Who guards the guardians? Social workers in an era of privatization

The article traces and assesses the impact of contracting out and outsourcing on the work environment of social workers in Israel. We argue that the ability of social workers to live up to their professional and ethical obligations is hampered due to outsourcing

Gender and Cutaneous Leishmaniasis in Israel

Leishmaniasis is estimated to be more common in males than in females. Our purpose was to evaluate differences in preponderance in relation to sex and gender across cutaneous and mucocutaneous leishmaniasis in Israel. An observational study was performed, including cases of endemic CL (cutaneous leishmaniasis) in Israel, and imported MCL (mucocutaneous leishmaniasis). CL is a notifiable disease and is supposed to be reported to the Ministry of Health (MOH). The MOH database shows that males as more likely to be infected by leishmania, with an incidence of 5/100,000 in males vs. 3.5/100,000 in females. However, while conducting a demographic house-to-house survey in several locations in Israel where CL is highly endemic, among 608 people who were screened only 49% were males in Leishmania major (L. major) endemic regions and 41% were males in Leishmania tropica (L. tropica) endemic regions, while among 165 cases of imported New-World cutaneous leishmaniasis in Israeli travelers freturning from abroad, 142 (86%) were males. It may be postulated that there is no real gender difference in leishmanial infection, but, perhaps, infections are more commonly seen in men because of referral/reported bias, due to more risk-taking behaviors by men or, perhaps, men are less likely to strictly adhere to recommended preventive measures and thus increase their risk of contracting the disease

Altered ubiquitin signaling induces Alzheimer’s disease-like hallmarks in a three-dimensional human neural cell culture model

Abstract Alzheimer’s disease (AD) is characterized by toxic protein accumulation in the brain. Ubiquitination is essential for protein clearance in cells, making altered ubiquitin signaling crucial in AD development. A defective variant, ubiquitin B + 1 (UBB+1), created by a non-hereditary RNA frameshift mutation, is found in all AD patient brains post-mortem. We now detect UBB+1 in human brains during early AD stages. Our study employs a 3D neural culture platform derived from human neural progenitors, demonstrating that UBB+1 alone induces extracellular amyloid-β (Aβ) deposits and insoluble hyperphosphorylated tau aggregates. UBB+1 competes with ubiquitin for binding to the deubiquitinating enzyme UCHL1, leading to elevated levels of amyloid precursor protein (APP), secreted Aβ peptides, and Aβ build-up. Crucially, silencing UBB+1 expression impedes the emergence of AD hallmarks in this model system. Our findings highlight the significance of ubiquitin signalling as a variable contributing to AD pathology and present a nonclinical platform for testing potential therapeutics