Background

Intraventricular rupture of brain abscesses (IVRBA) remains a catastrophic and fatal complication of bacterial brain abscess (BBA). However, no information has been reported about the risk factors that are predictive of intraventricular rupture.

Methods

This study was undertaken to determine the potential risk factors that are predictive of intraventricular ruptures in patients with BBA but without intraventricular rupture when arriving at the hospital. A comparison is also made between patients who already have IVRBA at the time of admission (initial IVRBA) and those who have the episode during hospitalisation (subsequent IVRBA).

Results

62 patients, including 45 who had initial IVRBA and 17 who had subsequent IVRBA, were examined. Stepwise logistic regression analysis showed that the adjusted risk of intraventricular rupture during hospitalisation for patients with multiloculated brain abscesses had an odds ratio (OR) of 4.2 (95% confidence interval (CI) 1.24 to 14.3; p = 0.02) compared with those without multiloculated brain abscesses (referent); a reduction of 1 mm in the distance between the ventricle and brain abscesses would increase the rupture rate by 10% (p = 0.006, OR 0.9, 95% CI 0.83 to 0.97).

Conclusion

This study shows that if the abscess is deep seated, multiloculated and close to the ventricle wall, a reduction of 1 mm in the distance between the ventricle and brain abscesses will increase the rupture rate by 10%. Despite aggressive medical and surgical management shown in this series, many patients continue to progress poorly.

Background

Hydrocephalus following spontaneous aneurysmal sub-arachnoid hemorrhage (SAH) is often associated with unfavorable outcome. This study aimed to determine the potential risk factors and outcomes of shunt-dependent hydrocephalus in aneurysmal SAH patients but without hydrocephalus upon arrival at the hospital.

Methods

One hundred and sixty-eight aneurysmal SAH patients were evaluated. Using functional scores, those without hydrocephalus upon arrival at the hospital were compared to those already with hydrocephalus on admission, those who developed it during hospitalization, and those who did not develop it throughout their hospital stay. The Glasgow Coma Score, modified Fisher SAH grade, and World Federation of Neurosurgical Societies grade were determined at the emergency room. Therapeutic outcomes immediately after discharge and 18 months after were assessed using the Glasgow Outcome Score.

Results

Hydrocephalus accounted for 61.9% (104/168) of all episodes, including 82 with initial hydrocephalus on admission and 22 with subsequent hydrocephalus. Both the presence of intra-ventricular hemorrhage on admission and post-operative intra-cerebral hemorrhage were independently associated with shunt-dependent hydrocephalus in patients without hydrocephalus on admission. After a minimum 1.5 years of follow-up, the mean Glasgow outcome score was 3.33 ± 1.40 for patients with shunt-dependent hydrocephalus and 4.21 ± 1.19 for those without.

Conclusions

The presence of intra-ventricular hemorrhage, lower mean Glasgow Coma Scale score, and higher mean scores of the modified Fisher SAH and World Federation of Neurosurgical grading on admission imply risk of shunt-dependent hydrocephalus in patients without initial hydrocephalus. These patients have worse short- and long-term outcomes and longer hospitalization.

Introduction

Serum concentrations of adhesion molecules may be connected to the pathogenesis of secondary brain injury after spontaneous intracerebral hemorrhage (ICH). This study posits the hypothesis that levels of adhesion molecules substantially increase after ICH and are decreased thereafter, and that they can predict treatment outcomes.

Methods

Two hundred and thirty-nine blood samples were collected from 60 consecutive patients admitted within 24 hours after onset of spontaneous ICH and 60 blood samples were collected from 60 volunteers. Additional samples were obtained on Days 4, 7, 10, and 14 after onset of ICH regardless of clinical deterioration.

Results

Upon discharge, the therapeutic outcomes of the 60 spontaneous ICH cases based on the modified Rankin Disability Scale (mMRS) showed that 17 had no disability while 8.3% developed delayed cerebral infarction (DCI). Statistical analysis of adhesion molecules between patient groups with good outcome (mMRS = 0 or 1) and poor outcome (mMRS ≥2) revealed significant differences in diabetes mellitus (P=0.049), hyperlipidemia (P=0.012), mentality change (P=0.043), ICH volume and intraventricular hemorrhage on admission (P=0.036 and 0.006, respectively), Glasgow Coma Scale (GCS) on admission (P≤0.001), neuro-surgical intervention (P=0.003), and sE-selectin and soluble intercellular cell adhesion-molecule-1 (sICAM-1) levels on admission (P=0.036 and 0.019, respectively). Multiple logistic regression analysis of these significant variables showed that GCS on admission, hyperlipidemia, and sICAM-1 (P=0.039, 0.042, and 0.022, respectively) were independently associated with outcome of acute spontaneous ICH.

Conclusion

Increased sICAM-1 and sE-selectin levels may imply poor therapeutic outcomes for the treatment of spontaneous ICH during hospitalization. These early inflammatory responses may cause whole-brain injury immediately after spontaneous ICH and offer a potential therapeutic target for such patients. The importance of these findings is that they offer a potential therapeutic target for patients with spontaneous ICH.

Anthraquinone compounds have been shown to induce apoptosis in different cancer cell types. Effects of chrysophanol, an anthraquinone compound, on cancer cell death have not been well-studied. The goal of this study was to examine if chrysophanol had cytotoxic effects and if such effects involved apoptosis or necrosis in J5 human liver cancer cells. Chrysophanol induced necrosis in J5 cells in a dose- and time-dependent manner. Non-apoptotic cell death was induced by chrysophanol in J5 cells and was characterized by caspase independence, delayed externalization of phosphatidylserine and plasma membrane disruption. Blockage of apoptotic induction by a general caspase inhibitor (z-VAD-fmk) failed to protect cells against chrysophanol-induced cell death. The levels of ROS production and loss of mitochondrial membrane potential (ΔΨm) were also determined to assess the effects of chrysophanol. However, reductions in ATP levels and increases in LDH activity indicated that chrysophanol stimulated necrotic cell death. In summary, human liver cancer cells treated with chrysophanol exhibited a cellular pattern associated with necrosis and not apoptosis.

FXYD proteins are novel regulators of Na+-K+-ATPase (NKA). In fish subjected to salinity challenges, NKA activity in osmoregulatory organs (e.g., gills) is a primary driving force for the many ion transport systems that act in concert to maintain a stable internal environment. Although teleostean FXYD proteins have been identified and investigated, previous studies focused on only a limited group of species. The purposes of the present study were to establish the brackish medaka (Oryzias dancena) as a potential saltwater fish model for osmoregulatory studies and to investigate the diversity of teleostean FXYD expression profiles by comparing two closely related euryhaline model teleosts, brackish medaka and Japanese medaka (O. latipes), upon exposure to salinity changes. Seven members of the FXYD protein family were identified in each medaka species, and the expression of most branchial fxyd genes was salinity-dependent. Among the cloned genes, fxyd11 was expressed specifically in the gills and at a significantly higher level than the other fxyd genes. In the brackish medaka, branchial fxyd11 expression was localized to the NKA-immunoreactive cells in gill epithelia. Furthermore, the FXYD11 protein interacted with the NKA α-subunit and was expressed at a higher level in freshwater-acclimated individuals relative to fish in other salinity groups. The protein sequences and tissue distributions of the FXYD proteins were very similar between the two medaka species, but different expression profiles were observed upon salinity challenge for most branchial fxyd genes. Salinity changes produced different effects on the FXYD11 and NKA α-subunit expression patterns in the gills of the brackish medaka. To our knowledge, this report is the first to focus on FXYD expression in the gills of closely related euryhaline teleosts. Given the advantages conferred by the well-developed Japanese medaka system, we propose the brackish medaka as a saltwater fish model for osmoregulatory studies.

The present study was to explore the biological responses of the newly compound, MJ-29 in murine myelomonocytic leukemia WEHI-3 cells in vitro and in vivo fates. We focused on the in vitro effects of MJ-29 on ER stress and mitochondria-dependent apoptotic death in WEHI-3 cells, and to hypothesize that MJ-29 might fully impair the orthotopic leukemic mice. Our results indicated that a concentration-dependent decrease of cell viability was shown in MJ-29-treated cells. DNA content was examined utilizing flow cytometry, whereas apoptotic populations were determined using annexin V/PI, DAPI staining and TUNEL assay. Increasing vital factors of mitochondrial dysfunction by MJ-29 were further investigated. Thus, MJ-29-provaked apoptosis of WEHI-3 cells is mediated through the intrinsic pathway. Importantly, intracellular Ca2+ release and ER stress-associated signaling also contributed to MJ-29-triggered cell apoptosis. We found that MJ-29 stimulated the protein levels of calpain 1, CHOP and p-eIF2α pathways in WEHI-3 cells. In in vivo experiments, intraperitoneal administration of MJ-29 significantly improved the total survival rate, enhanced body weight and attenuated enlarged spleen and liver tissues in leukemic mice. The infiltration of immature myeloblastic cells into splenic red pulp was reduced in MJ-29-treated leukemic mice. Moreover, MJ-29 increased the differentiations of T and B cells but decreased that of macrophages and monocytes. Additionally, MJ-29-stimulated immune responses might be involved in anti-leukemic activity in vivo. Based on these observations, MJ-29 suppresses WEHI-3 cells in vitro and in vivo, and it is proposed that this potent and selective agent could be a new chemotherapeutic candidate for anti-leukemia in the future.