Management of Spontaneously Ruptured Hepatocellular Carcinomas in the Radiofrequency Ablation Era

Background and aim

Spontaneous rupture of hepatocellular carcinoma (HCC) carries a high mortality. The use of radiofrequency ablation (RFA) in recent years has enriched the armamentarium for hemostasis of spontaneously ruptured HCCs but its results have not been documented. This study investigated the prognosis and outcome of spontaneous rupture of HCC as well as the results of using RFA for hemostasis.

Patients and method

From January 1991 to December 2010, 5283 patients were diagnosed with HCC at our hospital, and 189 of them had spontaneous rupture of HCCs. They were grouped under two periods: period 1, 1991–2000, n = 70; period 2, 2001–2010, n = 119. RFA was available in period 2 only.

Results

Hepatitis B virus infection was predominant in both periods. Surgical hemostasis was mainly achieved by hepatic artery ligation in period 1 and by RFA in period 2. The 30-day hospital mortality after surgical treatment was 55.6% (n = 18) in period 1 and 19.2% (n = 26) in period 2 (p = 0.012). Multivariate analysis identified 4 independent factors for better overall survival, namely, hemostasis by transarterial chemoembolization (hazard ratio 0.516, 95% confidence interval 0.354–0.751), hemostasis by RFA (hazard ratio 0.431, 95% confidence interval 0.236–0.790), having surgery as a subsequent treatment (hazard ratio 0.305, 95% confidence interval 0.186–0.498), and a serum total bilirubin level <19 umol/L (hazard ratio 1.596, 95% confidence interval 1.137–2.241).

Conclusion

The use of RFA for hemostasis during laparotomy greatly reduced the hospital mortality rate when compared with conventional hepatic artery ligation.     

Total C and N Pools and Fluxes Vary with Time,Soil Temperature,and Moisture Along an Elevation,Precipitation, and Vegetation Gradient in Southern Appalachian Forests

The interactions of terrestrial C pools and fluxes with spatial and temporal variation in climate are not well understood. We conducted this study in the southern Appalachian Mountains where complex topography provides variability in temperature, precipitation, and forest communities. In 1990, we established five large plots across an elevation gradient allowing us to study the regulation of C and N pools and cycling by temperature and water, in reference watersheds in Coweeta Hydrologic Laboratory, a USDA Forest Service Experimental Forest, in western NC, USA. Communities included mixed-oak pine, mixed-oak, cove hardwood, and northern hardwood. We examined 20-year changes in overstory productivity and biomass, leaf litterfall C and N fluxes, and total C and N pools in organic and surface mineral soil horizons, and coarse wood, and relationships with growing season soil temperature and precipitation. Productivity increased over time and with precipitation. Litterfall C and N flux increased over time and with increasing temperature and precipitation, respectively. Organic horizon C and N did not change over time and were not correlated to litterfall inputs. Mineral soil C and N did not change over time, and the negative effect of temperature on soil pools was evident across the gradient. Our data show that increasing temperature and variability in precipitation will result in altered aboveground productivity. Variation in surface soil C and N is related to topographic variation in temperature which is confounded with vegetation community. Data suggest that climatic changes will result in altered aboveground and soil C and N sequestration and fluxes.     

A human SHC-related sequence maps to chromosome 17, the SHC gene maps to chromosome 1

The SHC gene encodes a protein that is thought to act as an adapter in many signal transduction pathways; the SHC protein probably facilitates the activation of RAS proteins in response to a variety of factors. We have mapped the human SHC gene and have identified a new SHC-related sequence. We have sequenced the region corresponding to the SHC 3 UTR from both loci and have mapped cosmids by fluorescence in situ hybridization. The human SHC gene maps to the proximal long arm of chromosome 1 and the SHC-related sequence maps to the proximal long arm of chromosome 17. A number of cancers have been positioned in the proximal long arm of chromosome 1; this is of interest given the oncogenic potential of the SHC protein.     

Adverse effects of tempol on hidrosaline balance in rats with acute sodium overload

We studied the effects of tempol, an oxygen radical scavenger, on hydrosaline balance in rats with acute sodium overload. Male rats with free access to water were injected with isotonic (control group) or hypertonic saline solution (0.80 mol/l NaCl) either alone (Na group) or with tempol (Na-T group). Hydrosaline balance was determined during a 90 min experimental period. Protein expressions of aquaporin 1 (AQP1), aquaporin 2 (AQP2), angiotensin II (Ang II) and endothelial nitric oxide synthase (eNOS) were measured in renal tissue. Water intake, creatinine clearance, diuresis and natriuresis increased in the Na group. Under conditions of sodium overload, tempol increased plasma sodium and protein levels and increased diuresis, natriuresis and sodium excretion. Tempol also decreased water intake without affecting creatinine clearance. AQP1 and eNOS were increased and Ang II decreased in the renal cortex of the Na group, whereas AQP2 was increased in the renal medulla. Nonglycosylated AQP1 and eNOS were increased further in the renal cortex of the Na-T group, whereas AQP2 was decreased in the renal medulla and was localized mainly in the cell membrane. Moreover, p47-phox immunostaining was increased in the hypothalamus of Na group, and this increase was prevented by tempol. Our findings suggest that tempol causes hypernatremia after acute sodium overload by inhibiting the thirst mechanism and facilitating diuresis, despite increasing renal eNOS expression and natriuresis.     

Sulfidation of NiMn‐Layered Double Hydroxides/Graphene Oxide Composites toward Supercapacitor Electrodes with Enhanced Performance

Supercapacitors can deliver high‐power density and long cycle stability, but the limited energy density due to poor electronic and ionic conductivity of the supercapacitor electrode has been a bottleneck in many applications. A strategy to prepare microflower‐like NiMn‐layered double hydroxides (LDH) with sulfidation is delineated to reduce the charge transfer resistance of supercapacitor electrode and realize faster reversible redox reactions with notably enhanced specific capacitance. The incorporation of graphite oxide (GO) in NiMn LDH during sulfidation leads to simultaneous reduction of GO with enhanced conductivity, lessened defects, and doping of S into the graphitic structure. Cycling stability of the sulfidized composite electrode is enhanced due to the alleviation of phase transformation during electrochemical cycling test. As a result, this sulfidation product of LDH/GO (or LDHGOS) can reach a high‐specific capacitance of 2246.63 F g^?1 at a current density of 1 A g^?1, and a capacitance of 1670.83 F g^?1 is retained at a high‐current density of 10 A g^?1, exhibiting an outstanding capacitance and rate performance. The cycling retention of the LDHGOS electrode is also extended to ≈ 67% after 1500 cycles compared to only ≈44% of the pristine NiMn LDH.     

Experimental Persistent Infection of BALB/c Mice with Small-Colony Variants of Burkholderia pseudomallei Leads to Concurrent Upregulation of PD-1 on T Cells and Skewed Th1 and Th17 Responses

BackgroundBurkholderia pseudomallei (B. pseudomallei), the causative agent of melioidosis, is a deadly pathogen endemic across parts of tropical South East Asia and Northern Australia. B. pseudomallei can remain latent within the intracellular compartment of the host cell over prolonged periods of time, and cause persistent disease leading to treatment difficulties. Understanding the immunological mechanisms behind persistent infection can result in improved treatment strategies in clinical melioidosis.MethodsTen-day LD₅₀ was determined for the small-colony variant (SCV) and its parental wild-type (WT) via intranasal route in experimental BALB/c mice. Persistent B. pseudomallei infection was generated by administrating sub-lethal dose of the two strains based on previously determined LD₅₀. After two months, peripheral blood mononuclear cells (PBMCs) and plasma were obtained to investigate host immune responses against persistent B. pseudomallei infection. Lungs, livers, and spleens were harvested and bacterial loads in these organs were determined.ResultsBased on the ten-day LD₅₀, the SCV was ~20-fold less virulent than the WT. The SCV caused higher bacterial loads in spleens compared to its WT counterparts with persistent B. pseudomallei infection. We found that the CD4+ T-cell frequencies were decreased, and the expressions of PD-1, but not CTLA-4 were significantly increased on the CD4+ and CD8+ T cells of these mice. Notably, persistent infection with the SCV led to significantly higher levels of PD-1 than the WT B. pseudomallei. Plasma IFN-γ, IL-6, and IL-17A levels were elevated only in SCV-infected mice. In addition, skewed plasma Th1 and Th17 responses were observed in SCV-infected mice relative to WT-infected and uninfected mice.ConclusionB. pseudomallei appears to upregulate the expression of PD-1 on T cells to evade host immune responses, which likely facilitates bacterial persistence in the host. SCVs cause distinct pathology and immune responses in the host as compared to WT B. pseudomallei.