Today's organizations are operating in a highly competitive and changing environment that pushes them to continuously adapt their organizational structures to such environment. However, the success ...of change initiatives may face a barrier in the response of employees, especially when they lack readiness to change. While leadership can shape the culture of an organization and a culture of effectiveness can help increase employees' readiness to change, ethical leaders, who serve as a guide and offer support, can also make a difference by reducing uncertainty. Yet existing research on the role of ethical leadership in the enhancement of the employees' readiness to change is practically non-existent. Far less is the research that analyses the mechanisms that ethical leadership can use to foster employees' readiness to change. This study aims to investigate whether the ethical leadership of middle-lower echelons influences on employees' readiness to change positively (H1) and if this relationship is mediated through shaping an organizational culture of effectiveness (H2). Using data from 270 direct reports of middle-lower managers in public foreign trade Egyptian companies, the findings reveal that ethical leadership enhances employees' readiness to change and that this impact is partially mediated by an organizational culture of effectiveness. Thus, with these findings, new light is shed on the positive role of ethical leadership and the mechanisms it uses to enhance employees' readiness to change.
Preterm infants are at risk for poor neurodevelopmental outcomes, including deficits in learning and memory, disrupted sensory processing, attention deficit hyperactivity disorder, and autism ...spectrum disorder.1,2 Prematurity leads to a situation where critical in utero steps of brain development occur in an abnormal ex utero environment. This alters the quality and intensity of sensory stimuli that the premature infant experiences, and potentially affects normal maturation of sensory systems adversely. The identification of the impact of the NICU environment on the development of sensory systems may pave the way for the establishment of a comprehensive protocol of multisensory stimulation that can potentially ameliorate sensory deficits associated with prematurity.
The kidney is among the metabolic organs most susceptible to injury, particularly following exposure to xenobiotics and heavy metals. We aimed to explore the potential protective impacts of coenzyme ...Q10 (CoQ10) on lead acetate (PbAc)-induced nephrotoxicity in rats. Four experimental groups (
= 7) were applied as follows: control group, CoQ10 alone (10 mg/kg), PbAc alone (20 mg/kg), and PbAc with CoQ10. Exposure to PbAc led to the accumulation of Pb in the kidney and increased urea and creatinine serum levels. The deposition of Pb coupled with the elevation of malondialdehyde and nitrate/nitrite levels along with the upregulation of inducible nitric oxide synthase. Additionally, upon PbAc poisoning, glutathione content and the antioxidant enzymes were depleted along with the downregulation of Nrf2 and HO-1 expression. Moreover, PbAc injection increased the protein and mRNA levels of pro-inflammatory cytokines namely, tumor necrosis factor-alpha and interleukin-1 beta, while decreased the levels of interleukin-10, an anti-inflammatory cytokine, in the kidney. Furthermore, exposure to PbAc correlated with increased levels of pro-apoptotic markers, Bax and caspase-3, and reduced levels of the anti-apoptotic marker Bcl-2. The administration of CoQ10 alleviated the molecular, biochemical and histological changes following PbAc intoxication. Thus, CoQ10 reduces the deleterious cellular side effects of PbAc exposure due to its antioxidant, anti-inflammatory and anti-apoptotic effects.
The diversity and importance of Echinococcus species in domesticated animals in Saudi Arabia are poorly understood. In this study, 108 singular (hydatid) cysts were collected from goats (n = 25), ...sheep (n = 56) and camels (n = 27). DNA was extracted from the protoscoleces of individual fertile cysts and used for polymerase chain reaction (PCR) amplification of mitochondrial subunit 1 of the cytochrome c oxidase 1 (cox1) gene. Amplicon sequencing results revealed the presence of Echinococcus granulosus sensustricto (s.s.) (genotypes G1-G3) in 16 of the17 sheep cysts and 2 of the 27 camel cysts.of these samples, 18 (2 camel and 16 sheep) were divided into genotypes G1, G2, and G3.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
This study aimed to characterize the relationship between cannabis use, ACE score, and pregnancy outcomes. Pregnant patients in Baltimore, MD, completed the 17-point ACE checklist. Charts of the ...birth parent and neonate were reviewed for urine toxicology testing at initiation of care and delivery, prenatal care metrics, and birth statistics. Multivariable logistic regression analysis was performed to assess the relationship between ACE score, cannabis use, and pregnancy outcomes. Of 256 birth parents, 87 (34.0%) tested positive for cannabis at initial visit and 39 (15.2%) tested positive for cannabis at delivery. Testing positive for cannabis at initial visit or delivery was associated with higher ACE score (15.1 vs 13.7,
p
= 0.04; 16.2 vs 13.8,
p
= 0.01). Of those who tested positive for cannabis at initial visit, 39/87 (45.0%) tested positive at delivery. Continued cannabis use at delivery was associated with lower maternal weight gain (7.9 kg vs 13.3 kg,
p
= 0.003), fewer prenatal visits (7 vs 8,
p
= 0.010), and numerically higher mean ACE score. Cannabis use at delivery was associated with 10% lower birthweight (2665 g vs 3014 g
p
< 0.05) but not with pre-term birth. Total ACE score was not significantly associated with any birth outcome. Worse pregnancy outcomes were associated with cannabis use throughout pregnancy but not with cannabis use at prenatal care initiation. The interplay of ACE and continued cannabis use during pregnancy warrants further research on the physiologic effects of cannabis and interventions to decrease substance use during pregnancy.
Opioid use by pregnant women is an understudied consequence associated with the opioid epidemic, resulting in a rise in the incidence of neonatal opioid withdrawal syndrome (NOWS) and lifelong ...neurobehavioral deficits that result from perinatal opioid exposure. There are few preclinical models that accurately recapitulate human perinatal drug exposure and few focus on fentanyl, a potent synthetic opioid that is a leading driver of the opioid epidemic. To investigate the consequences of perinatal opioid exposure, we administered fentanyl to mouse dams in their drinking water throughout gestation and until litters were weaned at postnatal day (PD) 21. Fentanyl‐exposed dams delivered smaller litters and had higher litter mortality rates compared with controls. Metrics of maternal care behavior were not affected by the treatment, nor were there differences in dams' weight or liquid consumption throughout gestation and 21 days postpartum. Twenty‐four hours after weaning and drug cessation, perinatal fentanyl‐exposed mice exhibited signs of spontaneous somatic withdrawal behavior and sex‐specific weight fluctuations that normalized in adulthood. At adolescence (PD 35), they displayed elevated anxiety‐like behaviors and decreased grooming, assayed in the elevated plus maze and sucrose splash tests. Finally, by adulthood (PD 55), they displayed impaired performance in a two‐tone auditory discrimination task. Collectively, our findings suggest that perinatal fentanyl‐exposed mice exhibit somatic withdrawal behavior and change into early adulthood reminiscent of humans born with NOWS.
Perinatal fentanyl exposure induces spontaneous somatic withdrawal behavior.
At least 60% of the neonates with opioid withdrawal syndrome (NOWS) require morphine to control withdrawal symptoms. Currently, the morphine dosing strategies are empiric, not optimal and associated ...with longer hospital stay. The aim of the study was to develop a quantitative, model‐based, real‐world data‐driven approach to morphine dosing to improve clinical outcomes, such as reducing time on treatment. Longitudinal morphine dose, clinical response (Modified Finnegan Score (MFS)), and baseline risk factors were collected using a retrospective cohort design from the electronic medical records of neonates with NOWS (N = 177) admitted to the University of Maryland Medical Center. A dynamic linear mixed effects model was developed to describe the relationship between MFS and morphine dose adjusting for baseline risk factors using a split‐sample data approach (70% training: 30% test). The training model was evaluated in the test dataset using a simulation based approach. Maternal methadone and benzodiazepine use, and race were significant predictors of the MFS response. Positive autocorrelations of 0.56 and 0.12 were estimated between consecutive MFS responses. On an average, for a 1,000 μg increase in the morphine dose, the MFS decreased by 0.3 units. The model evaluation showed that observed and predicted median time on treatment were similar (13.0 vs. 13.8 days). A model‐based framework was developed to describe the MFS–morphine dose relationship using real‐world data that could potentially be used to develop an adaptive, individualized morphine dosing strategy to improve clinical outcomes in infants with NOWS.
Arsenic, a major environmental pollutant of global concern, is well-known for its reproductive toxicity. In this study, the protective potential of chlorogenic acid (CGA), a caffeoylquinic acid ...isomer abundantly found in many plants, was investigated against sodium arsenite (NaAsO2)-induced testicular dysfunctions. Adult male Swiss mice were either administered NaAsO2 alone at 5 mg kg−1 or co-treated with CGA at 100 mg kg−1 or 200 mg kg−1 body weight for 4 weeks. Results showed that NaAsO2-treated mice exhibited marked declines in testes weight, sperm count, and viability accompanied by decreases in sexual hormonal levels. Moreover, NaAsO2 toxicity evoked exhaustion of antioxidant markers (SOD, CAT, GPx, GR, and GSH), down-regulation of Nrf2 (nuclear factor erythroid 2–related factor 2) gene expression level, and elevations in malondialdehyde. Further, elevations in inflammatory cytokines (IL-1, TNF-α, and IL-6) together with the up-regulation of pro-apoptotic biomarkers (Bax and caspase- 3) and down-regulation of anti-apoptotic Bcl-2 were observed in NaAsO2 intoxication. Immunohistochemical analysis of testis sections of NaAsO2-treated mice showed high caspase-3 expression. These findings were well supported with testicular histopathological examination. However, pretreatment of mice with CGA resulted in noteworthy improvements in testicular damage induced by arsenic in a dose-dependent manner possibly mediated by the Nrf2 signaling pathway. Conclusively, CGA counteracted arsenic-induced testicular injury through its antioxidant, anti-inflammatory, and anti-apoptotic properties. Therefore, CGA could serve as a favorable intervention in the alleviation of arsenic-induced reproductive toxicity.
•Exposure to arsenic causes apoptosis, inflammation and oxidative stress in testis.•Chlorogenic acid inhibits arsenic-induced reproductive toxicity in rats.•Chlorogenic acid has antioxidant, antiinflammatory and antiapoptotic activities.
Heavy metal exposure, in lead (Pb) particularly, is associated with severe neuronal impairment though oxidative stress mediated by reactive oxygen species, and antioxidants may be used to abolish ...these adverse effects. This study investigated the potential neuroprotective role of coenzyme Q10 (CoQ
) against lead acetate (PbAc)-induced neurotoxicity. Twenty-eight male Wistar albino rats were divided into four equal groups (
= 7) and treated as follows: the control group was injected with physiological saline (0.9% NaCl); the CoQ
group was injected with CoQ
(10 mg/kg); PbAc group was injected with PbAc (20 mg/kg); PbAc + CoQ
group was injected first with PbAc, and after 1 h with CoQ
. All groups were injected intraperitoneally for seven days. PbAc significantly increased cortical lipid peroxidation, nitrate/nitrite levels, and inducible nitric oxide synthase expression, and decreased glutathione content, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase activity and mRNA expression, as well as nuclear factor erythroid 2-related factor 2 (Nrf2) and homoxygenase-1 (HO-1) expression. PbAc also promoted the secretion of interleukin-1ß and tumor necrosis factor-α, inhibited interleukin-10 production, triggered the activation of pro-apoptotic proteins, and suppressed anti-apoptotic proteins. Additionally, PbAc increased the cortical levels of serotonin, dopamine, norepinephrine, GABA, and glutamate, and decreased the level of ATP. However, treatment with CoQ
rescued cortical neurons from PbAc-induced neurotoxicity by restoring the balance between oxidants and antioxidants, activating the Nrf2/HO-1 pathway, suppressing inflammation, inhibiting the apoptotic cascade, and modulating cortical neurotransmission and energy metabolism. Altogether, our findings indicate that CoQ
has beneficial effects against PbAc-induced neuronal damage through its antioxidant, anti-inflammatory, anti-apoptotic, and neuromodulatory activities.
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