A rare case of meningeal carcinomatosis and internal auditory canal metastasis presenting with the deafness for gastric cancer.

BACKGROUND: Meningeal carcinomatosis is a very rare metastatic site of gastric cancer and meningeal carcinomatosis without other metastatic sites is much extremely rare. Herein, we report our experience with a very rare case of meningeal carcinomatosis which was difficult to diagnose the recurrence by general systemic examination and was found due to the deafness despite the sustained high tumor markers. CASE PRESENTATION: A 68-year-old man consulted a hospital with vomiting and hematemesis. Laboratory tests revealed severe anemia. He was referred to our hospital and underwent an emergency gastroscopy, which revealed Borrman type 3 tumor and oozing of blood. Biopsy specimen showed gastric cancer. After several examinations, total gastrectomy was performed and tegafur-gimeracil-oteracil potassium (S-1) was initiated as adjuvant chemotherapy one month after surgery. Tumor marker levels (CEA and CA19-9) remained high for three months after surgery. S-1 was continued while shortening the imaging study follow-up period. Nine months after surgery, he noticed difficulty in hearing with facial paralysis, dizziness, tinnitus, and appetite loss. He was diagnosed with meningeal carcinomatosis and bilateral internal auditory canal metastasis. He died approximately two months later. CONCLUSION: Meningeal carcinomatosis should be considered if bilateral deafness and vestibulopathy develop after gastrectomy, even if no recurrence is apparent in the abdominal cavity.

[Locally Advanced Rectal Cancer Curatively Resected after Modified FOLFOXIRI plus Bevacizumab Chemotherapy-A Case Report].

A 69-year-old man with dyschezia was diagnosed with locally advanced colorectal cancer invading the urinary bladder and pelvis. We performed ileostomy to avoid passage disturbance because curative resection was difficult. The patient received 2 courses of modified FOLFOXIRI plus bevacizumab. The size of the primary tumor and lymph nodes decreased after chemotherapy. High anterior resection with D3 lymph node dissection was performed. Histopathological analysis revealed that the tumor stage was pT3, N0, M0, StageⅡ. The patient has been receiving adjuvant chemotherapy with oral UFT/UZEL for 6months. No recurrence has been observed for the past 4 months.

Suprachiasmatic nucleus grafts restore circadian behavioral rhythms of genetically arrhythmic mice.

The mammalian master clock driving circadian rhythmicity in physiology and behavior resides within the suprachiasmatic nuclei (SCN) of the hypothalamus. SCN neurons contain a molecular oscillator composed of a set of clock genes that acts in intertwined negative and positive feedback loops [1]. In addition, all peripheral tissues analyzed thus far have been shown to contain circadian oscillators [2]. This raises the question of whether the central circadian pacemaker in the SCN is sufficient to evoke behavioral rhythms or whether peripheral circadian clockworks are also required. Mice with a mutated CLOCK protein (a transcriptional activator of E box-containing clock and clock output genes) or lacking both CRYPTOCHROMES, mCRY1 and mCRY2 proteins (inhibitors of E box-mediated transcription), lack circadian rhythmicity in behavior [3,4]. Here, we show that transplantation of mouse fetal SCN tissue into the hypothalamus restores free-running circadian behavioral rhythmicity in Clock mutant or mCry1/mCry2 double knockout mice. The periodicity of the emerged rhythms is determined by the genetic constitution (i.e., wild-type or mCry2 knockout) of the grafted SCN. Since transplanted mCry1/mCry2-deficient mice do not have functional circadian oscillators [5] other than those present in the grafted hypothalamus region, these findings suggest that the SCN can generate circadian behavioral rhythms in the absence of distant peripheral oscillators in the brain or elsewhere.