Serum adiponectin levels may be associated with the pathogenesis of hepatocellular carcinoma.

The aim of the meta-analysis described below was to investigate the correlation between serum levels of adiponectin (ADPN) and the pathogenesis of hepatocellular carcinoma (HCC). Relevant studies about serum ADPN levels and the pathogenesis of HCC were identified by searching electric databases and by manual search. The included studies were selected in strict accordance with the inclusion and exclusion criteria. Detailed criteria were described in "Materials and methods" section. Statistical analyses were conducted with the STATA 12.0 statistical software (StataCorp, College Station, TX, USA). A total of nine studies were incorporated into this meta-analysis after careful consideration, including 705 HCC patients and 1390 healthy controls. This meta-analysis demonstrated that the serum ADPN levels in HCC patients were significantly higher than those in healthy controls (standard mean difference (SMD) = 0.97, 95% confidence intervals (CI) = 0.02∼1.93, P < 0.05). The result of subgroup analysis by ethnicity revealed that serum ADPN levels in Caucasians and Asians were both obviously higher than those in healthy controls (Caucasians: SMD = 0.51, 95% CI = 0.30∼0.73, P < 0.001; Asians: SMD = 0.49, 95% CI = 0.06∼0.91, P < 0.05), but in Africans, the differences between HCC patients and controls had no statistical significance (SMD = 2.64, 95% CI = -3.01∼8.30, P = 0.36). The evidence obtained by this meta-analysis suggests that serum ADPN levels are associated with the pathogenesis of HCC. Further conclusion might be that increased serum levels of ADPN can inhibit tumor growth and play a protective role in the development of HCC.

[Dynamic changes of sciatic nerve conduction velocity in rats infected with Toxoplasma gondii].

OBJECTIVE: To observe the dynamic changes of sciatic nerve conduction velocity of Toxoplasma gondii-infected rats at different time points. METHODS: Twenty SD rats were randomly divided into control group and Toxoplasma gondii infection group. Rats in T. gondii infection group were intraperitoneal injected with 4x10(7) T. gondii tachyzoites, while those in control group were given equivalent normal saline. Motor and sensory nerve conduction velocities (MNCV, SNCV) in sciatic nerve were measured by Medtronic Keypoint4 Workstation electromyography at pre-infection, and 2, 4, 8, 12 months post-infection. RESULTS: Within two months after infection, there was no difference in SNCV and MNCV between control group and infection group (P>0.05). From 4 months after T. gondii injection, infected rats began to show the slowness of SNCV and MNCV, which progressed with the course of infection. At 4, 8, and 12 months after infection, SNCV and MNCV of infection group were (35.26±3.02) and (25.94±3.20) m/s, (33.57±2.27) and (22.75±2.31) m/s, and (32.38±2.38) and (22.03±2.08) m/s, respectively. Compared with control group, SNCV and MNCV of infection group reduced by (7.47±2.11)% and (12.57±1.89)%, (8.92±2.64)% and (13.72±2.65)%, and (12.18±1.94)% and (15.46±2.37)%, respectively (P<0.05). CONCLUSION: From 4 months after infection, Toxoplasma gondii-infected rats show a slowness of motor and sensory nerve conduction velocities in sciatic nerve.

[Recent Progress of Molecular Genetic Characteristics and Prognosis of Non-Hodgkin's Lymphoma--Review].

Lymphomas are traditionally divided into Hodgkin's lymphoma and non-Hodgkin's lymphoma(NHL), the NHL is a common hematological cancer, which represents a wide spectrum of illnesses from the most indolent to the most aggressive malignancies, and the detection of related molecular targets will be needed for diagosing each subtype of NHL. Advances in understanding the pathogenesis of NHL have improved the precision of diagnosis and the prognosis evaluation of patients with this disorder, such as chromosomal translocation leading to the up-regulation of oncogene expression. Besides, the deletion of several tumor suppressor genes may cause excessive proliferation in tumor cells, and the single nucleotide polymorphism (SNP) determines the differences of susceptibility, drug-resistance and prognosis of NHL. In addition, DNA methylation, histone modification, non-coding RNA and other epigenetic phenomena play an increasingly important role in the diagnosis, selection of clinical drugs and evaluation of prognosis of NHL. In this review, the recent progress of researches on chromosome translocation, deletion of tumor suppression genes, gene poly-morphism and epigenetics are summarized.

Serum CXCL12 Levels as a Novel Predictor of Future Stroke Recurrence in Patients with Acute Ischemic Stroke.

Previous studies had shown that CXC chemokine ligand-12 (CXCL12) plays a significant role in animal models of ischemic stroke, but its role in human stroke is unclear. The aim of this study was to test the relationship between elevated serum circulating CXCL12 levels and the 1-year stroke recurrence in Chinese patients with acute ischemic stroke (AIS). All consecutive patients with first-ever acute ischemic stroke from January 2011 to September 2013 were recruited to participate in the study. Serum levels of CXCL12 and National Institute of Health Stroke Scale (NIHSS) were measured at the time of admission. Logistic regression analysis was used to evaluate the stroke recurrence according to serum CXCL12 levels. Receiver operating characteristic (ROC) curve was used to evaluate the accuracy of serum CXCL12 in predicting stroke recurrence. Clinical follow-up was performed at 1 year. In our study, 248 patients finished the 1-year follow-up. At 1-year follow-up, 31 patients had a recurrence ischemic stroke. The median CXCL12 levels were significantly higher in those who sustained a recurrence ischemic stroke compared with those who did not [24.2 ng/mL (IQR 15.4-33.7) vs 6.5 ng/mL (IQR 3.4-10.2); Z = 8.258, P < 0.0001]. In multivariate analysis, there was an increased risk of stroke recurrence associated with serum CXCL12 levels ≥12.15 ng/mL (OR 9.122, 95 % CI 6.103-15.104) after adjusting for above possible confounders. The time to recurrence stroke distribution between patients with baseline CXCL12 levels ≥12.15 ng/mL and those with baseline CXCL12 levels <12.15 ng/mL were significantly different (P < 0.0001, log-rank test). Elevated circulating CXCL12 levels at admission are strongly associated with the future recurrence of ischemic stroke in Chinese patients with AIS. Further studies are warranted to confirm this association and define the role for CXCL12 as a novel predictor biomarker for stroke recurrence.

Nogo-A expression dynamically varies after spinal cord injury.

The mechanism involved in neural regeneration after spinal cord injury is unclear. The myelin-derived protein Nogo-A, which is specific to the central nervous system, has been identified to negatively affect the cytoskeleton and growth program of axotomized neurons. Studies have shown that Nogo-A exerts immediate and chronic inhibitory effects on neurite outgrowth. In vivo, inhibitors of Nogo-A have been shown to lead to a marked enhancement of regenerative axon extension. We established a spinal cord injury model in rats using a free-falling weight drop device to subsequently investigate Nogo-A expression. Nogo-A mRNA and protein expression and immunoreactivity were detected in spinal cord tissue using real-time quantitative PCR, immunohistochemistry and western blot analysis. At 24 hours after spinal cord injury, Nogo-A protein and mRNA expression was low in the injured group compared with control and sham-operated groups. The levels then continued to drop further and were at their lowest at 3 days, rapidly rose to a peak after 7 days, and then gradually declined again after 14 days. These changes were observed at both the mRNA and protein level. The transient decrease observed early after injury followed by high levels for a few days indicates Nogo-A expression is time dependent. This may contribute to the lack of regeneration in the central nervous system after spinal cord injury. The dynamic variation of Nogo-A should be taken into account in the treatment of spinal cord injury.