Objective Observe the injuries to the cranial nerves in cases of brain stem injury following head trauma;explore the mechanism of injuries and their relations to the mode and point of impact on the head. Method Brain stem specimens of 465 cases of head trauma were designed to take cross sections at the roots of the 3rd～12th cranial nerves. Among the 465 cases, 171 were proven to have contusion of the brain stem. On these cases, the cranial nerves were observed meticulously. Results Cranial nerve injuries were found in all cases suffering from brain stem contusion. The nerves included were: oculomotor nerve (120 cases, 70.2%), facial and acoustic nerve (92 cases, 53.8%), trigeminal nerve (85 cases, 49.7%), abducent nerve (45 cases, 26.3%), hypoglossal nerve (31 cases, 18.1%), vagus nerve (27 cases, 15.8%), glosso-pharyngeal nerve (24 cases, 14.0%), and trochlear nerve and accessory nerve (10 cases each, 5.8%). The nerve injuries may be unilateral or bilateral, involving single or multiple nerves in a case. The pathological changes included hemorrhage (42 cases, 24.6%), edema (26 cases, 15.2%), structural deformation at the root of the nerves (71 cases, 41.5%), tear of the nerve roots (32 cases, 18.7%). Conclusion Cranial nerve injury is an important part of the cranio-cerebral injury, and also an accompaniment of the brain stem injury. The features of interesting in the injuries were the higher frequencies in the nerves at the upper level and the nerves of larger diameter; of highest frequency were oculomotor nerve, facial nerve and acoustic nerve.

Objective To investigate the clinical manifestation, inherited pattern and the related factor of Hunting?ton disease families. Method The clinical data from 12 HD families was collected from 2013-2014. Patients received the genetic test and neurological evaluation including motor, cognitive and problem of behavior. Results There were 12 patients having the IT15 gene dynamic mutations, including 1 Juvenile Huntington disease patient and 3 pre-symptomat?ic mutant gene carriers. The average CAG repeats of these patients was between the range of 40 to 60, and the average on?set age ranged from 13 to 54 year-old. Positive family history and genetic anticipation could be observed. Patients pre?sented with different clinical manifestations at the early stage while had typical chorea movements, declined cognitive and psychiatric symptoms at the late stage of the illness. Conclusions There are typical triad symptoms in the late stage but not in the early stage nor pre-symptom stage illness. Clinical manifestation and the neuroimaging are both of great ref?erence value, and the genetic test is essential for final diagnosis.

OBJECTIVEPsoriasis is an autoimmune-related chronic inflammatory skin disease strongly associated with the dysfunction of Th17 cells. Retinoic acid-related orphan nuclear receptor γt (RORγt) plays a critical role in the differentiation and maturation of Th17 cells and in cell-derived immunologic derangement. We conducted this study to investigate potential mechanism by which the derivative of digoxin selectively antagonizes RORγt transcriptional activity.

METHODUsing molecular docking in combination with molecular electrostatic potential (MEP), we detected the interaction between the derivative of digoxin (Dhd) and ROR transcription factor (RORα,RORβ and RORγt), and the results were further confirmed by bioluminescent assay.

RESULTMolecular docking demonstrated that Dhd could exclusively inhibit the conformation of RORγt; bioluminescent assay further indicated that RORγt was selectively antagonized by Dhd in a dose- and time-dependent manner.

CONCLUSIONDhd can selectively suppress RORγt transcriptional activity.

Digoxin ; analogs & derivatives ; pharmacology ; Humans ; Models, Chemical ; Molecular Docking Simulation ; Nuclear Receptor Subfamily 1, Group F, Member 1 ; antagonists & inhibitors ; genetics ; Transcription, Genetic

Objetive Psoriasis is an autoimmune-related chronic inflammatory skin disease strongly associated with the dysfunction of Th17 cells. Retinoic acid-related orphan nuclear receptorγt (RORγt) plays a critical role in the differentiation and maturation of Th17 cells and in cell-derived immunologic derangement. We conducted this study to investigate potential mechanism by which the derivative of digoxin selectively antagonizes RORγt transcriptional activity. Method Using molecular docking in combination with molecular electrostatic potential (MEP), we detected the interaction between the derivative of digoxin (Dhd) and ROR transcription factor (RORα,RORβ and RORγt), and the results were further confirmed by bioluminescent assay. Result Molecular docking demonstrated that Dhd could exclusively inhibit the conformation of RORγt;bioluminescent assay further indicated that RORγt was selectively antagonized by Dhd in a dose- and time-dependent manner. Conclusion Dhd can selectively suppress RORγt transcriptional activity.

Objetive Psoriasis is an autoimmune-related chronic inflammatory skin disease strongly associated with the dysfunction of Th17 cells. Retinoic acid-related orphan nuclear receptorγt (RORγt) plays a critical role in the differentiation and maturation of Th17 cells and in cell-derived immunologic derangement. We conducted this study to investigate potential mechanism by which the derivative of digoxin selectively antagonizes RORγt transcriptional activity. Method Using molecular docking in combination with molecular electrostatic potential (MEP), we detected the interaction between the derivative of digoxin (Dhd) and ROR transcription factor (RORα,RORβ and RORγt), and the results were further confirmed by bioluminescent assay. Result Molecular docking demonstrated that Dhd could exclusively inhibit the conformation of RORγt;bioluminescent assay further indicated that RORγt was selectively antagonized by Dhd in a dose- and time-dependent manner. Conclusion Dhd can selectively suppress RORγt transcriptional activity.

Background::Arterial stiffening increases with age and blood pressure and is associated with cardiovascular disease (CVD), but the relationship between blood pressure lowering and arterial stiffening is still uncertain, especially in older people. This study aimed to evaluate the effect of intensive blood pressure treatment on the progression of arterial stiffness and risk of CVD in older patients with hypertension.Methods::The Strategy of Blood Pressure Intervention in the Elderly Hypertensive Patients (STEP) trial was a multicenter, randomized, controlled trial performed at 42 clinical centers throughout China, and 8511 patients aged 60–80 years with essential hypertension were enrolled and randomly assigned to systolic blood pressure (SBP) target of 110 mmHg to <130 mmHg (intensive treatment) or 130 mmHg to <150 mmHg (standard treatment). Patients underwent repeated examinations of the brachial-ankle pulse wave velocity (baPWV) and ankle-brachial index (ABI) at baseline, and the arterial stiffness was evaluated at the 3-year follow-up. A total of 5339 patients who had twice repeated measurements were included in this study. Changes in arterial stiffness between the intensive and standard treatment groups were analyzed using a multivariate linear regression model. The Cox proportional hazard regression model was used to evaluate the effect of intensive treatment on primary CVD outcomes.Results::The changes in baPWV were 61.5 cm/s (95% confidence interval [CI]: 49.8–73.2 cm/s) in the intensive treatment group and 98.4 cm/s (95% CI: 86.7–110.1 cm/s) in the standard treatment group ( P <0.001). Intensive treatment significantly delayed the progression of arterial stiffness, with an annual change of 23.1 cm·s –1·year –1vs. 36.7 cm·s –1·year -1 of baPWV in the intensive and standard treatment groups, respectively. During a median follow-up period of 3.36 years, primary CVD outcomes occurred in 77 (2.9%) patients in the intensive treatment group compared with 93 (3.5%) in the standard treatment group. Intensive treatment resulted in a significantly lower CVD risk in patients aged 70–80 years or with SBP <140 mmHg. Conclusion::Intensive blood pressure control with an SBP target of 110 mmHg to <130 mmHg could delay the progression of arterial stiffness and reduce the risk of CVD in older patients with hypertension.Clinical trial registration::http://www.clinicaltrials.gov; No. NCT03015311.