Separating acetylene from carbon dioxide is important but highly challenging due to their similar molecular shapes and physical properties. Adsorptive separation of carbon dioxide from acetylene can directly produce pure acetylene but is hardly realized because of relatively polarizable acetylene binds more strongly. Here, we reverse the CO2 and C2H2 separation by adjusting the pore structures in two isoreticular ultramicroporous metal-organic frameworks (MOFs). Under ambient conditions, copper isonicotinate (Cu(ina)2), with relatively large pore channels shows C2H2-selective adsorption with a C2H2/CO2 selectivity of 3.4, whereas its smaller-pore analogue, copper quinoline-5-carboxylate (Cu(Qc)2) shows an inverse CO2/C2H2 selectivity of 5.6. Cu(Qc)2 shows compact pore space that well matches the optimal orientation of CO2 but is not compatible for C2H2. Neutron powder diffraction experiments confirmed that CO2 molecules adopt preferential orientation along the pore channels during adsorption binding, whereas C2H2 molecules bind in an opposite fashion with distorted configurations due to their opposite quadrupole moments. Dynamic breakthrough experiments have validated the separation performance of Cu(Qc)2 for CO2/C2H2 separation.

BACKGROUND: Evidence has proven that liver fibrosis or even cirrhosis can be reversed by anti-HBV treatment. However, the difference of fibrosis regression rates in short-term and long-term antiviral therapy remain unclear. Therefore, we aimed to identify the dynamic changes in fibrosis regression rate in patients with three-time liver biopsies during 5 years antiviral therapy.
METHODS: CHB patients with three times of liver biopsies (baseline, after 1.5-year and 5-year antiviral therapy) from a prospective cohort were enrolled. All patients were biopsy-proved Ishak stage ≥ 3 at baseline (n = 92). Fibrosis regression was defined as Ishak stage decreased ≥ 1 or predominantly regressive categorized by P-I-R score.
RESULTS: Totals of 65.2% (60/92) and 80.4% (74/92) patients attained fibrosis regression after 1.5-year and 5-year therapy, respectively. Median HBV DNA level declined from 6.5 log IU/ml (baseline) to 0 log IU/ml (1.5 years and 5 years, P < 0.001). The mean level of Ishak fibrosis stage in all patients decreased from stage 4.1 (baseline) to 3.7 (1.5 years) then 3.2 (5 years). Fibrosis regression rates were 0.27 stage/year between baseline to year 1.5 and 0.14 stage/year between year 1.5 and year 5. Furthermore, for patients who attained fibrosis regression after 5-year antiviral therapy, the two-phase regression rates were 0.39 stage/year (0 year-1.5 years) and 0.20 stage/year (1.5 years-5 years). This two-phase feature of regression rate was further confirmed by fully-quantification assessment of liver fibrosis based on SHG/TPEF.
CONCLUSIONS: During the 5 years of long-term antiviral treatment, liver fibrosis rapidly regresses in the first 1.5 years before slowing down in the following 3.5 years.

Following the publication of the above article, an interested reader drew to the authors\' attention that, in Fig. 2 on p. 1408, the microscopic images shown for the light scope images (upper row) and the green fluorescence images (lower row) appeared to be overlapping, such that these images appeared to have been derived from the same original sources even though they were intended to portray the results from differently performed experiments. After having re‑examined their figures, the authors realized that this figure was assembled incorrectly. The revised version of Fig. 2, showing the correct data for all four experimental panels, is shown below. Note that the errors made during the assembly of these figures did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 37: 1405‑1411, 2016; DOI: 10.3892/ijmm.2016.2539].

Over the last few decades, although the age-standardized mortality rate (ASMR) of injury has shown a significant declining trend in China, this pattern has dramatically reversed recently.
We aimed to elucidate the geographical, demographic, and temporal trends of cause-specific injuries, the reversal phenomenon of these trends, and the fluctuations of injury burden from 2005 to 2019 in China.
A longitudinal observational study was performed using the raw data of injury deaths in the National Cause-of-Death surveillance data provided by the disease surveillance points system in 2005-2019. The cause-specific injuries were divided into disparate subgroups by sex, age, urban/rural region, and eastern/central/western areas of China. The burden of injury was assessed using potential years of life lost (PYLL), average years of life lost (AYLL), and PYLL rate (PYLLR). Temporal trends of mortality rates and burden were evaluated using best-fitting joinpoint models.
Injury deaths accounted for 7.51% (1,156,504/15,403,835) of all-cause deaths in China in 2005-2019. The crude mortality rate of all-cause injury was 47.74 per 100,000 persons. The top 3 injury types (traffic accident, falls, and suicide) accounted for 70.57% (816,145/1,156,504) of all injury-related deaths. The ASMR of all-cause injury decreased (P=.003), while the crude mortality rate remained unchanged (P=.52) during 2005-2019. A significant reverse trend in ASMR of all-cause injury was observed in urban older adults since 2013, mainly due to the inverted trend in injuries from falls. A reverse trend in ASMR of suicide was observed among individuals aged 10-24 years, with notable increases by 35.18% (annual percentage change 15.4%, 95% CI 4.1%-28.0%) in men since 2017. The AYLL and PYLLR of all-cause injury among older adults showed consistent ascending trends from 2005 to 2019 (average annual percentage change [AAPC] 6.1%, 95% CI 5.4%-6.9%, 129.04% increase for AYLL; AAPC 5.4%, 95% CI 2.4%-8.4%, 105.52% increase for PYLLR). The AYLL due to suicide for individuals aged 10-24 years showed a considerable upswing tendency (AAPC 0.5%, 95% CI 0.4%-0.7%, 8.02% increase).
Although the ASMR of all-cause injury decreased in China from 2005 to 2019, the trend in suicide among adolescents and young adults and falls among older adults has been on the rise in recent years. Interventions should be encouraged to mitigate the cause-specific burdens of injury death.

Two new (1, 2 viz Rubracin D and E) and sixteen known Glyceroglycolipids (3-18) in the saprophytic fungus Tubeufia rubra (PF02-2) from decaying wood in freshwater habitat were isolated and identified. Their chemical structures were elucidated via means of the extensive spectroscopic analyses of NMR, HR-ESI-MS and UV spectra, as well as comparison with literature data. The new compounds were assayed for the reversal activity of multidrug resistance (MDR) on MCF-7/ADM, K562/ADM and A549/ADM cell lines, and both compounds 1 and 2 reversed MDR in the three resistant cancer cell lines with concentration dependence. In the assay on K562/ADM, both new compounds had been proved to have remarkable MDR reversal effects, which were higher than those of the positive control viz Verapamil (Vrp). Meanwhile, in the assay on A549/ADM, compound 1 displayed significant MDR reversal effects, which were also higher than those of Vrp at certain concentrations. Furthermore, the Western blot assay proved that both new compounds reversed the MDR in the resistant cancer cell line viz MCF-7/ADM by inhibiting the overexpression of P-glycoprotein. This is the first report that the Glyceroglycolipids isolated firstly from the fungal genus Tubeufia reversed MDR in resistant cancer cells.

Genetic analyses showed nearly 30 amino acid mutations occurred in the spike protein of the Omicron variant of SARS-CoV-2. However, how these mutations occurred and changed during the generation and development of Omicron remains unclear. In this study, 6.7 million (all publicly available data from 2020/04/01 to 2022/04/01) SARS-CoV-2 genomes were analyzed to track the origin and evolution of Omicron variants and to reveal the genetic pathways of the generation of core mutations in Omicron. The haplotype network visualized the pre-Omicron, intact-Omicron, and post-Omicron variants and revealed their evolutionary direction. The correlation analysis showed the correlation feature of the core mutations in Omicron. Moreover, we found some core mutations, such as 142D, 417N, 440K, and 764K, reversed to ancestral residues (142G, 417K, 440N, and 764N) in the post-Omicron variant, suggesting the reverse mutations provided sources for the emergence of new variants. In summary, our analysis probed the origin and further evolution of Omicron sub-variants, which may add to our understanding of new variants and facilitate the control of the pandemic.

Background Heart failure with recovered ejection fraction (HFrecEF) has been a newly recognized entity since 2020. However, the concept has primarily focused on left ventricular ejection fraction improvement, with less focus on the recovery of the left atrium. In this study, we investigated changes in left atrial (LA) echocardiographic indices in HFrecEF. Methods and Results An inpatient cohort with heart failure with reduced ejection fraction (HFrEF) was identified retrospectively and followed up prospectively in a single tertiary hospital. The enrolled patients were classified into HFrecEF and persistent HFrEF groups. Alternations in LA parameters by echocardiography were calculated. The primary outcome was a composite of cardiovascular death or heart failure rehospitalization. A total of 699 patients were included (HFrecEF: n=228; persistent HFrEF: n=471). Compared with persistent HFrEF, the HFrecEF group had greater reductions in LA diameter, LA transverse diameter, LA superior-inferior diameter, LA volume, and LA volume index but not in LA sphericity index. Cox regression analysis showed that the HFrecEF group experienced lower risks of prespecified end points than the persistent HFrEF group after adjusting for confounders. Additionally, 136 (59.6%) and 62 (13.0%) patients showed LA reverse remodeling (LARR) for the HFrecEF and persistent HFrEF groups, respectively. Among the HFrecEF subgroup, patients with LARR had better prognosis compared with those without LARR. Multivariate logistic analysis demonstrated that age and coronary heart disease were 2 independent negative predictors for LARR. Conclusions In HFrecEF, both left ventricular systolic function and LA structure remodeling were improved. Patients with HFrecEF with LARR had improved clinical outcomes, indicating that the evaluation of LA size provides a useful biomarker for risk stratification of heart failure.

BACKGROUND: Myopia is recognized as a progressive eye disease. The aim of this study was to evaluate the frequency and associated factors of clinically significant axial length (AL) shortening among myopic children following repeated low-level red light (RLRL) therapy.
METHODS: The clinical data that were collected for the myopic children aged 3-17 years who received an RLRL therapy delivered by home-use desktop light device that emitted light at 650 nm for at least 1 year, were reviewed. The clinical data included AL, spherical equivalent refraction (SER), and visual acuity measured at baseline and follow-up. The primary outcomes were frequency of AL shortening of > 0.05 mm, > 0.10 mm, and > 0.20 mm per year, and associated factors of AL shortening per year.
RESULTS: A total of 434 myopic children with at least 12 months of follow-up data were included. The mean age of participants was 9.7 (2.6) years with SER of -3.74 (2.60) diopters. There were 115 (26.50%), 76 (17.51%), and 20 (4.61%) children with AL shortening based on cutoffs of 0.05 mm/year, 0.10 mm/year, and 0.20 mm/year, respectively. In the multivariable model, AL shortening was significantly associated with older baseline age, female gender, and longer baseline AL or greater spherical equivalent refraction (all P < 0.05). Among AL shortened eyes, the mean AL difference (standard deviation, SD) was -0.142 (0.094) mm/year. Greater AL shortening was observed among children who were younger and had longer baseline AL (all P < 0.05).
CONCLUSIONS: More than a quarter of children had AL shortening > 0.05 mm following RLRL therapy, and the overall mean AL change was -0.142 mm/year. Further studies should explore the mechanisms underlying AL shortening.

UNASSIGNED: Mammalian Target of rapamycin (mTOR) plays a central role in regulating cell growth, proliferation, and cell cycle. The key component of mTORC2 is highly expressed in docetaxel-resistant prostate cells. However, the underlying molecular effects on prostate cells remain unclear.
UNASSIGNED: A docetaxel-resistant human prostate cell line (PC-3/DTX) was constructed to investigate the role of mTORC2 in docetaxel resistance. The lentivirus was transfected into cells to knock down the expression of Rictor, and cell viability was measured by Cell Counting Kit 8 (CCK-8). Flow cytometry was used to analyze the cell cycle, and the changes in related signal cascades were assessed by immunohistochemistry (IHC) staining and Western blot.
UNASSIGNED: Docetaxel showed the lowest IC50 (50% inhibitory concentration) in PC-3/DTX cells with sh-RNA. Decreased Rictor expression resulted in a larger proportion of arrested cells in the G0/G1 phase in PC-3/DTX cells. The IC50 values of the AZD8055 group were lower than in the Rapamycin group when treated with docetaxel again. Furthermore, a larger proportion of PC-3/DTX cells were arrested in the G0/G1 phase in the AZD8055 group compared to the Rapamycin group. The IHC results of the prostate cancer tissues from a CRPC patient revealed the over expression of Rictor only, while Raptor expression was unaffected.
UNASSIGNED: We investigated the role of mTORC2 signaling on the acquired docetaxel -resistant PC-3 cells to identify potential methods for clinical treatment. MTORC2 expression is essential for docetaxel drug resistance of PC-3 cells. The mTORC1/2 inhibitor AZD8055 caused more significant disruption of mTORC2 kinase activity than the mTORC1 inhibitor Rapamycin, which lead to decreased docetaxel-mediated resistance. Therefore, reversing docetaxel resistance, may become a therapeutic option in the treatment of mCRPC patients.

Tumor recurrence and chemotherapy resistance are mainly responsible for poor prognosis in colorectal cancer (CRC) patients. Cancer stem cell (CSC) has been identified in many solid tumors, including CRC. Additionally, CSC cannot be completely killed during chemotherapy and develops resistance to chemotherapeutic drugs, which is the main reason for tumor recurrence. This study reviews the main mechanisms of CSC chemotherapy resistance in CRC, including activation of DNA damage checkpoints, epithelial-mesenchymal transition (EMT), inhibition of the overexpression of antiapoptotic regulatory factors, overexpression of ATP-binding cassette (ABC) transporters, maintenance of reactive oxygen species (ROS) levels, and the dormant state of CSC. Advances in research to reverse chemotherapy resistance are also discussed. Our study can provide the promising potential for eliminating CSC and preventing tumor progression for CRC treatment.