Protozoa exert a serious global threat of growing concern to human, and animal, and there is a need for the advancement of novel therapeutic strategies to effectively treat or mitigate the impact of associated diseases. Omega polyunsaturated fatty acids (ω-PUFAs), including Omega-3 (ω-3) and omega-6 (ω-6), are constituents derived from various natural sources, have gained significant attention for their therapeutic role in parasitic infections and a variety of essential structural and regulatory functions in animals and humans. Both ω-3 and ω-6 decrease the growth and survival rate of parasites through metabolized anti-inflammatory mediators, such as lipoxins, resolvins, and protectins, and have both in vivo and in vitro protective effects against various protozoan infections. The ω-PUFAs have been shown to modulate the host immune response by a commonly known mechanism such as (inhibition of arachidonic acid (AA) metabolic process, production of anti-inflammatory mediators, modification of intracellular lipids, and activation of the nuclear receptor), and promotion of a shift towards a more effective immune defense against parasitic invaders by regulation the inflammation like prostaglandins, leukotrienes, thromboxane, are involved in controlling the inflammatory reaction. The immune modulation may involve reducing inflammation, enhancing phagocytosis, and suppressing parasitic virulence factors. The unique properties of ω-PUFAs could prevent protozoan infections, representing an important area of study. This review explores the clinical impact of ω-PUFAs against some protozoan infections, elucidating possible mechanisms of action and supportive therapy for preventing various parasitic infections in humans and animals, such as toxoplasmosis, malaria, coccidiosis, and chagas disease. ω-PUFAs show promise as a therapeutic approach for parasitic infections due to their direct anti-parasitic effects and their ability to modulate the host immune response. Additionally, we discuss current treatment options and suggest perspectives for future studies. This could potentially provide an alternative or supplementary treatment option for these complex global health problems.

The emergence of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has affected many countries throughout the world. As urgency is a necessity, most efforts have focused on identifying small molecule drugs that can be repurposed for use as anti-SARS-CoV-2 agents. Although several drug candidates have been identified using in silico method and in vitro studies, most of these drugs require the support of in vivo data before they can be considered for clinical trials. Several drugs are considered promising therapeutic agents for COVID-19. In addition to the direct-acting antiviral drugs, supportive therapies including traditional Chinese medicine, immunotherapies, immunomodulators, and nutritional therapy could contribute a major role in treating COVID-19 patients. Some of these drugs have already been included in the treatment guidelines, recommendations, and standard operating procedures. In this article, we comprehensively review the approved and potential therapeutic drugs, immune cells-based therapies, immunomodulatory agents/drugs, herbs and plant metabolites, nutritional and dietary for COVID-19.

Mastitis is a major health problem for bovines and can be categorized as non-severe or severe, based on clinical symptoms. A severe case of clinical mastitis is usually defined by the cow being affected systemically. It is important to consider how to handle severe cases because these cases can be fatal and cause high production losses. However, there are generally few detailed treatment guidelines. By conducting a scoping review on the topic, we aimed to synthesize the information that is available on treatment and outcomes, as reported from clinical trials and observational studies. This was facilitated by following the PRISMA-guidelines with a stepwise systematic screening of scientific literature on the subject, retrieved via Pubmed and Web of Science, using pre-defined selection criteria. The results yielded a total of 14 reports of treatment and outcomes in cases of naturally occurring severe clinical mastitis. Cross-trial comparison was difficult due to the different exclusion criteria and outcome definitions. Many studies focused on cases caused by gram-negative bacteria treated with intensive antibiotic protocols, often containing antibiotics that are categorized as critical for human health. Few focused on severe cases caused by gram-positive bacteria or on the relative use of non-antibiotic treatment. In general, only a small number of statistically significant differences were found in trials comparing different treatment protocols, with no obvious trends across trials. Our findings emphasize the need for more research into the treatment efficacy of antibiotic and non-antibiotic options for clinically severe mastitis. Furthermore, consideration of how trial conditions relate to the practical circumstances in a field setting could improve the applicability of reported results. This could help to provide practitioners with the information needed to make evidence-based treatment decisions in cases of clinically severe mastitis.

The manuscript summarizes the consensus of the Austrian Society of Nephrology on the diagnosis and therapy of lupusnephritis, which is built on existing studies and literature. We discuss in detail the immunosuppressive treatment in proliferative forms of lupusnephritis (III and IV ± V) and in pure lupusnephritis V with nephrotic-range proteinuria. Furthermore, the supportive medication in lupusnephritis is summarized in the consensus. The figures were designed to provide the reader a guidance through the therapeutical approach in lupusnephritis for the daily practice.
UNASSIGNED: Das vorliegende Manuskript fasst die Empfehlungen der Österreichischen Gesellschaft für Nephrologie zur Diagnose und Therapie der Lupusnephritis zusammen und erläutert die Hintergründe der entsprechenden Empfehlungen anhand der vorhandenen Literatur. Wir besprechen im Detail die immunsuppressive Therapie in proliferativen Stadien der Lupusnephritis (Stadium III und IV mit/ohne Stadium V) und in der Lupusnephritis im reinen Stadium V mit großer Proteinurie. Zudem wird auch die konservative, supportive Therapie der Lupusnephritis detailliert besprochen. In den Abbildungen haben wir versucht, einen Leitfaden für die Praxis zur Therapie der Lupusnephritis zu erstellen.

The histopathological term focal-segmental glomerulosclerosis comprises different pathogenic processes with the unifying features of a high proteinuria and the name-giving glomerular lesion pattern seen on light microscopy. A differentiation according to the underlying cause into primary, secondary and genetic forms is therefore of utmost importance. The pathogenesis of primary focal-segmental glomerulosclerosis remains unknown but, like minimal-change disease, an autoimmune-mediated process leading to podocyte damage is assumed. Consequently, the unifying term \"podocytopathy\" is increasingly being used for both entities. Supportive treatment measures to preserve kidney function are important in all subtypes. In contrast, immunosuppressive treatment is only indicated in primary focal-segmental glomerulosclerosis. Steroid-dependence, steroid-resistance and frequently relapsing disease often complicate disease management and necessitate alternative treatment strategies. Here, the Austrian Society of Nephrology (ÖGN) provides consensus recommendations on how to best diagnose and manage patients with focal-segmental glomerulosclerosis.
UNASSIGNED: Der histopathologische Begriff fokal-segmentale Glomerulosklerose umfasst verschiedene Krankheitsprozesse mit dem gemeinsamen Kennzeichen einer großen Proteinurie und dem namensgebenden glomerulären Schädigungsmuster in der Lichtmikroskopie. Eine Einteilung in primäre, sekundäre und genetische Formen anhand der zugrundeliegenden Pathogenese ist daher von großer Relevanz. Die exakte Pathogenese der primären fokal-segmentalen Glomerulosklerose ist ungeklärt, allerdings wird – analog zur Minimal-change Glomerulopathie – eine autoimmun-vermittelte Schädigung der Podozyten angenommen. Angesichts des ähnlichen Pathomechanismus findet zunehmend die vereinende Bezeichnung „Podozytopathie“ Verwendung. Supportive Therapiemaßnahmen zum Erhalt der Nierenfunktion sind bei allen Formen angezeigt. Demgegenüber sollten immunsuppressive Therapien nur bei der primären fokal-segmentalen Glomerulosklerose zum Einsatz kommen. Komplizierte Verläufe umfassen steroid-abhängige, steroid-resistente und häufig relapsierende Formen und erfordern den Einsatz alternativer Therapiestrategien. Die Österreichische Gesellschaft für Nephrologie (ÖGN) stellt hier einen gemeinsamen Konsens darüber vor, wie erwachsene PatientInnen mit fokal-segmentaler Glomerulosklerose am besten diagnostiziert und behandelt werden können.

Immunoglobulin A nephropathy (IgAN) is the most common glomerulonephritis. It leads to end-stage kidney disease in about a third of the patients within 10 to 20 years. The pathogenesis of IgAN is incompletely understood. It is believed that a dysregulation of the mucosal immune system leads to undergalactosylation of IgA, followed by formation of IgG autoantibodies against undergalactosylated IgA, circulation of these IgG-IgA immune complexes, deposition of the immune complexes in the mesangium, ultimately resulting in glomerular inflammation. IgAN can occasionally be triggered by other diseases, these secondary causes of IgAN should be identified or ruled out (chronic inflammatory bowel disease, infections, tumors, rheumatic diseases). Characteristic findings of IgAN of variable extent are a nephritic urinary sediment (erythrocytes, acanthocytes, erythrocyte casts), proteinuria, impaired renal function, arterial hypertension, or intermittent painless macrohematuria, especially during infections of the upper respiratory tract. However, the diagnosis of IgAN can only be made by a kidney biopsy. A histological classification (MEST‑C score) should always be reported to be able to estimate the prognosis. The most important therapeutic measure is an optimization of the supportive therapy, which includes, among other things, a consistent control of the blood pressure, an inhibition of the RAS, and the administration of an SGLT2 inhibitor. A systemic immunosuppressive therapy with corticosteroids is discussed controversially, should be used restrictively and only administered after an individual benefit-risk assessment under certain conditions that speak for a progressive IgAN. New promising therapeutics are enteral Budesonide or the dual angiotensin-II-receptor- and endothelin-receptor-antagonist Sparsentan. Rapidly progressive IgAN should be treated with corticosteroids and cyclophosphamide like ANCA-associated vasculitis.
UNASSIGNED: Die Immunglobulin A Nephropathie (IgAN) ist die häufigste Glomerulonephritis weltweit und führt bei ungefähr einem Drittel der PatientInnen innerhalb von 10 bis 20 Jahren zur terminalen Nierenerkrankung. Die Pathogenese der IgAN ist nicht eindeutig geklärt. Vermutlich kommt es durch eine Dysregulation des mukosalen Immunsystems zu einer Untergalaktosylierung der IgA-Moleküle, Bildung von IgG Auto-Antikörpern und zur Zirkulation von IgG-IgA-Immunkomplexen, welche sich im Mesangium ablagern und schließlich zur Glomerulonephritis führen. Eine IgAN kann gelegentlich durch eine andere Erkrankung ausgelöst werden, deswegen sollten diese sekundären Ursachen einer IgAN identifiziert bzw. ausgeschlossen werden (chronisch entzündliche Darmerkrankungen, Infektionen, Tumore, rheumatische Erkrankungen). Charakteristische Befunde einer IgAN im variablen Ausmaß sind ein nephritisches Harnsediment (dysmorphe Erythrozyten, Akanthozyten, Erythrozytenzylinder), Proteinurie, eine Einschränkung der Nierenfunktion, eine arterielle Hypertonie, oder auch eine intermittierende schmerzlose Makrohämaturie, vor allem bei Infekten des oberen Respirationstraktes. Die Diagnose einer IgAN kann jedoch ausschließlich durch eine Nierenbiopsie gestellt werden. Dabei sollte eine histologische Klassifizierung (MEST‑C score) durchgeführt werden, um die Prognose abschätzen zu können. Die wichtigste therapeutische Maßnahme besteht in einer Optimierung der supportiven Therapie, das beinhaltet u. a. eine konsequente Kontrolle des Blutdrucks, eine Hemmung des RAS, und die Gabe eines SGLT2-Hemmers. Eine systemische immunsuppressive Therapie mit Kortikosteroiden wird kontroversiell diskutiert, sollte restriktiv gehandhabt und nur nach individueller Nutzen-Risiko-Abwägung unter bestimmten Bedingungen, die für eine progressive IgAN sprechen, verabreicht werden. Neue vielversprechende Therapeutika sind enterales Budesonid oder der duale Angiotensin-II-Rezeptor- und Endothelin-Rezeptor-Antagonist Sparsentan. Eine rapid-progressive IgAN sollte mit Kortikosteroiden und Cyclophosphamid ähnlich einer ANCA-assoziierten Vaskulitis behandelt werden.

Fat embolism syndrome (FES) is known to occur when fat macroglobules get embolized into the blood circulation, whereby they then get dispersed out to multiple organs including the brain. It\'s typically diagnosed when the patient sustains a neurological dysfunction, respiratory insufficiency, and petechial rash, the classical triad of FES. Cerebral fat embolism occurrence is rarely seen. In this case report, a 20-year-old male was admitted due to a closed left midshaft femur fracture from a motor vehicle accident, and sustained cerebral manifestation of fat embolism syndrome 32 hours post the incident. It was noted that the patient had the classical triad of FES and intubation was done for airway protection. MRI revealed features of cerebral fat embolism. Interlocking nail fixation of the left femur was done for this patient on day three after admission. On day 15 post trauma, the patient was successfully extubated. Adequate supportive management was given and the patient\'s prognosis improved. As a practitioner, it is important to recognize and diagnose cerebral fat embolism as early as possible so as to have a much better outcome and to avoid any unnecessary investigation.

Duchenne muscular dystrophy (DMD), the severest form of muscular dystrophy, is characterized by progressive muscle weakness with fatal outcomes most often before the fourth decade of life. Despite the recent addition of molecular treatments, DMD remains a disease without a cure, and the need persists for the development of supportive therapies aiming to help improve patients\' quality of life. This review focuses on the therapeutical potential of amino acid and derivative supplements, summarizing results obtained in preclinical studies in murine disease models. Several promising compounds have emerged, with L-arginine, N-acetylcysteine, and taurine featuring among the most intensively investigated. Their beneficial effects include reduced inflammatory, oxidative, fibrotic, and necrotic damage to skeletal muscle tissues. Improvement of muscle strength and endurance have been reported; however, mild side effects have also surfaced. More explorative, placebo-controlled and long-term clinical trials would need to be conducted in order to identify amino acid formulae that are safe and of true benefit to DMD patients.

Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative disorder affecting upper and lower motor neurons, with death resulting mainly from respiratory failure three to five years after symptom onset. As the exact underlying causative pathological pathway is unclear and potentially diverse, finding a suitable therapy to slow down or possibly stop disease progression remains challenging. Varying by country Riluzole, Edaravone, and Sodium phenylbutyrate/Taurursodiol are the only drugs currently approved in ALS treatment for their moderate effect on disease progression. Even though curative treatment options, able to prevent or stop disease progression, are still unknown, recent breakthroughs, especially in the field of targeting genetic disease forms, raise hope for improved care and therapy for ALS patients. In this review, we aim to summarize the current state of ALS therapy, including medication as well as supportive therapy, and discuss the ongoing developments and prospects in the field. Furthermore, we highlight the rationale behind the intense research on biomarkers and genetic testing as a feasible way to improve the classification of ALS patients towards personalized medicine.

Diffuse large B-cell lymphoma (DLBCL) accounts for approximately 24% of new cases of B-cell non-Hodgkin lymphoma in the US each year. Up to 50% of patients relapse or are refractory (R/R) to the standard first-line treatment option, R-CHOP. The anti-CD19 monoclonal antibody tafasitamab, in combination with lenalidomide (LEN), is an NCCN preferred regimen for transplant-ineligible patients with R/R DLBCL and received accelerated approval in the US (July 2020) and conditional marketing authorization in Europe (August 2021) and other countries, based on data from the L-MIND study. The recommended dose of tafasitamab is 12 mg/kg by intravenous infusion, administered in combination with LEN 25 mg for 12 cycles, followed by tafasitamab monotherapy until disease progression or unacceptable toxicity. Tafasitamab + LEN is associated with durable responses in patients with R/R DLBCL. The majority of clinically significant treatment-associated adverse events are attributable to LEN and can be managed with dose modification and supportive therapy. We provide guidelines for the management of patients with R/R DLBCL treated with tafasitamab and LEN in routine clinical practice, including elderly patients and those with renal and hepatic impairment, and advice regarding patient education as part of a comprehensive patient engagement plan. Our recommendations include LEN administration at a reduced dose if required in patients unable to tolerate the recommended dose. No dose modification is required for tafasitamab in special patient populations.