Impact of sarcopenia on variceal rebleeding in patients after endoscopic therapy: a multicenter retrospective cohort study based on propensity score matching.

BACKGROUND: Sarcopenia is a common complication of liver cirrhosis and can be used for predicting dismal prognostic outcomes. This study aimed to evaluate the role of sarcopenia in rebleeding and mortality of liver cirrhosis patients after endoscopic therapy. METHODS: The liver cirrhosis patients who received endoscopic treatment were enrolled. Propensity score matching (PSM) was used to overcome selection bias. Two-year rebleeding episodes and mortality after endoscopic therapy were recorded. RESULTS: A total of 109 (32.4%) sarcopenia patients were reported. Before PSM, the frequency of rebleeding was significantly higher in the sarcopenia group relative to the non-sarcopenia group (41.3% vs. 15.9%, p < 0.001). Moreover, the multivariable analysis revealed that sarcopenia (p < 0.001, HR:2.596, 95% CI 1.591-4.237) was independently associated with a 2-year rebleeding episode. After PSM, the sarcopenia group exhibited an increased rebleeding rate as compared with non-sarcopenia group (44.4% vs. 15.3%, p < 0.001). According to multivariable analysis, sarcopenia (p < 0.001, HR:3.490, 95% CI 1.756-6.938) was identified as a significant predictor for 2-year rebleeding. CONCLUSION: Sarcopenia was significantly associated with a high 2-year rebleeding rate in liver cirrhosis patients after endoscopic treatment. Therefore, the precise evaluation of a patient's nutritional status, including sarcopenia becomes mandatory before endoscopic treatment.

ERK signaling expands mammalian cortical radial glial cells and extends the neurogenic period.

The molecular basis for cortical expansion during evolution remains largely unknown. Here, we report that fibroblast growth factor (FGF)-extracellular signal-regulated kinase (ERK) signaling promotes the self-renewal and expansion of cortical radial glial (RG) cells. Furthermore, FGF-ERK signaling induces bone morphogenic protein 7 (Bmp7) expression in cortical RG cells, which increases the length of the neurogenic period. We demonstrate that ERK signaling and Sonic Hedgehog (SHH) signaling mutually inhibit each other in cortical RG cells. We provide evidence that ERK signaling is elevated in cortical RG cells during development and evolution. We propose that the expansion of the mammalian cortex, notably in human, is driven by the ERK-BMP7-GLI3R signaling pathway in cortical RG cells, which participates in a positive feedback loop through antagonizing SHH signaling. We also propose that the relatively short cortical neurogenic period in mice is partly due to mouse cortical RG cells receiving higher SHH signaling that antagonizes ERK signaling.

Rapid Silicification of a DNA Origami with Shape Fidelity.

High-fidelity patterning of DNA origami nanostructures on various interfaces holds great potential for nanoelectronics and nanophotonics. However, distortion of a DNA origami often occurs due to the strong interface interactions, e.g., on two-dimensional (2D) materials. In this study, we discovered that the adsorption of silica precursors in rapid silicification can prevent the distortion caused by graphene and generates a high shape-fidelity DNA origami-silica composite on a graphene interface. We found that an incubation time of 1 min and silicification time of 16 h resulted in the formation of DNA origami-silica composites with the highest shape fidelity of 99%. By comparing the distortion of the DNA origami on the graphene interface with and without silicification, we observed that rapid silicification effectively preserved the integrity of the DNA origami. Statistical analysis of scanning electron microscopy data indicates that compared to bare DNA origami, the DNA origami-silica composite has an increased shape fidelity by more than two folds. Furthermore, molecular dynamics simulations revealed that rapid silicification effectively suppresses the distortion of the DNA origami through the interhelical insertion of silica precursors. Our strategy provides a simple yet effective solution to maintain the shape-fidelity DNA origami on interfaces that have strong interaction with DNA molecules, expanding the applicable interfaces for patterning 2D DNA origamis.

Prevalence and risk factors for cirrhotic cardiomyopathy: a prospective cross-sectional study.

BACKGROUND: This study aimed to assess cardiac structure and function in patients with cirrhosis, to investigate the prevalence of cirrhotic cardiomyopathy (CCM) in patients with cirrhosis of different etiologies and to analyze the risk factors for the development of CCM. METHODS: This study selected cirrhotic patients aged 18-75 years who were hospitalized in Qilu Hospital of Shandong University. Patients with known heart disease, chronic lung disease, severe renal insufficiency, malignancy, thyroid disease, hypertension, diabetes or pregnancy were excluded. A total of 131 patients with cirrhosis were finally included. Based on the results of echocardiography, patients who met the diagnostic definition of CCM were included in the CCM group, otherwise, they were classified as the non-CCM group. The demographic and clinical data of the two groups were compared, and the clinical characteristics and risk factors of CCM were evaluated. RESULTS: The overall prevalence of CCM was 24.4%, and the occurrence of CCM was not related to the etiology of liver cirrhosis. The prevalence of CCM was significantly higher among cirrhotic patients complicated with ascites (31.4% vs. 16.4%; P  = 0.046) or with portal vein thrombosis (PVT) (42.9% vs. 17.1%; P  = 0.003). Older age [odds ratio (OR) = 1.058; 95% confidence interval (CI), 1.005-1.113; P  = 0.032] and PVT (OR = 2.999; 95% CI, 1.194-7.533; P  = 0.019) were independent risk factors for the development of CCM. CONCLUSION: The prevalence of CCM in cirrhotic patients was 24.4%, and the occurrence of CCM was not related to the etiology of cirrhosis. The prevalence of CCM was higher in cirrhotic patients with ascites or PVT. Older age and PVT are independent risk factors for CCM, but validation in larger sample studies is still needed.

Influence of subcutaneous adipose tissue index on prognosis in cirrhotic patients following endoscopic therapy: a retrospective cohort study.

BACKGROUND: The relation of adipose tissue depletion with prognostic outcome of variceal bleeding among cirrhotic patients is still inconclusive. The present work explored whether adipose tissue, which was measured based on computed tomography (CT), was valuable for analyzing rebleeding and mortality among patients with variceal bleeding who had undergone endoscopic therapy. METHODS: The study encompassed cirrhotic patients who underwent endoscopic therapy to prevent variceal rebleeding between January 2016 and October 2022. The L3-level CT images were obtained. Besides, impacts of subcutaneous adipose tissue index (SATI), visceral adipose tissue index (VATI), as well as total adipose tissue index (TATI) on rebleeding and mortality among cirrhotic patients following endoscopic therapy were examined. RESULTS: In this work, our median follow-up period was 31 months. Among those adipose tissue indexes, only SATI exhibited an independent relation to higher rebleeding (HR 0.981, 95% CI, 0.971-0.991, p < 0.001) and mortality (HR 0.965, 95% CI, 0.944-0.986, p = 0.001) risks. Upon multivariate Cox regression, low SATI (male < 30.15 cm2/m2, female < 39.82 cm2/m2) was independently linked to higher rebleeding risk (HR 2.511, 95% CI, 1.604-3.932, p < 0.001) and increased mortality risk (HR 3.422, 95% CI, 1.489-7.864, p = 0.004) after adjusting for other predictors. Furthermore, subgroups were created based on using nonselective ß-blockers (NSBBs), demonstrating that quantitatively assessing SATI exerts a vital role in evaluating rebleeding incidence in patients with or without NSBB therapy. CONCLUSION: This study underscores the potential of quantifying SATI as a means for achieving a more accurate risk classification for individual patients and identifying patients that can gain more benefits from nutritional intervention.

BMP7 expression in mammalian cortical radial glial cells increases the length of the neurogenic period.

The seat of human intelligence is the human cerebral cortex, which is responsible for our exceptional cognitive abilities. Identifying principles that lead to the development of the large-sized human cerebral cortex will shed light on what makes the human brain and species so special. The remarkable increase in the number of human cortical pyramidal neurons and the size of the human cerebral cortex is mainly because human cortical radial glial cells, primary neural stem cells in the cortex, generate cortical pyramidal neurons for more than 130 days, whereas the same process takes only about 7 days in mice. The molecular mechanisms underlying this difference are largely unknown. Here, we found that bone morphogenic protein 7 (BMP7) is expressed by increasing the number of cortical radial glial cells during mammalian evolution (mouse, ferret, monkey, and human). BMP7 expression in cortical radial glial cells promotes neurogenesis, inhibits gliogenesis, and thereby increases the length of the neurogenic period, whereas Sonic Hedgehog (SHH) signaling promotes cortical gliogenesis. We demonstrate that BMP7 signaling and SHH signaling mutually inhibit each other through regulation of GLI3 repressor formation. We propose that BMP7 drives the evolutionary expansion of the mammalian cortex by increasing the length of the neurogenic period.

Context-dependent regulation of Notch signaling in glial development and tumorigenesis.

In the mammalian brain, Notch signaling maintains the cortical stem cell pool and regulates the glial cell fate choice and differentiation. However, the function of Notch in regulating glial development and its involvement in tumorigenesis have not been well understood. Here, we show that Notch inactivation by genetic deletion of Rbpj in stem cells decreases astrocytes but increases oligodendrocytes with altered internal states. Inhibiting Notch in glial progenitors does not affect cell generation but instead accelerates the growth of Notch-deprived oligodendrocyte progenitor cells (OPCs) and OPC-related glioma. We also identified a cross-talk between oligodendrocytes and astrocytes, with premyelinating oligodendrocytes secreting BMP4, which is repressed by Notch, to up-regulate GFAP expression in adjacent astrocytes. Moreover, Notch inactivation in stem cells causes a glioma subtype shift from astroglia-associated to OPC-correlated patterns and vice versa. Our study reveals Notch's context-dependent function, promoting astrocytes and astroglia-associated glioma in stem cells and repressing OPCs and related glioma in glial progenitors.

The clinical characteristics of focal acute pancreatitis based on imaging diagnosis: comparison with non-localized acute pancreatitis- a preliminary result.

BACKGROUND: Focal acute pancreatitis is a special type of acute pancreatitis, which diagnosis is based on image showing a focal mass formation in the pancreas. For acute pancreatitis with or without focal inflammatory enlargement, little is known on differences between them. Our purpose was to find differences between focal acute pancreatitis and non-localized acute pancreatitis. METHODS: We reviewed the medical records of a total of 24 patients diagnosed with focal acute pancreatitis by imaging and clinical diagnosis, and 27 cases of acute pancreatitis which manifest non-localized pancreas inflammation were selected as the control group. The differences of the two groups were compared to describe their clinical characteristics. RESULTS: Differences in bloating (4.2% VS 29.6%,P = 0.026), abdominal tenderness (58.3% VS 85.2%,P = 0.032), peripheral blood neutrophil ratio (60.1 ± 23.3VS 75.9 ± 12.6,P = 0.004), serum D-Dimer (0.40(0.25,0.98) VS 1.59(0.49,4.63),P = 0.008), serum GGT (40(25,91) VS120(22,383),P = 0.046), serum amylase(435(241,718) VS 591(394,1333),P = 0.044) and lipase(988(648,1067) VS 1686(525,2675),P = 0.027) between focal acute pancreatitis and non-localized acute pancreatitis groups were statistically significant. However, difference of the severity of two groups was not statistically significant (P = 1.000). CONCLUSION: Compared with non-localized acute pancreatitis, changes in symptoms, signs and laboratory indicators of focal acute pancreatitis are non-obvious, however, there was no significant difference in the severity of two groups, indicating that we should pay more attention to diagnosis of focal acute pancreatitis in clinical practice.

Constructing Intrapenetrated Hierarchical Zeolites with Highly Complete Framework via Protozeolite Seeding.

Creation of intrapenetrated mesopores with open highway from external surface into the interior of zeolite crystals are highly desirable that can significantly improve the molecular transport and active sites accessibility of microporous zeolites to afford enhanced catalytic properties. Here, different from traditional zeolite-seeded methods that generally produced isolated mesopores in zeolites, nanosized amorphous protozeolites with embryo structure of zeolites were used as seeds for the construction of single-crystalline hierarchical ZSM-5 zeolites with intrapenetrated mesopores (mesopore volume of 0.51 cm3 g-1 ) and highly complete framework. In this strategy, in contrast to the conventional synthesis, only a small amount of organic structure directing agents and a low crystallization temperature were adopted to promise the protozeolites as the dominant growth directing sites to induce crystallization. The protozeolite nanoseeds provided abundant nucleation sites for surrounding precursors to be crystallized, followed by oriented coalescence of crystallites resulting in the formation of intrapenetrated mesopores. The as-prepared hierarchical ZSM-5 zeolites exhibited ultra-long lifetime of 443.9 hours and a high propylene selectivity of 47.92 % at a WHSV of 2 h-1 in the methanol-to-propylene reaction. This work provides a facile protozeolite-seeded strategy for the synthesis of intrapenetrated hierarchical zeolites that are highly effective for catalytic applications.

A multi-omics study to investigate the progression of the Correa pathway in gastric mucosa in the context of cirrhosis.

BACKGROUND: Patients with liver cirrhosis (LC) are prone to gastric mucosa damage. We investigated the alterations of gastric mucosa in LC patients and their possible mechanisms through multi-omics. RESULTS: We observed significant gastric mucosa microbial dysbiosis in LC subjects. Gastric mucosal microbiomes of LC patients contained a higher relative abundance of Streptococcus, Neisseria, Prevotella, Veillonella, and Porphyromonas, as well as a decreased abundance in Helicobacter and Achromobacter, than control subjects. The LC patients had higher levels of bile acids (BAs) and long-chain acylcarnitines (long-chain ACs) in serum. The gastric mucosal microbiomes were associated with serum levels of BAs and long-chain ACs. Transcriptome analyses of gastric mucosa revealed an upregulation of endothelial cell specific molecule 1, serpin family E member 1, mucin 2, caudal type homeobox 2, retinol binding protein 2, and defensin alpha 5 in LC group. Besides, the bile secretion signaling pathway was significantly upregulated in the LC group. CONCLUSIONS: The alterations in the gastric mucosal microbiome and transcriptome of LC patients were identified. The impaired energy metabolism in gastric mucosal cells and bile acids might aggravate the inflammation of gastric mucosa and even exacerbate the Correa's cascade process. The gastric mucosal cells might reduce bile acid toxicity by bile acid efflux and detoxification. TRIAL REGISTRATION: ChiCTR2100051070.

Partial splenic embolization combined with endoscopic therapies and vasoconstrictive drugs reduces rebleeding in cirrhosis patients with acute variceal bleeding and hypersplenism: a multicenter randomized controlled trial.

BACKGROUND: This study aimed to compare the efficacy of partial splenic embolization (PSE) combined with endoscopic therapy and endoscopic therapy alone in cirrhosis patients with acute variceal bleeding (AVB) and hypersplenism. METHODS: Cirrhosis patients with AVB who visited three hospitals from June 2016 to June 2022 were prospectively enrolled and randomly allocated to either the endoscopic therapy combined with PSE group (EP group) or the endoscopic intervention group (E group) in a 1:1 ratio. The primary endpoint of the study was re-bleeding of varices during follow-up, and the secondary endpoints were the recurrence of varices, death, and adverse events. RESULTS: One hundred and fourteen patients were prospectively included, of whom 110 completed the trial. The risk of variceal re-bleeding (19.3% vs. 40.4% (23/57), p = 0.013) and variceal recurrence (28.1% vs. 63.2%, p < 0.001) five years after treatment was significantly lower in the EP group than in the E group, and the EP treatment was the only significant independent risk factor affecting variceal re-bleeding and variceal recurrence in patients. The mortality rate was comparable between the EP and E groups. Peripheral blood counts and liver function all improved significantly in the EP group compared to the E group during the follow-up (p < 0.05). CONCLUSIONS: The rates of variceal re-bleeding and recurrence were significantly lower in cirrhosis patients with AVB and hypersplenism after combined endoscopic and PSE treatment compared to those who were provided endoscopic treatment only. The peripheral blood counts and liver function were also improved significantly in EP group (NCT02778425).

In situ subtotal spleen resection combined with selective pericardial devascularization for the treatment of portal hypertension.

BACKGROUND: Hypersplenism and esophageal varices bleeding are the major complications of portal hypertension (PHT). In recent years, increasing attention has been given to spleen preservation operations. The mode and long-term effects of subtotal splenectomy and selective pericardial devascularization for PHT remain controversial. AIM: To investigate the clinical efficacy and safety of subtotal splenectomy combined with selective pericardial devascularization for the treatment of PHT. METHODS: This was a retrospective study of 15 patients with PHT who underwent subtotal splenectomy not preserving the splenic artery or vein combined with selective pericardial devascularization in the Department of Hepatobiliary Surgery, Qilu Hospital of Shandong University from February 2011 to April 2022. Fifteen propensity score-matched patients with PHT who underwent total splenectomy at the same time served as the control group. The patients were followed for up to 11 years after surgery. We compared the postoperative platelet levels, perioperative splenic vein thrombosis, and serum immunoglobulin levels between the two groups. Abdominal enhanced computed tomography was used to evaluate the blood supply and function of the residual spleen. The operation time, intraoperative blood loss, evacuation time, and hospital stay were compared between the two groups. RESULTS: The postoperative platelet level of patients in the subtotal splenectomy group was significantly lower than that in the total splenectomy group (P < 0.05), and the postoperative portal system thrombosis rate in the subtotal splenectomy group was also much lower than that in the total splenectomy group. The levels of serum immunoglobulins (IgG, IgA, and IgM) showed no significant differences after surgery compared with before surgery in the subtotal splenectomy group (P > 0.05), but serum immunoglobulin IgG and IgM levels decreased dramatically after total splenectomy (P < 0.05). The operation time in the subtotal splenectomy group was longer than that in the total splenectomy group (P < 0.05), but there were no significant differences in the amount of intraoperative blood loss, evacuation time, or hospital stay between the two groups. CONCLUSION: Subtotal splenectomy not preserving the splenic artery or vein combined with selective pericardial devascularization is a safe and effective surgical treatment for patients with PHT, not only correcting hypersplenism but also preserving splenic function, especially immunological function.

Micron-Scale Fabrication of Ultrathin Amorphous Copper Nanosheets Templated by DNA Scaffolds.

Two-dimensional (2D) amorphous materials could outperform their crystalline counterparts toward various applications because they have more defects and reactive sites and thus could exhibit a unique surface chemical state and provide an advanced electron/ion transport path. Nevertheless, it is challenging to fabricate ultrathin and large-sized 2D amorphous metallic nanomaterials in a mild and controllable manner due to the strong metallic bonds between metal atoms. Here, we reported a simple yet fast (10 min) DNA nanosheet (DNS)-templated method to synthesize micron-scale amorphous copper nanosheets (CuNSs) with a thickness of 1.9 ± 0.4 nm in aqueous solution at room temperature. We demonstrated the amorphous feature of the DNS/CuNSs by transmission electron microscopy (TEM) and X-ray diffraction (XRD). Interestingly, we found that they could transform to crystalline forms under continuous electron beam irradiation. Of note, the amorphous DNS/CuNSs exhibited much stronger photoemission (∼62-fold) and photostability than dsDNA-templated discrete Cu nanoclusters due to the elevation of both the conduction band (CB) and valence band (VB). Such ultrathin amorphous DNS/CuNSs hold great potential for practical applications in biosensing, nanodevices, and photodevices.

Anticoagulation therapy early is safe in portal vein thrombosis patients with acute variceal bleeding: a multi-centric randomized controlled trial.

Portal vein thrombosis (PVT) and acute variceal bleeding (AVB) are frequent complications of cirrhosis. The efficacy, safety, and timing of anticoagulant treatment in cirrhotic patients with PVT and AVB are contentious issues. We aimed to establish the safety and efficacy of initiating nadroparin calcium-warfarin sequential (NWS) anticoagulation therapy early after esophageal variceal band ligation within PVT patients having cirrhosis and AVB. Cirrhotic patients having AVB and PVT who underwent EVL were included and randomly allocated to either the NWS therapy group (1-month nadroparin calcium by subcutaneous injection following 5-month warfarin through oral administration, n = 43) or the control group (without any anticoagulation therapy, n = 43). The primary endpoint was the rate of PVT recanalization. Secondary endpoints included major bleeding events mainly referring to variceal rebleeding (5-day failure, 14-day, 4-week, 6-week, and 6-month rebleeding rates) and mortality after EVL. The overall recanalization (complete and partial) rate in the NWS therapy group was significantly higher than that in the control group (67.4% vs. 39.5%, P = 0.009). Low Child-Pugh score (P = 0.039, OR: 0.692, 95% CI 0.488-0.982), D-dimer < 2.00 ug/mL (P = 0.030, OR: 3.600, 95% CI 1.134-11.430), and NWS anticoagulation therapy (P = 0.002, OR: 4.189, 95% CI 1.660-10.568) were the predictors of PVT recanalization through univariate analysis of binary logistic regression. NWS anticoagulation therapy (P = 0.003, OR: 4.506, 95% CI 1.687-12.037) was the independent factor of recanalization through multivariate analysis. Nobody bled except for variceal rebleeding. Five-day failure and 14-day rebleeding were zero. There were no significantly different in 4-week (2.3% vs. 4.7%, P = 1.000), 6-week (4.7% vs. 9.3%, P = 0.672) and 6-month rebleeding (18.6% vs. 20.9%, P = 0.787) between the two groups. There was no mortality during six months follow-up. Low serum albumin (P = 0.011, OR: 0.844, 95% CI 0.741-0.962), high MELD score (P = 0.003, OR: 1.564, 95% CI 1.167-2.097) and Child-Pugh score (P = 0.006, OR: 1.950, 95% CI 1.206-3.155) were predictors of rebleeding by univariate analysis of binary logistic regression analysis. The Child-Pugh score (7 [6-8] vs. 6 [5-7], P = 0.003) and albumin levels (33.93 ± 5.30 vs. 37.28 ± 4.32, P = 0.002) were improved in the NWS therapy group at six months. In PVT patients with cirrhosis and AVB, starting NWS anticoagulation therapy early after EVL was safe and effective. It has the potential to raise albumin levels and improve liver function.

Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice.

Introduction: Age is an established risk factor for neurodegenerative disorders. Aging-related cognitive decline is a common cause of memory impairment in aging individuals, in which hippocampal synaptic plasticity and hippocampus-dependent memory formation are damaged. Circular RNAs (circRNAs) have been reported in many cognitive disorders, but their role in aging-related memory impairment is unclear.Methods: In this study, we aimed to investigate the effects of circ-Vps41 on aging-related hippocampus-dependent memory impairment and explore the potential mechanisms. Here, D-galactose was used to produce a conventional aging model resulting in memory dysfunction. Results: Circ-Vps41 was significantly downregulated in D-galactose-induced aging in vitro and in vivo. The overexpression of circ-Vps41 could upregulate synaptophysin (Syp), thereby promoting the synaptic plasticity and alleviating cognitive impairment in aging mice. Mechanistically, we found that circ-Vps41 upregulated Syp expression by physically binding to miR-24-3p. Moreover, the miR-24-3p mimics reversed the circ-Vps41 overexpression-induced increase in Syp expression. Discussion: Overexpression of circ-Vps41 alleviated the synaptic plasticity and memory dysfunction via the miR-24-3p/Syp axis. These findings revealed circ-Vps41 regulatory network and provided new insights into its potential mechanisms for improving aging-related learning and memory impairment.

The transcription factor Zfp503 promotes the D1 MSN identity and represses the D2 MSN identity.

The striatum is primarily composed of two types of medium spiny neurons (MSNs) expressing either D1- or D2-type dopamine receptors. However, the fate determination of these two types of neurons is not fully understood. Here, we found that D1 MSNs undergo fate switching to D2 MSNs in the absence of Zfp503. Furthermore, scRNA-seq revealed that the transcription factor Zfp503 affects the differentiation of these progenitor cells in the lateral ganglionic eminence (LGE). More importantly, we found that the transcription factors Sp8/9, which are required for the differentiation of D2 MSNs, are repressed by Zfp503. Finally, sustained Zfp503 expression in LGE progenitor cells promoted the D1 MSN identity and repressed the D2 MSN identity. Overall, our findings indicated that Zfp503 promotes the D1 MSN identity and represses the D2 MSN identity by regulating Sp8/9 expression during striatal MSN development.

Association between the severity of metabolic dysfunction-associated fatty liver disease and the risk of colorectal neoplasm: a systematic review and meta-analysis.

BACKGROUND: The severity of metabolic dysfunction-associated fatty liver disease (MAFLD) reportedly plays a part in the etiology of colorectal tumors. However, there is no consensus. METHODS: Studies relevant with the impact of MAFLD severity on the risk of colorectal neoplasms published before 24th April 2022 were screened. The pooled odds ratio (OR) with corresponding 95% confidence intervals (95% CI) was obtained using standard and cumulative meta-analyses. Subgroup, meta-regression, and sensitivity analyses were carried out to identify heterogeneity. RESULTS: Fourteen studies with data from 37,824 MAFLD patients were included. The prevalence of colorectal neoplasms escalated with the progression of MAFLD compared to simple steatosis (OR = 1.93; 95% CI = 1.42-2.62). The magnitude and direction of the effect on these outcomes remained largely constant over time. Even after limiting the meta-analysis to 8 studies with available adjusted OR (aOR), the findings still suggested that MAFLD severity was positively related to colorectal neoplasms (aOR = 3.03; 95% CI = 2.02-4.53). Severe MAFLD was more likely to cause left colon tumors (OR = 3.86, 95% CI = 2.16-6.91) than right colon neoplasms (OR = 1.94, 95% CI = 1.15-3.28). CONCLUSION: The severity of MAFLD was independently related to colorectal neoplasms and severe MAFLD was more likely to cause left colon tumors.

DNA Methylation: An Important Biomarker and Therapeutic Target for Gastric Cancer.

Gastric cancer (GC) is a very common malignancy with a poor prognosis, and its occurrence and development are closely related to epigenetic modifications. Methylation of DNA before or during gastric cancer is an interesting research topic. This article reviews the studies on DNA methylation related to the cause, diagnosis, treatment, and prognosis of gastric cancer and aims to find cancer biomarkers to solve major human health problems.

Influence of Nonalcoholic Fatty Liver Disease on the Occurrence and Severity of Chronic Kidney Disease.

Nonalcoholic fatty liver disease (NAFLD) is reported to affect 20-30% of adults and is accompanied by various metabolic comorbidities, where the economic and clinical burden of NAFLD is attributed to the progression of liver disease as well as the presence of extrahepatic diseases. Chronic kidney disease (CKD), which has a high incidence rate, high morbidity and mortality rates, and high medical costs, has been linked to NAFLD. CKD is associated with some metabolism-related risk factors that overlap with metabolic comorbidities of NAFLD. Therefore, to investigate the potential factors that influence CKD occurrence, the association between NAFLD and CKD should be clarified. Some studies have confirmed that NAFLD influences the occurrence and severity of CKD, whereas some studies have indicated that there is no correlation. In this review, the results of a few studies have been discussed, the potential risk factors for CKD in NAFLD are explored, and the respective biological mechanisms are elaborated to help clinicians identify CKD in patients much earlier than it is diagnosed now and thus help in reducing the incidence of liver and kidney transplants.