Ultrastructural PathologyPub Date : 2025-03-04Epub Date: 2025-02-21DOI: 10.1080/01913123.2025.2468708
Guillermo A Herrera, Jiamin Teng, Chun Zeng, Luis Del Pozo-Yauner, Bing Liu, Elba A Turbat-Herrera
{"title":"Identifying gene expression and cellular pathways involved in glomerular AL-amyloidosis and correlation with experimental data: seeking novel therapeutic interventions.","authors":"Guillermo A Herrera, Jiamin Teng, Chun Zeng, Luis Del Pozo-Yauner, Bing Liu, Elba A Turbat-Herrera","doi":"10.1080/01913123.2025.2468708","DOIUrl":"10.1080/01913123.2025.2468708","url":null,"abstract":"<p><p>The prognosis of myeloma is based on controlling the plasma cell burden and thus, management of the production of monoclonal light chains has improved considerably, expanding survival and quality of life. However, the effects of the monoclonal light chains in the various organs result in alterations that may lead to renal failure. There is a crucial need to ameliorate or abolish renal damage. Organ-based therapies must be developed. Glomerulopathic light chains interact with mesangial cells using the SORL1 receptor and downstream effects lead to divergent mesangial alterations. While the multi-step process occurring when amyloidogenic light chains interact with mesangial cells has been elucidated in the laboratory, gene expression profiles and activated cellular pathways in human glomeruli have not been probed. Mesangial cells from five renal biopsies at different stages of glomerular amyloidosis were interrogated using spatial transcriptomics and compared with those from normal biopsy controls to identify cellular pathways and gene expression changes. The two most significant statistically overexpressed genes (FDR <0.05) when comparing control, early vs late cases were heat shock protein 90AB1 and HSPB1, known to be involved in protein misfolding and aggregation. The overexpressed genes exercise function and regulation over cellular pathways promoting apoptosis, vesicular transport, metalloproteinase activation, collagen degradation, gap junction degradation, GTPase cycle activation, and organelle biogenesis. This data confirmed the results previously reached in the research laboratory. Spatial transcriptomics demonstrated uniquely activated genes and cellular pathways in mesangial cells involved in the initiation and progression of glomerular amyloidosis, uncovering novel genes and new therapeutic targets.</p>","PeriodicalId":23430,"journal":{"name":"Ultrastructural Pathology","volume":" ","pages":"216-234"},"PeriodicalIF":1.1,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ultrastructural PathologyPub Date : 2025-01-02Epub Date: 2024-12-15DOI: 10.1080/01913123.2024.2441933
Elena G Pershina, Ksenia N Morozova, Nataliya P Bgatova
{"title":"Ultrastructural organization of the liver of rat pups in early postnatal ontogenesis when pregnant and lactating rats are kept on a low-protein diet.","authors":"Elena G Pershina, Ksenia N Morozova, Nataliya P Bgatova","doi":"10.1080/01913123.2024.2441933","DOIUrl":"10.1080/01913123.2024.2441933","url":null,"abstract":"<p><p>Protein deficiency in the diet during pregnancy and lactation has a serious impact on the offspring by programming a predisposition to such serious diseases as hypertension and type 2 diabetes mellitus. In our study, we examined liver ultrastructure of rat pups at ages 2, 21, and 40 days with maternal protein deficiency. Body weight of the pups progressively lagged behind the control throughout the experiment, and the timing of eye opening indicated a slowdown of development. In the liver of 2-day-old animals, the proportion of hematopoietic cells at early stages of differentiation was higher as compared to the control. At the ultrastructural level, no obvious pathological changes were revealed, but a decrease in the amount of organelles was observed simultaneously with accumulation of lipids and glycogen. In the course of the experiment, a progressive decrease in the amount of the rough endoplasmic reticulum and ribosomes and increasing accumulation of glycogen in the cytoplasm of hepatocytes were noted. The most pronounced difference in ultrastructure between periportal and pericentral hepatocytes of control rat pups was detected on the 40th day of development, whereas in the low-protein diet group, the difference was weakly pronounced throughout the experiment. Thus, we showed that with prenatal and early postnatal protein deficiency, the growth and development of rat pups slows down, and glycogen accumulates excessively in the liver concurrently with a decrease in the amount of organelles.</p>","PeriodicalId":23430,"journal":{"name":"Ultrastructural Pathology","volume":" ","pages":"93-107"},"PeriodicalIF":1.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ultrastructural PathologyPub Date : 2025-01-02Epub Date: 2024-12-24DOI: 10.1080/01913123.2024.2446231
Christopher-Rasheem Mcmillan
{"title":"Not so fast, we have to weight the cost.","authors":"Christopher-Rasheem Mcmillan","doi":"10.1080/01913123.2024.2446231","DOIUrl":"10.1080/01913123.2024.2446231","url":null,"abstract":"","PeriodicalId":23430,"journal":{"name":"Ultrastructural Pathology","volume":" ","pages":"108"},"PeriodicalIF":1.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ultrastructural PathologyPub Date : 2025-01-02Epub Date: 2024-11-17DOI: 10.1080/01913123.2024.2428703
Ida Perrotta
{"title":"Live and let die: analyzing ultrastructural features in cell death.","authors":"Ida Perrotta","doi":"10.1080/01913123.2024.2428703","DOIUrl":"10.1080/01913123.2024.2428703","url":null,"abstract":"<p><p>Cell death is an important process that supports morphogenesis during development and tissue homeostasis during adult life by removing damaged or unwanted cells and its dysregulation is associated with numerous disease states. There are different pathways through which a cell can undergo cell death, each relying on peculiar molecular mechanisms and morpho-ultrastructural features. To date, however, while molecular and genetic approaches have been successfully integrated into the field, cell death studies rarely incorporate ultrastructural data from electron microscopy. This review article reports a gallery of original transmission electron microscopy images to describe the ultrastructural features of cells undergoing different types of cell death programs, including necrosis, apoptosis, autophagy, mitotic catastrophe, ferroptosis, methuosis, and paraptosis. TEM has been an important technology in cell biology for well over 50 years and still continues to offer significant advantages in the area of cell death research. TEM allows detailed characterization of the ultrastructural changes within the cell, such as the alteration of organelles and subcellular structures, the nuclear reorganization, and the loss of membrane integrity that enable a distinction between the different forms of cell death based on morphological criteria. Possible pitfalls are also described.</p>","PeriodicalId":23430,"journal":{"name":"Ultrastructural Pathology","volume":" ","pages":"1-19"},"PeriodicalIF":1.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142649138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ultrastructural PathologyPub Date : 2025-01-02Epub Date: 2024-12-30DOI: 10.1080/01913123.2024.2446242
Fayza E Ahmed, Ebtahal Z Hassen, Fatma M E Mousa, Karima F Abdelfadeel
{"title":"Ameliorating role of co-administration of granulocyte colony stimulating factor and sodium bicarbonate on the skeletal muscle of a rat model of chronic kidney disease (A histological and immunohistochemical study).","authors":"Fayza E Ahmed, Ebtahal Z Hassen, Fatma M E Mousa, Karima F Abdelfadeel","doi":"10.1080/01913123.2024.2446242","DOIUrl":"https://doi.org/10.1080/01913123.2024.2446242","url":null,"abstract":"<p><p>Over half million individuals suffer from chronic kidney disease (CKD) worldwide. In addition to raising the possibility of cardiovascular diseases, skeletal myopathy remains a challenging complication that is highly correlated with mortality and a lower quality of life. Granulocyte-colony stimulating factor (G-CSF) is an active cytokine for mobilization of immunological and hematopoietic stem cells that can replace exogenous stem cell infusions. So, it is seen as a less expensive and noninvasive tool for regenerative medicine. Sixty three rats were divided into 4 groups: I control, II CKD induced, IIIa, IIIb treated and IV recovery groups. After induction of CKD in all rats, group II were sacrificed after 4 weeks. Rats of group IIIa received NaHCO<sub>3</sub>. Group IIIb rats were injected subcutaneously by G-CSF as 100 µg/kg/day for 5 successive days in addition to NaHCO<sub>3</sub> as group IIIa. Group IV rats were housed for 4 weeks without treatment. Serum urea, creatinine, tissue MDA& TNF-α were assessed. Renal and gastrocnemius muscle sections were evaluated for histological structure, CD34 and myogenin immune expression, morphometric and statistical analyses. The CKD group revealed a significant increase in MDA and TNF-α. Furthermore, features of renal injury, muscle degenerative changes, increased collagen and decreased CD34 and myogenin expression were observed. Alterations were partially attenuated by NaHCO<sub>3</sub>, while GCSF remarkably improved most parameters. The current results indicated that co-administration of GCSF and NaHCO<sub>3</sub> could ameliorate CKD myopathy via attenuating oxidative stress, immunomodulation, pro-angiogenic ability, myocyte regeneration. In addition to the reduction of mitochondrial stress and maintenance of cellular homeostasis.</p>","PeriodicalId":23430,"journal":{"name":"Ultrastructural Pathology","volume":"49 1","pages":"67-92"},"PeriodicalIF":1.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142915637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ultrastructural PathologyPub Date : 2025-01-02Epub Date: 2024-12-11DOI: 10.1080/01913123.2024.2440479
Mohammad Y Alshahrani, Fahad S Al Amri, Mohammed A Alzahrani, Abdulaziz S Alshahrani, Dina H Abdel Kader, Faris Almasabi, Hind Zafrah, Mohammad Dallak, Osama M Osman, Bahjat Al-Ani, Norah M Alzamil
{"title":"Metformin ameliorates diabetes-induced hepatic ultrastructural damage and the immune biomarker CD86 and inflammation in rats.","authors":"Mohammad Y Alshahrani, Fahad S Al Amri, Mohammed A Alzahrani, Abdulaziz S Alshahrani, Dina H Abdel Kader, Faris Almasabi, Hind Zafrah, Mohammad Dallak, Osama M Osman, Bahjat Al-Ani, Norah M Alzamil","doi":"10.1080/01913123.2024.2440479","DOIUrl":"10.1080/01913123.2024.2440479","url":null,"abstract":"<p><p>Diabetes is a known inducer of hepatic ultrastructural alterations, and the expression of the immune biomarker that involves in T-cell immunity, cluster of differentiation 86 (CD86) is increased in diabetic patients with liver cirrhosis. The antidiabetic drug metformin has not previously been used to protect against type 2 diabetes mellitus (T2DM)-induced alternations in hepatic ultrastructure and the induction of the hepatic CD86/inflammation axis in diabetic animal models induced by streptozotocin and a high fat diet. To test our hypotheses, T2DM was induced in rats (model group) and the protective animals were treated with the antidiabetic drug metformin (200 mg/kg) until being sacrificed at week 12. A profound ultrastructural damage to the hepatocytes and liver tissue injury was induced by T2DM as demonstrated by hepatocytes with dark shrunken irregular nuclei, rarefied cytoplasm with lipid droplets, mitochondria with disrupted cristae, as well as depletion of glycogen granules and damaged of liver architecture, which were effectively (<i>p</i> < .0001) protected with metformin. Metformin also suppressed diabetes-induced hepatic gene expression of CD86 and inflammation as well as glycemia and liver injury markers. Furthermore, a significant correlation between hepatocyte damage and CD86, inflammation, glycemia, and biomarkers of liver injury was observed. These findings demonstrate that diabetes is associated with the induction of the hepatic CD86/inflammation axis and hepatocyte ultrastructural alterations while being protected by metformin.</p>","PeriodicalId":23430,"journal":{"name":"Ultrastructural Pathology","volume":" ","pages":"58-66"},"PeriodicalIF":1.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142814240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ultrastructural PathologyPub Date : 2025-01-02Epub Date: 2024-12-09DOI: 10.1080/01913123.2024.2438382
Eman Saeed Mokhtar Tawfeek, Salwa Aly Abou Elez Gawish, Wafaa Saad Hamed, Samar A Asker
{"title":"Construction of an animal model of autism based on interaction between cerebellar histological, immunohistochemical, and biochemical changes in adult male albino rat.","authors":"Eman Saeed Mokhtar Tawfeek, Salwa Aly Abou Elez Gawish, Wafaa Saad Hamed, Samar A Asker","doi":"10.1080/01913123.2024.2438382","DOIUrl":"10.1080/01913123.2024.2438382","url":null,"abstract":"<p><strong>Methods: </strong>Twelve pregnant female rats were divided into a control group and a valproic acid (VPA) treated group (injected intraperitoneally on embryonic day 12 with 600 mg/kg body weight of VPA). Neurobehavioral tests were conducted on the offspring of both groups. The cerebellum was studied by light and electron microscopy as well as GFAP and caspase-3 immunohistochemical staining.</p><p><strong>Results: </strong>The VPA-treated group showed signs of neuronal degeneration, such as congested blood vessels, vacuolations, irregularly shrunken with dark small heterochromatic nuclei and numerous apoptotic blebs in the Purkinje and granule cells with vacuolated cerebellar glomeruli. The myelinated nerve fibers showed rarefaction and loss of their neurofilaments. GFAP and caspase-3 immune expression were significantly altered in the VPA-treated group.</p><p><strong>Conclusion: </strong>The VPA rat model can serve as an excellent model of autism at the structural level, which may be used as a validated model in preclinical studies to evaluate novel drugs.</p>","PeriodicalId":23430,"journal":{"name":"Ultrastructural Pathology","volume":" ","pages":"39-57"},"PeriodicalIF":1.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142802357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ultrastructural PathologyPub Date : 2025-01-02Epub Date: 2024-12-16DOI: 10.1080/01913123.2024.2438380
Sayed M El-Sayed, Gehan A El-Sayed, Mansour M A, Enas Haridy Ahmed, Sherif A Kamar
{"title":"A comparative study on the effect of melatonin and orlistat combination versus orlistat alone on high fat diet-induced hepatic changes in the adult male albino rats (a histological and morphometric study).","authors":"Sayed M El-Sayed, Gehan A El-Sayed, Mansour M A, Enas Haridy Ahmed, Sherif A Kamar","doi":"10.1080/01913123.2024.2438380","DOIUrl":"10.1080/01913123.2024.2438380","url":null,"abstract":"<p><strong>Background: </strong>Nonalcoholic fatty liver disease (NAFLD) is the extremely usual reason of chronic liver disease, extending from simple hepatic steatosis (HS), nonalcoholic steatohepatitis (NASH) to advanced hepatic fibrosis and cirrhosis. Though orlistat is a Food and Drug Administration (FDA) approved drug for long-duration management of obesity, few cases of severe hepatic insult were declared. Melatonin is an efficient antioxidant; it also regulates metabolic processes that lead to fat accumulation and obesity.</p><p><strong>Aim of the work: </strong>The current research aimed to compare the impact of orlistat, melatonin, and their combination on the structural changes of the hepatic tissue of adult male albino rats supplied with high fat diet (HFD).</p><p><strong>Material and methods: </strong>Thirty adult male albino rats divided into five groups. Liver specimens were divided into two parts. One-half was processed to obtain paraffin blocks, and the other half was processed to obtain semithin sections. Morphometric study and statistical analysis were done.</p><p><strong>Results: </strong>Hepatic tissue from the HFD group showed steatosis, ballooning, and inflammation and all these parameters were moderately improved - except for inflammation which worsened with therapy. Combined orlistat and melatonin-treated groups showed marked improvement of all parameters as well as marked improvement in the hepatic fibrosis.Orlistat/Melatonin combination therapy is both safe and effective in comparison to orlistat and melatonin monotherapy.</p>","PeriodicalId":23430,"journal":{"name":"Ultrastructural Pathology","volume":" ","pages":"20-38"},"PeriodicalIF":1.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ultrastructural PathologyPub Date : 2025-01-01Epub Date: 2025-04-23DOI: 10.1080/01913123.2025.2493116
I D Perrotta, Zh Taherzadeh, G A van Montfrans, L M Brewster
{"title":"Exosomes in ultrastructural resistance artery remodeling of human hypertension.","authors":"I D Perrotta, Zh Taherzadeh, G A van Montfrans, L M Brewster","doi":"10.1080/01913123.2025.2493116","DOIUrl":"https://doi.org/10.1080/01913123.2025.2493116","url":null,"abstract":"<p><p>We previously reported that human hypertension is associated with ultrastructural remodeling of systemic resistance arteries. Endothelial and smooth muscle cells (SMC) displayed mitochondrial and sarco-endoplasmic reticulum stress, accompanied by SMC migration toward the intima. Exosomes, nano-sized phospholipid bilayer-enclosed vesicles released from cells upon fusion of multivesicular bodies (MVB) with the plasma membrane, are thought to be involved in the endothelial-to-SMC communication regulating these adaptations. However, there is a dearth of ultrastructural studies on microvascular exosomes during hypertension. Therefore, we characterized and quantified exosomes in omental resistance-sized arteries (200-400 μm), obtained during surgery in 19 women (9 hypertensive), mean age 42 y (SE 1). The number of MVBs was around 7-fold higher in hypertensives, mean, 3.8 (SE 0.2)/cell vs 0.5 (0.1) in normotensives, with a shift from a scant dispersion of intracellular MVBs in normotensives, toward a prominent abluminal endothelial location in hypertensives. MVBs also contained significantly more exosomes in hypertensives, mean 7.9 (0.2) vs 5.0 (0.2)/MVB in normotensives.</p>","PeriodicalId":23430,"journal":{"name":"Ultrastructural Pathology","volume":"49 3","pages":"306-314"},"PeriodicalIF":1.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144050134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ultrastructural PathologyPub Date : 2025-01-01Epub Date: 2025-04-21DOI: 10.1080/01913123.2025.2488809
Josep Lloreta-Trull, Judith Marin-Corral, Nuria Juanpere, Sergi Pascual-Guardia, Javier Gimeno, Dolores Naranjo, Laura Segalés, Silvia Hernández, Mercedes Simón, Laia Serrano, Beatriz Casado, Belén Lloveras, Joaquim Gea
{"title":"Muscle disease in severe COVID-19 patients: a microangiopathic myopathy.","authors":"Josep Lloreta-Trull, Judith Marin-Corral, Nuria Juanpere, Sergi Pascual-Guardia, Javier Gimeno, Dolores Naranjo, Laura Segalés, Silvia Hernández, Mercedes Simón, Laia Serrano, Beatriz Casado, Belén Lloveras, Joaquim Gea","doi":"10.1080/01913123.2025.2488809","DOIUrl":"https://doi.org/10.1080/01913123.2025.2488809","url":null,"abstract":"<p><p>Patients surviving coronavirus disease of 2019 (COVID-19) often complain of skeletal muscle weakness that may be very limiting and long-lasting. There are almost no studies on the skeletal muscle of these patients, and electron microscopic data are scarce. We assessed the ultrastructural changes in the quadriceps of eight patients with COVID-19 and found a combination of features different from those reported in corticosteroid myopathy and acute relaxant-steroid myopathy. The most remarkable and constant changes involved the endothelial cells and consisted of massive amounts of pinocytotic vesicles, degenerative changes, platelet aggregates and, most characteristic of all, an increase in the external lamina thickness that seems to stem from reduplication due to successive bouts of endothelial cell damage and subsequent regeneration. Viral particles were not found in any of the cases. This distinct and quite common set of alterations defines the myopathy associated with infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This association seems to be the result of an inflammatory process that would arise in infected cells but could damage non-infected endomysial blood vessels, thus resulting in persistent changes of the microvasculature that would be related to long-standing myopathic clinical features.</p>","PeriodicalId":23430,"journal":{"name":"Ultrastructural Pathology","volume":"49 3","pages":"296-305"},"PeriodicalIF":1.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}