PHF-Core Tau as the Potential Initiating Event for Tau Pathology in Alzheimer’s Disease

FUNDING This work was supported by Fondo Nacional de Ciencia, Tecnologia, FONDOCyT, from the Ministry of Higher Education, Science and Technology, Dominican Republic (2015- 3A2-127 to MP-H and 2018-2019-2A3-208 to JL-M and MP-H). ACKNOWLEDGMENTS: We want to express our gratitude to the following: Dr. P. Davies (Albert Einstein College of Medicine, Bronx, NY, United States) and Lester I. Binder† (North Western, Chicago, IL, United States) for the generous gifts of mAbs TG3 and Alz-50, and Tau-1, Tau-5, and Tau-7, respectively; Tec. Amparo Viramontes Pintos for the handling of the brain tissue; Samadhi Moreno-Campuzano for her technical assistance/support in the confocal microscopy unit of CIIDIR Durango, Instituto Politécnico Nacional; Union Medical University Clinic, Dominican Republic, for their support and collaboration in the development of this research project. We also want to express our gratitude to the Mexican families who have donated the brain of their loved ones affected with Alzheimer’s disease and made our research possible. This work is dedicated to the memory of Professor Dr. José Raúl Mena López† .Peer reviewedPublisher PD

Tau Protein Phosphorylated at Threonine-231 Is Expressed Abundantly in the Cerebellum in Prion Encephalopathies

ACKNOWLEDGMENTS: The authors want to express their gratitude to the following: Dr. P. Davies † (Albert Einstein College of Medicine, Bronx, NY, USA) and Lester I. Binder † (North Western, Chicago, IL, USA) for the generous gift of mAbs TG-3 and Alz-50, and Tau-1, Tau-5 and Tau-7, respectively; Tec. Amparo Viramontes Pintos for the handling of the brain tissue; support in the confocal microscopy unit of CIIDIR Durango, Instituto Politécnico Nacional; Union Medica University Clinic, Dominican Republic, for their support and collaboration in the development of this research project. We also want to express our gratitude to the Mexican families who have donated the brain of their loved ones affected with Alzheimer's disease and made our research possible. This work is dedicated to the memory of Professor Dr. José Raúl Mena López †. †Deceased. This work was supported by Fondo Nacional de Ciencia y Tecnologia, FONDOCyT, from the Ministry of Higher Education, Science and Technology, Dominican Republic (2015-3A2-127 to MP-H) and (2018-2019-2A3-208 to JL-M and MP-H).Peer reviewedPublisher PD

Phospho-Tau Protein Expression in the Cell Cycle of SH-SY5Y Neuroblastoma Cells : A Morphological Study

ACKNOWLEDGMENTS Authors want to express their gratitude to Dr. P. Davies (Albert Einstein College of Medicine, Bronx, NY, USA); Lester I. Binder † (North Western, Chicago, IL, USA) for the generous gift of mAbs (TG-3, Alz-50) and (Tau-1, Tau-5, Tau-7), respectively; Tec. Amparo Viramontes Pintos for the handling of the brain tissue; M. en C. Samadhi Moreno-Campuzano for her technical assistance; M en C.J. Iván Gálvan for his support in confocal microscopy, and the confocal microscopy unit of Laboratorio Nacional de Servicios Experimentales (LaNSE), CINVESTAV. We also want to express our gratitude to the Mexican families who donated brains of loved ones affected with Alzheimer’s disease, and made our research possible. This work is dedicated to the memory of Professor Dr. José Raúl Mena López †. This work was financially supported by CONACyT grants, No. 142293 (to R.M.), 266492 (I.V-F), 239516 (J.S) and the Mancera-Reséndiz family.Peer reviewedPostprin

A modified supraclavicular approach to scalenotomy without first rib resection for the treatment of neurogenic thoracic outlet syndrome

Background: Current approaches to scalenectomy for brachial plexus decompression can cause nerve injuries in patients with neurogenic thoracic outlet syndrome (nTOS), especially when first rib resection (FRR) is performed. We describe a modified supraclavicular approach for scalenotomy that reduces the postoperative morbidity of nTOS patients. Methods: The patient is placed in supine position with the neck slightly extended and turned to the opposite side of the procedure. The modified incision begins above the clavicle 2.5 cm lateral to its first third, extends in medial direction, and turns upwards along the lateral edge of the sternocleidomastoid muscle (SCM) 2.5 cm from the clavicle. Skin flaps are elevated. The external jugular vein is dissected and retracted. The supraclavicular nerves and omohyoid muscle are conserved if found. The phrenic nerve is identified, dissected, and retracted. The anterior scalene muscle is divided, and the brachial plexus is freed. The clinical data and postoperative outcomes of patients that underwent surgery over the last three years were retrieved. The functionality of the arm after surgery was evaluated using the Disabilities of the Arm, Shoulder, and Hand questionnaire in Spanish (DASHe). Results: Sixteen nTOS patients received surgery with one bilateral procedure (17 procedures). Seventy-five percent were females with a median age of 53 years. Obesity and smoking were observed in 43.75% and 37.5% of patients, respectively. No postoperative complications occurred, except for one partial phrenic nerve palsy. All patients reduced their DASHe scores after surgery (mean reduction 41.09 ± 18.37). Conclusion: Our modified supraclavicular approach for scalenotomy is safe and improves outcomes in patients with nTOS, reducing the need for FRR

Phenotype of Peripheral NK Cells in Latent, Active, and Meningeal Tuberculosis

The mechanisms underlying the immunopathology of tuberculous meningitis (TBM), the most severe clinical form of extrapulmonary tuberculosis (TB), are not understood. It is currently believed that the spread of Mycobacterium tuberculosis (Mtb) from the lung is an early event that occurs before the establishment of adaptive immunity. Hence, several innate immune mechanisms may participate in the containment of Mtb infection and prevent extrapulmonary disease manifestations. Natural killer (NK) cells participate in defensive processes that distinguish latent TB infection (LTBI) from active pulmonary TB (PTB). However, their role in TBM is unknown. Here, we performed a cross-sectional analysis of circulating NK cellCID="C008" value="s" phenotype in a prospective cohort of TBM patients (n=10) using flow cytometry. Also, we addressed the responses of memory-like NK cell subpopulations to the contact with Mtb antigens in vitro. Finally, we determined plasma levels of soluble NKG2D receptor ligands in our cohort of TBM patients by enzyme-linked immunosorbent assay (ELISA). Our comparative groups consisted of individuals with LTBI (n=11) and PTB (n=27) patients. We found that NK cells from TBM patients showed lower absolute frequencies, higher CD69 expression, and poor expansion of the CD45RO+ memory-like subpopulation upon Mtb exposure in vitro compared to LTBI individuals. In addition, a reduction in the frequency of CD56brightCD16- NK cells characterized TBM patients but not LTBI or PTB subjects. Our study expands on earlier reports about the role of NK cells in TBM showing a reduced frequency of cytokine-producing cells compared to LTBI and PTB