[Para-Aortic Lymphadenectomy and Subsequent Chemotherapy after Resection of the Primary Lesion for Poorly Differentiated Adenocarcinoma of the Sigmoid Colon - A Case Report].

The patient was a 68-year-old male who had bloody stools. A colonoscopy revealed a sigmoid colon stricture, and a histological examination confirmed the presence of a poorly differentiated adenocarcinoma.Computed tomography revealed the involvement of a para-aortic lymph nodes, without other metastatic lesions. The patient underwent a sigmoidectomy (with regional lymph node dissection) and a para-aortic lymph node biopsy to prove the histological conformation. Subsequently, he was provided with 6 courses of modified FOLFOX6(mFOLFOX6) chemotherapy, resulting in a marked decrease in para-aortic lymph node involvement. He subsequently underwent a para-aortic lymphadenectomy. The resected specimen was mostly composed of fibrous degenerative tissue; viable cancer cells were observed only in a 2-mm² area. The patient was provided with 6 more courses of mFOLFOX6 chemotherapy, and has since been free of recurrence (for 6 years and 1 month after the second surgery).

Morel's laminar sclerosis showing apraxia of speech: distribution of cortical lesions in an autopsy case.

A 57-year old man with chronic alcoholism presented with apraxia of speech and disturbance of consciousness. He had a history of gastrectomy and had been drinking alcohol. The symptoms improved with administration of thiamine, but he later developed diarrhea and delirium, and died approximately 40 days after the onset. Autopsy findings were consistent with Wernicke's encephalopathy and pellagra encephalopathy. Furthermore, laminar cortical necrosis with vacuoles and astrocytosis was found in the second and third layers of the bilateral frontal cortices, suggesting Morel's laminar sclerosis. The lesions were mainly located in the bilateral primary motor cortices. Involvement of the lower part of the left primary motor cortex may be associated with apraxia of speech in our case.

Neuronal expression of cyclooxygenase-2, a pro-inflammatory protein, in the hippocampus of patients with schizophrenia.

Several types of evidence suggesting that the inflammatory response system is associated with pathophysiology of schizophrenia have been accumulated. Recently, a prospective double-blind study demonstrated that supplementary treatment with celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, produced significantly greater improvement in scores on the Positive and Negative Syndrome Scale (PANSS) and on all subscales during the acute phase in patients with schizophrenia compared with risperidone alone therapy. The therapeutic effect of celecoxib on the psychopathology of schizophrenia is speculated to be based on COX activity inhibition; however, the detailed pharmacological mechanisms are unclear. To clarify whether or not COX-2 expression is altered in schizophrenia, we examined neuronal COX-2 expression in the hippocampus from cases of schizophrenia (n = 17), normal controls (n = 22), and cases of Alzheimer's disease (AD) as a positive control (n = 17). Quantitative immunohistochemical analysis demonstrated that neuronal COX-2 expression was significantly up-regulated in each CA1-4 region in Alzheimer's disease compared with controls, and that the mean COX-2 immunointensity in CA1-4 was significantly correlated with Abeta load in cases of Alzheimer's disease. In contrast, COX-2 expression was not up-regulated in any subdivision of the hippocampus in the schizophrenia group. These results suggest that celecoxib may affect the pathophysiology of schizophrenia through COX-2-independent actions rather than by inhibiting activity of up-regulated COX-2 protein.

Increased expression of neuronal cyclooxygenase-2 in the hippocampus in amyotrophic lateral sclerosis both with and without dementia.

The pathophysiological basis of cognitive dysfunction, including frontotemporal dementia (FTD), in patients with amyotrophic lateral sclerosis (ALS) and ALS with dementia (ALSD) remains unclear. On the other hand, increased expression of cyclooxygenase-2 (COX-2) in the spinal cord is thought to play a pivotal role in motor neuron degeneration in ALS. In this study, to assess the relationship between the neuronal COX-2 expression in the cerebrum, the formation of tau- and alpha-synuclein-negative but ubiquitin-positive neuronal inclusions (UPIs), and dementia in motor neuron disease (MND), we examined neuronal COX-2 immunoreactivity in the frontal cortex and hippocampus of patients with non-demented ALS without UPIs ( n=11), ALSD with UPIs ( n=6), and normal controls ( n=24) using a quantitative immunohistochemical technique. Neuronal COX-2 expression in all CA1-4 in the hippocampus was significantly up-regulated in the ALSD group, and, to lesser degree but significantly, in the ALS group. Neuronal COX-2 expression in the frontal cortex was also significantly up-regulated in the ALSD group but not in the ALS group. These findings suggest that (1) the frontal cortex and hippocampus of MND are involved in the same pathogenic process associated with COX-2 induction that has been observed in spinal anterior horn cells, (2) COX-2 induction in the cerebrum is a pathogenic process that can occur even in the absence of UPI formation in MND, and (3) COX-2 expression in the cerebrum may be associated with cognitive dysfunction in MND.