Interorgan communication in neurogenic heterotopic ossification: the role of brain-derived extracellular vesicles

Brain-derived extracellular vesicles participate in interorgan communication after traumatic brain injury by transporting pathogens to initiate secondary injury.Inflammasome-related proteins encapsulated in brain-derived extracellular vesicles can cross the blood‒brain barrier to reach distal tissues.These proteins initiate inflammatory dysfunction,such as neurogenic heterotopic ossification.This recurrent condition is highly debilitating to patients because of its relatively unknown pathogenesis and the lack of effective prophylactic intervention strategies.Accordingly,a rat model of neurogenic heterotopic ossification induced by combined traumatic brain injury and achillotenotomy was developed to address these two issues.Histological examination of the injured tendon revealed the coexistence of ectopic calcification and fibroblast pyroptosis.The relationships among brain-derived extracellular vesicles,fibroblast pyroptosis and ectopic calcification were further investigated in vitro and in vivo.Intravenous injection of the pyroptosis inhibitor Ac-YVAD-cmk reversed the development of neurogenic heterotopic ossification in vivo.The present work highlights the role of brain-derived extracellular vesicles in the pathogenesis of neurogenic heterotopic ossification and offers a potential strategy for preventing neurogenic heterotopic ossification after traumatic brain injury.

Research Progress of Acupuncture Treatment of Neurogenic Bladder after Spinal Cord Injury

Neurogenic bladder (NB) mainly occurs in patients with spinal cord injury (SCI). The pathological basis of NB is the occurrence of lesions in the urination control center, which requires systematic treatment. Western medicine has many treatment methods for this disease, which can alleviate the symptoms of the disease. However, the radical effect is not ideal and there are many adverse reactions. In comparison, acupuncture can improve the residual urine volume of NB patients and regulate the related indexes of urodynamics. There are many kinds of acupuncture therapies, such as simple acupuncture and moxibustion, which can comprehensively improve the therapeutic effect and obtain a better disease prognosis. Therefore, this article elaborates on the pathogenesis of SCI complicated with NB, the treatment mechanism, and treatment methods of acupuncture and moxibustion to provide a reference for clinical treatment.

Rehabilitation care of patients with neurogenic bladder after spinal cord injury:A literature review

This article reviews the research progress of rehabilitation treatment and nursing care of patients with neurogenic bladder after spinal cord injury,in order to provide reference for the rehabilitation treatment and nursing care of patients.We reviewed recent medical literature on patients with neurogenic bladder,focusing on neurogenic bladder caused by spinal cord injury.We analyzed 30 recent of publications in patients with neurogenic bladder after spinal cord injury,in addition to reviewing and evaluating the commonly used rehabilitation nursing methods for neurogenic bladder.Psychological counseling is a vital aspect which cannot be neglected in the process of neurogenic bladder rehabilitation.Hitherto,the commonly used drug and surgical treatments may have negatively impacted the mental health of patients in varying degrees.However,in clinical practice,applying intermittent catheterization in patients who have neurogenic bladder with spinal cord injury may help improve patients’life quality,mitigate psychological burden,and reduce negative emotions.

MLL1 inhibits the neurogenic potential of SCAPs by interacting with WDR5 and repressing HES1

Mesenchymal stem cell(MSC)-based therapy has emerged as a promising treatment for spinal cord injury(SCI),but improving the neurogenic potential of MSCs remains a challenge.Mixed lineage leukemia 1(MLL1),an H3K4me3 methyltransferases,plays a critical role in regulating lineage-specific gene expression and influences neurogenesis.In this study,we investigated the role and mechanism of MLL1 in the neurogenesis of stem cells from apical papilla(SCAPs).We examined the expression of neural markers,and the nerve repair and regeneration ability of SCAPs using dynamic changes in neuron-like cells,immunofluorescence staining,and a SCI model.We employed a coimmunoprecipitation(Co-IP)assay,real-time RT-PCR,microarray analysis,and chromatin immunoprecipitation(ChIP)assay to investigate the molecular mechanism.The results showed that MLL1 knock-down increased the expression of neural markers,including neurogenic differentiation factor(NeuroD),neural cell adhesion molecule(NCAM),tyrosine hydroxylase(TH),βIII-tubulin and Nestin,and promoted neuron-like cell formation in SCAPs.In vivo,a transplantation experiment showed that depletion of MLL 1 in SCAPs can restore motor function in a rat SCI model.MLL1 can combine with WD repeat domain 5(WDR5)and WDR5 inhibit the expression of neural markers in SCAPs.MLL1 regulates Hairy and enhancer of split 1(HES1)expression by directly binds to HES1 promoters via regulating H3K4me3 methylation by interacting with WDR5.Additionally,HES1 enhances the expression of neural markers in SCAPs.Our findings demonstrate that MLL1 inhibits the neurogenic potential of SCAPs by interacting with WDR5 and repressing HES1.These results provide a potential therapeutic target for promoting the recovery of motor function in SCI patients.

Survey of spinal cord injury-induced neurogenic bladder studies using the Web of Science

OBJECTIVE：To identify global trends in research on spinal cord injury-induced neurogenic bladder, through a bibliometric analysis using the Web of Science. DATA RETRIEVAL：We performed a bibliometric analysis of studies on spinal cord injury-induced neurogenic bladder using the Web of Science.Data retrieval was performed using key words＂spinal cord injury＂,＂spinal injury＂,＂neurogenic bladder＂,＂neuropathic bladder＂,＂neurogenic lower urinary tract dysfunction＂,＂neurogenic voiding dysfunction＂,＂neurogenic urination disorder＂and ＂neurogenic vesicourethral dysfunction＂. SELECTION CRITERIA：Inclusion criteria：（a）published peer-reviewed articles on spinal cord injury-induced neurogenic bladder indexed in the Web of Science;（b）type of articles：original research articles and reviews;（c）year of publication：no limitation.Exclusion criteria：（a）articles that required manual searching or telephone access;（b）Corrected papers and book chapters. MAIN OUTCOME MEASURES：（1）Annual publication output;（2）distribution according to journals; （3）distribution according to subject areas;（4）distribution according to country;（5）distribution according to institution;and（6）top cited publications. RESULTS：There were 646 research articles addressing spinal cord injury-induced neurogenic bladder in the Web of Science.Research on spinal cord injury-induced neurogenic bladder was found in the Science Citation Index-Expanded as of 1946.The United States,Ireland and Switzerland were the three major countries contributing to studies in spinal cord injury-induced neurogenic bladder in the 1970s.However,in the 1990s,the United States,the United Kingdom,the Netherlands,Germany and Japan published more papers on spinal cord injury-induced neurogenic bladder than Switzerland,and Ireland fell off the top ten countries list.In this century,the United States ranks first in spinal cord injury-induced neurogenic bladder studies,followed by France,the United Kingdom,Germany,Switzerland and Japan.Subject categories including urology, nephrology and clinical neurology,as well as rehabilitation,are represented in spinal cord injury-induced neurogenic bladder studies. CONCLUSION：From our analysis of the literature and research trends,we conclude that spinal cord injury-induced neurogenic bladder is a hot topic that will continue to generate considerable research interest in the future.

Experimental study on the regulation effect of Qiaoqin Qingfei agent on cough variant asthma based on airway neurogenic inflammation

Objective:To investigate the mechanism of regulation of airway neurogenic inflammation by Qiaoqin Qingfei agent in rats with cough variant asthma(CVA).Methods:48 SD rats were randomly divided into blank group,model group,montelukast sodium group(1.05 mg/kg)and high,medium and low dose groups(26,13,6.5 g/kg),with 8 rats in each group.The rat CVA model was established by the method of ovalbumin(OVA)combined with aluminum hydroxide(Al(OH)3)sensitization and repeated stimulation.From the second day of sensitization,the rat CVA model was given by gavage for 28 days.The pathological changes of lung tissue were observed under microscope by HE staining.The content changes of nerve growth factor(NGF)and substance P(SP)in alveolar lavage fluid(BALF)were determined by double-antibody sandwich ABC-ELISA,and the protein expression levels of NGF and SP in lung tissue were detected by immunohistochemistry.Results:Pathological findings showed significant inflammatory manifestations in the model group,and the inflammatory infiltration in the high-dose,medium-dose and low-dose groups of Qiaoqin Qingfei agent and montelukast sodium groups were alleviated to varying degrees.Compared with blank group,the protein expression levels of NGF and SP in lung tissue of model group were significantly increased(P<0.01).Compared with model group,the protein expression levels of NGF and SP in lung tissue and the contents of NGF and SP in alveolar lavage fluid in high-dose,medium-dose and low-dose groups and montelukast sodium group were significantly decreased(P<0.05).Conclusion:Qiaoqin Qingfei agent may reduce airway inflammation and relieve cough variant asthma by regulating the protein expression levels of NGF and SP in airway neurogenic inflammation.

Neurogenic bowel dysfunction in patients with spinal cord injury, myelomeningocele, multiple sclerosis and Parkinson’s disease

Exciting new features have been described concerning neurogenic bowel dysfunction,including interactions between the central nervous system,the enteric nervous system,axonal injury,neuronal loss,neurotransmission of noxious and non-noxious stimuli,and the fields of gastroenterology and neurology.Patients with spinal cord injury,myelomeningocele,multiple sclerosis and Parkinson's disease present with serious upper and lower bowel dysfunctions characterized by constipation,incontinence,gastrointestinal motor dysfunction and altered visceral sensitivity.Spinal cord injury is associated with severe autonomic dysfunction,and bowel dysfunction is a major physical and psychological burden for these patients.An adult myelomeningocele patient commonly has multiple problems reflecting the multisystemic nature of the disease.Multiple sclerosis is a neurodegenerative disorder in which axonal injury,neuronal loss,and atrophy of the central nervous system can lead to permanent neurological damage and clinical disability.Parkinson's disease is a multisystem disorder involving dopaminergic,noradrenergic,serotoninergic and cholinergic systems,characterizedby motor and non-motor symptoms.Parkinson's disease affects several neuronal structures outside the substantia nigra,among which is the enteric nervous system.Recent reports have shown that the lesions in the enteric nervous system occur in very early stages of the disease,even before the involvement of the central nervous system.This has led to the postulation that the enteric nervous system could be critical in the pathophysiology of Parkinson's disease,as it could represent the point of entry for a putative environmental factor to initiate the pathological process.This review covers the data related to the etiology,epidemiology,clinical expression,pathophysiology,genetic aspects,gastrointestinal motor dysfunction,visceral sensitivity,management,prevention and prognosis of neurogenic bowel dysfunction patients with these neurological diseases.Embryological,morphological and experimental studies on animal models and humans are also taken into account.

Diet in neurogenic bowel management:A viewpoint on spinal cord injury

The aim of this review is to offer dietary advice for individuals with spinal cord injury(SCI)and neurogenic bowel dysfunction.With this in mind,we consider health conditions that are dependent on the level of lesion including skeletal muscle atrophy,autonomic dysreflexia and neurogenic bladder.In addition,SCI is often associated with a sedentary lifestyle,which increases risk for osteoporosis and diseases associated with chronic low-grade inflammation,including cardiovascular and chronic kidney diseases.The Mediterranean diet,along with exercise and dietary supplements,has been suggested as an anti-inflammatory intervention in individuals with SCI.However,individuals with chronic SCI have a daily intake of whole fruit,vegetables and whole grains lower than the recommended dietary allowance for the general population.Some studies have reported an increase in neurogenic bowel dysfunction symptoms after high fiber intake;therefore,this finding could explain the low consumption of plant foods.Low consumption of fibre induces dysbiosis,which is associated with bothendotoxemia and inflammation.Dysbiosis can be reduced by exercise and diet in individuals with SCI.Therefore,to summarize our viewpoint,we developed a Mediterranean diet-based diet and exercise pyramid to integrate nutritional recommendations and exercise guidelines.Nutritional guidelines come from previously suggested recommendations for military veterans with disabilities and individuals with SCI,chronic kidney diseases,chronic pain and irritable bowel syndrome.We also considered the recent exercise guidelines and position stands for adults with SCI to improve muscle strength,flexibility and cardiorespiratory fitness and to obtain cardiometabolic benefits.Finally,dietary advice for Paralympic athletes is suggested.

Long-term anodal block stimulation at sacral anterior roots promoted recovery of neurogenic bladder function in a rabbit model of complete spinal cord injury

A complete spinal cord injury model was established in experimental rabbits using the spinal cord clip compression method. Urodynamic examination was performed 2 weeks later to determine neurogenic bladder status. The rabbits were treated with anodal block stimulation at sacral anterior roots for 4 weeks. Electrical stimulation of sacral anterior roots improved urodynamic parameters of neurogenic bladder in rabbit models of complete spinal cord injury, effectively promoted urinary function, and relieved urinary retention. Immunohistochemistry results showed that a balance was achieved among expression of muscarinic receptor subunits M2, M3, ATP-gated ion channel P2X3 receptors, and 132-adrenergic receptor, and nerve growth factor expression decreased. These results suggested that long-term sacral anterior root stimulation of anodal block could＇be used to treat neurogenic bladder in a rabbit model of complete spinal cord injury.

Bibliometric profile of neurogenic bladder in the literature:a 20-year bibliometric analysis

Neurogenic bladder is a dysfunction of the lower urinary tract caused by nervous system disor- der. We investigated the trends in publication of articles under the topic ＂neurogenic bladder＂ using bibliometric analysis. Articles on neurogenic bladder, published between 1995 and 2014, were retrieved from the ISI Web of Science citation database. We analyzed the search results for authors, countries, institutions, journals, and top-cited papers. A total of 1,904 articles were re- trieved. There was a small increase in the number of articles on neurogenic bladder from 1995 （n = 43） to 2014 （n = 117）. The USA was the leading country in the total number of articles （n = 598）. However, the number of publications from China has rapidly increased, and China was ranked second in 2014. Emmanuel Chartier-Kastler （n = 65） was the most productive author, and University of Paris VI （Paris 6） （n = 61） was the most productive institution. The Journal of Urology published the greatest number of artides on this topic （n = 285）. Articles on neurogenic bladder were often published in a professional journal under the category Urology ＆ Nephrology, Neurosciences ＆ Neurology, or Rehabilitation. Visualization analysis based on co-citation networks was conducted using CiteSpace III. Visualization analysis revealed that the hot spots in neurogenic bladder were botulinum toxin-A, prazosin, bethanechol, and afferent pathways. These findings provide new insight into the publication trends and hot spots in neurogenic bladder.

Curative effect assessment of bandage contact lens in neurogenic keratitis

AIM: To observe the curative effect of bandage contact lens in neurogenic keratitis.METHODS: Twenty cases of neurogenic keratitis were studied at the Department of Ophthalmology, the First Affiliated Hospital of China Medical University, between October 2012 and June 2013. These included 13 males and 7 females, aged from 35 to 88 y. Patients were voluntarily divided into an experimental group(lens wearing group, n =10) and control group(drug therapy,n =10). In experimental group patients wore silicone hydrogel bandage soft contact lens. Both groups used the following eyedrops: 0.5% levofloxacin TID; 0.5%Sodium carboxymethyl cellulose QID; fibroblast growth factor BID; ganciclovir BID [cases complicated with herpes simplex virus(HSV)]; compound tropicamide BID(cases concurrent hypopyon). The healing time of corneal ulcer and complication rates were observed in the two groups.RESULTS: The healing time of corneal ulcer in the experimental group was 10.80±4.44 d versus 46.70±13.88 d in the control group(P 【0.05). No complications occurred in the experimental group, except for the lens falling off twice in one case, the patient recovered eight days after rewearing the lens. While in the control group, all cases vascularized, 2 cases were complicated with descemetocele that recovered with amniotic membrane transplantation and 1 case was complicated with corneal perforation that recovered by autologous conjunctival flap covering.CONCLUSION: Bandage contact lens is a safe and effective method of treating neurogenic keratitis andsignificantly shortened the healing time of corneal ulcer.

Clinical characteristics and treatment of severe encephalitis associated with neurogenic pulmonary edema caused by enterovirus 71 in China

BACKGROUND： Hand-foot-mouth disease has become a major public health issue in children in China. In the present prospective study we investigated the clinical characteristics and emergency management of children with severe encephalitis associated with NPE caused by enterovirus 71.METHODS： The study was conducted in 2 pediatric intensive care units （PICUs） over a 2-month period. Clinical records were reviewed of critically ill children with severe encephalitis associated with NPE caused by EV71 who were admitted to PICUs during the period of May to June 2008 in Fuyang.RESULTS： We reviewed the complete records of 36 children, of whom 23 （63.9%） were male and 13 （36.1%） female. Their age ranged from 4 to 48 months, with an average of 15.8 months. All children except one were under 3 years of age. The overall mortality in these children was 19.4%. The average duration of critical life threatening signs and symptoms was 2.1 days （12 hours-5 days）. Nervous system diseases included brainstem encephalitis in 27 children （75%）, brainstem encephalitis associated with myelitis in 6 children （16.7%）, and general encephalitis in 3 chidren （8.3%）, respectively. In 12 patients of NPE （33.3%） pink or bloody bubble sputum and asymmetric pulmonary edema or hemorrhage was the primary manifestation but no typical exanthema was observed. Five children died of acute onset of NPE and / or pulmonary hemorrhage with rapid progression of cardiopulmonary failure within hours after admission. Therapeutic management consisted of mechanical ventilation and administration of mannitol, methylprednisolone, intravenous immunoglobulin （IVIG） and vasoactive drugs, associated with the need of fluid volume resuscitation in 9 （25%） of the 36 children.CONCLUSION： In children less than 3 years of age found to be affected by severe EV71 encephalitis associated with NPE, one fifth may die. The major organ systems infected by severe EV71 include the central nervous system, the respiratory system, and the cardiovascular system. Early diagnosis and evaluation, respiratory support, treatment of intracranial hypertension, and mainttenance of function of the cardiovascular system are the most important therapeutic measures.

Midline synovial and ganglion cysts causing neurogenic claudication

Typically situated posterolateral in the spinal canal, intraspinal facet cysts often cause radicular symptoms. Rarely, the midline location of these synovial or ganglion cysts may cause thecal sac compression leading to neurogenic claudication or cauda equina syndrome. This article summarizes the clinical presentation, radiographic appearance, and management of three intraspinal, midline facet cysts. Three patients with symptomatic midline intraspinal facet cysts were retrospectively reviewed. Documented clinical visits, operative notes, histopathology reports, and imaging findings were investigated for each patient. One patient presented with neurogenic claudication while two patients developed partial, subacute cauda equina syndrome. All 3 patients initially responded favorably to lumbar decompression and midline cyst resection; however, one patient required surgical stabilization 8 mo later. Following the three case presentations, we performed a thorough literature search in order to identify articles describing intraspinal cystic lesions in lateral or midline locations. Midline intraspinal facet cysts represent an uncommon cause of lumbar stenosis and thecal sac compression. Such entities should enter the differential diagnosis of midline posterior cystic lesions. Midline cysts causing thecal sac compression respond favorably to lumbar surgical decompression and cyst resection. Though laminectomy is a commonly performed operation, stabilization may be required in cases of spondylolisthesis or instability.

Neurogenic nitric oxide facilitates the central nociceptive transmission of migraine attacks

Recent studies have shown that nitric oxide （NO） can induce migraine attacks at three possible sites of action： nitroxidergic nerves, the vascular endothelium, and the central nervous system. Most previous studies have focused on the former two sites of action. Several experiments using exogenic NO donors have suggested that nitroglycerin may induce migraine via central mechanisms. However, few studies have investigated the source of the NO involved in the central mechanisms of migraine. The present study used a cat model of migraine to represent migraine attacks in humans. We performed immunochemical staining of successive frozen sections of the brainstem and upper cervical spinal cord, and then used c-Fos protein expression to label nerve cell activation. We observed the effects of N^ω-nitro-L-arginine methyl ester （L-NAME）, a non-selective nitric oxide synthase （NOS） inhibitor, and 7-nitroindozole （7-NI）, a selective neuronal NOS inhibitor, on c-Fos and nNOS expression, which were induced by electrical stimulation to the dura mater near the superior sagittal sinus. The results demonstrated that c-Fos or nNOS immunoreactive cells was concentrated in the superficial layers （laminae Ⅰ and Ⅱ） of the spinal nucleus of trigeminal nerve. L-NAME and 7-NI pre-treatment significantly decreased c-Fos and neurogenic NOS expression; and there was a significant linear correlation between c-Fos and NOS expression （r = 0.858 2, P 〈 0.01）. These findings suggest that neurogenic NO could facilitate migraine nociceptive transmission to second-order neurons of the trigeminal nerve. However, L-NAME and 7-NI may block the activation of neurons in the spinal nucleus of the trigeminal nerve by inhibiting NO synthesis, and thereby attenuate acute migraine attacks.

Do neural precursor cells exist in a distal neurogenic region following cerebral hemorrhage?

BACKGROUND： Cerebral injury in adult mammals can induce neural precursor cells （NPCs） to proliferate and migrate towards the focal zone, but it is unclear whether endogenous NPCs can migrate towards regions distal to the hemorrhagic focus or whether NPCs differentiate in the peripheral hemorrhagic region. OBJECTIVE： To investigate the distribution of endogenous NPCs in different brain regions of rats with experimental cerebral hemorrhage, as well as NPC proliferation and differentiation with time. DESIGN, TIME AND SE＇B＇ING： A randomized, controlled animal experiment was performed at the Department of Neurobiology, Luzhou Medical College, between January 2007 and October 2008. MATERIALS： Bromodeoxyuridine （BrdU） was purchased from Roche, Germany. Mouse anti-rat BrdU monoclonal antibody, rabbit anti-nestin polyclonal antibody, rabbit anti-neuron specific enolase （NSE） polyclonal antibody were purchased from Wuhan Boster, China. Rabbit anti-glial fibrillary acidic protein （GFAP） polyclonal antibody was purchased from Sigma, USA. METHODS： Thirty-five adult Sprague Dawley rats were randomly divided into three groups： （1） cerebral hemorrhage group （n = 25）, rats were stereotaxically administered 50 p L autologous arterial blood via the dorsal caudate putamen to induce cerebral hemorrhage; （2） sham-surgery group （n = 5）, rats underwent surgery but did not receive blood injection; （3） blank control group （n = 5）, rats received no surgery and blood administration. At 2 hours after surgery, all rats were intraperitoneally administered BrdU. MAIN OUTCOME MEASURES： Distribution and proliferation of BrdU-positive cells were observed by immunohistochemical staining. BrdU-positive cell differentiation into neurons and glial cells in the peripheral hemorrhagic region was detected by double-label immunofluorescence. RESULTS： Immunohistochemistry results revealed that BrdU-positive cells existed not only in the peripheral hemorrhagic region, such as the subependymal layer and hippocampal dentate gyrus, but also in the lateral septal nucleus, diagonal band, habenular nucleus, and cerebral cortex. Following cerebral hemorrhage, BrdU-positive cells in the peripheral hemorrhagic region gradually increased （P 〈 0.05）, and peaked at 7 14 days. Double-label immunofluorescence showed that with time after cerebral hemorrhage, BrdU/nestin-positive cells decreased, but BrdU/GFAP- and BrdU/NSE-positive cells increased in the peripheral cerebral hemorrhagic region （P 〈 0.05）. CONCLUSION： Cerebral hemorrhage can induce the proliferation of endogenous NPCs, which peaks at 1-2 weeks after hemorrhage. NPCs can also migrate towards the regions distal to the hemorrhagic focus, such as a diagonal band or lateral septal nucleus. NPCs can gradually differentiate with increasing time after hemorrhage.

TAZ and myostatin involved in muscle atrophy of congenital neurogenic clubfoot

BACKGROUND Muscular atrophy is the basic defect of neurogenic clubfoot.Muscle atrophy of clubfoot needs more scientific and reasonable imaging measurement parameters to evaluate.The Hippo pathway and myostatin pathway may be directly correlated in myogenesis.In this study,we will use congenital neurogenic clubfoot muscle atrophy model to verify in vivo.Further,the antagonistic mechanism of TAZ on myostatin was studied in the C2C12 cell differentiation model.AIM To identify muscle atrophy in fetal neurogenic clubfoot by ultrasound imaging and detect the expression of TAZ and myostatin in gastrocnemius muscle.To elucidate the possible mechanisms by which TAZ antagonizes myostatin-induced atrophy in an in vitro cell model.METHODS Muscle atrophy in eight cases of fetal unilateral clubfoot with nervous system abnormalities was identified by 2D and 3D ultrasound.Western blotting and immunostaining were performed to detect expression of myostatin and TAZ.TAZ overexpression in C2C12 myotubes and the expression of associated proteins were analyzed by western blotting.RESULTS The maximum cross-sectional area of the fetal clubfoot on the varus side was reduced compared to the contralateral side.Myostatin was elevated in the atrophied gastrocnemius muscle,while TAZ expression was decreased.They were negatively correlated.TAZ overexpression reversed the diameter reduction of the myotube,downregulated phosphorylated Akt,and increased the expression of forkhead box O4 induced by myostatin.CONCLUSION Ultrasound can detect muscle atrophy of fetal clubfoot.TAZ and myostatin are involved in the pathological process of neurogenic clubfoot muscle atrophy.TAZ antagonizes myostatin-induced myotube atrophy,potentially through regulation of the Akt/forkhead box O4 signaling pathway.

Outcomes of bowel program in spinal cord injury patients with neurogenic bowel dysfunction

In this study, we aimed to determine gastrointestinal problems associated with neurogenic bowel dysfunction in spinal cord injury patients and to assess the efficacy of bowel program on gastrointestinal problems and the severity of neurogenic bowel dysfunction. Fifty-five spinal cord injury patients were included in this study. A bowel program according to the characteristics of neurogenic bowel dysfunction was performed for each patient. Before and after bowel program, gastrointestinal problems（constipation, difficult intestinal evacuation, incontinence, abdominal pain, abdominal distension, loss of appetite, hemorrhoids, rectal bleeding and gastrointestinal induced autonomic dysreflexia） and bowel evacuation methods（digital stimulation, oral medication, suppositories, abdominal massage, Valsalva maneuver and manual evacuation） were determined. Neurogenic bowel dysfunction score was used to assess the severity of neurogenic bowel dysfunction. At least one gastrointestinal problem was identified in 44（80%） of the 55 patients before bowel program. Constipation（56%, 31/55） and incontinence（42%, 23/55） were the most common gastrointestinal problems. Digital rectal stimulation was the most common method for bowel evacuation, both before（76%, 42/55） and after（73%, 40/55） bowel program. Oral medication, enema and manual evacuation application rates were significantly decreased and constipation, difficult intestinal evacuation, abdominal distention, and abdominal pain rates were significantly reduced after bowel program. In addition, mean neurogenic bowel dysfunction score was decreased after bowel program. An effective bowel program decreases the severity of neurogenic bowel dysfunction and reduces associated gastrointestinal problems in patients with spinal cord injury.

Neurogenic orthostatic hypotension with Parkinson's disease as a cause of syncope:A case report

BACKGROUND Syncope presents with diagnostic challenges and is associated with high healthcare costs.Neurogenic orthostatic hypotension(nOH)as one cause of syncope is not well established.We review a case of syncope caused by nOH in a patient with Parkinson's disease.CASE SUMMARY We describe a case of syncope caused by nOH in Parkinson's disease and review the literature.A 70-year-old man with Parkinson's disease had uncontrolled blood pressure for 1 mo,with blood pressure ranging from 70/40 to 220/112 mmHg,and once lost consciousness lasting for several minutes after getting up.Ambulatory blood pressure monitoring indicated nocturnal hypertension(up to 217/110 mmHg)and morning orthostatic hypotension(as low as 73/45 mmHg).Seated-to-standing blood pressure measurement showed that the blood pressure dropped from 173/96 mmHg to 95/68 mmHg after standing for 3 min from supine position.A diagnosis of nOH with supine hypertension was made.During the course of treatment,Midodrine could not improve the symptoms.Finally,the patient's blood pressure stabilized with simple strategies by strengthening exercises,reducing the duration of lying in bed in the daytime,and consuming water intake before getting up.CONCLUSION nOH is one of the causes of syncope.Ambulatory blood pressure monitoring is a cost-effective method for its diagnosis,and non-pharmacological measures are still the primary management methods.

How botulinum toxin in neurogenic detrusor overactivity can reduce upper urinary tract damage?

Intradetrusor injections of botulinum toxin are the cornerstone of medical treatment of neurogenic detrusor overactivity. The primary aim of this treatment is to ensure a low pressure regimen in the urinary bladder, but the mechanisms leading to long-term protection of the urinary tract remain poorly understood. In this paper, we highlight the potential benefts of intradetrusor injections of botulinum toxin regarding local effects on the bladder structures, urinary tract infections, stone disease, vesico ureteral refux, hydronephrosis, renal function based on a comprehensive literature review.

Giant neurogenic tumors of mediastinum: report of two cases and literature review

Neurogenic tumors are commonly found in the mediastinum, especially in the posterior mediastinum or in the chest wall, neurogenic tumors may reach large size before becoming symptomatic. If the neurogenic tumor occupied more than half size of the chest wall accompanied by mediastinal shift, tracheal compression, or superior vena reflux disorder, it may be called giant intrathoracic neurogenic tumors. Giant intrathoracic neurogenic tumors are relatively rare. Most of intrathoracic neurogenic tumors were benign or low-grade malignant tumors in nature. Complete surgical excision should be the rule for these patients. We report two cases of giant neurogenic tumors, and study the clinical manifestations, diagnostic methods, surgical management, and prognosis in the light of the most important published data.