Modeling effects of roadway lighting photometric criteria on nighttime pedestrian crashes on roadway segments.

INTRODUCTION: Nighttime crashes account for 74% of pedestrian fatalities in the United States, and reduced visibility is a significant cause of nighttime pedestrian crashes. Maintaining sufficient and uniform roadway lighting is an effective countermeasure to improve pedestrian visibility and prevent nighttime pedestrian crashes and injuries. Previous studies have not quantified the safety effects of roadway photometric patterns (i.e., average lighting level and uniformity) on nighttime pedestrian crashes on roadway segments. METHOD: This study investigated the association between two roadway photometric criteria (horizontal illuminance mean representing average lighting level and horizontal illuminance standard deviation representing lighting uniformity) and nighttime pedestrian crash occurrence in Florida roadway segments. The matched case-control method was used to decouple the confounding effects between the illuminance mean and standard deviation. Statistically-significant crash modification factors (CMFs) were developed to quantify the safety effects of the mean and standard deviation of horizontal illuminance on nighttime pedestrian crashes. RESULTS: The results show that if the average lighting level on a roadway segment is increased from a low illuminance mean (<0.2 foot-candle [fc]) to a medium illuminance mean [0.2 fc, 0.5 fc], a medium-high illuminance mean (0.5 fc, 1.0 fc], and a high illuminance mean (>1.0 fc), the relative likelihood of nighttime pedestrian crashes on midblock segments in Florida tends to be reduced by 77.5% (CMF = 0.225), 81.2% (CMF = 0.188), and 85.5% (CMF = 0.145), respectively. PRACTICAL APPLICATIONS: A poor uniformity (illuminance standard deviation ≥ 0.52 fc) is likely to increase the relative likelihood of nighttime pedestrian crashes on midblock segments in Florida by 80.3% (CMF = 1.803) compared to good uniformity (illuminance standard deviation < 0.52 fc).

The potential role of CpG oligodeoxynucleotides on diabetic cardiac autonomic neuropathy mediated by P2Y12 receptor in rat stellate ganglia.

Cardiac autonomic neuropathy has a high prevalence in type 2 diabetes, which increases the risk of cardiovascular system disorders. CpG oligodeoxynucleotide (CpG-ODN), a Toll-like receptor 9 (TLR9) ligand, has been shown to have cardioprotection and cellular protection. Our previous work showed that P2Y12 in stellate ganglia (SG) is involved in the process of diabetic cardiac autonomic neuropathy (DCAN). Here, we aim to investigate whether CpG-ODN 1826 plays a protective role in DCAN and whether this beneficial protection involves regulation of the P2Y12-mediated cardiac sympathetic injury. Our results revealed that CpG-ODN 1826 activated TLR9 receptor, improved the abnormal blood pressure (BP), heart rate (HR), heart rate variability (HRV) and sympathetic nerve discharge (SND) activity in diabetic rats and reduced the up-regulated NF-κB, P2Y12 receptor, TNF-α and IL-1ß in SG. Meanwhile, CpG-ODN 1826 significantly decreased the elevated ATP, nuclear receptor coactivator 4 (NCOA4), iron, ROS and MDA levels and increased GPX4 and GSH levels. In addition, CpG-ODN 1826 contributes to maintain normalization of mitochondrial structure in SG. Overall, CpG-ODN 1826 alleviates the sympathetic excitation and abnormal neuron-glial signal communication via activating TLR9 receptors to achieve a balance of autonomic activity and relieve the DCAN in rats. The mechanism may involve the regulation of P2Y12 receptor in SG by reducing ATP release and NF-κB expression, which counteract neuroinflammation and ferroptosis mediated by activated P2Y12 in SG.

DNA methylation regulator-based signature for predicting clear cell renal cell carcinoma prognosis.

OBJECTIVES: To investigate the role of DNA methylation regulators in the prognosis of clear cell renal cell carcinoma (ccRCC) and to construct a DNA methylation regulator-based signature for predicting patient outcome. METHODS: Data from the TCGA dataset were downloaded and analyzed to identify differentially expressed DNA methylation regulators and their interaction as well as correlation. Consensus clustering was used to establish groups of ccRCC with distinct clinical outcomes. A prognostic signature based on two sets of DNA methylation regulators was established and validated in an independent cohort. RESULTS: Our analysis revealed that the expression levels of DNMT3B, MBD1, SMUG1, DNMT1, DNMT3A, TDG, TET3, MBD2, UHRF2, MBD3, UHRF1, and TET2 were significantly upregulated in ccRCC samples, while UNG, ZBTB4, TET1, ZBTB38, and MECP2 were markedly downregulated. UHRF1 was identified as a hub gene in the DNA methylation regulator interaction network. Significant differences were found regarding overall survival, gender, tumor status, and grade between ccRCC patients in the two risk groups. The prognostic signature, based on two sets of DNA methylation regulators, was an independent prognostic indicator, and these findings were validated in an external, independent cohort. CONCLUSIONS: The study provides evidence that DNA methylation regulators play a significant role in the prognosis of ccRCC and the developed DNA methylation regulator-based signature could effectively predict patient outcome.

Central role of purinergic receptors with inflammation in neuropathic pain-related macrophage-SGC-neuron triad.

Adenosine triphosphate (ATP) acts on P2 purinergic receptors as an extracellular signaling molecule. P2 purinergic receptors include P2X ionotropic receptors and P2Y metabotropic receptors. Satellite glial cells (SGCs) and macrophages express P2X and P2Y receptors. Inflammatory cytokines and pro-nociceptive mediators are released by activated macrophages and SGCs, which can act on neurons to promote excitability and firing. In the primary sensory ganglia, in response to signals of injury, SGCs and macrophages accumulate around primary sensory neurons, forming a macrophage-SGC-neuron triad. In addition to affecting the pathological alterations of inflammation-related neuropathic pain, inflammatory cytokines and pro-nociceptive mediators are released by the action of ATP on P2X and P2Y receptors in macrophages and SGCs. Macrophages and SGCs work together to enhance and prolong neuropathic pain. The macrophage-SGC-neuron triad communicates with each other through ATP and other inflammatory mediators and maintains and promotes the initiation and development of inflammation related-neuropathic pain. This article is part of the Special Issue on "Purinergic Signaling: 50 years".

Durability Performance and Corrosion Mechanism of New Basalt Fiber Concrete under Organic Water Environment.

Under corrosive environments, concrete material properties can deteriorate significantly, which can seriously affect structural safety. Therefore, it has important engineering applications to improve the durability performance at a lower economic cost. This paper proposes a new, highly durable concrete using inexpensive construction materials such as basalt fiber, sodium methyl silicate, and inorganic aluminum salt waterproofing agent. With the massive application of sewage treatment projects, the problem of concrete durability degradation is becoming more and more serious. In this paper, five types of concrete are developed for the sewage environment, and the apparent morphology and fine structure of the specimens after corrosion in sewage were analyzed. The density, water absorption, and compressive strength were measured to investigate the deterioration pattern of concrete properties. It was found that ordinary concrete was subject to significant corrosion, generating large deposits of algae on the surface and accompanied by sanding. The new concrete showed superior corrosion resistance compared to conventional concrete. Among other factors, the inorganic aluminum salt waterproofing agent effect was the most prominent. The study found that the strength of ordinary concrete decreased by about 15% in the test environment, while the new concrete had a slight increase. Comprehensive evaluation showed that the combination of basalt fiber and inorganic aluminum salt waterproofing agent had the best effect. Its use is recommended.

Gallic Acid Improves Comorbid Chronic Pain and Depression Behaviors by Inhibiting P2X7 Receptor-Mediated Ferroptosis in the Spinal Cord of Rats.

Ferroptosis is an inflammatory programmed cell death process that is dependent on iron deposition and lipid peroxidation. The P2X7 receptor not only is involved in the pain process but also is closely related to the onset of depression. Gallic acid (3,4,5-trihydroxybenzoic acid), which is naturally found in a variety of plants, exhibits anti-inflammatory, antioxidant, and analgesic effects. This study established a rat model with the comorbidity of chronic constrictive injury (CCI) plus chronic unpredictable mild stress (CUMS) to explore the role and mechanism of gallic acid in the treatment of pain and depression comorbidity. Our experimental results showed that pain and depression-like behaviors were more obvious in the chronic constriction injury (CCI) plus chronic unpredictable mild stimulation (CUMS) group than they were in the sham operation group, and the P2X7-reactive oxygen species (ROS) signaling pathway was activated. The tissue iron concentration was increased, and mitochondrial damage was observed in the CCI plus CUMS group. These results were alleviated with gallic acid treatment. Therefore, we speculate that gallic acid inhibits the ferroptosis of the spinal microglia by regulating the P2X7-ROS signaling pathway and relieves the behavioral changes in rats with comorbid pain and depression.

Purinergic signaling: a potential therapeutic target for depression and chronic pain.

The comorbid mechanism of depression and chronic pain has been a research hotspot in recent years. Until now, the role of purinergic signals in the comorbid mechanism of depression and chronic pain has not been fully understood. This review mainly summarizes the research results published in PubMed during the past 5 years and concludes that purinergic signaling is a potential therapeutic target for comorbid depression and chronic pain, and the purinergic receptors A1, A2A, P2X3, P2X4, and P2X7and P2Y6, P2Y1, and P2Y12 may be important factors. The main potential pathways are as follows: A1 receptor-related G protein-dependent activation of introverted K+ channels (GIRKs), A2A receptor-related effects on the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) and MAPK/nuclear factor-κB (NF-κB) pathways, P2X3 receptor-related effects on dorsal root ganglia (DRG) excitability, P2X4 receptor-related effects on proinflammatory cytokines and inflammasome activation, P2X7 receptor-related effects on ion channels, the NLRP3 inflammasome and brain-derived neurotrophic factor (BDNF), and P2Y receptor-related effects on the phospholipase C (PLC)/inositol triphosphate (IP3)/Ca2+ signaling pathway. We hope that the conclusions of this review will provide key ideas for future research on the role of purinergic signaling in the comorbid mechanism of depression and chronic pain.

Pinocembrin Inhibits P2X4 Receptor-Mediated Pyroptosis in Hippocampus to Alleviate the Behaviours of Chronic Pain and Depression Comorbidity in Rats.

Neuroinflammation is critical to the comorbidity of chronic pain and depression. Pyroptosis is an inflammatory cell death that is different from apoptosis. Activation of the P2X4 receptor leads to inflammation and is involved in chronic pain and depression. Pinocembrin (5,7-dihydroxyflavanone) is a natural flavonoid compound with anti-inflammatory, antioxidant and neuroprotective effects. In this study, an animal model of chronic pain and depression comorbidity was used to explore the therapeutic effect of pinocembrin in P2X4-mediated pyroptosis. The results showed that nociceptive behaviours and depression-like behaviours were obvious in the model rats induced by chronic constrictive injury (CCI) and chronic unpredictable mild stimulus (CUMS). In the model rats, the mRNA and protein levels of the P2X4 receptor in the hippocampus were increased, and the coexpression of P2X4 and the astrocyte marker glial fibrillary acidic protein (GFAP) in the hippocampus was increased. The protein content of connexion 43 (Cx43), NOD-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and caspase-1 was increased. The serum content of IL-1ß and the mRNA and protein expression of IL-1ß were increased. The protein content of p-P38MAPK was increased. After treatment with pinocembrin in the model rats, these behavioural changes were improved, and the mRNA and protein levels of the above indicators were decreased. The results of molecular docking confirmed that the affinity of pinocembrin and the P2X4 receptor was - 7.8 (kcal/mol). At the same time, pinocembrin inhibited the ATP release and Ca2+ signal release in primary astrocytes and ATP-activated current of HEK293 cells transfected with the pcDNA3.0-EGFP-hP2X4 plasmid. Therefore, pinocembrin relieved nociceptive and depression-like behaviours in rats with chronic pain and depression comorbidity by inhibiting P2X4 receptor-mediated pyroptosis in the hippocampus. The mechanism of pinocembrin in treating rats with chronic pain and depression comorbidity. GJ stands for gap junction, and Cx43 is mainly expressed in astrocytes.

Beneficial Effects of lncRNA-UC.360+ shRNA on Diabetic Cardiac Sympathetic Damage via NLRP3 Inflammasome-Induced Pyroptosis in Stellate Ganglion.

Hyperglycemia is one of the common symptoms of diabetes, and it produces excessive reactive oxygen species (ROS). This study investigated whether the long noncoding RNA (lncRNA) UC.360+ is involved in diabetic cardiac autonomic neuropathy (DCAN) mediated by NLRP3 inflammasome-induced pyroptosis in the stellate ganglion (SG). Using a rat type 2 diabetes model, we found that lncRNA UC.360+ short hairpin RNA (shRNA) ameliorated the dyslipidaemia of type 2 diabetic rats and reduced serum adrenaline and ROS production in SG under hyperglycemia. In addition, UC.360+ shRNA also reduced the expression of nuclear factor kappa-B (NF-κB), NLRP3, ASC, caspase-1, interleukin-1ß (IL-1ß), and IL-18 in the SG of diabetic rats and inhibited the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK). Therefore, lncRNA-UC.360+ shRNA may modulate the NLRP3 inflammasome/inflammatory pathway in the SG, which in turn alleviates diabetic heart sympathetic nerve damage.

Implication of P2Y12 receptor in uc.48+-mediated abnormal sympathoexcitatory reflex via superior cervical ganglia in myocardial ischemic rats.

Purinergic 2Y12 (P2Y12) receptor antagonists are used as platelet aggregation inhibitors. Long non-coding RNAs (lncRNAs) play an important role in neuropathological events. Satellite glial cells (SGCs) in the superior cervical ganglia (SCGs) encircle the somata of neurons. This study explored if the upregulated P2Y12 receptor in SCGs was relevant to lncRNA uc.48+ during myocardial ischemia (MI). The results showed that upregulation of P2Y12 receptor was accompanied by increased expression of uc.48+ in the SCGs of MI rats which displayed abnormal changes in cervical sympathetic nerve activity, blood pressure, heart rate, electrocardiograms and cardiac tissue structure. The P2Y12 antagonist clopidogrel improved abnormal alterations in cardiac function and tissue structure in MI rats. Short hairpin RNA (shRNA) against uc.48+ significantly inhibited P2Y12 receptor upregulation and its co-expression with glial fibrillary acidic protein (GFAP) in SCGs, and ameliorated the cardiac dysfunction in MI rats. By contrast, overexpression of uc.48+ increased the expression of P2Y12 in SCGs and enhanced cervical sympathetic nerve activity in control rats. Direct interaction between uc.48+ and the P2Y12 receptor was predicted using the bioinformatic tool CatRAPID and confirmed by RNA immunoprecipitation. Moreover, overexpression of the P2Y12 receptor reversed the protective effect of uc.48+ shRNA on cardiac dysfunction in MI rats. Uc.48 shRNA treatment also inhibited the enhanced rise of intracellular free Ca2+ level ([Ca2+]i) evoked by the P2Y12 agonist 2-methylthio-adenosine-5'-diphosphate (2-MeSADP) in SGCs of SCGs after oxygen-glucose deprivation (OGD) treatment. These data demonstrated that uc.48+ shRNA could counteract the P2Y12 upregulation and improve P2Y12-implicated cardiac dysfunction due to MI.

Study of the Involvement of the P2Y12 Receptor in Chronic Itching in Type 2 Diabetes Mellitus.

Itching is a common clinical symptom in diabetic patients. This research is to carry out experiments on the pathological changes in the P2Y12 receptor in type 2 diabetes mellitus complicated with chronic itching. Changes in body weight, fasting blood glucose (FBG), thermal hyperalgesia, cold hyperalgesia, spontaneous itching, and sciatic nerve conduction velocity were detected. The content of reactive oxygen species (ROS) in the dorsal root ganglion was detected by chemical fluorescence. The expression of the P2Y12 receptor, NLRP3, ASC, interleukin-1ß (IL-1ß), and IL-18 was detected by Western blotting, real-time quantitative PCR, immunofluorescence double labelling, and enzyme-linked immunosorbent assay. Itching and pain behaviours of the mice in the type 2 diabetes mellitus + itch group were significantly increased, and the expression of P2Y12 and NLRP3 as well as the content of ROS increased, and these changes were significantly reversed by treatment with P2Y12 short hairpin RNA (shRNA) or P2Y12 antagonist ticagrelor. Upregulated P2Y12 receptor expression after the activation of satellite glial cells contributes to the increase in ROS content in vivo, followed by NLRP3 inflammasome activation, increased inflammatory cytokine release, and damage to peripheral nerves, which leads to chronic itching. Treatment with P2Y12 shRNA or ticagrelor can inhibit these pathological changes, thus improving itching behaviour. Development mechanism of diabetes mellitus complicated with chronic itching. Notes: The upregulation of P2Y12 receptor expression and the activation of SGCs lead to the increase of ROS content in vivo, followed by the activation of NLRP3 inflammasome, the increase of inflammatory cytokine release, the abnormal excitation of DRG neurons, and the damage of peripheral nerves, resulting in chronic itching. P2Y12 receptor-related inflammatory injury involves chronic itching in type 2 diabetes mellitus. Treatment with P2Y12 receptor shRNA or P2Y12 antagonist ticagrelor can inhibit these pathological changes and improve itching behaviour.

Catestatin enhances ATP-induced activation of glial cells mediated by purinergic receptor P2X4.

The activation of glial cells and its possible mechanism play an extremely important role in understanding the pathophysiological process of some clinical diseases, and catestatin (CST) is involved in regulating this activation. In this project, we found that CST could enhance the activation of satellite glial cells (SGCs) and microglial cells and that the expression of P2X4 was increased; the co-expression of the P2X4 receptor with glial fibrillary acidic protein (GFAP) and the P2X4 receptor with CD11b was also increased significantly in glial cells of the ATP + CST group, and TNF-α and IL-1ß also showed a rising trend; the expression of phosphorylated ERK1/2 was also increased in the ATP + CST group. In summary, we conclude that CST could enhance ATP-induced activation of SGCs and microglial cells mediated by the P2X4 receptor and that the ERK1/2 signaling pathway may be involved in this activation process.

Corrigendum: Long Non-coding RNA Uc.48+ Small Interfering RNA Alleviates Neuroinflammatory Hyperalgesia in Gp120-Treated Rats via the P2Y12 Receptor.

[This corrects the article DOI: 10.3389/fnins.2021.663962.].

Gallic Acid Alleviates Neuropathic Pain Behaviors in Rats by Inhibiting P2X7 Receptor-Mediated NF-κB/STAT3 Signaling Pathway.

Neuropathic pain is a complex disease with high incidence. Adenosine triphosphate (ATP) and its activated P2X7 receptor are involved in the signal transmission of neuropathic pain. Gallic acid (3,4,5-trihydroxybenzoic acid) is a traditional Chinese medicine obtained from natural plants that exhibit anti-inflammatory, analgesic, and antitumor effects. However, the underlying mechanism for gallic acid in analgesia remains unknown. This study aims to reveal how gallic acid alleviates neuropathic pain behaviors in a rat model with chronic constriction injury (CCI). Real-time PCR, western blotting, double-label immunofluorescence, molecular docking, and whole-cell patch clamp technology were used to explore the therapeutic action of gallic acid on neuropathic pain. The results showed that after CCI rats were treated with gallic acid for 1 week, the mechanical withdrawal threshold and thermal withdrawal latency were increased, accompanied by inhibition of the upregulated expression of P2X7 and TNF-α at both mRNA and protein levels, and reduced NF-κB and phosphorylated-STAT3 in the dorsal root ganglia. At the same time, gallic acid significantly decreased the coexpression of P2X7 and glial fibrillary acidic protein in the dorsal root ganglia. In addition, gallic acid could suppress ATP-activated current in human embryonic kidney 293 (HEK293) cells transfected with the plasmid expressing P2X7 but had no effect on ATP activation current of P2X7-mutant plasmid (with the point mutation sequence of the key site where gallic acid binds to the P2X7 receptor). Therefore, our work suggests that gallic acid may alleviate neuropathic pain in CCI rats by inhibiting the P2X7 receptor and subsequent activation of the TNF-α/STAT3 signaling pathway.

Development of crash modification factors for roadway illuminance: A matched case-control study.

Roadway lighting is used to ensure nighttime safety and security for multimodal road users. However, the absence of reliable quantitative analyses of the safety effects of roadway lighting photometric characteristics prevents accurate assessment of street lighting maintenance and retrofitting projects. This study aimed to investigate the relationship between nighttime crash risk and two critical photometric criteria, i.e., average lighting level and uniformity. To achieve this goal, high-resolution horizontal illuminance data were collected in Florida for 300 + center-miles from 2011 to 2014. Based on the data, a matched case-control study was conducted to address two major issues existing in previous studies: (1) the confounding effects of illuminance standard deviation on illuminance mean and (2) spatially-unrelated extreme values for ratio-based uniformity. By eliminating the confounding effects through a random matching strategy (one case, a segment with nighttime crashes, to one control, a segment without nighttime crashes at 1,046 strata), this study successfully isolated the negative effects of the standard deviation and developed more significant crash modification factors (CMFs) for average lighting levels: 0.679 for increasing the average lighting level from [0 fc, 0.5 fc] to (0.5 fc, 1.0 fc] and 0.581 for increasing the average lighting from [0 fc, 0.5 fc] to higher than 1.0 fc. Additionally, a CMF of 1.391 for a max-min ratio greater than 10 was identified by controlling the segment length at a short uniform unit (1,200 ft). The developed CMFs overcame the underestimation issue in previous studies and are implementable in current street lighting design and safety management.

Long Non-coding RNA Uc.48+ Small Interfering RNA Alleviates Neuroinflammatory Hyperalgesia in Gp120-Treated Rats via the P2Y12 Receptor.

Human immunodeficiency virus envelope glycoprotein 120 (gp120) leads to hyperalgesia. Long non-coding RNAs are characterized by the lack of a protein-coding sequence and may contribute to the development and maintenance of inflammatory and neuroinflammatory pain. Rats with neuroinflammatory pain were established by gp120 treatment, which is featured by intensified pain behaviors. Long non-coding RNA uc.48+ was increased in the dorsal root ganglia of gp120-treated rats, and small interfering RNA that targets uc.48+ markedly alleviated hyperalgesia in gp120-treated rats. Notably, uc.48+ overexpression increased P2Y12 expression in control rats dorsal root ganglia and induced hyperalgesia. Uc.48+ small interfering RNA inhibited P2Y12 expression in gp120-treated rats. Uc.48+ potentiated P2Y12 receptor functions in the neurons and heterologous cells. Therefore, uc.48+ siRNA treatment reduced the upregulation of P2Y12 expression and function in DRG neurons, and, hence, alleviated hyperalgesia in gp120-treated rats.

The P2X7 Receptor Is Involved in Diabetic Neuropathic Pain Hypersensitivity Mediated by TRPV1 in the Rat Dorsal Root Ganglion.

The purinergic 2X7 (P2X7) receptor expressed in satellite glial cells (SGCs) is involved in the inflammatory response, and transient receptor potential vanilloid 1 (TRPV1) participates in the process of neurogenic inflammation, such as that in diabetic neuropathic pain (DNP) and peripheral neuralgia. The main purpose of this study was to explore the role of the P2X7 receptor in DNP hypersensitivity mediated by TRPV1 in the rat and its possible mechanism. A rat model of type 2 diabetes mellitus-related neuropathic pain (NPP) named the DNP rat model was established in this study. The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) of DNP rats were increased after intrathecal injection of the P2X7 receptor antagonist A438079, and the mRNA and protein levels of TRPV1 in the dorsal root ganglion (DRG) were decreased in DNP rats treated with A438079 compared to untreated DNP rats; in addition, A438079 also decreased the phosphorylation of p38 and extracellular signal-regulated kinase 1/2 (ERK1/2) in the DNP group. Based on these results, the P2X7 receptor might be involved in DNP mediated by TRPV1.

Impact of postmortem degradation of cytoskeletal proteins on intracellular gap, drip channel and water-holding capacity.

The present study aimed to investigate the impact of the degradation of cytoskeletal proteins (desmin, integrin, vinculin, and talin) on the formation of intracellular gap and drip channel and water-holding capacity in pork. The intensity of intact cytoskeletal proteins and the width of intracellular gap and drip channel were measured in high drip loss and low drip loss groups. The data indicate that the width of intracellular gap and drip channel explained 17% and 62% variation in drip loss, respectively, while the intensity of intact desmin, integrin, and vinculin explained 47%, 34%, and 47% variation in drip loss, respectively. The postmortem formation of intracellular gap is mainly affected by the changes in integrin and vinculin, while the formation of the drip channel is influenced by the changes in desmin. These findings suggest that postmortem formation of wide intracellular gap and drip channels is linked to increased drip loss.