BACKGROUND: Pulmonary arterial hypertension (PAH) presents a significant health burden in Asia and remains a critical challenge. This study aims to delineate the PAH burden in Asia from 1990 to 2021. METHODS: Using the latest data from the Global Burden of Disease 2021, we evaluated and analyzed the distributions and patterns of PAH disease burden among various age groups, sexes, regions, and countries in Asia. Additionally, we examined the associations between PAH disease burden and key health system indicators, including the socio-demographic index (SDI) and the universal health coverage (UHC) index. RESULTS: In 2021, there were 25,989 new PAH cases, 103,382 existing cases, 13,909 PAH-associated deaths, and 385,755 DALYs attributed to PAH in Asia, which accounted for approximately 60% of global PAH cases. The age-standardized rates (ASRs) for prevalence and deaths were 2.05 (95% uncertainty interval [UI]: 1.66-2.52) per 100,000 population and 0.31 (95% UI: 0.23-0.38) per 100,000 population, respectively. From 1990 to 2021, Asia reported the lowest ASRs for PAH prevalence but the highest ASRs for deaths compared to other continents. While the ASRs for prevalence increased slightly, ASRs for mortality and DALYs decreased over time. This increasing burden of PAH was primarily driven by population growth and aging. The burden was especially pronounced among individuals aged ≥60 years and <9 years, who collectively accounted for the majority of deaths and DALYs. Moreover, higher SDI and UHC levels were linked to reduced incidence, but higher prevalence rates. CONCLUSIONS Although progress has been made in reducing PAH-related mortality and DALYs, the disease continues to impose a substantial burden in Asia, particularly among older adults and young children. Region-specific health policies should focus on improving early diagnosis, expanding access to treatment, and effectively addressing the growing PAH burden in the region.
Humans ; Global Burden of Disease ; Male ; Female ; Middle Aged ; Adult ; Asia/epidemiology* ; Prevalence ; Aged ; Pulmonary Arterial Hypertension/mortality* ; Adolescent ; Young Adult ; Child ; Child, Preschool ; Infant ; Hypertension, Pulmonary/epidemiology*

Objective To explore the impact of Qiangxin Tang on myocardial fibrosis in rats with chronic heart failure by mediating myocardial mitochondrial autophagy through the Bcl-2/adenovirus E1B 19kDa interacting protein 3/NIP3 like protein X and FUN14domain-containing protein 1.Methods Forty Sprague Dawley rats were divided into five groups randomly by the random number table:sham operation group,model group,Qiangxin Tang group,Captopril group,and Qiangxin Tang+Captopril group,with a total of eight rats in each group.Only the sham operation group threaded without ligating the left coronary artery of the heart.In all the other groups,CHF rat models were established after myocardial infarction by ligating the left coronary artery of the heart.From the day after successful modeling,each group was given corresponding drugs by gavage,and the left ventricular myocardial tissue of each group was de-tected.Western blot was used to detect the expression of NIX,BNIP3,and FUNDC1 proteins in each group.ELISA was used to detect brain natriuretic peptide and cardiac troponin T level.Mitochondrial morphology was observed under transmission electron microscopy.Masson staining was used to observe left ventricular myocardial fibrosis.Results Compared with the sham surgery group,the expression of NIX,BNIP3 and FUNDC1 proteins in the model group was significantly reduced,while the levels of BNP and cTnT were significantly increased(P＜0.05).The left ventricular myocardial tissue showed significant fibrosisand mitochondrial swelling.Compared with the model group,the expression of NIX,BNIP3,and FUNDC1 proteins was significantly increased in Qiangxin Tang group and Captopril group,while the levels of BNP and cTnT were significantly decreased(P＜0.05).The left ventricular myocardial tissue fibrosis was sig-nificantly reduced,and the mitochondrial morphology was mildly altered.Compared with Qiangxin Tang group and Captopril group,the Qiangxin Tang+Captopril group showed significant improvement in the above indicators,and there was no significant difference in the in-dicators between Qiangxin Tang group and Captopril group.Conclusion Qiangxin Tang may promote mitochondrial autophagy and ensure the morphology and function of mitochondrial by upregulating the expression of NIX,BNIP3 and FUNDC1,thereby reducing myocardial injury and fibrosis.In addition,the combination of Qiangxin Tang and Captopril has a better therapeutic effect on CHF.

BACKGROUND:Studies at home and abroad have shown that sarcopenia is closely related to metabolites.At present,the relationship between the latest 1400 blood metabolites and sarcopenia is still unknown.OBJECTIVE:To analyze the causal relationship between 1 400 metabolites and sarcopenia and its relevance with cardiovascular disease using Mendelian randomization.METHODS:Genome-wide association study(GWAS)data of sarcopenia-related characteristics(grip strength,limb muscle lean body mass,and walking speed)were obtained from the OPEN GWAS website as outcome data.A GWAS containing 1 400 metabolites was used as an exposure factor,and single nucleotide polymorphisms significantly associated with exposure factors were selected as instrumental variables.The causal association between 1 400 metabolites and sarcopenia was analyzed by"TwoSampleMR"and"gwasglue"packages of R software(V4.3.2).The research methods included inverse variance weighting,MR-Eggeer regression intercept,weighted median method,and simple mode.Heterogeneity,pleiotropic,sensitivity and other verification analysis were performed.Finally,reverse Mendelian randomization analysis was performed.RESULTS AND CONCLUSION:(1)The causal relationship between 1 400 serum metabolites and sarcopenia was analyzed by inverse variance weighting.The results showed that 1-linoleoyl-2-linoleoyl-GPC(18:2/18:3)and glycodeoxycholate 3-sulfate were protective factors,and the risk of disease decreased with the increase of metabolites(P＜0.01).(2)Two unknown metabolites(X-12822 and X-15486)and trans-3,4-methyleneheptanoate were risk factors.With the increase of two unknown metabolites(X-12822 and X-15486),the degree of low grip strength of male hands increased.Similarly,with the increase of trans-3,4-methylene heptanoate,the risk of disease also increased(P＜0.01).(3)To conclude,1-linoleoyl-2-linoleoyl-GPC(18:2/18:3)and glycodeoxycholate 3-sulfate have inhibitory effects on sarcopenia.Two unknown metabolites(X-12822 and X-15486)and trans-3,4-methyleneheptanoate can promote sarcopenia.This may be a new idea and new basis for sarcopenia research and treatment in the future.This study will also provide a reference for the study of the role of related metabolites in the Chinese population.

Objective To explore the impact of Qiangxin Tang on myocardial fibrosis in rats with chronic heart failure by mediating myocardial mitochondrial autophagy through the Bcl-2/adenovirus E1B 19kDa interacting protein 3/NIP3 like protein X and FUN14domain-containing protein 1.Methods Forty Sprague Dawley rats were divided into five groups randomly by the random number table:sham operation group,model group,Qiangxin Tang group,Captopril group,and Qiangxin Tang+Captopril group,with a total of eight rats in each group.Only the sham operation group threaded without ligating the left coronary artery of the heart.In all the other groups,CHF rat models were established after myocardial infarction by ligating the left coronary artery of the heart.From the day after successful modeling,each group was given corresponding drugs by gavage,and the left ventricular myocardial tissue of each group was de-tected.Western blot was used to detect the expression of NIX,BNIP3,and FUNDC1 proteins in each group.ELISA was used to detect brain natriuretic peptide and cardiac troponin T level.Mitochondrial morphology was observed under transmission electron microscopy.Masson staining was used to observe left ventricular myocardial fibrosis.Results Compared with the sham surgery group,the expression of NIX,BNIP3 and FUNDC1 proteins in the model group was significantly reduced,while the levels of BNP and cTnT were significantly increased(P＜0.05).The left ventricular myocardial tissue showed significant fibrosisand mitochondrial swelling.Compared with the model group,the expression of NIX,BNIP3,and FUNDC1 proteins was significantly increased in Qiangxin Tang group and Captopril group,while the levels of BNP and cTnT were significantly decreased(P＜0.05).The left ventricular myocardial tissue fibrosis was sig-nificantly reduced,and the mitochondrial morphology was mildly altered.Compared with Qiangxin Tang group and Captopril group,the Qiangxin Tang+Captopril group showed significant improvement in the above indicators,and there was no significant difference in the in-dicators between Qiangxin Tang group and Captopril group.Conclusion Qiangxin Tang may promote mitochondrial autophagy and ensure the morphology and function of mitochondrial by upregulating the expression of NIX,BNIP3 and FUNDC1,thereby reducing myocardial injury and fibrosis.In addition,the combination of Qiangxin Tang and Captopril has a better therapeutic effect on CHF.

BACKGROUND:Studies at home and abroad have shown that sarcopenia is closely related to metabolites.At present,the relationship between the latest 1400 blood metabolites and sarcopenia is still unknown.OBJECTIVE:To analyze the causal relationship between 1 400 metabolites and sarcopenia and its relevance with cardiovascular disease using Mendelian randomization.METHODS:Genome-wide association study(GWAS)data of sarcopenia-related characteristics(grip strength,limb muscle lean body mass,and walking speed)were obtained from the OPEN GWAS website as outcome data.A GWAS containing 1 400 metabolites was used as an exposure factor,and single nucleotide polymorphisms significantly associated with exposure factors were selected as instrumental variables.The causal association between 1 400 metabolites and sarcopenia was analyzed by"TwoSampleMR"and"gwasglue"packages of R software(V4.3.2).The research methods included inverse variance weighting,MR-Eggeer regression intercept,weighted median method,and simple mode.Heterogeneity,pleiotropic,sensitivity and other verification analysis were performed.Finally,reverse Mendelian randomization analysis was performed.RESULTS AND CONCLUSION:(1)The causal relationship between 1 400 serum metabolites and sarcopenia was analyzed by inverse variance weighting.The results showed that 1-linoleoyl-2-linoleoyl-GPC(18:2/18:3)and glycodeoxycholate 3-sulfate were protective factors,and the risk of disease decreased with the increase of metabolites(P＜0.01).(2)Two unknown metabolites(X-12822 and X-15486)and trans-3,4-methyleneheptanoate were risk factors.With the increase of two unknown metabolites(X-12822 and X-15486),the degree of low grip strength of male hands increased.Similarly,with the increase of trans-3,4-methylene heptanoate,the risk of disease also increased(P＜0.01).(3)To conclude,1-linoleoyl-2-linoleoyl-GPC(18:2/18:3)and glycodeoxycholate 3-sulfate have inhibitory effects on sarcopenia.Two unknown metabolites(X-12822 and X-15486)and trans-3,4-methyleneheptanoate can promote sarcopenia.This may be a new idea and new basis for sarcopenia research and treatment in the future.This study will also provide a reference for the study of the role of related metabolites in the Chinese population.

OBJECTIVE To investigate the effects and potential mechanism of Qiangxin decoction on mitochondrion of rats with chronic heart failure(CHF).METHODS The CHF model was established by ligating the left anterior descending branch of the coronary artery.Modeled rats were divided into model group,Qiangxin decoction low-dose and high-dose groups(12.25,24.50 g/kg,calculated by crude drug),and chemical medicine group(Sacubitril valsartan sodium tablets,10.42 mg/kg),with 10 rats in each group;control group was set up without treatment.Each group of rats was orally administered with the corresponding medication or normal saline twice a day for 28 consecutive days.After the last medication,the contents of N-terminal pro-brain natriuretic peptide(NT-proBNP)and adenosine triphosphate(ATP)in serum and phosphatidic acid(PA)and cardiolipin(CL)in myocardial tissue were all detected;the pathological damage and collagen fibrosis of rat myocardial tissue were observed;the apoptosis of myocardial cells was determined;the ultrastructure of myocardial tissue was observed;the protein expressions of mitofusin 1(Mfn1),Mfn2,optic atrophy protein 1(OPA1)and dynamin-related protein 1(Drp1)were all detected in myocardial tissue.RESULTS Compared with control group,the serum content of NT-proBNP,apoptotic rate of myocardial cells,and relative expressions of S-OPA1 and Drp1 proteins were all increased significantly;serum content of ATP,contents of PA and CL,and relative expressions of Mfn1,Mfn2 and L-OPA1 proteins were all significantly reduced(P＜0.05).There were abnormal membrane tissue structure in various layers of myocardial tissue,degeneration and necrosis of myocardial cells,and severe fibrosis;the mitochondria were swollen,with reduced or absent cristae,and uneven matrix density.After intervention with Qiangxin decoction,the levels of the aforementioned quantitative indicators in serum and myocardial tissue of rats(excluding CL content in the Qiangxin decoction low-dose group)were significantly reversed(P＜0.05);the pathological damage of myocardial tissue had significantly improved,fibrosis had significantly reduced,mitochondrial morphology tended to be normal,cristae had increased,and matrix density was uniform.CONCLUSIONS Qiangxin decoction can regulate myocardial mitochondrial function and structural integrity of CHF rats,thereby improving myocardial energy metabolism and antagonizing myocardial fibrosis,the mechanism of which may be associated with activating PA/Mfn/CL signaling pathway.

OBJECTIVE To investigate the effects of Qiangxin decoction on myocardial mitochondrial and energy metabolism in rats with chronic heart failure （CHF） based on mitophagy. METHODS Male SD rats were collected to establish CHF model by ligating the left anterior descending branch of coronary artery. The successful modeling rats were divided into model group， Qiangxin decoction group [12.25 g/（kg·d）， calculated by crude drug]， captopril group [10.38 mg/（kg·d）]， and Qiangxin decoction+captopril group （the same usage and dosage as single drug group） according to a random number table method， with 8 rats in each group. Another 8 normal rats were selected and received threading in the left anterior descending branch of the coronary artery without ligation as the sham operation group. Starting from the second day after successful modeling， the rats in administration groups were given relevant drug intragastrically， twice a day， for consecutive 28 days. After the last medication， the levels of adenosine triphosphate （ATP）， adenosine monophosphate （AMP） and free fatty acid （FFA） in infarcted myocardial tissues were detected， the pathological changes and mitochondrial morphology of the infarcted myocardial tissue were observed， as well as the protein expressions of B cell lymphoma-2 （Bcl-2）， Bcl-2 related X protein （Bax）， TANK-binding kinase 1 （TBK1）， p62 were detected in each group. RESULTS Compared with the sham operation group， the infarcted myocardial tissue fibrosis was changed evidently， with a large number of mitochondrial swelling and fusion， and internal cristae rupture； the levels of AMP and FFA， the protein expressions of Bax and p62 were all increased or up-regulated significantly in infarcted myocardial tissue， while the level of ATP， and the protein expressions of Bcl-2 and TBK1 were all decreased or down-regulated significantly （P＜0.05）. Compared with the model group， the pathological changes of infarcted myocardial tissue and mitochondrial swelling had been improved； the levels of AMP and FFA， and the protein expressions of Bax and p62 in infarcted myocardial tissue were significantly decreased or down-regulated in administration groups， while the level of ATP， and the protein expressions of Bcl-2 and TBK1 were increased or up-regulated significantly （P＜0.05）. And the effect of Qiangxin decoction+captopril group was better than that of single drug group. CONCLUSIONS Qiangxin decoction can alleviate myocardial fibrosis and mitochondrial swelling in CHF rats， and improve their myocardial energy metabolism， which may be related to regulating the expression of Bcl-2， Bax， TBK1 and p62 proteins and promoting myocardial mitophagy.

Objective:To explore the clinical phenotype and gene characteristics of a case of TSC2/PKD1 adjacency gene syndrome, so as to improve the clinical understanding of the disease.Methods:A case of TSC2/PKD1 adjacency gene syndrome diagnosed in the Department of Neurology of the Children′s Hospital Affiliated to Zhengzhou University was analyzed retrospectively. The clinical data, laboratory examination, imaging characteristics and gene variation characteristics of the child were summarized.Results:The patient was a 17 months old girl, with the main complaint of "intermittent convulsion with 17 months of underdevelopment". The clinical manifestations were epileptic seizures, which were in the form of a series of spastic seizures, absence seizures, focal seizures, and depigmentation spots can be seen in the trunk and neck. Cranial magnetic resonance imaging showed multiple patchy signals in the cortex and subcortical areas of the bilateral cerebral hemispheres, multiple small nodular shadows under the ependyma of the bilateral lateral ventricles, the heart color Doppler ultrasound showed patent foramen ovale and pericardial effusion, and the abdomen color Doppler ultrasound showed polycystic kidney. Ophthalmic color Doppler ultrasound showed that there were localized small swelling lesions around the optic disc of the left eye. The whole exon gene sequencing of the pedigree showed the proband had partial deletion of TSC2 gene (NM_000548) at chromosome position chr16: 2125799-2185690. The real-time quantitative detection system verified that exons 23-42 were deleted, and all exons of PKD1 gene were deleted (NM_001009944), and multiple ligation dependent probe amplification verified that exons 1-46 were deleted, and no downstream gene deletion was found. The overall deletion size was about 60 kb. Both of the girl's father and mother had normal phenotypes and were wild-type.Conclusions:TSC2/PKD1 adjacency gene syndrome is relatively rare. It can have clinical manifestations of tuberous sclerosis/autosomal dominant polycystic kidney disease. Most of the nervous system and kidney are seriously affected, and the prognosis is poor. TSC2/PKD1 gene deletion and variation is the genetic cause of the TSC2/PKD1 adjacency gene syndrome.

Objective:To correlate homocysteine (Hcy) and blood lipid levels with neurological function in patients with progressive ischemic stroke.Methods:A total of 400 patients with ischemic stroke who received treatment between June 2018 and June 2020 in Linhai Second People's Hospital were included in this study. Progressive ischemic stroke ( n = 126) and non-progressive ischemic stroke ( n = 274) groups were designated. Hcy level was determined by enzyme-linked immunosorbent assay. High-density lipoprotein cholesterol, triacylglycerol, low-density lipoprotein cholesterol and cholesterol levels were measured using a biochemical analyzer. Hcy and blood lipid levels as well as National Institute Health of Stroke Scale (NIHSS) score were determined in each group. Hcy and blood lipid levels were correlated with NIHSS score. Results:Hcy level in the progressive ischemic stroke group was significantly higher than that in the non-progressive ischemic stroke group [(28.39 ± 4.36) μmol/L vs. (20.17 ± 3.24) μmol/L, t = 18.894, P < 0.05]. Low-density lipoprotein cholesterol , triacylglycerol and TC levels in the progressive ischemic stroke group were (3.29 ± 0.45) mmol/L, (2.08 ± 0.34) mmol/L and (4.82 ± 0.79) mmol/L, respectively, which were significantly higher than those in the non-progressive ischemic stroke group [(2.48 ± 0.37) mmol/L, (1.56 ± 0.29) mmol/L and (4.08 ± 0.43) mmol/L, t = 17.644, 14.859, 9.860, P < 0.05]. High-density lipoprotein cholesterol level in the progressive ischemic stroke group was significantly lower than that in the non-progressive ischemic stroke group [(1.03 ± 0.13) mmol/L vs. (1.19 ± 0.14) mmol/L, t =11.158, P < 0.05]. NIHSS score in the progressive ischemic stroke group was significantly higher than that in the non-progressive ischemic stroke group [(21.72 ± 4.35) points vs. (15.52 ± 2.89) points, t = 14.582, P < 0.05]. Hcy, low-density lipoprotein cholesterol, cholesterol and triacylglycerol levels were linearly and positively correlated with NIHSS score ( r = 0.846, 0.724, 0.718, 0.765, all P < 0.05), while igh-density lipoprotein cholesterol level was linearly and negatively correlated with NIHSS score ( r = -0.710, P < 0.05). Conclusion:In patients with progressive ischemic stroke, Hcy level is increased and blood lipid level is obviously abnormal. Hcy and blood lipid levels are greatly correlated with neurological function.

The proportion of laparoscopic surgeries is continuously increasing in general surgeries. Along with the development and application, new image sensor and digital image processing technology accelerated the emergence of novel laparoscope in recent years. Stereoscopic laparoscope (3D) appearing make the space orientation more accurate. new imaging methods and new structure design satisfy more clinical requirements; combination with optical technology (NBI technique, PDD technique, ICG technique) make intraoperative diagnosis possible.
Image Processing, Computer-Assisted ; Laparoscopes ; Laparoscopy