Standardna lumbalna diskektomija nasuprot mikrodiskektomiji – razlike u ishodu liječenja i stopi reoperacije

Microdiscectomy (MD) is accepted nowadays as the operative method of choice for lumbar disc herniation, but it is not rare for neurosurgeons to opt for standard discectomy (SD), which does not entail the use of operating microscope. In our study, differences in disc herniation recurrence and clinical outcome of surgical treatment of lumbar disc herniation with and without the use of operating microscope were assessed. Our study included 167 patients undergoing lumbar disc surgery during a three-year period (SD, n=111 and MD, n=56). Clinical outcome assessments were recorded by patients via questionnaire forms filled out by patients at three time points. Operation duration, length of hospital stay and revision surgeries were also recorded. According to study results, after one-year follow up there was no statistically significant difference between the SD and MD groups in functional outcome. However, we recorded a statistically significant difference in leg pain reduction in favor of the MD group. According to the frequency of reoperations with the mean follow up period of 33.4 months, there was a statistically significant difference in favor of the MD group (SD 6.3% vs. MD 3.2%). There appears to be no particular advantage of either technique in terms of functional outcome since both result in good overall outcome. However, we choose MD over SD because it includes significantly lower recurrent disc herniation rate and higher reduction of leg pain.Mikrodiskektomija (MD) je danas prihvaćena kao operativna metoda izbora u liječenju lumbalne diskus hernije, ali se neurokirurzi nerijetko odlučuju za standardnu diskektomiju (SD) koja ne podrazumijeva upotrebu operativnog mikroskopa. U našoj studiji smo nastojali uočiti razlike vezano za rekurentnu diskus herniju i funkcionalni ishod kirurškog liječenja lumbalne diskus hernije uz uporabu operativnog mikroskopa i bez nje. Naša studija je uključila 167 bolesnika koji su podvrgnuti operaciji lumbalne diskus hernije tijekom trogodišnjeg razdoblja (SD, n=111 i MD, n=56). Ishod liječenja procjenjivao se pomoću upitnika koji su bolesnici ispunjavali u tri vremenske točke. Vrijeme trajanja operacije, dužina hospitalizacije i reoperacije su također bilježeni. Nakon godinu dana praćenja prema našim rezultatima nije bilo statistički značajne razlike između skupina SD i MD u funkcionalnom ishodu liječenja, ali je zabilježena statistički značajna razlika u smanjenju boli u nozi u korist skupine MD. Prema učestalosti reoperacija s prosječnim razdobljem praćenja od 33,4 mjeseca, utvrđena je statistički značajna razlika u korist skupine MD (SD, 6,3% i MD, 3,2%). Nijednoj operativnoj tehnici ne može se dati prednost u smislu funkcionalnog ishoda liječenja, jer obje daju odlične rezultate. Ipak, naš izbor je mikrodiskektomija zbog niže stope rekurentne diskus hernije i višeg stupnja smanjenja boli u nozi

Role of Galectin 3 in the pathogenesis of experimental autoimmune myocarditis

Miokarditis je inflamatorno oboljenje srčanog mišića, koje se karakteriše degeneracijom i/ili nekrozom kardiomiocita i prisustvom ćelijskog infiltrata u intersticijumu miokarda. Miokarditis se može manifestovati kao akutno, subakutno ili hronično zapaljenje miokarda, sa fokalnim ili difuznim ćelijskim infiltratom i može progredirati do fibroze, remodelovanja tkiva i gubitka kontraktilne funkcije. Najčešći uzročnici miokarditisa su virusi, bakterije i paraziti,međutim brojni dokazi ukazuju da ovo oboljenje može biti i autoimunske prirode. Eksperimentalni autoimunski miokarditis (EAM) predstavlja animalni model postinfektivnog miokarditisa i dilatacione kardiomiopatije. Galektin 3 (Gal-3) pripada familiji β-galaktozid-vezujućih lektina i eksprimiran je na mnogim ćelijama imunskog sistema i ima važnu ulogu u regulaciji inflamacije. Uloga Gal-3 jeispitivana u različitim autoimunskim i inflamatornim bolestima i pokazano je da Gal-3 može dvojako regulisati imunski odgovor, što zavisi od više faktora, kao što su specifični uslovi inflamacije, vrsta tkiva i nivo ekspresije ovog molekula kako u fiziološkim tako i u patološkim stanjima. Nema podtaka o ulozi i značaju Gal-3 u patogenezi EAM kod C57BL/6 miševa, koji su relativno rezistentni na peptidom indukovani EAM. Da bi se utvrdilo da li i na koji način delecija gena za Gal-3 utiče na patogenezu EAM korišćeni su miševi čistog soja WT- C57BL/6 i Gal-3KO miševi. Svi WT i Gal- 3KO miševi imunizovani su MyHCα334-352 peptidom 0. i 7. dana. Težina EAM određivana je 21-og dana eksperimenta, odnosno prilikom žrtvovanja životinja. Gal-3KO miševi su imali značajno veću hipertrofiju srca i veći patohistološki skor u poređenju sa WT miševima 21. dana nakon imunizacije. Gal-3KO miševi imali su značajno veću infiltraciju srčanog mišića CD45+ mononuklearnim ćelijama posebno F4/80+ makrofagama i CD3+ T limfocitima, kao i veću zastupljenost eozinofila u poređenju sa WT miševima. Serumske koncentracije Th2 citokina (IL-4 i IL-33) su bile više u serumima Gal-3KO u poređenju sa kontrolnim obolelim WT miševima. Delecija gena za Gal-3 je indukovala značajno veći influks Th1 i Th2 ćelija u srcu imunizovanih Gal-3KO u odnosu na WT miševe. Odsustvo ekspresije gena za Gal-3 značajno povećava ukupan broj F4/80+ ćelija i olakšava alternativnu aktivaciju makrofaga u srcu. U obolelom miokardu Gal-3KO miševa registrovana je značajno veća procentualna zastupljenost i ukupan broj: mijeloidnih CD11b+Ly6Chi makrofaga; i CD11c+ ćelija koje produkuju IL-13. U miokardu Gal-3KO miševa detektovan je veći broj IgG pozitivnih ćelija i veća količina IgG depozita u poređenju sa WT miševima. Delecija gena za Gal-3 povećava broj antifibrotskih ćelija koje produkuju IL-10 što se manifestuje značajno slabijim deponovanjem kolagena u srcu obolelih miševa. Delecija gena za Gal-3 povećava oštećenje tkiva u animalnom modelu autoimunskog miokarditisa indukovanog aplikacijom MyHCα334-352 peptida i ukida rezistenciju C57BL/6 miševa na indukciju bolesti.Myocarditis is an inflammatory heart muscle disease characterized by degeneration and necrosis of cardiomyocytes with presence of cellular infiltrates in the interstitium. Myocarditis can be manifested as acute, subacute or chronic myocardial inflammation with focal or diffuse cell infiltrates, it can progress to fibrosis, tissue remodeling and loss of contractile function. The most common causes of myocarditis are viruses, bacteria and parasites, however numerous evidence suggests that this disease can also be autoimmune. Experimental autoimmune myocarditis (EAM) is an animal model of postinfective myocarditis and dilated cardiomyopathy. Galectin 3 (Gal-3), which belongs to the family of β- galactoside-binding lectins is expressed on many cells of the immune system and plays an important role in regulation of inflammation. The role of Gal-3 was studied in various autoimmune and inflammatory diseases and it has been shown that Gal-3 can have a different effect on the immune response. Its role depends on several factors, such as the specific conditions of inflammation, the type of tissue, and the expression level of this molecule in pathological as well as in physiological conditions. There are no precise data on the role and significance of Gal-3 in the pathogenesis of EAM in C57BL/6 mice, which are relatively resistant to EAM-induced by peptide. Mice of the pure strain WT-C57BL/6 and Gal-3KO mice were used in order to determine whether and how the deletion of the Gal-3 gene affects the EAM pathogenesis. WT and Gal-3KO mice were immunized with the MyHCα334-352 peptide on day zero and day seven. Severity of EAM was determined on the 21st day of the experiment, during the sacrifice of animals. Gal-3KO mice had significantly higher cardiac hypertrophy and higher histopathological score compared to WT mice on the 21st day after immunization. Gal-3KO mice also had a significantly higher infiltration of heart muscle by CD45+ mononuclear cells, particulary with F4/80+ macrophages and CD3+T lymphocytes, and higher number of eosinophils compared to WT mice.Serum concentrations of Th2 cytokine (IL-4 and IL-33) were higher in Gal-3KO mice than in control diseased WT mice. The deletion of the Gal-3 gene also induced significantly higher influx Th1 and Th2 cells at the heart of the immunized Gal-3KO compared to WT mice. The absence of gene expression for Gal-3 significantly increases the total number of F4/80+ cells and facilitates alternative macrophage activation in the heart. In myocardium of Gal-3KO mice were significantly higher percentage of distribution and total number of: myeloid CD11b+Ly6Chi macrophages and CD11c+ cells producing IL-13. In the myocardium of Gal-3KO mice were detected a higher number of IgG positive cells and a larger amount of IgG deposits compared to WT mice. The deletion of Gal-3 gene increases the number of antifibrotic cells that produce IL-10, which is manifested by significantly less collagen storage in the heart of diseased mice. Gal-3 gene deletion increases tissue damage in animal model of autoimmune myocarditis induced by application of the MyHCα334-352 peptide and eliminates the resistance of C57BL/6 mice to induction of the disease

Role of Galectin 3 in the pathogenesis of experimental autoimmune myocarditis

Miokarditis je inflamatorno oboljenje srčanog mišića, koje se karakteriše degeneracijom i/ili nekrozom kardiomiocita i prisustvom ćelijskog infiltrata u intersticijumu miokarda. Miokarditis se može manifestovati kao akutno, subakutno ili hronično zapaljenje miokarda, sa fokalnim ili difuznim ćelijskim infiltratom i može progredirati do fibroze, remodelovanja tkiva i gubitka kontraktilne funkcije. Najčešći uzročnici miokarditisa su virusi, bakterije i paraziti,međutim brojni dokazi ukazuju da ovo oboljenje može biti i autoimunske prirode. Eksperimentalni autoimunski miokarditis (EAM) predstavlja animalni model postinfektivnog miokarditisa i dilatacione kardiomiopatije. Galektin 3 (Gal-3) pripada familiji β-galaktozid-vezujućih lektina i eksprimiran je na mnogim ćelijama imunskog sistema i ima važnu ulogu u regulaciji inflamacije. Uloga Gal-3 jeispitivana u različitim autoimunskim i inflamatornim bolestima i pokazano je da Gal-3 može dvojako regulisati imunski odgovor, što zavisi od više faktora, kao što su specifični uslovi inflamacije, vrsta tkiva i nivo ekspresije ovog molekula kako u fiziološkim tako i u patološkim stanjima. Nema podtaka o ulozi i značaju Gal-3 u patogenezi EAM kod C57BL/6 miševa, koji su relativno rezistentni na peptidom indukovani EAM. Da bi se utvrdilo da li i na koji način delecija gena za Gal-3 utiče na patogenezu EAM korišćeni su miševi čistog soja WT- C57BL/6 i Gal-3KO miševi. Svi WT i Gal- 3KO miševi imunizovani su MyHCα334-352 peptidom 0. i 7. dana. Težina EAM određivana je 21-og dana eksperimenta, odnosno prilikom žrtvovanja životinja. Gal-3KO miševi su imali značajno veću hipertrofiju srca i veći patohistološki skor u poređenju sa WT miševima 21. dana nakon imunizacije. Gal-3KO miševi imali su značajno veću infiltraciju srčanog mišića CD45+ mononuklearnim ćelijama posebno F4/80+ makrofagama i CD3+ T limfocitima, kao i veću zastupljenost eozinofila u poređenju sa WT miševima. Serumske koncentracije Th2 citokina (IL-4 i IL-33) su bile više u serumima Gal-3KO u poređenju sa kontrolnim obolelim WT miševima. Delecija gena za Gal-3 je indukovala značajno veći influks Th1 i Th2 ćelija u srcu imunizovanih Gal-3KO u odnosu na WT miševe. Odsustvo ekspresije gena za Gal-3 značajno povećava ukupan broj F4/80+ ćelija i olakšava alternativnu aktivaciju makrofaga u srcu. U obolelom miokardu Gal-3KO miševa registrovana je značajno veća procentualna zastupljenost i ukupan broj: mijeloidnih CD11b+Ly6Chi makrofaga; i CD11c+ ćelija koje produkuju IL-13. U miokardu Gal-3KO miševa detektovan je veći broj IgG pozitivnih ćelija i veća količina IgG depozita u poređenju sa WT miševima. Delecija gena za Gal-3 povećava broj antifibrotskih ćelija koje produkuju IL-10 što se manifestuje značajno slabijim deponovanjem kolagena u srcu obolelih miševa. Delecija gena za Gal-3 povećava oštećenje tkiva u animalnom modelu autoimunskog miokarditisa indukovanog aplikacijom MyHCα334-352 peptida i ukida rezistenciju C57BL/6 miševa na indukciju bolesti.Myocarditis is an inflammatory heart muscle disease characterized by degeneration and necrosis of cardiomyocytes with presence of cellular infiltrates in the interstitium. Myocarditis can be manifested as acute, subacute or chronic myocardial inflammation with focal or diffuse cell infiltrates, it can progress to fibrosis, tissue remodeling and loss of contractile function. The most common causes of myocarditis are viruses, bacteria and parasites, however numerous evidence suggests that this disease can also be autoimmune. Experimental autoimmune myocarditis (EAM) is an animal model of postinfective myocarditis and dilated cardiomyopathy. Galectin 3 (Gal-3), which belongs to the family of β- galactoside-binding lectins is expressed on many cells of the immune system and plays an important role in regulation of inflammation. The role of Gal-3 was studied in various autoimmune and inflammatory diseases and it has been shown that Gal-3 can have a different effect on the immune response. Its role depends on several factors, such as the specific conditions of inflammation, the type of tissue, and the expression level of this molecule in pathological as well as in physiological conditions. There are no precise data on the role and significance of Gal-3 in the pathogenesis of EAM in C57BL/6 mice, which are relatively resistant to EAM-induced by peptide. Mice of the pure strain WT-C57BL/6 and Gal-3KO mice were used in order to determine whether and how the deletion of the Gal-3 gene affects the EAM pathogenesis. WT and Gal-3KO mice were immunized with the MyHCα334-352 peptide on day zero and day seven. Severity of EAM was determined on the 21st day of the experiment, during the sacrifice of animals. Gal-3KO mice had significantly higher cardiac hypertrophy and higher histopathological score compared to WT mice on the 21st day after immunization. Gal-3KO mice also had a significantly higher infiltration of heart muscle by CD45+ mononuclear cells, particulary with F4/80+ macrophages and CD3+T lymphocytes, and higher number of eosinophils compared to WT mice.Serum concentrations of Th2 cytokine (IL-4 and IL-33) were higher in Gal-3KO mice than in control diseased WT mice. The deletion of the Gal-3 gene also induced significantly higher influx Th1 and Th2 cells at the heart of the immunized Gal-3KO compared to WT mice. The absence of gene expression for Gal-3 significantly increases the total number of F4/80+ cells and facilitates alternative macrophage activation in the heart. In myocardium of Gal-3KO mice were significantly higher percentage of distribution and total number of: myeloid CD11b+Ly6Chi macrophages and CD11c+ cells producing IL-13. In the myocardium of Gal-3KO mice were detected a higher number of IgG positive cells and a larger amount of IgG deposits compared to WT mice. The deletion of Gal-3 gene increases the number of antifibrotic cells that produce IL-10, which is manifested by significantly less collagen storage in the heart of diseased mice. Gal-3 gene deletion increases tissue damage in animal model of autoimmune myocarditis induced by application of the MyHCα334-352 peptide and eliminates the resistance of C57BL/6 mice to induction of the disease

To wait for a spontaneous recovery of the third cranial nerve palsy occurring after the coiling of a PcomA aneurysm or to implement surgical treatment? A case report

Introduction. In the last two decades a method of endovascular embolization has been imposed as a method of choice in the treatment of unruptured intracranial aneurysms. Therefore, the problem of treating posterior communicating artery (PComA) aneurysms presenting with the third cranial nerve (TCN) palsy has become even more complex. The case of a patient reported in the paper itself has presented a dilemma of whether to wait for spontaneous resolution of ophthalmoplegia developed after the coiling of a PComA aneurysm or whether to implement an early surgical treatment. Case report. An unruptured saccular aneurysm, directed inferolaterally in the right internal carotid artery (ICA) segment in the position of the PcomA origin, was diagnosed in a 58-year-old male patient. The aneurysm was measuring 9 mm in diameter while the neck was measuring 5 mm. The day before the planned embolization, the patient developed ipsilateral ophthalmoparesis, whereas the first day after the endovascular procedure was completed, the patient developed right-sided complete ophthalmoplegia. Ten weeks after the endovascular embolization our team decided to perform a microsurgical treatment including aneurysm clipping and coil extraction. Eighteen months after the surgery, the patient made a full recovery of the functions of musculus (m) levator palpabrae, m. rectus medialis and pupillary function, with a partial recovery of the functions of m. obliqus inferior, m. rectus inferior and m. rectus superior. Conclusion. According to medical research and literature, the partial recovery of the TCN palsy is expected to happen in the first few weeks after embolization. Despite the completion of endovascular treatment progression of ophthalmoparesis to ophthalmoplegia without any simptoms of clinical improvement after 10 weeks is considered to be an indicator of longstanding TCN compression, which can lead to irreversible nerve damage. Despite the increase in the use of an endovascular embolization method in the treatment of PComA aneurysms preceeded by the TCN palsy, neurosurgical treatment is believed to have been necessary. Still, there is one question left to be answered - did we react too late in this particular case

Histological characteristics and classifications of coarctation of the aorta

Coarctation of the thoracic aorta is defined as a congenital narrowing of the upper part of the descending aorta, adjacent to the place of joining of ductus arteriosum or ligament, which produces a difference in the pressure above the narrowing and below it. One of the most widely accepted classifications of the coarctation is its division on the basis of the age of patients. According to this classification, coarctation is divided into the neonatal and adult type. The neonatal type of coarctation is characterized by the presence of the ductal sling and coarctational shelf placed proximally in relation to the ductal orifice. In newborn babies and younger nurslings, the shelf and neighboring parts of coarctational segment contain ductal tissue. The ductal tissue forms a 'sling' which completely surrounds the juxtaductal aorta. Clinical characteristics of the neonatal type are heart insuficiency at infancy, diffused narrowing of the aortic arch, called tubular hypoplasia, together with the wide open ductus and other congenital heart diseases. In the adult type of coarctation, the histological findings shows cystic medial necrosis. It is characterized by necrosis of smooth muscle cells, presence of cysts in the elastic lamellae filled with basophile mucopolysaccharides, followed by fibrosis with irregular fibroelastic tissue in the media. The adult type is characterized by clearly limited external narrowing of a short aorta segment in the shape of a sandglass, usually in place of the connection of ductus or ligament, or just distal. Concomitant heart diseases are rarely found in this type of coarctation

AI-Driven Optimization of PCL/PEG Electrospun Scaffolds for Enhanced In Vivo Wound Healing

Here, an artificial intelligence (AI)-based approach was employed to optimize the production of electrospun scaffolds for in vivo wound healing applications. By combining polycaprolactone (PCL) and poly(ethylene glycol) (PEG) in various concentration ratios, dissolved in chloroform (CHCl3) and dimethylformamide (DMF), 125 different polymer combinations were created. From these polymer combinations, electrospun nanofiber meshes were produced and characterized structurally and mechanically via microscopic techniques, including chemical composition and fiber diameter determination. Subsequently, these data were used to train a neural network, creating an AI model to predict the optimal scaffold production solution. Guided by the predictions and experimental outcomes of the AI model, the most promising scaffold for further in vitro analyses was identified. Moreover, we enriched this selected polymer combination by incorporating antibiotics, aiming to develop electrospun nanofiber scaffolds tailored for in vivo wound healing applications. Our study underscores three noteworthy conclusions: (i) the application of AI is pivotal in the fields of material and biomedical sciences, (ii) our methodology provides an effective blueprint for the initial screening of biomedical materials, and (iii) electrospun PCL/PEG antibiotic-bearing scaffolds exhibit outstanding results in promoting neoangiogenesis and facilitating in vivo wound treatment