Maintain a pleasant expression, and avoid any fidgety habits that show your nervousness. The way you speak — including the use of positive language — is also a key evaluation factor for many AI programs. Vocal tone will also help you showcase confidence and affability so you can land the job. The diaphragm is key when expressing our natural voice, says Professor of Communication Studies Preston Ni. Developing this speaking style through breathing exercises or even a singing class can go a long way in impressing an AI program. Though the idea of allowing artificial intelligence to play a role in the hiring process may be intimidating to job seekers, it is essential to remember that this same technology is also used by companies that are actively trying to recruit new employees.
The result? Job seekers see the jobs they need to see, and are provided with the information essential to making an informed decision — meaning less wasted time and better matches for recruiter and job seeker alike. Upwardly-mobile Freshman students in the New York area are getting internship offers a year in advance before they even set foot on campus.
AI has enabled forward-thinking employers to sift through talent and engage with them faster. By taking care of most of the heavy lifting on your behalf, they give you a much greater chance of a successful outcome before you ever submit an application. Though artificial intelligence is already resulting in dramatic changes in how companies go about their hiring process, it is important to remember that many of the best practices for landing a job have remained largely unchanged.
You must learn to control your posture and facial expressions during an interview. At the end of the day, companies are looking for the same thing as always — high-performing employees who will stick around for the long haul.
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Do you want to take the lead in the digital era? Published October 11, — UTC. October 11, — UTC. Deletion of SF-1 in the VMH resulted in dysregulated insulin and leptin homeostasis and late onset obesity due to increased food intake under normal chow and high fat diet conditions. In addition, SF-1 ablation was accompanied by a marked reduction in energy expenditure and physical activity and this effect was significantly pronounced in the aged mice.
Taken together, our data indicates that SF-1 is a key component in the VMH-mediated regulation of energy homeostasis and implies that SF-1 plays a protective role against metabolic stressors including aging and high fat diet. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: All relevant data are within the paper and its Supporting Information files. Competing interests: The authors have declared that no competing interests exist. Steroidogenic factor 1 SF-1 is a nuclear receptor expressed in the adrenal glands, gonads, anterior pituitary, and ventromedial nucleus of the hypothalamus VMH [ 1 ]. SF-1 is vital not only for the development of the VMH but also for its physiological functions [ 2 , 3 ].
The VMH is an important hypothalamic nucleus critical for regulating feeding and maintaining whole body energy homeostasis. Lesions in the VMH alter feeding behavior and have been associated with hyperphagia and development of obesity [ 4 ]. Similarly, the VMH functions as a nutrient sensor and has been shown to respond to declining nutritional conditions such as hypoglycemia by inhibiting insulin production and stimulating glucagon and catecholamines release [ 5 ].
In addition, the expression of leptin receptors in the VMH depicts the importance of this nucleus in responding to leptin induced feeding, metabolism and energy balance regulation [ 6 , 7 ]. Whereas whole body SF-1 knockout is lethal due to adrenal insufficiency, corticosterone injection and adrenal transplants rescues the SF-1 knockout mice but is accompanied by severe obesity indicating that SF-1 deficiency alters energy metabolism [ 11 ]. Mice lacking leptin receptor in SF-1 expressing neurons specifically in the VMH exhibited metabolic syndrome features including obesity, elevated insulin and leptin levels and impaired glucose tolerance [ 8 , 12 ].
Moreover, insulin receptor knockout mice in SF-1 neurons showed improved glucose metabolism and were protected against high fat diet induced leptin resistance and weight gain and deletion of the transcription factor FoxO1 in SF-1 neurons showed increased energy expenditure and improved insulin sensitivity that exhibited an overall lean phenotype [ 9 , 13 ]. In addition, mice lacking vesicular glutamate transporter 2 Vglut2 in SF-1 neurons exhibited a modest increase in body weight when exposed to high fat diet HFD and also developed hypoglycemia during fasting due to impaired induction of the glucose raising hormone glucagon and the gluconeogenic enzymes PEPCK and G6Pase [ 14 ].
Although these studies point to the importance of SF-1 neurons in the maintenance of normal energy homeostasis in the VMH, the mechanism regulating this energy metabolism by SF-1 is not well understood. Further the role of SF-1 in modulating age-dependent energy homeostasis under different nutritional conditions has not been well elucidated. We previously reported that postnatal deletion of SF-1 in the VMH leads to high fat diet induced obesity due to impaired thermogenesis and blunted leptin signaling [ 15 ].
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Here, we report that deletion of SF-1 in the VMH leads to late onset of obesity that is largely associated with increased food intake, blunted energy expenditure and reduced physical activity in the aged KO mice. Additionally, the SF-1 KO mice showed dysregulated insulin and leptin homeostasis and a reduction in the activity of the brown adipose tissue BAT as indicated by decreased expression of uncoupling protein 1 UCP1.
Taken together, our data underpins the importance of SF-1 in the VMH-mediated energy balance regulation and implies that SF-1 is critical for protection against age-dependent and diet induced metabolic disorders. For metabolic cage studies, the mice were allowed to acclimatize in the metabolic chambers for 6 days and provided with food and water ad libitum. O 2 consumption, CO 2 production and heat generation were monitored for 5 days after acclimatization and the rearing and ambulatory movements monitored with infrared beams.
Mice were fasted overnight for 18h and provided with water ad libitum. The following morning, the mice were housed in individual cages and stabilized for one hour. Mice were acclimatized in individual cages and fasted for one hour and provided with water ad libitum. The plasma glucose, insulin and leptin levels were assayed in fed condition and after 24h fasting condition. Mice were decapitated after deep anesthesia with i.
In situ hybridization was carried out on the tissue sections following the protocol described previously [ 7 ]. Statistical analyses were performed using GraphPad Prism 5. Metabolic phenotypes were assessed in two different age groups, a young cohort aged 20—30 weeks young mice and an old cohort aged 45—55 weeks old mice. In the young cohort, the WT and KO mice had comparable body weight and fat components Fig 1A , however in the old cohort, the KO mice showed increased body weight indicated by the significant increase in fat content and marked decrease in lean mass Fig 1E and S1A Fig.
In addition, the daily food intake increased significantly in the old cohort, especially in the dark phase Fig 1F , but this increase in food intake was not observed in the young cohort Fig 1B. These results indicate that SF-1 is required for the regulation of normal energy balance in the aging process. A-D 20—30 weeks old male mice. E-H 45—55 weeks old male mice. The number of animals examined is expressed in the parenthesis. To gain mechanistic insight into the deteriorated metabolic profile and hence late onset of obesity in the aged KO mice, we analyzed their metabolic profiles using metabolic chambers.
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Different from the young cohort S1B—S1E Fig , the KO mice in the old cohort exhibited a marked reduction in energy expenditure and physical activity, suggesting that the obese phenotype in aged KO mice might be attributed to blunted energy expenditure and locomotor activity together with increased food intake Figs 1F and 2A—2D.
The aging process is accompanied by considerable changes in the efficiency of the metabolic process and aging in this sense could be considered as a metabolic stress condition [ 17 , 18 ]. We therefore postulated that SF-1 might be essential for maintaining normal body weight homeostasis in different metabolic stress conditions. As high fat diet HFD is a well-known metabolic stress condition, besides age, we set out to investigate the role of SF-1 in the regulation of energy homeostasis under HFD.
A O 2 consumption, B heat generation, C ambulatory movement, D rearing movement, E body weight, F blood insulin levels, G blood leptin levels, H glucose levels. A-D 45—55 weeks old male mice. E-H 20—30 weeks old male mice challenged with high fat diet for three weeks. Figures in parenthesis indicate number of animals studied.
BB, beam break. These results indicate that SF-1 expression in the VMH might be required for the regulation of body weight and hormonal homeostasis in metabolic stress conditions such as aging and high fat diet. We next performed metabolic cage studies with mice fed on normal chow diet then switched to high fat diet HFD during the study to investigate the underlying mechanism of the diet-induced obesity in KO mice. This data indicates that SF-1 is essential not only for regulation of late onset obesity but also for protection against diet induced obesity.
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A-F 20—30 weeks old male mice. HFD, high fat diet. Impaired glucose tolerance has been shown to develop with age due to a reduction in glucose induced insulin secretion or due to uncontrolled hepatic glucose output among other factors [ 19 ]. Having observed significant insulin and leptin resistance in young SF-1 KO mice Fig 1C and 1D , we speculated that hormonal dysregulation might already have occurred at a younger age before the development of obesity in aged KO mice. Therefore, we investigated the effect of SF-1 knockout in the VMH on glucose homeostasis and insulin action.
We first assayed plasma glucose level at fed and fasted conditions and observed a significant increase in the fed condition only in the old cohort Fig 4A and 4D. These results highly imply that SF-1 is required for normal hormonal regulation from a young age and that the hormonal dysregulation observed in the young mice might contribute, at least partially, to the deteriorated metabolic profile and obese phenotype observed in the aged mice. A-C 20—30 weeks old female mice.
D-F 45—55 weeks old female mice. The brown adipose tissue BAT is known to regulate whole body energy expenditure through sympathetically activated thermogenesis and therefore protect the body against diet-induced obesity [ 20 ]. Prompted by the altered energy expenditure in metabolic stress condition including HFD and age in SF-1 KO mice, we sought to explore the molecular mechanism regulating energy expenditure by assaying various genes mediating thermogenesis in the BAT.
It has been suggested that the VMH expresses high level of vesicular glutamate transporter 2 Vglut2 and the deletion of Vglut2 in SF-1 neurons was reported to induce obesity under high fat diet associated with hyperphagia and blunted response to hypoglycemia [ 14 ]. In the current study, SF-1 deletion in the VMH also induced hyperphagia, hormonal dysregulation and subsequent obesity development.
Obesity has remained a major public health concern with the prevalence rate rising rapidly over the last few decades. Recent studies have focused on understanding the molecular, environmental and social factors promoting obesity development. A major contributor to the development and pathology of obesity is an imbalance between energy intake and energy expenditure partly due to the modern sedentary lifestyle [ 21 ].
The central nervous system CNS regulates energy homeostasis by integrating and responding to nutritional signals generated by the peripheral organs such as the circulating insulin and leptin levels. The hypothalamus, particularly the VMH, is a well-known region of the CNS critical for regulating feeding and energy expenditure and therefore maintaining whole body energy homeostasis [ 22 ].
In this study, we sought to investigate the mechanism involved in the VMH-mediated energy regulation under different metabolic stress conditions including aging and high fat diet.