Objective To investigate the molecular biological mechanism of deposition of triglyceride(TG)in hepatocytes in alcoholic fatty liver disease(AFLD)and the pathogenesis of this condition by detecting the contents of serum tumor necrosis fac-tor-α(TNF-α),liver triglyceride(TG),peroxisome proliferator-activated receptorα(PPARα)and acyl-CoA oxidase(Acox1)mR-NAs,and liver PPARαprotein after intervention with bezafibrate,a PPARαagonist.Methods Sixty Wistar rats were randomly divided into three groups:control group(n=20),AFLD group(n=20),and bezafibrate group(n=20).Animals in control group were given distilled water by gavage once a day for 8 weeks.Those in AFLD group were given ethanol and fish oil(2.5 mL/kg) by gavage daily for the same period of time.In bezafibrate group,rats were treated by gavage with ethanol and fish oil(2.5 mL/kg)for the first 4 weeks and then with bezafibrate(100 mg/kg)for another 4 weeks.TG in the liver was measured by colorimet-ric method,serum TNF-αlevels by enzyme linked immunoabsorbent assay (ELISA),the mRNA expression of PPARαand Acox1 in hepatocytes by reverse transcription polymerase chain reaction(RT-PCR)and the expression of PPARαprotein in hep-atocytes by Western blot.Results A significant increase in TG[AFLD group(0.72±0.09)mmol/L vs.control group(0.28± 0.07)mmol/L,P<0.01]and TNF-α[AFLD group(3.01±0.31)ng/mL vs.control group(1.07±0.28)ng/mL,P<0.01]was found in AFLD group when compared with control group.After bezafibrate intervention,the contents of liver TG and serum TNF-αwere significantly decreased.The mRNA expression of PPARα[AFLD group(0.22±0.08)vs.control group(0.68± 0.13),P<0.01]and Acox1[AFLD group(0.43±0.12)vs.control group(1.14±0.21),P<0.01]was suppressed in AFLD group,which was significantly reversed by bezafibrate treatment[bezafibrate group(0.59±0.13)for PPARαmRNA vs.AFLD group,P<0.01;bezafibrate group(0.83±0.17)for Acox1 mRNA vs.AFLD group,P<0.01].The expression of PPARαpro-tein in hepatocyts was also found to decrease in AFLD group[AFLD group(0.19±0.07)vs.control group(0.48±0.11),P<0.01].After bezafibrate intervention,it was profoundly increased.Conclusion The down-expression of PPARαand Acox1 in the liver of rats with AFLD may suppress the fatty acid metabolism and lead to the TG deposition in the liver.The increase in serum TNF-αcontents also contributes to the development of AFL.Bezafibrate can prevent and treat AFL by activating PPARα,increasing the expression of PPARαand Acox1 ,promoting the metabolism of fatty acids,decreasing the TG deposition and the serum TNF-αcontents.

Inflammasome is a multi-protein complex which plays an important role in innate immune defense,and can adjust the activation of caspase-1 and promote the production of cytokines. NLRP3 is an important member of inflammasome Nod-like receptor(NLR)family,and its activation and expression occur mainly in macrophages and dendritic cells. NLRP3 can sense the pathogen associated molecular patterns(PAMPs)and damage associated molecular patterns(DAMPs)and initiate the inherent immune response,which plays an important role in the pathogenesis of autoimmune diseases. This article reviewed the advances in study on NLRP3 in autoimmune diseases.

Good doctor-patient communication is the most effective way to build a harmonious doctor-patient relationship and reduce medical disputes, where the communication skill is the key. In communication with the hospitalized patients, it should pay attention to the communication object choice;the choice of the communicator;communication time, location and the form; pay attention to the communication protocol; using a comprehensible language communication;stand in the perspective of patients in order to enhance the doctor-patient trust and im-prove the doctor-patient relationship.

Objective To investigate the effect of chronic stress on the mucin secretion and muc2 protein content in goblet cells of rat colonic mucosa. Methods 24 healthy Wistar rats were randomly divided into 2 groups. Control group moved freely, experimental group was forced to undergo 2-hour-long immobilization stress per day for 14 days. The number of goblet cells containing mucus was determined by AB/PAS histochemical staining. The expression of muc2 protein was detected by immuohistochemical staining. Results Chronic stress decreased the number of goblet cells containing mucus, and down-regulated the expression of muc2 protein in goblet cells in rat colonic mucosa. Conclusion Chronic stress damaged the colonic epithelial barrier and functions of colonic goblet cells.

BACKGROUND:Growth-associated protein-43 is the primary substance for constructing plasticity of central nervous system, which is recognized as the first molecular marker for studying growth and repairing injury of nerves. OBJECTIVE: To explore the expression of growth-associated protein-43 in rats with focal cerebral ischemia following bone marrow mesenchymal stem cells (MSCs) transplantation.DEISNG, TIME AND SETTING: A randomized, controlled, animal study was performed at the Laboratory of Department of Neurology, Renmin Hospital of Wuhan University and Doctoral Scientific Research Work Station of C-BONS Pharmacy, Hubei, China, from March 2006 to October 2007.MATERIALS: Sixty adult Sprague Dawley rats, with clean grade, irrespective of genders, weighing (180±20) g, were randomly divided into the model, sham operated, and MSCs transplantation groups, with 20 animals in each group. METHODS: Additional 4 Sprague Dawiey rats, aged 2 months, were selected to isolate and culture MSCs, which was labeled with 5-Bromo-2,-deoxyuridine (BrdU). In the sham operated group, the right internal carotids were deligated after anaesthesia. The remained rats were prepared for models of right middle cerebral artery ischemia. At 24 hours after model preparation, 20 μL culture solution containing 5×105/L MSCs was injected into the left lateral ventricle of rats in the MSCs group, the same volume of phosphate buffer saline was injected in the model group.MAIN OUTCOME MEASURES: The rats were sacrificed prior to and at days 7, 14, and 21 after transplantation. The expression of growth associated protein-43 at the infarcted areas, the survival and migration of transplanted cells were examined by immunohistochemistry, at the same time, neurological deficit scores were recorded.RESULTS: The transplanted MSCs migrated from the left lateral ventricle to the infracted areas. Seven days after transplantation, the expression of BrdU-positive cells was found, reached a peak at day 14, and gradually decreased, until disappeared at 28 days after transplantation. Results of immunohistochemistry image analysis showed that immunological activity of growth associated protein-43 around the infarcted area of the MSCs group was obviously greater than that of the model group at days 7 and 14 after transplantation (P<0.06). There was no neurological deficit in the sham operated group. Moreover, with time prolonged, the neurological deficit scores gradually decreased in the model and MSCs groups, which were significantly lower in the MSCs group compared to the model group at day 14 after transplantation (P<0.05).CONCLUSION: MSCs transplantation up-regulates the expression of growth associated protein-43 around the infarcted area, which is consistent with the recovery of neurological function.

Although current direct anti-hepatitis B virus (HBV) drugs have good effects in controlling viral replication and limiting the progression to liver cirrhosis, there is still a long way to go in the treatment of chronic hepatitis B (CHB). Immune tolerance and immune dysfunction may be the two most important immunopathogenic factors. With reference to the development of new strategies and new drugs for anti-HBV immunotherapy and the latest research findings around the world, this article reviews the research advances in immunotherapy for CHB in recent years.

Small for gestational age (SGA) infants are more likely to experience neurocognitive impairments compared to appropriate for gestational age (AGA) infants. This paper reviews recent research on the neurocognitive development of SGA children. SGA can lead to a "brain-sparing effect" due to growth restriction, which may affect cerebral blood flow and brain structure. However, this does not guarantee normal brain development. Restrictive blood flow can result in changes in brain structure, such as reduced total white matter and gray matter volume in various brain regions, including the cerebral cortex, hippocampus and cerebellum, ultimately leading to decreased head circumference. SGA children also exhibit lower scores in all neurocognitive domains, including intelligence, attention, memory, and executive function. This may result in poor academic performance and an increased risk of social, behavioral, and neurological problems, such as cerebral palsy, epilepsy, visual and hearing impairments, as well as comorbidities like attention deficit hyperactivity disorder(ADHD), autism spectrum disorder(ASD), anxiety, depression, and schizophrenia. Several risk factors for SGA-related neurocognitive impairments have been identified, including gestational hypertension, abnormal gestational weight, smoking, and catch-up growth. Studies have shown that the best interventions to improve cognitive dysplasia include nutrient supplementation, continued breastfeeding, high-quality education, and appropriate early intervention (responsive parenting) are effective in improving cognitive outcomes for SGA children.