Combined metabolomics and proteomics to reveal beneficial mechanisms of Dendrobium fimbriatum against gastric mucosal injury.

As a dietary and medicinal plant, Dendrobium fimbriatum (DF) is widely utilized in China for improving stomach disease for centuries. However, the underlying mechanisms against gastric mucosal injury have not been fully disclosed. Here, metabolomics and proteomics were integrated to clarify the in-depth molecular mechanisms using cyclophosphamide-induced gastric mucosal injury model in mice. As a result, three metabolic pathways, such as creatine metabolism, arginine and proline metabolism, and pyrimidine metabolism were hit contributing to DF protective benefits. Additionally, γ-L-glutamyl-putrescine, cytosine, and thymine might be the eligible biomarkers to reflect gastric mucosal injury tatus, and DF anti-gastric mucosal injury effects were mediated by the so-called target proteins such as Ckm, Arg1, Ctps2, Pycr3, and Cmpk2. This finding provided meaningful information for the molecular mechanisms of DF and also offered a promising strategy to clarify the therapeutic mechanisms of functional foods.

The interval between onset and admission predicts disease progression in COVID-19 patients.

BACKGROUND: The prognostic role of the interval between disease onset and hospital admission (O-A interval) was undetermined in patients with the coronavirus disease 2019 (COVID-19). METHODS: A total of 205 laboratory-confirmed inpatients admitted to Hankou hospital of Wuhan from January 11 to March 8, 2020 were consecutively included in this retrospective observational study. Demographic data, medical history, laboratory testing results were collected from medical records. Univariate and multivariate logistic regression models were used to evaluate the prognostic effect of the O-A interval (≤7 versus >7 days) on disease progression in mild-to-moderate patients. For severe-to-critical patients, the in-hospital mortality and the length of hospital stay were compared between the O-A interval subgroups using log-rank test and Mann-Whitney U test, respectively. RESULTS: Mild-to-moderate patients with a short O-A interval (≤7 days) are more likely to deteriorate to severe-to-critical stage compared to those with a long O-A interval (>7 days) [unadjusted odds ratio =2.93, 95% confidence interval (CI), 1.32-6.55; adjusted odds ratio =3.44, 95% CI, 1.20-9.83]. No association was identified between the O-A interval and the mortality or the length of hospital stay of severe-to-critical patients. CONCLUSIONS: The O-A interval has predictive values for the disease progression in mild-to-moderate COVID-19 patients. Under circumstances of the specific health system in Wuhan, China, the spontaneous healthcare-seeking behavior is usually determined by patients' own heath conditions. Hence, the O-A interval can be reflective of the natural course of COVID-19 to some extent. However, our findings should be validated further in other cohorts and in other health systems.

Clinical efficacy of low dose recombinant tissue-type plasminogen activator for the treatment of acute intermediate-risk pulmonary embolism.

OBJECTIVES: To investigate the efficacy and safety of initial thrombolysis by recombinant tissue-type plasminogen activator (rt-PA) in compared with anticoagulant therapy in patients with acute intermediate-risk pulmonary embolism (PE).  Methods: Sixty-six patients with acute intermediate-risk PE were randomly assigned to receive rt-PA or LMWH between June 2014 and June 2017 in our department. We obtained information regarding the difference in the right ventricle/left ventricle (RV/LV) ratio, pulmonary artery systolic pressure (PASP), clinical symptoms improvement, PE-related mortality, hemodynamic decompensation, recurrent PE, and major and minor bleeding.  Results: In the rt-PA group, the mean PASP was reduced from 52.0±12.2 at baseline to 34.8±9.4 (p less than 0.001) and the mean RV/LV ratio was reduced from 1.26±0.22 at baseline to 0.96±0.18 (p less than 0.001) at 24 hours. In the LMWH group, the mean PASP was 53.4±12.8 at baseline and 48.5±11.9 at 24 hours (p=0.11), and the mean RV/LV ratio was 1.22±0.19 at baseline and 1.17±0.21 at 24 hours (p=0.31). In comparison with the LMWH group, there was a significant reduction in PASP and an improvement in the symptom severity in the rt-PA group. At 90 days, there was no difference in mortality, recurrent venous thromboembolism and major bleeding as a safety outcome, but increased minor bleeding and decreased hemodynamic decompensation occurred in the rt-PA group. Conclusions: In patients with acute intermediate-risk PE, low dose thrombolytic therapy is considered safe and effective, it can be recommended as an alternative option in clinical treatment.

Aryl Hydrocarbon Receptor Suppresses the Prostate Cancer LNCaP Cell Growth and Invasion by Promoting DNA Damage Response Under Oxidative Stress.

Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that interacts with multiple signaling pathways during prostate development. In the present study, LNCaP cells were knocked down of AhR by siRNA, or treated with the AhR agonist 3-methylcholanthrene (3MC). The effects of AhR on LNCaP cells and the associated mechanisms were studied both under normal condition and under hydrogen peroxide (H2O2)-induced oxidative stress. MTT, transwell chamber assays and flow cytometry were employed to investigate cell proliferation, invasion, and apoptosis, respectively, whereas the DNA damage response (DDR) signaling (phosphorylation of ataxia-telangiectasia mutated [ATM], check-point kinase 2 [Chk2], histone H2AX, p53, and cleaved poly-ADP-ribose polymerase [PARP]) was detected by western blotting. Exposure of LNCaP cells to H2O2 inhibited their viability and migration, and induced apoptosis, at a greater extent compared with the culture under normal conditions. In addition, the oxidative stress increased p-ATM, p-Chk2, p-p53, and p-H2AX expression levels significantly. Knockdown of AhR attenuated the aforementioned effects caused by H2O2-induced oxidative stress. Activation of AhR by 3MC treatment, further aggravated these changes of LNCaP cells on oxidative stress. The findings indicated that AhR suppresses the viability and migration of LNCaP cells notably under oxidative stress, and this process is associated with positive regulation of the responses to oxidative DNA damage.

Neurogenic effect of VEGF is related to increase of astrocytes transdifferentiation into new mature neurons in rat brains after stroke.

To study the cellular mechanism of vascular endothelial growth factor (VEGF)-enhanced neurogenesis in ischemic brain injury, we used middle cerebral artery occlusion (MCAO) model to induce transient focal ischemic brain injury. The results showed that ischemic injury significantly increased glial fibrillary acidic protein immunopositive (GFAP(+)) and nestin(+) cells in ipsilateral striatum 3 days following MCAO. Most GFAP(+) cells colocalized with nestin (GFAP(+)-nestin(+)), Pax6 (GFAP(+)-Pax6(+)), or Olig2 (GFAP(+)-Olig2(+)). VEGF further increased GFAP(+)-nestin(+) and GFAP(+)-Pax6(+) cells, and decreased GFAP(+)-Olig2(+) cells. We used striatal injection of GFAP targeted enhanced green fluorescence protein (pGfa2-EGFP) vectors combined with multiple immunofluorescent staining to trace the neural fates of EGFP-expressing (GFP(+)) reactive astrocytes. The results showed that MCAO-induced striatal reactive astrocytes differentiated into neural stem cells (GFP(+)-nestin(+) cells) at 3 days after MCAO, immature (GFP(+)-Tuj-1(+) cells) at 1 week and mature neurons (GFP(+)-MAP-2(+) or GFP(+)-NeuN(+) cells) at 2 weeks. VEGF increased GFP(+)-NeuN(+) and BrdU(+)-MAP-2(+) newborn neurons after MCAO. Fluorocitrate, an astrocytic inhibitor, significantly decreased GFAP and nestin expression in ischemic brains, and also reduced VEGF-enhanced neurogenic effects. This study is the first time to report that VEGF-mediated increase of newly generated neurons is dependent on the presence of reactive astrocytes. The results also illustrate cellular mechanism of VEGF-enhanced neural repair and functional plasticity in the brains after ischemic injury. We concluded that neurogenic effect of VEGF is related to increase of striatal astrocytes transdifferentiation into new mature neurons, which should be very important for the reconstruction of neurovascular units/networks in non-neurogenic regions of the mammalian brain.

[Perineal urethrostomy plus secondary urethroplasty for ultralong urethral stricture: clinical outcomes and influence on the patient's quality of life].

OBJECTIVE: To investigate the outcomes of perineal urethrostomy plus secondary urethroplasty for ultralong urethral stricture and assess its influence on the patient's quality of life. METHODS: We retrospectively analyzed 54 cases of ultralong urethral stricture treated by perineal urethrostomy from 2000 to 2010. The mean age of the patients was 40 years, and the average length of stricture was 6.5 cm. We evaluated the patients'quality of life by questionnaire investigation and the clinical outcomes based on IPSS, Qmax, the necessity of urethral dilation and satisfaction of the patients. RESULTS: The mean Qmax of the 54 patients was (14.0 +/- 4.7) ml/min. Of the 34 cases that underwent secondary urethroplasty, 22 (64.7%) achieved a mean Qmax of (12.0 +/- 3.5) ml/min, 8 (23.5%) needed regular urethral dilatation and 4 (11.8%) received internal urethrotomy because of restenosis. IPSS scores were 5.4 +/- 2.1 and 8.5 +/- 5.8 after perineal urethrostomy and secondary urethroplasty, respectively. Fifty of the total number of patients (92.6%) were satisfied with the results of perineal urethrostomy, and 22 of the 34 (64.7%) with the results of secondary urethroplasty. CONCLUSION: Perineal urethrostomy plus secondary urethroplasty is safe and effective for ultralong urethral stricture, and affects very little the patient's quality of life.

New striatal neurons form projections to substantia nigra in adult rat brain after stroke.

Previous studies have demonstrated that newborn striatal neurons can functionally integrate with local neural networks in adult rat brain after injury. In the present study, we determined whether these newly generated striatal neurons can develop projections to the substantia nigra, a target of striatal projection neurons. We used 5'-bromodeoxyuridine (BrdU) and a retroviral vector expressing green fluorescent protein (GFP) combined with multiple immunostaining labels of newborn striatal neurons, and nigral microinjection of fluorogold (FG) to trace the striatonigral projection in adult rat brain at different weeks following a transient middle cerebral artery occlusion (MCAO). We found that FG positive (FG(+)) cells could be detected in newly generated neurons (BrdU(+)-NeuN(+) and GFP(+)-NeuN(+)) in ipsilateral striatum clearly at 12, but not 2 weeks after MCAO. The data suggest that ischemia-induced newborn striatal projection neurons could form long axons that targeted the substantia nigra (striatonigral projection pathway) and that have intact axonal transport from the nerve terminal to cell body. These new striatal neurons express glutamate NR2 and dopamine D2L receptors, which form the molecular basis for responding to the inputs from cortical glutamatergic and nigral dopaminergic projection neurons. Our data provide the first morphological evidence that newborn neurons in the striatum, a non-neurogenic region, can establish new striatonigral neural circuits, important pathways for the maintenance of motor function. These results help us to understand endogenous cellular mechanisms of brain repair, and suggest that increasing adult neurogenesis could be a practical strategy for enhancing the efficacy of rehabilitative therapy in stroke patients.

Reciprocal activation between PLK1 and Stat3 contributes to survival and proliferation of esophageal cancer cells.

BACKGROUND & AIMS: Aberrant activation of the signal transducer and activator of transcription (Stat)3 and overexpression of polo-like kinase (PLK)1 each have been associated with cancer pathogenesis. The mechanisms and significance of dysregulation of Stat3 and PLK1 in carcinogenesis and cancer progression are unclear. We investigated the relationship between Stat3 and PLK1 and the effects of their dysregulation in esophageal squamous cell carcinoma (ESCC) cells. METHODS: We used immunoblot, quantitative reverse-transcription polymerase chain reaction, immunochemistry, chromatin immunoprecipitation, mobility shift, and reporter assays to investigate the relationship between Stat3 and PLK1. We used colony formation, fluorescence-activated cell sorting, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling, and xenograft tumor assays to determine the effects of increased activation of Stat3 and PLK1 in proliferation and survival of ESCC cells. RESULTS: Stat3 directly activated transcription of PLK1 in esophageal cancer cells and mouse embryonic fibroblast cell NIH3T3. PLK1 then potentiated the expression of Stat3; ß-catenin was involved in PLK1-dependent transcriptional activation of Stat3. This mutual regulation between Stat3 and PLK1 was required for proliferation of esophageal cancer cells and resistance to apoptosis in culture and as tumor xenografts in mice. Furthermore, phosphorylation of Stat3 and overexpression of PLK1 were correlated in a subset of ESCC. CONCLUSIONS: Stat3 and PLK1 control each other's transcription in a positive feedback loop that contributes to the development of ESCC. Increased activity of Stat3 and overexpression of PLK1 promote survival and proliferation of ESCC cells in culture and in mice.

Oxalate impairs aminophospholipid translocase activity in renal epithelial cells via oxidative stress: implications for calcium oxalate urolithiasis.

PURPOSE: We evaluated the possible involvement of phospholipid transporters and reactive oxygen species in the oxalate induced redistribution of renal epithelial cell phosphatidylserine. MATERIALS AND METHODS: Madin-Darby canine kidney cells were labeled with the fluorescent phospholipid NBD-PS in the inner or outer leaflet of the plasma membrane and then exposed to oxalate in the presence or absence of antioxidant. This probe was tracked using a fluorescent quenching assay to assess the bidirectional transmembrane movement of phosphatidylserine. Surface expressed phosphatidylserine was detected by annexin V binding assay. The cell permeable fluorogenic probe DCFH-DA was used to measure the intracellular reactive oxygen species level. RESULTS: Oxalate produced a time and concentration dependent increase in phosphatidylserine, which may have resulted from impaired aminophospholipid translocase mediated, inward directed phosphatidylserine transport and from enhanced phosphatidylserine outward transport. Adding the antioxidant N-acetyl-L-cysteine significantly attenuated phosphatidylserine externalization by effectively rescuing aminophospholipid translocase activity. CONCLUSIONS: To our knowledge our findings are the first to show that oxalate induced increased reactive oxygen species generation impairs aminophospholipid translocase activity and decreased aminophospholipid translocase activity has a role in hyperoxaluria promoted calcium oxalate urolithiasis by facilitating phosphatidylserine redistribution in renal epithelial cells.

TGF-beta1 reverses inhibition of COX-2 with NS398 and increases invasion in prostate cancer cells.

Bone-derived transforming growth factor (TGF)-beta1 leads to tumor growth, osteoblastic lesions and more invasion. Degradation of basement membranes caused by cyclooxygenase (COX)-2 is known as a distinctive feature of invasive cells. We investigated inhibition of COX-2 with NS398 in PC-3 and LNCaP cell lines. TGF-beta1 and dmPGE2 were added in NS398 treated or untreated cells. COX-2 did not express in PC-3, after treatment with TGF-beta1, COX-2 appeared and accompanied with enhanced invasion. COX-2 expressed in LNCaP, undetectable after addition of NS398 along with decreased invasion. Addition of TGF-beta1 reversed inhibition of NS398 in both cell lines. DmPGE2 augmented invasion in both cell lines without alteration of COX-2. These results suggest that TGF-beta1 can increase invasion and reverse inhibition of COX-2 induced by NS398. We indicate that bone-derived TGF-beta1 might contribute to clinical unsatisfied effect of NSAIDs or COX-2 specific inhibitors adjuvant therapies. Our data provide a new potential therapy for fighting against prostate cancer.

[Study on the neurophysiologic of detrusor overactivity due to partial bladder outflow obstruction].

OBJECTIVE: To study the neurophysiologic of detrusor overactivity (DO) due to partial bladder outflow obstruction (PBOO). METHODS: Twenty four female Wistar rats with DO caused by PBOO were studied simultaneously with ten sham-operated rats. An electrophysiological multi-channel simultaneous recording system was used to record pelvic afferent fiber potentials as well as the pudendal nerve motor branch potentials, external urethral sphincter electromyogram (EUS EMG) and abdominal muscle EMG during filling cystometry. To test the effect of the unstable contraction in DO rats after the decentralization of the central nervous system, DO rats were studied the changes of the unstable contraction after transection of the spinal cord (T(8) level), pelvic nerve, the sympathetic trunk, and the pudendal nerve. RESULTS: The incidence of DO was 62.5% in filling cystometry. During filling cystometry, there are two type of DO contraction according to the changes of pelvic afferent fiber signals, the relevant nerves and muscles responses: the small pressure of the unstable contraction (S-DO) and the big pressure of the unstable contraction (B-DO). For the B-DO, there were significant changes in the recordings of pelvic afferent fiber, the motor branch of the pudendal nerve, EUS EMG, and abdominal muscle EMG. While all these differences have not been recorded during S-DO. Both the filling-voiding cycle and the unstable contraction of B-DO were eliminated and the base line of bladder pressure increased after T(8) spinal cord transection. While the S-DO was not affected by such transection. When bladder relevant nerves were transected by the sequence of the pelvic nerve, the sympathetic trunk, and the pudendal nerve, the filling-voiding cycle was eliminated. The base line of bladder pressure increased significantly. No B-DO was recorded, but the S-DO still existed. CONCLUSION: There are some bladder-genic factors take part in the DO contractions induced by PBOO.

[Efficacy evaluation of intersphincteric resection during anus-preserving operation for ultralow rectal carcinoma].

OBJECTIVE: To evaluate anorectal dynamics, function and efficacy of ultralow rectal carcinoma patients undergone intersphincteric resection(ISR). METHODS: From January 2004 to August 2007, 30 patients with ultralow rectal carcinoma(2.5-4.0 cm distance from anal edge) underwent ISR. All the patients received anorectal manometry before and after operation. The postoperative anal function was evaluated by Williams continence standard and the treatment outcome was followed up. RESULTS: After ISR operation, anal resting pressure, maximum squeeze pressure and maximum tolerance volume of the rectum decreased significantly (all P<0.01) and restored gradually, but not to normal. The rectal anal inhibitory reflex disappeared in 27 patients(90.0%) and was not improved. According to Williams continence standard, 86.7%, 93.3% and 96.7% of patients obtained acceptable anal function in 3, 6, and 12 months after operation respectively. During follow-up of 12 to 44 months, all the patients were still alive and no patient developed pelvis or local recurrence, distant metastasis and anastomotic leakage. Fecal eczema of anus occurred in 10 patients, colonic mucosa prolapse in 2 patients and stenosis of anal canal in one patient. CONCLUSION: ISR for ultralow rectal carcinoma can not only attain radical treatment outcome, but also preserve anal sphincter.

VEGF enhance cortical newborn neurons and their neurite development in adult rat brain after cerebral ischemia.

To study the effect of VEGF overexpression on development of cortical newborn neurons in the brains after stroke, we injected human VEGF(165)-expressive plasmids (phVEGF) into the lateral ventricle of rat brains with a transient middle cerebral artery occlusion (MCAO). An injection of phVEGF significantly promoted angiogenesis (BrdU(+)-von Willebrand's factor(+)) and reduced infarct volume in the rat brain after MCAO. Single labeling of 5'-bromodeoxyuridine (BrdU) and double staining of BrdU with lineage-specific neuronal markers were used to indicate the proliferated cells and maturation of newborn neurons in the brain section of rats at 2, 4, and 8 weeks after MCAO. The results showed that BrdU positive (BrdU(+)) cells existed in ipsilateral frontal cortex within 8 weeks after MCAO and reached the maximum at 2 weeks of reperfusion. The phVEGF treatment significantly increased BrdU(+) cells compared with the control plasmid (pEGFP) injection. Cortical neurogenesis was indicated by the presence of newborn immature (BrdU(+)-Tuj1(+)), newborn mature (BrdU(+)-MAP-2(+)), and newborn GABAergic (BrdU(+)-GAD67(+)) neurons. All these neurons declined within 8 weeks after MCAO in the controls. Injection of phVEGF significantly increased BrdU(+)-Tuj1(+) neurons at 2 weeks, and BrdU(+)-MAP-2(+) neurons and BrdU(+)-GAD67(+) neurons at 4 and 8 weeks, respectively after MCAO. Moreover, phVEGF treatment significantly increased neurite length and branch numbers of BrdU(+)-MAP-2(+) newborn neurons compared with pEGFP treatment. These results demonstrate that VEGF enhances maturation of stroke-induced cortical neurogenesis and dendritic formation of newborn neurons in adult mammalian brains.

[Cigarette smoking affects cyclogeny of spermatogenic cells in rats].

OBJECTIVE: To determine the effects of cigarette smoking on the cyclogeny of spermatogenic cells in rats. METHODS: Rat models of passive smoking were established using a self-made smoking device, and then allocated randomly into two passive smoking groups (A and B, n = 10) and two corresponding control groups (C and D, n = 10). Groups A and B were exposed to cigarette smoke for 8 weeks, followed by the sacrifice of the rats in Groups A and C. And the animals in Groups B and D were killed 48 days after the cessation of passive smoking. The spermatogenesis cycle of each group of rats was detected by flow cytometry, the levels of testosterone (T) and luteinizing hormone (LH) measured by radio-immunity method, and the testis histopathology analyzed by HE staining and transmission electron microscopy. RESULTS: Compared with Group C, Group A showed a significant decrease in the number of spermatids, spermatozoa ([18.76 +/- 3.58]%) and primary spermatocytes ([5.71 +/- 1.18]%) (P < 0.01), but an obvious increase in the spermatogonias ([55.98 +/- 5.35]%, P < 0.01), with a markedly decreased proliferation index ( P < 0.01). The rats of Group A also exhibited pycnosis of spermatocytes, nucleus aberration of Leydig cells, expansion and degranulation of the endoplasmic reticulum, decreased Golgi apparatus, increased lysosomes and fat drops of Sertoli cells, as well as a reduction in the thickness of the wall and the layers of seminiferous tubules and the number of spermatogonia. The T and LH levels were significantly lower in Group A than in C (P < 0.01). After the cessation of passive smoking, a remarkable increase was observed in the percentage of spermatozoa and primary spermatocytes and the levels of serum T and LH in Group B, although the latter were still lower than those of Group D. CONCLUSION: Smoking damages spermatogenic epithelia, Leydig cells and Sertoli cells, reduces the T and LH levels, and block the proliferation of spermatogenetic cells. These changes can be partially reversed after cessation of smoking.

[Morphological study on the role of ICC-like cells in detrusor neuro-modulation of rat urinary bladder].

OBJECTIVE: To investigate the role of ICC-like cells in bladder neuromodulation in rat urinary bladder. METHODS: 14 SD rats and 1 guinea pig were sacrificed in this study. The ultra structural relationships among interstitial cells, nerves and detrusor smooth muscle cells (DSMCs) of urinary bladder were investigated by transmission electron microscopy (TEM). c-kit immunofluorescence was used to identify ICC-like cells in SD rat urinary bladder and the structural relationship between ICC-like cells and nerve terminals was studied by immunofluorescence (double-label). RESULTS: Gap junction between ICC-like cells and DSMCs was confirmed by TEM. ICC-like cells were very close apposition with nerve terminals under TEM. ICC-like cells were identified to exist in sub-urothelium layer, along the longitude of smooth muscle bundles and among detrusor smooth muscle in SD rat urinary bladder by c-kit immunofluorescence. Double-labeled tissue with c-kit and PGP9.5 antibodies also showed that ICC-like cells were very close apposition with nerve terminals in SD rat bladder. CONCLUSIONS: Morphological study indicated that ICC-like cells in rat urinary bladder may play an important role in detrusor neuromodulation. Further study on function will be helpful for elucidating the mechanism of bladder neuromodulation clearly.

Functional integration of newly generated neurons into striatum after cerebral ischemia in the adult rat brain.

BACKGROUND AND PURPOSE: Ischemic injury can induce neurogenesis in the striatum. Those newborn neurons can express glutamic acid decarboxylase and choline acetyltransferase, markers of GABAergic and cholinergic neurons, respectively. The present study investigated whether these GABAergic and cholinergic new neurons could differentiate into functional cells. METHODS: Retrovirus containing the EGFP gene was used to label dividing cells in striatal slices prepared from adult rat brains after middle cerebral artery occlusion. EGFP-targeted immunostaining and immunoelectron microscopy were performed to detect whether newborn neurons could anatomically form neuronal polarity and synapses with pre-existent neurons. Patch clamp recording on acute striatal slices of brains at 6 to 8 weeks after middle cerebral artery occlusion was used to determine whether the newborn neurons could display functional electrophysiological properties. RESULTS: EGFP-expressing (EGFP(+)) signals could be detected mainly in the cell body in the first 2 weeks. From the fourth to thirteenth weeks after their birth, EGFP(+) neurons gradually formed neuronal polarity and showed a time-dependent increase in dendrite length and branch formation. EGFP(+) cells were copositive for NeuN and glutamic acid decarboxylase (EGFP(+)-NeuN(+)-GAD(67)(+)), MAP-2, and choline acetyltransferase (EGFP(+)-MAP-2(+)-ChAT(+)). They also expressed phosphorylated synapsin I (EGFP(+)-p-SYN(+)) and showed typical synaptic structures comprising dendrites and spines. Both GABAergic and cholinergic newborn neurons could fire action potentials and received excitatory and inhibitory synaptic inputs because they displayed spontaneous postsynaptic currents in picrotoxin- and CNQX-inhibited manners. CONCLUSIONS: Ischemia-induced newly formed striatal GABAergic and cholinergic neurons could become functionally integrated into neural networks in the brain of adult rats after stroke.

[Effects of graft and nitrogen supply level on water consumption and water use efficiency of solar greenhouse cucumber under traditional irrigation].

An experiment was conducted in solar greenhouse to study the effects of graft and different nitrogen (N) supply levels (0, 110, and 331 kg k x hm(-2)) on the water consumption and water use efficiency (WUE) of cucumber (Cucumis sativus L.) under traditional irrigation. The results showed that when topdressing 331 kg N x hm(-2), the water consumption of grafted cucumber was the highest, being 3350 m3 x hm(-2) and 2181 m3 x hm(-2) in winter-spring and autumn-winter cropping, so did the WUE, being 27.2 kg x m(-3) and 36.9 kg x m(-3), respectively. Comparing with those of self-rooted cucumber, the water consumption, economic yield, and WUE of grafted cucumber under the same N topdressing levels were increased by 3%-6%, 28%, and 20.9%, respectively, and the water consumption and WUE of grafted cucumber were increased with increasing N supply level. The water consumption of self-rooted cucumber also increased with increasing N supply level, but its WUE was the highest when the N supply was 110 kg graft could markedly promote the water consumption and WUE of cucumber, and the effect was more markedly with increasing N supply level. To increase N supply could also markedly promote the water consumption of self-rooted cucumber, but the WUE would be lower when excessive N was supplied.

Effects of alcohol intake on penile structure and function in rats.

OBJECTIVE: To investigate the effects of alcohol intake on penile structure and function in rats. METHODS: Thirty adult male Wistar rats were randomly divided into two groups: control group and alcohol intake group. They were administered with 2 mL of normal saline and 40% alcohol solution respectively through gastric tubes every day. Three months later, the animal model of alcohol intake was evaluated by modified Nayagida's method, and the effects of alcohol on the rats were studied by sexual behavior, the number of apomorphine-induced penile erection, level of testosterone in the sera, and the content of penile smooth muscle. RESULTS: The scores of animal model of alcohol intake evaluated by Nayagida's method were 0.66 +/- 2.05 in the control group and 9.26 +/- 5.50 in the alcohol intake group (P < 0.05), which indicated that an animal model of alcohol intake was successfully established. Sexual behavior, the number of apomorphine-induced penile erection, testosterone level in the sera, and the content of penile smooth muscle of the alcohol intake group were all statistically different as compared with the control group (P < 0.05). CONCLUSION: Alcohol intake induces sexual dysfunction in rats, which may be due to the decline of testosterone level in the sera and decline of penile smooth muscle.

[Neuroprotective mechanisms of vascular endothelial growth factor].

Vascular endothelial growth factor (VEGF), originally discovered in tumor cells, is an angiogenic factor essential for new blood vessel formation during embryogenesis and in many pathological conditions. There is a growing body of evidence that VEGF can act directly on neurons and plays a new role as a neuroprotective factor via multiple mechanisms. Moreover, VEGF modulates neurogenesis in constitutive neurogenic and non-neurogenic regions of adult mammalian brains, which is a promising therapeutic strategy for neuronal replacement in traumatic brain injury and neurodegenerative diseases. Here, we mainly reviewed the neuroprotection of VEGF against ischemic brain injury and its mechanisms.