Exploring pore-scale production characteristics of oil shale after CO_(2) huff‘n’puff in fractured shale with varied permeability

Recent studies have indicated that the injection of carbon dioxide(CO_(2))can lead to increased oil recovery in fractured shale reservoirs following natural depletion.Despite advancements in understanding mass exchange processes in subsurface formations,there remains a knowledge gap concerning the disparities in these processes between the matrix and fractures at the pore scale in formations with varying permeability.This study aims to experimentally investigate the CO_(2) diffusion behaviors and in situ oil recovery through a CO_(2) huff‘n’puff process in the Jimsar shale oil reservoir.To achieve this,we designed three matrix-fracture models with different permeabilities(0.074 mD,0.170 mD,and 0.466 mD)and experimented at 30 MPa and 91°C.The oil concentration in both the matrix and fracture was monitored using a low-field nuclear magnetic resonance(LF-NMR)technique to quantify in situ oil recovery and elucidate mass-exchange behaviors.The results showed that after three cycles of CO_(2) huff‘n’puff,the total recovery degree increased from 30.28%to 34.95%as the matrix permeability of the core samples increased from 0.074 to 0.466 mD,indicating a positive correlation between CO_(2) extraction efficiency and matrix permeability.Under similar fracture conditions,the increase in matrix permeability further promoted CO_(2) extraction efficiency during CO_(2) huff‘n’puff.Specifically,the increase in matrix permeability of the core had the greatest effect on the extraction of the first-cycle injection in large pores,which increased from 16.42%to 36.64%.The findings from our research provide valuable insights into the CO_(2) huff‘n’puff effects in different pore sizes following fracturing under varying permeability conditions,shedding light on the mechanisms of CO_(2)-enhanced oil recovery in fractured shale oil reservoirs.

3-Methyladenine potentiates paclitaxel-induced apoptosis and phosphorylation of cyclin-dependent kinase 1 at thr161 in nasopharyngeal carcinoma cell

Background:Nasopharyngeal carcinoma(NPC)exhibits a significant prevalence in the southern regions of China,and paclitaxel(PTX)is frequently employed as a medication for managing advanced NPC.However,drug resistance is typically accompanied by a poor prognosis.Exploring the synergistic potential of combining multiple chemotherapeutic agents may represent a promising avenue for optimizing treatment efficacy.Methods:This study investigated whether 3-Methyladenine(3-MA)could potentiated the effect of PTX and its potential molecular mechanism.Samples were divided into the following categories:Negative control(NC)with the solvent dimethyl sulfoxide(DMSO,0.5%v/v),PTX(400 nM),3-MA(4 mM),and PTX(400 nM)+3-MA(4 mM).The viability of NPC cells was assessed using both the cell counting kit-8(CCK-8)assay and the colony formation assay.Microscopic observation was performed to identify morphological cell changes.Flow cytometry was used to assess cell cycle status,mitochondrial membrane potential(MMP),and apoptotic cells.Western blotting was conducted to quantify the protein expression.Results:3-MA enhanced PTX-specific inhibition of NPC cell proliferation.PTX,either alone or in combination with 3-MA,caused cell cycle halt at the G2/M phase in the majority of NPC cells,and the combination treatment of PTX with 3-MA induced a higher rate of NPC cell death compared to PTX alone.Western blotting results revealed the combination of PTX with 3-MA heightened activation of cyclin-dependent kinase 1(CDK1),a key molecule in shifting cells from mitotic arrest to apoptosis,led to a reduction in Myeloid Cell Leukemia 1(MCL-1)expression and an increase in Poly(ADP-ribose)polymerase(PARP)cleavage.Conclusion:The concurrent administration of PTX with 3-MA effectively enhances PTX’s inhibitory impact on NPC and activates the apoptosis signal regulated by CDK1.

Trafficking abnormality and ER stress underlie functional deficiency of hearing impairmentassociated connexin-31 mutants

Hearing impairment(HI)affects 1/1000 children and over 2%of the aged population.We have previously reported that mutations in the gene encoding gap junction protein connexin-31(Cx31)are associated with HI.The pathological mechanism of the disease mutations remains unknown.Here,we show that expression of Cx31 in the mouse inner ear is developmentally regulated with a high level in adult inner hair cells and spiral ganglion neurons that are critical for the hearing process.In transfected cells,wild type Cx31 protein(Cx31wt)forms functional gap junction at cell-cell-contacts.In contrast,two HIassociated Cx31 mutants,Cx31R180X and Cx31E183K resided primarily in the ER and Golgi-like intracellular punctate structures,respectively,and failed to mediate lucifer yellow transfer.Expression of Cx31 mutants but not Cx31wt leads to upregulation of and increased association with the ER chaperone BiP indicating ER stress induction.Together,the HI-associated Cx31 mutants are impaired in trafficking,promote ER stress,and hence lose the ability to assemble functional gap junctions.The study reveals a potential pathological mechanism of HI-associated Cx31 mutations.