The survival potential of companies placed into administrative receivership

The paper focuses on a sample of companies, which have been placed into administrative receivership, and attempts to assess whether financial ratios used by lending banks can be identified and used to discriminate between companies which can be rescued and those which will fail. The distinctiveness of the paper lies in the fact that it applies conventional bank lending ratios, rather than prediction of failure ratios, to a sample of companies and is primarily concerned with the prediction of corporate survival rather than the prediction of corporate failure. The research compares two statistical classification techniques - Linear Discriminant Analysis and Logistic Regression - to ascertain which is the best at predicting eventual outcomes. A number of further issues, relating to which financial ratios are the most important in predicting future outcomes and the additional insight these financial ratios provide in helping to explain why companies move into crisis and why some companies are rescued and others fail, are also discussed in the paper

<i>ltd</i>, <i>ca</i> and <i>rb</i> affect lipid storage.

<p>(A) Lipid droplets in different eye pigment granule biogenesis mutants. Nile red staining of lipid droplets in wandering stage third instar larval fat body cells. <i>rb</i> mutants have small lipid droplets. Scale bar: 10 µm. (B) Quantification of lipid droplet size in different eye pigment granule biogenesis mutants and <i>rb;ltd</i> double mutants. The error bars represent the standard deviation. **: P<0.001. (C) The level of TAG is reduced in <i>ltd</i>, <i>ca</i> and <i>rb</i> mutant larvae. The error bars represent the standard deviation. *: P<0.01; **: P<0.001. (D) The level of TAG and glucose are reduced in <i>ltd¹</i> mutant adults. **: P<0.001. (E) Survival curve of adult flies under starvation. <i>ltd</i>, <i>ca</i> and <i>rb</i> mutants are sensitive to starvation.</p

<i>ltd</i> and <i>ca</i> genetically interact with the two lipolysis-related genes <i>bmm</i> and <i>plin2</i>.

<p>(A) Image and fluorescence intensity quantification of lipogenic reporter Gal4-SREBP>UAS-GFP in <i>ca</i> mutants and control. Scale bar: 20 µm. **: P<0.001. (B) Quantification of lipid droplet size in different genetic backgrounds. <i>ltd</i>;<i>plin2</i> or <i>ca</i>;<i>plin2</i> double mutants did not show an enhanced phenotype compared to single mutants. Overexpressing <i>plin2</i> suppresses <i>ca</i>. The error bars represent the standard deviation. **: P<0.001. (C) Quantification of lipid droplet size in different genetic backgrounds. <i>bmm</i> mutants suppress <i>ltd</i> mutants in a dosage-dependent manner. The error bars represent the standard deviation. **: P<0.001.</p

Genetic screen for Rabs that affect the size of lipid droplets.

<p>(A) Nile red staining of lipid droplets in wandering stage third instar larval fat body cells. Dominant-negative (DN) Rab expression reduces (DN-Rab1 and DN-Rab5) or increases (DN-Rab7 and DN-Rab10) lipid droplet size. Expressing DN-Rab18 does not affect the size of lipid droplets. Scale bar: 10 µm. (B) Quantification of the effects of all DN-Rabs. The error bars represent the standard deviation. Red dashed lines indicate the average variation in lipid droplet size in controls. *: P<0.01. (C) Nile red staining of lipid droplets in wandering stage third instar larval fat body cells. Constitutive-active (CA) Rab expression reduces (CA-Rab39) or increases (CA-Rab1, CA-Rab10, and CA-RabX4) lipid droplet size. Expressing CA-Rab18 does not affect the size of lipid droplets. <i>bmm</i> mutant was included as a comparison. Scale bar: 10 µm. (D) Quantification of the effects of all CA-Rabs. The error bars represent the standard deviation. Red dashed lines indicate the average variation in lipid droplet size in controls. *: P<0.01.</p

Autophagy is impaired in <i>ca</i> mutants and defective autophagy leads to small lipid droplets.

<p>(A) Autophagy marker EGFP-huLC3-positive puncta are greatly reduced in <i>ltd¹</i> and <i>ca¹</i> homozygous mutants compared to the <i>ca¹</i> heterozygous control. Scale bar: 20 µm. (B) Quantification of EGFP-huLC3-marked autophagosomes in <i>ca¹</i> heterozygous and <i>ltd¹</i> and <i>ca¹</i> homozygous mutants. The error bars represent the standard deviation. **: P<0.001. (C) tGPH reporter in control and <i>ltd¹</i> mutant salivary glands at 13.5 hr after pupae formation. tGPH cortical signal persists in <i>ltd¹</i> mutants. Scale bar: 50 µm. (D) Nile red staining of lipid droplets in wandering stage third instar larval fat body cells. Autophagy mutants or <i>Atg1</i> and <i>Atg6</i> RNAi animals have small lipid droplets. Scale bar: 20 µm. (E) Quantification of lipid droplet size in different genetic backgrounds. The error bars represent the standard deviation. *: P<0.001.</p

Lipid droplet size is reduced in <i>Rab32/ltd</i> and <i>Rab32 GEF/ca</i> mutants.

<p>(A) Nile red staining of lipid droplets in wandering stage third instar larval fat body cells. <i>Rab32/ltd</i> and <i>Rab32 GEF/ca</i> mutants have smaller lipid droplets compared to the control. Scale bar: 10 µm. (B) Quantification of the effects of <i>Rab32/ltd</i> and <i>Rab32 GEF/ca</i> single mutants and <i>ltd;ca</i> double mutants. The error bars represent the standard deviation. **: P<0.001.</p

Rab32 is localized to the lysosome and autophagosome.

<p>(A) The localization of WT, CA- and DN-Rab32-EYFP in wandering stage third instar larval fat body cells. WT and CA-Rab32-EYFP are localized to ring-like structures and do not colocalize with the lipid droplet marker PLIN1-mCherry. DN-Rab32-EYFP is located in the cytosol. Scale bar: 20 µm. (B) WT Rab32-EYFP appears as rings surrounding lysotracker-labeled lysosomes and RFP-Atg-8-marked autophagosomes. Scale bar: 20 µm.</p

Comparison of Rabs identified in this study with previous proteomic studies [13], [14].

*<p>Not available means the homolog can't be found.</p

A Novel Role for <i>DNA Methyltransferase 1</i> in Regulating Oocyte Cytoplasmic Maturation in Pigs

<div><p>Maternal factors are required for oocyte maturation and embryo development. To better understand the role of <i>DNA methyltransferase 1</i> (<i>Dnmt1</i>) in oocyte maturation and embryo development, small interfering RNA (siRNA) was conducted in porcine oocytes. In this study, our results showed that <i>Dnmt1</i> localized in oocyte cytoplasm and its expression displayed no obvious change during oocyte maturation. When siRNAs targeting <i>Dnmt1</i> were injected into germinal vesicle (GV) stage oocytes, <i>Dnmt1</i> transcripts significantly decreased in matured oocytes (P<0.05). After <i>Dnmt1</i> knockdown in GV stage oocytes, the significant reduction of glutathione content, mitochondrial DNA copy number, glucose-6-phosphate dehydrogenase activity and expression profiles of maternal factors and the severely disrupted distribution of cortical granules were observed in MII stage oocytes (P<0.05), leading to the impaired oocyte cytoplasm. Further study displayed that <i>Dnmt1</i> knockdown in GV stage oocytes significantly reduced the development of early embryos generated through parthenogenetic activation, <i>in vitro</i> fertilization and somatic cell nuclear transfer (P<0.05). In conclusion, <i>Dnmt1</i> was indispensable for oocyte cytoplasmic maturation, providing a novel role for <i>Dnmt1</i> in the regulation of oocyte maturation.</p></div

The expression and location of Dnmt1 in oocytes.

<p>A, the cytoplasmic location of Dnmt1 in GV and MII stage oocytes (×400), and B, relative Dnmt1 transcription levels during oocyte maturation. No obvious changes of Dnmt1 expression were observed in GV, GVBD, MI and MII stage oocytes. GV, GVBD, MI and MII stage oocytes were collected at 0 h, 19 h, 24 h and 42 h, respectively.</p