Chronic Diseases and Translational Medicine最新文献

{"title":"Direct cellular reprogramming and transdifferentiation of fibroblasts on wound healing—Fantasy or reality?","authors":"Juan Du,&nbsp;Xuelai Liu,&nbsp;Carol Wing Yan Wong,&nbsp;Kenneth Kak Yuen Wong,&nbsp;Zhixin Yuan","doi":"10.1002/cdt3.77","DOIUrl":"10.1002/cdt3.77","url":null,"abstract":"<p>Induced pluripotent stem cell (iPSC) technology is one of the de novo approaches in regeneration medicine and has led to new research applications for wound healing in recent years. Fibroblasts have attracted wide attention as the first cell line used for differentiation into iPSCs. Researchers have found that fibroblasts can be induced into different types of cells in variable mediums or microenvironments. This indicates the potential “stem” characteristics of fibroblasts in terms of direct cellular reprogramming compared with the iPSC detour. In this review, we described the morphology and biological function of fibroblasts. The stem cell characteristics and activities of fibroblasts, including transdifferentiation into myofibroblasts, osteogenic cells, chondrogenic cells, neurons, and vascular tissue, are discussed. The biological values of fibroblasts are then briefly reviewed. Finally, we discussed the potential applications of fibroblasts in clinical practice.</p>","PeriodicalId":32096,"journal":{"name":"Chronic Diseases and Translational Medicine","volume":"9 3","pages":"191-199"},"PeriodicalIF":0.0,"publicationDate":"2023-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e5/57/CDT3-9-191.PMC10497843.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10271451","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":"Association of blood pressure variability with target organ damage in older patients with essential hypertension","authors":"Zhiquan Jing,&nbsp;Gang Wang,&nbsp;Zeya Li,&nbsp;Shanshan Wu,&nbsp;Xiang Qiu,&nbsp;Rongchong Huang","doi":"10.1002/cdt3.73","DOIUrl":"10.1002/cdt3.73","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Although multiple measures of blood pressure variability (BPV) have been proposed, whether they are better than mean blood pressure in predicting target organs is unclear. We aimed to determine the relationship between short term BPV and target organ injury.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study was a retrospective study, and 635 inpatients in the Department of Cardiology from 2015 to 2020 were selected. We divided participants into four groups on the basis of the quartiles of BPV. One-way analysis of variance was used to compare the differences between the groups, and linear regression was used to analyze the relationship between BPV and target organ damage.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The average age of 635 patients was 74.36 ± 6.50 years old. Among them, 354 of 627 patients had diminished renal function (56.5%), 221of 604 patients had associated left ventricular hypertrophy (36.6%), and 227 of 231 patients had carotid plaque formation (98.3%). The baseline data indicated significant differences in fasting glucose, total cholesterol, low-density lipoprotein, creatinine, glomerular filtration rate, sex, calcium channel blocker use, and the rate of diminished renal function. Multiple linear regression analysis showed that BPV was negatively correlated with renal injury (creatinine: <i>r</i> = 0.306, <i>p</i> &lt; 0.01; estimated glomerular filtration rate: <i>r</i> = 0.058, <i>p</i> &lt; 0.01), and BPV is positively correlated with cardiac injury (<i>r</i> = 0.083, <i>p</i> &lt; 0.01). Elevated BPV was not found to be associated with vascular injury.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Renal function decreases with increasing BPV and left ventricular mass increases with increasing BPV.</p>\u0000 </section>\u0000 </div>","PeriodicalId":32096,"journal":{"name":"Chronic Diseases and Translational Medicine","volume":"9 4","pages":"320-328"},"PeriodicalIF":0.0,"publicationDate":"2023-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45686830","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":"Amyloid goiter secondary to familial Mediterranean fever with E148Q mutation: A unique case","authors":"Juan C. A. Moreno,&nbsp;Eduardo Eyzaguirre,&nbsp;Suimin Qiu","doi":"10.1002/cdt3.79","DOIUrl":"10.1002/cdt3.79","url":null,"abstract":"<p>Dear Editor,</p><p>Goiter is defined as the enlargement of the thyroid gland. It is currently divided into diffuse and nodular and subdivided into toxic (associated with hyperthyroidism) or nontoxic (associated with normal thyroid stimulating hormone [TSH] levels).<span>¹</span> The most common cause of goiter is iodine deficiency,<span>²</span> and other causes are increased levels of TSH, natural goitrogens, iron and vitamin A deficiency, genetic factors (<i>DICER1</i> syndrome and <i>PTEN</i> hamartoma tumor syndrome), and hereditary (Plummer syndrome) factors.<span>³</span></p><p>A rare entity known as familial Mediterranean fever (FMF) can present with amyloid goiter. This is an autoimmune disorder that affects the Mediterranean littoral.<span>⁴</span> These patients present with fevers and abdominal and chest pain. This condition can produce fibrillar depositions of amyloid protein, usually affecting the kidney<span>⁵</span> but rarely involving the thyroid. We present a case of a 21-year-old woman with no medical history who presented to our hospital with a nontoxic diffuse goiter with initial presentation and pathologically confirmed as amyloid deposition secondary to FMF.</p><p>The patient is a 21-year-old Asian American woman with no significant medical history. She presented to our institution with dyspnea and dysphagia. An ultrasound from an outside hospital revealed diffuse thyroid enlargement. Our in-house laboratory results showed normal TSH, T4, T3, and elevated TPO antibody and erythrocyte sedimentation rate. A CT scan was performed on the patient showing heterogenous thyromegaly wrapping around the trachea and esophagus (Figure 1). A fine needle aspirate was performed, which showed a fibroinflammatory lesion. The patient started on steroids with no improvement, and a total thyroidectomy was performed. Macroscopic examination revealed a poorly defined, firm mass with pale tan areas of discoloration (Figure 2). Microscopic examination revealed an atrophic thyroid parenchyma with diffuse adipose cell metaplasia and diffuse interfollicular deposition of acellular amorphous material consistent with amyloid (Figure 3). Multifocal areas of chronic inflammation were also seen. Congo red stain was positive for amyloid (Figure 4A) with apple-green birefringence under polarized light (Figure 4B). Liquid chromatography tandem mass spectrometry was performed on peptides extracted from the Congo red-positive/microdissected areas of the paraffin-embedded thyroid specimen. The detected peptide profile was consistent with AA (SAA)-type amyloid deposition. The patient consequently had genetic testing showing a homozygous E148Q mutation. This confirms the clinical syndrome of FMF. After continuous follow-up, 10 years later, she developed end-stage renal failure with a renal biopsy confirming Renal AA amyloidosis. Since then, she has been on hemodialysis and is now on the waiting list for a ","PeriodicalId":32096,"journal":{"name":"Chronic Diseases and Translational Medicine","volume":"9 3","pages":"266-268"},"PeriodicalIF":0.0,"publicationDate":"2023-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/37/d6/CDT3-9-266.PMC10497809.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10272900","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":"Vitamin D and hypertension: Is there any significant relation?","authors":"Naga P. Vakkalagadda,&nbsp;Sri H. Narayana,&nbsp;Gummadi S. Sree,&nbsp;Lakshmi D. Bethineedi,&nbsp;L. V. Simhachalam Kutikuppala,&nbsp;Gnana D. Medarametla","doi":"10.1002/cdt3.83","DOIUrl":"10.1002/cdt3.83","url":null,"abstract":"<p>Around a billion individuals worldwide have hypertension. Of these, 95% have essential hypertension, a type of undiagnosed hypertension.<span>¹</span> The regulation of blood pressure (BP) involves numerous signaling pathways. Among them, the Renin Angiotensin System is well known. All these pathways are regulated by modulation of renal salt handling and tone of vascular smooth muscle (VSM) tissue. Any of these mechanisms can become faulty and alter the resistance arteries’ VSM tone, which can elevate BP. However, since the exact origin of PH and its pathophysiology are unknown, less effective, and generic treatments are used.<span>²</span> The fact that more than 50% of hypertension patients in the USA do not have their BP under good control serves as an illustration of this. Antihypertensive treatment resistance affects an additional 5 million people and is defined as the inability to regulate BP despite the use of at least three antihypertensive drugs in combination.<span>³</span></p><p>Increasing age, racial variables, history in household members, obese status, physical inactivity, larger amounts of salt consumption, stress, tobacco use, and heavy alcohol use are some of the potential etiological factors for essential hypertension.<span>⁴</span> It has been examined in previous meta-analyses how vitamin D supplementation affects BP,<span>⁵</span> but it is still unclear whether this connection is causal in the general population. This study focused on finding out the effect of vitamin D3 deficiency on BP.</p><p>Vitamin D, a steroid hormone, promotes the calcium and phosphate absorption from the gastro-intestinal tract (GIT) and reabsorption from the renal tubules. At low levels, it causes bone mineralization. At high doses, it causes bone resorption. It contributes significantly to mineral metabolism and skeletal homeostasis in this way.<span>³</span></p><p>Up to 80% of human vitamin D comes from vitamin D3, which is produced in the skin by ultraviolet (UV) radiation from 7-dehydrocholesterol. Fish, egg yolk, fortified milk, cereal, juice, and yogurt are dietary sources of vitamin D that provide D2 as well as D3 forms and account for around 20% of the body's requirement. The significant vitamin D form, 25-hydroxyvitamin D [25(OH)D], is produced by the liver from D2 and D3 forms of vitamin D in the body. It is the most accurate measure of the action status and levels of vitamin D. It mostly depends on the serum vitamin D binding protein.<span>⁴</span></p><p>According to the Institution of Endocrinology clinical practice guidelines, blood 25-hydroxyvitamin D [25(OH)D] results below 20 ng/mL (or 50 nmol/L) are considered deficient levels of vitamin D. Inadequate vitamin D status is ubiquitous among Chinese.<span>⁴</span> Numerous studies have been published describing how vitamin D deficiency can lead to cancer,<span>^6-10</span> metabolic disor","PeriodicalId":32096,"journal":{"name":"Chronic Diseases and Translational Medicine","volume":"10 2","pages":"156-158"},"PeriodicalIF":0.0,"publicationDate":"2023-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cdt3.83","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43586708","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":"Posttreatment Lyme disease syndrome and myalgic encephalomyelitis/chronic fatigue syndrome: A systematic review and comparison of pathogenesis","authors":"Natalie A. Bai,&nbsp;Christie S. Richardson","doi":"10.1002/cdt3.74","DOIUrl":"10.1002/cdt3.74","url":null,"abstract":"<p>Lyme disease is the most common vector-borne illness in the United States and has been causing significant morbidity since its discovery in 1977. It is well-documented that about 10% of patients properly treated with antibiotics never fully recover, but instead go on to develop a chronic illness dubbed, posttreatment Lyme disease syndrome (PTLDS) characterized by severe fatigue, cognitive slowing, chronic pain, and sleep difficulties. This review includes 18 studies that detail the symptoms of patients with PTLDS and uses qualitative analysis to compare them to myalgic encephalitis/chronic fatigue syndrome (ME/CFS), a strikingly similar syndrome. In the majority of the PTLDS studies, at least four of the six major symptoms of ME/CFS were also noted, including substantial impairment in activity level and fatigue for more than 6 months, post-exertional malaise, and unrefreshing sleep. In one of the included PTLDS articles, 26 of the 29 ME/CFS symptoms were noted. This study adds to the expanding literature on the post-active phase of infection syndromes, which suggests that chronic illnesses such as PTLDS and ME/CFS have similar pathogenesis despite different infectious origins.</p>","PeriodicalId":32096,"journal":{"name":"Chronic Diseases and Translational Medicine","volume":"9 3","pages":"183-190"},"PeriodicalIF":0.0,"publicationDate":"2023-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4d/da/CDT3-9-183.PMC10497844.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10271445","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":"Cyclophilin D as a potential therapeutic target of liver ischemia/reperfusion injury by mediating crosstalk between apoptosis and autophagy","authors":"Mengjiao Yang,&nbsp;Zhihui Wang,&nbsp;Jin Xie,&nbsp;Md. Reyad-ul-Ferdous,&nbsp;Siying Li,&nbsp;Yongfeng Song","doi":"10.1002/cdt3.78","DOIUrl":"10.1002/cdt3.78","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Liver ischemia/reperfusion (I/R) injury is a complex and multifactorial pathophysiological process. It is well recognized that the membrane permeability transition pore (mPTP) opening of mitochondria plays a crucial role in cell death after I/R injury. Cyclophilin D (CypD) is a critical positive regulator of mPTP. However, the effect of CypD on the pathogenesis of liver I/R injury and whether CypD is a potential therapeutic target are still unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We constructed liver-specific CypD knockout and AAV8-peptidyl prolyl isomerase F (PPIF) overexpression mice. Then, a 70% liver I/R injury model was established in mice, with 90 min of ischemia and 6 h of reperfusion. The liver function was detected by the level of serum glutamic pyruvic transaminase (alanine transaminase) and glutamic oxaloacetic transaminase (aspartate aminotransferase), the liver damage score and degree of necrosis were measured by hematoxylin and eosin (H&amp;E) staining of liver tissues. Reactive oxygen species (ROS) staining, apoptosis, and autophagy-related molecules were used to detect apoptosis and autophagy during liver I/R.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The liver-specific knockout of CypD alleviated necrosis and dysfunction in liver I/R injury, by reducing the excessive production of ROS, and inhibiting cell apoptosis and autophagy. On the contrary, overexpression of CypD exacerbated I/R-induced liver damage.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>We found that the downregulation of CypD expression alleviated liver I/R injury by reducing apoptosis and autophagy through caspase-3/Beclin1 crosstalk; in contrast, the upregulation of CypD expression aggravated liver I/R injury. Therefore, interfering with the expression of CypD seems to be a promising treatment for liver I/R injury.</p>\u0000 </section>\u0000 </div>","PeriodicalId":32096,"journal":{"name":"Chronic Diseases and Translational Medicine","volume":"9 3","pages":"238-249"},"PeriodicalIF":0.0,"publicationDate":"2023-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/dd/31/CDT3-9-238.PMC10497823.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10321419","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":"Stroke-like presentation of acute toxic leukoencephalopathy due to capecitabine treatment with extensive intramyelinic edema","authors":"Julia Feige,&nbsp;Fritz Klausner,&nbsp;Johannes A. R. Pfaff,&nbsp;Eugen Trinka,&nbsp;Slaven Pikija,&nbsp;Mahdi Safdarian","doi":"10.1002/cdt3.72","DOIUrl":"10.1002/cdt3.72","url":null,"abstract":"<p>Capecitabine is an oral prodrug of 5-fluorouracil (5-FU), which is widely used for adjuvant and neoadjuvant chemotherapy of different solid tumors, particularly breast and colorectal cancers.<span>¹</span> Neurotoxicity of capecitabine has been consistently reported as capecitabine-induced toxic leukoencephalopathy, which includes bilateral lesions in the corpus callosum and corticospinal tract presenting as acute or delayed central nervous system toxicity.<span>²</span> This side effect requires discontinuation of chemotherapy<span>³</span>; however, neurological symptoms due to capecitabine are reported to be usually reversible upon drug withdrawal.<span>¹</span></p><p>The patients presenting with acute stroke-like symptoms with accompanied restricted diffusion outside typical vessel territory pose a significant diagnostic challenge. In the case of exclusively white matter involvement, the observed low apparent diffusion coefficient (ADC) could be due to the severe intramyelinic edema and not cell death, that is, cytotoxic edema. Multifocal leukoencephalopathy has been associated with capecitabine, but only a few cases have been reported in the literature.<span>⁴</span></p><p>A 51-year-old woman was admitted due to acute onset of dizziness, dysarthria, and right-sided central facial paresis. The patient had been diagnosed with bilateral breast cancer 5 years ago for which neoadjuvant chemotherapy was done as well as surgical and radiation therapy. The primary tumor was a moderately differentiated invasive breast carcinoma of nonspecific type (right breast: stadium cT1b, human epidermal growth factor receptor 2 [HER2] negative with Ki67 10%–20%, and left breast: Stadium cT1c cN1 cM0. HER2 negative. Ki67 10%). Neoadjuvant chemotherapy regime consisted of four cycles of epirubicin/cyclophosphamide (every 2 weeks [q2w]) afterwards four cycles of paclitaxel (q2w) with granulocyte-colony-stimulating factor (G-CSF) support for 4 months. In the follow-up fluorodeoxyglucose-positron emission tomography (FDG-PET) scan, a solitary osseous metastasis was detected in the sacrum, for which capecitabine and bevacizumab had been initiated.</p><p>At our department, the patient reported a feeling of dizziness and difficulties in swallowing 1 day after starting capecitabine and bevacizumab. The CT at admission showed no infarction or hemorrhage and she was also outside thrombolysis therapeutic window. In the evening that day, there was a sudden onset of motoric aphasia. MR-tomography showed a pronounced hyperintense white matter lesion affecting the splenium of the corpus callosum and the medullary beds with pronounced fiber rarefication in arcuate fasciculus (Figure 1A–C). There was a mild pleocytosis of 15 cells/μL in the CSF, with normal protein and lactate. A JC virus polymerase chain reaction (PCR) from the CSF was negative. Onco-neural and antineuronal antibodies were all negative (Table 1). Clinical","PeriodicalId":32096,"journal":{"name":"Chronic Diseases and Translational Medicine","volume":"9 3","pages":"258-262"},"PeriodicalIF":0.0,"publicationDate":"2023-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/19/13/CDT3-9-258.PMC10497845.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10271448","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":"Fruit and vegetable intake and the risk of arterial hypertension in China: A prospective cohort study","authors":"Zhi He,&nbsp;Yanhui Jia,&nbsp;Jianxin Li,&nbsp;Jie Cao,&nbsp;Fangchao Liu,&nbsp;Hongfan Li,&nbsp;Jichun Chen,&nbsp;Dongsheng Hu,&nbsp;Chong Shen,&nbsp;Yingxin Zhao,&nbsp;Xiaoqing Liu,&nbsp;Ling Yu,&nbsp;Jianfeng Huang,&nbsp;Xiangfeng Lu,&nbsp;Dongfeng Gu,&nbsp;Shufeng Chen","doi":"10.1002/cdt3.76","DOIUrl":"10.1002/cdt3.76","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Population-based epidemiological evidence regarding the association between fruit and vegetable intake and the incidence of hypertension is inconsistent. This prospective cohort study aimed to investigate the association between fruit and vegetable intake and the risk of new-onset hypertension.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Based on the project of Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR), 58,981 Chinese adults without hypertension at baseline were included. Information on fruit and vegetable intake was collected using a food-frequency questionnaire. Cox proportional hazards models were performed to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) of incident hypertension.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>During 640,795 person-years of follow-up, 21,008 new cases of hypertension were recorded. Compared with participants in the lowest quintile (Q1) of total fruit and vegetable (TFV) intake, the HRs (95% CIs) of incident hypertension were 0.90 (0.86–0.95), 0.85 (0.81–0.90), 0.82 (0.78–0.86), and 0.83 (0.78–0.88) for the Q2 to Q5 group (<i>p</i>_trend &lt; 0.001), respectively. In further analyses categorizing participants according to the recommended intake level (500 g/day), we found that increasing the intake of TFV, even though it was still insufficient for the recommendation, also had a protective effect against the incident hypertension. When considering the intake of fruit or vegetable separately, we found similar trends as the TFV intake.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These results suggest that a higher intake of fruit and vegetable is beneficial for preventing hypertension in Chinese adults.</p>\u0000 </section>\u0000 </div>","PeriodicalId":32096,"journal":{"name":"Chronic Diseases and Translational Medicine","volume":"9 4","pages":"309-319"},"PeriodicalIF":0.0,"publicationDate":"2023-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41860464","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":"Advances in immune response to pulmonary infection: Nonspecificity, specificity and memory","authors":"Jianqiao Xu,&nbsp;Lixin Xie","doi":"10.1002/cdt3.71","DOIUrl":"10.1002/cdt3.71","url":null,"abstract":"<p>The lung immune response consists of various cells involved in both innate and adaptive immune processes. Innate immunity participates in immune resistance in a nonspecific manner, whereas adaptive immunity effectively eliminates pathogens through specific recognition. It was previously believed that adaptive immune memory plays a leading role during secondary infections; however, innate immunity is also involved in immune memory. Trained immunity refers to the long-term functional reprogramming of innate immune cells caused by the first infection, which alters the immune response during the second challenge. Tissue resilience limits the tissue damage caused by infection by controlling excessive inflammation and promoting tissue repair. In this review, we summarize the impact of host immunity on the pathophysiological processes of pulmonary infections and discuss the latest progress in this regard. In addition to the factors influencing pathogenic microorganisms, we emphasize the importance of the host response.</p>","PeriodicalId":32096,"journal":{"name":"Chronic Diseases and Translational Medicine","volume":"9 2","pages":"71-81"},"PeriodicalIF":0.0,"publicationDate":"2023-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2e/d4/CDT3-9-71.PMC10249196.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9674228","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":"Prevalence of familial hypercholesterolemia and its association with coronary artery disease: A Chinese cohort study","authors":"Xiapikatijiang Aihaiti,&nbsp;Shufeng Chen,&nbsp;Jianxin Li,&nbsp;Zhennan Lin,&nbsp;Qingmei Cui,&nbsp;Xue Xia,&nbsp;Fangchao Liu,&nbsp;Chong Shen,&nbsp;Dongsheng Hu,&nbsp;Keyong Huang,&nbsp;Yingxin Zhao,&nbsp;Fanghong Lu,&nbsp;Xiaoqing Liu,&nbsp;Jie Cao,&nbsp;Ling Yu,&nbsp;Ying Li,&nbsp;Huan Zhang,&nbsp;Zhenyan Fu,&nbsp;Liancheng Zhao,&nbsp;Jianfeng Huang,&nbsp;Dongfeng Gu,&nbsp;Xiangfeng Lu","doi":"10.1002/cdt3.69","DOIUrl":"10.1002/cdt3.69","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Familial hypercholesterolemia (FH) is underrecognized, and its association with coronary artery disease (CAD) remains limited, especially in China. We aimed to investigate the prevalence of FH and its relationship with CAD in a large Chinese cohort.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>FH was defined using the Make Early Diagnosis to Prevent Early Death (MEDPED) criteria. The crude and age-sex standardized prevalence of FH were calculated based on surveys of the Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR) project during 2007−2008. The associations of FH with incident CAD and its major subtypes were estimated with the cohort-stratified multivariate Cox proportional hazard models based on the data from the baseline to the last follow-up (2018−2020).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among 98,885 included participants, 190 participants were defined as FH. Crude and age−sex standardized prevalence and 95% confidence interval (CI) of FH were 0.19% (0.17%–0.22%) and 0.13% (0.10%–0.16%), respectively. The prevalence varied across age groups and peaked in the group of 60–&lt;70 years (0.28%), and the peak prevalence (0.18%) in males was earlier, yet lower than the peak crude prevalence in females (0.41%). During a mean follow-up of 10.7 years, 2493 cases of incident CAD were identified. After multivariate adjustment, FH patients had a 2.03-fold greater risk of developing CAD compared to non-FH participants.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The prevalence of FH was estimated to be 0.19% in the participants, and it was associated with an elevated risk of incident CAD. Our study suggests that early screening of FH has certain public health significance for the prevention of CAD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":32096,"journal":{"name":"Chronic Diseases and Translational Medicine","volume":"9 2","pages":"134-142"},"PeriodicalIF":0.0,"publicationDate":"2023-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c1/e5/CDT3-9-134.PMC10249193.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9674229","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}