Diagnosis and Surgical Treatment of Renal Hydatid Disease: a Retrospective Analysis of 30 Cases

Echinococcosis (CE) is an infection which is caused by the larval stage of a tapeworm and is endemic in stockbreeding regions of developing countries. The kidney is the most commonly affected organ in the urinary tract. However, reports on renal hydatid disease are limited in the literature, and usually there are no specific clinical characteristics and promising operative methods. The purpose of this study is to assess the most appropriate surgical technique for the patient with urinary tract CE. We retrospectively analyzed thirty patients with renal hydatid cysts who received different surgical treatments in the urology department of the First Affiliated Hospital of Xinjiang Medical University from February 1985 to April 2010. Twenty patients were males and ten were females. The diagnostic accuracy was 74%, 87.5%, and 66.6% respectively by using of ultrasound, CT, and laboratory tests. Thirty patients were followed up for 1–15 years after surgery. One patient experienced a recurrence of renal CE. The ultrasound, CT, and immunological tests are an important means of diagnosis. The surgical treatment principle of renal hydatid should be based on residual renal function, hydatid cyst size, number, location, and surgical techniques to determine the surgical plan to retain the renal function.     

Oh,SNAP! How enteroviruses redirect autophagic traffic away from degradation

Picornaviruses, one of the major causes of human diseases ranging from the common cold to acute flaccid paralysis, have a short cytosolic lifecycle that, in cultured cells, ends in cell lysis. For years, the prevailing model was that these viruses exit from cells exclusively through cell lysis. However, over the last several years it has become apparent that for some picornaviruses, a macroautophagy/autophagy-related pathway can result in release of virus particles wrapped in a membrane containing autophagic markers. It has been proposed that this enveloped release predominates within hosts, allowing cell-to-cell movement of virus while minimizing exposure to the immune system. One reason that picornaviruses induce the autophagy pathway is to provide membrane scaffolds for RNA replication complexes. Perhaps more importantly, acidified autophagosomes (known as amphisomes) provide havens for maturation of new viral particles into infectious viruses. In back-to-back papers recently published in Cell Reports, our labs investigated a basic question: if picornavirus particles are maturing inside amphisomes, then how are they avoiding the typical degradative fate of autophagic cargo and exiting the cell intact?     

Tauroursodeoxycholic acid alleviates secondary injury in the spinal cord via up-regulation of CIBZ gene

Spinal cord injury (SCI) is generally divided into primary and secondary injuries, and apoptosis is an important event of the secondary injury. As an endogenous bile acid and recognized endoplasmic reticulum (ER) stress inhibitor, tauroursodeoxycholic acid (TUDCA) administration has been reported to have a potentially therapeutic effect on neurodegenerative diseases, but its real mechanism is still unclear. In this study, we evaluated whether TUDCA could alleviate traumatic damage of the spinal cord and improve locomotion function in a mouse model of SCI. Traumatic SCI mice were intraperitoneally injected with TUDCA, and the effects were evaluated based on motor function assessment, histopathology, apoptosis detection, qRT-PCR, and western blot at different time periods. TUDCA administration can improve motor function and reduce secondary injury and lesion area after SCI. Furthermore, the apoptotic ratios were significantly reduced; Grp78, Erdj4, and CHOP were attenuated by the treatment. Unexpectedly, the levels of CIBZ, a novel therapeutic target for SCI, were specifically up-regulated. Taken together, it is suggested that TUDCA effectively suppressed ER stress through targeted up-regulation of CIBZ. This study also provides a new strategy for relieving secondary damage by inhibiting apoptosis in the early treatment of spinal cord injury.     

云南多斑按蚊种团两亲缘种核型和异染色质区的比较观察

通过对多斑按蚊种团亲缘种中的达逻毗按蚊An．dravidicus和威氏按蚊An．willmori核型与异染色区比较,发现存在着明显差异：威氏按蚊的性染色体为亚中着丝点,x染色体的长臂上出现3条带;而达逻毗按蚊的性染色体为端着丝点,x染色体以2条带为主。表明利用染色体技术研究该种团亲缘种的鉴定有一定的价值。     

HSP25 down-regulation enhanced p53 acetylation by dissociation of SIRT1 from p53 in doxorubicin-induced H9c2 cell apoptosis

Heat shock proteins (HSPs) play important roles in cellular stress resistance. Previous reports had already suggested that HSP27 played multiple roles in preventing doxorubicin-induced cardiotoxicity. Although HSP25 might have biological functions similar to its human homolog HSP27, the mechanism of HSP25 is still unclear in doxorubicin-induced cardiomyocyte apoptosis. To investigate HSP25 biological function on doxorubicin-induced apoptosis, flow cytometry was employed to analyze cell apoptosis in over-expressing HSP25 H9c2 cells in presence of doxorubicin. Unexpectedly, the H9c2 cells of over-expressing HSP25 have no protective effect on doxorubicin-induced apoptosis. Moreover, no detectable interactions were detected by coimmunoprecipitation between HSP25 and cytochrome c, and HSP25 over-expression failed in preventing cytochrome c release induced by doxorubicin. However, down-regulation of endogenous HSP25 by a specific small hairpin RNA aggravates apoptosis in H9c2 cells. Subsequent studies found that HSP25, but not HSP90, HSP70, and HSP20, interacted with SIRT1. Knockdown of HSP25 decreased the interaction between SIRT1 and p53, leading to increased p53 acetylation on K379, up-regulated pro-apoptotic Bax protein expression, induced cytochrome c release, and triggered caspase-3 and caspase-9 activation. These findings indicated a novel mechanism by which HSP25 regulated p53 acetylation through dissociation of SIRT1 from p53 in doxorubicin-induced H9c2 cell apoptosis.     

Naringin in Ganshuang Granule suppresses activation of hepatic stellate cells for anti‐fibrosis effect by inhibition of mammalian target of rapamycin

A previous study has demonstrated that Ganshuang granule (GSG) plays an anti‐fibrotic role partially by deactivation of hepatic stellate cells (HSCs). In HSCs activation, mammalian target of rapamycin (mTOR)‐autophagy plays an important role. We attempted to investigate the role of mTOR‐autophagy in anti‐fibrotic effect of GSG. The cirrhotic mouse model was prepared to demonstrate the anti‐fibrosis effect of GSG. High performance liquid chromatography (HPLC) analyses were used to identify the active component of GSG. The primary mouse HSCs were isolated and naringin was added into activated HSCs to observe its anti‐fibrotic effect. 3‐methyladenine (3‐MA) and Insulin‐like growth factor‐1 (IGF‐1) was added, respectively, into fully activated HSCs to explore the role of autophagy and mTOR. GSG played an anti‐fibrotic role through deactivation of HSCs in cirrhotic mouse model. The concentration of naringin was highest in GSG by HPLC analyses and naringin markedly suppressed HSCs activation in vitro, which suggested that naringin was the main active component of GSG. The deactivation of HSCs caused by naringin was not because of the autophagic activation but mTOR inhibition, which was supported by the following evidence: first, naringin induced autophagic activation, but when autophagy was blocked by 3‐MA, deactivation of HSCs was not attenuated or reversed. Second, naringin inhibited mTOR pathway, meanwhile when mTOR was activated by IGF‐1, deactivation of HSCs was reversed. In conclusion, we have demonstrated naringin in GSG suppressed activation of HSCs for anti‐fibrosis effect by inhibition of mTOR, indicating a potential therapeutic application for liver cirrhosis.     

Spatial distributions of tree species in a subtropical forest of China

The spatial dispersion of individuals in a species is an important pattern that is controlled by many mechanisms. In this study we analyzed spatial distributions of tree species in a large-scale (20 ha) stem-mapping plot in a species-rich subtropical forest of China. O-ring statistic was used to measure spatial patterns of species with abundance >10. Ω_0–10, the mean conspecific density within 10 m of a tree, was used as a measure of the intensity of aggregation of a species. Our results showed: (1) aggregated distribution was the dominant pattern in the plot. The percentage of aggregated species decreased with increased spatial scale. (2) The percentages of significantly aggregated species decreased from abundant to intermediate and to rare species. Rare species was more strongly aggregated than common species. Aggregation was weaker in larger diameter classes. (3) Seed traits determined the spatial patterns of trees. Seed dispersal mode can influence spatial patterns of species, with species dispersed by both modes being less clumped than species dispersed by animal or wind, respectively. Considering these results, we concluded that seed dispersal limitation, self-thinning and habitat heterogeneity primarily contributed to spatial patterns and species coexistence in the forest.     

Propofol protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation

Propofol is a widely used intravenous anesthetic agent with antioxidant properties secondary to its phenol based chemical structure. Treatment with propofol has been found to attenuate oxidative stress and prevent ischemia/reperfusion injury in rat heart. Here, we report that propofol protects cardiac H9c2 cells from hydrogen peroxide (H₂O₂)-induced injury by triggering the activation of Akt and a parallel up-regulation of Bcl-2. We show that pretreatment with propofol significantly protects against H₂O₂-induced injury. We further demonstrate that propofol activates the PI3K-Akt signaling pathway. The protective effect of propofol on H₂O₂-induced injury is reversed by PI3K inhibitor wortmannin, which effectively suppresses propofol-induced activation of Akt, up-regulation of Bcl-2, and protection from apoptosis. Collectively, our results reveal a new mechanism by which propofol inhibits H₂O₂-induced injury in cardiac H9c2 cells, supporting a potential application of propofol as a preemptive cardioprotectant in clinical settings such as coronary bypass surgery.