Preventing Rupture: Clipping of Unruptured Intracranial Aneurysms

Unruptured intracranial aneurysms (UIAs) represent a major public health issue due to their unpredictable natural history. Whether to actively treat them or to maintain them under observation remains a hotly disputed topic. In this chapter, we present a review of the literature regarding the history of clipping and its use in UIAs, as well as the experience of our senior author in this field. We performed an extensive Medline and Google Academic search of the relevant literature. We have also made a retrospective analysis on patients harboring UIAs and multiple intracranial aneurysms (MIAs) clipped by the senior author between 1997 and 2017. About 89 patients had solitary UIAs, alongside 101 with MIAs possessing 257 individual aneurysms in total. All UIA patients were discharged with a favorable neurological outcome and no mortality. Concerning MIAs, the majority of cases had 2 aneurysms, the highest number being 6. And, 61 patients from this group had a favorable outcome. In the hands of experienced vascular neurosurgeons, clipping remains a safe option for both UIAs and MIAs. This procedure offers a long-lasting protection from aneurysmal rupture. In the future, new clip technologies and intraprocedural methods of verifying vessel patency and aneurysmal occlusion may further enhance postoperative results

HEMOLYTIC UREMIC SYNDROME – A CASE PRESENTATION

The presentation aims to illustrate in a didactic manner the clinical aspects, laboratory findings and the diagnostic steps in a case of hemolytic uremic syndrome (HUS), also pointing out the importance of differential diagnosis for the triad consisting of microangiopathic hemolytic anemia, thrombocytopenia and acute kidney injury. The clinician’s approach regarding the prognostic factors is also depicted, alongside the hallmarks concerning the treatment of HUS, the aspects of acute kidney injury monitoring and the need for a long term follow-up of HUS patients

Investigating the role of WT1-expressing progenitors and the function of WT1 in visceral adipose tissue angiogenesis

Unlike brown or subcutaneous white adipose tissue, visceral white adipose tissue (VWAT) is closely linked to cardiometabolic disease. The Wilms tumour 1 gene (WT1), an important developmental transcription factor, has been shown to be expressed in the progenitors of VWAT both in human and mouse. Moreover, adipose tissue expansion requires the formation of blood vessels and WT1 has previously been shown to be involved in angiogenesis during development and tumour formation. We were therefore interested in investigating the role of WT1 in VWAT angiogenesis by characterising the different WT1-expressing microvascular cell populations in VWAT and by focusing on the function of WT1 in angiogenesis. In order to look into the role of WT1 and WT1-expressing cells in vitro and in vivo, we used a lineage tracing (Wt1CreERT2; mTmG) mouse line and a reporter (Wt1GFP/+) line. Additionally, we used a conditional knock-out (CAGCreERT2; Wt1loxP/loxP) model, obtained by crossing CAGCreERT2 mice, where CreERT2 is expressed ubiquitously under the synthetic CAG promoter, with floxed Wt1loxP/loxP mice. We analysed WT1 expression in several main VWAT depots present in mice (epididymal, omental, mesenteric, perirenal and pericardial) and found that WT1 is expressed by CD31+ endothelial cells and PDGFRβ+ pericytes in several VWAT depots. Moreover, our lineage tracing experiments revealed that WT1-expressing cells give rise to cells which reside in the perivascular space of microvessels and that the contribution of WT1+ cells to the adipocyte population of VWAT is decreased in obesity. In humans, omental fat, which surrounds the intestines, is one of the most studied and easily accessible VWAT depots and our experiments on human omental VWAT showed that WT1-expressing cells are present in the perivascular area of microvessels and WT1 levels are increased during obesity. We further investigated the role of WT1, which we achieved by deleting WT1 in vitro in stromal vascular fraction cells and sorted pericytes. RNAi-mediated deletion of Wt1 did not show significant changes in in vitro angiogenic potential. Finally, we aimed to investigate the differences between WT1+ and WT1- pericytes in visceral adipose tissue, by using RNA sequencing to analyse the transcriptome of the two populations. Our data suggest that sub-populations of VWAT cells which express microvascular markers are derived from WT1-expressing cells, and also express WT1 in adulthood, which points to a potential role of WT1 in VWAT homeostasis and expansion. However, in our in vitro experiments, knocking down Wt1 in murine adipose-derived SVF cells and pericytes did not impair angiogenic potential

SINDROM HEMOLITIC UREMIC – PREZENTARE DE CAZ

Prezentarea dorește să ilustreze în mod didactic tabloul clinic, paraclinic și etapele stabilirii diagnosticului pozitiv în cazul sindromului hemolitic uremic (SHU), totodată ilustrând importanța diagnosticului diferențial pentru triada compusă din anemie hemolitică microangiopatică, trombocitopenie și insuficiență renală acută. S-a prezentat abordarea din punct de vedere al factorilor de prognostic, precum și particularitățile în ceea ce privește terapia SHU, aspecte ale evaluării insuficienței renale acute și necesitatea monitorizării pe termen lung a pacientului cu SH

Postpartum Acute Basilar Artery Occlusion Secondary to Vertebral Artery Dissection. Case Report and Literature Review

Female patients in the peripartum and postpartum periods have an increased risk of stroke than nonpregnant women. Cerebrovascular complications of pregnancy represent a significant cause of maternal mortality and morbidity and are potentially disabling. Acute basilar artery occlusion secondary to spontaneous vertebral artery dissection in the postpartum period is an infrequent entity and a major diagnostic and treatment challenge. In the present case, a 37-year-old female patient, eight weeks after caesarean delivery, presented with a history of sudden cervical pain, followed by headache and dizziness. Some hours later, she was found unconscious by her family and was transferred to the emergency department, where a neurological status assessment suggested vertebrobasilar stroke. The imagistic workup revealed right vertebral artery dissection and basilar artery occlusion without constituted ischemic lesions. The patient underwent endovascular intervention with dilation of the narrowed vertebral artery and stent retriever basilar artery thrombectomy, with a favourable clinical outcome. This report first presents the details of this case and the relevant literature data on postpartum arterial dissections and the subsequent ischemic complications and available treatment options

SINDROMUL NEFROTIC INFANTIL – PROVOCĂRI DE DIAGNOSTIC ŞI MANAGEMENT

Sindromul nefrotic infantil este caracterizat de proteinurie (> 40 mg/m2), hipoalbuminemie (2,5 mg/dl) și edeme cu debut între 4 şi 12 luni. Copiii cu sindrom nefrotic infantil nu prezintă simptomatologie la naștere, proteinuria apare ulterior, este tipic mai puţin severă decât în sindromul nefrotic de tip finlandez şi crește progresiv în primul sau al doilea an. Din punctul de vedere al etiologiei, sindromul nefrotic poate fi idiopatic, genetic sau secundar. Examenul histopatologic nu mai este considerat criteriu cheie în diagnosticul şi prognosticul sindromului nefrotic corticorezistent la copii, având valoare limitatã în delimitarea formelor genetice de alte etiologii. Podocitopatiile genetice au schimbat modul de abordare al diagnosticului, tratamentului şi prognosticului copiilor cu debut precoce al sindromului nefrotic corticorezistent. Deciziile terapeutice sunt luate în funcţie de etiologie

CHALLENGING INFANTILE NEPHROTIC SYNDROME – MANAGEMENT AND DIAGNOSTIC ISSUES

Infantile nephrotic syndrome (INS) is a kidney disorder characterized by nephrotic syndrome presenting between 4 and 12 months of age with hypoalbuminemia, ( 40 mg/m2 ) and edema. Children with infantile nephrotic syndrome appear normal at birth, proteinuria with a bland urine sediment develops postnatally, increasing progressively during the first or the second year of life. From the point of view of etiology, nephrotic syndrome may be idiopathic, genetic or secondary. Renal histopathology is not anymore a key criterion for diagnostic and prognostic in children with SRNS (steroid resistant nephrotic syndrome), having limited value in distinguishing genetic from nongenetic etiologies. Genetic podocytopathies changed diagnostic, prognostic judgment and therapeutic approaches in early onset SRNS. Therapeutic decisions are based on the underlying etiology

Arsenic trioxide plus cisplatin/interferon α-2b/doxorubicin/capecitabine combination chemotherapy for unresectable hepatocellular carcinoma

BACKGROUND AND OBJECTIVES: The failure of existing treatments for liver cancer has recently been attributed to the existence of cancer stem cells, which are difficult to kill using current drugs due to their chemoresistant properties as well as their ability to stimulate neoangiogenesis. The aim of the current study was to evaluate in vitro the antitumor efficacy of arsenic trioxide in combination with conventional chemotherapy, as proposed by the concept of “differentiation therapy” in anticancer research. MATERIALS AND METHODS: Cancer stem cells showed enhanced chemoresistance to cancer drugs (carboplatin and doxorubicin) and had the ability to exclude rhodamine 123 dye, proving the existence of the multidrug resistance efflux pump. Arsenic trioxide was added prior to a tyrosine kinase inhibitor or to a slightly modified Piaf regimen with capecitabine replacing 5-fluorouracil. We also compared both cancer and normal stem cell lines with the hepG2 non-stem liver cancer cell line to investigate the differences between differentiated and more anaplastic cells. Molecular characterization (immunocytochemistry and rt-PCr analysis) of all the cell lines was carried out. RESULTS: Initially, the cells had a high proliferative potential, even when cultured in a medium supplemented with cytostatics, eliminated rhodamine 123 immediately in culture and also formed spheroids in suspension. The molecular characterization showed the expression of albumin, α1-antitrypsin, α-fetoprotein, citokeratin-18, telomerase, CD90 and CD133. Low concentrations of arsenic trioxide lead to morphologic differentiation and differentiation-associated cytochemical features, like increased sensitivity to cytostatic drugs. CONCLUSION: Our study suggests that arsenic trioxide sensitizes liver stem-like cancer cells to conventional chemotherapy. Still, further studies on animal models will be needed before we implement this idea in human clinical trials