Exploration of optimal disinfection model based on groundwater risk assessment in disinfection process.

Under the influence of different types of disinfectants and disinfection environments, the removal level of pathogens and the formation potential of disinfection by-products (DBPs) will have a dual impact on the groundwater environment. The key points for sustainable groundwater safety management are how to balance the positive and negative relationship and formulate a scientific disinfection model in combination with risk assessment. In this study, the effects of sodium hypochlorite (NaClO) and peracetic acid (PAA) concentrations on pathogenic E. coli and DBPs were investigated using static-batch and dynamic-column experiments, as well as the optimal disinfection model for groundwater risk assessment was explored using quantitative microbial risk assessment and disability-adjusted life years (DALYs) models. Compared to static disinfection, deposition and adsorption were the dominant factors causing E. coli migration at lower NaClO levels of 0-0.25 mg/L under dynamic state, while disinfection was its migration factor at higher NaClO levels of 0.5-6.5 mg/L. In contrast, E. coli removed by PAA was the result of the combined action of deposition, adsorption, and disinfection. The disinfection effects of NaClO and PAA on E. coli differed under dynamic and static conditions. At the same NaClO level, the health risk associated with E. coli in groundwater was higher, whereas, under the same PAA conditions, the health risk was lower. Under dynamic conditions, the optimal disinfectant dosage required for NaClO and PAA to reach the same acceptable risk level was 2 and 0.85 times (irrigation) or 0.92 times (drinking) of static disinfection, respectively. The results may help prevent the misuse of disinfectants and provide theoretical support for managing twin health risks posed by pathogens and DBPs in water treatment.

Development and Verification Experiment of In-Situ Friction Experiment Device for Simulating UV Irradiation in Space.

In order to explore the influence of space ultraviolet radiation on spacecraft lubricating materials, an in-situ friction experimental device simulating space ultraviolet radiation was developed in the laboratory, and the experimental verification was carried out. This paper firstly introduced the design index, structure and working principle of the space ultraviolet irradiation simulation device, and then calibrated and tested the parameters of the whole device, and also conducted a virtual operation of the device's operation effect by simulation software, and the results showed that it met the design index. Finally, the validation tested of the ultraviolet irradiated in-situ friction experimental device were described in detail. By using the device to irradiate the samples, it was found that the in-situ ultraviolet irradiation device could achieve the expected irradiation effect, and the irradiation would lead to changes in the surface structure and properties of the PTFE material, while also achieving the need for in-situ spatial friction property testing of the material, providing favorable conditions for future testing.

Research on Atomic Oxygen Erosion Influence of Structural Damage and Tribological Properties of Mo/MoS2-Pb-PbS Thin Film.

To investigate atomic oxygen effects on tribological properties of Mo/MoS2-Pb-PbS film and further enlarge application range, atomic oxygen exposure tests were carried out for 5 h, 10 h, 15 h, and 20 h by the atomic oxygen simulator with atomic oxygen flux of 2.5 × 1015 atoms/cm2·s. The exposure time in test was equivalent to the atomic oxygen cumulative flux for 159.25 h, 318.5 h, 477.75 h, and 637 h at the height of 400 km in space. Then, the vacuum friction test of Mo/MoS2-Pb-PbS thin film was performed under the 6 N load and 100 r/min. By SEM, TEM, and XPS analysis of the surface of the film after atomic oxygen erosion, it was observed that atomic oxygen could cause serious oxidation on the surface of Mo/MoS2-Pb-PbS film, and the contents of MoS2, PbS, and Pb, which were lubricating components, were significantly reduced, and oxides were generated. From AES analysis and the variation in the main element content, Mo/MoS2-Pb-PbS thin film showed self-protection ability in an atomic oxygen environment. Hard oxide generated after atomic oxygen erosion such as MoO3 and Pb3O4 could cause the friction coefficient slight fluctuations, but the average friction coefficient was in a stable state.

Role of carbon and nutrient exports from different land uses in the aquatic carbon sequestration and eutrophication process.

The hydrochemical features affected by differing land uses play a key role in regulating both the primary production of aquatic photosynthetic organisms and the formation of autochthonous organic carbon (AOC); this impacts eutrophication and the global carbon cycle. In shallow water environments where phytoplankton and submerged plants coexist, the C-N-P limitations on the primary production of these aquatic organisms, and the mechanisms by which they promote the formation of AOC are poorly understood. In this study, over the hydrological year September 2018 to August 2019, a large-scale field simulation experiment at the Shawan Karst Test Site (SW China) with various types of land use was systematically conducted to investigate the C-N-P limitations on the primary production of phytoplankton and submerged plants. The results indicate that (1) phytoplankton are co-limited by nitrogen (N) and phosphorus (P) but with the N more important, while submerged plants are limited by carbon (C); (2) Chlorophyta and Bacillariophyta display a stronger competitive advantage than Cyanophyta in aqueous environments with high C but low N-P; (3) there is a seasonal difference in the contribution of phytoplankton and submerged plants to the formation of AOC, however, throughout the year, the contributions of phytoplankton (27%) and submerged plants biomass (28%) to AOC concentrations in the water were similar, combinedly accounting for approximately 17% of the formed AOC. It is concluded that natural restoration of vegetation, or injecting CO2 into water, which results in higher C but lower N-P loadings, may simultaneously help to mitigate eutrophication (with changes in biological structure and species) and increase C sequestration in surface waters.

The ballast effect controls the settling of autochthonous organic carbon in three subtropical karst reservoirs.

The change in hydrodynamics by damming facilitates the terrestrial biological­carbon-pump (BCP) effect and promotes the generation and burial of autochthonous organic carbon (OCauto). To constrain the burial fluxes of OCauto is crucial when assessing the role of inland waters in the global carbon cycle as OCauto originating mainly from weathering-derived dissolved inorganic carbon is overlooked in current global carbon budgeting. Here we examined the elemental and carbon isotopic compositions of the settling organic matter collected by sediment traps in three subtropical karst reservoirs (Hongfenghu, Pingzhai and Puding), SW China. The results show that 30- 60% of the settling OC in the studied reservoirs is autochthonous. The proportion of OCauto correlates inversely with OC's settling flux. Interestingly, Hongfenghu Reservoir, featured by the highest trophic state and POC concentration, has the highest fraction of OCauto but the lowest settling flux of OCauto among three reservoirs. The ballast effect of biogenic silica and lithogenic materials, rather than the aquatic primary productivity, is supposed to be the primary factor that governs the settling flux of OCauto in the studied reservoirs. Finally, it is estimated that the settling flux of OCauto in the three reservoirs is 47- 119 g C/m2/yr while the burial flux of OCauto is 10- 26 g C/m2/yr if assuming about 80% of OCauto is remineralized after sedimentation. This study demonstrates for the first time the role of biogenic silica and lithogenic materials' input in reservoir OC's settling which may be the further important due to the strengthening agricultural activity and the increasing fast-flow hydroelectric reservoirs.

Roflumilast, a phosphodiesterase-4 inhibitor, improves hyperoxia-induced lung injury via anti-inflammation.

Roflumilast is an inhibitor of phosphodiesterase-4 (PDE4) and can suppress the hydrolysis of cAMP in inflammatory cells, conferring anti-inflammatory effects. This study aimed to investigate the protective effects of roflumilast on hyperoxia-induced acute lung injury (HALI) in a rat model. Male Sprague-Dawley rats were randomly assigned into: control group; HALI group; 2.5 mg/kg roflumilast group; and 5 mg/kg roflumilast group. Rats were pressurized to 250 kPa with pure oxygen to induce lung injury. In the roflumilast groups, rats were orally administered with roflumilast at 2.5 or 5 mg/kg once before hyperoxia exposure and once daily for two days after exposure. Rats were sacrificed 72 hours after hyperoxia exposure. The lung tissues were collected for the detection of lung water content, inflammatory cytokines and NF-κB/p-NF-κB protein expression, and the bronchoalveolar lavage fluid was harvested for the measurement of protein concentration and lactate dehydrogenase activity. Results showed roflumilast at different doses could significantly reduce lung edema, improve lung pathology and reduce the expression of inflammatory cytokines in the lung. The protective effects seemed to be related to the dose of roflumilast. Our study indicates roflumilast has the potential as a medication for the treatment of HALI.

Neurocognitive sequelae after carbon monoxide poisoning and hyperbaric oxygen therapy.

Carbon monoxide (CO) has been the leading cause of poisoning mortality in many countries and hyperbaric oxygen (HBO) is a widely accepted treatment for CO poisoning. However, some patients with CO poisoning will still develop neurocognitive sequelae regardless of HBO therapy, which can persist since CO poisoning or be present days to weeks after a recovery from CO poisoning. HBO has been used in the prevention and treatment of neurocognitive sequelae after CO poisoning, and some mechanisms are also proposed for the potential neuroprotective effects of HBO on the neurocognitive impairment after CO poisoning, but there is still controversy on the effectiveness of HBO on neurocognitive sequelae after CO poisoning. In this paper, we briefly introduce the neurocognitive sequelae after CO poisoning, summarize the potential predictive factors of neurocognitive sequelae, and discuss the use of HBO in the treatment and prevention of neurocognitive sequelae after CO poisoning.

Association between tea consumption and gastroesophageal reflux disease: A meta-analysis.

BACKGROUND: Gastroesophageal reflux disease (GERD) is one of the most common digestive system diseases, which is associated with lifestyle and dietary factors. The main mechanism involved in GERD is affected by demographics, lifestyles, and dietary factors. Tea consumption is reported to be associated with GERD, especially in Asian population. However, the effect of tea drinking on GERD risk is still controversial. The aim of this study was to investigate the relationship between tea consumption and the risk of GERD by meta-analysis. METHODS: We searched the published research databases such as PubMed and Embase for studies that were published up to March 2018. The search results were reviewed by 2 authors, and studies that complied with the criteria were selected. Odds ratio (OR) and 95% confidence interval (CI) were used to assess the association between tea consumption and the risk of GERD. RESULTS: Twenty-three articles including 30 studies were included in the meta-analysis. The result of meta-analysis showed that tea drinking had no significant association with the risk of GERD. The odds ratio (OR) and 95% CI were 1.12 and (0.98-1.27). In subgroup analysis based on geographical region, tea consumption can increase the risk of GERD in East Asia (OR = 1.27, 95% CI = 1.07-1.51), while the risk of GERD was decreased in Middle Asia (OR = 0.77, 95% CI = 0.63-0.95). Besides, in the subgroup of study design, there was a significant association between tea intake and the GERD in cross-sectional study. In no symptom subgroup, the risk of GERD was increased (OR = 1.47, 95% CI = 1.11-1.93). CONCLUSIONS: There was no significant relationship between tea consumption and the risk of GERD overall. However, in subgroup analysis, tea drinking may increase the risk of GERD in East Asia and decrease in Middle Asia. To clarify the causality between tea intake and GERD, a more precise study design will be needed.

Clinicopathologic Characteristics of Thyroid-like Low-grade Nasopharyngeal Papillary Adenocarcinoma: A Case Report.

Thyroid-like low-grade nasopharyngeal papillary adenocarcinoma (TL-LGNPPA) is an extremely rare neoplasm. It morphologically resembles papillary thyroid carcinoma and is immunochemically positive for thyroid transcription factor 1. Herein, we reported a case of TL-LGNPPA in a female patient of 35 years old. She felt pharyngeal foreign body sensation of unknown cause and subsequently developed dyspnea after activities. Nasopharyngeal plain computerized tomography showed no abnormalities, but laryngoscopy showed a peanut-sized smooth neoplasm with a pedicel at the posterior edge of the nasal septum. The mass was completely resected by nasopharyngoscopy. Histologic examination showed the tumor was composed of papillary configuration and tubular glands; each papilla was covered with cuboidal or columnar epithelial cells; tubular architecture and spindle cell component were also observed; some tumor cells had psammoma bodies. Immunohistochemically, tumor cells were positive for CKpan, CK7, CK19, VIM, and thyroid transcription factor 1, but negative for thyroglobulin, CK20, S-100, P63, P40, smooth muscle actin, CDX-2, and glial fibrillary acidic protein. This patient was diagnosed with TL-LGNPPA and followed up for 16 months, and metastasis and recurrence were not observed.

Unusual location of the glomus tumour in the liver: A case report and literature review.

RATIONALE: Liver glomus tumor is very rare, and only 6 cases have been reported. Herein, we report another case of liver glomus tumor and the clinicopathological features are summarized. PATIENT CONCERNS: An 18-year-old male patient was admitted due to hypertension and arrhythmia for 4 days. DIAGNOSES: Abdominal enhanced CT revealed a 6.0-cm solid and cystic mass in the left liver lobe. The mass was collected by hepatic lobectomy. Microscopically, the tumor cells were round or oval, and had no malignant features and no evident atypia. Immumohistochemically, tumor cells were positive for positive for SMA and vimentin, but partially positive for syn, CD34 and desmin. He was pathologically diagnosed with liver glomus tumor. INTERVENTIONS: The patient underwent a left hepatic lobectomy. OUTCOMES: After surgery, this patient was followed up for 6 months, and metastasis/recurrence was not observed. LESSONS: Primary liver glomus tumor has no specific clinical manifestations, and imaging examinations have limitations for its diagnosis. Immunostaining for SMA and vimentin is necessary to prove the diagnosis. Complete resection is strongly advised and it has a favorable prognosis.

Sigma-1 receptor (σ1R) is downregulated in hepatic malignant tumors and regulates HepG2 cell proliferation, migration and apoptosis.

Sigma-1 receptor (σ1R), an important transmembrane structural protein, has been demonstrated to be overexpressed in various types of human cancer, and has been confirmed to be involved in many biological behaviors during tumorigenesis and tumor progression. The aim of the present study was to explore the essential role of σ1R in hepatic malignant tumors (HMTs), which, to the best of our knowledge, has not been reported to date. We assessed σ1R expression in hepatocellular carcinoma (HCC) tissues and found that σ1R was significantly decreased in HCC when compared with that in benign liver tissues (P<0.01). Additionally, the expression of σ1R was shown to be inversely correlated with HCC grade (r=-0.424, P=0.021, Kendall's τ-b-test). We further used a FLAG­SV40­neomycin­plasmid strategy to increase σ1R expression in the HepG2 hepatoblastoma cell line. Overexpression of σ1R impaired cell proliferation, inhibited cell migration, induced cell cycle arrest at G1 phase, and increased cell apoptosis in vitro. Furthermore, overexpression of σ1R decreased the expression levels of STAT-3 and NF-κB, which provided insight into the underlying mechanisms of σ1R-associated HMT development and progression. These findings suggest that the decreased expression of σ1R plays an essential role in hepatic tumorigenesis, and that it may serve as a potential predictive factor and therapeutic target for the treatment of HMTs.

Macrophage polarization is related to the pathogenesis of decompression induced lung injury.

Studies have shown that blood bubbles may be detectable and there is ultrasonic evidence of acute interstitial lung edema even after diving without protocol violation. Macrophages play a central role in the inflammation, and macrophage polarization is closely related to the pathogenesis some lung diseases. Available findings indicate that decompression may induce the production of pro-inflammatory cytokines, chemokines, and adhesion molecules in the blood and tissues, which are associated with the macrophage polarization, and hyperbaric treatment may exert therapeutic effects on decompression related diseases via regulating these factors. Thus, we hypothesize that the polarization of circulating and/or resident macrophages is involved in the pathogenesis of decompression induced lung injury.

Changes in angiotensin II and angiotensin-converting enzyme of different tissues after prolonged hyperoxia exposure.

Current study findings concerning changes in the renin-angiotensin system (RAS) in cases of hyperoxic acute lung injury (HALI) have shown conflicting results. This study aimed to detect the angiotensin II (Ang II) and angiotensin-converting enzyme (ACE) in a rat HALI model. Healthy male Sprague-Dawley rats were randomly assigned into three groups: the control group, HALI group and hyperbaric oxygen preconditioning (HBO2-PC) group. HALI was induced by exposure to pure oxygen at 250 kPa for six hours. In the HBO2-PC group, rats were exposed to oxygen at 250 kPa for 60 minutes twice daily for two consecutive days; HALI was induced at 24 hours after the last oxygen exposure.=After HALI, the lung, spleen and liver were harvested for HE staining and pathological examination. At one hour and 18 hours after HALI, the blood, liver, lung and spleen were collected for the detection of Ang II and ACE contents by enzyme-linked immunosorbent assay. Pathological examination showed the lung was significantly damaged and characteristics of HALI were observed, but there were no significant pathological changes in the liver and spleen. After HALI, Ang II and ACE contents of different tissues increased progressively over time, but the HBO2-PC group showed reductions in the Ang II and ACE contents to a certain extent, especially at 18 hours after injury. These findings suggest prolonged hyperoxia exposure may activate the RAS, which may be associated with the pathogenesis of HALI. HBO2-PC has a limited capability to inhibit RAS activation.

The association between XPG polymorphisms and cancer susceptibility: Evidence from observational studies.

BACKGROUND: Exposure to environmental carcinogens can cause damages to DNA. If not properly repaired, the DNA damages may increase the risk of carcinogenesis. Xeroderma pigmentosum group G (XPG) gene is an essential gene in the nucleotide excision repair (NER) pathway. The association between XPG polymorphisms and cancer susceptibility has been the focus of attention in the molecular epidemiology of cancer. However, the conclusions have been divergent. Therefore, we conducted a comprehensive meta-analysis to precisely evaluate the association of 3 frequently investigated XPG polymorphisms (rs751402, rs873601, and rs2296147) with cancer risk. METHODS: Pubmed, EMBASE, and Chinese National Knowledge Infrastructure (CNKI) were searched for relevant studies in English and Chinese. Odds ratio (OR) and 95% confidence interval (CI) were used to assess the association between XPG polymorphisms (rs751402, rs873601, and rs2296147) and cancer risk. RESULTS: Twenty-three studies were included. Overall, there was no significant association between rs751402 polymorphism and overall cancer risk under the 5 gene models. However, we observed strong correlation between rs751402 polymorphism and gastric cancer (C vs T: OR=1.21, 95% CI = 1.00-1.26, P = .045; TC vs CC: OR = 1.12, 95% CI = 1.00-1.24, P = .041; TC/TT vs CC: OR = 1.13, 95% CI = 1.02-1.26, P = .020). There was a significant correlation between rs873601 polymorphism and cancer risk under the homozygous model (GG vs AA: OR = 1.16, 95% CI = 1.07-1.26, P = .001). Moreover, significant association with breast cancer was detected for rs873601 polymorphism under the allele contrast model (G vs A: OR = 1.10, 95% CI = 1.02-1.20, P = .021). In the subgroup of Asian, rs873601 polymorphism was related to the susceptibility to cancer (G vs A: OR = 1.07, 95% CI = 1.03-1.12, P = .010; GG vs AA: OR = 1.15, 95% CI = 1.06-1.26, P = .001; AG/AA vs GG: OR = 1.08, 95% CI = 1.01-1.15, P = .031; AA vs AG/GG: OR = 1.13, 95% CI = 1.05-1.21, P = .001). Significant association between rs2296147 polymorphism and cancer risk were observed in Asian population (CT vs TT: OR = 0.93, 95% CI = 0.87-0.99, P = .036). CONCLUSIONS: Our meta-analysis suggested that the rs873601 polymorphism was significantly associated with overall cancer risk. The moderate effects of rs751402 and rs2296147 polymorphism on cancer susceptibility might be highly dependent on cancer type and ethnicity, respectively. Large studies are needed to validate our findings, especially in Caucasian and African population.

Polarization of macrophages in the blood after decompression in mice.

The veins are a major site of bubble formation after decompression and the lung is a target organ of bubbles. Bubble-induced inflammation has been implicated in the pathogenesis of decompression sickness (DCS). Macrophages play a central role in the inflammation, and macrophage polarization is closely related to the pathogenesis of some lung diseases. This study aimed to investigate the blood macrophage polarization in mice after decompression. BALB/c mice were exposed to hyperbaric air for 60 minutes, and rapid decompression was performed to induce DCS. Slow decompression and hyperoxia (150 kPa, 60 minutes) served as control groups, and hyperbaric oxygen (HBO; 250 kPa, 60 minutes) was employed for DCS treatment. Macrophage phenotype was determined by flow cytometry, and cytokines related to macrophage polarization were measured by enzyme-linked immunosorbent assay. Our results showed rapid decompression significantly induced the shift to M1 phenotype, which was not observed in slow decompression group, HBO and hyperoxia groups. These changes were consistent with the change in blood tumor necrosis factor α level. Moreover, any treatment could significantly increase the M2 macrophages, but blood interleukin-10 remained unchanged after different treatments. In addition, the blood and lung levels of monocyte chemoattractant protein-1 and intercellular adhesion molecule-1 increased significantly after rapid decompression, but reduced markedly after HBO treatment. Taken together, rapid decompression is able to induce the shift to M1 phenotype in blood macrophages, which may then migrate into the lung involving decompression-induced lung injury.

Nitric oxide and hyperoxic acute lung injury.

Hyperoxic acute lung injury (HALI) refers to the damage to the lungs secondary to exposure to elevated oxygen partial pressure. HALI has been a concern in clinical practice with the development of deep diving and the use of normobaric as well as hyperbaric oxygen in clinical practice. Although the pathogenesis of HALI has been extensively studied, the findings are still controversial. Nitric oxide (NO) is an intercellular messenger and has been considered as a signaling molecule involved in many physiological and pathological processes. Although the role of NO in the occurrence and development of pulmonary diseases including HALI has been extensively studied, the findings on the role of NO in HALI are conflicting. Moreover, inhalation of NO has been approved as a therapeutic strategy for several diseases. In this paper, we briefly summarize the role of NO in the pathogenesis of HALI and the therapeutic potential of inhaled NO in HALI.

Treatment of hyperoxic acute lung injury with stem cell transplantation in murine models: a brief review.

Hyperoxia has been a prominent clinical concern with the emergence of the intensive care unit and prolonged mechanical ventilation, along with the increasing use of hyperbaric oxygen therapy. Indeed, prolonged breathing of a high oxygen partial pressure may cause hyperoxic acute lung injury (HALI). To date, HALI has been a focus in the fields of pediatric and pulmonary medicine. However, no effective strategies have been developed for therapy for HALI due to the complicated mechanisms underlying the pathogenesis of HALI. In recent years, increasing studies have employed cell-based therapy for HALI. In this review, we summarize findings from available studies on therapy for HALI using stem cells in murine models and, based on concerns in this field, present our findings on cell-based therapy for HALI.

Application of hyperbaric oxygen in liver transplantation.

In recent years, hyperbaric oxygen (HBO) has been used in the treatment of a lot of diseases such as decompression sickness, arterial gas embolism, carbon dioxide poisoning, soft tissue infection, refractory osteomyelitis, and problematic wound, but little is known about its application in liver transplantation. Although several studies have been conducted to investigate the protective effects of HBO on liver transplantation and liver preservation, there are still some controversies on this issue, especially its immunomodulatory effect. In this short review, we briefly summarize the findings supporting the application of HBO during liver transplantation (including donors and recipients).

Hyperbaric oxygen preconditioning alleviates myocardial ischemic injury in rats.

It has been shown that after ischemia-reperfusion, application of hyperbaric oxygen (HBO) reduces cardiac injury. In this study we tested the hypothesis that HBO preconditioning reduces injury to the ischemic myocardium. One hundred and eight adult male Sprague-Dawley rats (250-280 g) were randomly divided into four groups: normoxia + sham surgery (CS), normoxia + permanent occlusion of the left anterior descending (LAD) coronary artery (CMI), HBO preconditioning + sham surgery (HS), and HBO preconditioning + permanent LAD occlusion (HMI). Rats receiving HBO preconditioning were intermittently exposed to 100% O(2) at 2.5 atmosphere absolute (ATA) for 60 min, twice daily for 2 days followed by 12 hrs of recovery in room air prior to the myocardial ischemic insult induced by LAD ligation. Rats in the normoxia group were time-matched with the HBO group and maintained under normoxic conditions prior to LAD occlusion. At 3 and 7 days after LAD occlusion, heart function parameters were measured by inserting a catheter into the left ventricle, infarct size was calculated using the method of TTC staining, myocardial capillary density was determined by immunohistochemical staining with a monoclonal anti-CD(31)/PECAM-1 antibody, and VEGF protein level was determined by Western blot analysis. At 3 days after LAD ligation, the infarct size of the HMI group was significantly smaller than that of the CMI group (26 +/- 2.5% vs. 38 +/- 3%, P < 0.05). The heart function parameters including left ventricular systolic pressure (LVSP), +dP/dt(max) and -dP/dt(max) were significantly improved in the HMI group compared to the CMI group at 3 and 7 days after LAD occlusion. Capillary density and VEGF protein levels were significantly increased in the ischemic myocardium pre-exposed to HBO. We conclude that HBO preconditioning alleviates myocardial ischemia in rat model.

Mechanism of hyperbaric oxygen preconditioning in neonatal hypoxia-ischemia rat model.

Hypoxic ischemic (HI) injury in neonates damages brain tissues. We examined the mechanism of hyperbaric oxygen preconditioning (HBO-PC) in neonatal HI rat model. Seven-day-old rat pups were subjected to left common carotid artery ligation and hypoxia (8% oxygen at 37 degrees C) for 90 min. HBO (100% O(2), 2.5 atmospheres absolute for 2.5 h) were administered by placing pups in a chamber 24 h before HI insult. Brain injury was assessed by the survival rate, 2,3,5-triphenyltetrazolium chloride (TTC), Nissl, TUNEL straining and caspase-3,caspase-9 activities after HI. In HBO preconditioned animals, survival rate was increased, infarct ratio was decreased, and the positive stained TUNEL cells were reduced, accompanied by the suppression of caspase-3 and -9 activities. These results indicate that a single HBO-PC appears to provide brain protection against HI insult via inhibition of neuronal apoptosis pathways.