Abstract. Social network data is often prohibitively expensive to collect, limiting empirical network research. Typical economic network mapping requires (1) enumerating a census, (2) eliciting the names of all network links for each individual, (3) matching the list of social connections to the census, and (4) repeating (1)- (3) across many networks. In settings requiring field surveys, steps (2)- (3) can be very expensive. In other network populations such as financial intermediaries or high-risk groups, proprietary data and privacy concerns may render (2)- (3) impossible. Both restrict the accessibility of high-quality networks research to investigators with considerable resources.We propose an inexpensive and feasible strategy for network elicitation using Aggregated Relational Data (ARD) -responses to questions of the form "How many of your social connections have trait k?" Our method uses ARD to recover the parameters of a general network formation model, which in turn, permits the estimation of any arbitrary node-or graph-level statistic. The method works well in simulations and in matching a range of network characteristics in real-world graphs from 75 Indian villages. Moreover, we replicate the results of two field experiments that involved collecting network data. We show that the researchers would have drawn similar conclusions using ARD alone. Finally, using calculations from J-PAL fieldwork, we show that in rural India, for example, ARD surveys are 80% cheaper than full network surveys. JEL Classification Codes: D85, C83, L14

Ascorbic acid (AA) is an essential micronutrient that has been safely used in the clinic for many years. The present study indicates that AA has an unexpected function in facilitating nerve regeneration. Using a mouse model of sciatic nerve crush injury, we found that AA can significantly accelerate axonal regrowth in the early stage [3 days post-injury (dpi)], a finding that was revealed by immunostaining and Western blotting for antibodies against GAP-43 and SCG10. On day 28 post-injury, histomorphometric assessments demonstrated that AA treatment increased the density, size, and remyelination of regenerated axons in the injured nerve and alleviated myoatrophy in the gastrocnemius. Moreover, the results from various behavioral tests and electrophysiological assays revealed that nerve injury-derived functional defects in motor and sensory behavior as well as in nerve conduction were significantly attenuated by treatment with AA. The potential mechanisms of AA in nerve regeneration were further explored by investigating the effects of AA on three types of cells involved in this process [neurons, Schwann cells (SCs) and macrophages] through a series of experiments. Overall, the data illustrated that AA treatment in cultured dorsal root ganglionic neurons resulted in increased neurite growth and lower expression of RhoA, which is an important inhibitory factor in neural regeneration. In SCs, proliferation, phagocytosis, and neurotrophin expression were all enhanced by AA. Meanwhile, AA treatment also improved proliferation, migration, phagocytosis, and anti-inflammatory polarization in macrophages. In conclusion, this study demonstrated that treatment with AA can promote the morphological and functional recovery of injured peripheral nerves and that this effect is potentially due to AA’s bioeffects on neurons, SCs and macrophages, three of most important types of cells involved in nerve injury and regeneration.

Spinal cord injury (SCI) often leads to impaired motor and sensory functions, partially because the injury-induced neuronal loss cannot be easily replenished through endogenous mechanisms. In vivo neuronal reprogramming has emerged as a novel technology to regenerate neurons from endogenous glial cells by forced expression of neurogenic transcription factors. We have previously demonstrated successful astrocyte-to-neuron conversion in mouse brains with injury or Alzheimer's disease by overexpressing a single neural transcription factor NeuroD1. Here we demonstrate regeneration of spinal cord neurons from reactive astrocytes after SCI through AAV NeuroD1-based gene therapy. We find that NeuroD1 converts reactive astrocytes into neurons in the dorsal horn of stab-injured spinal cord with high efficiency (~95%). Interestingly, NeuroD1-converted neurons in the dorsal horn mostly acquire glutamatergic neuronal subtype, expressing spinal cord-specific markers such as Tlx3 but not brain-specific markers such as Tbr1, suggesting that the astrocytic lineage and local microenvironment affect the cell fate after conversion. Electrophysiological recordings show that the NeuroD1-converted neurons can functionally mature and integrate into local spinal cord circuitry by displaying repetitive action potentials and spontaneous synaptic responses. We further show that NeuroD1-mediated neuronal conversion can occur in the contusive SCI model with a long delay after injury, allowing future studies to further evaluate this in vivo reprogramming technology for functional recovery after SCI. In conclusion, this study may suggest a paradigm shift from classical axonal regeneration to neuronal regeneration for spinal cord repair, using in vivo astrocyte-to-neuron conversion technology to regenerate functional new neurons in the gray matter.

RhoA, a member of Rho GTPases family, is known to play an important role in remodeling actin cytoskeleton. During the development of the peripheral nervous system (PNS), Schwann cells undergo proliferation, migration, and radial sorting and finally wrap the related axons compactly to form myelin sheath. All these processes involve actin cytoskeletal remodeling. However, the role of RhoA on Schwann cell during development is still unclear. To address this question, we first used a lentiviral vector-mediated short hairpin (sh) RNA targeting RhoA to knock down the expression of RhoA in the cultured Schwann cells in vitro. Effects of RhoA on Schwann cell proliferation and migration were examined by BrdU assay and transwell assay, respectively. Results of the present study indicated that downregulated RhoA expression in cultured Schwann cells significantly slacked the cells' capabilities of migration and proliferation. Then, we investigated the role of RhoA in the developing rat sciatic nerves. Immunohistology and Western blotting showed that RhoA was mainly expressed in Schwann cells in the sciatic nerves and was peaked at 2 weeks postnatal then kept in low level up to 8 weeks. In the subjected rats whose sciatic nerves were microinjected with lentiviral vectors at postnatal 3 days, we found that the lentiviruses mainly transfected Schwann cells, and the RhoA expression in the transfected Schwann cells was significantly knocked down. Four weeks after lentivirus microinjection, immunohistology and transmission electron microscopy illustrated that RhoA knockdown resulted in hypomyelination and significant decrease of the thickness of myelin in the transfected area. Overall data of current study suggested that RhoA plays a critical role in Schwann cell biology and is essential for myelination in developing peripheral nerve.

Peripheral blood mesenchymal stem cells (PBMSCs) may be easily harvested from patients, permitting autologous grafts for bone tissue engineering in the future. However, the PBMSC’s capabilities of survival, osteogenesis and production of new bone matrix in the defect area are still unclear. Herein, PBMSCs were seeded into a nanofiber scaffold of self-assembling peptide (SAP) and cultured in osteogenic medium. The results indicated SAP can serve as a promising scaffold for PBMSCs survival and osteogenic differentiation in 3D conditions. Furthermore, the SAP seeded with the induced PBMSCs was splinted by two membranes of poly(lactic)-glycolic acid (PLGA) to fabricate a composited scaffold which was then used to repair a critical-size calvarial bone defect model in rat. Twelve weeks later the defect healing and mineralization were assessed by H&E staining and microcomputerized tomography (micro-CT). The osteogenesis and new bone formation of grafted cells in the scaffold were evaluated by immunohistochemistry. To our knowledge this is the first report with solid evidence demonstrating PBMSCs can survive in the bone defect area and directly contribute to new bone formation. Moreover, the present data also indicated the tissue engineering with PBMSCs/SAP/PLGA scaffold can serve as a novel prospective strategy for healing large size cranial defects.

Objective: Addiction is a chronic relapsing brain disease. Brain structural abnormalities may constitute an abnormal neural network that underlies the risk of drug dependence. We hypothesized that individuals with Betel Quid Dependence (BQD) have functional connectivity alterations that can be described by long- and short-range functional connectivity density(FCD) maps. Methods: We tested this hypothesis using functional magnetic resonance imaging (fMRI) data from subjects of the Han ethnic group in Hainan, China. Here, we examined BQD individuals (n = 33) and age-, sex-, and education-matched healthy controls (HCs) (n = 32) in a rs-fMRI study to observe FCD alterations associated with the severity of BQD. Results: Compared with HCs, long-range FCD was decreased in the right anterior cingulate cortex (ACC) and increased in the left cerebellum posterior lobe (CPL) and bilateral inferior parietal lobule (IPL) in the BQD group. Short-range FCD was reduced in the right ACC and left dorsolateral prefrontal cortex (dlPFC), and increased in the left CPL. The short-range FCD alteration in the right ACC displayed a negative correlation with the Betel Quid Dependence Scale (BQDS) (r=-0.432, P=0.012), and the long-range FCD alteration of left IPL showed a positive correlation with the duration of BQD(r=0.519, P=0.002) in BQD individuals. Conclusions: fMRI revealed differences in long- and short- range FCD in BQD individuals, and these alterations might be due to BQ chewing, BQ dependency, or risk factors for developing BQD.

Recent studies suggest that heat exposure degrades work productivity, but such studies have not considered individual- and workplace-level factors. Forty-six tree fruit harvesters (98% Latino/a) from six orchards participated in a cross-sectional study in Central/Eastern Washington in 2015. The association between maximum measured work-shift Wet Bulb Globe Temperature (WBGTmax) and productivity (total weight of fruit bins collected per time worked) was estimated using linear mixed effects models, adjusting for relevant confounders. The mean (standard deviation) WBGTmax was 27.9 (3.6)° C in August and 21.2 (2.0) °C in September. There was a trend of decreasing productivity with increasing WBGTmax, but this association was not statistically significant. When individual- and workplace-level factors were included in the model, the association approached the null. Not considering individual, work, and economic factors that affect rest and recovery in projections of the impacts of climate change could result in overestimates of reductions in future productivity and underestimate risk of heat illness.

Objective: The brain functional alterations at regional and network levels in post-traumatic stress disorder patients are still unclear. This study explored brain functional alterations at regional and network levels in post-traumatic stress disorder patients with resting-state functional magnetic resonance imaging and evaluated the relationship between brain function and clinical indices in post-traumatic stress disorder. Methods: Amplitude of low-frequency fluctuation and seed-based functional connectivity analyses were conducted among typhoon survivors with (n = 27) and without post-traumatic stress disorder (n = 33) and healthy controls (n = 30) to assess the spontaneous brain activity and network-level brain function. Pearson correlation analyses were performed to examine the association of brain function with clinical symptom and social support. Results: Both the post-traumatic stress disorder group and the trauma-exposed control group showed decreased amplitude of low-frequency fluctuation in the dorsal anterior cingulate cortex relative to the healthy control group. The posttraumatic stress disorder group showed increased dorsal anterior cingulate cortex functional connectivity with the right paracentral lobule and bilateral precentral gyrus/postcentral gyrus relative to both control groups. Both traumatized groups exhibited decreased dorsal anterior cingulate cortex functional connectivity with the right hippocampus and left cerebellum relative to the healthy control group. More decreased dorsal anterior cingulate cortex functional connectivity with the right hippocampus was found in the post-traumatic stress disorder group. The Checklist-Civilian Version score positively correlated with functional connectivity between the dorsal anterior cingulate cortex and the right paracentral lobule as well as between the dorsal anterior cingulate cortex and the right precentral gyrus/postcentral gyrus. The social support was associated with functional connectivity between the dorsal anterior cingulate cortex and the bilateral precentral gyrus/postcentral gyrus as well as the dorsal anterior cingulate cortex and the left middle frontal gyrus. Conclusion: Trauma exposure may result in aberrant local and network-level functional connectivity in individuals with or without post-traumatic stress disorder. Altered amplitude of low-frequency fluctuation in the dorsal anterior cingulate cortex may be a predisposing risk factor for post-traumatic stress disorder development following trauma exposure. More prominent decreased dorsal anterior cingulate cortex functional connectivity with the right hippocampus might be specific in the post-traumatic stress disorder group. Improvement of social support might possibly be significant for post-traumatic stress disorder patients.