Proses Produksi Dan Pengemasan Yoghurtdicv. Cita Nasional Salatiga

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Synthesis of Five-Membered Osmacycles with Osmium–Vinyl Bonds from Hydrido Alkenylcarbyne Complexes

Treatment of the osmium hydrido butenylcarbyne complex [OsH­{CC­(PPh₃)CH­(Et)}­(PPh₃)₂Cl₂]­BF₄ (<b>1</b>) with excess 2-chloro-4-cyanopyridine in the presence of H₂O₂ generates the fused osmacyclopentadiene <b>2</b>. A detailed mechanism of the conversion has been investigated with the aid of in situ NMR experiments and the isolation of intermediates <b>3</b> and <b>4</b>. In contrast, reaction of <b>1</b> with the propiolic acid ester HCCCOOMe produces the osmafuran <b>5</b>. Analogous reactions of the osmium hydrido phenylethenylcarbyne complex [OsH­{CC­(PPh₃)CH­(Ph)}­(PPh₃)₂Cl₂]­BF₄ (<b>6</b>) with nitriles/CO or HCCCOOMe were also studied, which result in the formation of five-membered osmacycles [Os­{CHC­(PPh₃)­CH­(Ph)­(OH)}­(CH₃CN)­(PPh₃)₂CO]­(BF₄)₂ (<b>7</b>) and [Os­{CHC­(PPh₃)­CH­(Ph)­(OH)}­(PhCN)­(PPh₃)₂CO]­(BF₄)₂ (<b>8</b>). In the presence of NEt₃, <b>6</b> can convert to the osmium hydrido phenylethenylcarbyne complex OsH­{CCCH­(Ph)}­(PPh₃)₂Cl₂ (<b>9</b>) in wet acetonitrile, presumably involving P–C bond cleavage. Similarly, <b>9</b> can react with HCCCOOMe with the aid of HBF₄ to give osmafuran <b>10</b>

Synthesis of Five-Membered Osmacycles with Osmium–Vinyl Bonds from Hydrido Alkenylcarbyne Complexes

Treatment of the osmium hydrido butenylcarbyne complex [OsH­{CC­(PPh₃)CH­(Et)}­(PPh₃)₂Cl₂]­BF₄ (<b>1</b>) with excess 2-chloro-4-cyanopyridine in the presence of H₂O₂ generates the fused osmacyclopentadiene <b>2</b>. A detailed mechanism of the conversion has been investigated with the aid of in situ NMR experiments and the isolation of intermediates <b>3</b> and <b>4</b>. In contrast, reaction of <b>1</b> with the propiolic acid ester HCCCOOMe produces the osmafuran <b>5</b>. Analogous reactions of the osmium hydrido phenylethenylcarbyne complex [OsH­{CC­(PPh₃)CH­(Ph)}­(PPh₃)₂Cl₂]­BF₄ (<b>6</b>) with nitriles/CO or HCCCOOMe were also studied, which result in the formation of five-membered osmacycles [Os­{CHC­(PPh₃)­CH­(Ph)­(OH)}­(CH₃CN)­(PPh₃)₂CO]­(BF₄)₂ (<b>7</b>) and [Os­{CHC­(PPh₃)­CH­(Ph)­(OH)}­(PhCN)­(PPh₃)₂CO]­(BF₄)₂ (<b>8</b>). In the presence of NEt₃, <b>6</b> can convert to the osmium hydrido phenylethenylcarbyne complex OsH­{CCCH­(Ph)}­(PPh₃)₂Cl₂ (<b>9</b>) in wet acetonitrile, presumably involving P–C bond cleavage. Similarly, <b>9</b> can react with HCCCOOMe with the aid of HBF₄ to give osmafuran <b>10</b>

Table1_Role of ATG7-dependent non-autophagic pathway in angiogenesis.XLSX

ATG7, one of the core proteins of autophagy, plays an important role in various biological processes, including the regulation of autophagy. While clear that autophagy drives angiogenesis, the role of ATG7 in angiogenesis remains less defined. Several studies have linked ATG7 with angiogenesis, which has long been underappreciated. The knockdown of ATG7 gene in cerebrovascular development leads to angiogenesis defects. In addition, specific knockout of ATG7 in endothelial cells results in abnormal development of neovascularization. Notably, the autophagy pathway is not necessary for ATG7 regulation of angiogenesis, while the ATG7-dependent non-autophagic pathway plays a critical role in the regulation of neovascularization. In order to gain a better understanding of the non-autophagic pathway-mediated biological functions of the autophagy-associated protein ATG7 and to bring attention to this expanding but understudied research area, this article reviews recent developments in the ATG7-dependent non-autophagic pathways regulating angiogenesis.</p

Table2_Role of ATG7-dependent non-autophagic pathway in angiogenesis.XLSX

ATG7, one of the core proteins of autophagy, plays an important role in various biological processes, including the regulation of autophagy. While clear that autophagy drives angiogenesis, the role of ATG7 in angiogenesis remains less defined. Several studies have linked ATG7 with angiogenesis, which has long been underappreciated. The knockdown of ATG7 gene in cerebrovascular development leads to angiogenesis defects. In addition, specific knockout of ATG7 in endothelial cells results in abnormal development of neovascularization. Notably, the autophagy pathway is not necessary for ATG7 regulation of angiogenesis, while the ATG7-dependent non-autophagic pathway plays a critical role in the regulation of neovascularization. In order to gain a better understanding of the non-autophagic pathway-mediated biological functions of the autophagy-associated protein ATG7 and to bring attention to this expanding but understudied research area, this article reviews recent developments in the ATG7-dependent non-autophagic pathways regulating angiogenesis.</p

Representative images showing immunohistochemical staining for ATG-5 in non-tumorous and GC tumor tissues.

<p>(A) ATG-5 staining in non-cancerous gastric tissues scored 285(×200); (B) ATG-5 staining in GC tumor tissues scored 50(×400); (C) ATG-5 staining in GC tumor tissues scored 270(×400); (D) ATG-5 staining in GC tumor tissues scored 400(×200).</p

ATG-5 was upregulated in chemoresistant cells.

<p>(A) The level of ATG5 was detected in cell lines using western blot analysis. β -actin was used as internal controls.(B) The IC 25, IC50 and IC75 of SGC-7901 and SGC-7901/DDP cells were tested using the MTT assays after DPP treatment.</p

Silencing ATG-5 sensitized chemoresistant cells to drug treatment.

<p>(A) The mRNA level of ATG-5 was detected by real time PCR after treatment with siRNAs. GAPDH was used as internal controls. (B) The protein level of ATG-5 was detected by western blot after treatment with siRNAs. β -actin was used as internal controls. (C) The proliferation ability was tested using MTT assay 48 hours or 72 hours after different treatment.</p

Association between ATG-5 expression and clinicopathological characteristics of GC patients.

▴<p>Statistical analyses were carried out with the One-Way ANOVA test and others were carried out with the Pearson’s χ² test.</p><p>Association between ATG-5 expression and clinicopathological characteristics of GC patients.</p

Autophagy was involved in the drug resistant of DC cells.

<p>(A) The autophagy was detected by immunofluorescence assay of LC3B in the cells 48 hours after different treatment. (B) The protein levels of LC3A and LC3B were tested by western blot. β-actin was used as internal controls.</p