Primary osteoporosis （POP） is a metabolic bone disease characterized by reduced bone mass， degenerated bone microstructure， and increased bone fragility. Its pathogenesis involves the interaction of multiple factors such as genetics， aging， endocrine， and environment， which remain incompletely elucidated. Mitochondrial dysfunction can lead to insufficient adenosine triphosphate （ATP） production and abnormal accumulation of reactive oxygen species （ROS）， activating oxidative stress and inflammation pathways， thereby inhibiting osteoblast differentiation and promoting osteoclast activation， exacerbating the negative bone metabolism balance in POP. Mitochondrial autophagy， as the core mechanism of mitochondrial quality control， selectively identifies and clears damaged mitochondria to effectively reduce ROS accumulation and energy metabolism disorders， thus maintaining the balance between osteoblast and osteoclast differentiation. It plays a critical role in maintaining bone homeostasis and the prevention and treatment of POP. The traditional Chinese medicine （TCM） theory of Qi transformation shares similarities with the functions of mitochondria in energy generation and substance conversion. The pathological state of Qi deficiency and stagnation may be associated with mitochondrial autophagy dysfunction， and the pathogenic characteristics of combined phlegm and stasis align with the metabolic waste accumulation induced by obstructed autophagy flow. This article explores the correlation of the theory of Qi deficiency and stagnation with mitochondrial autophagy and elucidates its potential role in the pathogenesis of POP. Additionally， considering the pathogenesis features of POP， which involve deficiency causing stagnation and a mixture of deficiency and excess， this article proposes a novel therapeutic approach： tonifying Qi to support the body and unblocking collaterals to resolve stagnation from the perspective of mitochondrial autophagy. This article aims to provide theoretical support and research insights for further exploration of TCM in the prevention and treatment of POP.

Primary osteoporosis （POP） is a metabolic bone disease characterized by reduced bone mass， degenerated bone microstructure， and increased bone fragility. Its pathogenesis involves the interaction of multiple factors such as genetics， aging， endocrine， and environment， which remain incompletely elucidated. Mitochondrial dysfunction can lead to insufficient adenosine triphosphate （ATP） production and abnormal accumulation of reactive oxygen species （ROS）， activating oxidative stress and inflammation pathways， thereby inhibiting osteoblast differentiation and promoting osteoclast activation， exacerbating the negative bone metabolism balance in POP. Mitochondrial autophagy， as the core mechanism of mitochondrial quality control， selectively identifies and clears damaged mitochondria to effectively reduce ROS accumulation and energy metabolism disorders， thus maintaining the balance between osteoblast and osteoclast differentiation. It plays a critical role in maintaining bone homeostasis and the prevention and treatment of POP. The traditional Chinese medicine （TCM） theory of Qi transformation shares similarities with the functions of mitochondria in energy generation and substance conversion. The pathological state of Qi deficiency and stagnation may be associated with mitochondrial autophagy dysfunction， and the pathogenic characteristics of combined phlegm and stasis align with the metabolic waste accumulation induced by obstructed autophagy flow. This article explores the correlation of the theory of Qi deficiency and stagnation with mitochondrial autophagy and elucidates its potential role in the pathogenesis of POP. Additionally， considering the pathogenesis features of POP， which involve deficiency causing stagnation and a mixture of deficiency and excess， this article proposes a novel therapeutic approach： tonifying Qi to support the body and unblocking collaterals to resolve stagnation from the perspective of mitochondrial autophagy. This article aims to provide theoretical support and research insights for further exploration of TCM in the prevention and treatment of POP.

OBJECTIVE To monitor plasma concentration of anti-tuberculosis drugs in children, and explore the influencing factors and safety of anti-tuberculosis drugs, and promote the rational use of drugs. METHODS The plasma drug concentration monitoring results of isoniazid, rifampicin, pyrazinamide and ethambutol, the adverse drug reactions and the changes of various parameters before and after treatment in 40 children with tuberculosis were analyzed retrospectively in Zhejiang Hospital of Integrated Tradtional Chinese and Western Medicine. RESULTS The compliance rates of plasma drug concentration of isoniazid, rifampicin, pyrazinamide and ethambutol in chlidren with tuberculosis were 48.15%, 34.88%, 73.81%, 18.52%, respectively. Isoniazid(P=0.0250), rifampicin(P=0.0212) concentrations were positively correlated with daily dose. Age was also one of the factors affecting the concentrations of isoniazid(P=0.0430) and rifampicin(P=0.0057). Serum albumin(P=0.0475) and sex(P=0.0087) were correlated with rifampicin and pyrazinamide, respectively. Abnormal liver function(5/40, 12.50%) and rash(4/40, 10%) were the most common adverse drug reaction. Aspartate aminotransferase(AST), alanine aminotransferase(ALT) and uric acid levels increased after treatment with anti-tuberculosis drugs. CONCLUSION The plasma drug concentrations of isoniazid, rifampicin and ethambutol in children are low. The anti-tuberculosis drugs maybe related to the increase of AST, ALT and uric acid. Therefore, monitoring of serum drug concentration, renal fuction and liver function during anti-tuberculosis treatment is helpful to improve drug safety and implement individualized treatment.

The concept of the glial-vascular unit (GVU) was raised recently to emphasize the close associations between brain cells and cerebral vessels, and their coordinated reactions to diverse neurological insults from a "glio-centric" view. GVU is a multicellular structure composed of glial cells, perivascular cells, and perivascular space. Each component is closely linked, collectively forming the GVU. The central roles of glial and perivascular cells and their multi-level interconnections in the GVU under normal conditions and in central nervous system (CNS) disorders have not been elucidated in detail. Here, we comprehensively review the intensive interactions between glial cells and perivascular cells in the niche of perivascular space, which take part in the modulation of cerebral blood flow and angiogenesis, formation of the blood-brain barrier, and clearance of neurotoxic wastes. Next, we discuss dysfunctions of the GVU in various neurological diseases, including ischemic stroke, spinal cord injury, Alzheimer's disease, and major depression disorder. In addition, we highlight the possible therapies targeting the GVU, which may have potential clinical applications.
Humans ; Neuroglia ; Nervous System Diseases ; Blood-Brain Barrier ; Alzheimer Disease ; Glymphatic System

Objective To investigate the role of herpesvirus infection and the activation of Th cell subsets in rheumatoid arthritis (RA) patients.Methods Polymerase chain reaction (PCR) was used to determine herpes viral (HSV 1,HSV 2,EBV,CMV) DNA in whole blood (WB) and serum samples.ELISA used for measuring serum levels of IFN ? and IL 4.Results ① Thirty two WB samples and 32 serum samples from RApatients were tested for the viral DNA types.Of them 2 WB samples were positive for HSV 1 DNA and 1 serum sample did.In normal control samples one serum sample was positive for CMV DNA.There was no significant difference in rate of detection between control group and test group.② Comparing serum levels of IFN ? and the ratio of IFN ?/IL 4,it was found that RA patients had significantly higher values than the normal controls.Increased values directly correlated with severity of disease.[in RA patients IFN ? (21?33) pg/ml.TFN ?/IL 4 (25?20),in normal controls IFN ? (10 1?2 6) pg/ml, IFN ?/IL 4 (17?8)].Conclusion ① The rate of detection of herpes viral (EBV,CMV,HSV 1,HSV 2) DNA does not correlate with RA significantly.② Increased serum levels of Th1 derived inflammatory cytokine (IFN ?) and the impaired production of anti inflammatory Th2 derived cytokines (IL 4) indicate impaired activation of Th1 and Th2 in RA patients and may account for the chronic arthritis.