARS-CoV-2.

Hyperuricemia remains the most prevalent cause of gout. Gout patients present with joint inflammation and uric acid crystals deposition manifesting as tophi. The association of gout with increased risk of insulin resistance, diabetes, metabolic disorders, increased cardiometabolic risk, and kidney disease is well established. These factors influence the treatment plan, and current treatment options have limited cardiovascular risk reduction. So the need for novel treatments with a broad range of coverage for the complications is warranted. Sodium-glucose co-transporter 2 inhibitors are novel drugs approved for treating type-2 diabetes. They prevent glucose reabsorption and lower serum uric acid levels. Recently few studies have studied their association with reducing the risk of gout. They may help address the gout related complications through their recorded benefit with weight loss, improved insulin resistance, and cardiovascular benefits in recent studies. . SGLT2-Is may be useful to reduce the risk of gout in individuals with type 2 diabetes. Limited literature is available on the safety and efficacy of these novel antidiabetic drugs in patients with gout. This review is aimed to summarize the current knowledge on the role and effectiveness of novel antidiabetic medication as an early therapeutic option in gout patients.

Tetralogy of Fallot is the most common cyanotic heart disease in children. While doing echocardiographic examination of children with Tetralogy of Fallot, we observed that many older children with this condition had congestion in their bulbar conjunctiva, easily recognizable even from some distance. This observation led us to design and perform a research study in order to find out the presence of conjunctival congestion in children with Tetralogy of Fallot. 85% of children in the ≥ 5-years of age group had conjunctival congestion without any ocular symptom. This novel clinical finding can act as an adjunct clinical sign for recognizing Tetralogy of Fallot in older children.

Artificial intelligence (AI) has grown tremendously in the past decade. The application of AI in teledentistry can reform the way dental care, dental education, research, and subsequent innovations can happen remotely. Machine learning including deep learning-based algorithms can be developed to create predictive models of risk assessment for oral health related conditions, consequent complications, and patient stratification. Patients can be empowered to self-diagnose and apply preventive measures or self-manage some early stages of dental diseases. Applications of AI in teledentistry can be beneficial for both, the dental surgeon and the patient. AI enables better remote screening, diagnosis, record keeping, triaging, and monitoring of dental patients based on smart devices. This will take away rudimentary cases requiring run-of-the-mill treatments from dentists and enable them to concentrate on highly complex cases. This would also enable the dentists to serve a larger and deprived population in inaccessible areas. Its usage in teledentistry can bring a paradigm shift from curative to preventive personalised approach in dentistry. A strong asset to teledentistry could be a robust and comprehensive feedback mechanism routed through various channels proposed in this paper. This paper discusses the application of AI in teledentistry and proposes a feedback mechanism to enhance performance in teledentistry.