Correlation between cold pain of knee joint and subchondral bone marrow edema in patients with knee osteoarthritis / 中国骨伤

OBJECTIVE@#To investigate relationship between cold pain of knee joint and subchondral bone marrow edema (BME).@*METHODS@#From May 2018 to August 2019, 92 patients with knee osteoarthritis (KOA) associated with cold pain of knee were admitted, all patients were underwent MRI examination. The patients were divided into observation group (47 patients with BME) and control group(45 patients without BME). In observation group, there were 6 males and 41 females aged from 36 to 87 years old with an average of (63.2±12.3) years old. In control group, there were 10 males and 35 females, aged from 48 to 84 years old with an average of (62.7±8.3) years old. All patientswere treated with drugs. The degree of joint degeneration was evaluated by Kellgren-Lawrence (K-L) grading. Degree of cold pain of knee was evaluated by knee cold pain score, and degree of BME was evaluated according to WORMS. The correlation between cold pain of knee and K-L grading and BME was analyzed.@*RESULTS@#Score of cold pain in observation group (15.55±7.68) was higher than that of control group (9.42± 5.50), which had significant difference (@*CONCLUSION@#The cold pain of KOA patients is not related to K-L grading, but corelate with BME grading. The Cold pain of knee was more pronounced in KOA patients with BME, and the severity of BME is often related to degree of cold pain. It seemed to be a tendency:the more serious BME, the heavier coldpain.

Using molecular genetics to guide the diagnosis and treatment of hypertrophic cardiomyopathy / 中华心血管病杂志

Hypertrophy cardiomyopathy (HCM) is an autosomal dominant disorder characterized by increased heart mass that occurs without a defined stimulus (such as hypertension or valvular disease). It is commonly recognized through the widespread use of non-invasive imaging. Epidemiological studies indicate that 1 of 500 individuals has unexplained cardiac hypertrophy, an observation that predicts a considerable role for genetics in this enigmatic disorder. Indeed, to date, more than 500 mutations had been identified in more than 12 genes encoding components of the thick and thin filament of the sarcomere and other myofilament-related proteins. Intensive studies of HCM continue to take our understandings about this fascinating disease in new directions. Mechanistic analyses have provided insights into how mutational alterations in these structural proteins may trigger the hypertrophic remodeling processes and other associated clinical features of HCM. Based on these studies, investigations have been initiated to assess whether early pharmacological interventions could prevent or attenuate the development of the disease and its clinical sequelae. By combining pathophysiology with knowledge of genetic cause and molecular responses, HCM has begun to exemplify opportunities for predictive and personalized medicine. With the emergence of newer technologies that enable high-throughput sequencing of DNA, it is timely to review clinical manifestations and genetic causes of this unique disease, and how intertwining these insights can improve contemporary diagnosis and management of HCM and other genetic forms of cardiac hypertrophy.

Levels of PCDD/Fs, PCBs and PBDEs compounds in human placenta tissue / 中华预防医学杂志

<p><b>OBJECTIVE</b>To establish the methods of Polychlorinated Dibenzo-p-Dioxins and Dibenzofurans (PCDD/Fs), polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) compounds determination by isotope dilution HRGC/HRMS simultaneously in human placenta tissue from mothers, and assess the human exposure risk to dioxins and PBDEs in study.</p><p><b>METHODS</b>Concentrations of 17 PCDD/Fs and 12 dioxin-like PCBs as well as 7 PBDEs were measured in human placenta tissue samples by isotope dilution HRGC/HRMS. SigmaTEQ (PCDD + PCDFs + PCBs) concentration using WHO-TEF factor and PBDEs concentration was calculated respectively. Risk assessment of mother exposure to dioxins and PBDEs was evaluated.</p><p><b>RESULTS</b>Median of SigmaTEQ (PCDD + PCDFs + PCBs) concentration for six samples was 18.15 WHO-TEQ pg/g lipid, ranging from 5.14 - 67.01 WHO-TEQ pg/g lipid. Although the median of SigmaTEQ (PCDD + PCDFs + PCBs) was lower than that of human blood of EU and Japan, and close to that of Korea and Taiwan non-exposure as reported in the literatures, the highest SigmaTEQ (PCDD + PCDFs + PCBs) concentration of placenta sample exceeded the value of high dioxins exposure area subjects in Taiwan. The dominant contributor congener for WHO-TEQ were 2, 3, 4, 7, 8-PeCDF, 1, 2, 3, 7, 8-PeCDD, PCB126, totally accounted for 65 percent of SigmaWHO-TEQ. Median and average of PBDE concentration for six samples were 2.73 ng/g lipid and 7.17 ng/g lipid, respectively, ranging from 0.95 - 25.99 ng/g lipid. BDE47 was the dominant contributor congener for the total concentration, accounted for 35 percent.</p><p><b>CONCLUSION</b>The methods of PCDD/Fs, PCBs and PBDEs compounds determined by isotope dilution HRGC/HRMS simultaneously in human placenta tissue from mothers were established successfully, and the human exposure risk to PCDD/Fs, PCBs and PBDEs should be surveyed for the donor with the highest SigmaTEQ (PCDD + PCDFs + PCBs) and PBDEs concentration of placenta sample in the future.</p>