29 research outputs found
The Resolution Modules of A Space and Its Universal Covering Space
Let G be a finite group, Y a finite connected G-CW-complex, and let Ⅱ(Y) denote G-poset (in the sense of Oliver-Petrie) associated to Y. They defined the abelian group Ω(G,Ⅱ(Y)) consisting of all equivalent classes of Ⅱ(Y)-complexes. They also defined the subgroup Φ(G,Ⅱ(Y)) related to Ⅱ(Y)-resolutions. We call Φ(G,Ⅱ(Y)) the resolution module of Y. Applying the Oliver-Petrie theory to the universal covering space Y, we obtain the group Ω(G,Ⅱ(Y)), where G is a certain extension of G by π(1)(Y). Then the canonical homomorphism ν : Ω(G,Ⅱ(Y))→ Ω(G,Ⅱ(Y)) induced by the projection Y → Y is an isomorphism. In this paper, for G = Z(p)×Z(q) we construct a finite G-CW-complex Y such that π(1)(Y) Zq and ν(Φ(G,Ⅱ(Y)) ≠ Φ(G,Ⅱ(Y)), where p and q are arbitrary distinct primes
Identification of prothymosin-α1, the necrosis–apoptosis switch molecule in cortical neuronal cultures
We initially identified a nuclear protein, prothymosin-α1 (ProTα), as a key protein inhibiting necrosis by subjecting conditioned media from serum-free cultures of cortical neurons to a few chromatography steps. ProTα inhibited necrosis of cultured neurons by preventing rapid loss of cellular adenosine triphosphate levels by reversing the decreased membrane localization of glucose transporters but caused apoptosis through up-regulation of proapoptotic Bcl2-family proteins. The apoptosis caused by ProTα was further inhibited by growth factors, including brain-derived neurotrophic factor. The ProTα-induced cell death mode switch from necrosis to apoptosis was also reproduced in experimental ischemia-reperfusion culture experiments, although the apoptosis level was markedly reduced, possibly because of the presence of growth factors in the reperfused serum. Knock down of PKCβII expression prevented this cell death mode switch. Collectively, these results suggest that ProTα is an extracellular signal protein that acts as a cell death mode switch and could be a promising candidate for preventing brain strokes with the help of known apoptosis inhibitors
A surgical case of phlegmonous gastritis after endoscopic submucosal dissection for early gastric cancer
Phlegmonous gastritis is a rare inflammatory lesion in which bacterial infection occurs in the gastric wall. A 92-year-old man was admitted to the medical ward due to early gastric cancer. The patient received endoscopic submucosal dissection (ESD), and he complained of sudden-onset upper abdominal pain the day after ESD. On physical examination he showed rebound tenderness in the upper abdomen. The white blood cell count was 16,100/μl, and an abdominal CT-SCAN showed diffuse and irregular thickening of the gastric wall. At emergency operation, a subtotal gastrectomy was performed, and the patient had an uneventful recovery
体外式腹部超音波が診断に有用であった十二指腸巨大Brunner 腺過形成の一例
Brunner 腺過形成は十二指腸腫瘍性病変で,大きさが40mm を超えるものは10% 未満と稀である.医学中央雑誌で「腹部超音波」「Brunner 腺過形成」のキーワードで検索すると,関連した報告はない.体外式超音波検査(US)が診断に有用であったBrunner 腺過形成の一例を報告する.症例は50歳代,女性.食欲不振,心窩部痛とタール便を主訴に近医受診.貧血を認め,出血源検索目的に行った上部消化管内視鏡検査(EGD)で胃内に約 45 mm の腫瘤性病変を認め精査目的に当院紹介となった.血液生化学検査ではHb 9.1 g/dl,MCV 89.1 fl,MCH 30.0 pg と正球性正色素性貧血を認め,BUN/CRE 比は43.1と上昇していた.当院でのEGD では十二指腸球部に内腔をほぼ閉塞する45×40 mm の腫瘤性病変を認めた.腫瘤表面の異型性は目立たないが,oozing bleeding を伴ったびらん形成を認めた.粘膜下腫瘍を疑い生検も行われたが確定診断には至らなかった.単純造影CT では十二指腸球部に 45 mm 程度の腫瘤性病変を認め,辺縁は遷延性に造影された.内部は低吸収域が認められ,嚢胞変性や壊死が疑われた.周囲臓器への浸潤や転移を示唆する所見は認めず,粘膜下腫瘍が疑われたが癌は否定できなかった.US では十二指腸球部後壁の第2層から第3層に存在する約55 mm の粘膜下腫瘍が認められた.固有筋層は正常で,内部は大半が多房性嚢胞からなり,嚢胞間に充実成分がみられた.血流は比較的豊富であるが血管径や形状に明らかな不整は認めなかった.以上より十二指腸Brunner 腺過形成が疑われた.外科的切除の方針となり,開腹で十二指腸粘膜下層剥離術を行った.術材の組織診断はBrunner 腺過形成で超音波診断と矛盾しない所見であった.十二指腸粘膜下腫瘍の鑑別には超音波内視鏡が有用であるが,大きな病変では全体の描出が困難などの欠点もある.一方でUS は内視鏡侵襲なく,比較的大きな病変も描出可能で,特に本症例の様に前庭部付近は良好な観察が期待できるため,上部消化管の精査に応用できる.Brunner’s gland hyperplasia is a duodenal neoplastic lesion, and its lesions measuring >40 mm in diameter are rare, accounting for <10% of cases. A search of the Ichushi (Japana Centra Revuo Medicina) database using the keywords “abdominal ultrasound” and “Brunner’s gland hyperplasia” yielded no relevant articles. Here we report a case of Brunner’s gland hyperplasia in which transabdominal ultrasonography (US) was useful for diagnosis. A female in her 50s presented to a local hospital complaining of anorexia, epigastric pain and tarry stool. She had anemia and esophagogastroduodenoscopy (EGD), which was performed to identify the source of bleeding, revealed a mass lesion measuring approximately 45 mm in diameter in the stomach. She was referred to our hospital for further examination. Blood biochemistry showed a hemoglobin (Hb) level of 9.1 g/dL, mean corpuscular volume (MCV) of 89.1 fL and mean corpuscular hemoglobin (MCH) of 30.0 pg, indicating normocytic normochromic anemia. The blood urea nitrogen (BUN)/creatinine (CRE) ratio was as high as 43.1. In our hospital, EGD revealed a 45×40 mm mass lesion almost obstructing the lumen in the duodenal bulb. Atypia of the mass surface was not prominent, but erosion with oozing bleeding was observed. A submucosal tumor was suspected, and biopsy was performed but did not lead to a definitive diagnosis. Plain contrast-enhanced computed tomography (CT) revealed a mass lesion with prolonged peripheral enhancement measuring approximately 45 mm in diameter in the duodenal bulb. There was a low-density area inside the mass, raising the suspicion of cystic degeneration and necrosis. There were no findings suggesting infiltration or metastasis to the surrounding organs, raising the suspicion of a submucosal tumor, but cancer could not be ruled out. US revealed a submucosal tumor measuring approximately 55 mm in diameter in the second to third layer of the posterior wall of the duodenal bulb. The muscularis propria was normal and mostly composed of multilocular cysts with solid components in the space between the cysts. Blood flow was relatively abundant, but there were no obvious irregularities in the diameter or shape of blood vessels. The above findings raised the suspicion of duodenal Brunner’s gland hyperplasia. It was decided to perform surgical resection, and she underwent open duodenal submucosal dissection. Histology of the surgical specimen revealed Brunner’s gland hyperplasia, cons istent with the ultrasonographic findings. Endoscopic ultrasonography is useful in the differential diagnosis of duodenal submucosal tumors, but also has disadvantages such that it is difficult to visualize the entire lesion, when the lesion is large. On the other hand, US can be applied to the detailed examination of the upper gastrointestinal tract, because there are no invasive endoscopic procedures and US can visualize relatively large lesions and, in particular, can be expected to satisfactory observe around the vestibule, like in the present case
DOCK2 is involved in the host genetics and biology of severe COVID-19
「コロナ制圧タスクフォース」COVID-19疾患感受性遺伝子DOCK2の重症化機序を解明 --アジア最大のバイオレポジトリーでCOVID-19の治療標的を発見--. 京都大学プレスリリース. 2022-08-10.Identifying the host genetic factors underlying severe COVID-19 is an emerging challenge. Here we conducted a genome-wide association study (GWAS) involving 2, 393 cases of COVID-19 in a cohort of Japanese individuals collected during the initial waves of the pandemic, with 3, 289 unaffected controls. We identified a variant on chromosome 5 at 5q35 (rs60200309-A), close to the dedicator of cytokinesis 2 gene (DOCK2), which was associated with severe COVID-19 in patients less than 65 years of age. This risk allele was prevalent in East Asian individuals but rare in Europeans, highlighting the value of genome-wide association studies in non-European populations. RNA-sequencing analysis of 473 bulk peripheral blood samples identified decreased expression of DOCK2 associated with the risk allele in these younger patients. DOCK2 expression was suppressed in patients with severe cases of COVID-19. Single-cell RNA-sequencing analysis (n = 61 individuals) identified cell-type-specific downregulation of DOCK2 and a COVID-19-specific decreasing effect of the risk allele on DOCK2 expression in non-classical monocytes. Immunohistochemistry of lung specimens from patients with severe COVID-19 pneumonia showed suppressed DOCK2 expression. Moreover, inhibition of DOCK2 function with CPYPP increased the severity of pneumonia in a Syrian hamster model of SARS-CoV-2 infection, characterized by weight loss, lung oedema, enhanced viral loads, impaired macrophage recruitment and dysregulated type I interferon responses. We conclude that DOCK2 has an important role in the host immune response to SARS-CoV-2 infection and the development of severe COVID-19, and could be further explored as a potential biomarker and/or therapeutic target