The Evaluation of a Golden Period of Fasciotomy for High Voltage Electrical Burn Injury Patients With Compartment Syndrome.

Electrical burn injuries can cause various acute manifestations that require surgeons to make an early decision, such as fasciotomy for compartment syndromes. Early decompression can become a 'golden period'for limb salvation. This study evaluates the duration of burn to fasciotomy (B-F time) and amputation. A cross-sectional study was performed on medical records. Inclusion criteria were patients with high voltage electrical injuries and compartment syndrome. Exclusion criteria were patients whose extremities were already non-vital on admission and those lost to follow up. Demographic information, burn surface area and B-F time for patients amputated above the elbow (group A amputation), below the elbow (group B amputation), and no amputation (non-amputated) were investigated. More than 50% patients underwent amputation and 60% had less than 18 hours B-F time. Mean B-F time for non-amputated patients was 18 hours and for amputated patients 20.38 hours. Mean burn to amputation (B-A) time and fasciotomy to amputation (F-A) time in group B was about double compared to group A. The B-A time range of group Awas 4.2-7.3 days. Our study showed 18 hours maximum to be the golden period of burn to fasciotomy. The window period of muscle injury evaluation is maximum 7 days to permit limb salvation at the lowest level possible.

Les brûlures électriques peuvent entraîner des situations cliniques nécessitant une chirurgie urgente, en particulier une aponévrotomie pour syndrome de loge. Cette étude se penche sur l'évaluation de la corrélation entre le délai de réalisation d'une aponévrotomie après brûlure (délai B-A) et une amputation. Il s'agit d'une étude comparative rétrospective sur dossiers. Le critère d'inclusion était l'apparition d'un syndrome de loge après électrisation. Les critères d'exclusion étaient l'existence de nécrose distale d'emblée et les perdus de vue. Nous avons relevé les données démographiques, la surface brûlée, le délai B-A et comparé 3 groupes : amputation au bras (amp. A), amputation à l'avant- bras (amp. B) et sans amputation (amp. 0). Plus de la moitié des patients ont été amputés, et le délai B-A était de moins de 18 h pour 60% d'entre eux. Le délai B-F moyen de amp. 0 était de 18 h, et de 20,38 h pour les amputés. Les délais moyens entre brûlure et amputation (B-amp.) et entre aponévrotomie et amputation (A-Amp.) était presque le double chez amp. B que chez amp. A (de 4,2 à 7,3 jours dans ce groupe). Le délai maximal entre électrisation et aponévrotomie semble être de 18 h et le délai avant de décider du niveau d'amputation de 7 j.

Evaluation of the nano silica and nano waste materials on the corrosion protection of high strength steel embedded in ultra-high performance concrete.

Corrosion resistance of high strength steel (HHS) embedded in ultra-high performance concrete (UHPC) immersed in 3.5% NaCl solution is evaluated in the absence and presence of nano silica (NS), nano glass waste (NGW), nano rice husk ash (NRHA) and nano metakaolin (NMK) using open circuit potential, potentiodynamic polarization and electrochemical impedance spectroscopy (EIS) under normal and accelerated conditions. Data showed that the corrosion rate in the accelerated conditions is higher compared by the normal conditions due to the increasing in the rate of both anodic and cathodic reactions in the presence of anodic current. On the other hand, the presence of the studied nano materials decreases both the anodic and cathodic overpotentials, and shifts both the open circuit potential (Eocp) and corrosion potential (Ecorr) of HSS to more noble values, as well as decreases the values of the corrosion current densities (Icorr) in both normal and accelerated conditions. Furthermore, EIS analysis illustrates that the presence of these materials enhances both the concrete bulk resistance and the charge transfer resistance at HSS/UHPC interface, which retards the flow of the electrons between the anodic and cathodic sites, thus impeding the propagation of the corrosion process. The inhibitory effect of the studied nano materials for the corrosion of HSS is interpreted on the basis of the change in the microstructure and the compressive strength of the UHPC.

Characteristics Of Liquefied Petroleum Gas (Lpg) Related Burn Injuries In Hasan Sadikin Bandung General Hospital.

The number of liquefied petroleum gas (LPG) related burn injuries has increased over recent years in Indonesia, since the conversion of kerosene to LPG in 2007 (government policy). Based on studies in India and China, LPG-related burn injuries have become a serious public health issue. A 5-year retrospective study was conducted from medical records of patients with LPG-related burn injuries. The data included age, gender, place, occupation, LPG tank size, mechanism, burn classification, burn site and concurrent injury. A total of 169 patients with LPG-related burn were admitted. The yearly incidence was in the range of 24-46% of all burn injury cases. They mostly occurred in males (66.2%) aged 36-55 years (43.1%). The most common place was the home (83.4%) and the most common occupation was merchant (32%). LPG leakage (94.7%) was the main cause of burn, followed by LPG explosion (5.3%). A 3-kilogram LPG tank (96.4%) was the most common cause. Patient burn classification was mostly major burns (62.1%), with the most common site being the head and neck (73%), and concurrent with inhalational injury (16%). Our study showed that the increasing number of LPG-related burn injuries is alarming. The majority of the patients were males in the productive age and they suffered major burns. Some of them suffered inhalation injury that increases the risk of mortality. Since LPG leakage was the main cause and the most common place was the home, there must be regulation with government related prevention strategies.

Le nombre de brûlures par GPL a augmenté ces dernières années en Indonésie, suivant la loi sur la conversion kérosène/GPL de 2007. Les études indiennes et chinoises en font un problème de santé publique. Nous avons revu les dossiers des 169 patients admis pour de telles brûlures pendant 5 ans. Les données étudiées comprenaient l'âge, le sexe, le lieu, l'activité, la taille du réservoir de GPL, le mécanisme, la surface, la profondeur, les zones brûlées et les lésions associées. Ces brûlures représentaient 22 à 46% de l'ensemble. Elles touchaient préférentiellement des hommes (66,2%) de 36 à 55 ans (43,1%). Bien que survenant le plus souvent au domicile (83,4%), elles étaient liées à des activités commerciales dans 32% des cas. La fuite de GPL était la cause très largement majoritaire (94,7%), les explosions ne représentant que 5,3% des mécanismes, la bonbonne de 3kg étant impliquée dans 96,4% des accidents. Les brûlures étaient considérées comme graves dans 62,1% des cas ; la zone cervico- faciale était atteinte 3 fois sur 4 (73%). Une inhalation était observée dans 16% des cas. Notre étude montre l'augmentation préoccupante des brûlures graves par GPL, survenant chez des hommes actifs, certains d'entre eux souffrant en plus d'une inhalation, qui accroît le risque létal. La fuite de GPL en étant l'origine prédominante, une législation de prévention primaire doit être mise en place.

Possible Anticancer Mechanisms of Some Costus speciosus Active Ingredients Concerning Drug Discovery.

Costus speciosus is native to South East Asia, especially found in India, Srilanka, Indonesia and Malaysia. C. speciosus have numerous therapeutic potentials against a wide variety of complains. The therapeutic properties of C. speciosus are attributed to the presence of various ingredients such as alkaloids, flavonoids, glycosides, phenols, saponins, sterols and sesquiterpenes. This review presented the past, present, and the future status of C. speciosus active ingredients to propose a future use as a potential anticancer agent. All possible up-regulation of cellular apoptotic molecules as p53, p21, p27, caspases, reactive oxygen species (ROS) generation and others attribute to the anticancer activity of C. speciosus along the down-regulation of anti-apoptotic agents such as Akt, Bcl2, NFKB, STAT3, JAK, MMPs, actin, surviving and vimentin. Eventually, we recommend further investigation of different C. speciosus extracts, using some active ingredients and evaluate the anticancer effect of these chemicals against different cancers.

Expression of carbonic anhydrase 9, a potential intrinsic marker of hypoxia, is associated with poor prognosis in oesophageal squamous cell carcinoma.

Carbonic anhydrase 9 (CA9) is a protein to be upregulated under exposure to hypoxic conditions. Hypoxic conditions are known to be associated with resistance to chemotherapy and radiotherapy, and with poor cancer prognosis. We examined CA9 expression in surgical specimens from oesophageal squamous cell carcinoma (ESCC) patients (n=127) using immunohistochemistry and real-time RT-PCR. We also examined CA9 expression and cell proliferation in ESCC cell lines (TE-2, TE-8 and TE-15) and an immortalised human oesophageal cell line (CHEK-1) using real-time RT-PCR, Western blotting, ELISA and MTT assay. Immunohistochemistry, high expression of CA9 was found in 63 of the 127 primary tumour specimens and was correlated with poor outcome (P=0.0003) and more aggressive/less favourable clinicopathological parameters (tumour size (P=0.0235), tumour depth (P<0.0001), regional lymph node metastasis (P=0.0031), distant lymph node metastasis (P=0.0077), stage (P<0.0001) and blood vessel invasion (P=0.006)). In vitro, CA9 expression in cultured cells and culture medium was also induced by hypoxia (P<0.01). CA9 is correlated with poor prognosis and malignant phenotype in patients with ESCC, and was upregulated by hypoxia. It is suggested that control of CA9 expression might improve the effectiveness of chemotherapy and radiotherapy in ESCC.

Anticancer effects of gallic acid isolated from Indonesian herbal medicine, Phaleria macrocarpa (Scheff.) Boerl, on human cancer cell lines.

The natural antioxidant gallic acid (GA) was isolated from fruits of a medicinal Indonesian plant, Phaleria macrocarpa (Scheff.) Boerl. The structure was identified on the basis of spectroscopic analysis and comparison with authentic compound. GA demonstrated a significant inhibition of cell proliferation in a series of cancer cell lines and induced apoptosis in esophageal cancer cells (TE-2) but not in non-cancerous cells (CHEK-1). Observation of the molecular mechanism of apoptosis showed that GA up-regulated the pro-apoptosis protein, Bax, and induced caspase-cascade activity in cancer cells. On the other hand, GA down-regulated anti-apoptosis proteins such as Bcl-2 and Xiap. In addition, GA also induced down-regulation of the survival Akt/mTOR pathway. In non-cancerous cells, we observed delayed expression of pro-apoptosis related proteins. Our results suggest that GA might be a potential anticancer compound. However, in depth in vivo studies are needed to elucidate the exact mechanism.

RhoA and RhoC proteins promote both cell proliferation and cell invasion of human oesophageal squamous cell carcinoma cell lines in vitro and in vivo.

There is growing evidence that Rho proteins are deregulated by overexpression in tumours; and according to some reports, this correlates with disease progression. Our previous clinical study had demonstrated a correlation between RhoA expression and tumour progression in oesophageal squamous cell carcinoma (ESCC). These findings prompted us to study, using nude mice, pathological roles of Rho proteins in human ESCC cells. Western blot analysis in ESCC cell lines, in addition to cell proliferation and in vitro migration assays, were performed to observe the malignant potential of RhoA and RhoC in untransfected and transfected cells. Constitutively active RhoA, RhoC and dominant negative RhoA (dnRhoA) proteins were transfected to ESCC (TE-1 and TE-2) cells. The stably transfected cells were injected into nude mice, and the growth and metastasis of these cells to the lungs were analysed. Tumour tissues were then examined using immunohistochemical methods for proteins Ki-67 (MIB-1), FAK, MMP-1, MMP-9 and TIMP-3. Protein levels of RhoA and RhoC in ESCC cell lines were visualised by Western blotting, and showed highest expression in TE-2 cells. Results from the migration assay illustrated that both RhoA and RhoC play a role in migration of ESCC cells. In TE-2 transfected cells, RhoC showed greater migration compared to RhoA. By using an experimental metastasis model in nude mice, RhoA was found to promote more tumour growth than RhoC, whereas RhoC induced lung metastasis in comparison to RhoA. Ki-67 labelling index was used to evaluate the proliferation potential of tumour tissue inoculated from nude mice. In TE-2 cells RhoA gave a proliferation capacity of 24.8+/-0.5, which was significantly higher than those of TE-2 RhoC 10+/-0.4 (P<0.01). Strong immunoreactivity for FAK, MMP-1 and MMP-9 proteins was present in all tumour cells. By contrast, loss of TIMP-3 expression was observed in all tumour cells. In conclusion, our results indicate that pro-oncogenic Rho proteins are involved in promoting tumour growth, cell migration and metastasis in human ESCC cells in nude mice. The results from this study suggest that active Rho proteins may induce a transforming effect that leads to a malignant phenotype.

Inhibition of the mammalian target of rapamycin (mTOR) by rapamycin increases chemosensitivity of CaSki cells to paclitaxel.

Paclitaxel, a potent anti-neoplastic agent, has been found to be effective against several tumours, including cervical cancer. However, the exact mechanism underlying the cytotoxic effects of pacitaxel, especially in the survival-signalling pathway, is poorly understood. The aim of this study was to investigate the molecular pathway of the cytotoxic effect of paclitaxel in human cervical cancer cell lines. Four human cervical cancer cell lines were treated for 24 h with various concentration of paclitaxel, and the sensitivity was analysed by an MTT assay. The cell cycle progression and sub-G1 population were analysed by flow cytometry. Apoptosis was further measured by DNA fragmentation and microscope examination. The protein expression was determined by Western blot analysis. Our results showed that HeLa cells demonstrated the highest sensitivity to paclitaxel, whereas CaSki cells showed the lowest. In cervical cancer cells, paclitaxel induced apoptosis through an intrinsic pathway with prior G2/M arrest. In addition, we showed that paclitaxel downregulated the phosphorylation of Akt in both HeLa and CaSki cells. Interestingly, in CaSki cells, which were more suggestive of a resistant phenotype, paclitaxel induced the activation of mTOR as a downstream target of Akt. Pre-treatment with rapamycin inhibited activation of mTOR signalling and significantly enhanced the sensitivity of CaSki cells to paclitaxel by increasing apoptotic cell death. This effect was mediated, at least partly, through caspase activation. Overall, paclitaxel exerts its anti-tumour effects on cervical cancer cells by inducing apoptosis through intrinsic pathway, and rapamycin targeted to mTOR can sensitise paclitaxel-resistant cervical cancer cells.

Biochemical and histological studies on H2-receptor antagonist ranitidine-induced hepatotoxicity in rats.

This study was designed to investigate the hepatotoxicity of ranitidine treatment in dose levels of 10, 30, and 50 mg/kg b.wt. for 3 weeks period in male rats. The results showed some adverse changes in rats treated with either 10 or 30 mg/kg. Treatment with dose of 50 mg/kg produced marked increase in the activity of both acid phosphatase in liver and aspartate aminotransferase in serum and liver, with a tendency for increase in serum alanine aminotransferase activity. Also, a significant decrease in the serum activity of both amylase and alkaline phosphatase was noted. Microscopic examination of livers of the same animals revealed absence of some hepatic cells, pyknotic nuclei, dilatation of blood sinusoids, binucleated cells, and infiltration of lymphocytes. These biochemical and histological changes indicate that ranitidine when given chronically in high dose could produce hepatotoxicity in rats.

Correlation between RhoA overexpression and tumour progression in esophageal squamous cell carcinoma.

AIMS: The aim of this study was to clarify the clinico-pathologic outcome and prognostic significance of RhoA in esophageal squamous cell carcinoma (ESCC). METHODS: Immunohistochemical staining for RhoA was performed on surgical specimens obtained from 122 patients with ESCC. RESULTS: There were significant correlations among RhoA overexpression and TNM clinical classification (depth of invasion, P=0.028; presence of regional lymph node metastasis, P=0.009; presence of distant metastasis, P=0.003; staging P=0.006), lymphatic invasion (P=0.002), and blood-vessel invasion (P=0.004). The five-year survival rates for ESCC patients with RhoA overexpression were significantly lower than those in patients with RhoA under-expression (P=0.002). CONCLUSIONS: Our results demonstrated immunohistochemically that the expression of RhoA protein appeared to be correlated with tumour progression of ESCC. Patients with RhoA overexpression tended to have poor prognosis compared with patients with RhoA under-expression.

Expression of heat-shock protein Hsp60 correlated with the apoptotic index and patient prognosis in human oesophageal squamous cell carcinoma.

Cellular stress response and apoptosis are two highly conserved mechanisms for maintaining homeostasis. Hsp60 and Hsp90 have been shown to play pro- and anti-apoptotic roles, respectively. Our present study examined whether there is a correlation between the expression of Hsp60 and Hsp90, clinical parameters, the apoptotic index (AI), and the prognosis of patients with oesophageal squamous cell carcinoma (ESCC). We immunohistochemically stained cells for Hsp60, Hsp90, and single-stranded DNA (ssDNA), which acts as an apoptotic marker. In normal oesophageal epithelium tissue, Hsp60 and Hsp90 were expressed in the cytoplasm and membrane from the basal cell layer to the supra-basal cell layers. Hsp60 and Hsp90 positive stainings (+) were found in 63 of 123 cases (51%) and 62 of 123 cases (50%), respectively. There was no correlation between Hsp60 and Hsp90 expression levels and any of the clinical parameters examined. The five-year survival rate for ESCC patients with Hsp60 (+) expression was significantly higher than for those patients with Hsp60 (-) expression (P=0.0371). Five-year survival rates of patients with Hsp60 (+) and (-) were 49% and 33%, respectively. By contrast, Hsp90 expression failed to predict patient prognosis (P=0.7965). The high-AI group did not have a significantly better prognosis than the low-AI group (P=0.2218). Statistical analysis showed a significant correlation between the expression of Hsp60 and AI in ESCC patients (P=0.008). Thus, the five-year survival rate for the high-AI/Hsp60 (+) group was statistically significantly better than for the other groups (P=0.0281). The results obtained in this study indicate that positive Hsp60 expression is a good prognostic indicator. This may be due to its role as a chaperone in contributing to the induction of apoptosis. These data suggest that Hsp60 expression correlates with the AI and patient prognosis in human ESCC.

An immunohistochemical study of TIMP-3 expression in oesophageal squamous cell carcinoma.

Tissue inhibitor of metalloproteinase-3 (TIMP-3) inhibits the activity of matrix metalloproteinase, which may play an important role in carcinoma invasion and metastasis. We have investigated the relationship between TIMP-3 reduction and clinicopathological factors in oesophageal squamous cell carcinoma (ESCC). We examined tissue specimens that had been removed from 90 patients with thoracic oesophageal cancer who had undergone surgery between 1983 and 2001. Immunohistochemical staining was performed by the standard streptavidin-biotin method. Immunostaining of TIMP-3 was seen in the cytoplasm of cancer cells and normal oesophageal epithelial cells, particularly in cells located in shallow areas of the tumour. TIMP-3 preserved (+), moderate (+/-), and reduced (-) cases accounted for 30, 27, and 33 of the 90 patients, respectively (33, 30, 37%). Significant correlations were observed between TIMP-3 expression and depth of tumour invasion (P=0.001), number of lymph node metastases (P=0.003), infiltrative growth pattern (P=0.003), and disease stage (P=0.005). The survival rates of patients with TIMP-3 (-) cancer were significantly lower than those of patients with TIMP-3 (+) and TIMP-3 (+/-) cancer (P=0.0003). The mean 5-year survival rates of patients with TIMP-3 (+), (+/-), and (-) were 50, 58, and 21%, respectively. In conclusion, decreased expression of TIMP-3 protein correlates with invasive activity and metastasis. This makes the prognosis for patients with cancer that has lost TIMP-3 significantly less favourable than that for patients with cancer that has maintained TIMP-3.

Partial suppressive effect of melatonin on indomethacin-induced renal injury in rat.

Intramuscular injection of a single high dose of indomethacin (20 mg/kg) in fasted rats produced renal injury. The results showed increases in the level of lipid peroxidation and cholesterol, and activity of acid phosphatase and alkaline phosphatase in the kidney. Also, the renal contents of both reduced glutathione and activity of total adenosine triphosphatase were decreased by the toxicant. In serum, indomethacin increased activity of lactate dehydrogenase and acid phosphatase, and levels of creatinine and inorganic phosphorus. Paradoxically, administration of melatonin (0.75 mg/rat/day) alone for 7 days decreased significantly the activity of lipid peroxidation and acid phosphatase, and increased, but not significantly, the level of reduced glutathione in the kidney. Also, serum level of creatinine tended to decrease, but not significantly. Pretreatment with melatonin prevented the increase by subsequently administered indomethacin in the renal activity of lipid peroxidation and acid phosphatase. However, this pretreatment regimen partially suppressed the adverse changes in the remaining analyzed cytotoxic parameters induced by indomethacin in both serum and kidney. These results indicate that oral administration of melatonin at a low dose level exerted moderate antioxidant action, thereby it protected against some of the renal detrimental effects produced by indomethacin.