• Toxicological Research
• /
• 제17권
• /
• pp.117-125
• /
• 2001

Envenoming by Russells viper causes a broad spectrum of renal impairment. Renal failure is an important complication in patients bitten by Russells viper. Experimental work in animals and in vitro has elucidated pathophysiological mechanisms that contribute to life threatening complications and have suggested possibilities for therapeutic intervention. The evidence in experimental animals regarding mechanisms of venom action in relation to changes in either extrarenal or intrarenal factors is presented. The cardiovascular system and renal hemodynamics are affected by venom. Reductions of renal function including renal hemodynamics are associated directly with changes in general circulation during envenomation. Possible endogenous mechanisms for releasing the hormone inducing renal vasoconstriction after envenomation are evident. Hormonal factor such as the catecholamine, prostaglandin and renin angiotensin systems induce these changes. Direct nephrotoxicity of venom action is studied in the isolated per-fused kidney. Characteristic polarization of the cell membrane, changes of mitochondrial activity and Na-K ATPase in renal tubular cells are observed. Changes in renal function and the cardiovascular system are observed of ter envenomation and are reversed by the administration of Russells viper antivenom (purified equine immunoglobulin, $Fab_2$ fragment). The neutralizing effects are more efficient when the intravenous injection of antivenom is given within 30 min after the envenomation.

• Journal of Microbiology and Biotechnology
• /
• 제30권4호
• /
• pp.477-481
• /
• 2020

Viability plays an important role in the beneficial microbes (probiotics) to produce health benefits. However, this idea has been changed after the invention of the term "paraprobiotics," indicating that non-viable microbes could produce health benefits similar to those produced by live probiotics. Occasionally, it might be dangerous to administer live probiotics to people with weak immunity. In such cases, ingestion of paraprobiotics could be a potential alternative. The definition of paraprobiotics refers to the use of inactivated (non-viable) microbial cells or cell fractions to provide health benefits to the consumer. Paraprobiotics have attracted much attention because of their long shelf life, safety, and beneficial effects, such as modulation of immunity, modification of biological responses, reduction of cholesterol, anti-inflammatory, and antiproliferative properties. These features indicate that paraprobiotics may play a vital role in improving the health of the consumer by enhancing particular physiological functions, even though the exact underlying mechanisms have not yet been completely elucidated. In this mini-review, we briefly discuss the historical backgrounds of paraprobiotics and evidence of their health-promoting effects, prophylactic, and therapeutic properties.

• Journal of Korean Neurosurgical Society
• /
• 제58권5호
• /
• pp.401-411
• /
• 2015

More than 10 years have passed since lumbar total disc replacement (LTDR) was introduced for the first time to the world market for the surgical management of lumbar degenerative disc disease (DDD). It seems like the right time to sum up the relevant results in order to understand where LTDR stands on now, and is heading forward to. The pathogenesis of DDD has been currently settled, but diagnosis and managements are still controversial. Fusion is recognized as golden standard of surgical managements but has various kinds of shortcomings. Lately, LTDR has been expected to replace fusion surgery. A great deal of LTDR reports has come out. Among them, more than 5-year follow-up prospective randomized controlled studies including USA IDE trials were expected to elucidate whether for LTDR to have therapeutic benefit compared to fusion. The results of these studies revealed that LTDR was not inferior to fusion. Most of clinical studies dealing with LTDR revealed that there was no strong evidence for preventive effect of LTDR against symptomatic degenerative changes of adjacent segment disease. LTDR does not have shortcomings associated with fusion. However, it has a potentiality of the new complications to occur, which surgeons have never experienced in fusion surgeries. Consequently, longer follow-up should be necessary as yet to confirm the maintenance of improved surgical outcome and to observe any very late complications. LTDR still may get a chance to establish itself as a substitute of fusion both nominally and virtually if it eases the concerns listed above.

• Asian Pacific Journal of Cancer Prevention
• /
• 제15권23호
• /
• pp.10495-10500
• /
• 2015

Background: To evaluate the effects of bufalin in A549 human lung adenocarcinoma epithelial cells in vitro and assess the underlying mechanisms. Materials and Methods: Human A549 non-small cell lung cancer (NSCLC) cells were treated with various concentrations of bufalin. Cell proliferation was measured by CCK-8 assay, apoptotic cell percentage was calculated by flow cytometry and morphological change was observed by inverted phase contrast microscopy/transmission electron microscopy. In addition, the membrane potential of mitochondria was detected by JC-1 fluorescence microscopy assay, and the related protein expression of cytochrome C and caspase-3 was analyzed by Western blotting. Results: Bufalin could inhibit the proliferation of A549 cells via induction of apoptosis, with the evidence of characteristic morphological changes in the nucleus and mitochondria. Furthermore, bufalin decreased the mitochondrial membrane potential with up-regulation of cytochrome C in the cytosol, and activation of caspase-3. Conclusions: Bufalin inhibits the proliferation of A549 cells and triggers mitochondria-dependent apoptosis, pointing to therapeutic application for NSCLC.

• Asian Pacific Journal of Cancer Prevention
• /
• 제15권16호
• /
• pp.6485-6488
• /
• 2014

Research over the years has progressively and sequentially provided near complete resolution of regulators of the DNA repair pathways which are so important for cancer prevention. Ataxia-telangiectasia mutated kinase (ATM), a high-molecular-weight PI3K-family kinase has emerged as a master regulator of DNA damage signaling and extensive cross-talk between ATM and downstream proteins forms an interlaced signaling network. There is rapidly growing scientific evidence emphasizing newly emerging paradigms in ATM biology. In this review, we provide latest information regarding how oxidative stress induced activation of ATM can be utilized as a therapeutic target in different cancer cell lines and in xenografted mice. Moreover, crosstalk between autophagy and ATM is also discussed with focus on how autophagy inhibition induces apoptosis in cancer cells.

• The Korean Journal of Physiology and Pharmacology
• /
• 제22권2호
• /
• pp.193-201
• /
• 2018

Connective tissue growth factor (CTGF) is a novel fibrotic mediator, which is considered to mediate fibrosis through extracellular matrix (ECM) synthesis in diabetic cardiovascular complications. Statins have significant immunomodulatory effects and reduce vascular injury. We therefore examined whether fluvastatin has anti-fibrotic effects in vascular smooth muscle cells (VSMCs) and elucidated its putative transduction signals. We show that advanced glycation end products (AGEs) stimulated CTGF mRNA and protein expression in a time-dependent manner. AGE-induced CTGF expression was mediated via ERK1/2, JNK, and Egr-1 pathways, but not p38; consequently, cell proliferation and migration and ECM accumulation were regulated by CTGF signaling pathway. AGE-stimulated VSMC proliferation, migration, and ECM accumulation were blocked by fluvastatin. However, the inhibitory effect of fluvastatin was restored by administration of CTGF recombinant protein. AGE-induced VSMC proliferation was dependent on cell cycle arrest, thereby increasing G1/G0 phase. Fluvastatin repressed cell cycle regulatory genes cyclin D1 and Cdk4 and augmented cyclin-dependent kinase inhibitors p27 and p21 in AGE-induced VSMCs. Taken together, fluvastatin suppressed AGE-induced VSMC proliferation, migration, and ECM accumulation by targeting CTGF signaling mechanism. These findings might be evidence for CTGF as a potential therapeutic target in diabetic vasculature complication.

• Journal of Korean Neurosurgical Society
• /
• 제40권2호
• /
• pp.69-73
• /
• 2006

Objective : The optimal surgical treatment for symptomatic middle cranial fossa arachnoid cysts is controversial. Therapeutic options include endoscopic fenestration, excision, cyst shunting, and craniotomy for fenestration of basal cistern. We reviewed the results of surgically treated middle cranial fossa arachnoid cysts. Methods : We performed a retrospective study in 18 cases of middle cranial fossa arachnoid cysts who had been treated with microsurgical fenestration between 1995 to 2003. The analysis was based on the results of the patients' age, sex distribution, developed area, clinical symptoms, treatment method, and complications. Results : Eighteen surgical treated middle cranial fossa arachnoid cysts patients were evaluated. The age range of cyst development was between 2 years and 44 years with the average of 16.4 years. The follow-up periods averaged 31.48 months. There were 15 male and 3 female patients, with significantly more cyst development in males than females. The most common clinical symptom was headache, followed by seizure. In the entire series, 77.8% of patients demonstrated a decrease in cyst size In serial imaging studies. Of them, 67.3% demonstrated a complete cyst effacement. Overall, 100% of patients with Grade I cysts, 81.8% of patients with Grade II cysts, 60% of patients with Grade III cysts exhibited evidence of decrease in cyst size during long-term monitoring. Complications included headache, meningitis, and hydrocephalus. Conclusion : Patients who were treated with microsurgical fenestration showed good outcome with acceptable complications. We concluded that microsurgical fenestration is a safe and effective surgical method for middle cranial fossa arachnoid cysts.

• 대한한방내과학회지
• /
• 제19권2호
• /
• pp.219-232
• /
• 1998

Paljintanggagmbang has been used for cure of tumor as a traditional medicine without any experimental evidence to support the rational basis for its clinical use. This study was carried out to evaluate. the possible therapeutic or antitumoral effects of Paljintanggagmbang extract against tumor, and to carry out some mechanisms responsible for its effect. Experimental studis were performed for measurement of Humoral and Cellular Immune Response and Phagocytosis in Mice treated with mitomytion C(MMC) and Paljintanggagmbang alone and combination. The results obtained in this study were as follows 1. The adminstration of Paljintanggagmbang extract decresed size of tumors cell which MCA induced. 2. The adminstration of Paljintanggagmbang extract decresed growth of the tumors which S 180 transplant. 3. The adminstration of Paljintanggagmbang extract decresed reproduction of A549, Hep3b, 3LL cell and S 180 in vivo. 4. The adminstration of Paljintanggagmbang extract incresed activity of the NK cell. These results also suggested that effect of Paljintanggagmbang might be chiefly due to nonspecific enhancement of Humoral and Cellular Immune Response and Phagocytosis in Mice treated with MMC and Paljintanggagmbang alone and combination.

• IMMUNE NETWORK
• /
• 제12권2호
• /
• pp.48-57
• /
• 2012

Acute viral encephalitis caused by neurotrophic viruses, such as mosquito-borne flaviviruses, is an emerging and re-emerging disease that represents an immense global health problem. Considerable progression has been made in understanding the pathogenesis of acute viral encephalitis, but the immune-pathological processes occurring during the progression of encephalitis and the roles played by various molecules and cellular components of the innate and adaptive systems still remain undefined. Recent findings reveal the significant contribution of Toll-like receptors (TLRs) and regulatory $CD4^+$ T cells in the outcomes of infectious diseases caused by neurotrophic viruses. In this review, we discuss the ample evidence focused on the roles of TLRs and $CD4^+$ helper T cell subsets on the progression of acute viral encephalitis. Finally, we draw attention to the importance of these molecules and cellular components in defining the pathogenesis of acute viral encephalitis, thereby providing new therapeutic avenues for this disease.

• 대한본초학회지
• /
• 제21권4호
• /
• pp.93-101
• /
• 2006

Objectives : Increasing evidence has linked chronic inflammation to a number of neurodegenerative disorders including Alzheimer's disease(AD), Parkinson's disease(PD) and Huntington's disease(HD) in the inflammatory process. Uncontrolled activation of microglia may directly toxic to neurons by releasing various substances such as inflammatory cytokines ($TNF-{\alpha}$, $IL-1{\beta}$ and IL-6), NO, PEG2 and superoxide. In this study, the immunomodulatory effects of the herbal extract Panax notoginseng on cultured BV2 microglial cells and primary microglia were investigated to address potential therapeutic or toxic effects. Notoginseng radix extracts extracted from the root of the plant using Methanol. Methods : Cells were stimulated with LPS and treated with notoginseng at different concentrations. Results : Notoginseng significantly decreased LPS-induced production of $TNF-{\alpha}$ and IL-6 by the cultured microglial cells in a dose-dependent manner. The activation of iNOS mRNA and secretion of nitric oxide(NO) in microglial cells were inhibited in microglial cells in a dose-dependent manner by notoginseng. Conclusion : These results indicate that notoginseng inhibits LPS-induced activation of microglial cells and demonstrates notoginseng possess anti-inflammatory and immunosuppressive properties in vitro.