Prosthetic joint infection (PJI) is a common complication of the knee and hip arthroplasty and represents a huge challenge for physicians. PJI raises serious social, economic and clinical concerns in the public health that need a comprehensive approach to better focus on proven strategies for disease prevention and treatment. History and clinical signs on joint site are useful means for suspecting PJI that need to be confirmed through major and minor diagnostic criteria. The pathogen isolation and the resulting antibiogram are crucial to guide the correct antibiotic strategy and together with surgical treatment (prosthesis revision and spacer implantation) represent the cornerstones to eradicate the infection before attempting a new arthroplasty. External fixator with removal of the spacer may be an option before performing a new arthroplasty when the infection does not heal. Arthrodesis may also be considered if the arthroplasty is contraindicated. Limb amputation is the last chance when pathogen eradication failed and might lead to life-threatening situations.

Complex molecular and cellular mechanisms are involved in the pathway of liver fibrosis. Activation and transformation of hepatic stellate cells (HSCs) are considered the two main reasons for the cause and development of liver fibrosis. The peroxisome proliferator-activated receptors (PPARs) belonging to the family of ligand-activated transcription factors play a key role in liver homeostasis, regulating adipogenesis and inhibiting fibrogenesis in HSCs. Normal transcriptional function of PPARs contributes to maintain HSCs in quiescent phase. A reduced expression of PPARs in HSCs greatly induces a progression of liver fibrosis and an increased production of collagen. Here, we discuss role and function of PPARs and we take into consideration molecular factors able to reduce PPARs activity in HSCs. Finally, although further validations are needed, we illustrate novel strategies available from in vitro and animal studies on how some PPARs-agonists have been proved effective as antifibrotic substances in liver disease.

The most important species of Cryptosporidium in humans, C. parvum and C. hominis, cause severe and chronic life-threatening gastroenteritis in immunocompromised patients. Despite a certain efficacy shown by passive immunotherapy or by some chemotherapeutic agents (e.g. paromomycin and nitazoxanide), no significant benefit has been demonstrated. The use of highly active antiretroviral therapy (HAART) in persons with the acquired immunodeficiency syndrome drastically reduces the prevalence of Cryptosporidium infection. This result seems to be due to aspartyl protease inhibitors of the human immunodeficiency virus included in HAART, which directly interfere with the life cycle of the parasite. The identification of the C. parvum proteases involved in the host-cell interaction could lead to new therapeutic approaches using specific parasite protease inhibitors in immunocompromised persons.