Publications by authors named "Peilin Zheng"

Background: Glioma is one of the most common malignant brain tumors. It has a high rate of progression and a poor prognosis, and effective biomarkers still need to be identified. The solute carrier family 12 (SLC12) family has been reported to be involved in various physiological and pathological processes, but their functional roles in glioma remain unclear.

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In recent years, there has been a remarkable surge in the approval of therapeutic protein drugs, particularly recombinant glycoproteins. Drosophila melanogaster S2 cells have become an appealing platform for the production of recombinant proteins due to their simplicity and low cost in cell culture. However, a significant limitation associated with using the S2 cell expression system is its propensity to introduce simple paucimannosidic glycosylation structures, which differs from that in the mammalian expression system.

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Islet transplantation is a promising therapy for diabetes treatment. However, the molecular underpinnings governing the immune response, particularly T-cell dynamics in syngeneic and allogeneic transplant settings, remain poorly understood. Understanding these T cell dynamics is crucial for enhancing graft acceptance and managing diabetes treatment more effectively.

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CD5 is constitutively expressed on all T cells and is a negative regulator of lymphocyte function. However, the full extent of CD5 function in immunity remains unclear. CD5 deficiency impacts thymic selection and extra-thymic regulatory T cell generation, yet CD5 knockout was reported to cause no immune pathology.

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  • * Carotid endarterectomy (CEA) is the traditional treatment for severe blockages in the internal carotid artery, while carotid artery stenting (CAS) has been proposed as a viable alternative due to advancements in medical technology.
  • * This review focuses on the emerging knowledge regarding persistent hemodynamic depression (PHD) after CAS, aiming to enhance understanding and potentially improve prognostic and therapeutic strategies.
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  • - Nonalcoholic steatohepatitis (NASH) is a serious liver disease characterized by fat accumulation, inflammation, and damage, leading to increased cases of liver failure and transplants, with KLF10 playing a potential role in its development.
  • - In both mouse models and human patients, KLF10 expression was found to increase in NASH conditions compared to simpler fat accumulation (NAFL), influencing the severity of the disease.
  • - The study revealed that KLF10 contributes to NASH progression by enhancing fat buildup and inflammation via a mechanism involving zDHHC7 and the fatty acid transporter CD36, indicating its critical role in the transition from NAFL to NASH.
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Background: This study aimed to determine the effect of PKM2 knockout in STZ induced type 1 diabetes mellitus (T1D) mouse models and to explore the possible mechanism.

Method: PKM2fl/fl C57BL/6 mouse was backcrossed with Ins-1cre C57BL/6 mouse to generate β-cell-specific PKM2 knockout mouse after tamoxifen administration. The expression level of PKM2 in pancreas tissues was detected by quantitative reverse-transcription polymerase chain reaction and western blot analysis.

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Lower limb ischemia caused by diabetic foot (DF) is one of the most serious complications of diabetes. The therapeutic role of VEGF in DF is well documented. However, the mechanism for action of VEGF is still not clear.

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Background: we demonstrated that disulfide-bond A oxidoreductase-like protein (DsbA-L) was involved in the progression of renal fibrosis. However, the precise function of DsbA-L in acute kidney injury (AKI), and the mechanisms involved, have yet to be elucidated.

Methods: We illustrate the DsbA-L interacted with VDAC1 by co-IP (co-immunoprecipitation) in vitro and vivo, and found the interaction parts of them by mutation experiment.

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Aims: High physical capability reduces risk of diabetes, but the association of its changes with risk of diabetes and glycemic control is unclear in older adults. This study aimed to quantify their association.

Methods: A total of 1,667 participants without diabetes and aged ≥ 60 years from the China Health and Retirement Longitudinal Study were included and followed over 4 years.

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Aims/hypothesis: Type 2 diabetes is associated with a reduction in skeletal muscle mass; however, how the progression of sarcopenia is induced and regulated remains largely unknown. We aimed to find out whether a specific microRNA (miR) may contribute to skeletal muscle atrophy in type 2 diabetes.

Methods: Adeno-associated virus (AAV)-mediated skeletal muscle miR-193b overexpression in C57BLKS/J mice, and skeletal muscle miR-193b deficiency in db/db mice were used to explore the function of miR-193b in muscle loss.

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Article Synopsis
  • Pancreatic beta cell failure is central to type 1 diabetes (T1D), and new research highlights the role of pathogen recognizing receptors (PRRs) in beta cell survival and function.
  • The study specifically focuses on alpha-protein kinase 1 (ALPK1) and its effect on MIN6 pancreatic beta cells, finding that ALPK1 expression increases with pro-inflammatory cytokines but does not trigger apoptosis on its own.
  • Activation of ALPK1 worsens cytokine-induced apoptosis by enhancing TNF-α signaling, suggesting a potential target for new treatments to protect beta cells in T1D.
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In this study, we investigated the role of circular RNA_30032 (circRNA_30032) in renal fibrosis and the underlying mechanisms. The study was carried out using TGF-β1-induced BUMPT cells and unilateral ureteral obstruction (UUO)-induced mice, respectively, as and models. CircRNA_30032 expression was significantly increased by 9.

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Nuclear receptors (NRs) are a superfamily of transcription factors which sense hormonal signals or nutrients to regulate various biological events, including development, reproduction, and metabolism. Here, this study identifies nuclear receptor subfamily 2, group F, member 6 (NR2F6), as an important regulator of hepatic triglyceride (TG) homeostasis and causal factor in the development of non-alcoholic fatty liver disease (NAFLD). Adeno-associated virus (AAV)-mediated overexpression of NR2F6 in the liver promotes TG accumulation in lean mice, while hepatic-specific suppression of NR2F6 improves obesity-associated hepatosteatosis, insulin resistance, and methionine and choline-deficient (MCD) diet-induced non-alcoholic steatohepatitis (NASH).

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Quantum compiling, a process that decomposes the quantum algorithm into a series of hardware-compatible commands or elementary gates, is of fundamental importance for quantum computing. We introduce an efficient algorithm based on deep reinforcement learning that compiles an arbitrary single-qubit gate into a sequence of elementary gates from a finite universal set. It generates near-optimal gate sequences with given accuracy and is generally applicable to various scenarios, independent of the hardware-feasible universal set and free from using ancillary qubits.

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  • Recent research shows that the DsbA-L protein can help prevent kidney damage caused by high lipid levels in diabetic nephropathy, but its role in renal tubulointerstitial fibrosis (TIF) is still not well understood.
  • The study revealed that mice lacking DsbA-L in proximal tubules had reduced TIF, kidney cell death, and inflammation when subjected to surgical obstruction.
  • The mechanism involves DsbA-L interacting with another protein, Hsp90, which activates pathways that lead to tissue growth factors, ultimately increasing fibrosis in kidney tissues, a finding also confirmed in biopsies from patients with kidney obstruction.
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Purpose: Neuroendocrine differentiation (NED) may serve as a prognostic factor in colorectal cancer; however, the prognostic relevance of NED remains controversial. The aim of the present study was to determine whether NED influenced the survival of patients in colorectal cancer while exploring its potential interactions with other clinicopathological features.

Methods: Patients with primary stage I to IV colorectal adenocarcinoma ranging between 2010 and 2015 were identified using the Surveillance, Epidemiology, and End Results database.

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  • - The study investigates how tumor deposits in stage III colon cancer affect patient survival, comparing those with only lymph node metastasis (LNM) to those with both LNM and tumor deposits.
  • - Analysis of over 23,000 patients revealed that having both LNM and tumor deposits was linked to a significantly worse overall survival rate.
  • - When combining the number of tumor deposits with lymph nodes, the prognostic impact seemed similar to having LNM alone, suggesting that tumor deposits should be treated as LNM in these patients.
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The prediction of mortality for septic acute kidney injury (AKI) has been assessed by a number of potential biomarkers, including long noncoding RNAs (lncRNAs). However, the validation of lncRNAs as biomarkers, particularly for the early stages of septic AKI, is still warranted. Our results indicate that the lncRNA TCONS_00016233 is upregulated in plasma of sepsis-associated non-AKI and AKI patients, but a higher cutoff threshold (9.

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  • - The study developed and validated a nomogram to predict cancer-specific survival (CSS) in elderly patients with stages I-III colon cancer using data from the SEER database from 2010 to 2015.
  • - Key factors like tumor grade, stage, node involvement, and treatment options were identified as independent predictors of CSS, and the nomogram demonstrated a C-index of 0.728, outperforming traditional staging methods.
  • - Validation results indicated that the nomogram effectively stratified patients into risk groups, providing valuable insights for patient counseling and clinical decision-making regarding long-term survival.
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Type 1 diabetes (T1D) is an autoimmune disease caused by the dysfunction of immune system and consequently the destruction of insulin-producing β cells. In past decades, numerous studies have uncovered that CD4 T cell subsets are critical in the pathogenesis of T1D, manifesting that type 1 T helper (Th1) and Th17 cells are pathogenic, while regulatory T (Treg) cells and Th2 cells are protective. More recently, the pathogenic role of another subset, follicular helper T (Tfh) cells that essentially regulate germinal center (GC) formation and humoral responses, has also been demonstrated in T1D and many other autoimmune diseases.

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Purpose: A coding variant in PTPN22 (C1858T) is one of the most important genetic risk factors in type 1 diabetes (T1D). The role of the PTPN22 risk allele in B cells is still incompletely understood and has not been investigated directly in T1D. This study aimed to explore the role of PTPN22 in the homeostasis of B cells and its influence in T1D.

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Background: The clinical characteristics of stage III colon cancer and the prognostic significance of tumor deposits were investigated, to construct a prognostic nomogram.

Methods: The data of patients were retrieved from the Surveillance, Epidemiology, and End Results database. Patients were randomized to a training or validation cohort.

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Type 1 diabetes (T1D) is an autoimmune disease characterized by the immune-mediated destruction of insulin-producing β cells. Recent studies showed that in addition to malaria, artemisinin and its derivative, artesunate (AS), could alleviate several autoimmune diseases. However, whether AS has a role in the prevention or treatment of T1D is still unknown.

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