Purpose-Aims to study the role tacit knowledge plays in shaping the knowledge base of the knowledge-intensive growing organizations using the storytelling method. Design/methodology/approach-Stories were collected from eight human resource professionals working in eight different knowledge-intensive growing organizations in New Zealand. Interviews containing loosely structured questions were used for collecting stories. These stories were deconstructed on the knowledge grid. This grid attempted to depict a complex interplay of tacit knowledge with the important subsystems (referred to as threads) of organization. Findings-Tacit knowledge seemed to be a major concern for the human resource professionals in knowledge-intensive growing organizations. It plays a significant role in shaping the knowledge base of an organization by interacting with the important subsystems of organization. Research limitations/implications-There is a need to study ways of reducing the risk of being dependent on tacit knowledge of a few employees. Technology is needed that would be able to effectively capture the multidimensional interplay of tacit knowledge with important subsystems of organization. Practical implications-Knowledge being a strategic input in knowledge-intensive growing organizations, there is a need to address major concerns related to tacit knowledge that these organizations specifically face due to their knowledge-intensive nature. Originality/value-Tacit knowledge interacts with the important subsystems of an organization, thereby shaping its knowledge base. This paper attempts to demonstrate that tacit knowledge operates in multidimensional contexts.

Hydralazine is a commonly prescribed antihypertensive agent. Some of its labelled adverse reactions include lupus-like syndrome, tachycardia, headache and fever. Despite its well-known side effects, little is known about hydralazine’s hepatotoxic effects. We report the case of a 54-year-old female patient who was started on hydralazine for hypertension management but later presented with hydralazine-induced liver injury. Her initial presentation consisted of non-specific symptoms and a hepatocellular injury pattern. Liver biopsy revealed hepatic steatosis. Three weeks after discontinuation of hydralazine, the patient’s liver enzymes normalised, and her symptoms resolved. Few studies have examined the incidence and mechanism by which hydralazine induces a liver injury pattern. With this case, we review the literature, the pathogenesis involved and the eventual management of hydralazine-induced liver injury. We propose close monitoring of liver enzymes for patients on hydralazine throughout their treatment course.

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Stress during adolescence clearly impacts brain development and function. Sex differences in adolescent stress-induced or exacerbated emotional and metabolic vulnerabilities could be due to sex-distinct gene expression in hypothalamic, limbic and prefrontal brain regions. However, adolescent stress-induced gene expression changes in these key brain regions were unclear. RNA extraction from whole brain regions, instead of discrete nuclei, dilutes gene expression results. In this study, female and male adolescent Sprague Dawley rats received one-hour restraint stress every day from postnatal day (PD) 32 to PD44, their plasma corticosterone levels were measured, and their body weights, food intake and body composition were monitored. On PD44, their brains and blood samples were collected. Circulating levels of adioposity hormones (leptin and insulin) and sex hormones (estradiol and testosterone) were measured. Gene expression in nine subregions was measured using RNA sequencing (RNA-Seq). Differentially expressed (DE) genes were analyzed using bootstrapped receiver operating characteristic (bROC) approach. The results indicated that sex differences in stress-induced DE genes were widespread, being identified in the hypothalamus, limbic system, and prefrontal cortex of adolescent brains. Additionally, this study revealed canonical pathways enriched in stress compared to nonstress rats, which were predictive of well-known sex-distinct maladies in the literature, providing examples of the DE genes likely involved in producing sex-distinct and stress-induced diseases. In summary, findings from this study suggest sex biases in stress-induced transcriptional changes during adolescence, indicating a molecular basis for sex differences witnessed in stress-induced or exacerbated emotional and metabolic disorders throughout life. Future studies are warranted to test the implications of the DE genes identified in this study in sex-distinct stress-induced susceptibilities.