Mutations in the fused in sarcoma/translated in liposarcoma gene (FUS/TLS, FUS) have been identified in sporadic and familial forms of amyotrophic lateral sclerosis (ALS). FUS is an RNA-binding protein that is normally localized in the nucleus, but is mislocalized to the cytoplasm in ALS, and comprises cytoplasmic inclusions in ALS-affected areas. However, it is still unknown whether the neurodegeneration that occurs in ALS is caused by the loss of FUS nuclear function, or by the gain of toxic function due to cytoplasmic FUS aggregation.
Alloantibody can be a major barrier to successful organ transplantation; however, therapy to control antibody production or to alter its impact on the allograft remains limited. The goal of this review is to examine the regulatory steps that are involved in the generation of alloreactive B cells, with a specific emphasis on how known mechanisms relate to clinical situations in transplant recipients. Thus, we will examine the process of activation of mature, naÔve B cells and how this relates to de novo antibody production.
Huntington's disease (HD) is a lethal, neurodegenerative disorder caused by expansion of the polyglutamine repeat in the Huntingtin gene (HTT), leading to mutant protein misfolding, aggregation, and neuronal death. Feeding a Drosophila HD model cystamine, or expressing a transgene encoding the anti-htt intracellular antibody (intrabody) C4-scFv in the nervous system, demonstrated therapeutic potential, but suppression of pathology was incomplete.
The purpose of this study was to confirm a previous finding that homosexual males with older brothers weigh less at birth than do heterosexual males with older brothers. The subjects comprised 250 feminine boys referred to a child psychiatry service because of extreme cross-gender wishes or behavior and assumed, on the basis of previous research, to be prehomosexual, plus 739 control boys and 261 control girls referred to the same service for reasons unrelated to sexual orientation or gender identity disorder and assumed, from base-rate probabilities, to be preheterosexual.
The immunomodulatory activity of an Indian Ayurvedic medicinal preparation, Ashwagandna (Withania somnifera (L. Dunal)) was studied in mice with myelosuppression induced by one or more of the following three compounds: cyclophosphamide, azathioprin, or prednisolone. The assessment of immunomodulatory activity was carried out by hematological and serological tests. A significant modulation of immune reactivity was observed in all the three animal models used. Ashwagandha prevented myelosuppression in mice treated with all three immunosuppressive drugs tested.
Bacopa monnieri (L.) Wettst. (Brahmi) is a medicinal plant used as a memory enhancer in Ayurvedic medicines. Its active components are triterpenoid glycosides namely pseudojujubogenin and jujubogenin glycosides. In order to analyze these saponin glycosides, an enzyme-linked immunosorbant assay (ELISA) was developed using polyclonal antibodies against bacopaside I, one of the pseudojujubogenin glycosides found in the plant. Bacopaside I was conjugated with a bovine albumin serum (BSA) to prepare an immunogen.
Caesalpinia bonducella FLEMING (Caesalpiniaceae) is a plant well known for its medicinal value in Indian Ayurveda. However, to prove its efficiency for the clinical utilization, more experimental data will be beneficial. AIMS OF THE STUDY: The present study involved the investigation of immunomodulatory activities of ethanolic extract of Caesalpinia bonducella seeds.
Cancer is responsible for millions of deaths each year worldwide. Pharmacological intervention with plant-derived products alone or in combination to reverse, suppress, or prevent the cancer progression plays a key role in the fight against this terrible disease. Aerva lanata is an important medicinal plant widely used in traditional systems of medicine like ayurveda and siddha. Ethanolic extract of whole plant of A. lanata exhibited immunomodulatory and antitumor activity.
Multiple death signals influence mitochondria during apoptosis, yet the critical initiating event for mitochondrial dysfunction in vivo has been unclear. tBID, the caspase-activated form of a "BH3-domain-only" BCL-2 family member, triggers the homooligomerization of "multidomain" conserved proapoptotic family members BAK or BAX, resulting in the release of cytochrome c from mitochondria. We find that cells lacking both Bax and Bak, but not cells lacking only one of these components, are completely resistant to tBID-induced cytochrome c release and apoptosis.
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience
Huntington's disease (HD) results from polyglutamine expansion in huntingtin (htt), a protein with several consensus caspase cleavage sites. Despite the identification of htt fragments in the brain, it has not been shown conclusively that htt is cleaved by caspases in vivo. Furthermore, no study has addressed when htt cleavage occurs with respect to the onset of neurodegeneration. Using antibodies that detect only caspase-cleaved htt, we demonstrate that htt is cleaved in vivo specifically at the caspase consensus site at amino acid 552.