大学での生活科授業改善報告 : 幼小接続を大切にした「おもちゃをつくりあそぼう」の授業実践

調査報告　本稿は、大学での生活科授業実践の報告とその改善報告を行うことが目的である。現時点において大学での具体的な生活科授業実践を報告する例は少なく、生活科の学会においても報告対象そのものから外れている例がある。しかし、教員養成課程の生活科授業は、将来の生活科授業を担う授業者の採用期における力量を高めることに直結しており、授業改善を図ることの意義は極めて高いと言える。　そこで、具体的な単元「おもちゃをつくりあそぼう」での授業改善をどのように図ったのかを改善策の導入前後で報告したい。　改善策導入前は、幼小接続の視点を重視した授業実践を行った。幼児期「遊び」と小学校「学習とを円滑に接続するために「道具」、「ルールの把握（指し手とコマ）」、「幼児期の終わりまでに育ってほしい姿（10 の姿）」を視点として授業を行った。その結果、学生の評価は、５段階評価で4.5 程度を示し高い評価と言えた。しかし、「表現」項目は、3.6 と他の項目と比べ低かった。「理解」と「表現」の円滑な接続が課題となった。　改善策導入後は、課題として位置付けた「理解」と「表現」の間に、改善策として「反応」を入れた。具体的には、「聞き手の反応」を促す「逆説明」過程を取り入れた。その結果、学生の評価は、他の項目同様高い評価へと上昇した。「逆説明」の効果は、「表現」への直接的な効果だけでなく、おもちゃ作製と遊び方に関する改善への意欲面にも効果があり、有効な改善策となった

The HIV-1 Vpr displays strong anti-apoptotic activity

AbstractMutations in the human immunodeficiency virus type 1 (HIV-1) vpr gene only slightly reduce the replication rate of the virus. To study the role of HIV-1 Vpr in biological effects on cells, HEp-2 cells, which express HIV-1 Vpr constitutively but at a low level, were established. While control HEp-2 cells underwent apoptosis when incubated with sorbitol, the morphological and biochemical apoptotic changes were inefficiently induced in the HIV-1 Vpr-expressing cells by the same treatment. These results clearly indicate that HIV-1 Vpr has anti-apoptotic activity, and raise the possibility that Vpr acts as a weak activator of virus replication through anti-apoptosis

Growth characteristics of T-cell tropic HIV-1 vpu gene mutants in human peripheral blood mononuclear cells

A mutant designated NL-E65, which lacks the expression of entire vpu gene, was constructed from T-cell tropic wild-type (wt) human immunodeficiency virus type1(HIV-1) clone and monitored for its replication property in human cells, along with a mutant NL-Ss which expresses a C-terminal truncated Vpu. The mutant NL-Ss could grow in two cell lines and in all peripheral blood mononuclear cell (PBMC) preparations to some extent, with kinetics similar to those of wt virus. Likewise, the mutant NL-E65exhibited a replication property typical to the vpu mutant in the two cell lines and in all PBMC cultures, growing at a low level. Along with the results previously reported, these data indicate that HIV-1 Vpu is dispensable for virus replication in any of the types of cells so far tested

Is Adjuvant Chemotherapy Necessary in Patients with Early Endometrial Cancer?

Background: We investigated whether there was a difference in prognosis between patients with stage IA endometrial cancer with and without lymphovascular space invasion. Methods: We enrolled patients with stage IA (pT1aN0M0) endometrial cancer admitted to our hospital from 2009 to 2018. All patients underwent hysterectomy, bilateral salpingo-oophorectomy, and systematic pelvic lymphadenectomy. We immunopathologically evaluated the presence or absence of lymphovascular space invasion in the tumor tissue using hematoxylin and eosin, Elastica-van Gieson, and podoplanin staining. We analyzed disease-free and overall survival and calculated patients’ survival distribution using the Kaplan–Meier method and log-rank test. The multivariate analysis was performed to determine the prognostic factors. Results: A total of 116 patients were included. The median age of the patients was 57 (range, 30–78) years, and the histological subtype revealed 98 and 18 cases of types 1 and 2, respectively. The median follow-up period was 71.9 (range, 10.8–149) months, and the 3-year disease-free and 3-year overall survival rates were 94% and 99%, respectively. The disease-free and overall survival rates were significantly shorter in type 2 patients than in type 1 patients (type 2 vs. type 1; 77% vs. 97%, P < 0.01, 94% vs. 100%, P = 0.014, respectively). The univariate and multivariate analyses showed that there were no significant differences in disease-free survival between the lymphovascular space invasion-positive and -negative groups among type 1 cases. Conclusion: There was no difference in prognosis between patients with stage IA and type 1 endometrial cancer with and without lymphovascular space invasion

Role of virus-induced apoptosis in a host defense mechanism against virus infection

Many animal viruses are known to induce apoptosis in infected cells. This virus-induced apoptosis has been often described as a mechanism of host defense against virus infection, based on the finding that mutants of an insect virus with the ability to induce extensive apoptosis in some cells cannot grow in the same cells. In animal virus infection, we have shown that (1) viruses can somehow overcome this defense mechanism and that (2) virus multiplication in the apoptotic cells is not as completely suppressed as in the insect virus infection. These results suggest that, in the case of animal viruses, the virus-induced apoptosis does not play the same role in the host defense system as in insect cells. However, by examining the virus infection under the conditions comparable to the infection in vivo, we demonstrated the defensive role of apoptosis in animal virus infection