Duodenal Gastrointestinal Stromal Tumor Treated by Wedge Resection in a Patient with Neurofibromatosis Type 1: Report of a Case and Review of the Japanese Literature

A case of duodenal gastrointestinal stromal tumor (GIST) treated by wedge resection in a patient with neurofibromatosis type 1 (NF-1) is reported. A 55-year-old man with a history of NF-1 was admitted for surgery for a duodenal tumor. Upper gastrointestinal endoscopy revealed a 2.5 cm duodenal submucosal tumor. Abdominal computed tomography showed a homogenously enhanced mass in the third portion of the duodenum. The patient successfully underwent wedge resection of the duodenal tumor. Histological examination revealed proliferation of spindle tumor cells arranged in a bundle pattern. This tumor was immunohistochemically positive for c-Kit and CD34, and negative for S-100 and α-SMA. A mitotic count showed 3 mitoses per 50 high-power fields. The tumor was diagnosed as a low-risk GIST. The patient's postoperative course was uneventful. GIST in a patient with NF-1 is rare, only 27 cases being reported in the Japanese literature

Effect of clonidine on the release of serotonin from the rat hippocampus as measured by microdialysis

The purpose of the present study is to clarify the effect of clonidine on the release of serotonin from the rat hippocampus in vivo. For this purpose, endogenous serotonin release was measured by brain microdialysis. Potassium-evoked serotonin release from the hippocampus of freely moving rats was significantly inhibited when clonidine (10-5 M) was added to the perfusion solution, while the 5-hydroxyindoleacetic acid output remained unchanged. In catecholaminergically denervated rats, clonidine (10-5 M) also inhibited the potassium-evoked serotonin release from the hippocampus and the 5-hydroxyindoleacetic acid output was unaffected by clonidine. These results suggest that the inhibitory effect of clonidine on serotonin release from the hippocampus might reflect the activation of [alpha]2-adrenoceptors which are localized on the serotonergic nerve terminals.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/30049/1/0000417.pd

Opioid receptor regulation of 5-hydroxytryptamine release from the rat hippocampus measured by in vivo microdialysis

The modulation of serotonin (5-HT) release by opioid receptors in the hippocampus of the awake, unrestrained rat was evaluated by use of in vivo microdialysis. The hippocampus was perfused with Ringer's solution (2 [mu]l/min), and extracellular levels of 5-HT and its major metabolite, 5-hydroxyindoleacetic acid (5-HIAA) were estimated by assaying their concentration in the dialysate by HPLC-ECD. Addition of potassium (K+, 60 and 120 mM) to the perfusate evoked a concentration-dependent release of 5-HT, but did not alter extracellular 5-HIAA levels. Co-perfusion of morphine (0.1 to 10 [mu]M) with K+ (120 mM) produced a concentration-dependent reduction of 5-HT release. Naltrexone (0.03 to 3 mg/kg, i.p.), a relatively selective [mu]-opioid receptor antagonist, blocked in a dose-dependent manner the morphine (10 [mu]M)-induced inhibition of 5-HT release. Naltrexone alone did not alter significantly either extracellular 5-HT levels or the release of 5-HT evoked by K+. Neither co-perfusion with [-Pen2, -Pen5]-enkephalin (DPDPE, 1 to 10 [mu]M), an agonist selective for [delta]-opioid receptors, nor with U-69593 (10 [mu]M), an agonist selective for [kappa]-opioid receptors, modified the K+ (120 mM)-evoked release of 5-HT. These findings indicate that [mu]-opioid receptors modulate the physiological release of 5-HT from serotonergic neurons in the rat hippocampus.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/30746/1/0000396.pd

Gauss decomposition for Chevalley groups, revisited

In the 1960's Noboru Iwahori and Hideya Matsumoto, Eiichi Abe and Kazuo Suzuki, and Michael Stein discovered that Chevalley groups $G=G(\Phi,R)$ over a semilocal ring admit remarkable Gauss decomposition $G=TUU^-U$, where $T=T(\Phi,R)$ is a split maximal torus, whereas $U=U(\Phi,R)$ and $U^-=U^-(\Phi,R)$ are unipotent radicals of two opposite Borel subgroups $B=B(\Phi,R)$ and $B^-=B^-(\Phi,R)$ containing $T$. It follows from the classical work of Hyman Bass and Michael Stein that for classical groups Gauss decomposition holds under weaker assumptions such as \sr(R)=1 or \asr(R)=1. Later the second author noticed that condition \sr(R)=1 is necessary for Gauss decomposition. Here, we show that a slight variation of Tavgen's rank reduction theorem implies that for the elementary group $E(\Phi,R)$ condition \sr(R)=1 is also sufficient for Gauss decomposition. In other words, $E=HUU^-U$, where $H=H(\Phi,R)=T\cap E$. This surprising result shows that stronger conditions on the ground ring, such as being semi-local, \asr(R)=1, \sr(R,\Lambda)=1, etc., were only needed to guarantee that for simply connected groups $G=E$, rather than to verify the Gauss decomposition itself

Inhibitory effects of clonidine on serotonergic neuronal activity as measured by cerebrospinal fluid serotonin and its metabolite in anesthetized rats

Clonidine-induced changes in the serotonergic neuronal activity of the central nervous system were estimated by measuring the concentrations of serotonin (5-HT) and its major metabolite, 5-hydroxyindole-3-acetic acid (5-HIAA), in the cerebrospinal fluid (CSF) of anesthetized rats. Clonidine (30 and 300 [mu]g/kg, i.v.) led to 74% and 60% reductions in the concentration of 5-HT in the CSF 60 min after administration. CSF 5-HIAA concentrations were also decreased to 77% and 66%, respectively. Clonidine-induced (30 [mu]g/kg, i.v.) decreases in CSF 5-HT and 5-HIAA concentrations were attenuated by pretreatment with idazoxan (5 mg/kg, i.p.). Idazoxan by itself did not alter the CSF 5-HT and 5-HIAA concentrations. Decreased CSF 5-HT and 5-HIAA concentrations after i.v. administration of clonidine (30 [mu]g/kg) were abolished by noradrenergic denervation after pretreatment with 6-hydroxydopamine (200 [mu]g/rat, i.c.v.). These results suggest the possibility that clonidine acts to inhibit the serotonergic neuronal activity, which is mediated via the [alpha]2-adrenoceptors. It indicates, moreover, that noradrenergic nervous systems are involved in the clonidine-induced inhibition of serotonergic neuronal activity. Therefore, noradrenergic neurons play a significant role in mediating the actions of clonidine on serotonergic neuronal activity in the rat brain.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/31094/1/0000771.pd

APOBEC3B is preferentially expressed at the G2/M phase of cell cycle

APOBEC3B (A3B) is a cytosine deaminase that converts cytosine to uracil in single-stranded DNA. Cytosine-to-thymine and cytosine-to-guanine base substitution mutations in trinucleotide motifs (APOBEC mutational signatures) were found in various cancers including lymphoid hematological malignancies such as multiple myeloma and A3B has been shown to be an enzymatic source of mutations in those cancers. Although the importance of A3B is being increasingly recognized, it is unclear how A3B expression is regulated in cancer cells as well as normal cells. To answer these fundamental questions, we analyzed 1276 primary myeloma cells using single-cell RNA-sequencing (scRNA-seq) and found that A3B was preferentially expressed at the G2/M phase, in sharp contrast to the expression patterns of other APOBEC3 genes. Consistently, we demonstrated that A3B protein was preferentially expressed at the G2/M phase in myeloma cells by cell sorting. We also demonstrated that normal blood cells expressing A3B were also enriched in G2/M-phase cells by analyzing scRNA-seq data from 86, 493 normal bone marrow mononuclear cells. Furthermore, we revealed that A3B was expressed mainly in plasma cells, CD10+ B cells and erythroid cells, but not in granulocyte-macrophage progenitors. A3B expression profiling in normal blood cells may contribute to understanding the defense mechanism of A3B against viruses, and partially explain the bias of APOBEC mutational signatures in lymphoid but not myeloid malignancies. This study identified the cells and cellular phase in which A3B is highly expressed, which may help reveal the mechanisms behind carcinogenesis and cancer heterogeneity, as well as the biological functions of A3B in normal blood cells

イガン ジュツゴ ニ チョクチョウ テンイ オ キタシタ 1レイ

We report a case of rectal metastasis from gastric cancer. The patient was a 69-year-old man with diarrhea as his major symptoms, who underwent a distal gastrostomy for gastric cancer 2 years previously. We suspected primary or metastatic rectal cancer from colonoscopic examination and barium enema. A lower anterior resection was performed. Postoperative historical examination identified poorly differentiated adenocarcinoma and signet cell carcinoma identical to the gastric cancer. Finally the lesion was diagnosed as metastatic rectal cancer from gastric cancer that showed same pattern in PAS stain. There were only 40 cases in reports in the literature from 2002 to 2012, to our knowledge. We report a rare case