98 research outputs found
Harmful organisms in greenhouse production on vegetables and flowers in Äakovo 2016
Istraživanje je provedeno u plastenicima Srednje strukovne Å”kole Antuna Horvata u Äakovu u 2016. godini. Cilj istraživanja je bio praÄenje Å”tetnika u plasteniÄkom uzgoju povrÄa i cvijeÄa, te utjecaj razliÄitih supstrata na visinu presadnica. Pojava Å”tetnih kukaca pratila se vizualnim pregledom biljaka i uz pomoÄ Å¾utih i plavih ljepljivih ploÄa. Vizualnim pregledom biljaka utvrÄena je pojava lisnih uÅ”i na paprici i krastavcima te je provedeno tretiranje kemijskim pripravkom Mospilan 20 SP u koncentraciji 0,03% koje je uspjeÅ”no suzbilo ovog Å”tetnika. Na Engleskim pelargonijama se pojavio cvjetni Å”titasti moljac, zaÅ”tita protiv ovog Å”tetnika nije primjenjena. Na kadificama su se pojavili puževi koji su uklonjeni mehaniÄkim putem. U buduÄnosti, trebalo bi se voditi viÅ”e brige o pojavi Å”tetnika, pratiti okoliÅ” plastenika kako s tih povrÅ”ina ne bi doÅ”lo do napada puževa.The study was conducted in greenhouses Secondary vocational school Antun Horvat in Äakovo in 2016.The aim of this research was pests monitoring in greenhouse cultivation of vegetables and flowers, and the influence of different substrates on the height of seedlings. The appearance of harmful insects was followed by visual examination of plants, and also with yellow and blue sticky boards. It was found aphids on peppers and cucumbers and it was applied chemical preparation Mospilan 20 SP in a concentration of 0.03%, which successfully suppress this pest. In English geraniums appeared flower whitefly protection against this pest not applied. On Tagetes appeared the slugs, and they are removed mechanically. In the future, should pay more attention of the appearance of pests, monitor the environment greenhouses to prevent aslugs attac
The significance of alarmins ininflammatory rheumatic diseases
Razumijevanje imunopatogeneze upalnih reumatskih bolesti joÅ” uvijek je nepotpuno. Iako je opisana uloga alarmina u razliÄitim upalnim i autoimunim bolestima,kliniÄka ispitivanja iz tog podruÄja joÅ” uvijek su rijetka. U radu je prikazana literatura koja govori o znaÄenju trinajÄeÅ”Äa alarmina: proteina visoke pokretljivosti iz skupine 1 (HMGB1, engl. high mobility group box 1), proteina koji vežu kalcij S100A8/9 i S100A12 (S100A8/9, S100A12, engl. calcium-binding protein S100A12) i njihova topljiva receptora za krajnje produkte uznapredovale glikozilacije sRAGE (RAGE, engl. soluble receptor for advanced glycation end products) u upalnim reumatskim bolestima.Prema dosadaÅ”njim spoznajama smatra se da HMGB1, kao medijator priroÄene imunosti, u interakciji sa sRAGE sudjeluje u imunopatogenezi upalnih reumatskih bolesti te može služiti kao biomarker za odreÄivanje aktivnosti i moguÄa meta u lijeÄenju navedene skupine bolesnika.Our understanding of the imunopathogenesis of inflammatory rheumatic diseases is still incomplete. The involvement of alarmins in various inflammatory and autoimmune diseases has been documented but clinical trials on the contribution of this molecules are basically absent. In this article we summarized the literature about the significance of the three most common alarmins: high mobility group box 1 (HMGB1), calcium-binding proteins S100A8/9 and S100A12 and their soluble receptor for advanced glycation end products (sRAGE) in inflammatory rheumatic diseases. According to our previous knowledge, it is considered that HMGB1 through interactions with sRAGE contributes to imunopathogenesis of inflammatory rheumatic diseases. Furthermore, HMGB1 may serve as a biomarker for determining disease activity and a potential target of therapy in systemic inflammatory rheumatic diseases patients
Rituximab in Treatment of Children with Refractory Vasculitis and Systemic Lupus Erythematosus ā Single Center Experience in Croatia
The aim of this study was to present our experience
in rituximab therapy in patients with childhood-onset systemic
lupus erythematosus, lupus nephritis, and ANCA-associated vasculitis.
We conducted a retrospective clinical chart review of all
patients treated with rituximab in the time period from January
2009 to December 2015. Eight patients (3 boys and 5 girls)
aged 8 to 15 at the onset of disease were treated with rituximab.
Remission of disease was accomplished in 4 patients with childhood-
onset systemic lupus erythematosus and lupus nephritis, a
partial improvement was achieved in 1 patient with childhoodonset
systemic lupus erythematosus and lupus nephritis as well
as in 2 patients with vasculitis, while in one patient with vasculitis
treatment with rituximab showed no effect and the patient
died due to Candida sepsis. Reduction of corticosteroid doses
was enabled by rituximab treatment. Rituximab appeared to be
a safe and efficient therapeutic option in severe cases of childhood-
onset systemic lupus erythematosus or ANCA-associated
vasculitis that failed to respond to conventional therapy or as a
rescue therapy in life-threatening conditions
KADA POSUMNJATI NA AUTOINFLAMATORNU BOLEST?
Autoinflammatory diseases are clinical disorders caused by a deficiency or dysregulation of innate immunity, characterized by recurrent or persistent inflammation (increased levels of acute phase reactants) and the absence of a primary pathogenic role of adaptive immunity (autoreactive T lymphocytes or antibody production). They are clinically manifested by recurrent episodes of systemic inflammation due to the activation of an intense nonspecific inflammatory reaction with no apparent or sufficient cause. In terms of pathogenesis, autoinflammatory diseases can be divided into monogenic, or those that are caused by a mutation in a well-defined gene, and non-monogenic, also referred to as unclassified. According to the three main pathogenic patterns of emergence in monogenic autoinflammatory diseases described to date, they are divided into inflammasomopathies, interferonopathies, and ubiquitinopathies. Clinically, inflammasomopathies are most commonly manifested by fever (often periodic type), rash, serositis, hepatosplenomegaly, and lymphadenopathy. The therapeutic approach in many of these diseases is based on the use of an interleukin-1 inhibitor. Interferonopathies are most commonly manifested as acral and lung vasculopathy and fibrosis, with an onset of skin changes like chilblains,
intracranial calcifications, and myositis. Janus kinase inhibitors are used in the treatment. Ubiquitinopathies are most commonly manifested by granuloma, ulceration, uveitis, and immunodeficiency. The therapeutic approach in these diseases is based on the use of tumor necrosis factor-alpha inhibitors. Unclassified autoinflammatory diseases include diseases that meet the clinical and biological criteria for autoinflammatory diseases but to date have no detected genetic background (for example, syndrome of periodic fever, aphthous stomatitis, pharyngitis and cervical adenitis, Schnitzler syndrome, or systemic-onset juvenile idiopathic arthritis), and some multifactorial diseases that are polygenic or caused by complex interactions of multiple genes and environmental factors and not associated with Mendelian inheritance patterns (eg., gout, Behcet disease). In the diagnosis of patients with suspected autoinflammatory disease, it is necessary to exclude infections, malignancies, immunodeficiencies, and rheumatic diseases. The main indication for genetic testing is the presence of clinical symptoms that meet the criteria for one or more autoinflammatory diseases. There are a number of unanswered questions in genetic diagnostics, the main problem being the interpretation of the results.Autoinflamatorne bolesti kliniÄki su poremeÄaji uzrokovani nedostatkom ili poremeÄajem regulacije priroÄene
imunosti, a obilježavaju ih ponavljana ili stalna upala (poviŔeni reaktanti akutne faze) i odsutnost primarne patogenetske
uloge steÄene imunosti (autoreaktivni T-limfociti ili proizvodnja protutijela). KliniÄki se manifestiraju ponavljanim
epizodama sustavne upale zbog aktivacije intenzivne nespecifiÄne upalne reakcije bez oÄitog ili dovoljnog uzroka.
U patogenetskom smislu mogu se podijeliti na monogenske, odnosno na one koje su uzrokovane mutacijom u
jednom, dobro definiranom genu i na one koje nisu monogenske, a oznaÄavaju se i kao neklasificirane. Prema tri glavna
patogenetska obrasca nastanka, do danas opisane monogenske autoinflamatorne bolesti dijele se na inflamasomopatije,
interferonopatije i ubikvitinopatije. KliniÄki se inflamasomopatije najÄeÅ”Äe manifestiraju vruÄicom (nerijetko
periodiÄna tipa), osipima, serozitisom, hepatosplenomegalijom i limfadenopatijom. Terapijski pristup u velikom broju
ovih bolesti temelji se na primjeni inhibitora interleukina 1. Interferonopatije se najÄeÅ”Äe manifestiraju vaskulopatijama
ekstremiteta i pluÄa, nastankom fibroznih promjena, kožnih promjena nalik na ozebline, intrakranijalnim kalcifikacijama
i miozitisom. U lijeÄenju se rabe inhibitori Janusove kinaze. Ubikvitinopatije se najÄeÅ”Äe oÄituju nastankom
granuloma, ulceracija, uveitisa te imunodeficijencijom. Terapijski pristup u ovim bolestima temelji se na primjeni
inhibitora
Äimbenika tumorske nekroze alfa.
U skupinu neklasificiranih autoinflamatornih bolesti ubrajaju se bolesti koje zadovoljavaju kliniÄko-bioloÅ”ke kriterije
za autoinflamatorne bolesti, ali do danas nemaju otkrivenu gensku podlogu (primjerice, sindrom periodiÄne
vruÄice, aftoznog stomatitisa, faringitisa i adenitisa, Schnitzlerin sindrom, sustavni oblik juvenilnog idiopatskog artritisa),
kao i neke multifaktorske bolesti koje su poligenske, odnosno uvjetovane složenim interakcijama veÄeg broja
gena i okoliÅ”nih Äimbenika te nisu povezane s mendelovskim obrascem nasljeÄivanja (primjerice, giht, BehƧetova
bolest).
Pri obradi bolesnika sa sumnjom na autoinflamatornu bolest potrebno je iskljuÄiti infekcije, zloÄudne bolesti,
imunodeficijencije i reumatske bolesti. Glavna je indikacija za gensko testiranje prisutnost kliniÄkih simptoma koji
ispunjavaju kriterije za jednu ili viŔe autoinflamatornih bolesti. U genskoj dijagnostici postoji niz neodgovorenih pitanja,
meÄu kojima je glavni problem interpretacija nalaza
VASCULITIDES IN CHILDHOOD
Primarni sistemski vaskulitisi u djece relativno su rijetke bolesti, veÄinom nepoznate etiologije, kojima
je zajedniÄko obilježje upala u stijenci krvne žile. TeÅ”ko ih je dijagnosticirati jer su zahvaÄeni mnogi organi, a simptomi
su uglavnom nespecifi Äni. U posljednjih 10 godina postignut je znatan napredak u podruÄju vaskulitisa u djeÄjoj dobi:
defi nirani su i validirani klasifi kacijski kriteriji, razvijeni i validirani upitnici za procjenu aktivnosti bolesti i ishoda,
pedijatrijski bolesnici ukljuÄeni su u meÄunarodna multicentriÄna istraživanja vezana uz terapiju vaskulitisa, zapoÄeta
su kliniÄka istraživanja izuzetno rijetkih vaskulitisa i izdvojena je zasebna skupina rijetkih monogenskih vaskulitisa.
Ovim radom želimo upoznati Äitaoce s velikim iskorakom u podruÄju vaskulitisa u djeÄjoj dobi, nastalim na osnovi
mukotrpnog rada pedijatrijskih reumatologa u radnim skupinama za vaskulitise.Primary systemic vasculitides in children are relatively rare diseases. In most cases, they have an unknown
etiology and are defi ned as the presence of infl ammation in the blood vessel wall. Establishing the diagnosis of
vasculitis is oft en challenging, since the disorder is multisystem in nature with mostly nonspecifi c symptoms. Th e last
10 years have seen signifi cant advances in the fi eld of pediatric vasculitis: the development and validation of classifi cation
criteria as well as tools to assess clinical disease activity and disease outcome, the inclusion of pediatric patients in
international multicentre randomized controlled trial designs for therapies of vasculitis, clinical trials for very rare
pediatric vasculitides, and identifi cation of a special group of monogenic vasculitides. In this paper we want to introduce
readers to the giant leap in the fi eld of pediatric vasculitis as a result of the hard work of pediatric rheumatologists
in vasculitis work groups
The presence of high mobility group box-1 and soluble receptor for advanced glycation end-products in juvenile idiopathic arthritis and juvenile systemic lupus erythematosus
BACKGROUND:
The involvement of high mobility group box-1 (HMGB1) in various inflammatory and autoimmune diseases has been documented but clinical trials on the contribution of this pro-inflammatory alarmin in children with juvenile idiopathic arthritis (JIA) and systemic lupus erythematosus (SLE) are basically absent. To address the presence of HMGB1 and a soluble receptor for advanced glycation end products (sRAGE) in different subtypes of JIA and additionally in children with SLE, we enrolled a consecutive sample of children harvested peripheral blood as well as synovial fluids (SF) at diagnosis and correlated it with ordinary acute-phase reactants and clinical markers. ----- METHODS:
Serum and synovial fluids levels of HMGB1 and sRAGE in total of 144 children (97 with JIA, 19 with SLE and 27 healthy controls) were determined by ELISA. ----- RESULTS:
The children with JIA and those with SLE were characterised by significantly higher serum levels of HMGB1 and significantly lower sRAGE levels compared to the healthy controls. A positive correlation between serum HMGB1 and ESR, CRP, Ī±2 globulin was found while serum sRAGE levels were inversely correlated with the same inflammatory markers in children with JIA. Additionally, high level of serum HMGB1 was related to hepatosplenomegaly or serositis in systemic onset JIA. ----- CONCLUSION:
The inverse relationship of the HMGB1 and its soluble receptor RAGE in the blood and SF indicates that inflammation triggered by alarmins may play a role in pathogenesis of JIA as well as SLE. HMGB1 may serve as an inflammatory marker and a potential target of biological therapy in these patients. Further studies need to show whether the determination of HMGB1 levels in patients with JIA can be a useful guideline for detecting disease activity
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