Perubahan Harga Lahan dalam Kaitannya dengan Pembangunan Pertanian di Pedesaan Lampung

IndonesianDalam pembangunan pertanian diperlukan empat faktor penggerak yaitu sumberdaya lahan, sumberdaya manusia, teknologi dan kelembagaan. Keempat faktor diatas saling terkait satu sama lain, sehingga bila salahsatu faktor diatas mengalami hambatan sulit tercapai sasaran yang diinginkan. Pesatnya laju pembangunan beberapa tahun terakhir, menyebabkan sumberdaya lahan terasa semakin terbatas. Hal ini disebabkan oleh terjadinya Perubahan fungsi lahan untuk kepentingan pembangunan itu sendiri. Bertitik tolak dari permasalahan diatas, sumberdaya lahan khususnya lahan pertanian dapat merupakan permasalahan pada masa mendatang. Sumberdaya lahan untuk pertanian akan merupakan suatu komoditi langka dan mempunyai nilai yang tinggi. Kondisi seperti ini akan banyak membawa dampak, baik terhadap nilai lahan, kelembagaan pertanian dan lain sebagainya. Prubahan-Perubahan yang terjadi sudah tentu akan mempengaruhi pembangunan pertanian pada masa mendatang

Effects of thiazolidinediones on palmitate-induced ER stress and apoptotic signaling pathways.

<p>RAW264.7 cells were pretreated with pioglitazone (10 μmol/L) or rosiglitazone (10 μmol/L) for 6 hours and stimulated with or without palmitate (400 μmol/L) for 16 hours.Western blot analyses for phospho (P)-PERK (A), CHOP (B), Phospho (P)-JNK (C) and Cleaved caspase-3 (D) were performed. The bar graphs indicates the ratio of P-PERK to PERK, CHOP to α-tubulin, P-JNK to JNK, and cleaved caspase-3 to α-tubulin, respectively. *P<0.05, ** P<0.01 vs control (palmitate (-), pioglitazone (-) and rosiglitazone (-)), #P<0.05, ## P<0.01 vs palmitate. n = 4.</p

PPARγ Agonists Attenuate Palmitate-Induced ER Stress through Up-Regulation of SCD-1 in Macrophages - Table 1

<p>PPARγ Agonists Attenuate Palmitate-Induced ER Stress through Up-Regulation of SCD-1 in Macrophages - Table 1 </p

Effects of pioglitazone treatment on SCD-1 and LXRα mRNA expression.

<p>RAW264.7 cells were pretreated with pioglitazone (10 μmol/L) for 6 hours and stimulated with or without palmitate (400 μmol/L) for 16 hours. Expression of SCD-1 (A), LXRα, Abca1 (C) and Abcg1 (D) mRNA was determined by qRT-PCR. Expression of SCD-1, LXRα, Abca1, and Abcg1 mRNA was presented as the relative level to that of 18S rRNA. **p<0.01, *p<0.05 vs palmitate, ##p<0.01 vs control (palmitate (-) and pioglitazone (-)). n = 4.</p

Reversion of the anti-ER stress and anti-apoptotic effects of pioglitazone by GW9662.

<p>RAW264.7 cells were pretreated with GW9662 (1, 5, 10 μmol/L) for 1 hour and incubated with pioglitazone (10 μmol/L) for 6 hours. Then, cells were stimulated with palmitate (400 μmol/L) for 16 hours. Western blot analyses for phospho (P)-PERK (A), CHOP (B), phospho (P)-JNK (C), cleaved caspase-3 (D) were performed. The bar graphs indicate the ratio of P-PERK to PERK, CHOP to α-tubulin, P-JNK to JNK, and cleaved caspase-3 to α-tubulin, respectively. *P<0.05, ** P<0.01 vs control (palmitate (-), Pioglitazone (-) and GW9662 (-)), #P<0.05 vs palmitate, †P<0.05, ††P<0.01 vs Palmitate+Pioglitazone. n = 4.</p

Effects of palmitate on ER stress and apoptotic signaling pathways.

<p>RAW264.7 cells were treated with various concentrations (μmol/L) of palmitate (Black bar) or corresponding amount of BSA (White bar) for 16 hours. Western blot analyses for Phospho (P)-PERK (A), CHOP (B), Phospho (P)-JNK (C), cleaved caspase-3 (D) were performed. (E) The effect of palmitoleate on PERK phosphorylation was compared with that of palmitate in RAW264.7 cells. The bar graphs indicate the ratio of P-PERK to PERK, CHOP to α-tubulin, P-JNK to JNK, and cleaved caspase-3 to α-tubulin, respectively. *P<0.05, ** P<0.01 vs control. n = 4. (F) The effect of palmitate on PERK phosphorylation was examined in peritoneal macrophages. The effects of pioglitazone and SCD-1 inhibitor were also examined. **p<0.01 vs control (palmitate (-), pioglitazone (-)), ##P<0.01 vs palmitate, ††P<0.01 vs Palmitate+Pioglitazone. n = 4.</p

Immunostaining of the thoracic cage and lung parenchyma in <i>Pdpn</i>^KO1st mice for podoplanin (PDPN).

<p>In the hematoxylin-eosin (HE) staining, atrophy is observed in the <i>Pdpn</i>^-/- mice. The expression of podoplanin (arrowheads) is observed in the lung of the wild type <i>Pdpn</i>^+/+ mice and <i>Pdpn</i>^+/- mice, but not in the <i>Pdpn</i>^-/-. It is observed that the PDPN-positive areas are the mesothelia (arrowheads) of diaphragmatic pleura, costal pleura, and visceral pleura. It is also observed that costal bone (arrows) and lung parenchyma (asterisks) are PDPN positive. Staining densities of parenchyma PDPN are weaker in the <i>Pdpn</i>^+/- mice than in the <i>Pdpn</i>^+/+ mice. Bar: 1 mm.</p

Morphological study of tooth development in podoplanin-deficient mice

<div><p>Podoplanin is a mucin-type highly <i>O</i>-glycosylated glycoprotein identified in several somatyic cells: podocytes, alveolar epithelial cells, lymphatic endothelial cells, lymph node stromal fibroblastic reticular cells, osteocytes, odontoblasts, mesothelial cells, glia cells, and others. It has been reported that podoplanin-RhoA interaction induces cytoskeleton relaxation and cell process stretching in fibroblastic cells and osteocytes, and that podoplanin plays a critical role in type I alveolar cell differentiation. It appears that podoplanin plays a number of different roles in contributing to cell functioning and growth by signaling. However, little is known about the functions of podoplanin in the somatic cells of the adult organism because an absence of podoplanin is lethal at birth by the respiratory failure. In this report, we investigated the tooth germ development in podoplanin-knockout mice, and the dentin formation in podoplanin-conditional knockout mice having neural crest-derived cells with deficiency in podoplanin by the <i>Wnt1</i> promoter and enhancer-driven Cre recombinase: <i>Wnt1-Cre;Pdpn</i>^<i>Δ/Δ</i>mice. In the <i>Wnt1-Cre;Pdpn</i>^<i>Δ/Δ</i>mice, the tooth and alveolar bone showed no morphological abnormalities and grow normally, indicating that podoplanin is not critical in the development of the tooth and bone.</p></div

Immunostaining of the 2-week <i>Wnt1-Cre;Pdpn</i>^<i>Δ/Δ</i> mouse lower incisor sagittal section for podoplanin (PDPN).

<p>In the left images at higher magnification of the parts highlighted by box (a) in Fig 12, expression of podoplanin is observed in the inner enamel epithelial cells (IEE), and in the epithelial cells of the apical bud (Ap), but not in dental pulp fibroblasts (DP) including odontoblasts, or in the osteocytes of the alveolar bone (AB). In the right images by confocal microscopy at the higher magnification of an area of the left images, expression of PDPN is observed in the inner enamel epithelial cells (IEE) and in the outer enamel epithelial cells (OEE), but not in the odontoblasts (Ob). Bar: left 100μm, right 10μm.</p

Immunostaining of the 2-week <i>Wnt1-Cre;Pdpn</i>^<i>Δ/+</i> mouse lower incisor sagittal section for podoplanin (PDPN).

<p>In the left images at the higher magnification of the parts highlighted by box (c) in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0171912#pone.0171912.g007" target="_blank">Fig 7</a>, the expression of PDPN is observed in the odontoblasts (Ob), in the inner enamel epithelial cells (IEE), and in the outer enamel epithelial cells (OEE), but not in the pre-odontoblasts (pOb). There is no expression of PDPN observed in the dental pulp fibroblasts (DP). In the right images, by confocal microscopy at a higher magnification of the area of the left images, the expression of PDPN is observed on the cell membrane of odontoblasts (Ob) and inner enamel epithelial cells (IEE). Bar: left 100μm, right 10μm.</p