After peripheral nerve injury, nerve regeneration is slow, and skeletal muscles gradually atrophy due to long-term lack of nerve innervation, nutrient deficiency, and lack of stimulation of nerve electrical stimulation. Neuregulin-1 (NRG-1) and epidermal growth factor receptor (ErbB) can activate multiple complex intracellular signaling networks to affect the nerves and muscles. This article reviews the regulatory effect of NRG-1/ErbB signaling pathway on peripheral nerves, muscles, and neuromuscular junctions, aiming to provide references for finding new therapeutic target for denervated muscle atrophy.

Osteoporosis is highly prevalent and a leading cause of disability and death in the elderly. Bone metabolism homeostasis is maintained through the coupling of osteoblasts and osteoclasts. While current treatments can reduce bone loss, they may cause side effects such as gastrointestinal discomfort. Neuroboneology has gained attention as the nervous system, both directly and indirectly, influences bone metabolism, remodeling, and formation. Studies have also highlighted the role of peripheral nerves and blood vessels in bone health. Neuropeptides, small signaling molecules produced by neurons, regulate vascular function and bone homeostasis. These neuropeptides may offer new insights into the "peripheral nerve-angiogenesis-bone homeostasis" regulation theory. This study explores the impact of peripheral nerves on osteoporosis through neuropeptides.

Osteoporosis is highly prevalent and a leading cause of disability and death in the elderly. Bone metabolism homeostasis is maintained through the coupling of osteoblasts and osteoclasts. While current treatments can reduce bone loss, they may cause side effects such as gastrointestinal discomfort. Neuroboneology has gained attention as the nervous system, both directly and indirectly, influences bone metabolism, remodeling, and formation. Studies have also highlighted the role of peripheral nerves and blood vessels in bone health. Neuropeptides, small signaling molecules produced by neurons, regulate vascular function and bone homeostasis. These neuropeptides may offer new insights into the "peripheral nerve-angiogenesis-bone homeostasis" regulation theory. This study explores the impact of peripheral nerves on osteoporosis through neuropeptides.

After peripheral nerve injury, nerve regeneration is slow, and skeletal muscles gradually atrophy due to long-term lack of nerve innervation, nutrient deficiency, and lack of stimulation of nerve electrical stimulation. Neuregulin-1 (NRG-1) and epidermal growth factor receptor (ErbB) can activate multiple complex intracellular signaling networks to affect the nerves and muscles. This article reviews the regulatory effect of NRG-1/ErbB signaling pathway on peripheral nerves, muscles, and neuromuscular junctions, aiming to provide references for finding new therapeutic target for denervated muscle atrophy.

Osteoarthritis （OA） is characterized by articular cartilage degeneration， synovial hyperplasia， hyperosteogeny， and narrowing of joint space， which can be caused by trauma， inflammation， and other factors. With the increasing global population aging， the incidence of OA is rising year by year， making it a major public health problem that urgently needs to be addressed. Exploring effective treatment schemes is particularly important. The pathogenesis of OA is complex， including oxidative stress， autophagy， and apoptosis. Recent studies have found that ferroptosis， a new type of cell death， is also an important pathogenic factor in OA， characterized by a series of complex changes such as iron ion accumulation， glutathione （GSH） depletion， and mitochondrial dysfunction. Research shows that inhibiting ferroptosis in chondrocytes can promote chondrocyte proliferation， delay extracellular matrix （ECM） degradation， and reduce synovial hyperplasia and inflammation. Targeting ferroptosis is a new direction in the treatment of OA. OA treatment includes intra-articular injections of steroids or hyaluronic acid and artificial joint replacement， but there are limitations. Traditional Chinese medicine （TCM） has been widely used in the treatment of various diseases because of its low cost， low drug resistance， and few side effects. Cell and animal experiments have further confirmed that TCM can intervene in the treatment of OA with ferroptosis from multiple targets， multiple levels， and aspects， but the mechanism of its treatment of OA based on ferroptosis has not been clarified. This paper discussed iron metabolism， lipid peroxidation， cysteine/glutamate transporter system Xc^- （system Xc^-）/GSH/glutathione peroxidase 4 （GPX4） pathway， nicotinamide adenine dinucleotide phosphate（NADPH）/ferroptosis suppressor protein 1 （FSP1）/coenzyme Q₁₀ （CoQ₁₀） pathway， tumor protein p53 in OA， and related molecular targets of Chinese medicine monomers and compounds on ferroptosis inhibition. Their potential therapeutic mechanisms were further analyzed to provide theoretical guidance for the treatment of OA by TCM and useful reference for the research and development of related drugs.

Peripheral nerve injury(PNI),caused by contusions,fractures,and other traumas,may lead to abnormal sensory function,limited motor capabilities,neuropathic pain,and muscle atrophy,which can severely impact the patient's quality of life.Post-PNI,Wallerian degeneration occurs,involving axonal degeneration and myelin sheath collapse.Notably,the dorsal root ganglia(DRG),as the primary sensory neurons in pain signal transmission,are crucial targets in neuropathic pain(NP)induced by PNI,and changes in these targets trigger a series of complex signaling pathway alterations.Among these,the phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt)signaling pathway,as a vital regulator of cell survival and death,promotes Schwann cell proliferation and migration,thereby enhancing axonal growth and myelination to facilitate nerve regeneration,and supports the survival of DRG neurons to alleviate NP.Current treatment method,including stem cell transplantation and neurotrophic medications,all have certain limitations.Traditional Chinese medicine(TCM)has the advantages of low cost and few side effects,and is widely used for the treatment of PNI.This article reviews the relationship between oxidative stress,apoptosis,autophagy,inflammation,angiogenesis,the cell cycle,and other pathophysiological mechanisms in PNI and the PI3K/Akt signaling pathway,as well as its associated molecular targets.We also discuss the potential mechanisms of action of TCM monomers,compound formulas,and acupuncture based on the PI3K/Akt signaling pathway in the treatment of PNI,aiming to provide systematic and standardized theoretical guidance for the healing of PNI with TCM and a useful reference for the development of related medications.

Peripheral nerve injury(PNI),caused by contusions,fractures,and other traumas,may lead to abnormal sensory function,limited motor capabilities,neuropathic pain,and muscle atrophy,which can severely impact the patient's quality of life.Post-PNI,Wallerian degeneration occurs,involving axonal degeneration and myelin sheath collapse.Notably,the dorsal root ganglia(DRG),as the primary sensory neurons in pain signal transmission,are crucial targets in neuropathic pain(NP)induced by PNI,and changes in these targets trigger a series of complex signaling pathway alterations.Among these,the phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt)signaling pathway,as a vital regulator of cell survival and death,promotes Schwann cell proliferation and migration,thereby enhancing axonal growth and myelination to facilitate nerve regeneration,and supports the survival of DRG neurons to alleviate NP.Current treatment method,including stem cell transplantation and neurotrophic medications,all have certain limitations.Traditional Chinese medicine(TCM)has the advantages of low cost and few side effects,and is widely used for the treatment of PNI.This article reviews the relationship between oxidative stress,apoptosis,autophagy,inflammation,angiogenesis,the cell cycle,and other pathophysiological mechanisms in PNI and the PI3K/Akt signaling pathway,as well as its associated molecular targets.We also discuss the potential mechanisms of action of TCM monomers,compound formulas,and acupuncture based on the PI3K/Akt signaling pathway in the treatment of PNI,aiming to provide systematic and standardized theoretical guidance for the healing of PNI with TCM and a useful reference for the development of related medications.

【Objective】 To evaluate the safety and efficacy of long-term indwelling of Allium ureteral stent in the treatment of ureteral stricture. 【Methods】 The clinical data of patients who underwent endoscopic Allium ureteral stent implantation for ureteral stricture in our hospital during Aug.2020 and Dec.2022 were retrospectively analyzed, and the surgical conditions and adverse events were recorded. The data of serum creatinine, blood urea nitrogen, glomerular filtration rate (GFR) and renal pelvis width under ultrasound were compared before surgery and 1, 3, 6 and 12 months after surgery. 【Results】 A total of 52 patients with ureteral stricture of 1.1 (0.7, 2.0)cm were included. All operations were successful. The operation time was 82.5 (70, 114)min, intraoperative blood loss 20 (10, 20)mL, and postoperative hospitalization stay 1 (1, 2) day. During the follow-up of (13.2±7.8) months, 14 patients had stent displacement, 5 had stone obstruction of stent tubes, 7 had occasional hematuria after movement, 9 had intermittent lumbar and abdominal pain, and 1 had recurrent urinary tract infection. The serum creatinine, blood urea nitrogen and renal pelvis width of 1 month, 3, 6 and 12 months after surgery were significantly decreased, while GFR was significantly increased. 【Conclusion】 Long-term indwelling of Allium ureteral stent is effective in the treatment of ureteral stricture, but the high incidence of stent displacement should arouse attention.

ObjectiveTo observe the effect of Jiaji electroacupuncture combined with neurodynamic mobilization on nerve conduction velocity and the expression of Netrin-1, Slit2 and Rho GTPases after sciatic nerve injury in rabbits. MethodsA total of 216 New Zealand rabbits were randomly divided into nomal control group (NC), vector virus group (VV), Jiaji electroacupuncture combined with neurodynamic mobilization group (EN), Netrin-1 group (N1), Slit2 group (S2) and N1+S2 group. Each group was divided into three subgroups according to the postoperative treatment time points (one, two and four weeks), with twelve rabbits in each subgroup. The rabbit model of Sunderland Ⅲ degree injury of the left sciatic nerve was established by clamping method. There was no intervention in NC, and virus was injected during the preparation of the model. Jiaji electroacupuncture and neurodynamic mobilization were administrated three days after operation in EN group. Nerve conduction velocity of sciatic nerve was measured with electromyography. The sciatic nerve and L_4-6 spinal cords were obtained, the expression of Netrin-1 and Slit2 mRNA were detected real-time quantitative polymerase chain reaction and immunofluorescence double staining, and the expression of Rac1, Cdc42 and RhoA protein were observed via Western blotting. ResultsOne, two and four weeks after modeling, the nerve conduction velocity was more in EN group and N1+S2 group than in N1 group and S2 group (P < 0.05); the Netrin-1 and Slit2 mRNA expression were higher in the EN group and N1+S2 group than in the VV group and NC group (P < 0.05); the protein expression of Rac1 and Cdc42 were higher, and the protein expression of RhoA was lower in EN group and N1+S2 group than in N1 group, S2 group and VV group (P < 0.05). ConclusionJiaji electroacupuncture combined with nerve mobilization may promote the axonal regeneration by regulating the expression of Netrin-1 and Slit2, adjusting the imbalance of Rho GTPases enzyme system, and then promoting cytoskeleton reorganization and peripheral nerve regeneration after injury.

China is a big country with liver diseases, and various hepatitis viruses, drug poisons, and alcohol can cause liver injury and even liver failure. The key to the prognosis of patients with liver failure is liver self-repair and regeneration. Alpha-fetoprotein (AFP) has been extensively studied as a tumor marker in liver cancer, but its role in liver regeneration in patients with liver failure awaits further studies. This article summarizes the basic research on AFP in liver regeneration and the clinical research on AFP in acute liver failure and acute-on-chronic liver failure (ACLF), as well as the previous research findings of our group that AFP is an important prognostic index and regeneration factor for liver regeneration after hepatitis B virus-related ACLF. The analysis shows that further studies on the role of AFP in the prognosis of various types of liver failure and the mechanism of liver regeneration will help deepen our understanding of AFP and liver regeneration, thereby providing new ideas and methods for the clinical diagnosis, treatment, and prognostic evaluation of patients with various types of liver failure.