Intravenous administration of human amnion-derived mesenchymal stem cells improves gait and sensory function in mouse models of spinal cord injury.

Introduction: Spinal cord injury (SCI) leads to severe disabilities and remains a significant social and economic challenge. Despite advances in medical research, there are still no effective treatments for SCI. Human amnion-derived mesenchymal stem cells (hAMSCs) have shown potential due to their anti-inflammatory and neuroprotective effects.

Unilateral Stereotactic Radiofrequency Lesioning as a Surgical Treatment Option for Meige Syndrome.

Background Meige syndrome is a segmental dystonia affecting the head and neck, with bilateral blepharospasm as the primary symptom. First-line treatment typically involves Botox injections. For cases resistant to this treatment, bilateral deep brain stimulation of the globus pallidus internus (GPi) is considered.

Management of an Uncommon Complication: Anterior Choroidal Artery Occlusion by Posterior Clinoid Process Detected Through Intraoperative Monitoring After Clipping of Paraclinoid Aneurysm: 2-Dimensional Operative Video.

Despite technological advances in endovascular therapy, surgical clipping of paraclinoid aneurysms remains an indispensable treatment option and has an acceptable profile risk. Intraoperative monitoring of motor and somatosensory evoked potentials has proven to be an effective tool in predicting and preventing postoperative motor deficits during aneurysm clipping.1,2 We describe the case of a 61-yr-old Japanese woman with a history of hypertension and smoking.

Microsurgical resection of unruptured cerebellar arteriovenous malformation presenting with trigeminal neuralgia.

Cerebellar arteriovenous malformations (AVMs) represent 10%-15% of all intracranial AVMs and are associated with a greater risk for hemorrhagic presentation compared with supratentorial AVMs. When they reach the cerebellopontine angle cistern, neurovascular compression syndromes, including trigeminal neuralgia and hemifacial spasm, can occur. Due to the aggressive natural history of cerebellar AVM, an effective treatment strategy is required.

TACI deficiency enhances antibody avidity and clearance of an intestinal pathogen.

The transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) controls differentiation of long-lived plasma cells, and almost 10% of individuals with common variable immunodeficiency (CVID) express either the C104R or A181E variants of TACI. These variants impair TACI function, and TACI-deficient mice exhibit a CVID-like disease. However, 1%-2% of normal individuals harbor the C140R or A181E TACI variants and have no outward signs of CVID, and it is not clear why TACI deficiency in this group does not cause disease.

TACI deficiency impairs sustained Blimp-1 expression in B cells decreasing long-lived plasma cells in the bone marrow.

Deficiencies in transmembrane activator and CAML interactor (TACI) result in common variable immune deficiency, a syndrome marked by recurrent infections with encapsulated microorganisms, impaired production of antibodies, and lymphoproliferation. How TACI promotes antibody production and inhibits lymphoproliferation is not understood. To answer this question, we studied the generation of immunity to protein antigens in both TACI-deficient and TACI-proficient mice.

A functional family-wide screening of SP/KLF proteins identifies a subset of suppressors of KRAS-mediated cell growth.

SP/KLF (Specificity protein/Krüppel-like factor) transcription factors comprise an emerging group of proteins that may behave as tumour suppressors. Incidentally, many cancers that display alterations in certain KLF proteins are also associated with a high incidence of KRAS (V-Ki-ras2 Kirsten rat sarcoma viral oncogene homologue) mutations. Therefore in the present paper we investigate whether SP/KLF proteins suppress KRAS-mediated cell growth, and more importantly, the potential mechanisms underlying these effects.

Novel functions of B cells in transplantation.

Purpose Of Review: This manuscript reviews current knowledge and recent findings regarding antibody-independent functions of B cells in transplantation.

Recent Findings: Until recently the functions of B cells in transplantation have been attributed almost entirely to the antibodies they produce. However, the results of recent trials of B-cell-depleting agents for treatment of antibody-mediated rejection as well as auto-immune disease raised awareness that B cells mediate functions independent of antibody synthesis.

N-cadherin expression and epithelial-mesenchymal transition in pancreatic carcinoma.

Purpose: Loss of intercellular adhesion and increased cell motility promote tumor cell invasion. In the present study, E- and N-cadherin, members of the classical cadherin family, are investigated as inducers of epithelial-to-mesenchymal transition (EMT) that is thought to play a fundamental role during the early steps of invasion and metastasis of carcinomas. Cell growth factors are known to regulate cell adhesion molecules.

Endogenous decoy receptor 3 blocks the growth inhibition signals mediated by Fas ligand in human pancreatic adenocarcinoma.

Many cancers are resistant to Fas-mediated apoptosis despite the expression of Fas. To investigate the mechanisms by which Fas signals are attenuated, we focused on decoy receptor 3 (DcR3). DcR3 is a soluble receptor against Fas ligand belonging to the tumor necrosis factor receptor superfamily and overexpresses in some forms of cancers.

RECK expression in pancreatic cancer: its correlation with lower invasiveness and better prognosis.

Background: The reversion-inducing cysteine-rich protein with Kazal motifs (RECK) gene was initially isolated as a transformation suppressor gene. The RECK gene is expressed widely in normal organs but is undetectable in many tumor-derived cell lines. When artificially expressed in such cell lines, RECK negatively regulates at least matrix metalloprotease (MMP)-9, MMP-2, and MT1-MMP activation and suppresses the invasive and metastatic potentials of these cells.

Expression of IL-6 receptor in pancreatic cancer: involvement in VEGF induction.

Background: Vascular endothelial growth factor (VEGF) is one of the most potent angiogenic growth factors and its expression is correlated with MVD (microvascular density) in malignant tumors, including pancreatic adenocarcinoma. On the other hand, serum interleukin-6 (IL-6) is elevated in many patients with pancreatic cancer in accordance with their disease progression. In this study, we examined whether IL-6 and its receptors have any involvement in the induction of VEGF in pancreatic cancer.

All-trans retinoic acid induces differentiation of ducts and endocrine cells by mesenchymal/epithelial interactions in embryonic pancreas.

Retinoids during the embryonic period act as a mesenchymal inducer in many organs, including kidney, lung, central nervous system, and gut. Retinoic acid (RA) demonstrates insulinotropic effects in adult pancreas, but only a limited study has elucidated its role in pancreatic organogenesis. In this study, we have analyzed the existence of RA-signaling machinery in embryonic pancreas and evaluated its role using in vitro tissue culture experiments.