Boldness Predicts Aggressiveness, Metabolism, and Activity in Black Rockfish Sebastes schlegelii

Animal personality refers to individual behavioral and physiological differences that are consistent over time and across context. Recently, the fish personality has gained increasing attention, especially from the perspective of aquaculture production. Here, we used an important aquaculture species, black rockfish Sebastes schlegelii, as the target animal, and conducted a series of experiments to explore the relationships among fish boldness, aggressiveness, locomotor activity, opercular beat rate, standard metabolic rate, and cortisol level. Generally, the results showed that the boldness of black rockfish was significantly, positively correlated with fish aggressiveness, stressed locomotor activity, and standard metabolic rate, while was negatively correlated with stressed opercular beat rate. Bold fish had significantly higher aggressiveness, standard metabolic rate, and stressed locomotor activity but lower stressed opercular beat rate. However, there were no significant correlations between boldness and basal locomotor activity or between boldness and basal cortisol level. These results preliminarily constructed the behavioral and physiological spectrum of black rockfish in the context of fish personality and clearly indicated that the boldness could be used as a discrimination tool to predict fish aggressiveness and metabolic rate, which may have valuable applications for decreasing fish harmful aggression and increasing fish welfare in the aquaculture industry.

Knockout of the hsd11b2 Gene Extends the Cortisol Stress Response in Both Zebrafish Larvae and Adults

The Hsd11b2 enzyme converts cortisol into its inactive form, cortisone and regulates cortisol levels, in particular in response to stress. Taking advantage of CRISPR/Cas9 technology, we generated a hsd11b2 zebrafish mutant line to evaluate the involvement of this gene in stress response regulation. The absence of a functional Hsd11b2 affects survival of zebrafish, although homozygous hsd11b2−/− mutants can reach adulthood. Reproductive capability of hsd11b2−/− homozygous adult males is almost completely abrogated, while that of females is reduced. Interestingly, basal cortisol levels and glucocorticoid-dependent transcriptional activities are not affected by the mutation. In agreement with basal cortisol results, we also demonstrated that basal response to light (LMR-L/D) or mechanical (VSRA) stimuli is not significantly different in wild-type (hsd11b2+/+) compared to mutant larvae. However, after exposure to an acute stressor, the cortisol temporal patterns of synthesis and release are prolonged in both 5 days post fertilization larvae and one-year-old adult hsd11b2−/− zebrafish compared to wild-type siblings, showing at the same time, at 5 dpf, a higher magnitude in the stress response at 10 min post stress. All in all, this new zebrafish model represents a good tool for studying response to different stressors and to identify mechanisms that are induced by cortisol during stress response.

Evaluation of adrenal reserve in patients with differential thyroid cancer receiving thyroid hormone suppression therapy- case-control comparative study

Background Patients with differentiated thyroid cancer (DTC) are exposed to subclinical exogenous hyperthyroidism for the suppression of thyroid-stimulating hormone (TSH). In this study, we aimed to evaluate the adrenal reserve in DTC patients receiving suppression therapy. Materials and Methods The study included 55 DTC patients on suppression therapy and 32 healthy volunteers. Basal serum cortisol of all participants and adrenocorticotropic hormone (ACTH) of the patient group were measured. A standard-dose ACTH test (0.25 mg) was performed in patients with a basal cortisol < 14.5 mcg/dL. Results In the patient group, TSH was lower, free thyroxine (fT4) was higher, and free triiodothyronine (fT3) was similar to those of the control group (p < 0.01, p < 0.01, p = 0.140, respectively). The serum cortisol of the patient group was significantly lower than the control group (12.14 ± 5.12 mcg/dL vs 18.00 ± 5.56 mcg/dL, p < 0.001). 34 (61.8%) patients with DTC had a basal cortisol < 14.5 mcg/dL. Prolonged TSH suppression (≥ 5 years vs < 5 years) was associated with lower basal cortisol (7.46 ± 2.63 mcg/dL vs 9.48 ± 2.65 mcg/dL, p = 0.022). The ACTH stimulation test showed that 2 (5.8%) patients had a cortisol response < 18 mcg/dL. The rate of adrenal insufficiency was 3.6% in DTC patients. A moderate negative correlation was found between ACTH and fT3 of patients with low basal cortisol (r = − 0.358, p = 0.038) Conclusion Patients with DTC receiving TSH suppression therapy are at risk for adrenal insufficiency. The duration and severity of suppression might increase this possibility. Dynamic testing with synthetic ACTH can be used to reveal insufficient cortisol response in case of clinical suspicion.

Methylprednisolone stimulated gene expression (GILZ, MCL-1) and basal cortisol levels in multiple sclerosis patients in relapse are associated with clinical response

Glucocorticoids (GCs) are the main treatment of relapse in multiple sclerosis (MS). Decreased sensitivity to GCs in MS patients has been associated with lack of the suppressive effect of GCs on inflammatory molecules as well as increased resistance to apoptosis. We investigated GC-sensitivity by measuring the effect of intravenous methylprednisolone (IVMP) treatment on transactivation of anti-inflammatory and apoptotic genes (GILZ, MCL-1 and NOXA respectively), in accordance to clinical outcome. Thirty nine MS patients were studied: 15 with clinically isolated syndrome (CIS), 12 with relapsing remitting (RRMS) and 12 with secondary progressive (SPMS) under relapse. Patients underwent treatment with IVMP for 5 days. Blood was drawn before IVMP treatment on day 1 and 1 h after IVMP treatment on days 1 and 5. GIlZ, MCL-1 and NOXA were determined by qPCR. The Expanded Disability Status was evaluated and patients were divided according to their clinical response to IVMP. GILZ and MCL-1 gene expression were significantly higher following first IVMP treatment in responders, compared to non-responders. Furthermore, serum basal cortisol and 1,25-OH Vitamin D levels were significantly higher in clinical-responders as compared to non-clinical responders. Our findings suggest that the differential GILZ and MCL-1 gene expression between clinical-responders and non-clinical responders may implicate the importance of GILZ and MCL-1 as possible markers for predicting glucocorticoid sensitivity and response to GC-therapy in MS patients following first IVMP injection.

The syndrome of inappropriate antidiuresis after vaccination against COVID-19: case report

Background The Syndrome of Inappropriate Antidiuresis (SIADH) has been described to be associated with a multitude of conditions and medications, including the severe acute respiratory syndrome coronavirus 2. We describe the case of a patient with newly diagnosed and symptomatic SIADH after receiving the second COVID-19 vaccination not explained otherwise. Case presentation A 79-year-old male person was admitted to the emergency department due to a worsening of his general health state expressed by weakness, fatigue and anorexia. Vital signs and clinical findings were normal, in particular the patient was considered to be euvolemic. Laboratory investigations revealed a serum sodium of 117 mmol/L, a serum osmolality of 241 mosm/kg and a urea of 1.2 mmol/L with creatinine within normal range. Urine chemistry showed a urine osmolality of 412 mosm/kg and urine sodium of 110 mmol/L. TSH, C-reactive protein, and basal cortisol levels were normal. Under therapy with balanced crystalloid fluids, hyponatremia worsened and in absence of diuretic medications, diagnosis of SIADH was made. Since fluid restriction was not sufficiently effective, oral urea was administered. Under this therapy regimen hyponatremia resolved. Conclusions Local as well as systemic reactions have been described for the new mRNA-based vaccines including pain and fever. Therefore, it is imaginable that the vaccine might trigger SIADH in some patients.

Selective Glucocorticoid Replacement Following Unilateral Adrenalectomy for Hypercortisolism and Primary Aldosteronism

Background An institutional study previously demonstrated that cosyntropin stimulation testing on postoperative day 1 (POD1-CST) identified patients at risk for adrenal insufficiency (AI) following unilateral adrenalectomy (UA) for adrenal-dependent hypercortisolism (HC) and primary aldosteronism (PA), allowing for selective glucocorticoid replacement (GR). This study reevaluates the need for GR following UA for patients with HC and PA in a larger cohort. Methods A prospective database identified 108 patients who underwent UA for mild autonomous cortisol excess (MACE) (n=47), overt hypercortisolism (OH) (n=27), PA (n=22), and concurrent PA/HC (n=12) from 9/2014-10/2020; all underwent preoperative evaluation for HC. MACE was defined as 1mg dexamethasone suppression test (DST) cortisol &gt;1.8 (μg/dL), with ≥5 defined as OH. GR was initiated for basal cortisol ≤5 or stimulated cortisol ≤14 (≤18 prior to 4/2017) on POD1-CST. Results Fifty-one (47%) patients had an abnormal POD1-CST; 54 (50%) were discharged on GR (27 MACE, 20 OH, 1 PA, 6 PA/HC). Median duration of GR was OH: 6.0 months, MACE: 2.1 months, PA: 1 month, PA/HC: 0.8 months. Overall, 26% (n=7) of OH patients and 43% (n=20) of MACE patients did not require GR. Two (2%) OH patients had normal POD1-CST but developed AI several weeks postoperatively requiring GR. None experienced life-threatening AI. Conclusion POD1-CST identifies HC patients at risk for AI after UA, allowing for selective GR. One-quarter of OH patients and nearly half of MACE patients can forego GR after UA. PA patients do not require evaluation for AI if concurrent HC has been excluded preoperatively.