Sub-Rayleigh dark-field imaging via speckle illumination.

We demonstrate sub-Rayleigh dark-field imaging via speckle illumination. Imaging is achieved with second-order autocorrelated measurement by illuminating objects with hollow conical pseudothermal light. Our scheme can work well for highly transparent amplitude objects, pure phase objects, and even more complex transparent objects. The autocorrelated dark-field images show better resolution than intensity-averaged images and an ability in filtering out low-frequency noises.

Observation of positive-negative sub-wavelength interference without intensity correlation calculation.

We report an experimental demonstration of positive-negative sub-wavelength interference without correlation. Typically, people can achieve sub-wavelength effects with correlation measurement no matter by using bi-photon or thermal light sources. In this paper, we adopt a thermal light source, and we count the realizations in which the intensities of the definite symmetric points are above or below a certain threshold. The distribution of numbers of these realizations which meet the restriction will show a sub-wavelength effect. With proper constrictions, positive and negative interference patterns are demonstrated.

Dark-field ghost imaging.

Ghost imaging is a promising technique for shape reconstruction using two spatially correlated beams: one beam interacts with a target and is collected with a bucket detector, and the other beam is measured with a pixelated detector. However, orthodox ghost imaging always provides unsatisfactory results for unstained samples, phase objects, or highly transparent objects. Here we present a dark-field ghost imaging technique that can work well for these "bad" targets. The only difference from orthodox ghost imaging is that the bucket signals rule out the target's unscattered beam. As experimental proof, we demonstrate images of fine copper wires, quartz fibers, scratched and damaged glass plates, a pure phase object, and biospecimens.

Protective effects of mesenchymal stem cells overexpressing extracellular regulating kinase 1/2 against stroke in rats.

OBJECTIVE: Although transplantation of bone marrow-derived mesenchymal stem cells (MSCs) has shown beneficial effects on stroke, lower survival of MSCs limits effects. Extracellular regulating kinase 1/2 signaling (ERK1/2) is crucial for cell survival, differentiation, and proliferation. This study was designed to explore whether MSCs modified by over-expressing ERK1/2 may reinforce beneficial effects on stroke in rats. METHODS: rat MSCs transfected with ERK1/2 and empty lentivirus to generate MSCs overexpressing ERK1/2 (ERK/MSCs) and MSCs (as a control), respectively. In vitro, ERK/MSCs were plated and exposed to glutamate-induced condition, and viability of ERK/MSCs was measured. Furthermore, neural induction of ERK/MSCs was investigated in vitro. Cerebral ischemic rats were induced by occluding middle cerebral artery, and then were stereotaxically injected into ipsilateral right lateral ventricle with ERK/MSCs or MSCs 3 days after stroke and survived for 7 or 14 days after injection. RESULTS: ERK/MSCs showed better viability in physiological and glutamate-induced neurotoxic conditions compared to MSCs. After neural induction, more neurons were be differentiated from ERK/MSCs than from MSCs. After transplantation, more numbers of grafted cells and improved functional recovery were observed in ERK/MSCs-treated rats compared with MSCs-treated rats. Compared with MSCs treatment, ERK/MSCs treatment significantly increased proliferation of neural stem cells in the subventricle zone (SVZ) and the MAP2/nestin double-labeled cells adjacent to the SVZ, enhanced the numbers of reactive astrocytes while suppressed microglial activation. Besides, TNF-α level was elevated in ERK/MSCs-treated rats. CONCLUSION: ERK/MSCs transplantation showed better functional recovery after stroke in rats, likely in part through enhancing survival of MSCs and possibly by modulating the proliferation, neuronal de-differentiation and neuroinflammation.

Ginsenoside Rg1 protects against neurodegeneration by inducing neurite outgrowth in cultured hippocampal neurons.

Ginsenoside Rg1 (Rg1) has anti-aging and anti-neurodegenerative effects. However, the mechanisms underlying these actions remain unclear. The aim of the present study was to determine whether Rg1 affects hippocampal survival and neurite outgrowth in vitro after exposure to amyloid-beta peptide fragment 25-35 (Aß25-35), and to explore whether the extracellular signal-regulated kinase (ERK) and Akt signaling pathways are involved in these biological processes. We cultured hippocampal neurons from newborn rats for 24 hours, then added Rg1 to the medium for another 24 hours, with or without pharmacological inhibitors of the mitogen-activated protein kinase (MAPK) family or Akt signaling pathways for a further 24 hours. We then immunostained the neurons for growth associated protein-43, and measured neurite length. In a separate experiment, we exposed cultured hippocampal neurons to Aß25-35 for 30 minutes, before adding Rg1 for 48 hours, with or without Akt or MAPK inhibitors, and assessed neuronal survival using Hoechst 33258 staining, and phosphorylation of ERK1/2 and Akt by western blot analysis. Rg1 induced neurite outgrowth, and this effect was blocked by API-2 (Akt inhibitor) and PD98059 (MAPK/ERK kinase inhibitor), but not by SP600125 or SB203580 (inhibitors of c-Jun N-terminal kinase and p38 MAPK, respectively). Consistent with this effect, Rg1 upregulated the phosphorylation of Akt and ERK1/2; these effects were reversed by API-2 and PD98059, respectively. In addition, Rg1 significantly reversed Aß25-35-induced apoptosis; this effect was blocked by API-2 and PD98059, but not by SP600125 or SB203580. Finally, Rg1 significantly reversed the Aß25-35-induced decrease in Akt and ERK1/2 phosphorylation, but API-2 prevented this reversal. Our results indicate that Rg1 enhances neurite outgrowth and protects against Aß25-35-induced damage, and that its mechanism may involve the activation of Akt and ERK1/2 signaling.

Neuroprotective effects of ginsenoside Rb1 on hippocampal neuronal injury and neurite outgrowth.

Ginsenoside Rb1 has been reported to exert anti-aging and anti-neurodegenerative effects. In the present study, we investigate whether ginsenoside Rb1 is involved in neurite outgrowth and neuroprotection against damage induced by amyloid beta (25-35) in cultured hippocampal neurons, and explore the underlying mechanisms. Ginsenoside Rb1 significantly increased neurite outgrowth in hippocampal neurons, and increased the expression of phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2. These effects were abrogated by API-2 and PD98059, inhibitors of the signaling proteins Akt and MEK. Additionally, cultured hippocampal neurons were exposed to amyloid beta (25-35) for 30 minutes; ginsenoside Rb1 prevented apoptosis induced by amyloid beta (25-35), and this effect was blocked by API-2 and PD98059. Furthermore, ginsenoside Rb1 significantly reversed the reduction in phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2 levels induced by amyloid beta (25-35), and API-2 neutralized the effect of ginsenoside Rb1. The present results indicate that ginsenoside Rb1 enhances neurite outgrowth and protects against neurotoxicity induced by amyloid beta (25-35) via a mechanism involving Akt and extracellular signal-regulated kinase 1/2 signaling.

Plasma levels of omentin-1 and visfatin in senile patients with coronary heart disease and heart failure.

OBJECTIVE: To investigate the alteration of plasma levels of omentin-1 and visfatin in elderly patients with coronary heart disease (CHD) and heart failure. METHODS: Plasma omentin-1 and visfatin levels were measured in 90 subjects (29 stable angina pectoris (SAP) cases, 30 unstable angina pectoris (UAP) cases and 31 age- and sex-matched healthy controls (age ≥ 60 years) by enzyme-linked immunosorbent assay methods. According to the New York Heart Association classification, 59 CHDs were divided into three groups: functional I class, 11 cases; functional II/III class, 36 cases; and functional IV class, 12 cases. RESULTS: The plasma level of omentin-1 in CHD patients was significantly lower than that of the control group. Omentin-1in SAP group and UAP group were significantly lower compared to the control group (there was no statistical significance between UAP group and SAP group; P >0.05). The plasma level of visfatin in CHD patients was significantly higher than that of the control group. Similarly, visfatin in SAP group and UAP group were all significantly higher compared to the control group, while there was no statistical significance between UAP group, and SAP group. The plasma omentin-1 level was negatively correlated with SBP (r=-0.264, P<0.05), positively correlated with HDL-c level (r=0.271, P<0.05); the plasma visfatin level was positively correlated with TC (r=0.292,P<0.05), negatively correlated with HDL-c level (r=-0.266,P<0.05). There was a negative correlation between plasma omentin-1 and visfatin levels (r=-0.280, P<0.05). Moreover, multiple linear stepwise regression analysis showed that omentin-1 and visfatin levels might be affected by HDL-c level. Logistic regression analysis showed that visfatin could be an independent risk factor of CHD. CONCLUSIONS: Decreased levels of omentin-1 and increased levels of visfatin may be involved in the occurrence and development of CHD. Omentin-1 and visfatin, independently, may be protective and pro-inflammatory cytokines. Additionally, both omentin-1 and visfatin may be related to lipid metabolism. Visfatin may be an independent risk factor of CHD.

Cell apoptosis and proliferation in rat brains after intracerebral hemorrhage: role of Wnt/ß-catenin signaling pathway.

BACKGROUND/AIM: To investigate the role of Wnt/ß-catenin signaling pathway in cell apoptosis and proliferation in intracerebral hemorrhage (ICH) in rats. MATERIALS AND METHODS: The ICH rats were established by stereotaxic infusion of 50 µL autologous arterial blood into the right striatum. Pathological characteristics of brain tissue was assessed by hematoxylin and eosin and TUNEL staining, and the expressions of proliferating cell nuclear antigen (PCNA) and Wnt3a/ß-catenin/cyclin D1 were investigated by immunohistochemistry or reverse-transcription polymerase chain reaction. RESULTS: The number of apoptotic cells and PCNA-positive cells kept increasing from the day following the ICH induction and reached a peak on the 3rd and 14th days, respectively. Some of the PCNA-positive cells could coexpress neurofilament protein-200 or glial fibrillary acidic protein. Wnt3a, ß-catenin, cyclin D1, and PCNA mRNAs reached maximal expression levels on the 3rd, 7th, 7th, and 14th days, respectively. Moreover, the number of apoptotic cells was significantly positively correlated with the expressions of Wnt3a and ß-catenin mRNAs, and negatively correlated with the number of PCNA-positive cells. CONCLUSION: Our results suggest that the Wnt/ß-catenin signaling pathway is associated with cell apoptosis and expression of PCNA in the ICH rat brain and regulates the balance between cell apoptosis and proliferation.