ObjectiveThe controllability changes of structural brain network were explored based on the control and brain network theory in young smokers, this may reveal that the controllability indicators can serve as a powerful factor to predict the sleep status in young smokers. MethodsFifty young smokers and 51 healthy controls from Inner Mongolia University of Science and Technology were enrolled. Diffusion tensor imaging (DTI) was used to construct structural brain network based on fractional anisotropy (FA) weight matrix. According to the control and brain network theory, the average controllability and the modal controllability were calculated. Two-sample t-test was used to compare the differences between the groups and Pearson correlation analysis to examine the correlation between significant average controllability and modal controllability with Fagerström Test of Nicotine Dependence (FTND) in young smokers. The nodes with the controllability score in the top 10% were selected as the super-controllers. Finally, we used BP neural network to predict the Pittsburgh Sleep Quality Index (PSQI) in young smokers. ResultsThe average controllability of dorsolateral superior frontal gyrus, supplementary motor area, lenticular nucleus putamen, and lenticular nucleus pallidum, and the modal controllability of orbital inferior frontal gyrus, supplementary motor area, gyrus rectus, and posterior cingulate gyrus in the young smokers’ group, were all significantly different from those of the healthy controls group (P<0.05). The average controllability of the right supplementary motor area (SMA.R) in the young smokers group was positively correlated with FTND (r=0.393 0, P=0.004 8), while modal controllability was negatively correlated with FTND (r=-0.330 1, P=0.019 2). ConclusionThe controllability of structural brain network in young smokers is abnormal. which may serve as an indicator to predict sleep condition. It may provide the imaging evidence for evaluating the cognitive function impairment in young smokers.

The chemical constituents in dried roots of Atractylodes macrocephala were investigated in this study. Through utilizing normal-phase silica gel and ODS column chromatography, TLC, and semi-preparative HPLC, 4 new sesquiterpenoids were purified from the ethyl acetate extract of A. macrocephala. By various spectroscopic techniques, such as 1D and 2D NMR, HR-ESI-MS, IR, UV, and CD, their structures were identified as atractylmacron A (1), 9β-hydroxyasterolide (2), atractylenolide H (3), atractylenolide J (4). Compound 1 possesses a rare 6/7 bicyclic skeleton.

The Golgi apparatus (GA) is a key membranous organelle in eukaryotic cells, acting as a central component of the endomembrane system. It plays an irreplaceable role in the processing, sorting, trafficking, and modification of proteins and lipids. Under normal conditions, the GA cooperates with other organelles, including the endoplasmic reticulum (ER), lysosomes, mitochondria, and others, to achieve the precise processing and targeted transport of nearly one-third of intracellular proteins, thereby ensuring normal cellular physiological functions and adaptability to environmental changes. This function relies on Golgi protein quality control (PQC) mechanisms, which recognize and handle misfolded or aberrantly modified proteins by retrograde transport to the ER, proteasomal degradation, or lysosomal clearance, thus preventing the accumulation of toxic proteins. In addition, Golgi-specific autophagy (Golgiphagy), as a selective autophagy mechanism, is also crucial for removing damaged or excess Golgi components and maintaining its structural and functional homeostasis. Under pathological conditions such as oxidative stress and infection, the Golgi apparatus suffers damage and stress, and its homeostatic regulatory network may be disrupted, leading to the accumulation of misfolded proteins, membrane disorganization, and trafficking dysfunction. When the capacity and function of the Golgi fail to meet cellular demands, cells activate a series of adaptive signaling pathways to alleviate Golgi stress and enhance Golgi function. This process reflects the dynamic regulation of Golgi capacity to meet physiological needs. To date, 7 signaling pathways related to the Golgi stress response have been identified in mammalian cells. Although these pathways have different mechanisms, they all help restore Golgi homeostasis and function and are vital for maintaining overall cellular homeostasis. It is noteworthy that the regulation of Golgi homeostasis is closely related to multiple programmed cell death pathways, including apoptosis, ferroptosis, and pyroptosis. Once Golgi function is disrupted, these signaling pathways may induce cell death, ultimately participating in the occurrence and progression of diseases. Studies have shown that Golgi homeostatic imbalance plays an important pathological role in various major diseases. For example, in Alzheimer’s disease (AD) and Parkinson’s disease (PD), Golgi fragmentation and dysfunction aggravate the abnormal processing of amyloid β-protein (Aβ) and Tau protein, promoting neuronal loss and advancing neurodegenerative processes. In cancer, Golgi homeostatic imbalance is closely associated with increased genomic instability, enhanced tumor cell proliferation, migration, invasion, and increased resistance to cell death, which are important factors in tumor initiation and progression. In infectious diseases, pathogens such as viruses and bacteria hijack the Golgi trafficking system to promote their replication while inducing host defensive cell death responses. This process is also a key mechanism in host-pathogen interactions. This review focuses on the role of the Golgi apparatus in cell death and major diseases, systematically summarizing the Golgi stress response, regulatory mechanisms, and the role of Golgi-specific autophagy in maintaining homeostasis. It emphasizes the signaling regulatory role of the Golgi apparatus in apoptosis, ferroptosis, and pyroptosis. By integrating the latest research progress, it further clarifies the pathological significance of Golgi homeostatic disruption in neurodegenerative diseases, cancer, and infectious diseases, and reveals its potential mechanisms in cellular signal regulation.

Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder affecting a substantial proportion of women of reproductive age. It is frequently associated with ovulatory dysfunction, infertility, and an increased risk of chronic metabolic diseases. A hallmark pathological feature of PCOS is the arrest of follicular development, closely linked to impaired intercellular communication between the oocyte and surrounding granulosa cells. Transzonal projections (TZPs) are specialized cytoplasmic extensions derived from granulosa cells that penetrate the zona pellucida to establish direct contact with the oocyte. These structures serve as essential conduits for the transfer of metabolites, signaling molecules (e.g., cAMP, cGMP), and regulatory factors (e.g., microRNAs, growth differentiation factors), thereby maintaining meiotic arrest, facilitating metabolic cooperation, and supporting gene expression regulation in the oocyte. The proper formation and maintenance of TZPs depend on the cytoskeletal integrity of granulosa cells and the regulated expression of key connexins, particularly CX37 and CX43. Recent studies have revealed that in PCOS, TZPs exhibit significant structural and functional abnormalities. Contributing factors—such as hyperandrogenism, insulin resistance, oxidative stress, chronic inflammation, and dysregulation of critical signaling pathways (including PI3K/Akt, Wnt/β‑catenin, and MAPK/ERK)—collectively impair TZP integrity and reduce their formation. This disruption in granulosa-oocyte communication compromises oocyte quality and contributes to follicular arrest and anovulation. This review provides a comprehensive overview of TZP biology, including their formation mechanisms, molecular composition, and stage-specific dynamics during folliculogenesis. We highlight the pathological alterations in TZPs observed in PCOS and elucidate how endocrine and metabolic disturbances—particularly androgen excess and hyperinsulinemia—downregulate CX43 expression and impair gap junction function, thereby exacerbating ovarian microenvironmental dysfunction. Furthermore, we explore emerging therapeutic strategies aimed at preserving or restoring TZP integrity. Anti-androgen therapies (e.g., spironolactone, flutamide), insulin sensitizers (e.g., metformin), and GLP-1 receptor agonists (e.g., liraglutide) have shown potential in modulating connexin expression and enhancing granulosa-oocyte communication. In addition, agents such as melatonin, AMPK activators, and GDF9/BMP15 analogs may promote TZP formation and improve oocyte competence. Advanced technologies, including ovarian organoid models and CRISPR-based gene editing, offer promising platforms for studying TZP regulation and developing targeted interventions. In summary, TZPs are indispensable for maintaining follicular homeostasis, and their disruption plays a pivotal role in the pathogenesis of PCOS-related folliculogenesis failure. Targeting TZP integrity represents a promising therapeutic avenue in PCOS management and warrants further mechanistic and translational investigation.

Objective To compare the effects of 20 mg qd and 10 mg bidadministration of iprrazole enteric-coated tablets on the control of gastric acid in healthy subjects.Methods A randomized,single-center,parallel controlled trial was designed to include 8 healthy subjects.Randomly divided into 2 groups,20 mg qd administration group:20 mg enteric-coated tablets of iprrazole in the morning;10 mg bid administration group:10 mg enteric-coated tablets of iprrazole in the morning and 10 mg in the evening.The pH values in the stomach of the subjects before and 24 h after administration were monitored by pH meter.The plasma concentration of iprazole after administration was determined by HPLC-MS/MS.The main pharmacokinetic parameters were calculated by Phoenix WinNonlin(V8.0)software.Results The PK parameters of iprrazole enteric-coated tablets and reference preparations in fasting group were as follows:The Cmax of 20 mg qd group and 10 mg bid group were(595.75±131.15)and(283.50±96.98)ng·mL-1;AUC0-t were(5 531.94±784.35)and(4 686.67±898.23)h·ng·mL-1;AUC0-∞ were(6 003.19±538.59)and(7 361.48±1 816.77)h·ng·mL-1,respectively.The mean time percentage of gastric pH＞3 after 20 mg qd and 10 mg bid were 82.64％and 61.92％,and the median gastric pH within 24 h were 6.25±1.49 and 3.53±2.05,respectively.The mean gastric pH values within 24 h were 5.71±1.36 and 4.23±1.45,respectively.The correlation analysis of pharmacokinetic/pharmacodynamics showed that there was no significant correlation between the peak concentration of drug in plasma and the inhibitory effect of acid.Conclusion Compared with the 20 mg qd group and the 10 mg bid group,the acid inhibition effect is better,the administration times are less,and the safety of the two administration regimes is good.

Objective To explore the therapeutic material basis and antitussive mechanism of Ganke Formula.Methods Ultra-high performance liquid chromatography-quadrupole-time of flight mass spectrometry(UPLC-Q-TOF/MS)technology was used to analyze and identify the components of Ganke Formula in serum.30 rats were randomly divided into control group,model group,experimental-L group,experimental-M group and experimental-H group,6 rats per group.Acute bronchitis rat model was established by smoke inhalation and cold stimulus.The experimental-L,-M,-H groups were respectively given 1.86,4.66,9.32 g·kg-1(crude drug/weight)dose of Ganke Formula per day by intragastric administration for 7 days.The control group and model group were given the equal amount of normal saline.The contents of interleukin-1β(IL-1β)and tumor necrosis factor-α(TNF-α)in rat lung tissue were determined by enzyme-linked immunosorbent assay.The expressions of phosphatidylinositol 3-kinase(PI3K)and phosphorylated protein kinase B(p-Akt)in lung were detected by Western blotting.Results Twenty-six absorbed components have been identified by UPLC-Q-TOF/MS.The contents of IL-1β in control group,model group,experimental-M,-H group were(57.80±7.67),(186.48±8.50),(166.05±9.90)and(143.19±6.31)pg·mL-1;TNF-α contents were(47.14±8.55),(316.22±9.49),(68.93±7.94)and(65.93±7.10)pg·mL-1;the relative expression levels of PI3K in lung tissues were 0.38±0.05,0.97±0.10,0.68±0.15 and 0.56±0.10;the relative expression levels of p-Akt were 0.34±0.14,0.93±0.05,0.63±0.16 and 0.49±0.14,respectively.Compared with the model group,the above indicators in the experimental-H group and control group were statistically different(P＜0.01 or P＜0.05).Conclusion Ganke Formula can intervene in the expression of inflammatory and immune regulatory factors by regulating PI3K/Akt signaling pathway,improve airway inflammation,and thus exert cough relieving effects.

Objective To evaluate the efficacy and safety of Shenbao tablet in the treatment of kidney-yang deficiency syndrome.Methods Patients with kidney-yang deficiency syndrome,will were treated with Shenbao Tablets orally,3 tablets once,3 times a day,and the course of treatment was 56 days or 84 days,depending on the condition.By comparing the clinical efficacy,the changes of symptom scores and syndrome scores before and after treatment,and symptoms remission time,the effectiveness of Shenbao tablet in the treatment of kidney-yang deficiency syndrome was evaluated.The safety was evaluated by adverse reactions.Results There were 339 patients in the 56-day group and 345 patients in the 84-day group.After treatment,the clinical effective rates of the 56-day group and the 84-day group were 91.74％and 97.97％,respectively,and the difference was statistically significant(P＜0.05).In the 56-day group and the 84-day group,the excellent rate were 58.41％and 59.13％,clinical control rates were 18.58％and 27.54％,and the progress rates were 14.75％and 11.30％,respectively.After treatment,the symptom scores of kidney-yang deficiency syndrome were significantly reduced respectively within both groups(P＜0.05).In the 56-day group and the 84-day group,the nocturia scores of were 0.89±1.27 and 0.60±1.03,the soreness of waist scores were 1.31±1.19 and 0.72±1.00,the morning diarrhea scores were 0.28±0.74 and 0.19±0.61,the anaphrodisia scores were 0.65±1.13 and 0.53±0.98,the low spirits scores were 0.29±0.81 and 0.08±0.40,the cold limbs score were 1.09±1.20 and 0.55±0.93,the edema scores were 0.14±0.55 and 0.05±0.30,the bright pale complexion scores were 0.20±0.59 and 0.24±0.65,respectively.There were significant differences in the reduction of each symptom score between the two groups(P＜0.05);the 56-day group had a more significant decrease in the score of cold limbs than the 84-day group.The remaining symptom scores decreased more significantly in the 84-day group.After treatment,the syndrome scores of kidney-yang deficiency syndrome in the two groups were significantly lower than those before treatment(all P＜0.05);the change rates of score in the 56-day group and the 84-day group were(-72.33±24.57)％and(-78.77±19.53)％,respectively,and the difference was statistically significant(P＜0.05).The self-reported time to first symptom relief was(14.85±7.18)days in the 56-day group and(14.10±7.78)days in the 84-day group,with no significant difference(P＞0.05).The incidence of adverse reactions of Shenbao tablets was 5.37％,mainly reflected in hepatobiliary system diseases,gastrointestinal system diseases and various examination abnormalities.Conclusions After taking Shenbao tablets for 2 to 3 months,the clinical symptoms of kidney-yang deficiency were better improved,and the improvement was more significant after 3 months of treatment.The security of Shenbao Tablets was good.

Objective To explore the effect of sevelamer carbonate on blood phosphorus,vascular calcification,and parathyroid function in maintenance hemodialysis(MHD)patients.Methods MHD patients were selected as the research subjects and divided into treatment group and control group according to the treatment plan using a cohort method.The control group was given calcium carbonate chewable tablets orally at a dose of 1.25 g,bid,while the treatment group was given sevelamer carbonate tablets orally at a dose of 0.8 g,tid;the duration of treatment for both groups was 6 months.The clinical efficacy,blood phosphorus,blood calcium,coronary artery calcification score,parathyroid function[intact parathyroid hormone(iPTH),parathyroid volume],and levels of inflammatory factors[C-reactive protein(CRP),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)]were compared between the two groups,and the occurrence of adverse drug reactions was recorded.Results The total effective rates of the treatment group and the control group were 92.45％(49 cases/53 cases)and 77.55％(38 cases/49 cases)respectively,showing statistically significant difference(P＜0.05).After 6 months of treatment,the blood phosphorus levels of the treatment group and the control group were(1.63±0.31)and(2.07±0.36)mmol·L-1,respectively;blood calcium levels were(2.31±0.17)and(2.47±0.12)mmol·L-1,respectively;coronary artery calcification scores were 71.81±15.45 and 86.03±17.49,respectively;iPTH expression levels were(223.59±64.85)and(304.25±74.61)pg·mL-1,respectively;parathyroid volumes were(1.03±0.26)and(1.17±0.21)cm3,respectively;CRP expression levels were(5.12±1.35)and(6.59±1.66)mg·L-1,respectively;IL-6 expression levels were(16.32±2.81)and(19.84±3.62)ng·L-1,respectively;TNF-αexpression levels were(18.54±3.88)and(22.69±4.89)ng·L-1,respectively.The differences in the above indicators between the treatment group and the control group were all statistically significant(all P＜0.05).The total incidence of adverse drug reactions in the treatment group and the control group were 9.43％(5 cases/53 cases)and 6.12％(3 cases/49 cases),respectively,with no statistically significant difference(P＞0.05).Conclusion Sevelamer carbonate can reduce blood phosphorus levels in MHD patients,has minimal effect on blood calcium concentration,improves parathyroid function in patients,delays vascular calcification,and has good clinical application effects.

Objective To investigate the effect of Jichuan decoction on defecation in rats with slow transit constipation(STC).Methods A total of 36 SD rats were divided into model group,experimental group and control group.Except the control group,STC rat models were established in the other two groups by gavage of 2％rhein acid suspension.The experimental group was given 170％Jichuan decoction of 10 mL·kg-1 by gavage,while the control group and model group were given with 0.9％NaCl by gavage,once a day for 30 days.Fecal dry-wet weight ratio and colon transport time were observed by fecal weighing and recording of first fecal discharge time;substance P(SP)and vasoactive peptide(VIP)contents in plasma were detected by kit;changes in intestinal flora were detected by real-time fluorescent quantitative polymerase chain reaction(qRT-PCR).Results The dry-wet ratio of feces in control group,model group and experimental group were(44.86±4.40)％,(53.44±3.52)％and(44.28±4.33)％,respectively;the colon transport time were(340.17±34.91),(424.67±37.26)and(377.36±38.87)min,respectively;plasma SP were(79.86±7.56),(60.30±2.41)and(78.84±5.83)pg·mL-1,respectively;plasma VIP were(30.56±2.87),(23.38±6.62)and(28.39±2.37)pg·mL-1,respectively;the numbers of Bifidobacterium were 7.77±0.04,5.19±0.09 and 7.45±0.03,respectively;the numbers of Lactobacillus were 6.40±0.07,4.10±0.05 and 6.36±0.08,respectively.There were statistically significant differences in the above indexes between model group and control group,and between experimental group and model group(P＜0.01,P＜0.05).Conclusion Jichuan decoction can improve the defecation of rats with slow transit constipation.

Objective:To explore the clinical and electrophysiological characteristics of peripheral neuropathy in prediabetic patients.Methods:Subjects aged 20-65 years with high-risk factors of impaired glycemia enrolled in Beijing Tiantan Hospital, Capital Medical University from 2019 to 2022 were recruited to conduct oral glucose tolerance test, after excluding other causes of neuropathy or radiculopathy. Patients with impaired fasting glucose or impaired glucose tolerance were defined by American Diabetes Association criteria. These patients were divided into clinical polyneuropathy (PN) and clinical non-PN groups, according to the 2010 Toronto consensus criteria and the presence of PN symptoms and signs or not. Nerve conduction studies (NCS), F wave, sympathetic skin response (SSR), R-R interval variation (RRIV) and current perception thresholds (CPT) were performed and the abnormal rate was compared between different electrodiagnostic methods and between clinical subgroups.Results:Among the 73 prediabetic patients ultimately enrolled, only 20 (27.4%) can be diagnosed as clinical PN according to the Toronto consensus criteria. The abnormal rate of CPT (68.5%, 50/73) was significantly higher than those of F wave (2.7%, 2/73), lower limb NCS (0, 0/73), upper limb NCS changes of carpal tunnel syndrome (26.0%, 19/73), SSR (6.8%, 5/73) and RRIV (5.5%, 4/73; McNemar test, all P<0.001). With sinusoid-waveform current stimuli at frequencies of 2 000 Hz, 250 Hz and 5 Hz, the CPT device was used to measure cutaneous sensory thresholds of large myelinated, small myelinated and small unmyelinated sensory fibers respectively. CPT revealed a 21.9% (16/73) abnormal rate of unmyelinated C fiber in the hands of prediabetic patients, significantly higher than that of large myelinated Aβ fibers [8.2% (6/73), χ2=5.352, P=0.021]. Both abnormal rates of small myelinated Aδ [42.5% (31/73)] and unmyelinated C fibers [39.7% (29/73)] in the feet of prediabetic patients were significantly higher than that of large myelinated Aβ fibers [11.0% (8/73), χ2=18.508, 15.965, both P<0.001]. Compared with the clinical non-PN group, the abnormal rates of CPT [90.0% (18/20) vs 60.4% (32/53), χ2=5.904, P=0.015] and SSR [20.0% (4/20) vs 1.9% (1/53), P=0.016) were significantly higher in the clinical PN group. Conclusions:Peripheral neuropathies in prediabetic patients are usually asymptomatic or subclinical, and predispose to affect unmyelinated and small myelinated sensory fibers. Selective electrodiagnostic measurements of small fibers help to detect prediabetic neuropathies in the earliest stages of the disease.