Results 61 to 70 of about 1,253,950 (267)
MECHANISM OF ALCOHOLIC TESTICULAR DAMAGE
To observe the mechanism of alcoholic testicular damage, in a previous experiment we used weanling male SD rats aged 45 days, weighing about 200 g, and fed a liquid diet (Lieber's) containing 5% ethanol. The latter accounted for 36% of total caloric intake for 7 weeks, but did not result in testicular atrophy.
Shirai, Takashi, Ikemoto, Isao
openaire +3 more sources
Reciprocal control of viral infection and phosphoinositide dynamics
Phosphoinositides, although scarce, regulate key cellular processes, including membrane dynamics and signaling. Viruses exploit these lipids to support their entry, replication, assembly, and egress. The central role of phosphoinositides in infection highlights phosphoinositide metabolism as a promising antiviral target.
Marie Déborah Bancilhon, Bruno Mesmin
wiley +1 more source
Phosphatidylinositol 4‐kinase as a target of pathogens—friend or foe?
This graphical summary illustrates the roles of phosphatidylinositol 4‐kinases (PI4Ks). PI4Ks regulate key cellular processes and can be hijacked by pathogens, such as viruses, bacteria and parasites, to support their intracellular replication. Their dual role as essential host enzymes and pathogen cofactors makes them promising drug targets.
Ana C. Mendes +3 more
wiley +1 more source
Mechanisms of Toxic Damage to Spermatogenesis [PDF]
Azoospermia and long-lasting testicular atrophy are common adverse consequences of cancer treatment. Chemotherapeutic agents may disrupt spermatogenesis by targeting various testicular cell types (Leydig cells, Sertoli cells, and germ cells) and by activating numerous molecular pathways involved in germ cell life-and-death decision making.
openaire +2 more sources
Protein pyrophosphorylation by inositol pyrophosphates — detection, function, and regulation
Protein pyrophosphorylation is an unusual signaling mechanism that was discovered two decades ago. It can be driven by inositol pyrophosphate messengers and influences various cellular processes. Herein, we summarize the research progress and challenges of this field, covering pathways found to be regulated by this posttranslational modification as ...
Sarah Lampe +3 more
wiley +1 more source
We identified a systemic, progressive loss of protein S‐glutathionylation—detected by nonreducing western blotting—alongside dysregulation of glutathione‐cycle enzymes in both neuronal and peripheral tissues of Taiwanese SMA mice. These alterations were partially rescued by SMN antisense oligonucleotide therapy, revealing persistent redox imbalance as ...
Sofia Vrettou, Brunhilde Wirth
wiley +1 more source
In this study, we found that human cervical‐derived adipocytes maintain intracellular iron level by regulating the expression of iron transport‐related proteins during adrenergic stimulation. Melanotransferrin is predicted to interact with transferrin receptor 1 based on in silico analysis.
Rahaf Alrifai +9 more
wiley +1 more source
Structural insights into an engineered feruloyl esterase with improved MHET degrading properties
A feruloyl esterase was engineered to mimic key features of MHETase, enhancing the degradation of PET oligomers. Structural and computational analysis reveal how a point mutation stabilizes the active site and reshapes the binding cleft, expading substrate scope.
Panagiota Karampa +5 more
wiley +1 more source
Mechanisms of Brain Damage in Twins [PDF]
SUMMARY:The brains of 18 twins dying in the perinatal period showed a variety of lesions. Eleven had subependymal cell plate hemorrhage which had ruptured into the lateral ventricles in five. Five had periventricular damage. Three had anoxic neuronal damage. One acardiac monster had bilateral cerebral infarction.
openaire +2 more sources
Gut microbiome and aging—A dynamic interplay of microbes, metabolites, and the immune system
Age‐dependent shifts in microbial communities engender shifts in microbial metabolite profiles. These in turn drive shifts in barrier surface permeability of the gut and brain and induce immune activation. When paired with preexisting age‐related chronic inflammation this increases the risk of neuroinflammation and neurodegenerative diseases.
Aaron Mehl, Eran Blacher
wiley +1 more source

