Honeybees balance essential fatty acids and suffer cognitively from deficiency

Abstract Background and aims. Epidemiological data on autoimmune hepatitis (AIH) are scarce. In this study, we determined the clinical and epidemiological characteristics of AIH patients in the Netherlands (16.7 million inhabitants). Methods. Clinical characteristics were collected from 1313 AIH patients (78% females) from 31 centers, including all eight academic centers in the Netherlands. Additional data on ethnicity, family history and symptoms were obtained by the use of a questionnaire. Results. The prevalence of AIH was 18.3 (95% confidential interval [CI]: 17.3-19.4) per 100,000 with an annual incidence of 1.1 (95% CI: 0.5-2) in adults. An incidence peak was found in middle-aged women. At diagnosis, 56% of patients had fibrosis and 12% cirrhosis in liver biopsy. Overall, 1% of patients developed HCC and 3% of patients underwent liver transplantation. Overlap with primary biliary cirrhosis and primary sclerosing cholangitis was found in 9% and 6%, respectively. The clinical course did not differ between Caucasian and non-Caucasian patients. Other autoimmune diseases were found in 26% of patients. Half of the patients reported persistent AIH-related symptoms despite treatment with a median treatment period of 8 years (range 1-44 years). Familial occurrence was reported in three cases. Conclusion. This is the largest epidemiological study of AIH in a geographically defined region and demonstrates that the prevalence of AIH in the Netherlands is uncommon. Although familial occurrence of AIH is extremely rare, our twin data may point towards a genetic predisposition. The high percentage of patients with cirrhosis or fibrosis at diagnosis urges the need of more awareness for AIH

Adverse events related to low dose corticosteroids in autoimmune hepatitis

Background: Autoimmune hepatitis requires long‐term therapy, and systemic cor‐ ticosteroids are the backbone of therapeutic management. Prolonged use of corti‐ costeroids may lead to adverse events but data from long‐term studies are mainly derived from studies in rheumatic diseases. Aim: To assess cataract, diabetes and fractures in relation to corticosteroid doses in the long‐term maintenance treatment of patients with autoimmune hepatitis. Methods: We retrospectively collected data on 476 patients (77% women) with an established diagnosis of autoimmune hepatitis. Binary logistic regression with a gen‐ eralised estimating equation was used to analyse the association between current corticosteroid use and the incidence of cataract, diabetes and fractures with onset after autoimmune hepatitis diagnosis. We corrected for sex, age, cirrhosis at diagno‐ sis and predniso(lo)ne use in the prior 3 years to account for possible ongoing effects. Results: A total of 6634 years, with a median of 13 (range 1‐40) per patient were recorded. The median age at diagnosis was 44 years (range 2‐88). Adverse events were documented in 120 (25%) patients. Low‐dose predniso(lo)ne (0.1‐5.0 mg/d) in‐ creased the odds of fractures whereas higher doses (>5.0 mg/d) increased the odds of cataracts and diabetes. Budesonide increased the odds of cataract and fractures; this effect was independent of predniso(lo)ne use in the prior 1, 2 or 3 years. Conclusions: Even low doses of corticosteroids frequently lead to substantial ad‐ verse events refuting the assumption that adverse events are prevented by adminis‐ tering low doses

Studenten slaaf van internet?

It's impossible to imagine life today without a computer. EspeciaLly the introduction of the World Wide Web caused a breakthrough. However, excessive use of computers may cause physical, psychological and/or social problems, which might effect the daily life of those who are afflicted. Especially students may be vulnerable for these kinds of problems. The sudden and sometimes drastic changes in their lives may cause psychosocial problems (loneliness, lack of control, low self-esteem). It can be expected that part of these students will not be able to cope in an adequate way with this situation. Easy access to the Internet, provided by the university, may offer these students unique tools to escape from the daily problems. Research carried out in Groningen under 874 students showed that the mean Internet use among students was 7 hours a week. Ten percent used the computer over 16 hours a week (excessive Internet users). Most of the students did not experience serious problems. About 10-30% of the students reported various physical complaints because of (over)utilisation of the computer. Fifteen percent reported many internetrelated problems. (symptoms of 'addiction'). A group of 6% was qualified as 'users at risk' (>16 hours a week and many internetrelated problems). They were mainly lonely male students, who were able to make use of a cableconnection to chat, e-mail and to visit erotic sites. It is suggested to pay more and permanent attention to computer-related health problems, and to inform students properly about the possible risks of overfrequent computer utilization.

On the Dissimilarity of 5′-AMP Induced Hypothermia and Torpor in Mice

Administration of adenosine-5′-monophosphate (5′-AMP) can induce an artificial but endogenously reversible torpor-like state in mice. The dynamics of body temperature and the relation between body temperature and metabolic rate may indicate the (dis)similarity of this artificial torpor-like state to natural torpor in intact animals. We investigated these in C57BL/6J mice by (1) comparing cooling rates during 5′-AMP induced hypothermia to cooling rates during high workload induced torpor, and by (2) estimating the relative contributions of metabolic suppression and passive temperature (Q 10) effects in the 5′-AMP induced hypothermic state. We did the latter by back-extrapolating the relation between body temperature and metabolic rate in hypothermic conditions to the euthermic temperature level, using calculated Q 10-values. The data indicate that (1) cooling rate in 5′-AMP induced hypothermia is about 1.8 times faster than in natural torpor in workload conditions, and that (2) Q 10 effects can entirely explain the metabolic reduction of 5′-AMP induced hypothermia, indicating that active metabolic suppression may be lacking. Together, this suggests fundamental differences between 5′-AMP induced hypothermia and natural torpor, limiting the validity of the paradigm to the study of effects of hypothermic conditions and temperature related metabolic effects

Restoring the infected powerhouse: Mitochondrial quality control in sepsis

Sepsis is a dysregulated host response to an infection, characterized by organ failure. The pathophysiology is complex and incompletely understood, but mitochondria appear to play a key role in the cascade of events that culminate in multiple organ failure and potentially death. In shaping immune responses, mitochondria fulfil dual roles: they not only supply energy and metabolic intermediates crucial for immune cell activation and function but also influence inflammatory and cell death pathways. Importantly, mitochondrial dysfunction has a dual impact, compromising both immune system efficiency and the metabolic stability of end organs. Dysfunctional mitochondria contribute to the development of a hyperinflammatory state and loss of cellular homeostasis, resulting in poor clinical outcomes. Already in early sepsis, signs of mitochondrial dysfunction are apparent and consequently, strategies to optimize mitochondrial function in sepsis should not only prevent the occurrence of mitochondrial dysfunction, but also cover the repair of the sustained mitochondrial damage. Here, we discuss mitochondrial quality control (mtQC) in the pathogenesis of sepsis and exemplify how mtQC could serve as therapeutic target to overcome mitochondrial dysfunction. Hence, replacing or repairing dysfunctional mitochondria may contribute to the recovery of organ function in sepsis. Mitochondrial biogenesis is a process that results in the formation of new mitochondria and is critical for maintaining a pool of healthy mitochondria. However, exacerbated biogenesis during early sepsis can result in accumulation of structurally aberrant mitochondria that fail to restore bioenergetics, produce excess reactive oxygen species (ROS) and exacerbate the disease course. Conversely, enhancing mitophagy can protect against organ damage by limiting the release of mitochondrial-derived damage-associated molecules (DAMPs). Furthermore, promoting mitophagy may facilitate the growth of healthy mitochondria by blocking the replication of damaged mitochondria and allow for post sepsis organ recovery through enabling mitophagy-coupled biogenesis. The remaining healthy mitochondria may provide an undamaged scaffold to reproduce functional mitochondria. However, the kinetics of mtQC in sepsis, specifically mitophagy, and the optimal timing for intervention remain poorly understood. This review emphasizes the importance of integrating mitophagy induction with mtQC mechanisms to prevent undesired effects associated with solely the induction of mitochondrial biogenesis