Enhanced Wolf Pack Algorithm (EWPA) and Dense-kUNet Segmentation for Arterial Calcifications in Mammograms

Breast Arterial Calcification(BAC)is a mammographic decision dissimilar to cancer and commonly observed in elderly women.Thus identifying BAC could provide an expense,and be inaccurate.Recently Deep Learning(DL)methods have been introduced for automatic BAC detection and quantification with increased accuracy.Previously,classification with deep learning had reached higher efficiency,but designing the structure of DL proved to be an extremely challenging task due to overfitting models.It also is not able to capture the patterns and irregularities presented in the images.To solve the overfitting problem,an optimal feature set has been formed by Enhanced Wolf Pack Algorithm(EWPA),and their irregularities are identified by Dense-kUNet segmentation.In this paper,Dense-kUNet for segmentation and optimal feature has been introduced for classification(severe,mild,light)that integrates DenseUNet and kU-Net.Longer bound links exist among adjacent modules,allowing relatively rough data to be sent to the following component and assisting the system in finding higher qualities.The major contribution of the work is to design the best features selected by Enhanced Wolf Pack Algorithm(EWPA),and Modified Support Vector Machine(MSVM)based learning for classification.k-Dense-UNet is introduced which combines the procedure of Dense-UNet and kU-Net for image segmentation.Longer bound associations occur among nearby sections,allowing relatively granular data to be sent to the next subsystem and benefiting the system in recognizing smaller characteristics.The proposed techniques and the performance are tested using several types of analysis techniques 826 filled digitized mammography.The proposed method achieved the highest precision,recall,F-measure,and accuracy of 84.4333%,84.5333%,84.4833%,and 86.8667%when compared to other methods on the Digital Database for Screening Mammography(DDSM).

Myosteatosis is associated with coronary artery calcification in patients with type 2 diabetes

BACKGROUND Myosteatosis,rather than low muscle mass,is the primary etiologic factor of sarcopenia in patients with type 2 diabetes mellitus(T2DM).Myosteatosis may lead to a series of metabolic dysfunctions,such as insulin resistance,systematic inflammation,and oxidative stress,and all these dysfunctions are closely associated with the acceleration of T2DM and atherosclerosis.AIM To investigate the association between myosteatosis and coronary artery calcification(CAC)in patients with T2DM.METHODS Patients with T2DM,who had not experienced major cardiovascular events and had undergone both abdominal and thoracic computed tomography(CT)scans,were included.The mean skeletal muscle attenuation was assessed using abdominal CT images at the L3 level.The CAC score was determined from thoracic CT images using the Agatston scoring method.Myosteatosis was diagnosed according to Martin’s criteria.Severe CAC(SCAC)was defined when the CAC score exceeded 300.Logistic regression and decision tree analyses were performed.RESULTS A total of 652 patients with T2DM were enrolled.Among them,167(25.6%)patients had SCAC.Logistic regression analysis demonstrated that myosteatosis,age,duration of diabetes,cigarette smoking,and alcohol consumption were independent risk factors of SCAC.Myosteatosis was significantly associated with an increased risk of SCAC(OR=2.381,P=0.003).The association between myosteatosis and SCAC was significant in the younger patients(OR=2.672,95%CI:1.477-4.834,P=0.002),but not the older patients(OR=1.456,95%CI:0.863-2.455,P=0.188),and was more prominent in the population with lower risks of atherosclerosis.The decision tree analyses prioritized older age as the primary variable for SCAC.In older patients,cigarette smoking was the main contributing factor for SCAC,while in younger patients,it was myosteatosis.CONCLUSION Myosteatosis is a novel risk factor for atherosclerosis in patients with T2DM,especially in the population with younger ages and fewer traditional risk factors.

A novel mouse model of calcific aortic valve stenosis

Background:Calcific aortic valve stenosis(CAVS)is one of the most challenging heart diseases in clinical with rapidly increasing prevalence.However,study of the mecha-nism and treatment of CAVS is hampered by the lack of suitable,robust and efficient models that develop hemodynamically significant stenosis and typical calcium deposi-tion.Here,we aim to establish a mouse model to mimic the development and features of CAVS.Methods:The model was established via aortic valve wire injury(AVWI)combined with vitamin D subcutaneous injected in wild type C57/BL6 mice.Serial transthoracic echocardiography was applied to evaluate aortic jet peak velocity and mean gradi-ent.Histopathological specimens were collected and examined in respect of valve thickening,calcium deposition,collagen accumulation,osteogenic differentiation and inflammation.Results:Serial transthoracic echocardiography revealed that aortic jet peak velocity and mean gradient increased from 7 days post model establishment in a time depend-ent manner and tended to be stable at 28 days.Compared with the sham group,sim-ple AVWI or the vitamin D group,the hybrid model group showed typical pathological features of CAVS,including hemodynamic alterations,increased aortic valve thicken-ing,calcium deposition,collagen accumulation at 28 days.In addition,osteogenic dif-ferentiation,fibrosis and inflammation,which play critical roles in the development of CAVS,were observed in the hybrid model.Conclusions:We established a novel mouse model of CAVS that could be induced efficiently,robustly and economically,and without genetic intervention.It provides a fast track to explore the underlying mechanisms of CAVS and to identify more effec-tive pharmacological targets.

Animal Model of Aortic Valve Calcification: Their Methodology Helps Us Understand Aortic Valve Calcification

Aortic valve calcification disease (CAVD) is the most prevalent degenerative valve disease in humans, leading to significant morbidity and mortality. Despite its common occurrence, our understanding of the underlying mechanisms remains incomplete, and available treatment options are limited and risky. A more comprehensive understanding of the biology of CAVD is essential to identify new therapeutic strategies. Animal models have played a crucial role in advancing our knowledge of CAVD and exploring potential treatments. However, these models have inherent limitations as they cannot fully replicate the complex physiological mechanisms of human CAVD. In this review, we examine various CAVD models ranging from pigs to mice, highlighting the unique characteristics of each model to enhance our understanding of CAVD. While these models offer valuable insights, they also have limitations and shortcomings. We propose that the guide wire model shows promise for future CAVD research, and streamlining the methodology could enhance our understanding and expand the research scope in this field.

Animal models of tendon calcification:Past,present,and future

Tendon calcification is a common clinical condition that frequently occurs as a complication after tendon injury and surgery,or as an expression of fibrodysplasia ossificans progressiva.This condition can be referred to by various names in clinical practice and literature,including tendon ossification,tendon mineralization,heterotopic ossification,and calcific tendonitis.The exact pathogenesis of tendon calcification remains uncertain,but current mainstream research suggests that calcification is mostly cell mediated.To further elucidate the pathogenesis of tendon calcification and to better simulate the overall process,selecting appropriate experimental animal models is important.Numerous animal models have been utilized in various clinical studies,each with its own set of advantages and limitations.In this review,we have discussed the advancements made in research on animal models of tendon calcification,with a focus on the selection of experimental animals,the sites of injury in these models,and the methods employed for modeling.

Asymmetric expression of CA2 and CA13 linked to calcification in the bilateral mandibular condyles cause crossed beaks in chickens

Crossed beak is a complex mode of inheritance with prevalence ranging from 0.2 to 7.4% in at least 12 chicken strains worldwide.To reveal the intrinsic factors causing crossed beaks,genes expression patterns in bilateral mandibular condyle between affected and normal birds were characterized by RNA sequencing analysis in the present studies.Crossed beak was induced by short length of unilateral mandibular ramus,and a total of 110differentially expressed genes were up-or down-regulated in the affected(short)mandibular condyle side as compared to the normal side.Carbonic anhydrase 2(CA2)and Carbonic anhydrase 13(CA13)were enriched in the carbonate dehydratase activity,and high-expressed in mandibular condyle and osteoblasts(P<0.05).However,both were low-expressed in short mandibular condyle side of affected birds(P<0.05).The carbonate dehydratase inhibitor experiments confirmed that there is positive association between the calcification and carbonic anhydrase isoenzymes.Quantitative analysis with cetylpyridinium chloride showed a decrease in calcification when the cells were transfected with an anti-CA13 shRNA.Our research suggested that CA2 and CA13 are down-calcified in shortside mandibular condyle,and caused mandibular ramus to grow slowly.CA2 and CA13 have the critical role in crossed beaks by regulating calcification of mandibular condyle.

Vascular Calcification:Where is the Cure?

With the progress of aging,the incidence of vascular calcification(VC)gradually increases,which is correlated with cardiovascular events and all-cause death,aggravating global clinical burden.Over the past several decades,accumulating approaches targeting the underlying pathogenesis of VC have provided some possibilities for the treatment of VC.Unfortunately,none of the current interventions have achieved clinical effectiveness on reversing or curing VC.The purpose of this review is to make a summary of novel perspectives on the interventions of VC and provide reference for clinical decision-making.

Complicated calcified alloplastic implants in the nasal dorsum:A clinical analysis

BACKGROUND In rhinoplasty,calcification around silicone implants is frequently observed in the tip dorsum(TD)area.Additionally,based on a review of various literature,it is presumed that calcification in silicone implants occurs due to both inflammatory chemical reactions and physical friction against the tissue.The calcification of nasal silicone implants not only results in the functional loss of the implants,but also leads to material deformation.However,there is a lack of research on calcification of nasal silicone implants in the current literature.AIM To elucidate various clinical characteristics of calcification around nasal silicone implants,using histological and radiological analysis.METHODS This study analyzed data from 16 patients of calcified nasal implants,who underwent revision rhinoplasty for various reasons after undergoing augmentation rhinoplasty with silicone implants.The collected data included information on implant duration,implant types,location of calcification,presence of inflammatory reactions,and computed tomography(CT)scans.RESULTS The most common location of calcification,as visually analyzed,was in the TD area,accounting for 56%.Additionally,the analysis of CT scans revealed a trend of increasing Hounsfield Unit values for calcification with the duration of implantation,although this trend was not statistically significant(P=0.139).CONCLUSION Our study shows that reducing the frequency of calcification may be achievable by using softer silicone implants and by minimizing the damage to perioperative tissues.

Calcification-associated molecular traits and therapeutic strategies in hormone receptor-positive HER2-negative breast cancer

Objective:Mammographic calcifications are a common feature of breast cancer,but their molecular characteristics and treatment implications in hormone receptor-positive(HR+)/human epidermal growth factor receptor 2-negative(HER2−)breast cancer remain unclear.Methods:We retrospectively collected mammography records of an HR+/HER2−breast cancer cohort(n=316)with matched clinicopathological,genomic,transcriptomic,and metabolomic data.On the basis of mammographic images,we grouped tumors by calcification status into calcification-negative tumors,tumors with probably benign calcifications,tumors with calcification of lowmoderate suspicion for maligancy and tumors with calcification of high suspicion for maligancy.We then explored the molecular characteristics associated with each calcification status across multiple dimensions.Results:Among the different statuses,tumors with probably benign calcifications exhibited elevated hormone receptor immunohistochemical staining scores,estrogen receptor(ER)pathway activation,lipid metabolism,and sensitivity to endocrine therapy.Tumors with calcifications of high suspicion for malignancy had relatively larger tumor sizes,elevated lymph node metastasis incidence,Ki-67 staining scores,genomic instability,cell cycle pathway activation,and may benefit from cyclin-dependent kinase 4 and 6(CDK4/6)inhibitors.Conclusions:Our research established links between tumor calcifications and molecular features,thus proposing potential precision treatment strategies for HR+/HER2−breast cancer.

Giant cavernous aneurysms occluded by aneurysmal thrombosis,calcification,parent artery occlusion:A case report and review of literature

BACKGROUND Patients with giant intracranial aneurysms(GIAs)are at a high risk of rupture,morbidity,and mortality even after surgical or endovascular treatment.We described a case of a spontaneously occluded GIA secondary to gradual growth of the GIA,continuously progressed aneurysmal thrombosis,complete aneurysmal calcification and complete occlusion of the parent artery-the right internal carotid artery(RICA).CASE SUMMARY A 72-year-old female patient complained of sudden pain in her right eye upon admission to our hospital.She had been diagnosed with a GIA[30 mm(axial)×38 mm(coronal)×28 mm(sagittal)]containing an aneurysmal thrombus located in the cavernous sinus segment of RICA diagnosed by magnetic resonance imaging(MRI),enhanced MRI,and magnetic resonance angiography more than 14 years ago.Later,with slow growth of the cavernous carotid GIA,aneurysmal thrombosis progressed continuously,spontaneous occlusion of the RICA,complete aneurysmal calcification,and occlusion of the GIA occurred gradually.She had no history of subarachnoid hemorrhage but missed the chance for endovascular therapy at an early stage.As a result,she was left with severe permanent sequelae from the injuries to the right cranial nerves Ⅱ,Ⅲ,Ⅳ,V1/V2,and Ⅴ.CONCLUSION The risk of rupture of the cavernous carotid GIAs was relatively low and possibly further be reduced by the stasis flow and spontaneous occlusion of the parent artery internal carotid artery(ICA)induced by the mass effect of the cavernous carotid GIAs and the extremely rare aneurysmal calcification.However,nowadays,it is advisable to recommend early endovascular treatment for the cavernous carotid GIAs to prevent injuries to the surrounding intracranial nerves and occlusion of the ICA,mainly caused by the mass effect of the cavernous carotid GIAs.

Potential efficacy and mechanism of medicinal plants on chronic kidney disease-associated vascular calcification:a review

Vascular calcification is a crucial risk factor that affects the incidence and mortality of cardiovascular disease in chronic kidney disease patients.Modern medicine relies on calcium-phosphorus binding agents,calcium mimetics,active vitamin D,and hemodialysis to prevent and treat vascular calcification,however,their efficacy is unsatisfactory and adverse reactions often occur.Medical plant therapy can act as an integrative regulator in patients with chronic kidney disease-associated vascular calcification,which can significantly improve patients’symptoms,but its specific mechanism has not been fully elucidated yet.In this paper,we reviewed the domestic and international theoretical studies on the pathogenesis mechanism of chronic kidney disease-associated vascular calcification in recent years,summarized eight active ingredients of medicinal plants as well as four compound formulas for improving chronic kidney disease-associated vascular calcification,and explored the mechanism of action of herbal medicine,which will provide a new strategy for promoting the prevention and treatment of vascular calcification.

Relationship between severity of venous calcifications and symptoms of phlebosclerotic colitis

AIM: To examine the correlation between the severity of venous calcifications and the clinical symptoms of phlebosclerotic colitis.METHODS: This was a retrospective study.The data,including the numbers of episodes of active disease,were collected from the medical records at Taipei Veterans General Hospital and Wei Gong Memorial Hospital in Taiwan between January 2005 and December 2014.All computed tomography images with or without contrast enhancement were obtained using a multiple detector computed tomography scanner.The scanning range reached from the dome of the diaphragm to the pelvis.The severity of calcification at the tributaries of the portal vein was measured using a four-grade scoring system of the calcification of phlebosclerotic colitis.The episodes of active disease were defined as symptoms of fever,abdominal pain,severe constipation,bowel obstruction,vomiting or diarrhea based on a review of the medical records.Spearman's correlation analysis was used to examine the correlation between the numbers of episodes of active disease and the severity of the calcification of the mesenteric veins.RESULTS: More than 3000 cases were reviewed from 2005 to 2014,and a total of 12 patients from Taipei Veterans General Hospital and Wei Gong Memorial Hospital were enrolled according to our inclusion criteria.Among these 12 patients,the mean age of the six males and the six females was 61.8 ± 11.5 years.All patients exhibited typical imaging characteristics,consisting of threadlike calcifications and colonic wall thickening in the standard radiographs and calcifications along the colonic and mesenteric vessels or associated with colonic wall thickening and adjacent fat stranding in the computed tomography images.The median score of the severity of the venous calcifications was 18 ± 13,and the median number of active disease episodes was 1 ± 1.75.Spearman's correlation analysis revealed that the number of episodes of active phlebosclerotic colitis disease significantly positively correlated with the severity of the calcification of the mesenteric veins(r = 0.619,P < 0.05).CONCLUSION: The extent of mesenteric venous calcification is strongly associated with the number of episodes of active disease among patients with phlebosclerotic colitis.

Pentoxifylline treatment and penile calcifications in men Nith Peyronie＇s disease

This retrospective cohort study from a single clinical practice enrolled patients with evidence of calcified Peyronie＇s disease （PD） plaques detected on penile ultrasound at the time of initial presentation. The primary objective was to describe the effect of pentoxifylline （PTX） treatment on subtunical calcifications in men with PD. A PD-specific questionnaire was administered and sonographic evaluations were performed at baseline and follow-up visits. Descriptive statistics and X2 analysis were used to characterize the effect of PTX on calcified tunical plaques. In all, 71 men （mean age： 51.9 years） with PD and sonographic evidence of calcification were identified. Of them, 62 of these men were treated with PTX for a mean duration of I year, and nine with vitamin E or no treatment. Improvement or stabilization in calcium burden at follow-up was noted in 57 （91.9%） of men treated with PTX versus four （44,4%） of those not treated with PTX （P〈0.001）. PTX users were much less likely to have a subjective worsening of their clinical condition （25.0% versus 78.3%, P=0.002）. Treatment with PTX appeared to stabilize or reduce calcium content in PD plaques. A randomized controlled trial is warranted to further explore this effect.

Extensive calcifications in portal venous system in a patient with hepatocarcinoma

Calcification of the portal venous system is a rare entity that can be incidentally discovered during computed tomography (CT). We describe a case of extensive calcifications in the portal venous system in a middle-aged male patient with hepatocellular carcinoma (HCC). This patient presented with epigastric pain that had no obvious origin prior to admission. Laboratory examinations were positive for hepatitis B surface antigen and &#x003b1;-fetoprotein, and severe esophageal and gastric varices were detected during gastroscopy. Abdominal X-ray plain film showed well-defined linear and track-like calcification, with irregular margins directed along the course of the portal venous system. CT revealed extensive calcifications along the course of the portal, splenic, superior mesenteric and gastroesophageal veins. He underwent splenectomy 22 years ago due to splenomegaly and partial hepatectomy seven months before because of HCC of low-grade differentiation, confirmed by pathology. Finally, the patient was diagnosed with postoperative recurrent HCC and extensive portal venous system calcification after selective hepatic angiography under digital subtraction angiography.

Determinants of Detection of Stones and Calcifications in the Hepatobiliary System on Virtual Nonenhanced Dual-energy CT

Objective To retrospectively determine the features of stones and calcifications in hepatobiliary system on virtual nonenhanced (VNE) dual-energy computed tomography (CT), and to evaluate the possibility of VNE images in diagnosis for those lesions. Methods A total of 128 gall stones and calcifications of the liver found in 110 patients were examined with triple phase abdominal CT scan from July 2007 to December 2011, in which true nonenhanced (TNE) phase and arterial phase were performed with single-energy CT (120 kVp) and portal venous phase was performed with dual-energy CT (100 kVp and 140 kVp). VNE images were generated from the portal venous phase dual-energy CT data sets by using commercially VNC software. The mean CT values for the stone, liver, bile and paraspinal muscle, mean lesion density and size in area dimension, contrast-to-noise ratio (CNR) of lesion to the liver or bile, and image noise were assessed and compared between VNE and TNE images. The effective dose and size-specific dose estimate (SSDE) were also calculated. Results The mean CT values of the lesions measured on VNE images declined significantly compared with those measured on TNE images (164.51±102.13vs. 290.72±197.80 HU,P<0.001), so did the lesion-to-liver CNR (10.80±11.82vs.18.81±17.06,P<0.001) and the lesion-to-bile CNR (17.24±14.41 vs. 21.32±17.31,P<0.001). There was no significant difference in size of lesions area between VNE and TNE images (0.69±0.88vs.0.72±0.85 cm2,P=0.062). Compared to the 128 lesions found in TNE images, VNE images showed the same density in 30 (23.4%) lesions, lighter density in 88 (68.8%) lesions, while failed to show 10 (7.8%) lesions, and showed the same size in 61 (47.7%) lesions and smaller size in 57 (44.5%)&nbsp;lesions. The CT cutoff values of lesion and size were 229.21 HU and 0.15 cm2, respectively. The total effective dose for triple phase scan protocol with TNE images was 19.51±7.03 mSv, and the SSDE was 39.84±11.10 mGy. The effective dose for dual phase scan protocol with VNE images instead of TNE images was 13.29±4.89 mSv, and the SSDE was 27.83±9.99 mGy. Compared with TNE images, the effective dose and SSDE of VNE images were down by 32.05%±3.69 % and 30.63%±2.34 %, respectively. Conclusions Although the CT values and CNR of the lesions decreased in VNE images, the lesions of which attenuation greater than 229.21 HU and size larger than 0.15 cm2could be detected with good reliability and obvious dose reduction. There was good consistency in the size of stones and calcifications in hepatobiliary system between VNE images and TNE images, which ensured the possibility of the clinical application of VNE images.

Assessment of Arterial Stiffening and Vascular Calcifications in End‐Stage Renal Disease Patients

Background and Objective: Epidemiological and clinical studies have shown that vascular calcification and arterial vascular stiffness are associated with all-cause and cardiovascular (CV) mortality in the general populations and end-stage renal disease (ESRD) patients. The objective of this study was the assessment of arterial stiffness and vascular calcification in ESRD patients in Sohag University Hospital. Patients and Methods: In this cross-sectional descriptive study, 100 patients with ESRD (63 males and 37 females) were included. The patients were on regular hemodialysis (HD) for 65.18 ± 50.25 months. Arterial stiffness was measured by brachial pulse pressure (PP). A simple vascular calcification score (SVCS) based on plain radiographic films of pelvis and hands was used for assessment of vascular calcification. The patients undergoing clinical evaluation and serum calcium, phosphorus and parathyroid hormone (PTH) were obtained. Results: PP > 70 mmHg was observed in 24 patients (24%) and vascular calcifications were detected in 50 patients (50%). SVCS ≥ 3 was observed in 36 patients (36%) and 10 patients (10%) had both SVCS ≥ 3 and PP > 70 mmHg. PP > 70 was significantly associated with presence of vascular disease (odds ratio;5, 95% CI = 1.56 - 16.01;P = 0.007). In multivariate analysis, PP > 70 was independently associated with elevated systolic blood pressure (odds ratio;1.34, 95% CI = 1.11 - 1.6;P = 0.002) and serum PTH (odds ratio;1.004, 95% CI = 1 - 1.008;P = 0.03). SVCS ≥ 3 was association with age (odds ratio;1.05, 95% CI = 1.02 - 1.09;P = 0.003) and presence of vascular disease (odds ratio;3.19, 95% CI = 1.3 - 7.85;P = 0.01). Elevated systolic blood pressure was independently associated with SVCS ≥ 3 (odds ratio;1.08, 95% CI = 1.03 - 1.14;P = 0.002). Conclusion: Arterial stiffness and vascular calcifications are common in patients with ESRD on regular hemodialysis. PP and SVCS are simple and inexpensive methods in assessment of vascular calcifications and arterial stiffness in hemodialysis patients. PP and SVCS may provide important information that may guide the management of these patients.

Caseous mitral annular calcifications: Multimodality imaging characteristics

The authors report herein a series of 3 patients with caseous mitral annular calcifications (MAC). One of the patients presented with mass-like, caseous MAC as an incidental finding on a staging computed tomography (CT) for metastatic colorectal carcinoma. Another patient presented with a nodule on a chest radiograph, which was later found on CT to be due to caseous MAC. In the third patient, caseous MAC was initially detected on echocardiography, and was further evaluated with CT and cardiac magnetic resonance imag-ing. In all three patients, the appearances posed a diagnostic dilemma. The appearance of caseous MAC is dissimilar to non-caseous MAC and is usually seen as an ovoid, mass-like structure, with homogeneous hyperattenuation, representing a liquefied form of calcium and proteinaceous fluid. This homogeneous center is surrounded by peripheral, shell-like calcifications. Caseous MAC is likely an under-recognized entity and may present a diagnostic dilemma at CT, magnetic resonance imaging, or echocardiography.

Modifications of Coronay Artery Calcifications (CAC) and Correlations with C Reactive Protein (CRP) Levels in Renal Recipients after the First Year of Transplantation

The purpose of the present study was to determine the association between presence and progression of Coronary Artery Calcifications (CAC) quantified with Agatston Score (AS) and inflammatory index as CRP and other parameters in unselected renal transplant recipients. Forty-five patients were underwent a baseline Multislice CT (MSCT) at the time of renal transplant and a repeat evaluation 12 - 16 months later. After second MSCT recipients were divided in three groups: Gr1 (26 patients) with absence of CAC at basal and second MSCT, Gr2 (11 patients) with reduction of CAC after one year and Gr3 (8 patients) with increased values of CAC after one year. Mean +/- Standard deviation of basal and after one year values of AS and CRP were respectively: Gr1: 2 +/-3;2 +/- 5 and 0.4 +/- 0.3;0.55 +/- 0.67;Gr2: 317 +/- 288;212 +/- 242 and 0.9 +/- 1.1;0.55 +/- 0.6;Gr3: 854 +/- 1168;1032 +/- 1153 and 0.8 +/- 0.8;1.1 +/-?0.96. We found capacity of renal transplantation to protect against development of new calcium deposits in recipients without CAC at time of transplantation. While we confirmed association in Gr2 between reduction of CAC with reduction of CRP levels and in Gr3 between increased levels of CRP with increasing of CAC. Conclusion: In this preliminary study, renal transplantation appears to slow down or increasing CAC, in strict association with modifications of CRP levels. Long term studies are needed to confirm our preliminary data and to determine the effects of CAC on cardiovascular morbidity and mortality in renal transplant recipients.

Gastric cancer with calcifications: A case report

BACKGROUND Mucinous gastric carcinoma(MGC)is a rare histological type of gastric carcinoma.Calcifications,seen on imaging and histopathological preparations,and which are infrequent in other types of gastric carcinoma,are characteristic of MGC.We present a patient with MGC with calcifications of the gastric wall and describe the computerized tomography(CT)features of the lesion and changes in the calcifications before and after chemotherapy.CASE SUMMARY A 61-year-old man was admitted to our hospital in May 2020 because of a large,tender abdominal mass.Abdominal CT showed diffuse,irregular thickening of the gastric walls,with miliary and punctate calcifications.There were metastases to the perigastric and retroperitoneal lymph nodes and also peritoneal seeding.Histological examination of a specimen obtained by endoscopic biopsy showed poorly differentiated calcified signet-ring cell gastric cancer.The patient was clinically staged with T4N+M1 disease.He was treated with docetaxel,cisplatin,and fluorouracil as first-line therapy,irinotecan combined with S-1 as second-line chemotherapy,and programmed cell death protein 1 as third-line therapy.The patient underwent a total of nine cycles of chemotherapy.Follow-up CT scans every 3 mo showed continually increasing calcifications.As of this writing,the patient has survived almost 1 year.CONCLUSION In this case report,we describe the histopathological and imaging characteristics of a patient with gastric cancer receiving chemotherapy.Multiple punctate calcifications were seen,which gradually increased during chemotherapy.Several possible mechanisms for the calcifications are described,but further research is needed.Future findings may lead to new approaches for the evaluation and treatment of such tumors.

Post-traumatic cauda equina nerve calcification:A case report

BACKGROUND Post-traumatic cauda equina nerve calcification is extremely rare in clinical practice,and its etiology,pathogenesis,treatment and prognosis are unclear.There are few studies and reports on Post-traumatic cauda equina nerve calci-fication,and this review reports a case of Post-traumatic cauda equina nerve calcification for reference.CASE SUMMARY A 52-year-old patient presented to our hospital with a history of lumbar spinal stenosis and a lumbar vertebral fracture caused by trauma.The patient's right lower limb had weakness in hip flexion,knee extension and plantarflexion with muscle strength grade 3,right ankle dorsiflexion and thumb dorsiflexion with muscle strength grade 0.The patient's skin sensation below the right knee plane disappeared.The patient's Computed tomography(CT)data showed signs of cauda equina nerve calcification and the terminal filaments in the plane of the third to fifth lumbar vertebrae.After treatment the patient's symptoms were slightly relieved.CONCLUSION We provide an extremely rare case of Post-traumatic cauda equina nerve calcification and offer a conservative treatment plan.However,the etiology,mechanism and treatment of Post-traumatic cauda equina nerve calcification are still unclear.This requires scholars to conduct more research and exploration in this area.