Intracranial or extracranial artery stenosis is the major reason of ischemic stroke,which leads to insufficient cerebral blood flow perfusion and triggers cerebral dysfunction.The detection rate of unruptured intracranial aneurysm(UIA)combined with intracranial or extracranial artery stenosis is increasing with advances in diagnostic techniques for cerebrovascular disease.Due to the complexity of location and hemodynamic implications,there is no consensus on the treatment of UIA combined with intracranial or extracranial artery stenosis.This article summarized several types of UIA combined with intracranial or extracranial artery stenosis in terms of anatomical location,hemodynamics,and therapy strategies,aiming to provide references for clinical interventionalists.

Objective To observe the clinical effect of doing Huatuo five-animal play treating blood-stasis-type silent myocardial ischemia(SMI)and its influence on coronary hemodynamics.Methods Ninety patients diagnosed as silent myocardial ischemia were randomly divided into a five-animal play group(n=45,age:51.56±11.00 years,24 males and 21 females)and a regular exercise group(n=45,age:52.44±7.19 years old,24 males and 21 females)according to a random number table.The five-animal play group practised the traditional five-animal play,while the regular exercise group con-ducted daily 30-minute moderate-intensity treadmill aerobic exercise,five times a week,for 4 weeks.The changes in the number of abnormal ST-T segment occurrences,myocardial oxygen consumption(CMO),coronary ischemia threshold(CIT),and blood smoothness index(BSD)within 24-hour ambu-latory electrocardiogram before and after the intervention were observed in both groups,with the thera-peutic effect and hemodynamic characteristics of both groups evaluated.Results The average number of ST-T segment abnormalities decreased after intervention in both groups(P<0.001),with significantly greater improvement in the five-animal play group than the regular exercise group(P<0.001).More-over,the average CMO decreased significantly,while the average CMR and BSD increased significant-ly in both groups after intervention(P<0.05),with significantly greater improvement in the five-ani-mal play group than the other group.Meanwhile,the total effective rate in the five-animal play group was significantly higher than the regular exercise group(P<0.01).Conclusion Undergoing the five-ani-mal play and moderate intensity treadmill aerobic exercise both are effective in treating silent myocardi-al ischemia.However,the former therapy is superior to the latter in bettering CMO,CIT and BSD.

Hilar cholangiocarcinoma(HCCA)is a common malignant tumor of the biliary system.Radical HCCA resection with combined vascular resection and reconstruction can help achieve R0 resection,improve tumor resectability,and enhance patient outcomes.With the increasing popularity of minimally invasive surgical techniques such as laparoscopy and robotic surgery,more and more centers are beginning to experiment with minimally invasive HCCA resection with combined vascular resection and reconstruction.However,due to the complex anatomy of the hilum and the limitations of minimally invasive techniques,completing HCCA revascularization and reconstruction under minimally invasive conditions is particularly challenging.The author has accumulated considerable experience in minimally invasive HCCA vascular resection and reconstruction.This article will discuss the technical challenges of minimally invasive HCCA vascular resection and reconstruction,indication selection,established revascularization techniques,reconstructive skills,and remedial measures after reconstruction failure.

Objective To explore the correlation between triglyceride-glucose(TyG)index and hyperuricemia in men with normal fasting blood glucose(FPG)levels.Methods A total of 309 men with normal FPG who participated in a health examination at the Ninth Medical Center of the People's Liberation Army General Hospital in April 2024 were enrolled in this study.All the subjects were divided into the normal uric acid(NUA,n=218)group and the hyperuricemia(HUA,n=91)group according to serum uric acid(SUA)levels.Results Scr,TG,weight,SBP,DBP,BMI,ALT,AST,γ-GGT,and TyG index were higher in the HUA group than in the NUA group(P<0.05).Pearson and Spearman correlation analysis showed that SUA were positively correlated with Scr,eGFR,TG,weight,SBP,DBP,BMI,ALT,AST,γ-GGT and TyG(P<0.05),and negatively correlated with HDL-C(P<0.05).Logistic regression analysis showed that after adjusting for confounding factors,TyG index remained an important influencing factor for HUA.ROC curve analysis showed that the area under the ROC curve of TyG index predicting hyperuricemia in men with normal FPG was 0.665,with an cutoff value of 8.45.Conclusions TyG index in men with normal FPG are influencing factors for hyperuricemia,indicating that hyperuricemia has a close association with insulin resistance,and is an important component of metabolic syndrome.

Objectives: Hypoparathyroidism (HP) is a rare endocrine disorder caused by parathyroid hormone (PTH) defi ciency. The PTH is a candidate gene for familial isolated hypoparathyroidism (FIH). This study aimed to investigate the pathogenicity of two novel rare variants (RVs) ofPTH through in vitro functional study. Methods: Targeted next-generation sequencing was used to identify candidate gene mutations. Clinical data were retrospectively collected. Wild-type (WT) PTH was used as a template for site-directed mutagenesis to create mutant eukaryotic expression plasmids, which were transfected into cells. Treated with or without 4-phenylbu tyric acid (4-PBA), the levels of intact PTH (iPTH) and PTH (1-84) were measured by chemiluminescence, and protein expression was assessed using Western blotting. Results: Two patients carrying PTH mutations (c.154G > A: p.Val52Ile, c.270G > T: p.Leu90Phe) were identified.Patient 1, a 45-year-old male, presented with carpal and pedal numbness, muscle cramps, and low serum calcium (1.29 mmol/L). Patient 2, a 12-year-old female, had muscle twitches, convulsions, low calcium (1.50 mmol/L), and iPTH of 4 pg/mL. The iPTH or PTH (1-84) levels in the medium transfected with mutant Val52Ile and Leu90Phe PTH decreased by 31%–38%, and 51%–96% compared to WT (allP < 0.05), which were not rescued by 4-PBA. No significant changes in intracellular PTH expression were observed. Conclusions In this study, two novel RVs of PTH(Val52Ile and Leu90Phe) were identified that may impair hormone synthesis and secretion. Our study has broadened the mutation spectrum of the PTH and shed light on potential mechanisms underlying FIH.

Objectives: Hypoparathyroidism (HP) is a rare endocrine disorder caused by parathyroid hormone (PTH) defi ciency. The PTH is a candidate gene for familial isolated hypoparathyroidism (FIH). This study aimed to investigate the pathogenicity of two novel rare variants (RVs) ofPTH through in vitro functional study. Methods: Targeted next-generation sequencing was used to identify candidate gene mutations. Clinical data were retrospectively collected. Wild-type (WT) PTH was used as a template for site-directed mutagenesis to create mutant eukaryotic expression plasmids, which were transfected into cells. Treated with or without 4-phenylbu tyric acid (4-PBA), the levels of intact PTH (iPTH) and PTH (1-84) were measured by chemiluminescence, and protein expression was assessed using Western blotting. Results: Two patients carrying PTH mutations (c.154G > A: p.Val52Ile, c.270G > T: p.Leu90Phe) were identified.Patient 1, a 45-year-old male, presented with carpal and pedal numbness, muscle cramps, and low serum calcium (1.29 mmol/L). Patient 2, a 12-year-old female, had muscle twitches, convulsions, low calcium (1.50 mmol/L), and iPTH of 4 pg/mL. The iPTH or PTH (1-84) levels in the medium transfected with mutant Val52Ile and Leu90Phe PTH decreased by 31%–38%, and 51%–96% compared to WT (allP < 0.05), which were not rescued by 4-PBA. No significant changes in intracellular PTH expression were observed. Conclusions In this study, two novel RVs of PTH(Val52Ile and Leu90Phe) were identified that may impair hormone synthesis and secretion. Our study has broadened the mutation spectrum of the PTH and shed light on potential mechanisms underlying FIH.

Objectives: Hypoparathyroidism (HP) is a rare endocrine disorder caused by parathyroid hormone (PTH) defi ciency. The PTH is a candidate gene for familial isolated hypoparathyroidism (FIH). This study aimed to investigate the pathogenicity of two novel rare variants (RVs) ofPTH through in vitro functional study. Methods: Targeted next-generation sequencing was used to identify candidate gene mutations. Clinical data were retrospectively collected. Wild-type (WT) PTH was used as a template for site-directed mutagenesis to create mutant eukaryotic expression plasmids, which were transfected into cells. Treated with or without 4-phenylbu tyric acid (4-PBA), the levels of intact PTH (iPTH) and PTH (1-84) were measured by chemiluminescence, and protein expression was assessed using Western blotting. Results: Two patients carrying PTH mutations (c.154G > A: p.Val52Ile, c.270G > T: p.Leu90Phe) were identified.Patient 1, a 45-year-old male, presented with carpal and pedal numbness, muscle cramps, and low serum calcium (1.29 mmol/L). Patient 2, a 12-year-old female, had muscle twitches, convulsions, low calcium (1.50 mmol/L), and iPTH of 4 pg/mL. The iPTH or PTH (1-84) levels in the medium transfected with mutant Val52Ile and Leu90Phe PTH decreased by 31%–38%, and 51%–96% compared to WT (allP < 0.05), which were not rescued by 4-PBA. No significant changes in intracellular PTH expression were observed. Conclusions In this study, two novel RVs of PTH(Val52Ile and Leu90Phe) were identified that may impair hormone synthesis and secretion. Our study has broadened the mutation spectrum of the PTH and shed light on potential mechanisms underlying FIH.

Objectives: Hypoparathyroidism (HP) is a rare endocrine disorder caused by parathyroid hormone (PTH) defi ciency. The PTH is a candidate gene for familial isolated hypoparathyroidism (FIH). This study aimed to investigate the pathogenicity of two novel rare variants (RVs) ofPTH through in vitro functional study. Methods: Targeted next-generation sequencing was used to identify candidate gene mutations. Clinical data were retrospectively collected. Wild-type (WT) PTH was used as a template for site-directed mutagenesis to create mutant eukaryotic expression plasmids, which were transfected into cells. Treated with or without 4-phenylbu tyric acid (4-PBA), the levels of intact PTH (iPTH) and PTH (1-84) were measured by chemiluminescence, and protein expression was assessed using Western blotting. Results: Two patients carrying PTH mutations (c.154G > A: p.Val52Ile, c.270G > T: p.Leu90Phe) were identified.Patient 1, a 45-year-old male, presented with carpal and pedal numbness, muscle cramps, and low serum calcium (1.29 mmol/L). Patient 2, a 12-year-old female, had muscle twitches, convulsions, low calcium (1.50 mmol/L), and iPTH of 4 pg/mL. The iPTH or PTH (1-84) levels in the medium transfected with mutant Val52Ile and Leu90Phe PTH decreased by 31%–38%, and 51%–96% compared to WT (allP < 0.05), which were not rescued by 4-PBA. No significant changes in intracellular PTH expression were observed. Conclusions In this study, two novel RVs of PTH(Val52Ile and Leu90Phe) were identified that may impair hormone synthesis and secretion. Our study has broadened the mutation spectrum of the PTH and shed light on potential mechanisms underlying FIH.

A 20-year-old male patient presented to the Department of Dermatology of Peking Union Medical College Hospital with complaints of an 8-year history of facial scarring, swelling of the lower limbs, and a 4-year history of scalp thickening. Physical examination showed thickening furrowing wrinkling of the skin on the face and behind the ears, ciliary body hirsutism, blepharoptosis, and cutis verticis gyrate. Both lower limbs were swollen, especially the knees and ankles. The skin of the palms and soles of the feet was keratinized and thickened. Laboratory examination using bone and joint X-ray showed periostosis of the proximal middle phalanges and metacarpals of both hands, distal ulna and radius, tibia and fibula, distal femurs, and metatarsals.Genetic testing revealed two variants in SLCO2A1, c.1658T > A and c.96+4A > C.Through multidisciplinary consultation, we confirmed the diagnosis of pachydermoperiostosis.

Objectives: Hypoparathyroidism (HP) is a rare endocrine disorder caused by parathyroid hormone (PTH) defi ciency. The PTH is a candidate gene for familial isolated hypoparathyroidism (FIH). This study aimed to investigate the pathogenicity of two novel rare variants (RVs) ofPTH through in vitro functional study. Methods: Targeted next-generation sequencing was used to identify candidate gene mutations. Clinical data were retrospectively collected. Wild-type (WT) PTH was used as a template for site-directed mutagenesis to create mutant eukaryotic expression plasmids, which were transfected into cells. Treated with or without 4-phenylbu tyric acid (4-PBA), the levels of intact PTH (iPTH) and PTH (1-84) were measured by chemiluminescence, and protein expression was assessed using Western blotting. Results: Two patients carrying PTH mutations (c.154G > A: p.Val52Ile, c.270G > T: p.Leu90Phe) were identified.Patient 1, a 45-year-old male, presented with carpal and pedal numbness, muscle cramps, and low serum calcium (1.29 mmol/L). Patient 2, a 12-year-old female, had muscle twitches, convulsions, low calcium (1.50 mmol/L), and iPTH of 4 pg/mL. The iPTH or PTH (1-84) levels in the medium transfected with mutant Val52Ile and Leu90Phe PTH decreased by 31%–38%, and 51%–96% compared to WT (allP < 0.05), which were not rescued by 4-PBA. No significant changes in intracellular PTH expression were observed. Conclusions In this study, two novel RVs of PTH(Val52Ile and Leu90Phe) were identified that may impair hormone synthesis and secretion. Our study has broadened the mutation spectrum of the PTH and shed light on potential mechanisms underlying FIH.