Cruzterry1568

Median LOS decreased from 10 to 8days during the study period (p < 0.001), 36% were males, and 50% required blood transfusion. High-grade complications occurred in 15% of patients and were associated with bowel diversion [odds ratio (OR) 1.6, 95% confidence interval (CI) 1.1-2.4], disseminated cancer (OR 1.8, 95% CI 1.4-2.3), and gynecologic cancers (OR 2.9, 95% CI 1.8-4.7). Mortality was 2% and was associated with disseminated cancer (OR 2.2, 95% CI 1.1-4.3) and male sex (OR 2.4, 95% CI 1.3-4.4).

TPE is associated with high rates of complications, however mortality rates remain low. Preoperative and perioperative outcomes differ depending on the origin of the primary malignancy.

TPE is associated with high rates of complications, however mortality rates remain low. Preoperative and perioperative outcomes differ depending on the origin of the primary malignancy.Stem cell-based therapy has shown exciting efficacy in pre-clinical studies on different neurodegenerative diseases (NDs). However, no clinically applicable stem-cell-derived neurons are available to the patients with NDs. There exist some obstacles associated with stem cell therapy, which need to be overcome in future clinical studies. In this chapter, more challenges and new strategies will be explored to accelerate the clinical translation of a human embryonic stem cell (hESC)/induced pluripotent stem cell (iPSC)-derived neural cell product to patients with NDs.In the past decade, progress in the research on human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs) has provided the solid basis to derive retinal pigment epithelium, photoreceptors, and ganglion cells from hESCs/iPSCs for transplantation therapy of retinal degenerative diseases (RDD). Recently, the iPSC-derived retinal pigment epithelium cells have achieved efficacy in treating patients with age-related macular degeneration (AMD). However, there is still much work to be done about the differentiation of hESCs/iPSCs into clinically required retinal cells and improvement in the methods to deliver the cells into the retina of patients. Here we will review the research advances in stem cell transplantation in animal studies and clinical trials as well as propose the challenges for improving the clinical efficacy and safety of hESCs/iPSCs-derived retinal neural cells in treating retinal degenerative diseases.Spinal muscular atrophy (SMA) is a devastating neurodegenerative disease characterized by the degeneration of lower motor neurons in the spinal cord, leading to progressive paralysis and early death in the severe cases. SMA is primarily caused by the mutations in the gene of SMN (survival motor neuron). More research has focused on the development of SMN-targeted replacement therapy for SMA. The first US Food and Drug Administration (FDA)-approved modified antisense oligonucleotide (nusinersen) to treat SMA is to reverse intronic splicing silencer of SMN to produce fully functional SMN2. Recently, stem cell transplantation has shown the potential to repair the injured tissue and differentiate into neurons to rescue the phenotypes of SMA in animal models. In this chapter, we first review the clinical, genetic, and pathogenic mechanisms of SMA. Then, we discuss current pharmacological treatments and point out the therapeutic efficacy of stem cell transplantation and future directions and priorities for SMA.Multiple sclerosis (MS) is the most frequent demyelinating disease of the central nervous system (CNS) associated with inflammatory plaques of white matter demyelination, oligodendrocyte destruction, reactive gliosis and axonal degeneration. In this chapter, we first review the pathological process of axonal degeneration in MS and discuss how these changes cause clinical symptoms of MS. We then discuss the pharmacological treatment to improve the clinical symptoms. Finally, we highlight how the autologous hematopoietic stem cell transplantation (AHSCT) can be effective for aggressive MS patients, who fail to respond to drug therapies, and also propose the future challenges of AHSCT.Amyotrophic lateral sclerosis (ALS) is a motor neuronal degeneration disease, in which the death of motor neurons causes lost control of voluntary muscles. The consequence is weakness of muscles with a wide range of disabilities and eventually death. Most patients died within 5 years after diagnosis, and there is no cure for this devastating neurodegenerative disease up to date. Stem cells, including non-neural stem cells and neural stem cells (NSCs) or neural progenitor cells (NPCs), are very attractive cell sources for potential neuroprotection and motor neuron replacement therapy which bases on the idea that transplant-derived and newly differentiated motor neurons can replace lost motor neurons to re-establish voluntary motor control of muscles in ALS. Our recent studies show that transplanted NSCs or NPCs not only survive well in injured spinal cord, but also function as neuronal relays to receive regenerated host axonal connection and extend their own axons to host for connectivity, including motor axons in ventral root. This reciprocal connection between host neurons and transplanted neurons provides a strong rationale for neuronal replacement therapy for ALS to re-establish voluntary motor control of muscles. In addition, a variety of new stem cell resources and the new methodologies to generate NSCs or motor neuron-specific progenitor cells have been discovered and developed. SP2509 Together, it provides the basis for motor neuron replacement therapy with NSCs or NPCs in ALS.Huntington's disease (HD) is an inherited neurodegenerative disorder which is characterised by a triad of highly debilitating motor, cognitive, and psychiatric symptoms. While cell death occurs in many brain regions, GABAergic medium spiny neurons (MSNs) in the striatum experience preferential and extensive degeneration. Unlike most neurodegenerative disorders, HD is caused by a single genetic mutation resulting in a CAG repeat expansion and the production of a mutant Huntingtin protein (mHTT). Despite identifying the mutation causative of HD in 1993, there are currently no disease-modifying treatments for HD. One potential strategy for the treatment of HD is the development of cell-based therapies. Cell-based therapies aim to restore neuronal circuitry and function by replacing lost neurons, as well as providing neurotropic support to prevent further degeneration. In order to successfully restore basal ganglia functioning in HD, cell-based therapies would need to reconstitute the complex signalling network disrupted by extensive MSN degeneration.