ObjectiveTo investigate the molecular mechanisms of Mahuang Fuzi Gancao Tang and its pungent single herbs， Ephedrae Herba and Aconiti Lateralis Radix Praeparaia， in repairing podocyte injury based on the sweat pore theory， with a focus on the podocyte cytoskeletal transient receptor potential canonical 5 （TRPC5）-Ras-related C3 botulinum toxin substrate 1 （RAC1） feedforward loop. MethodsAn animal model with puromycin aminonucleoside （PAN）-induced overexpression of TRPC5 was established. Interventions included Mahuang Fuzi Gancao Tang， Ephedrae Herba alone， and Aconiti Lateralis Radix Praeparaia alone. Biochemical parameters ， histopathological changes， and podocyte ultrastructure were analyzed. Western blotting was performed to determine the expression of cytoskeletal protein synaptopodin and mechanism-related proteins TRPC5， RAC1-GTP， and RAC1 in the kidney. Primary podocytes were isolated and cultured for three-dimensional imaging of foot processes， cytoskeletal fluorescence analysis， and TRPC5-RAC1 co-staining via immunofluorescence. ResultsCompared with the model group， Mahuang Fuzi Gancao Tang， Ephedrae Herba alone， and Aconiti Lateralis Radix Praeparaia alone increased serum albumin （ALB）， decreased UPCR， reduced podocyte foot process fusion rate， upregulated synaptopodin expression， and downregulated TRPC5， RAC1-GTP， and RAC1 expression （P<0.05）. Moreover， the interventions increased the phalloidin fluorescence area/field area ratio （P<0.01） and mean fluorescence intensity （P<0.05）， while decreasing the proportion of TRPC5-RAC1 co-stained double-positive cells/total cells per field （P<0.01） in primary podocytes. ConclusionMahuang Fuzi Gancao Tang and its pungent single herbs， Ephedrae Herba and Aconiti Lateralis Radix Praeparaia， ameliorated podocyte injury in the model with PAN-induced TRPC5 overexpression by reducing proteinuria and suppressing the TRPC5-RAC1 feedforward loop-mediated podocyte cytoskeletal damage.

ObjectiveTo investigate the molecular mechanisms of Mahuang Fuzi Gancao Tang and its pungent single herbs， Ephedrae Herba and Aconiti Lateralis Radix Praeparaia， in repairing podocyte injury based on the sweat pore theory， with a focus on the podocyte cytoskeletal transient receptor potential canonical 5 （TRPC5）-Ras-related C3 botulinum toxin substrate 1 （RAC1） feedforward loop. MethodsAn animal model with puromycin aminonucleoside （PAN）-induced overexpression of TRPC5 was established. Interventions included Mahuang Fuzi Gancao Tang， Ephedrae Herba alone， and Aconiti Lateralis Radix Praeparaia alone. Biochemical parameters ， histopathological changes， and podocyte ultrastructure were analyzed. Western blotting was performed to determine the expression of cytoskeletal protein synaptopodin and mechanism-related proteins TRPC5， RAC1-GTP， and RAC1 in the kidney. Primary podocytes were isolated and cultured for three-dimensional imaging of foot processes， cytoskeletal fluorescence analysis， and TRPC5-RAC1 co-staining via immunofluorescence. ResultsCompared with the model group， Mahuang Fuzi Gancao Tang， Ephedrae Herba alone， and Aconiti Lateralis Radix Praeparaia alone increased serum albumin （ALB）， decreased UPCR， reduced podocyte foot process fusion rate， upregulated synaptopodin expression， and downregulated TRPC5， RAC1-GTP， and RAC1 expression （P<0.05）. Moreover， the interventions increased the phalloidin fluorescence area/field area ratio （P<0.01） and mean fluorescence intensity （P<0.05）， while decreasing the proportion of TRPC5-RAC1 co-stained double-positive cells/total cells per field （P<0.01） in primary podocytes. ConclusionMahuang Fuzi Gancao Tang and its pungent single herbs， Ephedrae Herba and Aconiti Lateralis Radix Praeparaia， ameliorated podocyte injury in the model with PAN-induced TRPC5 overexpression by reducing proteinuria and suppressing the TRPC5-RAC1 feedforward loop-mediated podocyte cytoskeletal damage.

[Objective]To discuss the pathogenesis,hierarchy,treatment and medication rules of deficiency of Yang with hyperactivity of Yin syndrome in Treatise on Febrile Diseases.[Methods]Combining with the medical theory of later physicians,this paper clarifies the pathogenesis and syndrome of deficiency of Yang with hyperactivity of Yin syndrome,explains the mechanism of Yang deficiency and Yin excess syndrome from the perspective of pathophysiology.This paper also analyzes the differences among the various versions of the text of the Shaoyin Chapter including the variations in disease location,the pathogen nature,stomach Qi and body fluid,and inducts the implicit therapeutic principles in the Shaoyin Chapter.[Results]The principle of differentiation and treatment for deficiency of Yang with hyperactivity of Yin syndrome is"protecting stomach Qi and preserving body fluids",which can be subdivided into Taiyin damp earth disease,Shaoyin monarch fire disease,and Jueyin wind wood disease.Through careful observation,questioning,smelling and palpation,combined with the pathological and physiological basis of modern medicine,it can accurately diagnose deficiency of Yang with hyperactivity of Yin syndrome.Shaoyin plays a crucial role in Treatise on Febrile Diseases.The structure of the Shaoyin Chapter is well-organized and can dynamically reflect the changes in the pathogenesis of Shaoyin syndrome,the combination of Shaoyin and Taiyin or Jueyin,or the tri-coordination syndrome of these location.From the text,it can be inferred that the location of the disease begins on the surface and gradually extends to the interior.The treatment methods will include moxibustion,warming the meridians,warming Yang and dredging Yang.The severity of the illness and the presence of phlegm-fluid determine the treatment,which may involve dispersing cold,dispersing fluids,and promoting urination.The degree of exhaustion of bodily fluids may require either reviving Yang for resuscitation or nourishing Yin.[Conclusion]From a pathological and physiological perspective,the mechanisms behind the changes in the primary symptoms of traditional Chinese medicine can be explained.When treating deficiency of Yang with hyperactivity of Yin syndrome,the selection of herbal prescriptions should be based on factors such as the disease location,the pathogen nature,stomach Qi and body fluids.The treatment principles for deficiency of Yang with hyperactivity of Yin syndrome have instructive significance for the treatment of other syndromes as well.

The"lipid nephrotoxicity"hypothesis introduces the lipid metabolism disorders into the field of kidney disease research.Fatty acids as important components of lipids can be ectopic deposition in various cells of the kidney in pathological status,and are involved in the occurrence and progression of acute kidney in-jury(AKI)and chronic kidney disease(CKD).The mechanism of abnormal fatty acid metabolism in tubular epithelial cells(TEC)and its function change are closely associated with kidney injury.This article summa-rized the relationship between fatty acid metabolism in TEC with AKI and CKD,elaborated the specific mech-anism of fatty acid metabolism disorders leading to TEC injury,and discussed the treatment strategies based on regulating fatty acid metabolism disorders to improve kidney injury.

Objective: To observe the clinical effect and infra-red thermogram changes for acute lumbar sprain. Methods: All 295 cases with acute lumbar sprain were randomly divided into an electroacupuncture group (147 cases) and medication group (148 cases). The cases in electroacupuncture group were treated by needling Houxi (SI 3), whereas those in the medication group were treated with Meloxicam tablet. The infra-red thermogram was observed before and after treatment. Results: The recovery and effective rates in the electroacupuncture group were 71.4% and 93.9%, whereas the rates in the medication groups were 42.6% and 87.2% (P＜0.01). The temperature differences via the thermogram in the electroacupuncture and medication groups were 2.52℃ and 0.80℃ (P＜0.01), indicating a significant difference.Conclusion: Both electroacupuncture and medication could obtain significant effect for acute lumbar sprain; however, electroacupuncture obtained a better overall effect and a more substantial temperature-raising effect in the thermogram than medication.

Objective: To observe the effect of treatment for proliferative knee osteoarthritis (KOA) using combined acupuncture and medicated compression. Method: All 328 cases were randomized into an observation and control group, 164 cases in each. Combined acupuncture and medicated compression were adopted in the observation group, while oral administration of Zhui Feng Tou Gu Wan (Wind-removing and Bone-penetrating Pills) were adopted in the control group. The clinical effects in the two groups were evaluated 40 days after the treatment. Result: There were significant differences in both marked and total effective rates (P<0.05). Conclusion: Combined acupuncture and medicated compression can obtain better effect for KOA than oral administration of the Wind-Removing and Bone-Penetrating pills.

Objective To study the effects of verussurinine (VSRN), an alkaloid isolated from Veratrum nigrum var. ussuriense alkaloids (VnA), against thrombosis and its platelet aggregation inhibitory activity in rats in order to find out whether VSRN is the antithrombotic active ingredient of VnA. Methods The electrically induced rat carotid artery thrombosis and stasis-induced rat inferior vena cava thrombosis models were used to evaluate the anti-arterial and anti-venous thrombosis effect of VSRN, respectively. Borns turbidimetric method was used to examine the in vivo and in vitro anti-platelet effect so as to investigate the antiplatelet aggregation of VSRN. Results In comparison with saline, VSRN in five different doses (1.25—20.00 ?g/kg) showed significantly and dose-dependently prolonged occlusion time (OT) of carotid artery injured by electrical stimulation and reduced thrombus dry weight of inferior vena cava ligated for 4 h to cause stasis. Platelet aggregation was found to be inhibited by VSRN in the doses of 1.25—5.00 ?g/kg and at the concentration of 6.25—50 ?g/L in both in vivo and in vitro test. Conclusion VSRN has powerful arteriovenous antithrombosis and antiplatelet aggregation of rats. The antithrombotic effect of VSRN is related to its platelet aggregation inhibitory activity. The above findings indicate that VSRN is an antithrombotic active ingredient of VnA.