In 145 previously healthy non-critically ill young adults, coronavirus disease 2019 (COVID-19)-related symptoms, risk factors for thrombosis, coagulation and inflammatory parameters were compared, with 29 patients reporting unusual thrombotic events (UTEs) and 116 not having thrombotic events. The inflammatory indices, coagulation and prothrombotic platelet phenotype (PTPP) were significantly higher in patients with UTEs versus those without. Patients with UTEs were categorised according to detection of thrombophilic genes (TGs), coagulation and inflammatory markers to the non-TG and TG subcohort. A total of 38 UTEs were identified, which included splanchnic vein thrombosis (SVT; 11), stroke (six), cerebral vein thrombosis (five), thrombotic microangiopathy (four), limb ischaemia and inferior vena cava thrombosis (three each), ST-segment elevation myocardial infarction (two), superior vena cava thrombosis (two), upper limb deep venous thrombosis and retinal vein thrombosis, one each. We found a 55% prevalence of TGs mainly heterozygous coagulation factor II, thrombin (FII)-G20210A, Janus kinase 2 (JAK2)-V617F, protein-S, and antithrombin III deficiency with a high (76Á9%) prevalence of venous UTEs, multiple vessels thrombosis, and recurrence rate among the TG versus non-TG subcohort. The presence of JAK2-V617F, and FII-G20210A mutations was linked with SVT. Thrombosis in the non-TG subcohort was associated with more haemorrhagic problems, thrombosis progression and a significantly higher level of inflammatory markers, PTPP, mean platelet volume, von Willebrand factor, and factor VIII, which remained high for up to 6 months, as well as elevated D-dimer. Acquired and inherited thrombophilia with endotheliopathy appeared to be a relevant mechanism to explain the occurrence of UTEs that are not correlated to COVID-19 severity.

Background: Gliomas represent the most frequent primary tumors of central nervous system (CNS), contributing to more than half of the incidence of brain tumors. Cancer stem cell markers (CSC) identify a group of patients at high risk for progression. Nestin is an intermediate fi lament (IF) protein was fi rst described as a neural stem cell/progenitor cell marker. Nestin-positive neuroepithelial stem cells are detected in the subventricular zone of the human adult brain and they remain mitotically active throughout adulthood. The expression of Nestin in gliomas has been suggested to be related to dedifferentiation, improved cell motility, invasive potential and increased malignancy. This study aims to investigate Nestin immunohistochemical expression in different types of glioma and its correlation with different clinicopathological parameters. Materials and Methods:Nestin immunostaining was studied in 60 specimens of glioma using avidinbiotin peroxidase method.Results: Nestin was strongly expressed in 11/60 (18.33%), moderately expressed in 29/60 (48.33%) and weekly expressed in 15/60 (25%) of studied gliomas. A signifi cant positive correlation was found between Nestin expression and histologic type (p< 0.001) and increasing grade of gliomas (p< 0.001). Conclusion:Increased Nestin expression is correlated with tumor progression, increasing grade, and poor prognostic parameter of glioma. Nestin is a useful marker for detection of CSC in high-grade glioma which is responsible for resistance to chemo-radiotherapy and may serve as a predictor for patient outcomes.

Summary A total of 244 patients with hereditary haemolytic anaemias (HHA) were screened for acute symptomatic human parvovirus B19 infection (HPV‐B19) in a prospective study. To assess the risks associated with HPV‐B19 infection, patients were classified into Group I and Group II according to presence or absence (symptoms, signs and specific serology) of acute HPV‐B19 infection respectively. In all, 131 (53·7%) patients had β‐thalassaemia, 75 (30·7%) hereditary spherocytosis (HS), 27 (11·1%) sickle cell anaemia (SCA) and 11 (4·5%) glucose‐6‐phosphate dehydrogenase (G6PD) deficiency. Of 33 (13·5%) patients who presented with symptomatic HPV‐B19 infection, 19 (57·5%) had HS, nine (27·3%) had β‐thalassaemia and five (15·2%) had SCA. In Group I, there were significant differences in the mean white blood cell, red blood cell and platelet counts, haemoglobin concentration, total bilirubin (TB), alanine aminotransferase, aspartate aminotransferase and serum creatinine (all P < 0·001) compared to Group II. In all, 27 (81·8%) patients had arthropathy and bone marrow failure (BMF); 13 (39·4%) had acute kidney injury (AKI), more in SCA (80%); and 12 (36·4%) patients had hepatitis, more in HS (66·8%). Five (15·2%) patients with HS had BMF, AKI, nervous system involvement and extreme hyperbilirubinaemia (TB range 26·3–84·7 mg/dl). Five (15·2%) patients had haemophagocytic syndrome. Two patients with HS combined with Type‐I autoimmune hepatitis presented with transient BMF. Complete recovery or stabilisation was noted at 12 months in every patient except for one patient with SCA who died during the infection. HPV‐B19 must be suspected and screened in patients with HHA with typical and atypical presentations with careful follow‐up.

Background: Meningioma is a common intracranial tumor arising from the meningothelial (arachnoid) cells. Meningiomas are divided into 15 histological subtypes and three grades, including benign (grade I), atypical (grade II) and anaplastic (grade III). It is important to correctly decide whether a meningioma isbrain-invasive or not. Tumor invasion can be described as a stepwise process involving the degradation of the extracellular matrix (ECM), tumor cell adhesion to resident cells or components, increased proliferation, and cell migration into new intracellular/ECM space. It is believed that expression of Matrix metalloproteinases (MMPs) can be related with this process, especially the matrix metalloproteinase-9 (MMP9). Objectives: Investigation of matrix metalloproteinase-9 expression in different grades of meningioma and correlate this expression with brain invasion. Patients and methods: Matrix metalloproteinase-9 immunostaining was studied in 50 specimens of meningioma using avidin-biotin peroxidase method. Results: The percentage of brain invasive was 5% as regard to MMP9 score 1 ,5% as regard MMP9 score 2,20% as regard MMP9 score 3,70% as regard MMP9 score 4. A significant positive correlation was found between MMP9score and brain invasion (p< 0.001). Conclusion: Increased MMP9 expression is correlated with brain invasion.

Pterygium is one of the most commonly seen disease in ophthalmology.. Anatomically, the pterygium is composed of body, neck, head and a white-gray avascular subepithelial cap called (Fuch's Islands) (Chow et al., 2008).Despite being a very common disease, the exact pathogenesis of pterygium is still not clearly understood. Historically, pterygia were Considered a degenerative disorder. The most widely recognized etiological factor is ultraviolet radiation (Weinstein et al., 2002). Some authors described pterygia as a proliferative disorder resembling an aberrant wound healing (Di Girolamo et al., 2004).However at 2010, pterygium was described as an uncontrolled cellular proliferation of the conjunctiva (Tsai et al., 2010). Almost at that date, it was hypothesized that it may be due to loss of limbal stem cells in its niche and their Abstract:Background: Pterygium is one of the most commonly occurring eye diseases. It is widely regarded as a degenerative condition. Pterygium shares some similarities with tumors, as active cell proliferation.. P63, a member of the p53 gene family is a transcription factor that is crucial for the development and maintenance of stem cells in stratified epithelia. It is present in the limbus and sustains the proliferative potential of limbal stem cells. This study aims to evaluate the pattern of p63 expression in cases of pterygia, and to correlate this pattern with their clinicopathological parameters.Materials and methods: p63 immunostaining was studied in 52 specimens of nasal pterygia using avidin-biotin peroxidase method.Results: p63 was expressed in 61.5% of cases with variation in its expression, strong 25%, moderate 21.1%, and mild in 15.4% of cases. There was significant increase in p63 expression in recurrent pterygia than in primary (p<0.03). Conclusion:Pterygium is a disease of limbal stem cells as reinforces of P63 gene in the pathogenesis of pterygium could explain the triangular shape of pterygium and the high amount of recurrence.