MASSIVE EDEMA OF OVARY-PSEUDOTUMOR: A CASE REPORT

Massive ovarian oedema is defined by WHO as formation of tumour like enlargement of one or both ovaries by oedema fluid in the stroma It is a benign lesion with age distribution varying from a neonate at six months of age to postmenopausal women up to 60-years-old. The differential diagnosis are ovarian fibromatosis, ovarian fibroma, sclerosing stromal tumour and ovarian myxoma. The common management of massive oedema of ovary is unilateral salpingo-oophorectomy, as the lesion is mistaken for primary ovarian neoplasm at laparotomy. Diagnosing MOE is of great importance to prevent unnecessary aggressive treatment in young patients to prevent infertility .We report this case of Massive Oedema of Ovary for its uncommonness.

Assessment of a Novel Method for Non-invasive Sampling of the Distal Airspace in Acute Respiratory Distress Syndrome Patients Receiving Inhaled Sedation with Sevoflurane: the ANAISS Study Protocol

ABSTRACTIntroductionRecently, fluid collected from the heat-and-moisture-exchange filters, which are commonly used in most mechanically ventilated patients under intravenous sedation, has been reported as a potential surrogate for fluid in the distal airspace. Therefore, collection of this fluid represents a promising, non-invasive method for sampling the distal airspace in patients with acute respiratory distress syndrome (ARDS) and for facilitating a mechanistic understanding of this devastating disease. The current study protocol was constructed to assess whether this fluid could be sampled from a dedicated device (Anaesthetic Conserving Device [AnaConDa-S], Sedana Medical, Danderyd, Sweden) used to deliver inhaled sevoflurane for sedation in patients with ARDS.Methods and analysisA total of 30 adult patients within 24 hours of meeting the Berlin criteria for moderate-severe ARDS and receiving inhaled sevoflurane as standard sedation in participating centres will be eligible for inclusion into this investigator-initiated, exploratory, prospective, bicentre study. After at least 12 h of inhaled sedation, a sample of directly aspirated, undiluted pulmonary oedema fluid will be collected concurrently with fluid from the AnaConDa-S device. Levels of proinflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α and sTNFr-1) and markers of lung endothelial (Ang-2) and epithelial (sRAGE) injury will be measured in both fluids by Multiplex. The primary endpoint is the correlation between protein markers (IL-1β, IL-6, IL-8, TNF-α, sTNFr-1, Ang-2 and sRAGE) measured in the undiluted pulmonary oedema fluid versus the AnaConDa-S fluid.Ethics and disseminationThe study was approved by the appropriate ethics committee (CPP Est I). Informed consent is required. The fluid collection from the AnaConDa-S has potential to foster our understanding of the potential effects of inhaled sedation in clinical ARDS and to open up novel perspectives for prognostic and predictive enrichment in future trials. The results will be published in a peer-reviewed journal.Registration numberNCT03964155.

Necrotic enteritis and its management in 13-week old commercial pullets in Katsina, Nigeria

Necrotic enteritis is rarely reported because it is often misdiagnosed as coccidiosis due to similarity in clinical and pathological features. A field outbreak of necrotic enteritis in a flock of 13 weeks old 4,500 commercial pullets was investigated, the onset of the disease, morbidity and mortality rates were recorded. Post mortem examinations were conducted and gross lesions were documented. Tissues were collected and fixed in 10 % neutral buffered formalin and processed for histopathological examinations. Clinical signs observed were ruffled feathers, weakness, somnolence, loss of weight and diarrhoea; while the gross lesions observed were emaciated carcasses, lean abdominal fat, enlarged, pale and haemorrhagic liver; enlarged, mottled and congested spleen; mucus and diphtheritic membrane on the jejunal mucosa and enlarged kidneys. The histopathological findings of the intestine were diffused necrotic epithelial cells with marked mononuclear cells infiltration in the mucosa with severe oedema fluid. The necrotic enteritis was diagnosed based on clinical signs, pathology as well as isolation and identification of Clostridium perfringes. Triplesulfa® (sulfadimidine sodium, sulfadiazine sodium and sulfamerazine sodium); Tridox® L.A (20% Oxytetracycline long acting) and Enterocillin® (Amoxycillintrihydrate and Colistin sulphate) were ineffective, while copper sulphate at 1g/5L of drinking water was found to be effective for the treatment of the disease. The haematological values indicated lymphocytosis due to damage of the tissue caused by C. perfringes and the toxins produced. Keywords: Necrotic enteritis, Commercial pullets, Copper sulphate, Clostridium perfringens

Plasmin improves oedematous blood-gas barrier by cleaving epithelial sodium channels

ABSTRACTBackground and PurposeLung oedema in association with suppressed fibrinolysis is a hallmark of lung injury. We aimed to test whether plasmin cleaves epithelial sodium channels (ENaC) to resolve lung oedema fluid.Experimental ApproachesHuman lungs and airway acid-instilled mice were used for analysing fluid resolution. In silico prediction, mutagenesis, Xenopus oocytes, immunoblotting, voltage clamp, mass spectrometry, protein docking, and alveolar fluid clearance were combined for identifying plasmin specific cleavage sites and benefits.Key ResultsPlasmin led to a marked increment in lung fluid resolution in both human lungs ex vivo and injured mice. Plasmin specifically activated αβγENaC channels in oocytes in a time-dependent manner. Deletion of four consensus proteolysis tracts (αΔ432-444, γΔ131-138, γΔ178-193, and γΔ410-422) eliminated plasmin-induced activation significantly. Further, immunoblotting assays identified 7 cleavage sites (K126, R135, K136, R153, K168, R178, K179) for plasmin to trim both furin-cleaved C-terminal fragments and full-length human γENaC proteins. In addition to confirming the 7 cleavage sites, 9 new sites (R122, R137, R138, K150, K170, R172, R180, K181, K189) in synthesized peptides were found to be cleaved by plasmin with mass spectrometry. These cleavage sites were located in the finger and the thumb, particularly the GRIP domain of human ENaC 3D model composed of two proteolytic centres for plasmin. Novel uncleaved sites beyond the GRIP domain in both α and γ subunits were identified to interrupt the plasmin cleavage-induced conformational change in ENaC channel complexes. Additionally, plasmin could regulate ENaC activity via the G protein signal.Conclusion and ImplicationsWe demonstrate that plasmin could cleave ENaC to benefit the blood-gas exchange by resolving oedema fluid as a potent fibrinolytic therapy for oedematous pulmonary diseases.Bullet point summaryWhat is already knowSerine proteases proteolytically cleave epithelial sodium channels, including plasmin and uPA acutely.Activity of epithelial sodium channels is increased post proteolysis.What this study addsPlasmin cleaves up to 16 sites composed of two proteolytic centres in both full-length and furin-cleaved human γ subunit of epithelial sodium channels in hours.Non-proteolytic sites in both α and γ subunits interrupt the plasmin cleavage-induced channel gating.Intratracheally instilled plasmin facilitates alveolar fluid clearance in normal human and injured mouse lungs.Clinical significanceActivation of human lung epithelial sodium channels by plasmin may benefit lung oedema resolution as a novel therapy for ARDS.