[Purpose] This study was performed to investigate the acid-base and ion balance at rest and after exercise in healthy males under normoxia, moderate hypoxia, and severe hypoxia. [Methods] Ten healthy Korean males completed three different trials on different days, comprising exercise under normoxia (FiO2 = 20.9%, N trial), moderate hypoxia (FiO2 = 16.5%, MH trial), and severe hypoxia (FiO2 = 12.8%, SH trial). They undertook endurance exercise for 30 min on a cycle ergometer at the same relative exercise intensity equivalent to 80% maximal heart rate under all conditions. Capillary blood samples were obtained to determine acid-base and ion balance at rest and after exercise. [Results] Exercise-induced blood lactate elevations were significantly increased as hypoxic conditions became more severe; SH > MH > N trials (P = 0.003). After exercise, blood glucose levels were significantly higher in the SH trial than in the N and MH trials (P = 0.001). Capillary oxygen saturation (SCO2) levels were significantly lowered as hypoxic conditions became more severe; SH > MH > N trials (P < 0.001). The pH levels were significantly lower in the MH trial than that in the N trial (P = 0.010). Moreover, HCO3- levels were significantly lower in the SH trial than in the N trial, with significant interaction (P = 0.003). There were no significant differences in blood Na+, K+, and Ca2+ levels between the trials. [Conclusion] MH and SH trials induced greater differences in glucose, lactate, SCO2, pH, and HCO3- levels in capillary blood compared to the N trial. Additionally, lactate, SCO2, and HCO3- levels showed greater changes in the SH trial than in the MH trial. However, there were no significant differences in Na+, K+, and Ca2+ levels in MH and SH trials compared to the N trial.
This study was carried out at 5 sites 11 times over two years to identify the variation of benthic environments and benthic polychaetous community and analyze the benthic healthiness in Dangdong Bay, a small semi-enclosed inner bay of Jinhae Bay. The temperature of bottom water showed the typical temporal fluctuation of a temperate zone and was in the range of 5.94 ~ 23.94℃. The salinity did not change significantly during the study period and was in the range of 32.93 ~ 35.72 psu. The concentration of dissolved oxygen of bottom water fluctuated a great deal and was in the range of 0.31 ~ 10.20 mg/L. The lowest DO value was recorded in July 2015, as 0.31±0.04 mg/L corresponding to the hypoxic water mass. The hypoxic water mass was formed continuously at some sites also in July and August 2016. The mean grain size was in the range of 7.57 ~ 9.81Ø and the average was 8.89±0.20Ø. The surface sediments were mainly composed of fine sediment (mud) above 85%. The mean of TOC was 3.09±0.22% and LOI was 13.30±0.47%, showing very high levels in Korean coastal waters. The concentration of AVS was in the range of 0.33 ~ 1.28 mgS/g-dry. The high values of organic contents and AVS indicated that there had been the serious organic enrichment in Dangdong Bay. The number of species and the density of the benthic polychaetous community in Dangdong Bay were in the range of 2 ~ 38 species and 2 ~ 2,185 ind./㎡ during the study period. The number of species and density were highly sustained in winter and spring, and then decreased gradually with the formation of a hypoxic water mass in summer, and the lowest number of species and density were recorded in autumn. In September and November 2015, the dead zone expanded to almost the whole study area. Dominant polychaetous species were Capitella capitata, Lumbrineris longifolia, Paraprionospio patiens and Sigambra tentaculata, each known as opportunistic species and potential organic pollutant indicator species. In particular, Paraprionospio patiens showed a very high population density of 2,019 ind./㎡ in December 2016. Polychaetous communities at each sampling time were classified into 4 temporal groups according to dominant species in each period by cluster analysis and nMDS. 'Period Group AI' was formed in winter and spring of 2015, dominated by Capitella capitata, 'Period AII' in summer dominated by Lumbrineris longifolia, 'Period B' in autumn with no fauna in the dead zone, and particularly 'Period C' in winter of 2016 dominated by Paraprionospio patiens. As a result of analysis of benthic healthiness, the study area was estimated to be in a Fair~Very Poor condition by AMBI and in a Poor~Very Poor condition by BPI during the study period. Both AMBI and BPI showed that the study area was in a Very Poor condition in September and November 2015, and when the dead zone occurred. In Dongdong Bay, the fact that the formation of a hypoxic water mass occurred in summer and a dead zone in autumn were confirmed. In addition, the dominance of opportunistic and organic pollutant indicator species was also observed clearly. The benthic healthiness indexes such as AMBI and BPI showed that organic enrichment was serious in Dangdong Bay.
Seo, Min-Ae;Lee, Hyun-Ju;Choi, Eun-Jin;Kim, Jin-Kyung;Chung, Hai-Lee;Kim, Woo-Taek
Neonatal Medicine
/
v.17
no.2
/
pp.181-192
/
2010
Purpose: Current studies have demonstrated the neuroprotective effects of dizocilpine (MK-801) in many animal models of brain injury, including hypoxic-ischemic (HI) encephlopathy, trauma and excitotoxicity, but limited data are available for those during the neonatal periods. Here we investigated whether dizocilpine can protect the developing rat brain from HI injury via anti-apoptosis. Methods: In an in vitro model, embryonic cortical neuronal cell culture of Sprague-Dawley (SD) rats at 18-day gestation was done. The cultured cells were divided into three groups: normoxia (N), hypoxia (H), and hypoxia treated with dizocilpine (HD). The N group was prepared in 5% $CO_2$ incubators and the other groups were placed in 1% $O_2$ incubators (94% N2, 5% $CO_2$) for 16 hours. In an in vivo model, left carotid artery ligation was done in 7-day-old SD rat pups. The animals were divided into six groups; hypoxia (N), hypoxia (H), hypoxia with sham-operation (HS), hypoxia with operation (HO), HO treated with vehicle (HV), and HO treated with dizocilpine (HD). Hypoxia was made by exposure to a 2 hour period of hypoxic incubator (92% N2, 8% $O_2$). Results: In the in vitvo and in vivo models, the expressions of Bcl-2 in the hypoxia groups were reduced compared to the normoxia group. whereas those in the dizocilpine-treated group were increased compared to the hypoxia group. However. the expressions of Bax and caspase-3 and the ratio of Bax/Bcl-2 were revealed reversely. Conclusion: Dizocilpine has neuroprotective property over perinatal HI brain injury via anti-apoptosis.
Purpose : Transforming growth factor (TGF)-${\beta}1$ reportedly increases neuronal survival by inhibiting the induction of inducible nitric oxide synthase (NOS) in astrocytes and protecting neurons after excitotoxic injury. However, the neuroprotective mechanism of $TGF-{\beta}1$ on hypoxic-ischemic (HI) brain injury in neonatal rats is not clear. The aim of this study was to determine whether $TGF-{\beta}1$ has neuroprotective effects via a NO-mediated mechanism and N-methyl-D-aspartate (NMDA) receptor modulation on perinatal HI brain injury. Methods : Cortical cells were cultured using 19-day-pregnant Sprague-Dawley (SD) rats treated with $TGF-{\beta}1$ (1, 5, or 10 ng/mL) and incubated in a 1% O2 incubator for hypoxia. Seven-day-old SD rat pups were subjected to left carotid occlusion followed by 2 h of hypoxic exposure (7.5% $O_2$). $TGF-{\beta}1$ (0.5 ng/kg) was administered intracerebrally to the rats 30 min before HI brain injury. The expressions of NOS and NMDA receptors were measured. Results : In the in vitro model, the expressions of endothelial NOS (eNOS) and neuronal NOS (nNOS) increased in the hypoxic group and decreased in the 1 ng/mL $TGF-{\beta}1-treated$ group. In the in vivo model, the expression of inducible NOS (iNOS) decreased in the hypoxia group and increased in the $TGF-{\beta}1$-treated group. The expressions of eNOS and nNOS were reversed compared with the expression of iNOS. The expressions of all NMDA receptor subunits decreased in hypoxia group and increased in the $TGF-{\beta}1$-treated group except NR2C. Conclusion : The administration of $TGF-{\beta}1$ could significantly protect against perinatal HI brain injury via some parts of the NO-mediated or excitotoxic mechanism.
Tooth movement by orthodontic force effects great tissue changes within the periodontium, especially by shifting the blood flow in the pressure side and resulting in a hypoxic state of low oxygen tension. The aim of this study is to elucidate the possible mechanism of apoptosis in response to hypoxia in MC3T3El osteoblasts, the main cells in bone remodeling during orthodontic tooth movement. MC3T3El osteoblasts under hypoxic conditions ($2\%$ orygen) resulted in apoptosis in a time-dependent manner as estimated by DNA fragmentation assay and nuclear morphology stained with fluorescent dye, Hoechst 33258. Pretreatment with Z-VAD-FMK, a pancaspase inhibitor, or Z-DEVD-CHO, a specific caspase-3 inhibitor, completely suppressed the DNA ladder in response to hypoxia. An increase in caspase-3-like protease (DEVDase) activity was observed during apoptosis, but no caspase-1 activity (YVADase) was detected. To confirm what caspases are involved in apoptosis, Western blot analysis was performed using anti-caspase-3 or -6 antibodies. The 10-kDa protein, corresponding to the active products of caspase-3, and the 10-kDa protein of the active protein of caspase-6 were generated in hypoxia-challenged cells in which the processing of the full length form of caspase-3 and -6 was evident. While a time course similar to this caspase-3 and -6 activation was evident, hypoxic stress caused the cleavage of lamin A, which was typical of caspase-6 activity. In addition, the stress elicited the release of cytochrome c into the cytosol during apoptosis. Furthermore, we observed that pre-treatment with SB203580, a selective p38 mitogen activated protein kinase inhibitor, attenuated the hypoxia-induced apoptosis. The addition of SB203S80 suppressed caspase-3 and -6-like protease activity by hypoxia up to $50\%$. In contrast, PD98059 had no effect on the hypoxia-induced apoptosis. To confirm the involvement of MAP kinase, JNK/SAPK, ERK, or p38 kinase assay was performed. Although p38 MAPK was activated in response to hypoxic treatment, the other MAPK -JNK/SAPK or ERK- was either only modestly activated or not at all. These results suggest that p38 MAPK is involved in hypoxia-induced apoptosis in MC3T3El osteoblasts.
From August, 1986 to December, 1989, mitral valve replacement was performed in 93 patients. Of the valve implanted, 42 were Duromedics, 35 St. Jude Medical, 15 Carpenter-Edwards and 1 Ionescu-Shiley. The hospital mortality rate was 3.2%[3 patients] and the late mortality rate was 4.3% [4 patients]. The causes of hospital death were LV rupture in 1, renal failure in 1 and hypoxic brain damage in l. The causes of late death were congestive heart failure in 1 and sudden death in 3. Follow-up was done on 78 surviving patients; mean follow-up period was 29.22$\pm$9.09 months. The actual survival rate was 91.8% at 4 years. We concluded, therefore, that good clinical results could be achieved with mitral valve replacement in short-term follow-up, and long-term follow-up is also necessary.
Changing trends in anticancer research have altered the treatment paradigm to the extent that it is difficult to investigate any anticancer drugs without mentioning immunotherapy. Thus, we are finally contemplating tumour regression using magic bullets known as immunotherapy drugs. This review explores the possible options and pitfalls in tumour regression by first elucidating the features of cancer and the importance of tumour microenvironments. Next, we evaluated the trends of anticancer therapeutics regulating tumour microenvironment. Finally, we introduced the concept of tumour regression and various targets of tumour microenvironment, which can be used in combination with current immunotherapy for tumour regression. In particular, we emphasize the importance of regulating the neurological manifestations of tumour microenvironment (N) in addition to inflammation (I) and hypoxia (H) in cancer.
Objectives : This study was designed to investigate the protective mechanisms of Palmul-tang on hypoxia-induced cytotoxicity in H9c2 cardiomyoblast cells. Methods : In this study, we used H9c2 cells. Cells were subjected to hypoxia in the absence and presence of $1000\mu\textrm{g}/ml$ Palmul-tang for 24 hrs. Cells were treated with various concentrations of Palmul-tang for 24 hrs. Cell viability was measured by MTT assay. Hypoxia markedly decreased the viability of H9c2 cells, which was characterized with apparent apoptotic features such as chromatin condensation as well as fragmentation of genomic DNA and nuclei. Results : Palmul-tang significantly reduced hypoxia-induced cell death and apoptotic characteristics. Also, Palmul-tang prevented mitochondrial dysfunction including the disruption of mitochondrial membrane permeability transition (MPT) and an increase in expression of apoptogenic Bcl-2 proteins in hypoxia-H9c2 cells. Conclusions; This study suggests that the protective effects of Palmul-tang against hypoxic damages may be mediated by the modulation of Bcl-2, Bax expression.
The immature neonatal brain is susceptible to the development of seizures. Seizures occur in 1% to 5% of infants during the neonatal period. Neonatal seizures are most commonly associated with serious acute illnesses, such as hypoxic-ischemic encephalopathy, birth trauma, metabolic disturbances, or infections. Thus, newborn infants with seizures are at risk for neonatal death and survivors are at risk for neurologic impairment, developmental delay, and subsequent epilepsy. Experimental data have also raised concerns about the potential adverse effects of the currently used anticonvulsants in neonates on brain development. Therefore, in the management of neonatal seizures, confirmatory diagnosis and optimal, but shorter, duration of anticonvulsant therapy is essential. Nevertheless, there has been substantial progress in understanding the developmental mechanisms that influence seizure generation and responsiveness to anticonvulsants. The currently used therapies have limited efficacy and the treatment of neonatal seizures has not significantly changed in the past several decades, This review includes an overview of current approaches to the treatment of neonatal seizures.
A 53-year-old man arrived at the trauma center with a steel bar penetrating from the epigastrium to the right scapula. He was hypotensive and hypoxic, and immediate resuscitation and basic evaluation were performed. An emergency operation was performed due to an unstable hemodynamic state. Multiple injuries were confirmed in the right lower lobe, posterior chest wall, diaphragm, and liver lateral segment. Right lower lobectomy and liver lateral sectionectomy were performed following removal of the bar. The patient recovered without additional hemorrhage after the surgery, and was transferred to a rehabilitation institution with periodic follow-up.
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