Objective　To observe the morphological changes of brain and to analyze the cause of coma after open-heart surgery in cases suffered from congenital heart disease.　Methods　Twenty six autopsy cases were collected from Jan. 1973 to Sep. 1999 in Fuwai Hospital. Their duration of coma was 1 day to 40 days and all of them died earlier later following cardiac surgery. Their surgical procedure, extracorporeal circulation time, and other clinical records and autopsy findings were reviewed. 　Results　The brain lesions included intracranial hemorrhages (n＝11), cerebral edema (n＝11), encephalitis and encephalomingitis (n＝3), and cerebromalacia (n＝1). Intracranial hemorrhages occurred in epidural (n＝3), subdural (n＝3), subarachoid spaces (n＝4), and intracerebral parenchyma (n＝1). The causes of coma were deduced as follows: lower cardiac output (n＝7), air embolism (n＝3), pneumonia (n＝3) and other infections (n＝2), pulmonary hypertension (n＝2), and the unknown causes of coma (n＝9). But the 6 out of the last 9 cases showed longer duration (more than 100 min) of extracorporeal circulation. Intracranial hemorrhages occurred more frequently in cases with waking period than those without after cardiac operation, and vice versa the cerebral edema. 　Conclusion　Intracranial hemorrhage and cerebral edema were the main changes of brain in the patients suffered from coma, but its causes were complex and difficult to analyze. These results suggest that further improved heart preservation, shorter time of extracorporeal circulation and effective treatment of infection would be benefit to the prevention of coma.

Aim To investigate the inhibitory effects of urocortin2 (UCN2) on ventral tegmental area (VTA) nervous activity of morphine addiction rats and the mechanism. Methods Morphine addiction rats and the microiontophoresis method were used to observe the effects of UCN2 on VTA neuron′s spontaneous dis-charge changing rule, as well as the inhibitory effects of UCN2 on DA neuron′s cluster spontaneous dis-charge, to identify UCN2 and DA on the same VTA neuron. Morever, the inhibitor of corticotropin-regula-ting factor′s receptor ( CRF-2 R ) and the blocker of protein kinase A ( PKA ) , AST-2 B and H89 , were used to investigate the effects of UCN2 on VTA neuron′s of morphine addiction rats. Results UCN2 could inhibit the firing rate 82% (31/38) of the tested VTA neuron ( P<0. 01 ) , the discharge frequency changed from (20. 89 ± 2. 86) Hz to (13. 66 ± 3. 93) Hz (P<0. 01). Further, the inhibitor of PKA, AST-2B and H89 could ablolish the inhibitory effects of UCN2 . Morever, the excitatory firing of VTA neurons was at-tenuated by addition of UCN2 , while AST application could inhibit the UCN2′s inhibitory effects. Conclu-sion UCN2 could regulate the effects of VTA via PKA pathway and may thereby contribute to the improvement of drug addiction.

Objective To observe the protective and regeneration-promoting effects of Ruyi Zhenbao Pill (RZP) on nerve injury in zebrafish.Methods The zebrafish model of central nervous injury was induced by mycophenolate mofetil,the model of peripheral motor nerve and axonal injury was induced by ethanol,and the model of myelin damage was induced by ethidium bromide.The variations of central nerve,axon and myelin sheath fluorescence intensity,and peripheral motor nerve length in zebrafish,which exposed to the different concentration (10.0,33.3,and 100.0 μ.g/mL) of RZP,were observed with fluorescence microscope.The effective protection rates of RZP on zebrafish central nerve and axone,and the regeneration-promoting effect on peripheral motor nerve and myelin sheath were analyzed and calculated with the image processing software NIDS-Element's.Results In 10.0,33.3,and 100.0 μg/mL RZP groups,the zebrafish central nervous injury protective rates were 2％,24％,and 50％ (P ＜ 0.001),respectively,the peripheral nerve regeneration promoting rates were 44％ (P ＜ 0.05),49％ (P ＜ 0.01),and 93 ％ (P ＜ 0.001),the axonal injury recovery rates were 3％,29％ and 48％ (P ＜ 0.05),and the myelin sheath regeneration promoting rates were 36％ (P ＜ 0.01),37％ (P ＜ 0.001),and 41％ (P ＜ 0.001),compared with model group.Conclusions RZP could not only protect the central nervous and axonal injury,but also promote the regeneration of peripheral nerve and myelin sheath in zebrafish.

We described chemical composition in Cangzhu in recent years, volatile oil is the important chemical composition, The beta-eudesmol, hinesol are active ingredient in volatile oil and there are 38 kind of glycosides. At the same time, we overview the applying of RAPD technology in atractylodes lancea. The results is that there are correlation in chemical composition, genetic differentiation and geographical distribution, there is some truth in bounded by a territorial division of the north-south Cangzhu, and genetic differentiation has been happened in atractylodes lancea to adapting the environment. We described advances of pharmacological in dampness spleen, cardiovascular system, genitourinary system, nervous system, and the results show that there are pharmacological activity in digestive system, cardiovascular system, genitourinary system of atractylodes lancea.
Animals ; Atractylodes ; chemistry ; genetics ; China ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; Humans ; Molecular Biology

OBJECTIVETo explore the differences of the main pharmacological action in wild and cultivated Atractylodes lancea.

METHODStudy the effect of the 70% ethanol extracts from the wild and the culticated A. lancea on the mice with gastriculcer induced by absolute ethyl alcohol or HCl. Stdudy the effect on intestinal propulsive function in mice by measuring the length of intestine and distance of Indian ink. Observe anti-bacteria effect in vitro of the A. lancea by determining the minimum inhibitory concentrations.

RESULTThe pharmacological action, which made a little difference in the sane productive places, and made significant differences in different productive places. Compared to Jurong, it has better actions in Luotian on small intestinal propulsive function and bacteriostatic action. There was not an obvious difference in protective effect on gastric ulcer induced by absolute ethyl alcohol and 0.6 mol x L(-1) HC1 between different locations.

CONCLUSIONTo the main effect, cultvated A. lancea had no significant difference on the whole but having better result in some respects, which can provide the pharmacodynamics evidence of cultivated A. lancea being used instead of the wild.

Animals ; Atractylodes ; chemistry ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; Gastrointestinal Motility ; drug effects ; Humans ; Male ; Mice ; Stomach Ulcer ; chemically induced ; drug therapy ; pathology ; physiopathology

OBJECTIVETo investigate the histopathological features of primary restrictive cardiomyopathy (PRCM).

METHODSNine extransplanted hearts from heart transplantation recipients were examined. Gross and histopathological findings were observed, photographed and final pathological diagnosis was compared to clinical diagnosis. The myocardial ultrastructure changes were determined using transmission electron microscopy.

RESULTSThe hallmark pathologic feature of PRCM was distinguished by myocardial cell degeneration and hyperplastic collagen fibrils around the myocardial cells.Fibrosis was severer in left ventricle free wall than in ventricular septum and right ventricle. The degree of myocardial cell degeneration and poloidal disorder were severer in patients with reduced ejection fraction (EF) than in patients with preserved EF. Transmission electron microscope evidenced severe interstitial fibrosis, myofibrillar changes of sarcomere structure, abnormalities both on intercalated disc number and distribution.

CONCLUSIONSPRCM is characterized by hyperplastic collagen fibrils around the cardiomyocytes. Fibrosis is severer in left ventricle than in right ventricle. Sarcomere dysplasia is the main cause of PRCM, and ultrastructural examination is helpful for PRCM diagnosis.

Cardiomyopathy, Restrictive ; surgery ; Fibrosis ; Heart Transplantation ; Heart Ventricles ; Humans ; Myocardium ; pathology ; Myocytes, Cardiac ; Sarcomeres

Objective:To analyze the case characteristics and outcomes of 12 idiopathic giant cell myocarditis(IGCM)cases after heart transplantation(HT).Methods:From June 2004 to May 2022, clinical data were retrospectively reviewed for 12 cases with pathologically confirm IGCM after HT at Fuwai Hospital.General characteristics, clinical manifestations, pathological examinations and postoperative follow-ups are recorded.Results:From June 2004 to May 2022, a total of 1 143 HT operations are performed at Fuwai Hospital and 12 cases of IGCM(1.05%)are confirmed by postoperative pathology.The age is(47.6±7.3)years.There are 5 boys and 7 girls.Initial presenting manifestations are congestive heart failure(7 cases, 58.3%)and arrhythmia(4 cases, 33.3%). Median time from symptom onset to HT is 6 months.All of them are undiagnosed pre-operation.And dilated cardiomyopathy(5 cases, 41.7%)and arrhythmogenic right ventricular cardiomyopathy(3 cases, 25%)are confirmed.The follow-up period is(4~142)months post-HT.One death occurred during perioperative period and another is due to heart failure at 68 months post-HT.Only 1 case of grade 1R transplant heart rejection occurrs at 9 years post-HT and there is no case of recurrence.According to Kaplan-Meier survival analysis, cumulative survival rates of 1/5/10 years post-HT in IGCM patients are 91.7%, 91.7% and 73.3% respectively.No significant difference exist in survival rate for other etiologies post-HT(Log-rank P=0.265). Conclusions:HT is efficacious for end-stage IGCM.Regular and sufficient postoperative immunosuppression is vital for preventing heart transplant rejection and recurrent IGCM.Most IGCM patients have a decent prognosis post-HT.

Mitochondrial autophagy is a process to clear dysfunctional mitochondria in the cytoplasm to maintain the integrity of mitochondrial function and cell homeostasis. Mitochondrial autophagy is a complex physiological process， which can maintain the balance of mitochondrial quality and quantity， cell survival under starvation and harsh conditions， and the stability of the intracellular environment. Its molecular mechanism involves a variety of proteins. Many factors can induce mitochondrial autophagy， such as starvation， oxidative stress， hypoxia， depolarization， and other stresses. The accumulation of unfolded proteins can also induce mitochondrial autophagy. In recent years， as a research hotspot， the abnormality of mitochondrial morphology and function is closely related to the occurrence of a variety of diseases. The research on mitochondrial autophagy and the pathogenesis of clinical diseases has attracted more attention， such as tumors， cardiovascular diseases， liver diseases， nervous system diseases， and glucose metabolism disorders. It has been found that regulating mitochondrial autophagy may inspire the treatment of some diseases. Meanwhile， clinical researchers have paid more attention to traditional Chinese medicine （TCM）. As revealed by in-depth research， Chinese medicine has a certain value in regulating mitochondrial autophagy. The research on the pathogenesis of mitochondrial autophagy in related diseases and the intervention of Chinese medicine has found that there are many reports on the regulation of mitochondrial autophagy by Chinese medicine in tumors， cardiovascular diseases， and nervous system diseases. However， the mechanism of mitochondrial autophagy， the balance of mitochondrial autophagy， and the difference in the activation or inhibition of mitochondrial autophagy by Chinese medicine remain unclear. The regulation of mitochondrial autophagy has become a new research target strategy of Chinese medicine in the prevention and treatment of diseases. This paper reviewed the available literature in recent years to provide reference materials for the regulation of mitochondrial autophagy by Chinese medicine and ideas for the follow-up research of Chinese medicine in mitochondrial autophagy.