The Concepts of Social Space and Social Value: An Interpretation of Clinical Nursing Practice in Vietnam Các khái niem ve không gian xã hoi và giá tri xã hoi: dien giai ve thuc hành dieu dÆ°ong lâm sàng o Viet Nam.

This research draws on broader inquiry that explores the construction of the spatial positioning of nurses in Vietnam and how power structures sustained that positioning. Observations and individual interviews were undertaken with 32 registered nurses. Analysis of participant data and relevant policy documents moved beyond coding to theorising and thus to the abstraction of key concepts. Social space and social value were significant concepts developed in the research. The concept of space reflected the ways in which nurses constantly engaged in processes of negotiation to embed a sense of control over their practice. The related concept of social value brought focus to a power structure whereby the fiscal priorities of health care managers reinforced a disconnect between the use and exchange values of nurses. An interpretation of power relations that underpinned the material and symbolic spaces in which nurses worked was framed within the historical context of Vietnam. Tóm lÆ°Æ°oc Bài báo này dua trên nghiên cuu voi qui mô lon hÆ¡n nham tìm hieu vi the cua nghành dieu dÆ°ong tai Viet Nam. PhÆ°Æ¡ng pháp quan sát và phong van cá nhân dÆ°oc thuc hien voi 32 nhân viên dieu dÆ°ong làm viec tai tám khoa cua mot benh vien o Viet Nam. Viec phân tích du lieu cua ngÆ°oi tham gia và các tài lieu ve chính sách liên quan dã vÆ°ot ra khoi pham vi mã hóa du lieu dÆ¡n thuan, mo rong sang hoc thuyet và chuyen sang truu tÆ°ong hóa các khái niem chính. Không gian xã hoi và giá tri xã hoi là nhung khái niem quan trong dÆ°oc phát trien trong nghiên cuu này. Khái niem ve không gian phan ánh cách thuc mà các nhân viên dieu dÆ°ong liên tuc tham gia vào các quá trình thÆ°Æ¡ng lÆ°ong de kiem soát dÆ°oc viec thuc hành cua ho. Khái niem liên quan ve giá tri xã hoi tap trung vào cÆ¡ cau quyen luc, theo dó Æ°u tiên tài chính cua các nhà quan lý cham sóc suc khoe góp phan làm gián doan moi liên ket giua giá tri su dung và giá tri trao doi mà ngành dieu dÆ°ong mang lai. Lý giai ve các moi quan he quyen luc dã dÆ°oc cung co trong không gian thuc và không gian mang tính bieu tÆ°ong nÆ¡i các dieu dÆ°ong làm viec, dÆ°oc dinh hình trong boi canh lich su cua Viet Nam.

[Mechanism of advanced glycation end products inhibiting the proliferation of peripheral blood mononuclear cells and osteoblasts in rats].

OBJECTIVE: To explore the mechanism of nuclear factor-kappa B (NF-κB), phosphatidylinositol 3-kinase (PI3K)/protein kinase B(PKB/Akt) and mitogen-activated protein kinase (MAPK) signaling pathways after intervention of advanced glycosylation end products (AGEs) in peripheral blood mononuclear cells (PBMCs) and osteoblasts (OB) in rats, so as to provide certain experimental basis and theoretical basis for further research on the clinical treatment of periodontal tissue inflammation caused by diabetes mellitus. METHODS: AGEs were prepared, PBMCs and OB were isolated and cultured in vitro. CCK-8 was used to detect the cell viability intervened by different concentrations and time of AGEs. Western blot and qRT-PCR were used to detect the expression changes of genes related to NF-κB, PI3K/PKB and MAPK signaling pathways. RESULTS: OB and PBMCs were successfully isolated and cultured in vitro. The activity of PBMCs and OB cells was significantly correlated with the concentration, time and interaction of AGEs. With the increase of AGEs concentration and time, the activity of PBMCs and OB cells significantly decreased (P < 0.001). AGEs stimulation significantly increased the expression of NF-κB in PBMCs and the contents of tumor necrosis factor α(TNF-α), interleukin-1ß(IL-1ß) (P < 0.01). TNF-α, IL-1ß levels were significantly reduced after inhibition of NF-κB pathway (P < 0.01). NF-κB p65, JNK, and p38 phosphorylated and non-phosphorylated proteins increased significantly after AGEs stimulation of OB (P < 0.05). The phosphorylated protein expression of IκB was significantly increased, while the expression of non-phosphorylated protein was decreased (P < 0.01).The expressions of NF-κB p65, JNK, and IκB were significantly increased at the mRNA levels, and the expressions of IκB mRNA were significantly decreased (P < 0.05). There was no difference in the expression of Akt in either phosphorylated or non-phosphorylated proteins or at the mRNA level (P>0.05). With the addition of MAPK signaling pathway inhibitors, the phosphorylation and non-phosphorylated protein expressions of NF-κB p65, p38 and JNK were significantly reduced, and the phosphorylated protein of IκB was significantly decreased and the non-phosphorylated protein was significantly increased compared with the group with AGEs alone (P < 0.05). The results of qRT-PCR showed that the expression of IκB increased significantly after the addition of the JNK pathway blocker (P < 0.05), and the expression of NF-κB p65, p38 and JNK decreased, but the difference was not significant (P>0.05). While NF-κB p65, p38 and JNK were significantly decreased and IκB was significantly increased in the AGEs group after the addition of the p38 pathway blocker (P < 0.05). At this time, there was still no significant change in the expression of Akt at the protein level and mRNA level (P>0.05). CONCLUSION: AGEs inhibit the proliferation of PBMCs and OB, and the NF-κB and MAPK pathways are likely involved in regulating this process, but not the PI3K/PKB pathway.

[The etiological analysis of 260 hospitalized cases with bilateral adrenal lesions].

Objective: To summarize the etiologies of bilateral adrenal lesions and the changes of the disease profile in hospitalized patients. Methods: Bilateral adrenal lesion screening was conducted in all patients admitted to Peking University Third Hospital from 1994 to 2017. The etiologies and disease profiles of bilateral adrenal lesions were retrospectively analyzed. Results: A total of 260 patients with bilateral adrenal lesions were included in the study. There were 146 males and 114 females with a mean age of (55.4±16.2) years. The most common adrenal lesion was bilateral adrenal hyperplasia (75 cases, 28.8%), followed by bilateral adrenal adenomas (71 cases, 27.3%), metastatic carcinoma (51 cases, 19.6%), discordant bilateral adrenal lesions (27 cases, 10.4%), bilateral pheochromocytomas (13 cases, 5.0%), and others. The clear data of endocrine function evaluation could be found in 184 patients. Among them, 111 cases (60.3%) were nonfunctioning lessions, 34 cases (18.5%) with primary aldosteronism, 15 cases (8.1%) with pheochromocytoma, 13 cases (7.1%) with congenital adrenal hyperplasia, 6 cases (3.3%) with primary hypoadrenocorticism, and 5 cases (2.7%) with Cushing syndrome. Using every 8 years as a period of time, the number of hospitalized patients with bilateral adrenal lesions increased with years in three periods (8, 41 and 211 cases, respectively). Conclusions: The most common cause of bilateral adrenal lesions is adrenal hyperplasia in the hospitalized patients. More than half of bilateral adrenal lesions are nonfunctioning. In functional bilateral lesions, primary aldosteronism and pheochromocytoma account for a large proportion.

Paired box 6 (PAX6) regulates glucose metabolism via proinsulin processing mediated by prohormone convertase 1/3 (PC1/3).

AIMS/HYPOTHESIS: Human patients with aniridia caused by heterozygous PAX6 mutations display abnormal glucose metabolism, but the underlying molecular mechanism is largely unknown. Disturbed islet architecture has been proposed as the reason why mice with complete inactivation of paired box 6 (PAX6) in the pancreas develop diabetes. This is not, however, the case in human aniridia patients with heterozygous PAX6 deficiency and no apparent defects in pancreatic development. We investigated the molecular mechanism underlying the development of abnormal glucose metabolism in these patients. METHODS: A human aniridia pedigree with a PAX6 R240Stop mutation was examined for abnormal glucose metabolism using an OGTT. The underlying mechanism was further investigated using Pax6 R266Stop mutant small-eye mice, which also have abnormal glucose metabolism similar to that in PAX6 R240Stop mutation human aniridia patients. RESULTS: Paired box 6 (PAX6) deficiency, both in aniridia patients with a heterozygous PAX6 R240Stop mutation and in mice with a heterozygous Pax6 R266Stop mutation, causes defective proinsulin processing and abnormal glucose metabolism. PAX6 can bind to the promoter and directly upregulate production of prohormone convertase (PC)1/3, an enzyme essential for conversion of proinsulin to insulin. Pax6 mutations lead to PC1/3 deficiency, resulting in defective proinsulin processing and abnormal glucose metabolism. CONCLUSIONS/INTERPRETATION: This study indicates a novel function for PAX6 in the regulation of proinsulin processing and glucose metabolism via modulation of PC1/3 production. It also provides an insight into the abnormal glucose metabolism caused by heterozygous PAX6 mutations in humans and mice.

Adversarial search by evolutionary computation.

In this paper, we consider the problem of finding good next moves in two-player games. Traditional search algorithms, such as minimax and alpha-beta pruning, suffer great temporal and spatial expansion when exploring deeply into search trees to find better next moves. The evolution of genetic algorithms with the ability to find global or near global optima in limited time seems promising, but they are inept at finding compound optima, such as the minimax in a game-search tree. We thus propose a new genetic algorithm-based approach that can find a good next move by reserving the board evaluation values of new offspring in a partial game-search tree. Experiments show that solution accuracy and search speed are greatly improved by our algorithm.

Interleukin-18 mRNA, but not interleukin-18 receptor mRNA, is constitutively expressed in islet beta-cells and up-regulated by interferon-gamma.

Interleukin-18 (IL-18) mRNA is expressed in islets of NOD mice during the early stages of insulitis and IL-18 has therefore been implicated as a contributing factor in immune-mediated beta-cell destruction. However, a recent study failed to show any effect of human IL-18 on the function of isolated rat islets. Since species differences have been shown between human and murine IL-18, the aims of this study were to investigate 1) if species homologous IL-18 alone or following IL-12 pre-exposure affected rat islet function, 2) if IL-18 dose-dependently modulated IL-1 beta or interferon-gamma (IFN-gamma) + tumor necrosis factor-alpha (TNF-alpha) actions on islet function, and 3) if IL-18 and IL-18 receptor (IL-18R) were expressed in rat islet beta-cells. Insulin release and nitric oxide (NO) production from isolated rat islets were measured after incubation with or without cytokines. RT-PCR was used to quantitate mRNA expression of IL-18 and the IL-18R signaling chain (IL-18R beta). There were no significant effects of 0.625-10 nM recombinant murine (rm) IL-18 alone on accumulated or glucose-challenged insulin release or NO production after 24 hours. Fifteen pg/ml of recombinant human (rh) IL-1 beta as well as 200 U/ml recombinant rat (rr) IFN-gamma + 250 U/ml rhTNF-alpha significantly increased islet NO production and inhibited both accumulated and glucose-challenged islet insulin release. However, rmIL-18 failed to modulate these effects of IL-1 beta or IFN-gamma + TNF-alpha. Although IL-12 induces IL-18R expression in Th1 and B lymphocytes, 24-hours rmIL-12 preincubation neither sensitized islets to effects of 10 nM of rm or rrIL-18 alone nor primed the islets to IL-1 beta actions on insulin release and NO production. IL-18R beta mRNA, which was expressed in human peripheral blood mononuclear cells (PBMC), was not expressed in rat insulinoma (RIN) cells or in isolated rat islets, even after exposure to IL-1 beta and/or IFN-gamma + TNF-alpha or IL-12. IL-18 mRNA was constitutively expressed in RIN cells, in FACS-purified rat beta-cells and in intact rat and mouse islets, and was up-regulated by IFN-gamma in an interferon regulatory factor-1- IRF-1) and NO - independent manner. However, IL-18 protein was undetectable in lysates and supernates of RIN cells by ECL, Western blotting and immunoprecipitation. In conclusion, we show for the first time that IL-18 but not IL-18R is expressed in rodent islet beta-cells. The physiological importance and pathological role of IL-18 originating from islet beta-cells deserve further investigation.

[Effects of different thyroid states on 5-HT1A receptor in adult rat brain].

The effects of dysthyroidism on central 5-HT1A receptor subtype in adult Wistar rats were investigated. Hyperthyroidism and hypothyroidism were respectively produced with the administration of T3 and propylthiouracil (PTU) via gavage for 2 weeks. Heart rate, oxygen consumption, anal temperature and plasma T3 concentration were increased in hyperthyroid rats and decreased in hypothyroid rats significantly. Radioligand binding assay showed that the specific binding of [3H] 8-hydroxy-2-(di-n-propylamino) tetralin ([3H] 8-OH-DPAT) at 0.6 nmol/L concentration was highest in hippocampus, next in cerebral cortex, and lowest in hypothalamus, brain stem and corpus striatum in euthyroid rats. Hyperthyroidism increased the binding significantly in hippocampus but decreased in cortex. No change was found in the other brain regions. Scatchard analyses revealed that the Bmax was increased in hippocampus and decreased in cortex, whereas the KD was not consistently affected in hyperthyroid rats in comparison with that in euthyroid rats. However, there were no significant changes mentioned above in all these brain regions of hypothyroid rats. Our results indicate that there seems to exist an imbalance of the serotonergic activity mediated via 5-HT1A receptor between hippocampus and cerebral cortex in hyperthyroids. This might be one of the mechanisms leading to psychoneural disorders in hyperthyroidism.