HIF-1 expression in retinal ganglion cells and optic nerve axons in glaucoma

Glaucoma is a result of increased intraocular pressure leading to damage to retinal ganglion cells andoptic nerve axons. The aim of this study was to evaluate HIF-1 expression in optic nerve axons and retinalganglion cells in 42 eyes enucleated because of complete glaucoma compared to eyes removed because of injury.The immunohistochemical reaction was done and specimens were examined under a light microscope. 57% ofcases presented HIF-1 expression in the optic nerve axons, and 52.3% in the retinal ganglion cells. 20 out of 42(47.6%) cases were HIF-1 positive both in the optic nerve axons and in the retinal ganglion cells, and the stainingwas evident mostly in the nuclear and perinuclear area. Our present results indicate that HIF-1 expression inhypoxic conditions in glaucoma might be a very crucial stage in damage to retinal ganglion cells and optic nerveaxons, and might be a successful target for the implementation of neuroprotective drugs.Glaucoma is a result of increased intraocular pressure leading to damage to retinal ganglion cells andoptic nerve axons. The aim of this study was to evaluate HIF-1 expression in optic nerve axons and retinalganglion cells in 42 eyes enucleated because of complete glaucoma compared to eyes removed because of injury.The immunohistochemical reaction was done and specimens were examined under a light microscope. 57% ofcases presented HIF-1 expression in the optic nerve axons, and 52.3% in the retinal ganglion cells. 20 out of 42(47.6%) cases were HIF-1 positive both in the optic nerve axons and in the retinal ganglion cells, and the stainingwas evident mostly in the nuclear and perinuclear area. Our present results indicate that HIF-1 expression inhypoxic conditions in glaucoma might be a very crucial stage in damage to retinal ganglion cells and optic nerveaxons, and might be a successful target for the implementation of neuroprotective drugs

Przypadek chorego z postacią zlokalizowanią choroby Castlemana: 10-letnia obserwacja

Castleman disease (CD) is a rare atypical lymphoproliferative process of obscure pathogenesis. An intracranial localization of the condition is extremely rare. We present a case of a 29-year-old man, who harbored an intracranial plasma cell variant of CD in the form of a tumor mimicking meningioma and was followed up to 10 years after surgical excision of the lesion. The histopathological examination showed massive infiltration of mononuclear cells, composed mainly of lymphocytes and matured plasmocytes, as well as many small thin-walled vessels surrounded with plasma cells and lymphocytes. This picture was consistent with a plasma cell type of CD. Ten-year follow-up supports a notion that total surgical excision of the solitary intracranial infiltration is curative in plasma cell type of CD.Choroba Castlemana jest rzadkim, atypowym procesem limfoproliferacyjnym o niejasnej etiologii i patogenezie. Postać o lokalizacji wewnątrzczaszkowej rozpoznaje się nadzwyczaj rzadko. W pracy zaprezentowano przypadek 29-letniego mężczyzny, u którego przedoperacyjnie stwierdzono zmianę „oponiakopodobną”, jednak badanie histopatologiczne ujawniło wewnątrzczaszkową postać choroby Castlemana o typie plazmatycznokomórkowym. Chorego obserwowano przez 10 lat po usunięciu guza. W badaniu histopatologicznym stwierdzono naciek zapalny złożony głównie z limfocytów oraz dojrzałych plazmocytów, a także liczne cienkościenne naczynia otoczone komórkami plazmatycznymi i limfocytami. Obraz histopatologiczny jednoznacznie wskazywał na postać plazmatycznokomórkową choroby Castlemana. Dziesięcioletnia obserwacja po usunięciu zmiany wskazuje, że całkowite wycięcie guza może zapewnić trwały efekt leczniczy

AgNOR, Ki-67 and PCNA expression in fibroepithelial tumours of the breast in correlation with morphological features

The authors retrospectively reviewed the cytological slides of 44 histopathologically confirmed fibroepithelial lesions of the breast, of which 11 were fibroadenoma (FA), 19 benign phyllodes tumours (PTLGM), 8 borderline (PTBM) and 6 malignant (PTHGM). The 2 FA misdiagnosed as PTLGM in cytological smears were both of cellular type. NORS were quantified in a series of the above cases using the silver-colloid method. Expression of Ki-67 and PCNA were evaluated by immunohistochemistry on sections from the corresponding paraffin blocks. The results were compared with morphological parameters. In phyllodes tumours (PT), the AgNOR scores showed a tendency to increase with degrees of malignancy. There was significant correlation between Ag- NOR counts and proliferation rates as determined by Ki-67 and PCNA immunostaining. Ki-67 and PCNA expression correlated with mitotic count, stromal overgrowth, cellularity and atypia in PT. Determination of the AgNOR number per cell revealed an overlap between FA and PTLGM. The proliferating activity determined by immunohistochemistry with Ki-67 and PCNA antibodies did not reveal any significant difference between FA and PTLGM. In summary, Ki-67 and PCNA expression is suggested as a marker of stromal element proliferation. The results obtained confirm the diagnostic difficulties in distinguishing PTLGM from FA of the cellular type using fine needle aspiration cytology

Mast cells evaluation in meningioma of various grades

Introduction: Meningioma is a heterogenous group of primary brain tumors. The progression or recurrence is relatively very common; however there is lack of prognostic factors which may indicate those events. The aim of the study was to evaluate the presence of mast cells within the low grade and high grade meningiomas. Material and Methods: The immunohistochemical reaction was done. The tryptase expression was estimated in slides of meningiomas of various grades in 10 random fields under the light microscope. Results: The expression of tryptase was observed in 31,8% low grade meningiomas and in 85,9% high grade meningiomas. The immunostaining was observed next to the blood vessels. Conclusion: The presence of mast cells might be a significant prognostic factor for the recurrence or the worse prognosis of meningiomas

Expression of connexin 43 in breast cancer in comparison with mammary dysplasia and the normal mammary gland

Gap junctional intercellular communication (GJIC) plays a critical role in tissue development and differentiation and probably in carcinogenesis. The purpose of the study was to evaluate the expression and localisation of Cx43 in 40 cases of mammary dysplasia and 29 cases of breast cancer (without primary chemotherapy). The tissue sections were investigated for Cx43 expression by immunohistochemistry. In the normal mammary gland there was an intercellular, punctate staining pattern, mainly between myoepithelial cells, characteristic of functional gap junctions. In dysplasias there was mainly mixed (cytoplasmic and intercellular) staining and in most cases of breast cancer we observed diffuse or granular, but cytoplasmic, staining of Cx43. Our results demonstrated that expression of Cx43 in dysplasias and breast cancer is changed and GJIC is probably impaired because of disruption of functional gap junction formation especially between breast cancer cells

An evaluation of Ki-67 and PCNA expression in conjunctival and eyelid tumours

The aim of our study was an evaluation of the expression of cell proliferation markers (PCNA and Ki-67) in conjunctival and eyelid papillomas and squamous and basal cell cancers. A series of 9 cases of squamous cell cancer (SCC), 15 cases of basal cell cancer (BCC) and 43 cases of squamous cell papilloma (SCP) were assessed using the immunohistochemical method with monoclonal antibodies. PCNA overexpression was observed in 100% of SCP, in 88.8% of SCC and in 100% of BCC cases. Ki-67 overexpression was seen in 32.5% of cases of SCP, in 22.2% of SCC and in 66.6% of BCC. The results showed that an evaluation of Ki-67 expression is the most valuable cell proliferation marker

Original paper expressiOn pattern Of isl-1, ttf-1 and pax5 in OlfactOry neurOblastOma

Olfactory neuroblastoma (ONB) is a rare neoplasm of the sinonasal area with neuroendocrine differentiation. ISL-1, TTF-1 and PAX5 are transcription factors that are frequently upregulated in tumors showing neuroendocrine differentiation. The aim of our study was to evaluate these markers in a group of ONBs. We included 11 ONBs from 4 large university hospitals. Immunohistochemical expression of TTF-1, PAX5 and ISL-1 was evaluated. TTF-1, ISL-1 and PAX5 were expressed in 3/11 cases (27.27%, h-score: 3-45), 7/11 cases (63.64%, h-score: 23-200), and in 3/11 cases (27.77%, h-score 3-85), respectively. The patient with the strongest PAX5 reactivity exhibited an aggressive clinical course with rapid dissemination to the spine and death shortly after the diagnosis. No significant correlation in the expression of PAX5 and TTF-1 (ρ = 0.43; p = 0.18) was observed. ISL-1 is widely expressed in tumors with neuroendocrine differentiation and therefore of limited value in their differential diagnosis. TTF-1 positivity does not exclude the diagnosis of primary ONB, although usually only a small percentage of cells are positive. PAX5 expression is infrequent (27.27%) in ONB; however, if present it can be associated with a very aggressive clinical course

The correlation of clinical and chromosomal alterations of benign meningiomas and their recurrences

Meningiomas (MGs) are the frequent benign intracranial tumors. Their complete removal does not always guarantee relapse-free survival. Recurrence-associated chromosomal anomalies in MGs haves been proposed as prognostic factors in addition to the World Health Organisation (WHO) grading, tumor size and resection rate. The aim of this study was to evaluate the frequency of deletions on chromosomes in sporadic MGs and to correlate them with the clinical findings and tumor behaviour. Along with survival, the tumor recurrence was the main endpoint. Chromosomal loss of heterozygosity (LOH) was studied. 46 benign MGs were subjected to the analysis, complete tumor resection was intended and no early mortalities were observed. Incomplete removal was related to parasagittal location and psammomatous hisptopathology (p<0.01). Chromosomal alterations were present in 82.6% of cases; LOH at 22q (67.4%) and 1p (34.8%) were the most frequent and associated with male sex (p=0.04). Molecular findings were not specific for any of the histopathologic grade. Tumor recurrence (14 of 46) correlated with tumor size (≥35mm), LOH at 1p, 14q, coexistence of LOH at 1p/14q, 10q/14q, ‘complex karyotype’ status (≥2 LOHs excluding 22q), patient age (younger <35), and Simpson grading of resection rate (≥3 of worse prognosis). The last 3 variables were independent significant prognostic factors in multivariate analysis and of the same importance in recurrence prediction (Receiver Operating Characteristic curves comparison p>0.05). Among the cases of recurrence, tumor progression was observed in 3 of 14. In 2 cases, LOH on 1p and/or coexistence of LOH 1p/14q correlated with anaplastic transformation

Extracellular Vimentin as a Target Against SARS-CoV-2 Host Cell Invasion

Infection of human cells by pathogens, including SARS-CoV-2, typically proceeds by cell surface binding to a crucial receptor. The primary receptor for SARS-CoV-2 is the angiotensin-converting enzyme 2 (ACE2), yet new studies reveal the importance of additional extracellular co-receptors that mediate binding and host cell invasion by SARS-CoV-2. Vimentin is an intermediate filament protein that is increasingly recognized as being present on the extracellular surface of a subset of cell types, where it can bind to and facilitate pathogens’ cellular uptake. Biophysical and cell infection studies are done to determine whether vimentin might bind SARS-CoV-2 and facilitate its uptake. Dynamic light scattering shows that vimentin binds to pseudovirus coated with the SARS-CoV-2 spike protein, and antibodies against vimentin block in vitro SARS-CoV-2 pseudovirus infection of ACE2-expressing cells. The results are consistent with a model in which extracellular vimentin acts as a co-receptor for SARS-CoV-2 spike protein with a binding affinity less than that of the spike protein with ACE2. Extracellular vimentin may thus serve as a critical component of the SARS-CoV-2 spike protein-ACE2 complex in mediating SARS-CoV-2 cell entry, and vimentin-targeting agents may yield new therapeutic strategies for preventing and slowing SARS-CoV-2 infection

Histologiczna ocena tkanek podniebienia miękkiego u pacjentów z zaburzeniami oddychania podczas snu

Wstęp: Sen to stan fizjologiczny, który jest niezbędny do prawidłowego funkcjonowania organizmu. Jedną z przyczyn jego zaburzeń jest zespół obturacyjnych bezdechów podczas snu (OSAS). Cel: Celem pracy jest ocena histologiczna błony śluzowej podniebienia miękkiego u pacjentów z różnymi postaciami OSAS. Materiał i metoda: Grupę badaną stanowili pacjenci z zaburzeniami oddychania podczas snu o charakterze chrapania pierwotnego lub OSAS. Pacjenci z przewlekłym zapaleniem migdałków podniebiennych, bez wywiadu zaburzeń oddychania podczas snu zostali włączeni do grupy porównawczej. Fragmenty błony śluzowej języczka podniebiennego (grupa badana) i łuku podniebienno-językowego (grupa porównawcza) były pobierane do badań histologicznych podczas zabiegów operacyjnych. W badanej tkance, przy użyciu metod histologicznych, histochemicznych i immunohistochemicznych, oceniano: obecność i nasilenie stanu zapalnego (CD3, CD20, CD68), strukturę włókien nerwowych (S-100) oraz wielkość naczyń krwionośnych (CD34). Wyniki: U pacjentów z OSAS rozwijał się miejscowy proces zapalny w obrębie tkanek gardła środkowego (silniejsza ekspresja CD3, CD20, CD68 u pacjentów z OSAS). Nasilenie reakcji immunohistochemicznej z CD3 korelowało ze stopniem zaawansowania OSAS. Wykazano wyższy stopień włóknienia, wyższą ekspresję receptora CD34 oraz S-100 u chorych z OSAS w stosunku do pacjentów chrapiących i z grupy porównawczej. Wnioski: Chrapanie, poprzez przewlekłą wibrację tkanek, najprawdopodobniej prowadzi do uszkodzenia włókien nerwowych w obszarze podniebienia miękkiego, co może nasilać epizody spłyceń oddechowych podczas snu oraz zwiększać liczbę pojawiających się bezdechów