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

Distribution of TLR2-positive cells in diabetic mouse kidneys.

<p>The immunostained sections were re-stained by HE staining. The HE staining shows that renal tubules are expanded in the cortex of the kidneys of STZ-induced type I diabetic ICR mice (ICR-STZ) and of HF-induced type II diabetic KK/Ta mice (KK/Ta-HF). In the non-diabetic ICR mouse kidney section, all of the glomeruli were immunostained with the antibody for the podocyte marker, podoplanin (PDPN, arrows, staining red), while there were no cells reacting with anti-TLR2. In the ICR-STZ and KK/Ta-HF mouse kidney sections, there are areas immunostained by anti-TLR2 (arrowheads, staining green) in all of the podoplanin-positive glomeruli. In the KK/Ta mouse kidney sections, podoplanin-negative proximal tubules which are more strongly stained with eosin than the distal tubules are also immunostained by anti-TLR2 (white arrowheads, staining green). In the ICR-STZ and KK/Ta-HF mouse kidney sections, distal tubules, collecting tubules, and blood vessels outside glomeruli are not stained. Bar: 100 µm.</p

Cytokine induction by <i>Porphyromonas gingivalis</i> LPS in the diabetic mouse kidneys.

<p>(A) Immunohistochemistry for the expression of cytokines and podoplanin (PDPN) in glomeruli by laser-scanning confocal microscopy. The IL-6, TNF-α, and TGF-β were detected in the glomeruli of STZ-induced type I diabetic ICR mice with the repeated intraperitoneal administration of <i>Porphyromonas gingivalis</i> LPS (STZ+LPS) whereas the no cytokines were detected in the kidneys of the diabetic mice without LPS (STZ). Bar: 20 µm. (B) Tissue RT-PCR for cytokine mRNAs in mouse kidneys. The amplicons of IL-6, TNF-α, and TGF-β mRNAs were detected from both the renal cortex of STZ-induced type I diabetic ICR mice with the repeated intraperitoneal administrations of <i>Porphyromonas gingivalis</i> LPS (STZ+LPS) and cultured mouse macrophage J774.1 with LPS, whereas they were not detected from the diabetic mice without LPS (STZ). (C) Tissue real-time PCR for cytokine mRNAs in mouse kidneys. The gene expression amounts of IL-6, TNF-α, and TGF-β were statistically significantly larger in the kidney tissue of STZ-induced type I diabetic ICR mice with the repeated intraperitoneal administrations of <i>Porphyromonas gingivalis</i> LPS (STZ+LPS) than in the diabetic mice without LPS (STZ) and in the non-diabetic ICR mice with LPS (LPS). Data are expressed as means+SD. *Significantly different (<i>p</i><0.01).</p

Localization of TLR2 in the glomeruli of STZ-induced type I diabetic ICR mouse kidneys.

<p>The HE staining showed that glomeruli (Gl) of the diabetic mice are subject to sclerosis. In the laser-scanning confocal microscopy, the region reacting with anti-podoplanin (PDPN, arrowhead) does not coincide with the region reacting with anti-TLR2 (arrows) in the merged image while the regions reacting with VE-cadherin and anti-PECAM-1 (arrowheads) coincide with the regions reacting with anti-TLR2 (arrows) in the merged images (rightmost column). Bar: 20 µm.</p

Localization of TLR2 in the glomeruli of HF-induced type II diabetic KK/Ta mouse kidneys.

<p>The HE staining showed that glomeruli (Gl) of the KK/Ta-HF mice are subject to sclerosis. In the laser-scanning confocal microscopy, epithelial cells of proximal tubules (PT) did not react with anti-podoplanin (PDPN) but reacted with anti-TLR2 (arrows) at the inside. The regions reacting with VE-cadherin and anti-PECAM-1 (arrowheads) coincided with the regions reacting with anti-TLR2 (arrows) in the merged images. Bar: 20 µm.</p

Immunostaining for TLR2, PECAM-1, podoplanin, and VE-cadherin.

<p>Mouse and human leukocyte cell line J774A.1 and HL60 were immunostained with both anti-PECAM-1 (CD31) and anti-TLR2, and nuclei were stained by DAPI. In the mouse heart section, lymphatic vessels (arrowheads) were immunostained by anti-podoplanin (PDPN) and a blood vessel (arrows) was stained by anti-VE-cadherin (VE-cad). In the human kidney section with type II diabetic nephropathy, there are glomerular endothelial cells immunostained with both anti-PECAM-1 (CD31) and anti-TLR2 (arrows), and cells that are only immunostained with anti-TLR2 (arrowheads). Bar: 20 µm.</p

Quantitative analysis for TLR2 gene expression in the diabetic mouse kidneys and the effects of <i>Porphyromonas gingivalis</i> LPS on diabetic nephropathy.

<p>(A) Tissue PCR for TLR2 mRNA of the mouse renal cortex. The RT-PCR and real-time PCR analysis show that the mRNA amounts were larger in the STZ-induced type I diabetic ICR mice (STZ) than in the non-diabetic ICR mice (ICR). *Significantly different (p<0.05) (B) Survival curve of the STZ-induced type I diabetic ICR mice with repeated intraperitoneal administrations of <i>Porphyromonas gingivalis</i> LPS. All of the 6 diabetic mice with LPS (red curve) died within the survival period of all of the diabetic mice without LPS and the non-diabetic mice with LPS (blue curve). (C) Urinalysis for STZ-induced type I diabetic ICR mice with LPS at the 8th week of survival. Urine reagent strips show sugar, protein, and bleeding in the mouse urine of non-diabetic ICR mice (ICR), non-diabetic ICR mice with LPS (LPS), STZ-induced type I diabetic ICR mice without LPS (STZ), and the diabetic mice with LPS (STZ+LPS). Extensive amounts of urinary sugar was observed in the diabetic mice and the diabetic mice with LPS, and the urinary protein level was higher in the diabetic mice with LPS than in the diabetic mice without LPS.</p

<i>In situ</i> hybridization for TLR2 mRNA of the diabetic mouse kidneys.

<p>DAB signals for the genes hybridized with the probe for TLR2 mRNA (closed arrowheads) are present weakly at the glomeruli (Gl) of non-diabetic ICR and KK/Ta mice, and strongly at the glomeruli of STZ-induced type I diabetic ICR mice (ICR-STZ) and HF-induced type II diabetic KK/Ta mice (KK/Ta-HF). DAB signals are also positive at the proximal tubules (PT) of ICR-STZ and KK/Ta-HF. There are leukocytes with DAB signals on the internal peroxidase (open arrowheads) in the blood vessels (BV) of the non-diabetic ICR mouse section (top left). Bar: 20 µm.</p

Sequence of primers.

<p>Sequence of primers.</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