Glassy cell carcinoma is a histologic subtype of cervical cancer with distinct pathologic features and it has an aggressive biologic course. It was first described by Glucksmann and Cherry in 1956 as a poorly differentiated adenoquamous carcinoma and commented on its poor prognosis, unresponsiveness to traditional modes of therapy, and often associated with pregnancy. The characteristic histologic features are defined as follows: 1) cells with a moderate amount of cytoplasm resembling ground glass, 2) a fairly distinct cell membrane that stains with eosin or PAS, 3) large nuclei with prominent nucleoli. We present two cases of glassy cell carcinoma of the cervix successfullyl treated by neoadjuvant chemotherapy and radical hyterectorny, with a brief review of literatures.
Cell Membrane ; Cervix Uteri* ; Coloring Agents ; Cytoplasm ; Drug Therapy* ; Eosine Yellowish-(YS) ; Female ; Glass ; Hysterectomy* ; Pregnancy ; Prognosis ; Prunus ; Uterine Cervical Neoplasms

The incidence of intracranial complications of otitis media, including lateral sinus thrombophlebitis, has been significantly reduced since the advent of antibiotics. This entity is rarely encountered in clinical practice, and delay in its diagnosis and institution of appropriate therapy may lead to serious, or even fatal, consequences. The signs and clinical course of lateral sinus thrombophlebitis are non-specific and the final diagnosis rests upon radiological investigations including CT-scans and MRI. We have experienced a case of middle fossa and posterior fossa epidural abscess formation, lateral sinus thrombophlebitis that has developed secondary chronic otitis media with cholesteatoma in a 47 year-old female patient. We report this case which was successfully treated by middle fossa dura and posterior fossa dura drainage, lateral sinus thrombectomy with open mastoidectomy.
Anti-Bacterial Agents ; Cholesteatoma* ; Diagnosis ; Drainage ; Epidural Abscess* ; Female ; Humans ; Incidence ; Lateral Sinus Thrombosis* ; Magnetic Resonance Imaging ; Middle Aged ; Otitis Media* ; Otitis* ; Thrombectomy ; Transverse Sinuses*

Background: Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disease.Although murine studies have demonstrated that type 2 innate lymphoid cells (ILCs) mediate type 2 skin inflammation, their role in skin fibrosis in AD remains unclear. This study investigated whether type 2 ILCs are involved in skin fibrosis using an AD-like murine model. Methods: C57BL/6 mice were treated epicutaneously with Aspergillus fumigatus (Af) for 5 consecutive days per week for 5 weeks to induce skin fibrosis. Mature lymphocyte deficient Rag1−/− mice were also used to investigate the role of type 2 ILCs in skin fibrosis. Results: The clinical score and transepidermal water loss (TEWL) were significantly higher in the AD group than in the control group. The AD group also showed significantly increased epidermal and dermal thicknesses and significantly higher numbers of eosinophils, neutrophils, mast cells, and lymphocytes in the lesional skin than the control group. The lesional skin of the AD group showed increased stain of collagen and significantly higher levels of collagen than the control group (10.4 ± 2.2 µg/mg vs. 1.6 ± 0.1 µg/mg, P < 0.05). The AD group showed significantly higher populations of type 2 ILCs in the lesional skin compared to the control group (0.08 ± 0.01% vs. 0.03 ± 0.01%, P < 0.05). These findings were also similar with the AD group of Rag1−/− mice compared to their control group. Depletion of type 2 ILCs with anti-CD90.2 monoclonal antibodies significantly improved clinical symptom score, TEWL, and infiltration of inflammatory cells, and significantly decreased levels of collagen were observed in the AD group of Rag1−/− mice (1.6 ± 0.0 μg/mg vs. 4.5 ± 0.3 μg/mg, P < 0.001). Conclusion In the Af-induced AD-like murine model, type 2 ILCs were elevated, with increased levels of collagen. Additionally, removal of type 2 ILCs resulted in decreased collagen levels and improved AD-like pathological findings. These findings suggest that type 2 ILCs play a role in the mechanism of skin fibrosis in AD.

Background: Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disease.Although murine studies have demonstrated that type 2 innate lymphoid cells (ILCs) mediate type 2 skin inflammation, their role in skin fibrosis in AD remains unclear. This study investigated whether type 2 ILCs are involved in skin fibrosis using an AD-like murine model. Methods: C57BL/6 mice were treated epicutaneously with Aspergillus fumigatus (Af) for 5 consecutive days per week for 5 weeks to induce skin fibrosis. Mature lymphocyte deficient Rag1−/− mice were also used to investigate the role of type 2 ILCs in skin fibrosis. Results: The clinical score and transepidermal water loss (TEWL) were significantly higher in the AD group than in the control group. The AD group also showed significantly increased epidermal and dermal thicknesses and significantly higher numbers of eosinophils, neutrophils, mast cells, and lymphocytes in the lesional skin than the control group. The lesional skin of the AD group showed increased stain of collagen and significantly higher levels of collagen than the control group (10.4 ± 2.2 µg/mg vs. 1.6 ± 0.1 µg/mg, P < 0.05). The AD group showed significantly higher populations of type 2 ILCs in the lesional skin compared to the control group (0.08 ± 0.01% vs. 0.03 ± 0.01%, P < 0.05). These findings were also similar with the AD group of Rag1−/− mice compared to their control group. Depletion of type 2 ILCs with anti-CD90.2 monoclonal antibodies significantly improved clinical symptom score, TEWL, and infiltration of inflammatory cells, and significantly decreased levels of collagen were observed in the AD group of Rag1−/− mice (1.6 ± 0.0 μg/mg vs. 4.5 ± 0.3 μg/mg, P < 0.001). Conclusion In the Af-induced AD-like murine model, type 2 ILCs were elevated, with increased levels of collagen. Additionally, removal of type 2 ILCs resulted in decreased collagen levels and improved AD-like pathological findings. These findings suggest that type 2 ILCs play a role in the mechanism of skin fibrosis in AD.

Background: Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disease.Although murine studies have demonstrated that type 2 innate lymphoid cells (ILCs) mediate type 2 skin inflammation, their role in skin fibrosis in AD remains unclear. This study investigated whether type 2 ILCs are involved in skin fibrosis using an AD-like murine model. Methods: C57BL/6 mice were treated epicutaneously with Aspergillus fumigatus (Af) for 5 consecutive days per week for 5 weeks to induce skin fibrosis. Mature lymphocyte deficient Rag1−/− mice were also used to investigate the role of type 2 ILCs in skin fibrosis. Results: The clinical score and transepidermal water loss (TEWL) were significantly higher in the AD group than in the control group. The AD group also showed significantly increased epidermal and dermal thicknesses and significantly higher numbers of eosinophils, neutrophils, mast cells, and lymphocytes in the lesional skin than the control group. The lesional skin of the AD group showed increased stain of collagen and significantly higher levels of collagen than the control group (10.4 ± 2.2 µg/mg vs. 1.6 ± 0.1 µg/mg, P < 0.05). The AD group showed significantly higher populations of type 2 ILCs in the lesional skin compared to the control group (0.08 ± 0.01% vs. 0.03 ± 0.01%, P < 0.05). These findings were also similar with the AD group of Rag1−/− mice compared to their control group. Depletion of type 2 ILCs with anti-CD90.2 monoclonal antibodies significantly improved clinical symptom score, TEWL, and infiltration of inflammatory cells, and significantly decreased levels of collagen were observed in the AD group of Rag1−/− mice (1.6 ± 0.0 μg/mg vs. 4.5 ± 0.3 μg/mg, P < 0.001). Conclusion In the Af-induced AD-like murine model, type 2 ILCs were elevated, with increased levels of collagen. Additionally, removal of type 2 ILCs resulted in decreased collagen levels and improved AD-like pathological findings. These findings suggest that type 2 ILCs play a role in the mechanism of skin fibrosis in AD.

Background: Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disease.Although murine studies have demonstrated that type 2 innate lymphoid cells (ILCs) mediate type 2 skin inflammation, their role in skin fibrosis in AD remains unclear. This study investigated whether type 2 ILCs are involved in skin fibrosis using an AD-like murine model. Methods: C57BL/6 mice were treated epicutaneously with Aspergillus fumigatus (Af) for 5 consecutive days per week for 5 weeks to induce skin fibrosis. Mature lymphocyte deficient Rag1−/− mice were also used to investigate the role of type 2 ILCs in skin fibrosis. Results: The clinical score and transepidermal water loss (TEWL) were significantly higher in the AD group than in the control group. The AD group also showed significantly increased epidermal and dermal thicknesses and significantly higher numbers of eosinophils, neutrophils, mast cells, and lymphocytes in the lesional skin than the control group. The lesional skin of the AD group showed increased stain of collagen and significantly higher levels of collagen than the control group (10.4 ± 2.2 µg/mg vs. 1.6 ± 0.1 µg/mg, P < 0.05). The AD group showed significantly higher populations of type 2 ILCs in the lesional skin compared to the control group (0.08 ± 0.01% vs. 0.03 ± 0.01%, P < 0.05). These findings were also similar with the AD group of Rag1−/− mice compared to their control group. Depletion of type 2 ILCs with anti-CD90.2 monoclonal antibodies significantly improved clinical symptom score, TEWL, and infiltration of inflammatory cells, and significantly decreased levels of collagen were observed in the AD group of Rag1−/− mice (1.6 ± 0.0 μg/mg vs. 4.5 ± 0.3 μg/mg, P < 0.001). Conclusion In the Af-induced AD-like murine model, type 2 ILCs were elevated, with increased levels of collagen. Additionally, removal of type 2 ILCs resulted in decreased collagen levels and improved AD-like pathological findings. These findings suggest that type 2 ILCs play a role in the mechanism of skin fibrosis in AD.

A 63-year-old woman developed left leg weakness, bilateral sensorineural hearing loss and headache. Brain MRI showed a hypointense rim on the surfaces of the cerebellum, brainstem, and cerebral cortex indicating superficial siderosis. Further examination showed an intramedullary ependymoma at the level of T12-L2. We report a patient with a spinal cord ependymoma resulting in superficial siderosis of the central nervous system.
Brain ; Brain Stem ; Central Nervous System ; Cerebellum ; Cerebral Cortex ; Ependymoma* ; Female ; Headache ; Hearing Loss, Sensorineural ; Humans ; Leg ; Magnetic Resonance Imaging ; Middle Aged ; Siderosis* ; Spinal Cord*

BACKGROUND: Epithelial-mesenchymal transition (EMT) is critical for morphogenesis during embryonic development and is also implicated in the conversion of early-stage tumors into invasive malignancies. Recently, Twist has been identified to play an important role in EMTmediated metastatic progression of several types of human cancer. The present study examined the expression of Twist and evaluated its clinicopathologic significance in urothelial carcinoma of upper urinary tract. METHODS: Immunohistochemical staining for Twist expression was performed on 70 upper urinary tract urothelial carcinomas (UUT-UCs) using tissue microarray. RESULTS: Immunohistochemical staining for Twist was positive in 31/70 cases (44.3%) of UUT-UCs. Twist expression was associated with high-grade and advanced-stage (ISUP grade, p<0.01; stage, p=0.045). The patients with Twist positive-tumors revealed lower disease free survival rate than those with Twist negative-tumors (p<0.01). The overall survival for patients with Twist positive-tumors was slightly worse than the patients with Twist negative- tumors, but the difference was not statistically significant (p=0.12). CONCLUSION: Our results suggest that Twist is a novel marker for advanced UUT-UC.
Carcinoma, Transitional Cell ; Disease-Free Survival* ; Embryonic Development ; Epithelial-Mesenchymal Transition ; Female ; Humans ; Morphogenesis ; Pregnancy ; Twist Transcription Factor ; Urinary Tract*

Hydrothcrax can be a cause of respiratory insufficiency and is needed adequate management and therapy. In this report, a patient of respiratory distress due to hydrothorax that occurred during explo-laparotomy and drainage of liver absceas under general anesthesia was treated with water seal drainage insertion in the 7th intercostal space and general management. Literatures was reviewed, and the importance of early recognition and vigorous treatment has been stressed.
Anesthesia, General* ; Drainage ; Humans ; Hydrothorax* ; Liver ; Respiratory Insufficiency ; Water

In order to explore the existence and distribution of phospholipase (PLC) isozymes in the rat retina, immunohistochemical staining was applied using monoclonal antibodies against PLC isozymes (PLC beta; K92, PLC gamma; D7, F7, PLC delta; R32, S11). For immunohistochemical detection, avidin-biotin peroxidase complex (ABC) method was performed on frozed tissue sections of rat retina. Our study showed that PLC isozymes have particular distributional patterns in the retina. Namely, PLC beta is broadly distributed in the outer and inner segments of photoreceptor cell layer, nuclear layer and ganglion cell layer. PLC gamma is mainly appeared in the nerve fiber layer, ganglion cell layer and inner nuclear layer. PLC delta is confined only in the ganglion cell layer. These results clearly demonstrate the PLC isozymes may have their own role in the transduction of light pathway in the retina. However, further studies will be required to verify theirs precise role in the photoreception.
Animals ; Antibodies, Monoclonal ; Ganglion Cysts ; Immunohistochemistry ; Isoenzymes* ; Nerve Fibers ; Peroxidase ; Phospholipase C beta ; Phospholipases* ; Photoreceptor Cells ; Rats* ; Retina* ; Type C Phospholipases*