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BACKGROUND Although arachnoid cysts are common lesions, the pathogenesis of their continuous growth remains unclear. We aimed to identify the role of aquaporins in arachnoid cyst specimens. CASE REPORT We selected 3 cases from our own facility and examined arachnoid cyst wall specimens, which were sampled intraoperatively. Patients presented with variable symptoms, a 52-year-old man with a \"heavy sensation\" in the head and dysesthesia on the left hand, a 68-year-old man with unsteady gait, and finally a 26-year-old woman with a history of intermittent headaches for 10 years. Intraoperative specimens were obtained and examined. Evaluation techniques were light microscopy, immunohistochemical staining for aquaporin, and electron microscopy. Light microscopy showed that cells were arranged in epithelium-like structures forming several thick lamellae, with visible connective tissue among them. Under electron microscopic examination, cells with many or few cell organelles and with spindle-like nuclei were arranged in lamellar or flattened structures. Many vacuolizations were seen in between. Interdigitation of cells and many desmosomes were observed. All 3 cases were positive for aquaporin 1. CONCLUSIONS Our study showed that water transportation through aquaporin 1 has a potential role in the formation and expansion of arachnoid cysts.

Ciliated epithelial cells have been rarely observed in urothelium lined mucosa. Only extremely rare reports in the literature have described this phenomenon and no cases have been described in other sites than the male urethra. Herein, we illustrate the finding of ciliated pseudostratified columnar cells in the renal calyx mucosa adjacent to an area of urothelial invasive carcinoma in an 82 year-old man with previous history of nephrolithiasis. The ciliated cells covered a linear extension of 0.5 cm: they were positive for keratin 7 and keratin 8/18 and negative for keratin 20. Alcian blue staining was positive in some vacuoles in the apical cytoplasm of the same cells whereas PAS (Periodic Acid-Schiff) staining was negative. GATA3 resulted negative in ciliated cells except for a layer in the basal portion of the epithelium, just above the basal membrane. The actual prevalence of ciliated epithelia in the urinary tract is not well documented and the current knowledge on the subject is limited to electron scanning microscopy studies. The significance of this phenomenon remains unknown: it could be either a developmental abnormality or more probably a metaplastic change. Associated urolithiasis, which has been described in both a previous report and in the present one, could hypothetically represent a possible trigger for this unusual cell change. However, this hypothesis needs to be confirmed through further investigation.

Immunologically different types of glomerulopathies show varied symptoms and clinical courses. Unlike in lupus nephritis, repeated biopsy is rarely performed in cases of mesangial glomerulonephritis. We reviewed 200 cases wherein rebiopsy was performed in patients with diagnosed mesangial glomerular pathology over a 30-year period and analyzed the symptoms follow-up in these cases. Further, we evaluated the morphological changes between the first and final biopsies to identify cases of histological progression and histological remission and examined the correlation between such changes and clinical symptoms. The time between the first and last biopsies ranged from 7 months to 35 years. The most common for the initial biopsy was nephrotic syndrome, followed by non-nephrotic proteinuria; other symptoms occurred rarely. Histological progression occurred at various stages of observation, ranging from within a few months to after several years. Histological progression and remission were detected in 118 and 3 patients, respectively, whereas there was no difference in morphological findings between the first and last biopsies in 79 patients. Rebiopsy is useful in patients who do not respond adequately to treatment, and especially in those with increased clinical symptoms. Moreover, electron microscopic examination is necessary to discover early signs of histological progression.

A case of poorly differentiated tubular gastric adenocarcinoma with tumor-associated tissue eosinophilia (TATE) is studied by light and electron microscopy, focusing on membrane interactions between eosinophils and tumor cells. 29.2% of the eosinophils in contact with tumor cells showed intact granules, 28.3% exhibited piecemeal degranulation (PMD), 40% were characterized by coexistence of PMD and compound exocytosis in the same granulocyte, whereas classical exocytosis was found in 2.5% of the eosinophils with PMD. Eosinophil Sombrero Vesicles (EoSVs), important tubulovesicular carriers for delivery of cytotoxic proteins from the specific granules during PMD, were also studied at the ultrastructural level. In activated eosinophils, EoSVs and specific granules with ultrastructural signs of degranulation were polarized toward tumor cells. Ultrastructural changes in paraptosis-like cell death, such as mitochondrial swelling, dilation of the nuclear envelope, cytoplasmic vacuoles, and nuclear chromatin condensation, but without margination of the chromatin, were observed in these tumor cells. Our data support the notion that eosinophils may exert an antitumoral role in gastric cancer. Finally, the case reported provides, for the first time, ultrastructural evidence of classical and compound exocytosis of eosinophils in the tumor stroma of human adenocarcinoma.

The localization of viral nucleic acids in the cell is essential for understanding the infectious cycle. One of the strategies developed for this purpose is the use of nucleotide analogs such as bromodeoxyuridine (BrdU, analog to thymine) or bromouridine (BrU, analog of uridine), which are incorporated into the nucleic acids during replication or transcription. In adenovirus infections, BrdU has been used to localize newly synthesized viral genomes in the nucleus, where it is key to distinguish between host and viral DNA. Here, we describe our experience with methodological variations of BrdU labeling to localize adenovirus genomes in fluorescence and electron microscopy. We illustrate the need to define conditions in which most of the newly synthesized DNA corresponds to the virus and not the host, and the amount of BrdU provided is enough to incorporate to the new DNA molecules without hampering the cell metabolism. We hope that our discussion of problems encountered and solutions implemented will help other researches interested in viral genome localization in infected cells.

Lafora disease is a severe form of progressive myoclonic epilepsy with autosomal recessive inheritance diagnosed by inclusion body in biopsy. A 26-year-old woman was admitted due to complaints of frequent twitches and fainting. The 0.5x0.3x0.3 cm axillary skin punch biopsy was subjected to routine histopathological evaluation. Cytoplasmic PAS-positive inclusion bodies were observed at the basal side of the eccrine and apocrine glands. The diagnosis of Lafora disease can also be made by the observation of the polyglycosan cytoplasmic inclusion bodies in the brain, liver and skeletal muscle biopsies. Although we need more work to understand the etiopathogenesis of Lafora disease, we would like to draw attention to the importance of skin biopsy in the differential diagnosis of young patients with clinically refractory epilepsy, myoclonus, and cognitive decline.

Since the Coronavirus Disease 2019 (COVID-19) outbreak, there is accumulating data on the clinical characteristics, treatment strategies and prognosis of COVID-19 in patients with concurrent renal disease. Postmortem investigations reveal renal involvement in COVID-19, and most recently, several biopsy researches reveal that acute tubular injury, as well as glomerular nephropathy such as collapsing glomerulopathy were common histological findings. However, to our best knowledge, there is limited data regarding IgA nephropathy in the setting of COVID-19.
In the present case, we report a 65-year old Chinese woman who presented with dark-colored urine, worsening proteinuria and decreased renal function after COVID-19 infection. She received a renal biopsy during COVID-19 infection. The renal biopsy revealed IgA nephropathy without any evidence for SARS-Cov-2. The findings suggest that the renal abnormalities were a consequence of exacerbation of this patient\'s underlying glomerular disease after COVID-19 infection. After a regimen of 3-day course of glucocorticoid and angiotensin II receptor blocker therapy, the patient recovered and remained stable upon follow-up.
It is important to consider the underlying glomerular disease exacerbation as well as virus induced injury when dealing with renal abnormalities in patients with COVID-19. A kidney biopsy may be indicated to exclude a rapidly progressive glomerular disease.

Glomerular involvement in rheumatoid arthritis has been known to be associated with treatment side effects from medications and secondary amyloidosis. However, limited basic science and clinical studies have been performed to address the potential disease specific immune-mediated mechanisms causing secondary glomerular pathology, its various types of presentation, and the potential treatments.
A 41-year-old man with chronic active rheumatoid arthritis presented with nephrotic syndrome and was found to have membranous nephropathy with eosinophilic intracapillary thrombi on renal biopsy. Proteinuria persisted despite complete withdrawal from non-steroidal anti-inflammatory drugs (NSAIDs) and disease-modifying anti-rheumatic drugs (DMARDs). Throughout the disease course, he developed cryoglobulinemic vasculitis and pulmonary sarcoidosis, both of which achieved clinical resolution with glucocorticoids. However, only partial improvement was observed in proteinuria with treatment of steroids and Rituximab.
Our case presented a unique and complicated clinical phenotype of active rheumatoid arthritis, with clinical features of cryoglobulinemic vasculitis, histopathologic features of membranous and cryoglobulinemic nephropathy in the absence of DMARDs use, as well as pulmonary sarcoidosis. We speculate that there is a wider spectrum of glomerular disease in patients with untreated rheumatoid arthritis. In addition, the potential association between rheumatoid arthritis and cryoglobulinemic vasculitis should probably be revisited and requires further studies to elucidate the underlying mechanisms and treatment options.

Idiopathic membranous nephropathy (MN) is one of the major glomerulonephritis that cause nephrotic syndrome. The phospholipase A2 receptor (PLA2R) has recently been identified as an endogenous antigen of idiopathic MN. Thrombotic thrombocytopenic purpura (TTP) is a disorder characterized by schistocytes, hemolytic anemia, thrombocytopenia, and organ dysfunction which occurs as a result of thrombi. Patients with acquired TTP have autoantibodies against a disintegrin and metalloprotease with thrombospondin type 1 motif 13 (ADAMTS13). These autoantibodies act as an inhibitor and cause ADAMTS13 deficiency. Idiopathic MN and acquired TTP are usually considered as independent autoimmune diseases. We experienced a patient who developed TTP during the conservative treatment of idiopathic MN, with the coexistence of ADAMTS13 inhibitor and anti-PLA2R antibody.
A 73-year-old man presented with thrombocytopenia, hemolytic anemia, disturbance of consciousness, and acute kidney injury after 4-year course of biopsy-proven idiopathic MN. ADAMTS13 activity was undetectable and the ADAMTS13 inhibitor was identified. Additionally, he was positive for anti-PLA2R antibody. The patient did not have any diseases that could cause secondary thrombotic microangiopathy, and he was diagnosed with acquired TTP. Steroid therapy and plasma exchange were initiated and the acquired TTP resolved. MN achieved remission 3 months after the anti-PLA2R antibody disappeared.
This is the first reported case of acquired TTP developed during conservative treatment of idiopathic MN, with both ADAMTS13 inhibitor and anti-PLA2R antibody positive at the onset of the TTP. The present case suggests that idiopathic MN might be associated with the development of some cases of acquired TTP.