Premigratory neural crest stem cells generate enteric neurons populating the mouse colon and regulating peristalsis in tissue-engineered intestine.

Hirschsprung's disease (HSCR) is a common congenital defect. It occurs when bowel colonization by neural crest-derived enteric nervous system (ENS) precursors is incomplete during the first trimester of pregnancy. Several sources of candidate cells have been previously studied for their capacity to regenerate the ENS, including enteric neural crest stem cells (En-NCSCs) derived from native intestine or those simulated from human pluripotent stem cells (hPSCs).

Insulin-Like Growth Factor-1 Down-Regulates the Phosphorylation of FXYD1 and Rescues Behavioral Deficits in a Mouse Model of Rett Syndrome.

Rett syndrome (RTT) is a neurodevelopmental disease in children that is mainly caused by mutations in the gene, which codes for a transcriptional regulator. The expression of insulin-like growth factor-1 (IGF-1) is reduced in RTT patients and animal models, and IGF-1 treatment is a promising therapeutic strategy for RTT. However, the mechanism underlying the effects of IGF-1 remains to be further explored.

[Research advances in the biomarkers of brain damage in preterm infants].

While the survival rate of preterm infants has continually increased with the development of perinatal and neonatal monitoring techniques, the incidence of brain injury in preterm infants has been increasing, resulting in varying degrees of cognitive impairment and movement disorders. Measuring the biomarkers of brain damage is an important means to diagnose brain injury. The biomarkers can be divided into neuroglial damage markers, neuronal damage markers and other markers according to the features of injured cells.

Evaluation of Whole Blood Trace Element Levels in Chinese Children with Autism Spectrum Disorder.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder, which has increased markedly during the last decades. Essential trace elements play an important role in neurological function and their imbalances are common in children with ASD. The objective of the present study was to investigate whole blood levels of trace elements including zinc (Zn), copper (Cu), iron (Fe), and magnesium (Mg) in Chinese children with ASD.

Heat shock protein 70 downregulation inhibits proliferation, migration and tumorigenicity in hepatocellular carcinoma cells.

The overexpression of heat shock protein 70 (HSP70), a major stress-inducible heat shock protein, has been identified to enhance the proliferation, survival, invasion and metastasis of diverse types of human cancer. However, its role in hepatocellular carcinoma (HCC) remains poorly understood. The present study demonstrated that HSP70 expression was higher in tested HCC cell lines, compared with the normal hepatocyte LO2, and the suppression of HSP70 significantly inhibited the proliferation of SMMC-7721 and Hep3B cells.

Effect of saracatinib on pulmonary metastases from hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Src is involved in multiple processes of cancer metastasis; however, its significance in HCC is not well defined. In the present study, overexpression of Src phosphorylation (Y416) was observed in the highly metastatic MHCC97H cell line; additionally, through inhibition of Src kinase activation, HCC cell proliferation, migration, invasion and colony formation were significantly reduced in vitro.

Clinically mild encephalitis/encephalopathy with a reversible splenial lesion associated with Mycoplasma pneumoniae infection.

Background: Clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) is a clinico-radiological syndrome characterized by transient mild symptoms of encephalopathy and a reversible lesion in the splenium of the corpus callosum on magnetic resonance imaging (MRI). It is often triggered by infection. The common pathogens of MERS are viruses, especially influenza virus.

Novel mutations of the ATP7B gene in Han Chinese families with pre-symptomatic Wilson's disease.

Background: Wilson's disease (WD) is an autosomal recessive genetic disorder of copper metabolism, caused by mutations in the ATP7B gene, resulting in copper accumulation in the liver, brain, kidney, and cornea and leading to significant disability or death if untreated. Early diagnosis and proper therapy usually predict a good prognosis, especially in pre-symptomatic WD. Genetic testing is the most accurate and effective diagnostic method for early diagnosis.

Reversible bilateral striatal lesions following Mycoplasma pneumoniae infection associated with elevated levels of interleukins 6 and 8.

Background: Reversible bilateral striatal necrosis associated with Mycoplasma pneumoniae (M. pneumoniae) infection is a rare neurological disease. The exact pathogenic mechanism remains unknown.

TLR4 signaling is involved in the protective effect of propofol in BV2 microglia against OGD/reoxygenation.

Propofol exhibits neuroprotective effects against hypoxic-ischemic brain injury, but the underlying mechanisms are still not clear. Toll-like receptor 4 (TLR4) plays a considerable role in the induction of innate immune and inflammatory responses. The purposes of this study are to investigate the effect of propofol on the oxygen and glucose deprivation (OGD)/reoxygenation (OGD/R) BV2 microglia and to explore the role of TLR4/myeloid differentiation protein 88 (MyD88)/nuclear factor-kappa B (NF-κB) pathway in the neuroprotective effects of propofol.

Toll-like receptor 4 signaling is involved in PACAP-induced neuroprotection in BV2 microglial cells under OGD/reoxygenation.

Object: The neuroprotective effects of pituitary adenylate cyclise-activating polypeptide (PACAP) have been well documented in vivo and in vitro. However, the mechanisms by which PACAP protected microglia from ischemic/hypoxic injury via inhibition of microglia activation remain unclear. Toll-like receptor 4 (TLR4) plays a considerable role in the induction of innate immune and inflammatory responses.

Exogenous administration of PACAP alleviates traumatic brain injury in rats through a mechanism involving the TLR4/MyD88/NF-κB pathway.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is effective in reducing axonal damage associated with traumatic brain injury (TBI), and has immunomodulatory properties. Toll-like receptor 4 (TLR4) is an important mediator of the innate immune response. It significantly contributes to neuroinflammation induced by brain injury.

Effects of pituitary adenylate cyclase activating polypeptide on CD4(+)/CD8(+) T cell levels after traumatic brain injury in a rat model.

Background: The effect of pituitary adenylate cyclase activating polypeptide (PACAP) during traumatic brain injury (TBI) and whether it can modulate secondary injury has not been reported previously. The present study evaluated the potential protective effects of ventricular infusion of PACAP in a rat model of TBI.

Methods: Male Sprague Dawley rats were randomly divided into 3 treatment groups (n=6, each): sham-operated, vehicle (normal saline)+TBI, and PACAP+TBI.

[Research advance of the protective role of PACAP in the nervous system diseases].

In the central nervous system, pituitary adenylate cyclase-activating polypeptide (PACAP) exerts different actions as neurotransmitter, neuromodulator, neurotrophic and neuroprotective factors via multiple signaling pathways. PACAP plays an important protective role in the nervous system diseases, such as focal cerebral ischemia, traumatic brain injury (TBI), schizophrenia, anxiety disorders Parkinson's disease and Alzheimer's disease. Now, we reviewed the research advances about the protective role of PACAP in the nervous system diseases.

miR-340 inhibition of breast cancer cell migration and invasion through targeting of oncoprotein c-Met.

Background: Different microRNAs have been shown to have oncogenic and tumor-suppressive functions in human cancers. Detection of their expression may lead to identifying novel markers for breast cancer.

Methods: The authors detected miR-340 expression in 4 human breast cell lines and then focused on its role in regulation of tumor cell growth, migration, and invasion and target gene expression.

MiR-339-5p inhibits breast cancer cell migration and invasion in vitro and may be a potential biomarker for breast cancer prognosis.

Background: MicroRNAs (miRNAs) play an important role in the regulation of cell growth, differentiation, apoptosis, and carcinogenesis. Detection of their expression may lead to identifying novel markers for breast cancer.

Methods: We profiled miRNA expression in three breast cancer cell lines (MCF-7, MDA-MB-231, and MDA-MB-468) and then focused on one miRNA, miR-339-5p, for its role in regulation of tumor cell growth, migration, and invasion and target gene expression.

Specific activation of 2'-5'oligoadenylate synthetase gene promoter by hepatitis C virus-core protein: a potential for developing hepatitis C virus targeting gene therapy.

Aim: To examine whether 2'-5'oligoadenylate synthetase (OAS) gene promoter can be specifically activated by hepatitis C virus (HCV)-core protein.

Methods: Human embryo hepatic cell line L02 was transfected with pcDNA3.1-core plasmid and selected by G418.

[Evaluation of right ventricular function by quantitative tissue velocity imaging and tissue tracking imaging in neonates with congenital hypothyroidism].

Objective: Although several reports documented the association of congenital hypothyroidism (CH) and left ventricular (LV) function in infants or neonates, right ventricular (RV) function in neonates with CH has not been previously studied. The aim of the present study was to assess RV function in neonates with CH before and after thyroxine substitution therapy by quantitative tissue velocity imaging (QTVI) and tissue tracking imaging (TTI).

Methods: Fifty-two neonates aged 18-28 days (25 males and 27 females) with CH and 35 healthy neonates aged 18-28 days (16 males and 19 females) were studied by QTVI, TTI as well as conventional pulsed-wave Doppler echocardiography (PWD).

[A study on the social adjustment and its affective factors in Down syndrome children].

Objective: To explore the social adjustment status and affected factors thereof in Down syndrome children.

Methods: The family environment, cognitive development and social adjustment were examined in 36 Down syndrome children aged 52 - 167 months, 30 mental age-matched children aged 20 - 65 months, and 40 chronological age-matched children aged 43 - 144 months with questionnaire of family influential factors, Peabody Picture Vocabulary Test (PPVT) and Infants-Junior Middle School Students' Social-Life Abilities Scale from September 2004 to July 2006. The gender and general family environment were matched among the three groups.

Study on the social adaptation of Chinese children with down syndrome.

Purpose: To evaluate social adjustment and related factors among Chinese children with Down syndrome (DS).

Patients And Methods: A structured interview and Peabody Picture Vocabulary Test (PPVT) were conducted with a group of 36 DS children with a mean age of 106.28 months, a group of 30 normally-developing children matched for mental age (MA) and a group of 40 normally-developing children matched for chronological age (CA).

[Expression of androgen receptor gene in cerebral cortex and hippocampus of rats with perinatal hypothyroidism].

Objective: To investigate the effects of perinatal thyroid hormone deficiency on the expression of androgen receptor (AR) mRNA in cerebral cortex and hippocampus of rats.

Methods: Perinatal hypothyroidism was induced by the administration of propylthiouracil (PTU) solution to the dams by gavage (50 mg/d) beginning at embryonic d15 throughout the lactational period. In the T(4) injected group hypothyroid rats were injected intraperitoneally with levothroxine (L-T(4)) 2 microg/100 g BW daily, starting from the day of birth.

[Left ventricular function in congenital hypothyroidism neonates before and after thyroxine substitution therapy].

Objective: To evaluate left the systolic and diastolic functions in neonates with congenital hypothyroidism (CH) as well as the effect of thyroxine substitution therapy on left ventricular function and its correlation with thyroid hormones serum levels.

Methods: M-mode echocardiography was used to examine the left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), pulse wave Doppler was used to examine the peak early diastolic mitral inflow velocity (E(m)) and peak late diastolic mitral inflow velocity (A(m)), quantitative tissue velocity imaging (QTVI) was used to examine the systolic peak mitral annular velocity (s(m)), early diastolic peak mitral annular velocity (E(m)), and the late diastolic peak mitral annular velocity (a(m)), and tissue tracking imaging (TTI) was used to detect the systolic mitral annular displacement (MAD) in 40 neonates with congenital hypothyroidism aged 15-28 days before and after 1-month levothyroxine substitution treatment. Thirty normal neonates were used as controls.

[Influence of congenital hypothyroidism on left ventricular function of neonates].

Objective: To evaluate left ventricular function in neonates with congenital hypothyroidism (CH) and its correlation with thyroid hormones serum levels.

Methods: M-mode echocardiography [left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS)], pulse wave Doppler [the peak early diastolic mitral inflow velocity (Em), the peak late diastolic mitral inflow velocity (Am)], quantitative tissue velocity imaging (QTVI) [the systolic peak mitral annular velocity (sm), the early diastolic peak mitral annular velocity (em), the late diastolic peak mitral annular velocity (am)] and tissue tracking imaging (TTI) [the systolic mitral annular displacement (MAD)] were evaluated in 35 neonates with congenital hypothyroidism aged 15-28 days and 30 normal neonates in this study. Correlation analysis was also made between left ventricular function and serum TT3, TT4 and TSH levels.