Polystyrene nanoplastics induce cardiotoxicity by upregulating HIPK2 and activating the P53 and TGF-ß1/Smad3 pathways.

Nanoplastics (NPs) pollution has become a global environmental problem, raising numerous health concerns. However, the cardiotoxicity of NPs exposure and the underlying mechanisms have been understudied to date. To address this issue, we comprehensively evaluated the cardiotoxicity of polystyrene nanoplastics (PS-NPs) in both healthy and pathological states. Briefly, mice were orally exposed to four different concentrations (0 mg/day, 0.1 mg/day, 0.5 mg/day, and 2.5 mg/day) of 100-nm PS-NPs for 6 weeks to assess their cardiotoxicity in a healthy state. Considering that individuals with underlying health conditions are more vulnerable to the adverse effects of pollution, we further investigated the cardiotoxic effects of PS-NPs on pathological states induced by isoprenaline. Results showed that PS-NPs induced cardiomyocyte apoptosis, cardiac fibrosis, and myocardial dysfunction in healthy mice and exacerbated cardiac remodeling in pathological states. RNA sequencing revealed that PS-NPs significantly upregulated homeodomain interacting protein kinase 2 (HIPK2) in the heart and activated the P53 and TGF-beta signaling pathways. Pharmacological inhibition of HIPK2 reduced P53 phosphorylation and inhibited the activation of the TGF-ß1/Smad3 pathway, which in turn decreased PS-NPs-induced cardiotoxicity. This study elucidated the potential mechanisms underlying PS-NPs-induced cardiotoxicity and underscored the importance of evaluating nanoplastics safety, particularly for individuals with pre-existing heart conditions.

Vitamin B12 and iron-rich sludge-derived biochar enhanced PFOA biodegradation: Importance of direct inter-species electron transfer and functional microbes.

Owing to the strong C-F bond in nature and the rigidity of the poly-fluoroalkyl chain, perfluorooctanoic acid (PFOA) is difficult to be eliminated by reactive species and microbes in environments, thus posing a serious threat to ecosystems. Vitamin B12 as a cofactor for enzymes, and biochar as the electron providers and conductors, were integrated to enhance PFOA biodegradation. The raw material of biochar was the sludge after dewatering by adding 50 mg/g DS of Fe(III). After pyrolysis under high temperature (800 °C), biochar (SC800) detected high content of Fe(II) (197.64 mg/g) and abundant oxygen-containing functional groups, thus boosting PFOA biodegradation via donating electrons. 99.9% of PFOA could be removed within 60 d as 0.1 g/L SC800 was presented in the microbial systems containing vitamin B12. Moreover, vitamin B12 facilitated the evolution of Sporomusa which behaved the deflorination. Via providing reactive sites and mediating direct inter-species electron transfer (DIET), SC800 boosted PFOA biodegradation. Corresponding novel results in the present study could guide the development of bioremediation technologies for PFOA-polluted sites.

Gut Microbiota Participates in Polystyrene Microplastics-Induced Hepatic Injuries by Modulating the Gut-Liver Axis.

Dietary pollution by polystyrene microplastics (MPs) can cause hepatic injuries and microbial dysbiosis. Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, exerts beneficial effects on the liver by modulating the gut microbiota. However, the role of microbiota in MPs-induced hepatic injuries and the protective effect of EGCG have not been clarified. Here, 5 µm MPs were orally administered to mice to induce hepatic injuries. Subsequently, antibiotic cocktail (ABX) and fecal microbial transplant (FMT) experiments were performed to investigate the underlying microbial mechanisms. Additionally, EGCG was orally administered to mice to explore its protection against MPs-induced hepatic injuries. Our results showed that MPs activated systemic and hepatic inflammation, promoted fibrosis, and altered the liver metabolome; meanwhile, MPs damaged the gut homeostasis by disturbing the gut microbiome, promoting colonic inflammation, and impairing the intestinal barrier. Notably, MPs reduced the abundance of the probiotics Akkermansia, Mucispirillum, and Faecalibaculum while increasing the pathogenic Tuzzerella. Interestingly, the elimination of gut microbiota mitigated MPs-induced colonic inflammation and intestinal barrier impairment. Moreover, ABX ameliorated MPs-induced systemic and hepatic inflammation but not fibrosis. Correspondingly, microbiota from MPs-administered mice induced colonic, systemic, and hepatic inflammation, while their profibrosis effect on the liver was not observed. Finally, EGCG elevated the abundance of probiotics and effectively repressed MPs-induced colonic inflammation. MPs-induced systemic and hepatic inflammation, fibrosis, and remodeling of the liver metabolome were also attenuated by EGCG. These findings illustrated that gut microbiota contributed to MPs-induced colonic and hepatic injuries, while EGCG could serve as a potential prevention strategy for these adverse consequences.

Particle Design and Inhalation Delivery of Iodine for Upper Respiratory Tract Infection Therapy.

Diseases caused by upper respiratory tract (URT) and pulmonary infections have been a serious threat to human health for millennia and lack of targeted effective therapeutic techniques. In this study, two kinds of cyclodextrin particles with typical particle shapes of nanocubes and microbars were synthesized through a facile process. Subsequently, the particles were used as carriers for loading and stabilizing iodine and characterizations were performed to demonstrate the loading mechanism. Next-generation impactor (NGI) experiments showed that iodine-loaded microbars (I2@microbars) had a deposition rate of 79.75% in URT, while iodine-loaded nanocubes (I2@nanocubes) were delivered to the deep lungs with a fine particle fraction (FPF) of 46.30%. Minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC) indicated that the iodine-loaded nanocubes and microbars had similar bactericidal effect to povidone iodine solution. Cell viability studies and extracellular pro-inflammatory factor (TNF-α, IL-1ß, IL-6) evaluations demonstrate noncytotoxic effects of the blank carriers and anti-inflammatory effects of iodine-loaded samples. The irritation of the rat pharynx by I2@microbars was evaluated for the behavioral observations, body weight changes, histopathological studies, and TNF-α, IL-1ß, and IL-6 levels in pharyngeal tissues. The results showed that I2@microbars had no irritation to rat pharyngeal tissues at therapeutic doses. In conclusion, the present study provides novel treatment of URT infections via supramolecular cyclodextrin carriers for URT local therapy with iodine loading by a solvent-free method, which enhances the stability and reduces the inherent irritation without inhibiting their antimicrobial effects. Two kinds of cyclodextrin particles with typical shapes of microbars and nanocubes were synthesized by a facile process. Subsequently, iodine was successfully loaded into the particles by gas-solid interaction. The iodine-loaded microbars showed air dynamics characteristics for inhalation delivery to the upper respiratory tract with little alveolar deposition in the lungs.

Efficient capture and stabilization of iodine via gas-solid reaction using cyclodextrin metal-organic frameworks.

For treatment of wound infection with stabilized iodine, potassium iodide cyclodextrin metal-organic frameworks (KI-CD-MOF) was prepared to carry iodine via gas-solid reaction. Apart from highly ordered porous frameworks, KI-CD-MOF contains uniformly distributed iodide ions which stabilize iodine (I2). X-ray photoelectron spectroscopy and potentiometric titration were utilized to confirm the formation of I3- in the highly porous KI-CD-MOF as I2@KI-CD-MOF. Molecular simulation and characterizations of the synchrotron radiation Fourier transform infrared spectroscopy, differential scanning calorimeter, powder X-ray diffraction and N2 adsorption were conducted to illustrate the inclusion mechanism of iodine in I2@KI-CD-MOF. The apparent solubility of iodine in water was 3.86 times enhanced. The stability and antibacterial activity tests demonstrated that the highly-dispersed iodide ions in KI-CD-MOF are crucial in improvement to the solubility, stability, and bacteriostatic effects of active iodide. Therefore, KI-CD-MOF has broad application prospects and advantages in efficiently capturing and stabilizing iodine.

SnRK2 subfamily I protein kinases regulate ethylene biosynthesis by phosphorylating HB transcription factors to induce ACO1 expression in apple.

Ethylene (ETH) controls climacteric fruit ripening and can be triggered by osmotic stress. However, the mechanism regulating ETH biosynthesis during fruit ripening and under osmotic stress is largely unknown in apple (Malus domestica). Here, we explored the roles of SnRK2 protein kinases in ETH biosynthesis related to fruit ripening and osmoregulation. We identified the substrates of MdSnRK2-I using phosphorylation analysis techniques. Finally, we identified the MdSnRK2-I-mediated signaling pathway for ETH biosynthesis related to fruit ripening and osmoregulation. The activity of two MdSnRK2-I members, MdSnRK2.4 and MdSnRK2.9, was significantly upregulated during ripening or following mannitol treatment. Overexpression of MdSnRK2-I increased ETH biosynthesis under normal and osmotic conditions in apple fruit. MdSnRK2-I phosphorylated the transcription factors MdHB1 and MdHB2 to enhance their protein stability and transcriptional activity on MdACO1. MdSnRK2-I also interacted with MdACS1 and increased its protein stability through two phosphorylation sites. The increased MdACO1 expression and MdACS1 protein stability resulted in higher ETH production in apple fruit. In addition, heterologous expression of MdSnRK2-I or manipulation of SlSnRK2-I expression in tomato (Solanum lycopersicum) fruit altered fruit ripening and ETH biosynthesis. We established that MdSnRK2-I functions in fruit ripening and osmoregulation, and identified the MdSnRK2-I-mediated signaling pathway controlling ETH biosynthesis.

Prognostic and Clinicopathological Correlations of Pretreatment Prognostic Nutritional Index in Renal Cell Carcinoma: A Meta-Analysis.

INTRODUCTION: Prognostic nutritional index (PNI) was indicted as a potential prognostic biomarker for cancer. However, the conclusion remains uncertain for renal cell carcinoma (RCC). This study was to confirm the association of PNI with prognosis and clinicopathological features in RCCs. METHODS: The PubMed, EMBASE, Cochrane Library, CNKI, and Wan Fang databases were searched to retrieve eligible studies. Hazard ratios (HRs) and 95% confidence intervals (CIs) were pooled to assess the strength of the association. RESULTS: Fifteen studies were included. The results showed a low pretreatment PNI level was significantly associated with poor overall survival (HR = 1.67, 95% CI: 1.45-1.92), progression-free survival (HR = 1.72, 95% CI: 1.23-2.42), cancer-specific survival (HR = 1.17, 95% CI: 1.09-1.26), disease-free survival (HR = 1.28, 95% CI: 1.09-1.26), and recurrence-free survival (HR = 2.14, 95% CI: 1.38-3.31). This prognostic role of PNI was almost not changed by subgroup analysis based on study design, HR source, RCC type, sample size, cutoff, follow-up, treatment, and country. Furthermore, low PNI was correlated with old age, large tumor size and high T stage, Fuhrman grade, lymph node, and distant metastases. CONCLUSION: Pretreatment PNI might be a promising indicator to beforehand predict the progression and prognosis for RCC patients.

The effect of capsule tension ring on posterior capsule opacification: A meta-analysis.

BACKGROUND: Posterior capsule opacification is one of the most common complications after cataract surgery. Studies have suggested that the introduction of a capsule tension ring might play a critical role in the prevention of capsule opacification, yet quantitative evidence is still lacking. This work consists of a meta-analysis on available data in order to explore the influence of a capsule tension ring on posterior capsule opacification. METHODS: A comprehensive review of the literature on capsule tension ring and posterior capsule opacification was carried out using the Embase, Pubmed, Web of Science, and Cochrane electronic databases. The selected studies included randomized controlled trials, retrospective studies and prospective studies published before June 2020. The studies of interest were selected by two reviewers independently from the included studies. Odds ratios (ORs) and standardized mean differences (SMD) were used in order to assess the association. A fixed-effects model or a random-effects model was applied to combine data according to heterogeneities. Sensitivity analysis was used to assess the heterogeneity of the studies. Publication bias was estimated using the Egger test. Statistical analysis was performed using the stata15.1 software. RESULTS: The meta-analysis included in total 8 studies involving 379 cases and 333 controls. There was a statistically significant difference of Nd:YAG laser capsulotomy rate (OR=0.241, 95% CI: 0.145, 0.400 I2=42.1%) between the capsule tension ring group and the control group, indicating that the tension ring reduced the Nd:YAG laser capsulotomy rate. Further studies with continuous data also revealed that the use of capsule tension ring was associated with a lower posterior capsule opacification score (SMD = -1.402, 95% CI: -2.448, -0.355 I2=95.0%). The sensitivity analysis suggested that the result of the re-combined analysis did not change notably, indicating that the result was reliable and stable. Both pooled analysis showed no evidence of publication bias. CONCLUSION: The findings of this meta-analysis confirmed that capsule tension ring might reduce capsule opacification. Further studies should be made to validate the result.

Selection and validation of reference genes for quantitative gene expression normalization in Taxus spp.

Quantitative real-time PCR (qRT-PCR) is commonly used to measure gene expression to further explore gene function, while suitable reference genes must be stably expressed under different experimental conditions to obtain accurate and reproducible data for relative quantification. Taxol or paclitaxel is an important anticancer compound mainly identified in Taxus spp. The molecular mechanism of the regulation of taxol biosynthesis is current research goal. However, in the case of Taxus spp., few reports were published on screening suitable reference genes as internal controls for qRT-PCR. Here, eight reference genes were selected as candidate reference genes for further study. Common statistical algorithms geNorm, NormFinder, BestKeeper, ΔCt, and RefFinder were used to analyze the data from samples collected from a cell line of Taxus × media under various experimental conditions and from tissues of Taxus chinensis var. mairei. The expression patterns of TcMYC under salicylic acid treatment differed significantly, with the best and worst reference genes in the cell line. This study screened out suitable reference genes (GAPDH1 and SAND) under different treatments and tissues for the accurate and reliable normalization of the qRT-PCR expression data of Taxus spp. At the same time, this study will aid future research on taxol biosynthesis-related genes expression in Taxus spp., and can also be directly used to other related species.

Luteolin alleviates methamphetamine-induced neurotoxicity by suppressing PI3K/Akt pathway-modulated apoptosis and autophagy in rats.

Methamphetamine (METH) is a highly addictive stimulant that results in serious and persistent neurotoxic effects. Studies have indicated that luteolin, a flavonoid, may confer neuroprotection against neurotoxicity. Nevertheless, the effects of luteolin on METH-induced neurotoxicity have not been sufficiently verified. In the present study, Sprague Dawley rats were pretreated with luteolin (100 mg/kg) or sodium dodecyl sulfate water, followed by administration of METH (15 mg/kg) or saline. Rat striata were then collected for RNA-sequencing and subsequent analyses. A total of 347 differentially expressed genes (DEGs) were identified in the METH group with 20 pathways, including the phosphoinositol 3 kinase (PI3K)/protein kinase B (Akt), found to be enriched by the KEGG analysis. Seventy-five of the 347 DEGs were modulated in luteolin-pretreated rats, which were enriched into 12 pathways, containing the PI3K/Akt. Results further showed that luteolin pretreatment significantly repressed the METH-induced increases of PI3K, Akt, p-Akt, p53, Bax, caspase 3, normalized the ratio of p-Akt/Akt, and autophagy-related proteins (Beclin1, Atg5 and LC3-II) expression. Taken together, these findings indicate that luteolin attenuates METH-induced apoptosis and autophagy by suppressing the PI3K/Akt pathway. In this case, it exerts protection against METH-induced neurotoxicity. This provides a platform for development of potential therapies for METH treatment.

The C-terminal domain of feline and bovine SAMHD1 proteins has a crucial role in lentiviral restriction.

SAM and HD domain-containing protein 1 (SAMHD1) is a host factor that restricts reverse transcription of lentiviruses such as HIV in myeloid cells and resting T cells through its dNTP triphosphohydrolase (dNTPase) activity. Lentiviruses counteract this restriction by expressing the accessory protein Vpx or Vpr, which targets SAMHD1 for proteasomal degradation. SAMHD1 is conserved among mammals, and the feline and bovine SAMHD1 proteins (fSAM and bSAM) restrict lentiviruses by reducing cellular dNTP concentrations. However, the functional regions of fSAM and bSAM that are required for their biological functions are not well-characterized. Here, to establish alternative models to investigate SAMHD1 in vivo, we studied the restriction profile of fSAM and bSAM against different primate lentiviruses. We found that both fSAM and bSAM strongly restrict primate lentiviruses and that Vpx induces the proteasomal degradation of both fSAM and bSAM. Further investigation identified one and five amino acid sites in the C-terminal domain (CTD) of fSAM and bSAM, respectively, that are required for Vpx-mediated degradation. We also found that the CTD of bSAM is directly involved in mediating bSAM's antiviral activity by regulating dNTPase activity, whereas the CTD of fSAM is not. Our results suggest that the CTDs of fSAM and bSAM have important roles in their antiviral functions. These findings advance our understanding of the mechanism of fSAM- and bSAM-mediated viral restriction and might inform strategies for improving HIV animal models.

miR-135a deficiency inhibits the AR42J cells damage in cerulein-induced acute pancreatitis through targeting FAM129A.

Acute pancreatitis (AP) is a common clinical critical disease with high mortality and the exact pathogenesis is not fully elucidated. The present study aimed to uncover the function of miR-135a in the proliferation, apoptosis, and inflammatory characteristics of diseased pancreatic cells and the potential molecular mechanisms. The expression patterns of miR-135a and family with sequence similarity 129 member A (FAM129A) in patients with AP were analyzed on the basis of the GEO database. The transfection efficiency and expression level of miR-135a in AR42J cells were determined by qRT-PCR. The biological characteristics of AR42J cells treated with cerulein were detected by cell counting kit-8 (CCK-8), flow cytometry, and western blot assays. The potential interaction between miR-135a and FAM129A was confirmed by bioinformatics prediction softwares and luciferase reporter assay. MiR-135a inhibitor and pcDNA3.1-FAM129A were co-transfected to determine the regulation of miR-135a/FAM129A on inflammatory AR42J cell injury. We observed that miR-135a was highly expressed in AP samples. Depletion of miR-135a could alleviate the condition so that the AR42J cells proliferation increased, apoptosis decreased, and the expression of inflammatory cytokines enhanced. In addition, mRNA and protein expression of FAM129A were negatively regulated by miR-135a, and over-expression of FAM129A could strengthen the relief effect of miR-135a inhibitor in AP induced by cerulein. In summary, our data demonstrates that silencing miR-135a reduces AR42J cells injury and inflammatory response in AP induced by cerulein through targeting FAM129A.

ATF3 mRNA, but not BTG2, as a possible marker for vital reaction of skin contusion.

The detection of vitality of wounds, especially when the wounds are inflicted very close to the time of death, is one of the most challenging issues in forensic pathology. This study investigated expression levels of ATF3 and BTG2 in mouse and human skin wounds. Protein levels examined by western blot showed that there was no significant change in ATF3 and BTG2 between wounded and intact skins. However, mRNA levels demonstrated higher expression of ATF3 and BTG2 in ante-mortem contused mouse skins, compared with the intact and postmortem contused skins. Increased ATF3 and BTG2 in the level of mRNA could also be detected until 96h and 48h after death, respectively. Human wounded skin samples from forensic autopsy cases were also examined. Increased ATF3 mRNA levels were detected until 48h after autopsy in 5 of 6 cases. However, no differences were observed between wounded and intact skins for BTG2. These findings suggest that the detection of mRNA levels of ATF3, but not BTG2, can be considered as a potential marker for vital reaction of skin contusion. Postmortem human samples should be used in order to validate the availability of markers screened by animal experiment.

METH-Induced Neurotoxicity Is Alleviated by Lactulose Pretreatment Through Suppressing Oxidative Stress and Neuroinflammation in Rat Striatum.

Abuse of methamphetamine (METH) results in neurological and psychiatric abnormalities. Lactulose is a poorly absorbed derivative of lactose and can effectively alleviate METH-induced neurotoxicity in rats. The present study was designed to investigate the effects of lactulose on METH-induced neurotoxicity. Rats received METH (15 mg/kg, 8 intraperitoneal injections, 12-h interval) or saline and received lactulose (5.3 g/kg, oral gavage, 12-h interval) or vehicle 2 days prior to the METH administration. Reactive oxygen species (ROS) and malondialdehyde (MDA) were measured. Protein levels of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), tumor necrosis factor receptor associated factor 6 (TRAF6), nuclear factor κB (NFκB), interleukin (IL)-1ß, IL-6, TNF-α, cleaved caspase 3, and poly(ADP-ribose) polymerase-1 (PARP-1) were determined by western blotting. mRNA expressions of nuclear factor erythroid 2-relatted factor-2 (Nrf2), p62, and heme oxygenase-1 (HO-1) were assessed by RT-qPCR. The lactulose pretreatment decreased METH-induced cytoplasmic damage in rat livers according to histopathological observation. Compared to the control group, overproduction of ROS and MDA were observed in rat striatums in the METH alone-treated group, while the lactulose pretreatment significantly attenuated the METH-induced up-regulation of oxidative stress. The lactulose pretreatment significantly repressed over-expressions of proteins of TLR4, MyD88, TRAF6, NFκB, IL-1ß, IL-6, TNF-α, cleaved caspase 3, PARP-1. The lactulose pretreatment increased mRNA expressions of Nrf2, p62, and HO-1. These findings suggest that lactulose pretreatment can alleviate METH-induced neurotoxicity through suppressing neuroinflammation and oxidative stress, which might be attributed to the activation of the Nrf2/HO-1 axis.

Nurse-led interventions on quality of life for patients with cancer: A meta-analysis.

BACKGROUND: To compare the quality of life outcome between nurse-led and non-nurse-led interventions for patients with cancer using a meta-analysis. METHODS: A systematic literature review was performed by searching randomized controlled trials about nurse-led interventions in PubMed, EMBASE, and Cochrane Library databases until June 2017. Pooled summary estimates for quality of life outcome was calculated as standardized mean difference (SMD) either on a fixed- or random-effect model via Stata 13.0 software. RESULTS: Seven literatures involving 1110 patients (554 in the nurse-led group and 556 in the control group) were included. Pooled analysis showed there were no differences in the global quality of life, cognitive, emotional, role, social and physical functions, appetite loss, diarrhea, and dyspnea scales of Quality of Life Questionnaire C30 version 3.0 core (QLQ-C30) questionnaires between the nurse-led and control groups. However, the nurse-led management program significantly decreased the occurrence of constipation (SMD = -0.36, 95% CI = -0.71 to -0.00; P = .001) and insomnia (SMD = -0.33, 95% CI = -0.99 to 0.32; P = .011) and reduced the financial difficulty (SMD = -0.34, 95% CI = -0.65 to -0.03; P = .033) for patients with cancer. CONCLUSION: The nurse-led disease management strategy seemed to be effective to improve constipation, insomnia, and financial impacts for patients with cancer in quality of life assessment.

IL-6 and IL-20 as potential markers for vitality of skin contusion.

The detection of vitality of wounds is very important in forensic practice. This study is performed using quantitative real-time reverse transcriptase polymerase chain reaction (RT-qPCR) in both mouse and human skin wounds for the application of IL-6 and IL-20 in order to differentiate intravital wounds from postmortem wounds. RT-qPCR analysis of contused mouse skin showed that increased IL-6 and IL-20 mRNA levels were found in comparison to intact skin tissues. The increased mRNA expressions of IL-6 and IL-20 were observed until 72 h after death in contused mouse skin, whereas there were no marked changes in these two cytokines in the postmortem contusion group. The alterations of IL-6 and IL-20 can also be detected in human skin wound samples. These finding suggest that mRNA levels of IL-6 and IL-20 might be used as potential markers for vital reaction.

CXCL1 and CXCR2 as potential markers for vital reactions in skin contusions.

Detection of the vitality of wounds is one of the most important issues in forensic practice. This study investigated mRNA and protein levels of CXCL1 and CXCR2 in skin wounds in mice and humans. Western blot analysis of CXCL1 and CXCR2 protein levels showed no difference between wounded and intact skin. However, mRNA levels demonstrated higher expression of CXCL1 and CXCR2 in contused mouse and human skin, compared with intact skin. At postmortem there were no remarkable changes in CXCL1 and CXCR2 mRNA levels in contused mouse skin. Increased mRNA expression was observed in contused mouse skin up to 96 h and 72 h after death for CXCL1 and CXCR2 respectively. In human samples of wounded skin, increased CXCL1 mRNA levels were detected up to 48 h after autopsy in all 5 cases, while increased CXCR2 mRNA levels were observed 48 h after autopsy in 4 of 5 cases. These findings suggest that the levels of CXCL1 and CXCR2 mRNA present in contused skin can be used as potential markers for a vital reaction in forensic practice.

Laser-induced electron diffraction for probing rare gas atoms.

Recently, using midinfrared laser-induced electron diffraction (LIED), snapshots of a vibrating diatomic molecule on a femtosecond time scale have been captured [C.I. Blaga et al., Nature (London) 483, 194 (2012)]. In this Letter, a comprehensive treatment for the atomic LIED response is reported, a critical step in generalizing this imaging method. Electron-ion differential cross sections (DCSs) of rare gas atoms are extracted from measured angular-resolved, high-energy electron momentum distributions generated by intense midinfrared lasers. Following strong-field ionization, the high-energy electrons result from elastic rescattering of a field-driven wave packet with the parent ion. For recollision energies ≥100 eV, the measured DCSs are indistinguishable for the neutral atoms and ions, illustrating the close collision nature of this interaction. The extracted DCSs are found to be independent of laser parameters, in agreement with theory. This study establishes the key ingredients for applying LIED to femtosecond molecular imaging.