Objective To investigate the effects of complement component 1q subcomponent B(C1QB) on neural repair and the phosphatidylinositol 3-kinase/protein kinase B(PI3K/AKT) signaling pathway in rats with spinal cord injury(SCI).Methods From March 2024 to October 2024, experiments were conducted in the laboratory of Xuzhou Medical University. An SCI rat model was established, and successfully modeled rats were randomly assigned to the model group(SCI group), si-NC group, si-C1QB group, and si-C1QB + PI3K/AKT signaling pathway inhibitor group(si-C1QB + LY294002 group), with 12 rats in each group. Additionally, 12 normal healthy SD rats were used as the blank control group(Control group). At the end of the treatment, the BBB score was assessed. Enzyme-linked immunosorbent assay(ELISA) was used to detect inflammatory factors in spinal cord tissue. Hematoxylin-eosin(HE) staining was used to observe pathological damage in spinal cord tissue. Terminal deoxynucleotidyl transferase-mediated d UTP nick end labeling(TUNEL) staining was used to detect apoptosis of spinal cord neurons. Immunohistochemistry was used to detect the expression of ionized calcium-binding adapter molecule 1(IBA-1) and glial fibrillary acidic protein(GFAP). Western blot was used to detect the expression of proteins related to the PI3K/AKT signaling pathway.Results Compared with the Control group, the spinal cord tissue structure in the SCI group was more disordered, with extensive cavitation due to loss of integrity, severe neuronal damage, disorganized nerve fiber arrangement, and prominent inflammatory cell infiltration. The BBB score, IL-10 level, and p-PI3K/PI3K and p-AKT/AKT expression were decreased(t/P=23.859/<0.001, 13.739/<0.001, 13.418/<0.001, 13.191/<0.001), while TNF-αand IL-6 levels, neuronal apoptosis rate, and expression of C-caspase-3, C-caspase-9, IBA-1, and GFAP were increased(t/P=14.325/<0.001, 14.820/<0.001, 18.653/<0.001, 13.191/<0.001, 12.269/<0.001, 13.168/<0.001, 14.795/<0.001). Compared with the si-NC group, the si-C1QB group showed better structural and morphological repair of spinal cord tissue, with noticeable reduction in cavitation, relatively clear gray and white matter boundaries, orderly nerve fiber arrangement, and reduced inflammatory cell infiltration. The BBB score, IL-10 level, and p-PI3K/PI3K and p-AKT/AKT expression were increased(t/P=21.430/<0.001, 11.692/<0.001, 11.393/<0.001, 13.182/<0.001), while TNF-αand IL-6 levels, neuronal apoptosis rate, and expression of C-caspase-3, C-caspase-9, IBA-1, and GFAP were decreased(t/P=11.889/<0.001, 12.385/<0.001, 3.846/0.003,12.187/<0.001, 9.242/<0.001, 12.050/<0.001, 11.900/<0.001). Compared with the si-C1QB group, the si-C1QB+LY294002 group showed more severe spinal cord tissue damage. The BBB score, IL-10 level, and p-PI3K/PI3K and p-AKT/AKT expression were decreased(t/P=14.543/<0.001, 9.647/<0.001, 10.735/<0.001, 12.187/<0.001), while TNF-αand IL-6 levels,neuronal apoptosis rate, and expression of C-caspase-3, C-caspase-9, IBA-1, and GFAP were increased(t/P=10.708/<0.001,10.678/<0.001, 3.149/0.010, 10.694/<0.001, 8.832/<0.001, 10.681/<0.001, 10.614/<0.001).Conclusion Silencing C1QB can promote neural repair in rats with spinal cord injury, which is associated with activation of the PI3K/AKT signaling pathway.

This article systematically elaborates the theoretical and clinical value of establishing a system for syndrome differentiation and treatment of pulmonary collateral diseases. Based on the historical coordinates and the intersection of the times of the theory of collateral disease, the theory of visceral outward manifestation, and the development of the syndrome differentiation of the viscera, this article clarifies the historical mission of constructing syndrome differentiation and treatment of pulmonary collateral diseases. This article clearly defines the core concepts and physiological functions of the pulmonary collateral and the pulmonary airways. It briefly elaborates on the causes, the basic pathogenesis, the main clinical manifestations, the therapeutic principles and methods, the treatment formulas, as well as the syndrome differentiation and treatment of pulmonary collateral diseases. This article presents some examples of representative research achievements in prevention and treatment of major chronic diseases such as respiratory communicable or infectious diseases and COPD, which are acquired under the guidance of syndrome differentiation and treatment of pulmonary collateral diseases. Thus, the significant theoretical and clinical value of the syndrome differentiation and treatment system of pulmonary collateral diseases are demonstrated.

This article reported a rare case of a patient with cardiac sarcoidosis combined with atrial septal defect, and conducted a literature review.

To report a case of acute inflammatory demyelinating polyradiculoneuropathy(AIDP) with treatmentrelated fluctuation(TRF), presenting with elevated intracranial pressure and positivity for anti-sulfatide antibody in cerebrospinal fluid and anti-GM3 antibody in serum, along with a literature review.

Romiplostim, as a thrombopoietin receptor agonist, is approved for use in patients with immune thrombocytopenia(ITP) in the United States, Australia, and several countries in European, Africa and Asia, and in patients with refractory aplastic anemia(AA) in Japan and South Korea. Romiplostim binds to and activates TPO receptors on megakaryocyte precursors, promoting cell proliferation and viability, leading to increased platelet production. Through this mechanism, Romiplostim reduces the reliance for other treatments and reduces bleeding events in patients with thrombocytopenia.This article reviews the mechanism of action, pharmacodynamics, pharmacokinetics and clinical application research progress of romiplostim.