A New Practical Method Based on MRI to Individually Localize the Transverse-Sigmoid Sinus Junction in Retrosigmoid Craniotomy: A Retrospective Before-After Study.

Background: Although the asterion has long been used as a skeletal surface marker of the transverse-sigmoid sinuses junction (TSSJ) point in the retrosigmoid approach, abundant evidence shows that the relationship between asterion and TSSJ point varies greatly. In recent years, new technologies have been developed, such as neuronavigation and three-dimensional volume rendering imaging, that can guide in exposing the TSSJ point individually. However, they are not only expensive but also difficult to apply in emergency surgery. Objective: To introduce a quick, practical, and low-cost new method for locating the TSSJ point precisely. Methods: In this retrospective before-after study, the test group located the TSSJ point with our new method during a 6-month period, while the control group used asterion as a surface landmark to estimate the TSSJ during the preceding 6 months. The primary outcome is the immediate exposure rate of the TSSJ point by the initial burr hole. Results: There were 60 patients in both control and test groups as no significant difference in the general clinical characteristics of both groups were observed. The new three-step method significantly increased the TSSJ exposure rate by initial burr hole compared with the control group (96.67% vs. 53.33%, P = 0.0002). Moreover, the total bone loss and craniotomy duration were significantly reduced by the new method. Incidence of sinus injury (10% vs. 6.6%), post-operation infection (3.33% vs. 3.33%), and CSF leakage (3.33% vs. 0%) were similar. Conclusions: The novel three-step approach accurately locates TSSJ points in retrosigmoid craniotomy, reduces bone defects, saves time, and does not increase the risk of sinus injury, infection, and CSF leakage.

Apocynin prevents reduced myocardial nerve growth factor, contributing to amelioration of myocardial apoptosis and failure.

Reduced nerve growth factor (NGF) is associated with cardiac sympathetic nerve denervation in heart failure (HF) which is characterized by increased oxidative stress. Apocynin is considered an antioxidant agent which inhibits NADPH oxidase activity and improves reactive oxygen species scavenging. However, it is unclear whether apocynin prevents reduced myocardial NGF, leading to improvement of cardiac function in HF. In this study, we tested the hypothesis that apocynin prevents reduced myocardial NGF, contributing to amelioration of myocardial apoptosis and failure. Rabbits with myocardial infarction (MI) or sham operation were randomly assigned to receive apocynin or placebo for 4 weeks. MI rabbits exhibited left ventricular (LV) dysfunction, and elevation in oxidative stress, as evidenced by a decreased reduced-to-oxidized glutathione ratio and an increased 4-hydroxynonenal expression, and reduction in NGF and NGF receptor tyrosine kinase A (TrKA) expression in the remote non-infarcted myocardium. Apocynin treatment ameliorated LV dysfunction, reduced oxidative stress, prevented decreases in NGF and TrKA expression and reduced cardiomyocyte apoptosis after MI. In cultured H9C2 cardiomyocytes, hypoxia or hydrogen peroxide decreased NGF expression, and apocynin normalized hypoxia-induced reduction of NGF. Recombinant NGF attenuated hypoxia-induced apoptosis. Apocynin prevented hypoxia-induced apoptosis, and the suppressive effect of apocynin on apoptosis was abolished by NGF receptor TrKA inhibitor K252a. We concluded that apocynin prevented reduced myocardial NGF, leading to attenuation of cardiomyocyte apoptosis and LV remodelling and dysfunction in HF after MI. These findings suggest that strategies to prevent NGF reduction by inhibition of oxidative stress may be of value in amelioration of LV dysfunction in HF.

Research on Treatment of Oily Sludge from the Tank Bottom by Ball Milling Combined with Ozone-Catalyzed Oxidation.

Difficult separation of oil-solid phase and high fine content of the recovered oil were two problems in the treatment of oily sludge from the tank bottom by the hot water-based extraction process. To solve the problems, one technology with "ball milling + ozone-catalyzed oxidation" as the core was studied, and the process parameters of ball milling and ozone-catalyzed oxidation were respectively optimized. After ball milling treatment, the oil content of dry oily sludge decreased from 33.9 to 10.2%. Then, an ozone catalytic oxidation treatment technology with aluminum ore as the catalyst was developed to further treat this stubborn oily sludge. Under the optimal conditions, the oil content of oily sludge could be further reduced to 0.28%, which met the treatment and disposal requirements stipulated in GB4284-2018. For further research on the contribution of the catalyst to the ozone catalytic oxidation system, the reaction activation energy and reaction rates of ozone oxidation and ozone catalytic oxidation were compared from the perspective of kinetics. The results showed that, with the catalyst addition, the reaction rate constants increased about three times and the reaction activation energy reduced 82.26%, which showed the effectiveness of the catalyst on the kinetics quantitatively. The combined process with "ball milling + ozone-catalyzed oxidation" as the core can solve the two problems in the treatment of oily sludge from the tank bottom by hot water-based extraction and provides a reference for the harmless and resourceful treatment of oily sludge from the tank bottom.

A novel 15-spiro diterpenoid dimer from Andrographis paniculata with inhibitory potential against human carboxylesterase 2.

The phytochemical investigation of Andrographis paniculata resulted in the isolation of a novel 15-spiro diterpenoid dimer bisandrographolide G (1). Its structure was determined by 1D and 2D NMR, HRESIMS, electronic circular dichroism (ECD), and TD DFT calculations of ECD spectra. It showed potent inhibitory activity against human carboxylesterase 2 (CES 2) with an IC50 value of 4.61 ± 0.23 µM, and it was defined as a mixed-competitive type inhibitor with a Ki value of 8.88 µM based on the inhibition kinetics result. This finding gave us a hit to develop new generation of human CES 2 inhibitors.

The NADPH oxidase inhibitor apocynin improves cardiac sympathetic nerve terminal innervation and function in heart failure.

NEW FINDINGS: What is the central question of this study? Does NADPH oxidase activation mediate cardiac sympathetic nerve denervation and dysfunction in heart failure. What is the main findings and its importance? Cardiac sympathetic nerve terminal density and function were reduced in heart failure after myocardial infarction in rabbits. The NADPH oxidase inhibitor apocynin prevented the reduction in cardiac sympathetic nerve terminal density and function in heart failure. This suggest that NADPH oxidase activation mediates cardiac sympathetic nerve terminal abnormalities in heart failure. NADPH oxidase may be a potential therapeutic target for cardiac sympathetic denervation and dysfunction in heart failure. ABSTRACT: Congestive heart failure (CHF) is characterized by cardiac sympathetic nerve terminal abnormalities, as evidenced by decreased noradrenaline transporter (NAT) density and cardiac catecholaminergic and tyrosine hydroxylase (TH) profiles. These alterations are associated with increased reactive oxygen species (ROS). NADPH oxidase is a major source of ROS in CHF. In this study, we tested the hypothesis that NADPH oxidase activation mediates cardiac sympathetic nerve terminal abnormalities in CHF. CHF was produced by myocardial infarction (MI) in rabbits. Rabbits with MI or a sham operation were randomized to orally receive an NADPH oxidase inhibitor, apocynin (6 mg kg-1  day-1 ), or placebo for 30 days. MI rabbits exhibited left ventricular dilatation, systolic dysfunction, and increases in NADPH oxidase activity and 4-hydroxynonenal expression in the remote non-infarcted myocardium, all of which were prevented by treatment with apocynin. Cardiac catecholaminergic histofluorescence profiles and immunostained TH and PGP9.5 expression were decreased, and the decreases were ameliorated by apocynin treatment. NAT, TH and PGP9.5 protein and mRNA expression were reduced and the reduction was mitigated by apocynin treatment. The effects of apocynin were confirmed by utilizing the NADPH oxidase inhibitor diphenyleneiodonium in a separate experiment. In conclusion, the NADPH oxidase inhibitor apocynin attenuated increased myocardial oxidative stress and decreased cardiac sympathetic nerve terminals in CHF after MI in rabbits. These findings suggest that the activation of NADPH oxidase mediates cardiac sympathetic nerve terminal abnormalities in CHF, and the inhibition of NADPH oxidase may be beneficial for the treatment of heart failure.

[Effects of bergapten on damages of osteocytes MLO-Y4 induced by TCP wear particles and its mechanism].

OBJECTIVE: To study the effects of bergapten (BP) on damages of osteocytes MLO-Y4 induced by tricalcium phosphate (TCP) wear particles and its mechanism. ;Methods: MLO-Y4 cells were treated with TCP wear particles for 48 h to establish the model of osteocytes injuries in vitro. The MLO-Y4 cells were divided into the following five groups: control group, TCP wear particles treated (0.1 mg/ml) group, bergapten (1, 5 and 20 µmol/L) treated groups. MTT assay and Calcein-AM staining were used to determine the viability of MLO-Y4 cells; Hoechst 33342 staining and the flow cytometry were applied to detect the apoptosis of MLO-Y4; real-time PCR was performed to examine the mRNA levels of dentin matrix protein1 (DMP-1), sclerostin (SOST) and fibroblast growth factor23 (FGF23); Western blot was performed to examine protein expressions of glucose-regulated protein 78 (GRP78), protein kinase R-like ER kinase (PERK) phospho-PERK (p-PERK), eukaryotic initiation factor 2α (eIF2α), phospho-eIF2α (p-eIF2α), activating transcription factor 4 (AFT4), C/EBP homologous protein (CHOP) and caspase-3 in MLO-Y4 cells. ;Results: Compared with control group, the MLO-Y4 viability and DMP-1 mRNA level in TCP group were decreased significantly (P＜0.05), while the percentage of apoptosis and mRNA levels of SOST and FGF23 were obviously increased (P＜0.05), and protein expressions of GRP78, AFT4, CHOP, p-PERK/PERK and p-eIF2α/eIF2α were up-regulated significantly in MLO-Y4 cells (P＜0.05). Compared with TCP group, the damages of MLO-Y4 and cell apoptosis in bergapten treated groups were decrease obviously (P＜0.05), the expressions of GRP78, AFT4, CHOP, p-PERK/PERK and p-eIF2α/eIF2α were down-regulated remarkably (P＜0.05). ;Conclusion: Bergapten can inhibit osteocytes damages induced by TCP wear particles, which may be related to reducing ER stress and PERK pathway activation.

Antioxidant N-acetylcysteine inhibits maladaptive myocyte autophagy in pressure overload induced cardiac remodeling in rats.

Increased oxidative stress and myocyte autophagy co-exist in cardiac remodeling. However, it is unclear whether oxidative stress mediates maladaptive myocyte autophagy in pathological ventricular remodeling. In this study, we tested the hypothesis that antioxidants prevent maladaptive myocyte autophagy in pressure overload-induced left ventricular (LV) remodeling. Sprague-Dawley rats underwent abdominal aortic constriction (AAC) or sham operation. The animals were randomized to receive an antioxidant N-acetylcysteine (NAC), an autophagy inhibitor 3-methyladenine (3-MA) or placebo treatment for 2 weeks. We measured LV structure and function by echocardiography and hemodynamics, myocyte autophagy and oxidative stress assessed by 8-hydroxy-2-deoxyguanosine (8-OHdG). AAC rats exhibited increased LV hypertrophy assessed by LV wall thickness and myocyte cross-sectional area. NAC prevented LV hypertrophy in AAC rats. There were no significant differences in LV fractional shortening, end-diastolic dimension and the maximal rate of LV pressure rise among the groups. AAC rats showed an increase in myocardial 8-OHdG that was prevented by NAC. The expression of LC3 II protein, a marker of autophagy, was increased at 2 weeks after AAC. Immunohistochemical scores further confirmed the increase in LC3 expression in AAC rats. The expression of autophagic proteins Beclin1 and Atg12 and ERK activity were also increased in AAC rats. NAC prevented the increases in LC3 II protein, LC3 scores, Beclin1, Atg12 and ERK activity in AAC rats. Inhibition of autophagy by 3-MA prevented LV hypertrophy after pressure overload. These findings suggest that antioxidants may be of value to prevent pressure overload-induced cardiac remodeling through inhibition of maladaptive myocyte autophagy.

Effect of adenosine on GLAST expression in the retina of a chronic ocular hypertension rat model.

This study was performed to evaluate the effect of adenosine and an adenosine receptor antagonist on the expression of the L-glutamate/L-aspartate transporter (GLAST) in the retina of a chronic ocular hypertension (COH) rat model. COH models were established via the cauterization of three episcleral veins. Measurements of the intraocular pressure of the right eye (COH eye) were taken weekly by a handheld digital tonometer. A total of 10 µM adenosine or 10 µM adenosine + 100 nM SCH442416 solution (2 µl) was injected into the rat vitreous space. The reverse transcription-quantitative polymerase chain reaction, western blotting and immunohistochemistry were used to detect GLAST expression. Compared with the COH group, GLAST mRNA expression was decreased by 33.6% in the group treated with adenosine (n=6, P=0.020) and was increased by 159.6% in the group treated with SCH442416 (n=6, P=0.001). Administration of adenosine decreased GLAST protein expression by 34.7% (n=6, P<0.001), while treatment with the adenosine A2A receptor antagonist SCH442416 increased GLAST protein expression by 48.3% compared with the control COH group (n=6, P<0.001). Immunohistochemical experiments showed that administration of adenosine decreased GLAST protein expression, as compared with expression in the control COH rat retina. Administration of SCH442416 markedly increased GLAST protein expression. The results of the present study may provide a novel method for retinal neuron protection.

The effect of ROCK-1 activity change on the adhesive and invasive ability of Y79 retinoblastoma cells.

BACKGROUND: Retinoblastoma (Rb) is the most common intraocular tumor in childhood worldwide. It is a deadly pediatric eye cancer. The main cause of death in Rb patients is intracranial and systemic metastasis. ROCK is the main downstream effector of Ras-homologous (Rho) family of GTPases which are involved in many cellular functions, such as cell proliferation, invasion and metastasis. Overexpression of ROCK promotes invasion and metastasis of many solid tumors. However, the effect of ROCK in Rb is largely unknown. METHODS: ROCK-1 and ROCK-2 mRNA expression in Y79 cell lines were examined by RT-PCR. Protein expression in the Y79 cell line were examined by western blot analyses. ROCK-1 and ROCK-2 siRNA were transfected into Y79 cells with Lipofectamine 2000. Cell proliferation was evaluated by CCK-8 assay after exposure to ROCK inhibitor (Y-27632). We examined the effect of ROCK inhibitors (Y-27632, ROCK-1 and ROCK-2 siRNA) on Y79 cell adhesive capacity by cell adhesion assay. Cell invasion assay through matrigel was used to study the effect of ROCK inhibitors on Y79 cell invasive capacity. RESULTS: The expression of mRNA of ROCK-1 was more than that of ROCK-2 in the Y79 cell line. The protein expression levels of ROCK-1 and ROCK-2 were downregulated in the cells transfected with siRNA. Y-27632 treatment didn't lead to any changes of Y79 cells proliferation. Adhesive ability of Y79 cells was enhanced following Y-27632 or ROCK-1 siRNA treatment. The invasive capacity of Y79 cells showed an inverse relationship with increasing Y-27632 concentration. Invasiveness of Y79 cells also decreased in Y79 cells transfected with ROCK-1 siRNA. However, there was no change in adhesive ability or invasive capacity in Y79 cells transfected with siRNA against ROCK-2. CONCLUSIONS: The findings of this study demonstrate that ROCK-1 protein plays a key role in regulating metastasis and invasion of Y79 cells, suggesting that the ROCK-1 dependent pathway may be a potential target for therapy of Rb.

Effect of Y-27632 on the cultured retinal neurocytes of rats.

AIM: To investigate the effect of Y-27632 on the survival and neurite outgrowth of the cultured retinal neurocytes. METHODS: After the postnatal day 2-3, Sprague-Dawley retinal neurocytes were cultured for 48 hours, the culture media was replaced with serum-free media (control group) and serum-free media contained 30µmol/L Y-27632 (Y-27632 group), and the cells were continually cultured another 48 hours. The cultured retinal neurocytes were identified with anti-neuron specific enolase (NSE) immunocytochemistry. The survival state of those cells was estimated by MTT assay, and the neurite outgrowth of those cells was evaluated by the computerized image-analysis system. RESULTS: Compared with the control group, the absorbance values of cells survival in Y-27632 group increased 12.90% and 33.33% respectively after 72 and 96 hours culture. Y-27632 had no significant effect on the diameter of cultured retinal neurocytes. Compared with the control group, Y-27632 induced a stable improvement of neurite outgrowth of retinal neurocytes after 72 and 96 hours culture (P=0.001). CONCLUSION: Y-27632 could promote the survival and neurite outgrowth of the early postnatal cultured retinal neurocytes.

Evaluation of a partial optic nerve crush model in rats.

This study was performed to determine whether a partial optic nerve crush (PONC) model in rats is effective and reliable for the study of optic nerve protection and regeneration. Bilateral superior colliculus (SC) retrograde 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI) labeling of retinal ganglion cells (RGCs; n=3) and unilateral SC retrograde labeling of RGCs (n=3) were performed in adult Sprague-Dawley (SD) rats and the results were compared with the bilateral and unilateral SC retrograde-labeled RGCs. Another 40 adult SD rats, three days after bilateral SC retrograde DiI labeling of RGCs underwent crushing with a non-invasive vascular clip (40 gram power) 1 mm behind the right optic nerve head for 5, 10 and 30 sec (n=10 each), and a sham-operated control group (n=10) was used as a control. The retinas of all 40 rats were flattened by four radial cuts, mounted vitreal side-up on gelatin-coated slides, and the number of labeled RGCs was counted in four distinct regions per retinal quadrant at three different eccentricities of 1/6, 3/6 and 5/6 of the retinal radius three days later. Bilateral SC retrograde DiI injection labeled the majority of normal RGCs, while unilateral SC injections only labeled a small part of the RGCs; the majority of RGCs were not labeled. In the mild crush (5 sec) injury group, the bilateral SC retrograde DiI injection labeled the majority of RGCs. The RGC densities at 1/6, 3/6 and 5/6 of the retinal radius showed no significant difference compared with the RGC densities at the corresponding region of the retinal radius in the sham-operated control group (P=0.734, 0.461, 0.273, respectively). In the moderate crush injury (10 sec) group, the number of labeled RGCs was significantly lower compared to that of the sham-operated control group, and the RGC densities at 1/6, 3/6, 5/6 of the retinal radius were significantly lower compared to the RGC densities at the corresponding retinal radius in the sham-operated control group (P<0.001). In the severe crush injury (30 sec) group the number of labeled RGCs was significantly decreased, and the labeled RGCs were not observed in the region at 5/6 of the retinal radius. The RGC densities at 1/6 and 3/6 of the retinal radius were significantly lower compared to the RGC densities at the corresponding retinal radius region in the sham-operated control group (P<0.001). Compared with the mild and severe optic nerve crush injury models, the moderate crush injury model is more suitable for the study of optic nerve damage and regeneration.

Impact of positive end-expiratory pressure on cerebral injury patients with hypoxemia.

BACKGROUND: Traumatic brain injury or intracranial hemorrhage patients with acute lung injury/acute respiratory distress syndrome need mechanical ventilation. The use of positive end-expiratory pressure (PEEP) in this situation remains controversial. This study explored the impact of PEEP on intracranial pressure (ICP), cerebral perfusion pressure (CPP), central venous pressure (CVP), and mean arterial pressure (MAP) in cerebral injury patients. METHODS: Nine cerebral injury patients with lung injury who needed mechanical ventilation and met the criteria for ICP monitoring were included in this study. Intraventricular catheters were positioned in 1 of the bilateral ventricles and connected to pressure transducers. Invasive arterial pressure and CVP were monitored continuously. Pressure control ventilation was applied during this clinical trial in a stepwise recruitment maneuver (RM) with 3 cm H2O intermittent increments and decrements of PEEP. RESULTS: A total of 28 RMs were completed in 9 patients. Mean values of MAP, CVP, ICP, and CPP 5 minutes after RMs showed no significant differences compared with baseline (P > 0.05). Correlation analysis of all the mean values of MAP, CVP, ICP, and CPP showed significant correlation between MAP and CPP, PEEP and CVP, PEEP and ICP, and PEEP and CPP with all P values less than 0.05. CONCLUSION: The impact of PEEP on blood pressure, ICP, and CPP varies greatly in cerebral injury patients. Mean arterial pressure and ICP monitoring is of benefit when using PEEP in cerebral injury patients with hypoxemia.

[The impact of positive end-expiratory pressure on cerebral perfusion pressure and hemodynamics in patients receiving lung recruitment maneuver].

OBJECTIVE: To explore the impact of lung recruitment maneuver (RM) on intracranial pressure (ICP), cerebral perfusion pressure (CPP) and mean arterial pressure (MAP). METHODS: RM was performed and ICP, MAP, central venous pressure (CVP), saturation of arterial oxygen (SpO2) were monitored continuously in 6 severe cerebral injury patients combined with lung injury, who were indicated for mechanical ventilation and meeting the criteria for intracranial pressure monitoring. RM included pressure control ventilation with stepwise increase in positive end-expiratory pressure (PEEP). RESULTS: RM was performed for 22 times in 6 patients, among them two were moribund due to sharp drop of blood pressure and CPP. In the remaining 20 attempts, the mean values of MAP, CVP, ICP, CPP measured at each PEEP level showed no significant difference compared with baseline values (all P>0.05). MAP was significantly correlated with CPP (r=0.706, P=0.000). In the remaining RMs, a correlation between MAP and CPP accounted for 85% (17/20) of total RMs, that between PEEP and CVP accounted for 75% (15/20), that between PEEP and ICP accounted for 75% (15/20), and that between PEEP and CPP existed in 40% (8/20). In a total of 22 cases, there were 6 patterns of response of MAP to alteration in PEEP: MAP maintained relatively stable in 8 case, MAP decreased when PEEP increased and increased when PEEP decreased in 6 case; in 2 cases MAP elevated with increase in PEEP, and drop to baseline with decrease in PEEP, in 2 cases it fell with increase in PEEP but it did not rise with decrease in PEEP, in 2 cases it rose with increase in PEEP but remained at a high level with PEEP decreased to baseline, in 2 cases, MAP dropped abruptly with increase in PEEP resulting in termination of RM. In 11 cases, ICP increased with increase in PEEP and decreased with lowering of PEEP. ICP maintained stable in 6 cases, and ICP maintained at a high level and did not return to baseline after RM in 3 cases. CPP decreased with increase in PEEP and increased when PEEP decreased, and it returned to baseline when PEEP was back to baseline in 12 case. CPP kept constant in 6 case. In 2 cases, CPP remained at a low level, and it returned to baseline 10-20 minutes after PEEP was lowered to baseline. CONCLUSION: There is considerable individual difference in impact of RM on MAP, ICP and CPP in patients with cerebral. ICP monitoring is helpful to assure safety of RM in patients with cerebral injury complicated with lung injury.

[The analysis of 252 episodes of recruitment maneuver during mechanical ventilation in surgery intensive care unit].

OBJECTIVE: To analyze the clinical effects of recruitment maneuver and the impacts on blood pressure and oxygen saturation in patients with mechanical ventilation. METHODS: To analyze all related data from 252 episodes of recruitment maneuver of 46 patients admitted from July 2005 to February 2007. Recruitment maneuver method: the drive pressure constant was kept at 15 cm H(2)O (1 cm H(2)O=0.098 kPa) and the positive end-expiratory pressure (PEEP) level was increased gradually. RESULTS: Of the 252 episodes of recruitment maneuver, this procedure was effective in 91% of the patients, with pneumothorax and pneumo-mediastinum occurred in a patient with legionnaire pneumonia, and no improvement of oxygen saturation in one patient with patent foramen ovale. The value of effective PEEP used ranged from a minimum of 8 cm H(2)O to a maximum of 30 cm H(2)O and the duration of satisfactory oxygen saturation ranged from a minimum of 0.4 hour to a maximum of 368 hours. On average, each patient received 5.48 episodes of recruitment maneuver with one of the patients received 16 episodes of recruitment maneuver. Twenty-three out of the 46 patients (50%) had experienced an episode of hypoxemia. One hundred and one episodes of hypoxemia occurred in 252 recruitment maneuver (40%) and the minimum PEEP inducing hypoxemia is 8 cm H(2)O, and the maximum PEEP was 22 cm H(2)O, with an average value of 12.7 cm H(2)O. Twenty-five of the 46 patients (54%) had experienced transient hypotension with 93 episodes of hypoxemia in 252 episodes of recruitment maneuver (37%), and the minimum PEEP inducing hypotension was 6 cm H(2)O and the maximum PEEP was 23 cm H(2)O, with an average value of 13.9 cm H(2)O. CONCLUSION: Recruitment maneuver could effectively improve oxygenation while the value of PEEP used should be individualized according to clinical condition.

[Perioperative nitric oxide inhalation therapy for open heart surgery patients with pulmonary hypertension].

OBJECTIVE: To investigate effectiveness and safety of perioperative nitric oxide (NO) inhalation therapy for open heart surgery patients with pulmonary hypertension. METHODS: Servo 300A and Pulmonox Aeronox were used for NO delivery and monitoring. NO was used perioperatively in 27 adult and 1 pediatric open heart surgery patients with pulmonary hypertension which were not effectively relieved by conventional treatment. At the beginning of NO inhalation therapy, the dose of NO was (5-10) x 10(-6), and mildly elevated to 20 x 10(-6). Pulmonary arterial pressure (PAP), arterial pressure (AP), pulmonary vascular resistance (PVR) and oxygenation index (PaO(2)/FiO(2)) of patients were monitored before and after treatment. Criterion for NO responsiveness was: AP/PAP or PaO(2)/FiO(2) improved more than 20% within 1 hour. NO inhalation therapy was discontinued if there was no response within 1.5 hours. RESULTS: Responsive rate in these adult patients was 77.8% (21/27 cases). Duration of NO therapy was 12-96 (32.6+/-10.3) hours. One 4-year-old atrial septal defect child with medium severity of pulmonary artery hypertension showed deterioration of pulmonary hypertension with serious hypoxemia [PaO(2)/FiO(2)=40 mm Hg (1 mm Hg=0.133 kPa), fractional concentration of inspired oxygen (FiO(2)) was 1.00] post operatively. NO inhalation therapy showed a very marked response and effect. The child was weaned from mechanical ventilation in four days. No adverse event was detected in patients and caregivers during and after NO inhalation therapy. CONCLUSION: NO inhalation therapy is effective in cardiac surgery patients with deteriorating pulmonary artery hypertension perioperatively. Further clinical investigation is urgently needed for promoting it to become a clinical routinely available therapy.

[Experimental study of fast diagnosis of mycotic keratitis using molecular biology technical].

OBJECTIVE: To establish a method for fast diagnosis of mycotic keratitis using multi-PCR system. METHODS: Detecting 9 important medical fungi species (Fusarium solani, Fusarium moniliform, Fusarium equiseti, Fusarium graminum, Aspergillus fumigatus, Aspergillus flavus, Aspergillus niger, Penicillium implicatum and Curvularia lunata) through a multi-PCR system. This method was used to identify the clinical cultured isolates and clinical samples. RESULTS: In this multi-PCR system, Fusarium species amplified a fragment of 360 bp, Aspergillus species amplified a fragment of 430 bp, Penicillium implicatum species amplified a fragment of 245 bp, and Curvularia lunata species amplified a fragment of 300 bp. Human DNA and DNA of other microorganism in human ocular infection obtained negative results in this multi-PCR system. The sensitivity of the multi-PCR system was 10 fg. CONCLUSIONS: Important clinical fungi could be detected and identified by the multi-PCR system. The multi-PCR method was proved to be a fast, sensitive and specific technology and has a good prospect in clinical application.