The impacts of corruption on firm performance: some lessons from 40 African countries

The current evidence-base regarding the impacts of corruption on firm performance is based largely on studies of individual countries and contains mixed results. Therefore, the aim of this paper is to achieve a better insight into this relationship by reporting the results of a firm-level analysis of the impacts of corruption on firm performance using World Bank Enterprise Survey (WBES) data across 40 African countries. The clear result is that corruption significantly enhances rather than harms annual sales, employment and productivity growth rates. The outcome is to re-theorize participation in acts of corruption as beneficial for the individual firms engaged in such activity, while recognizing the wider evidence that this is not an optimal strategy at the aggregate country level. The outcome will be to advance knowledge about how corruption needs to be tackled. To eliminate corruption, it is shown here to be necessary for public authorities to recognize that corruption is an efficient strategy at the firm level and to adopt measures to alter the cost/benefit ratio confronting individual enterprises, and at the same time, to address the country-level formal institutional deficiencies that characterize many developing countries and result in the prevalence of corruption

Firms cash management, adjustment cost and its impact on firms’ speed of adjustment-A cross country analysis

We investigate the firms’ specific attributes that determine the difference in speed of adjustment (SOA) towards the cash holdings target in the Scandinavian countries: Denmark, Norway and Sweden. We examine whether Scandinavian firms maintain an optimal level of cash holdings and determine if the active cash holdings management is associated with the firms’ higher SOA and lower adjustment costs. Our findings substantiate that a higher level of off-target cost induces professional managers to rebalance their cash level towards the optimal balance of cash holdings. Our results reveal that Scandinavian firms accelerate SOA towards cash targets primarily for the precautionary motive. Moreover, our results show that SOA is heterogeneous across Scandinavian firms based on adjustment cost and deviate cash holdings towards the target mainly with the support of internal financing. Furthermore, our empirical findings show that the SOA of Norwegian firms is significantly higher than the Danish and Swedish firms

Silencing Nuclear Pore Protein Tpr Elicits a Senescent-Like Phenotype in Cancer Cells

Background: Tpr is a large coiled-coil protein located in the nuclear basket of the nuclear pore complex for which many different functions were proposed from yeast to human. Methodology/Principal Findings: Here we show that depletion of Tpr by RNA interference triggers G0–G1 arrest and ultimately induces a senescent-like phenotype dependent on the presence of p53. We also found that Tpr depletion impairs the NES [nuclear export sequence]-dependent nuclear export of proteins and causes partial co-depletion of Nup153. In addition Tpr depletion impacts on level and function of the SUMO-protease SENP2 thus affecting SUMOylation regulation at the nuclear pore and overall SUMOylation in the cell. Conclusions: Our data for the first time provide evidence that a nuclear pore component plays a role in controlling cellular senescence. Our findings also point to new roles for Tpr in the regulation of SUMO-1 conjugation at the nuclear pore and directly confirm Tpr involvement in the nuclear export of NES-proteins

Antineuronal antibodies and 8-OHdG an indicator of cerebellar dysfunction in autism spectrum disorder: a case–control study

Objectives: Autism spectrum disorder (ASD) is a neurodevelopmental disorder, that starts in early childhood and presents with deficiencies in social-communicational domains along with restricted and repetitive behaviours/interests. While genetic factors are dominant in its pathogenesis, many factors, including neurological, environmental and immunological have been identified. Furtheremore, although cerebellar dysfunction in the etiology of autism has been shown in different studies, the possible causes of the dysfunction and the role of neuroinflammation among these causes have not been clarified yet. Anti-Yo, anti-Hu, anti-Ri and anti-Amphiphysin antibodies have been found to be associated with cerebellar degeneration. The aim of the present study was to compare anti-Yo, anti-Hu, anti-Ri and anti- Amphiphysin antibodies and 8-OHdG values in blood using the ELISA method between ASD patients and healthy children to demonstrate the role of neuroinflammation as a potential cause of cerebellar dysfunction and DNA damage and evaluate the relationship between Childhood Autism Rating Scale (CARS) scores in children diagnosed with ASD and these parameters. Methods: Thirty-five consecutive children between the ages of 3 and 12 referred to the Child and Adolescent Psychiatry Outpatient Clinic of Harran University Hospital and diagnosed with ASD according to the DSM-5 diagnostic criteria were included in the study. The children did not have any chronic physical disorders and were treatment naive. Thirty-three healthy children between the ages of 3 and 12 without any physical or psychiatric disorders were included as the healthy control group. For psychiatric evaluation, a sociodemographic form and to measure the severity of autism, CARS was used. In the study, anti-Yo, anti-Hu, anti-Ri and anti-Amphiphysin antibodies and 8-OHdG values in blood were investigated using the ELISA method. Results: Thirty-five cases with autism (62.9% males) and thirty-three healthy controls (72.7% males) were included in the present study (p = 0.385). The median age was 6.0 in the ASD group and 7.0 in the control group (p = 0.146). Among ASD patients, anti-Ri antibody positivity was detected, while no anti-Ri antibody positivity was found in the control group (p = 0.002). In the ASD group, the anti-Hu and 8-OHdG values were found to be significantly higher than those of the controls (p < 0.001, p = 0.001); no significant difference was found between the ASD and control groups with regard to the anti-Yo and anti-Amphiphysin values (p = 0.113, p = 0.275). Conclusions: The results of the present study suggest that antibodies against cerebellum may be present among children with ASD and DNA damage may occur due to oxidative stress. © 2019, © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group

Inactivation of Plasma Membrane-Localized CDPK-RELATED KINASE5 Decelerates PIN2 Exocytosis and Root Gravitropic Response in Arabidopsis.

CRK5 is a member of the Arabidopsis thaliana Ca2+/calmodulin-dependent kinase-related kinase family. Here, we show that inactivation of CRK5 inhibits primary root elongation and delays gravitropic bending of shoots and roots. Reduced activity of the auxin-induced DR5-green fluorescent protein reporter suggests that auxin is depleted from crk5 root tips. However, no tip collapse is observed and the transcription of genes for auxin biosynthesis, AUXIN TRANSPORTER/AUXIN TRANSPORTER-LIKE PROTEIN (AUX/LAX) auxin influx, and PIN-FORMED (PIN) efflux carriers is unaffected by the crk5 mutation. Whereas AUX1, PIN1, PIN3, PIN4, and PIN7 display normal localization, PIN2 is depleted from apical membranes of epidermal cells and shows basal to apical relocalization in the cortex of the crk5 root transition zone. This, together with an increase in the number of crk5 lateral root primordia, suggests facilitated auxin efflux through the cortex toward the elongation zone. CRK5 is a plasma membrane-associated kinase that forms U-shaped patterns facing outer lateral walls of epidermis and cortex cells. Brefeldin inhibition of exocytosis stimulates CRK5 internalization into brefeldin bodies. CRK5 phosphorylates the hydrophilic loop of PIN2 in vitro, and PIN2 shows accelerated accumulation in brefeldin bodies in the crk5 mutant. Delayed gravitropic response of the crk5 mutant thus likely reflects defective phosphorylation of PIN2 and deceleration of its brefeldin-sensitive membrane recycling