{"title":"Interstitial cells of Cajal in gastrointestinal inflammatory diseases.","authors":"Noriyuki Kaji, Masatoshi Hori","doi":"10.1540/jsmr.59.1","DOIUrl":"https://doi.org/10.1540/jsmr.59.1","url":null,"abstract":"<p><p>The gastrointestinal (GI) tract is a vital organ that digests food, absorbs nutrients, and excretes waste. Normal GI motility is the basis for these functions. The interstitial cells of Cajal (ICC) in the GI muscularis layer promote GI motility together with the enteric nervous system and smooth muscle cells. Since GI motility results from complex coordination of these heterogeneous cells, failure of any one of them can lead to GI dysmotility. Knowledge about ICC in physiological conditions has accumulated in recent decades, while the pathophysiology of ICC in GI inflammatory diseases, such as inflammatory bowel disease, is not well understood. In this review, we summarize the previous studies about the pathophysiological changes of ICC in inflammatory diseases and discuss the inflammatory mediators that induce ICC dysfunction.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"59 ","pages":"1-13"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/50/6e/jsmr-59-001.PMC9926098.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10777836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Direct active Fyn-paxillin interaction regulates vascular smooth muscle cell migration.","authors":"Ying Zhang, Hiroko Kishi, Sei Kobayashi","doi":"10.1540/jsmr.59.58","DOIUrl":"https://doi.org/10.1540/jsmr.59.58","url":null,"abstract":"<p><p>Vascular smooth muscle cell (VSMC) migration plays an important role in cardiovascular diseases, including atherosclerotic plaque formation and restenosis after vascular intervention. The mechanisms involved in VSMC migration are complex and have not been fully elucidated. Recently, we discovered a novel interaction, direct binding of active Fyn-paxillin at focal adhesions, which plays an important role in actin stress fiber formation and migration in VSMCs. In this review, we highlight paxillin as an intermediate signaling molecule that mediates actin stress fiber formation and VSMC migration through the Fyn/paxillin/Rho-kinase signaling pathway by directly binding to active Fyn. We also discuss the inhibition of VSMC migration by blocking the active Fyn-paxillin interaction and the potential of this interaction as a therapeutic target for cardiovascular diseases.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"59 ","pages":"58-66"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10336424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10192250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sex differences in the central regulation of colorectal motility in response to noxious stimuli.","authors":"Kazuhiro Horii, Tomoya Sawamura, Natsufu Yuki, Takahiko Shiina, Yasutake Shimizu","doi":"10.1540/jsmr.59.28","DOIUrl":"https://doi.org/10.1540/jsmr.59.28","url":null,"abstract":"<p><p>Distinct sex differences in the prevalence and symptoms of abnormal bowel habits in patients with irritable bowel syndrome (IBS) have been reported. We have elucidated the sex differences in the regulation of colorectal motility via the central nervous system. Noxious stimuli in the colorectum of anesthetized male rats enhance colorectal motility by activating monoaminergic neurons in descending pain inhibitory pathways from the brainstem to the lumbosacral spinal cord. These monoaminergic neurons release serotonin and dopamine into the lumbosacral spinal cord, resulting in the increment of colorectal motility. In female rats, in contrast, noxious stimuli in the colorectum have no effect on colorectal motility. We clarified that GABAergic inhibition in the lumbosacral spinal cord masks the enhancement of colorectal motility induced by monoamines in female animals. Considering that IBS patients often show visceral hypersensitivity and hyperalgesia, our studies suggest that differences in the descending neurons that respond to painful stimuli are involved in various sex differences in abnormal bowel habits.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"59 ","pages":"28-33"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4e/cf/jsmr-59-028.PMC10131095.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10069032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Glucose-6-phosphate dehydrogenase and MEG3 controls hypoxia-induced expression of serum response factor (SRF) and SRF-dependent genes in pulmonary smooth muscle cell","authors":"Atsushi Kitagawa, C. Jacob, S. Gupte","doi":"10.1540/jsmr.58.34","DOIUrl":"https://doi.org/10.1540/jsmr.58.34","url":null,"abstract":"Although hypoxia induces aberrant gene expression and dedifferentiation of smooth muscle cells (SMCs), mechanisms that alter dedifferentiation gene expression by hypoxia remain unclear. Therefore, we aimed to gain insight into the hypoxia-controlled gene expression in SMCs. We conducted studies using SMCs cultured in 3% oxygen (hypoxia) and the lungs of mice exposed to 10% oxygen (hypoxia). Our results suggest hypoxia upregulated expression of transcription factor CP2-like protein1, krüppel-like factor 4, and E2f transcription factor 1 enriched genes including basonuclin 2 (Bcn2), serum response factor (Srf), polycomb 3 (Cbx8), homeobox D9 (Hoxd9), lysine demethylase 1A (Kdm1a), etc. Additionally, we found that silencing glucose-6-phosphate dehydrogenase (G6PD) expression and inhibiting G6PD activity downregulated Srf transcript and hypomethylation of SMC genes (Myocd, Myh11, and Cnn1) and concomitantly increased their expression in the lungs of hypoxic mice. Furthermore, G6PD inhibition hypomethylated MEG3, a long non-coding RNA, gene and upregulated MEG3 expression in the lungs of hypoxic mice and in hypoxic SMCs. Silencing MEG3 expression in SMC mitigated the hypoxia-induced transcription of SRF. These findings collectively demonstrate that MEG3 and G6PD codependently regulate Srf expression in hypoxic SMCs. Moreover, G6PD inhibition upregulated SRF-MYOCD-driven gene expression, determinant of a differentiated SMC phenotype.","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"58 1","pages":"34 - 49"},"PeriodicalIF":0.0,"publicationDate":"2022-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43880956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The TRPM8 channel as a potential therapeutic target for bladder hypersensitive disorders","authors":"Naoki Aizawa, T. Fujita","doi":"10.1540/jsmr.58.11","DOIUrl":"https://doi.org/10.1540/jsmr.58.11","url":null,"abstract":"In the lower urinary tract, transient receptor potential (TRP) channels are primarily involved in physiological function, especially in cellular sensors responding to chemical and physical stimuli. Among TRP channels, TRP melastatin 8 (TRPM8) channels, responding to cold temperature and/or chemical agents, such as menthol or icilin, are mainly expressed in the nerve endings of the primary afferent neurons and in the cell bodies of dorsal root ganglia innervating the urinary bladder (via Aδ- and C-fibers); this suggests that TRPM8 channels primarily contribute to bladder sensory (afferent) function. Storage symptoms of overactive bladder, benign prostatic hyperplasia, and interstitial cystitis are commonly related to sensory function (bladder hypersensitivity); thus, TRPM8 channels may also contribute to the pathophysiology of bladder hypersensitivity. Indeed, it has been reported in a pharmacological investigation using rodents that TRPM8 channels contribute to the pathophysiological bladder afferent hypersensitivity of mechanosensitive C-fibers. Similar findings have also been reported in humans. Therefore, a TRPM8 antagonist would be a promising therapeutic target for bladder hypersensitive disorders, including urinary urgency or nociceptive pain. In this review article, the functional role of the TRPM8 channel in the lower urinary tract and the potential of its antagonist for the treatment of bladder disorders was described.","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"58 1","pages":"11 - 21"},"PeriodicalIF":0.0,"publicationDate":"2022-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45328311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Agnaldo Bruno Chies, Maria Angélica Spadella, Carla Patrícia Carlos, Carla Brigagão Pacheco da Silva, Carlos Renato Tirapelli
{"title":"Orchiectomy but not adjuvant-induced arthritis induces structural modifications in rat aortas.","authors":"Agnaldo Bruno Chies, Maria Angélica Spadella, Carla Patrícia Carlos, Carla Brigagão Pacheco da Silva, Carlos Renato Tirapelli","doi":"10.1540/jsmr.58.63","DOIUrl":"https://doi.org/10.1540/jsmr.58.63","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to verify whether Adjuvant-Induced Arthritis (AIA) and/or Orchiectomy (ORX) modify the expression of the Nox1, Nox2 and Nox4 isoforms, the endothelial function or the structure of rat aortas.</p><p><strong>Methods: </strong>Sixty-three Wistar rats were distributed into four groups: 1) Control; 2) ORX; 3) AIA; 4) Orchiectomy plus to Arthritis-induction (ORX/AIA). Thus, 21 days after the onset of AIA (by intradermal injection of Mycobacterium tuberculosis), the presence of Nox1, Nox2 and Nox4, the acetylcholine (ACh)-induced relaxation and the media layer thickness were assessed in the aorta taken from these animals.</p><p><strong>Results: </strong>The Nox1, Nox2 and Nox4 were immunostained in intima, media and adventitia layers of aortas taken from all studied groups and AIA apparently increased this immunostaining. These modifications of Nox1, Nox2 or Nox4 expression, however, were not confirmed by Western blotting. In addition, neither AIA nor ORX changed the endothelial function, but ORX increased the media layer thickness in the studied aortas.</p><p><strong>Conclusion: </strong>The present study showed weak clues of increased expression of Nox1, Nox2 and Nox4 as a result of AIA, as well as of Nox1 reduction caused by ORX. In addition, the endothelial function was not modified in the aortas of these animals by both AIA and/or ORX. On the other hand, ORX increased significantly the aorta media layer thickness in the studied animals, which was apparently mitigated by AIA.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":" ","pages":"63-77"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/77/71/jsmr-58-063.PMC9364264.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40597605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shahnawaz Ahmad Wani, Luqman Ahmad Khan, Seemi Farhat Basir
{"title":"Quercetin and resveratrol ameliorate nickel-mediated hypercontraction in isolated Wistar rat aorta.","authors":"Shahnawaz Ahmad Wani, Luqman Ahmad Khan, Seemi Farhat Basir","doi":"10.1540/jsmr.58.89","DOIUrl":"https://doi.org/10.1540/jsmr.58.89","url":null,"abstract":"<p><strong>Purpose: </strong>The ameliorative potential of quercetin and resveratrol on isolated endothelium-intact aortic rings incubated with nickel was examined.</p><p><strong>Method: </strong>The effect of varying concentrations of quercetin and resveratrol was investigated on isolated Wistar rat aortic rings using an organ bath system over vasoconstrictor phenylephrine (PE) at 1 µM. To delineate the mechanism of action, isolated aortic rings were pre-incubated with pharmacological modulators, such as verapamil 1 µM, apocynin 100 µM, indomethacin 100 µM or N-G-nitro-L-arginine methyl ester (L-NAME) 100 µM, separately, before incubation with 100 µM quercetin and 30 µM resveratrol. To assess the ameliorative and prophylactic potentials of quercetin and resveratrol, aortic rings were also incubated with quercetin or resveratrol for 40 min, followed by incubation with nickel for 40 min.</p><p><strong>Results: </strong>At 100 µM, quercetin caused 29% inhibition of contraction, while resveratrol at 30 µM caused 55% inhibition of contraction in aortic rings compared with control. Aortic rings incubated with contractile modulators, such as verapamil, apocynin, indomethacin or N-G-nitro-L-arginine methyl ester (L-NAME), along with quercetin or resveratrol at their concentrations producing maximum relaxant effect, showed that both of these natural compounds exert their relaxant effect by inhibiting the generation of reactive oxygen species (ROS) from endothelial and smooth muscle cells, blocking voltage-gated calcium channels, and increasing the release of nitric oxide (NO). The mediation of hypercontraction by nickel is due to the increased ROS and the influx of calcium through voltage-dependent calcium channels. These natural compounds are shown to counter the nickel-induced effects, appearing as effective ameliorators.</p><p><strong>Conclusion: </strong>In this study, we found that quercetin and resveratrol act as ameliorators of nickel-mediated hypercontraction by decreasing ROS and enhancing NO release from endothelial cells.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"58 ","pages":"89-105"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e2/b7/jsmr-58-089.PMC9748311.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10818597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Possible roles of N- and C-terminal unstructured tails of CPI-17 in regulating Ca<sup>2+</sup> sensitization force of smooth muscle.","authors":"Masumi Eto, Shuichi Katsuki, Minami Ohashi, Yui Miyagawa, Yoshinori Tanaka, Kosuke Takeya, Toshio Kitazawa","doi":"10.1540/jsmr.58.22","DOIUrl":"https://doi.org/10.1540/jsmr.58.22","url":null,"abstract":"<p><p>CPI-17 regulates the myosin phosphatase and mediates the agonist-induced contraction of smooth muscle. PKC and ROCK phosphorylate CPI-17 at Thr38 leading to a conformational change of the central inhibitory domain (PHIN domain). The N- and C-terminal tails of CPI-17 are predicted as unstructured loops and their sequences are conserved among mammals. Here we characterized CPI-17 N- and C-terminal unstructured tails using recombinant proteins that lack the potions. Recombinant CPI-17 proteins at a physiologic level (10 µM) were doped into beta-escin-permeabilized smooth muscle strips for Ca<sup>2+</sup> sensitization force measurement. The ectopic full-length CPI-17 augmented the PDBu-induced Ca<sup>2+</sup> sensitization force at pCa6.3, indicating myosin phosphatase inhibition. Deletion of N- and C-terminal tails of CPI-17 attenuated the extent of PDBu-induced Ca<sup>2+</sup>-sensitization force. The N-terminal deletion dampened phosphorylation at Thr38 by protein kinase C (PKC), and the C-terminal truncation lowered the affinity to the myosin phosphatase. Under the physiologic conditions, PKC and myosin phosphatase may recognize CPI-17 N-/C-terminal unstructured tails inducing Ca<sup>2+</sup> sensitization force in smooth muscle cells.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"58 0","pages":"22-33"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/48/9b/jsmr-58-022.PMC9006046.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9199708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mari Endo, Tetsuro Oikawa, Miki Tonooka, Toshihiko Hanawa, Hiroshi Odaguchi, Masatoshi Hori
{"title":"Hangekobokuto, a traditional Japanese herbal medicine, ameliorates postoperative ileus through its anti-inflammatory action.","authors":"Mari Endo, Tetsuro Oikawa, Miki Tonooka, Toshihiko Hanawa, Hiroshi Odaguchi, Masatoshi Hori","doi":"10.1540/jsmr.58.78","DOIUrl":"https://doi.org/10.1540/jsmr.58.78","url":null,"abstract":"Background/Aims: Gastroprokinetic agents are used for patients with postoperative ileus (POI), and the Japanese traditional herbal medicine daikenchuto (DKT) is one such agent used in the clinical setting. POI is caused by inflammation. DKT and rikkunshito have anti-inflammatory abilities in addition to their gastroprokinetic effects. The efficacy of Kampo formulations, including hangekobokuto (HKT), in patients with POI has been reported recently. Several authors have described the efficacy of honokiol, the primary component of Magnoliae Cortex, in HKT in mouse models of POI. We therefore analyzed the effect of HKT on POI model mice to determine the similarities in the mechanism of action between HKT and DKT. Methods: HKT was administered orally to each mouse before and after intestinal manipulation was performed on the distal ileum. The gastrointestinal transit in vivo, leukocyte infiltration, and levels of inflammatory mediators, such as cytokines and chemokines, were analyzed. Results: HKT significantly inhibited the infiltration of neutrophils and macrophages and led to the recovery of delayed intestinal transit. In addition, it significantly decreased inducible nitric oxide synthase (iNOS) as well as honokiol levels, suggesting anti-inflammatory activity. However, it did not inhibit the increase in levels of interleukin (IL)-1beta and IL-6, which are related to iNOS induction. In contrast, HKT increased levels of nerve growth factor (NGF) and suppressed those of nuclear factor-κB (NFκB), which are related to iNOS induction, suggesting the possibility of a neuronal anti-inflammatory mechanism. Conclusions: HKT exerted a POI-relieving effect similar to DKT in a murine POI model, and findings suggest that it may exert its anti-inflammatory activity through NGF.","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":" ","pages":"78-88"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f1/c2/jsmr-58-078.PMC9537061.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33498981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Disturbed gastric motility in patients with long-standing diabetes mellitus.","authors":"Takeshi Kamiya, Hidekatsu Fukuta, Hiromi Hagiwara, Michiko Shikano, Takashi Kato, Kenro Imaeda","doi":"10.1540/jsmr.58.1","DOIUrl":"https://doi.org/10.1540/jsmr.58.1","url":null,"abstract":"<p><strong>Purpose: </strong>Gastric dysmotility has been reported in patients with long-standing diabetes mellitus (DM). Some patients with DM are diagnosed as diabetes gastroparesis and have several upper gastrointestinal (GI) symptoms such as appetite loss and abdominal pain. This study aimed to identify the relationship between gastric motility and upper GI symptoms in patients with long-standing DM.</p><p><strong>Method: </strong>This study was conducted among 23 patients with DM and 15 healthy controls. All the patients with DM were receiving insulin treatment and had at least one history of incidence of diabetic nephropathy, retinopathy or neuropathy. Gastric motility was evaluated using electrogastrography (EGG) and gastric emptying using the <sup>13</sup>C-acetic acid breath test. The most severe upper gastrointestinal symptoms were assessed in all patients.</p><p><strong>Results: </strong>Compared to healthy controls, patients with long-standing DM showed a significantly lower percentage of normogastria at the postprandial state with a lower power ratio in EGG. Gastric emptying was significantly delayed in patients with DM in the overall analysis. Sixteen patients with DM (69.6%) demonstrated abnormalities in either gastric myoelectrical activity or gastric emptying. Among patients with abnormal EGG or delayed gastric emptying, 12 had some GI symptoms, compared with 3 patients with normal gastric motility. No significant correlation was observed between the gastric emptying parameters and HbA1c values.</p><p><strong>Conclusion: </strong>Patients with long-standing DM showed gastric dysmotility, including impaired gastric myoelectrical activity and delayed gastric emptying. Gastric dysmotility appears to be closely correlated with upper GI symptoms in patients with long-standing DM.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":" ","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/53/8e/jsmr-58-001.PMC8844815.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39930224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}