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Patients with serious mental illness are a high-risk category of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Patients with schizophrenia are not participatory and have increased mortality and morbidity, patients with dementia cannot be cared for while depression, anxiety, bipolar tubing are associated with low immune status. Social stress is amplified by social isolation, amplifying depression and the mechanisms of decreased immunity. Hygiene measures and prophylactic behavior are impossible to put into practice in conditions of chronic mental illness. In coronavirus disease 2019 (COVID-19), the risk for severe development is associated with the presence of comorbidities and immune system deficiency. Prothrombotic status, cytokine storm and alveolar destruction are mechanisms that aggravate the evolution of patients, especially in the context in which they have dysfunction of the autonomic system. The activity of proinflammatory cytokines is accentuated by hyperglutamatergia, which potentiates oxidative stress and triggers the mechanisms of neural apoptosis by stimulating microglial activation. Activation of M1-type microglia has an important role in pathogenesis of major psychiatric disorders, such as major depression, schizophrenia or bipolar disorder, and may associate hippocampal atrophy and disconnection of cognitive structures. Memantine and Amantadine, N-methyl-D-aspartate (NMDA) glutamate receptor inhibitors, have demonstrated, through their pharmacological profile, psychotropic effects but also antiviral properties. In the conditions of the COVID-19 pandemic, based on these arguments, we suggest that they can be associated with the therapy with the basic psychotropics, Memantine or Amantadine, for the control of neuropsychiatric symptoms but also as adjuvants with antiviral action.

Holoprosencephaly (HPE) is a dramatic human brain malformation sequence with an extreme variable phenotypic spectrum and genetic heterogeneity, variable degree of severity and unknown etiology, in many cases. HPE is classified into syndromic, chromosomal, and non-syndromic, non-chromosomal. The most cases of HPE are syndromic. We present an atypical case of syndromic alobar HPE associated with digynic triploidy fetus, prenatally diagnosed, early at 18 weeks of gestation, by ultrasound (US) and complex genetic investigations. The US examination was performed with a specialized US machine, General Electric Voluson E10 OLED BT18, using two-dimensional (2D) scanning, three-dimensional (3D) image reconstruction, four-dimensional (4D) spatiotemporal image methodology and the highest power Doppler US technology. A detailed US examination of the fetus revealed several major abnormalities of the fetal head and severe facial malformations. Based on the antenatal US findings, the fetus was diagnosed with alobar HPE. After a careful examination and genetic counseling, additional cytogenetic investigations and molecular genetic analyses were performed, which revealed an abnormal number of 69 chromosomes, digynic triploidy (69,XXY). Two days later, the parents choose to interrupt the current gestation because of major fetal malformations. The pathological examination of the embryo reaffirmed the antenatal diagnostics.

Background: Type 2 diabetes mellitus (T2DM) is associated with increased mortality and morbidity, including cardiovascular diseases and obstructive sleep apnea (OSA). The aim of this study was to assess the associations between cardiovascular risk, chronic diabetes complications and the risk of OSA in adult patients with T2DM. Methods: The study included 529 patients with T2DM in whom moderate-to-severe OSA risk was assessed using the STOP-Bang questionnaire, dividing the subjects into two groups: group 1: STOP-Bang score

Metabolic dysfunction-associated fatty liver disease (MAFLD) is a new term that no longer excludes patients that consume alcohol or present other liver diseases, unlike nonalcoholic fatty liver disease (NAFLD). The aim of this study was to evaluate the role of different biomarkers as predictors of MAFLD in patients with type 2 diabetes mellitus (T2DM). In this regard, a cross-sectional, non-interventional study was conducted over a period of 8 months in patients with T2DM. Liver steatosis displayed by abdominal ultrasound certified the MAFLD diagnosis. A percentage of 49.5% of the studied patients presented MAFLD. Through logistic regression adjusted for gender, age, T2DM duration, lipid-lowering therapy, smoking status, nutritional status, we demonstrated that elevated triglycerides (TG) levels, high non-high-density-lipoprotein (HDL)-cholesterol-to-HDL-cholesterol (non-HDL/HDL) ratio, high atherogenic index of plasma (AIP), and increased Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) had predictive value for MAFLD in patients with T2DM. Furthermore, we calculated the optimal cut-off values for these biomarkers (184 mg/dL for TG, 0.615 for AIP, 3.9 for the non-HDL/HDL ratio, and 2.01 for HOMA-IR) which can predict the presence of MAFLD in patients with T2DM. To our knowledge, this is the first study to assess the predictive value of the non-HDL/HDL ratio for MAFLD in patients with T2DM.

Gestational diabetes mellitus (GDM) is a major public health issue of our century due to its increasing prevalence, affecting 5% to 20% of all pregnancies. The pathogenesis of GDM has not been completely elucidated to date. Increasing evidence suggests the association of environmental factors with genetic and epigenetic factors in the development of GDM. So far, several metabolomics studies have investigated metabolic disruptions associated with GDM. The aim of this review is to highlight the usefulness of maternal metabolites as diagnosis markers of GDM as well as the importance of both maternal and fetal metabolites as prognosis biomarkers for GDM and GDM’s transition to type 2 diabetes mellitus T2DM.

Behcet's disease is a systemic vasculitis of unknown aetiology with cardiac involvement as well as damage to other organs. Whether the sterile valvular inflammation which occurs in this autoimmune disease predisposes to bacterial adhesion and infective endocarditis is not yet established. We present the case of a patient with Behcet disease in which transthoracic echocardiography showed mobile masses on the aortic, tricuspid, and mitral valves, leading to multivalvular infective endocarditis diagnosis, possibly in the context of valvular inflammation. The case presented in this article confirms observation of other studies, namely that ultrasonography plays an important role in the diagnosis and evaluation of rheumatic diseases and permits optimal management in daily practice.

Objective. To identify qualitative and quantitative changes involving coagulation factors engaged in maternal and fetal complications, to determine the level of correlation between them, and to highlight the involvement of hereditary thrombophilia among pregnant women. Material and method. The article is based on 92 publications from 1995 to 2017, including a total of 49,127 thrombophilic patients, of whom 1272 were controls, with inclusion criteria as preeclampsia, intrauterine growth retardation, or early or late pregnancy loss. Results. 31 studies based on preeclampsia- demonstrate the involvement of G1691A factor V Leiden gene mutation, G20210A Prothrombin gene mutation and/or C677T and A1298C MTHFR gene mutation as the main factors in the development of this complication. 10 studies focuses on the intrauterine growth restriction place G20210A Factor V Leiden gene mutation, G20210A Prothrombin gene mutation, C677T and A1298C MTHFR gene mutation, protein C and protein S deficiency as the main factors involved. Another 32 studies cite the involvement of factor V Leiden mutation, Prothrombin mutation and MTHFR mutation in the development of early or late pregnancy losses. Conclusion. Based on 92 rigorously selected publications, we were able to demonstrate the relationship between medium/increased risk thrombophilia and pregnancy outcome, especially due to the presence of factor V Leiden gene mutation, Prothrombin gene mutation but also MTHFR gene mutation homozygous status.

Obiectiv. Identificarea modificărilor calitative şi cantitative ale mutaţiile factorilor de coagulare implicate în complicaţii materne şi fetale, determinarea nivelului de corelaţie dintre acestea şi gradul de implicare al trombofiliei ereditare în rândul femeilor însărcinate. Material şi metodă. Articolul se bazează pe 92 de publicaţii din 1995 până în 2017, incluzând 49.127 de paciente cu trombofilie, dintre care 1.272 au fost martori, având drept criterii de includere în studiu prezenţa preeclampsiei, retardul de creştere intrauterină sau pierderea timpurie sau tardivă a sarcinii. Rezultate. 31 studii bazate pe preeclampsie demonstrează implicarea mutaţiei genei G1691A factor V Leiden, a mutaţiei genei G20210A a protrombinei şi a mutaţiei genei C677T şi A1298C MTHFR ca factori principali în dezvoltarea acestei complicaţii. 10 studii se concentrează asupra gradului de restricţie de creştere intrauterine, iar mutaţia genei G20210A a factorului V Leiden, mutaţia genei G20210A a protrombinei, mutaţia genei C677T şi A1298C MTHFR, deficitul de proteina C şi proteină S fiind principalii factori implicaţi. Alte 32 de studii citează implicarea mutaţiei factorului V Leiden, a mutaţiei protrombinei şi a mutaţiei MTHFR în dezvoltarea pierderilor de sarcină precoce sau tardive. Concluzii. Pe baza a 92 de publicaţii riguros selectate, am putut demonstra relaţia dintre trombofilia cu risc mediu/crescut şi rezultatul sarcinii, în special din cauza prezenţei mutaţiei genei factor V Leiden, a mutaţiei genei protrombinei, dar şi a statusului homozigot al mutaţiei genei MTHFR.

Systemic involvement in autoimmune diseases is often unclear and organ changes are confounding, thus making it difficult to have an early accurate diagnosis. In those situations, both clinical and paraclinical findings might orientate the diagnosis, but only histological or immunohistochemistry changes might be accurate enough. The skin histological changes are relevant and sometimes might have a tremendous role in the accurate diagnosis of autoimmune rheumatic diseases, due to the correlation with the clinical systemic manifestations of the diseases and through the accessibility of biopsy. In the same time, muscle biopsy can provide important support for physicians improving diagnosis and optimizing management of connective tissue diseases.

Myocardial fibrosis is one of the most common histopathological lesions found in chronic heart diseases. Progressive development of myocardial fibrosis will cause heart failure, an extremely debilitating and life threatening condition. The correlation between the severity of fibrosis and myocardial microcirculation is an important prognostic factor in this disease entity. In our study, myocardial microvascular density evaluation of the patients with high blood pressure (hypertension), atrial fibrillation (AF), coronary heart disease, and heart failure showed a significant decrease of the values of this parameter, which means that myocardial fibrosis is the direct result of stimulation of myocardial fibroblasts induced by local hypoxia.

Background and Aims. Diabetes mellitus (DM) is a chronic disease which can evolve towards devastating micro- and macrovascular complications. DM is the most frequent cause of chronic kidney disease (CKD). Insulin resistance plays an important role in the natural history of type 1 diabetes. The purpose of the study was to determine the prevalence of CKD in T1DM and the correlation with insulin resistance (IR) in patients with CKD.Materials and Methods. The study was conducted over a period of three years (2010–2013) and included patients with DM registered in the Clinical Centre of Diabetes, Nutrition and Metabolic Diseases of Dolj county. The study design was an epidemiological, transversal, noninterventional type. Finally, the study group included 200 subjects with type 1 DM. Insulin resistance (IR) was estimated by eGDR. The subjects with eGDR ≤ 7.5 mg/kg/min were considered with insulin resistance.Results. CKD was found in 44% of the patients. Analyzing statistically the presence of CKD, we found highly significant differences between patients with CKD and those without CKD regarding age and sex of the patients, the duration of diabetes, glycosylated hemoglobin (HbA1c), the estimated glucose disposal rate (eGDR), and the presence of hypertension, dyslipidemia, and hyperuricaemia. In patients with CKD, age and diabetes duration are significantly higher than in those who do not have this complication. CKD is more frequent in males than in females (50.9% men versus 34.5% women,p=0.022). From the elements of metabolic syndrome, high blood pressure, hyperuricemia, and dyslipidemia are significantly increased in diabetic patients with CKD. eGDR value (expressed as mg·kg−1·min−1) is lower in patients with CKD than in those without CKD (15.92 versus 6.42,p<0.001) indicating the fact that patients with CKD show higher insulin resistance than those without CKD.Conclusions.This study has shown that insulin resistance is associated with an increased risk of CKD, but, due to the cross-sectional design, the causal relationship cannot be assessed. However, the existence of this causality and the treatment benefit of insulin resistance in type 1 diabetes are issues for further discussion.

Hepatic steatosis is a progressive liver disease, frequently met in chronic virus C hepatitis, playing an important role in its evolution towards fibrosis, necroinflammation and the final stage the hepatocellular carcinoma. The present paper studies the correlation between clinico-epidemiological parameters and the pathology test outcome in patients with hepatic biopsies carried out before they began the antiviral treatment. We used the classical histological staining and the immunolabeling. The presence of steatosis is not directly associated with clinico-epidemiological parameters and with the degree of fibrosis and inflammation.

The purpose of this study was in vitro evaluation and comparison of the adhesion of self-etch (SE) adhesive systems applied on normal and sclerotic dentin. For this study, Class 5 cavities were prepared on sound teeth as well as on teeth with sclerotic dentin. They were then restored by means of the SE 2-step OptiBond XTR (Kerr) and SE 1-step Bond Force (Tokuyama Dental) adhesive systems, as well as the Estelite Sigma Quick (Tokuyama Dental) composite resin. For teeth with sclerotic dentin, the hypermineralized superficial layer was removed by means of round bur on low speed, than the adhesive systems and composite resin were applied. These teeth were prepared for microscopic study according to the protocol specific to each microscope. SEM (scanning electron microscopy) examination reveals that on normal and sclerotic dentin, OptiBond XTR and Bond Force form hybrid layers with about the same thickness, greater in normal dentin, but only OptiBond XTR pervades into the dentinal tubules, both in normal and sclerotic dentin. However, TEM (transmission electron microscopy) examination of Bond Force reveals that it penetrates into the dentinal tubules as well, but only in the case of normal dentin. The thickness of the hybrid layers resulting from the application of the SE adhesive systems to sound dentin is different from the thickness of the hybrid layers obtained when the same adhesive systems have been applied to sclerotic dentin.

Hepatic steatosis is a common histological finding in chronic liver diseases. One of the pathological entities in which hepatic steatosis has been found is chronic hepatitis C. The prevalence of steatosis in these patients ranges from 40% to 86%, with an average of 55%, which is two times higher than the steatosis seen in adults uninfected with hepatitis C. Many studies have shown that hepatic steatosis is a medical condition that may progress to steatohepatitis, progressive hepatic failure, hepatic cirrhosis, and is a risk factor for development of hepatocellular carcinoma. We have proposed to evaluate the severity of steatosis in patients with chronic hepatitis C and to correlate it with necroinflammatory processes and fibrosis. We included 259 patients diagnosed with chronic hepatitis C and proven histological steatosis. Age of patients with hepatic steatosis varied from 20 to 69 years. Most cases of steatosis associated with chronic hepatitis C (47.87%) were diagnosed in the age group 50-59 years. Of 259 patients, 141 (54.44%) were female and 118 (45.56%) male. Slight steatosis was identified in 130 cases (50.19%), moderate fatty changes were present in 54 (20.85%) patients and severe steatosis in 75 (28.96%) patients. The appearance of steatosis was macrovesicular and predominantly affected the third zone of the hepatic lobe. Most cases of hepatic steatosis were associated with necroinflammatory activity and low and moderate fibrosis. Cases of marked steatosis associated with intense activity accounted for about 10%, while marked steatosis was associated with severe fibrosis in less than 5% of cases.