Changes of neuropeptides and electrolytes in patients with acute traumatic brain injury

AIM: To investigate the levels of neuropeptides and electrolytes in the patients with acute traumatic brain injury.METHODS: Seventy-eight patients with acute brain injury were divided into mild, moderate and severe groups according to their GCS scores. The serum levels of arginine vasopressin (AVP) and angiotensin II (Ang II) were measured on day 1, 3 and 7 after injury. The serum levels of electrolytes were also measured on day 1. Forty-one subjects who received healthy check-up served as normalcontrols. RESULTS: Compared with normal control group, the serum levels of AVP and Ang II significantly increased in the patients with traumatic brain injury (P<0.01), depending on the severity of brain injury. Both neuropeptides reached the peak on day 3 after injury. The concentrations of serum potassium and calcium decreased in the patients with acute brain injury(P<0.01),also showing a severity-dependent tendency. No significant change of serum sodium in the patients with brain injury was observed. CONCLUSION: The serum levels of arginine vasopressin and angiotensin II canalso be used as the severity indicators of traumatic brain injuries. Decrease in serum potassium and calcium can also be used to evaluate the severity in patients with acute traumatic brain injury.     

Effect of respiratory syncytial virus on apoptosis and expressions of FasL,Fas, Bcl-2 and Bax

AIM: To study the relationship between respiratory syncytial virus (RSV) infection and apoptosis, between RSV infection and expressions of FasL, Fas, Bcl-2 and Bax. METHODS: Apoptotic cells were examined by flow cytometry and transmission electron microscope. Immunohistochemical analysis was used to detect the expressions of apoptosis-associated gene FasL, Fas, Bcl-2 and Bax in A549 cells during RSV infection. RESULTS: Apoptotic index increased at 72 h and 120 h postinfection. Apoptotic cells were detected by transmission electron microscope. High-expressions of FasL, Fas and Bax genes and low-expression of Bcl-2 gene were detected by immunohistochemical staining. CONCLUSION: Apoptosis in A549 cells was induced by RSV infection. This apoptosis may be induced by up-regulating the expression of FasL, Fas, Bax genes and down-regulating the expression of Bcl-2 gene.     

Inhibitory effect of Naja naja venom components on proliferation of human glioma U251 cells

AIM: To study the inhibitory effect of Naja naja venom components on the proliferation of human glioma U251 cells.METHODS: MTT assay was used to compare the inhibitory effect of various kinds of Naja naja venom components on human glioma U251 cells and the efficient components were selected. Flow cytometry was performed to detect apoptotic rate and cell cycle. The morphological changes of human glioma U251 cells were observed under laser scanning confocal microscope and transmission electron microscope.RESULTS: Eleven components of Naja naja venom were tested. The growth-inhibiting effects of them on U251 cells were observed, among which the component KD II-3 showed the inhibitory effect on U251 cells in a dose- and time-dependent manner. After treated with KD II-3 at the concentrations of 1 mg/L, 3.75 mg/L, 7.5 mg/L and 15 mg/L, the apoptotic rates of U251 cells were 13.3%, 17.7%, 20.0% and 22.4%, respectively. U251 cells were blocked in G₀/G₁ phase and the peak of sub-G₁ phase appeared. Under laser scanning confocal microscope, U251 cells showed shrinkage of the cell membrane, chromatin condensation and fragmentation after treated with KD II-3 at the concentration of 7.5 mg/L for 24 h, and karyopyknosis and chromatin condensation in U251 cells were found under transmission electron microscope.CONCLUSION: Component KD II-3 of Naja naja venom inhibits the proliferation of U251 cells and promotes apoptosis.     

Effects of Arg-Gly-Asp-Ser tetrapeptide on proliferation and apoptosis of hepatic stellate cells in vitro

AIM:To investigate the effects of Arg-Gly-Asp-Ser (RGDS) tetrapeptide on proliferation, apoptosis and caspase 3 expression in FN-stimulated HSCs in vitro. METHODS:[³H]-thymidine incorporation, Annexin-V/Propidium Iodide double-labeled flow cytometry(FCM), TUNEL, scanning electron microscope and transmission electron microscopy were employed to estimate the influence of RGDS on proliferation and apoptosis of HSCs. The adhesion rates were observed by toluidine blue colorimetric assay. The expression of caspase-3 protein was detected by FCM. RESULTS:①Compared with control and FN groups, RGDS tetrapeptide at concentrations of 25 mg·L^-1, 50mg·L^-1 and 100 mg·L^-1 inhibited the proliferation of HSCs (P<0.01), and the inhibition rates of 100 mg·L^-1 at 12 h, 24 h and 48 h were 62.73%, 74.23%, 80.22%, respectively.②RGDS tetrapeptide induced the HSC apoptosis in dose-dependent and time-dependent manners(P<0.01). Observed with scanning electron microscope, the cell bodies and cellular processes of HSCs exposed to RGDS tetrapeptide were seen to be diminished. Microvilli on the cell surface decreased, became short even disappeared. Observed with transmission electron microscopy, the chromatins condensed, shrunk and aggregated along inside of nuclear membrane to exist in the form of ball, petal and crescent. Sometimes, apoptotic bodies formed. ③After exposure of HSCs to RGDS tetrapeptide for 2 h, the inhibition rates of adhesion were 8.82%, 29.41% and 45.59%, respectively, but that of RGES group was only 4.41%, P<0.01. ④ The expression of caspase 3 was obviously higher in RGDS tetrapeptide group than that in FN group, RGES tetrapeptide. CONCLUSION: These results suggest that RGDS tetrapeptide may inhibit proliferation and induce apoptosis of HSCs in both dose- dependent and time- dependent manners in vitro, which may be related to the abrogation of cell adhesion and caspase 3.     

Effects of NGF on collagen secretion and morphology of hepatic stallete cells

AIM: To investigate the effects of nerve growth factor (NGF) on the changes of collagen secretion and morphology of hepatic stallete cells(HSCs). METHODS: Rat HSCs were incubated with different concentrations of NGF for 24 h. Collagen I and III in the supernatants of culture medium secreted by HSCs were detected by enzyme-linked immunosorbent assay. The morphological changes of HSCs were observed under inverted microscope with acridine orange staining and under transmission electronic microscope. RESULTS: When HSCs was incubated with NGF at concentrations of 100, 200 or 400 μg/L for 24 h, the content of collagen I and collagen III in the culture supernatants were significantly reduced compared with control group (P<0.05). After stimulated with NGF at the concentration of 100 μg/L for 24 h, the growth of the HSCs was inhibited and the morphous of the cells became round or oval gradually. The morphological changes of apoptotic cells were also observed by acridine orange staining and transmission electronic microscopy. CONCLUSION: NGF inhibits HSCs to synthesize collagen I and collagen III. Inhibition of collagen production and promotion of apoptosis in HSCs may be the possible mechanisms of NGF to reverse liver fibrosis.     

Effects of dust particles on autophagy of macrophages

AIM: To investigate the changes of autophagy of macrophages after phagocytizing dust particles and explore the mechanisms of dust particle-induced autophagy of the cells. METHODS: The bronchopulmonary lymph nodes were collected from patients with lung operation. The paraffin sections were prepared and then stained with Wilder′s method. The tissue structures were viewed. Peritoneal macrophages were harvested from rats and then treated with carbon particles. Influences of carbon particles in autophagic activities of macrophages were examined. The ultrathin sections of the lymph nodes and the cells phagocytized carbon particles were prepared. The structures and distribution of phagosomes, autophagosomes and lysosomes were viewed. The apoptotic cells in the dust cells of the lymph nodes and the cells having phagocytized carbon particles were examined using transmission electron microscope and TUNEL staining. RESULTS: In adult lymph nodes, dust particles were deposited significantly in macrophages, collagen fibres and density of microvessels increased. There were autophagosome precursors, autophagosomes, autophagolysosomes as well as phagosomes in the dust cells and the cells phagocytized carbon particles. In autophagosomes, mitochondrion, dust particle or carbon particle were usually observed. There were positive cells by TUNEL staining in the dust cells and the cells phagocytized carbon particles. Nuclear condensation or apoptotic body in the apoptotic cells were observed under transmission electron microscope. CONCLUSION: Deposition of dust particles induces enhancement of autophagic activities and apoptosis of macrophages. Autophagy plays an important role in cleaning dust particles and the injured mitochondria.     

Protective effect of pentoxifylline against spinal cord ischemia/reperfusion injury in rabbits

AIM: To investigate the protection of pentoxifylline against spinal cord ischemia/reperfusion injury.METHODS: Rabbits sustained spinal cord ischemia with 45 min cross-clamping of the infrarenal aorta. Groups were as follows: sham operation (n=8); ischemic control (n=20), receiving only vehicle; PTX A (n=20), receiving PTX before clamping and PTX B (n=20), receiving PTX at the onset of reperfusion. Rabbits were evaluated for hind-limb motor function with the Tarlov scoring system at 48 h. Serum was assayed with ELISA for TNF-α and spinal cords were harvest for MPO activity, histopathologic analysis and TUNEL staining. Immunohistochemistry was used for PECAM-1 and caspase-3 detection, and the numbers of necrosic and apoptotic neuron were counted at 12 h, 24 h, 48 h and 72 h of reperfusion. The necrotic and apoptotic neurons were also observed with transmission electron microscope.RESULTS: Improved Tarlov scores were observed in PTX-treated rabbits as compared with ischemic control rabbits at 48 h. The significant reductions of TNF-α in serum, activity of MPO, immunoreactivity of the PECAM-1 and caspase-3 were found in PTX-treated rabbits. The numbers of necrosic and apoptotic neuron were higher in PTX-treated rabbits than that in the ischemic control rabbits (P<0.05). No necrosic and apoptotic neuron were found in the sham operation group. CONCLUSION: PTX induces protection against ischemia/reperfusion injury in the spinal cord, thereby preventing both necrosis and apoptosis.     

Expression and subcellular localization of urocortin in syncytiotrophoblast of human term placenta

AIM: To obverse the expression and localization of urocortin on ultrathin cryosections of syncytiotrophoblast of human term placenta with immunocytochemistry technique under transmission electron microscope. METHODS: The human term placenta tissue from Cesarean delivery and normal labor were fixed in 4% paraformaldehyde, and then divided into two parts. One part was for regular immunocytochemistry under microscope, and the other part was used to prepare ultrathin cryosections for immunocytochemistry under transmission electron microscope. RESULTS: 1.Uroncortin mainly distributed in cytoplasm of syncytiotrophoblast of human term placenta under microscope. Urocortin also appeared in cytoplasm in some stromal cells. 2. Under transmission electron microscope, the anti-urocortin gold particles were observed in cytoplasm of syncytioptrophoblast ultrathin cryosections and sited on rough-surfaced endoplasmic reticulum. The anti-urocortin gold particles also appeared on nucleus and nuclear membrane of syncytiotrophoblast. CONCLUSION: Syncytiotrophoblast of human term placenta synthesized and secreted urocortin. The internalization of urocortin within syncytiotrophoblast nuclear indicates that urocortin may act as intracrine.     

Morphology and growth capacity of bone marrow stromal cells in vitro from APBSCT patients post pretreatment

AIM: To investigate the morphology and capacity of bone marrow colony forming unity-fibroblast (CFU-F) from APBSCT patients before and after pretreatment. METHODS: 21 case peripheral blood stem cell transplantation (PBSCT) patients were treated with pretreatment. The changes of morphology of the bone marrow stromal cells were assayed by light microscope and electron microscope, respectively. The numbers of CFU-F were assayed by Dexter type. RESULTS: The bone marrow stromal cells occured different types of morphology from PBSCT patients treated with chemotherapy or chemotherapy-TBI pretreatment, respectively, compared with controls. The transmission electron microscope showed that the endoplasmic reticula was dilated, the matrix of mitochondria appeared pale and the cristae of mitochondria became shorter in stromal cells from chemotherapy-TBI patients compared with those of controls. The structure of mitochondria from combined chemotherapy-TBI pretreatment appeared severe degeneration and disorder. The numbers of CFU-F from combined radiation-chemotherapy injury were significantly decreased compared with that before pretreatment and the chemotherapy injury (P<0.01), respectively. CONCLUSION: The change of cell morphology and capacity of CFU-F for bone marrow stromal cells is one of impairment injury mechanism of bone marrow hematopoietic inductive microenvironment from PBSCT patients post pretreatment.     

茄链格孢菌侵染马铃薯叶片过程的细胞学观察

采用光学显微镜和电镜技术系统研究了茄链格孢菌对马铃薯叶片的侵染过程及超微结构特征。结果表明：接种2 h后,分生孢子开始萌发,分生孢子各个位置都可萌发产生芽管|接种6 h后,菌丝顶端出现附着孢|接种8 h后,菌丝从细胞间凹陷处直接侵入感病品种东农303叶片表皮细胞内|接种24 h后,受侵染寄主细胞中的菌丝向相邻细胞扩展蔓延,感病品种细胞内含物及各类细胞器基本完全消解。在抗病品种克新1号上,茄链格孢菌的侵染情况与感病品种基本一致,但发生时间明显较感病品种推迟,寄主细胞内的菌丝数量明显少于感病品种|并且在接种24 h后出现细胞壁加厚的防卫反应,在感病品种上没有观察到防卫反应现象。说明抗病品种对茄链格孢菌具有一定的抗侵入和抗扩展能力。     

Establishment of autophagy model of rat gastric interstitial cells of Cajal induced by glutamic acid

AIM: To establish an autophagy model of glutamic acid-induced rat gastric interstitial cells of Cajal (ICCs) in vitro. METHODS: Glutamic acid was added to the medium of cultured ICCs in vitro at different concentrations (high, medium and low concentrations were 10 mmol/L, 5 mmol/L and 2.5 mmol/L, respectively) for different periods (3 h, 6 h and 24 h). The cell viability was measured by CCK-8 assay. The protein expression of microtubule-associated protein 1 light chain 3 (LC3) in the ICCs after cultured with glutamic acid at different concentrations for different periods was determined by Western blot. The ultrastructure and autophagic vacuoles of ICCs were observed under electron microscope, and immunofluorescence technique was used to measure the fluorescence intensity of autophagic protein LC3 after co-cultured with glutamic acid at medium concentration. RESULTS: Compared with control group, glutamic acid significantly inhibited the viability of ICCs (P<0.01). The ratios of LC3-Ⅱ/LC3-I in medium and high concentration groups at 3 h, 6 h and 24 h were significantly increased as compared with control group and low concentration group (P<0.01), and that in medium concentration group at 3 h was the best to increased the ratio of LC3-Ⅱ/LC3-I (P<0.01). Under electron microscope, the ICCs in glutamic acid group showed obvious autophagic vacuoles and cytoplasmic vacuoles. The fluorescence intensity of autophagic protein LC3 in the ICCs of glutamic acid group was significantly enhanced (P<0.01). CONCLUSION: Glutamic acid successfully induces autophagy in ICCs. The optimum condition of glutamic acid was 5 mmol/L for 3 h.     

Inhibitory effect of 5-fluorouracil on ultra-microstructure and insulin secretion of pancreatic β cells

AIM: To investigate the molecular mechanisms of β cell dysfunction induced by 5-fluorouracil (5-FU) in islet β cell line (NIT-1 cells). METHODS: The NIT-1 cells were treated with different concentrations of 5-FU. The content of insulin in the culture medium was determined by radioimmunoassay. Cell apoptosis was observed by flow cytometry with annexin V/PI staining. The ultra-microstructural changes of NIT-1 cells were observed under transmission electron microscope. The expression of pancreatic and duodenal homeobox protein 1(PDX-1) at mRNA and protein levels in NIT-1 cells was examined by RT-PCR and Western blotting, respectively. RESULTS: Exposed to the low glucose concentration (5.6 mmol/L), insulin secretion in NIT-1 cells was not significantly decreased following a 24 h treatment with 5.0 to 40.0 mg/L 5-FU (P>0.05). On the contrary, the high glucose (16.7 mmol/L)-stimulated insulin secretion in NIT-1 cells was inhibited by 5.0 to 40.0 mg/L of 5-FU in a dose-dependent manner after 24 h of incubation (P<0.01). The apoptosis rate of NIT-1 cells was significantly increased as compared to those in the control levels(P<0.05). The structural changes of mitochondria were the main apoptotic changes under transmission electron microscope. Significant down-regulation of PDX-1 expression at mRNA and protein levels was observed in NIT-1 cells treated with 5-FU at the concentration of 10.0 mg/L to 40.0 mg/L(P<0.05).CONCLUSION: 5-FU inhibits the insulin secretion in islet β cell induced by high glucose. A relative deficiency in insulin secretion following 5-FU treatment is related to the changes of β cell ultra-microstructure and the reduction of β cell numbers, by which an increase in apoptosis of pancreatic β cells is induced. Down-regulation of PDX-1 expression may play a pivotal role in increasing the apoptosis of pancreatic β cells induced by 5-FU in high-glucose condition.     

Energy metabolism and apoptotic effect of microwave radiation on rat myocardial cells

AIM: To investigate the effect of microwave radiation at different intensities on the rat myocardium and its possible mechanism.METHODS: The rats were radiated by the intensity of 500, 1 000, 1 500 and 2 000 W/m² with 2 450 MHz microwave for 6 min. The heart tissue was collected 6 h after microwave radiation. ATP and mitochondria complex Ⅳ and Ⅴ were measured. The changes of the tissue structures were observed under transmission electron microscope. The apoptosis of the myocardial cells was detected by a cell analyzer. The protein level of cleaved caspase-3 was determined by Western blotting.RESULTS: The concentration of ATP and activity of mitochondria complex Ⅳand Ⅴ signi-ficantly decreased compared with control group in the cardiac tissues. The decreased number, morphological abnormalities such as dissolved cavitation, matrix and obvious tumefaction of mitochondria were observed under transmission electron microscope. The microwave radiation induced the apoptosis of myocardial cells in the rats. The cell apoptotic rate and the protein level of cleaved caspase-3 increased with increasing intensity of microwave radiation(P<0.05).CONCLUSION: Microwave radiation has obvious injury effect on the rat heart, which can cause cardiac energy metabolism dysregulation and cardiac myocyte apoptosis.     

Effects of capsaicin on cognitive impairment and mitochondria-associated endoplasmic reticulum membranes in rats with chronic cerebral hypoperfusion

AIM:To observe the effects of capsaicin on cognitive impairment and mitochondria-associated endoplasmic reticulum membranes (MAMs) of hippocampal CA1 area in the rats with chronic cerebral hypoperfusion (CCH), and to investigate the underlying molecule mechanism of cognitive defects induced by ischemia. METHODS:Healthy male Sprague-Dawley (SD) rats(n=48) were randomly divided into sham operation (sham) group,CCH model (CCH) group, capsaicin group,and solvent group, 12 rats in each group. Capsaicin at 2.5 mg/kg was intraperitoneally injected twice a week for 4 weeks, starting on the 7th day after surgery. The rats in solvent group were given the same amount of solvent at the same time and under the same conditions. Morris water maze, object recognition test and open field test were conducted to analyze the cognitive related behavior performance on the 4th week after surgery. The changes of MAMs in the hippocampal CA1 region were observed under transmission electron microscope, the co-localization of the MAMs was observed by immunofluorescence double-labeling, and the expression of mitofusin 2 (Mfn2) in the hippocampal tissue was determined by Western blot.RESULTS:Four weeks after the operation, the behavior tests showed that the cognitive function of CCH rats was impaired compared with sham operation group. Compared with solvent group, spatial learning and memory in capsaicin group was improved significantly. The results of transmission electron microscope and confocal microscope showed that the distance of MAMs in the hippocampal CA1 area of CCH rats was increased compared with sham operation group, and the co-localization of the contacts was decreased (P<0.05). Compared with solvent group, the correlation between the mitochondria and ER in capsaicin group was increased (P<0.05). The protein level of Mfn2 in CCH group was significantly lower than that in sham group (P<0.05). Compared with solvent group, the protein level of Mfn2 in capsaicin group was higher (P<0.05). CONCLUSION:CCH rats showed decreased cognitive function and loosen MAMs. Capsaicin improves the cognitive behavior of CCH rats by up-regulation of MAMs.     

Experimental study on how brain-dead state affects the heart structure and function of Ba-Ma mini pigs and the mechanism

AIM:To investigate how brain-dead state affects the heart structure and function and the effect of PKC-α in BA-Ma mini pigs.METHODS:Ten Ba-Ma mini pigs were randomized into 2 groups: brain-dead group (n=5),and control group (n=5). The brain-dead model was made by increasing intracranial pressure,while the control group was maintained anesthesia for 24 h. The concentrations of cTnT,TNF-α,IL-1β and IL-6 in serum were determined at 6,12 and 24 h after brain death. At 24 h,heart tissues were observed by HE staining and electron microscope. The expression of PKC-α was detected by immunohistochemistry and RT-PCR.RESULTS:(1) Histological changes of myocardium: flaky bleeding under endocardium and dissolution of myocardium were found in optical microscope. In electron microscope dropsical mitochondria and confluent muscle fiber were found. (2) Changes of serum cTnT: serum cTnT for brain-dead group began to increase gradually since 6 h,and were significantly higher at each time point than those in control group (P<0.05). (3) Changes of inflammatory factors: IL-1β,IL-6,and TNF-α in brain-dead group began to increase gradually since 6 h,and were significantly higher at each time point than those in control group (P<0.05). (4) Changes of PKC-α expression: PKC-α mRNA and protein expressions in brain-dead group increased significantly at 24 h (P<0.05).CONCLUSION:Brain death may evoke heart structure and functional injury,and increase the levels of inflammatory factors and PKC-α. The activation of PKC-α may participate in the process of heart injury.     

Ultrastructural characteristics of neural stem cells derived from adipose-derived stromal cells during their differentiation into neurons and astrocytes

AIM: To observe the ultrastructural characteristics of neural stem cells derived from adipose-derived stromal cells (ADSC) differentiating into neurons and astrocytes. METHODS: ADSC were cultured, amplified and induced with β-mercaptoethanol or 3-isobutyl-1-methylxanthine (IBMX). The expression of nestin in the induced cells was determined by the method of immunofluorescence. The ultrastructure of the induced neural stem cells was observed under transmission electron microscope.RESULTS: The expression of nestin reached the peak at 3 h in β-mercaptoethanol group and at 14 d in IBMX group, and the positive rate of the former (86%) was significantly higher than that of the latter (23%). However, the duration of the induction in IBMX group was obviously longer than that in β-mercaptoethanol group. The ultrastructure of the induced neural stem cells in the two groups was similar under the transmission electron microscope, only with some differences in organelles.CONCLUSION: In the process of ADSC differentiating into astrocytes or neurons with the induction of β-mercaptoethanol or IBMX, the different changes of ultrastructure in ADSC-derived neural stem cells occur in some organelles in cytoplasm, not in nucleus.     

Effect of exogenous hydrogen sulfide on lipophagy in mouse primary hepatocytes

AIM: To evaluate the effect of exogenous hydrogen sulfide (H₂S) from GYY4137 on lipophagy in mouse primary hepatocytes. METHODS: The C57BL/6 mouse primary hepatocytes isolated and cultured by 2-step in situ perfusion method were divided into 4 groups: the cells in control group were incubated with normal medium; the cells in model group were incubated with 1.2 mmol/L oleic acid (OA) for 48 h; the cells in H₂S group or propargylglycine (PAG) group were incubated with 1.2 mmol/L OA for 48 h followed by serum-free phenol red-free RPMI-1640 medium which contained 1 mmol/L GYY4137 or 200 μmol/L PAG for 6 h. The cells were collected to conduct immunofluorescence staining of LC3 and photography under fluorescence microscope, phase-contrast microscope or transmission electron microscope. The protein expression of LC3-Ⅰ/Ⅱ in the hepatocytes was determined by Western blot. RESULTS: In contrast with the model group, the fluorescent particles of LC3, the protein expression of LC3, the number of autophagic lysosome and vacuoles in hepatocytes in H₂S group increased. CONCLUSION: In steatosis hepatocytes, exogenous H₂S promotes the lipophagy.     

Activating effect of astragalus saponin on mouse peritoneal macrophages in vitro

AIM: To investigate the immunomodulatory effect of astragalus saponin (AS) on macrophages and explore the mechanism of its immunomodulation. METHODS: By adding different concentrations of AS into cultured mouse peritoneal macrophages in vitro, the influence of AS on the synthesis of nitro oxide (NO) was detected by NO kit (enzymatic method). MTT assay was used to determine the cytotoxicity of macrophages induced by AS. The morphological changes of macrophages were observed under transmission electron microscope. LSCM and specificity fluorescent probe Fluo-3/AM were applied to observe the change of Ca2+ in macrophages induced by AS. RESULTS: AS significantly increased NO synthesis, enhanced the effects of mouse peritoneal macrophages on killing carcinoma cells. Cell surface projection exhibited multiplication, becoming thickening and growth longer via transmission electron microscope. Increase in intracellular Ca2+ in macrophages was also observed. CONCLUSION: AS enhances the immune function of macrophages by increasing NO synthesis and enhancing cytotoxicity. The increased intracellular Ca2+ may be the mechanism of immunomodulatory effect of AS.     

Effects of type III hysterectomy on lower urinary tract function

AIM: To analyze the urodynamic data and assess the alterations of lower urinary tract function in the patients before and after radical hysterectomy (type III). METHODS: The patients who underwent type III hysterectomy without complications and other diseases were enrolled in the study. Urodynamic examination was performed in the patients before operation and 12~14 d after surgery. The examination was carried out again 3 months post-operation. RESULTS: Post-void residual (PVR), flow time (FT), first desire to void volume (FDV) and maximum vesical pressure (Pvesmax) were increased in the patients 12~14 d after operation. Maximum flow rate (Qmax), average flow rate (Qave), voided volume (VV), maximum cystometric capacity (MCC), bladder compliance (BC), detrusor pressure (Pdet), maximum urethral pressure (MUP) and maximum urethral closure pressure (MUCP) were significantly decreased compared with preoperative data (P<0.05). PVR, FT, FDV and Pvesmax in 3 months post-hysterectomy were increased, and Qmax, Pdet, BC, MUP and MUCP were decreased compared with preoperative data (P<0.05). Qmax, Qave, VV, MCC, BC and Pdet in 3 months post-hysterectomy increased significantly, while PVR and Pvesmax were decreased compared with the data 12~14 d after operation (P<0.05). CONCLUSION: Most of the patients with type III hysterectomy show severe lower urinary tract dysfunction 12~14 d after operation, such as bladder storage dysfunction due to sharply decrease in bladder compliance, voiding function decline caused by deletion of detrusor contractility, and low urinary continence caused by decrease in urethral closure pressure. The bladder storage and voiding function can partially recover in 3 months.