The SAPPI Ngodwana mill is the largest integrated pulp and paper mill in Africa and is situated in the Elands River catchment in the Mpumalanga province. A need has arisen at the mill to reduce effluent volumes requiring discharge. The combined mill effluent is currently irrigated onto pastures and over the years percolation of attenuated effluent has resulted in elevated chloride levels in the Elands River. Elevated chloride levels in the river have in turn impacted on the tobacco farmers downstream of the mill. Reclamation of Kraft Liner Board effluent was identified as a means of reducing the hydraulic load onto the irrigation pastures and at the same time reduce the intake of fresh water into the mill. Two possible uses for the reclaimed effluent, namely washing of bleached or unbleached pulp, were identified. The major reclaimed water quality variables of concern for re-use are; biodegradable organic material, colour and suspended solids. Approximately 9 months of pilot-scale activated sludge treatment of the effluent demonstrates that sufficient organic material can be removed for re-use, as wash water. Removal of the organic material was not influenced by sludge age in the range 2 to 8 days. A high degree of colour removal was achieved, which is contrary to reports in the literature. Even with the high colour removal achieved, however, insufficient colour was removed to allow washing of bleached pulp. Pulp and paper effluents are often reported to result in filamentous bulking activated sludges. This was confirmed in the testwork. Severe sludge settleability problems were experienced throughout the pilot-scale testwork. Filamentous bulking was identified as the cause of poor sludge settleability and preventative or control strategies would have to be implemented on full-scale. / Dissertation (MEng)--University of Pretoria, 2010. / Chemical Engineering / unrestricted

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目的：主要通過對激痛點相關文獻的收集與分析，初步探究激痛點治療慢性頭痛的針刺取穴方案，同時與傳統針灸的取穴和治療方案進行對比，以總結出兩者的區別和聯繫，為進一步提高治療頭痛的臨床水準提供依據，並為治療慢性頭痛拓寬臨床思路。方法：本文通過對國內外期刊文獻資料庫（ Pubmed 、CNKI 等）進行檢索，搜集激痛點及傳統針灸治療頭痛的有關內容，從頭頂痛、頭後部疼痛、最頁部頭痛及額部頭痛四個部位進行歸納總結。激痛點將從不同肌肉引起相關部位頭痛著手，而傳統針灸將從陽明經頭痛、太陽經頭痛、厥陰經頭痛及少陽經頭痛的取穴方案進行分類。結果： 1 、激痛點治療頭頂痛主要針刺胸鎖乳突肌胸骨部、頭夾肌、枕額肌的激痛點。傳統針灸療法治療頭頂痛局部選穴為百會、後頂、前頂﹔遠端選穴為合穀、中院、足三裡、公孫、太沖、內關。在治療頭頂痛時，巔頂為厥陰經走行之處，但與激痛點相近的穴位中無歸厥陰經的穴位。但頭夾肌的激痛點（與風池相近）為常見治療各部位頭痛的選穴之一。2 、激痛點治療頭後部疼痛主要針刺斜方肌TrPl 、胸鎖乳突肌胸骨部、胸鎖乳突肌鎖骨部、頭半棘肌、頸半棘肌、頸夾肌、枕部下肌肉群、枕肌、二腹肌及舌骨上肌群、顳肌TrP4 的激痛點。傳統針灸療法治療頭後部疼痛局部選穴為天柱、風池、風門、風府、大椎、百會﹔遠端取穴為申脈、後溪、昆侖。激痛點療法與傳統針灸在天柱、風池穴有位置的相近或重合。3 、激痛點治療顳部頭痛主要針刺斜方肌TrPl 、胸鎖乳突肌胸骨部、顳肌（ TrP1、2 、3 ）、頸夾肌、枕部下肌肉群、頭半棘肌的激痛點。傳統針灸療法治療顛部疼痛局部選穴為太陽、絲竹空、角孫、率谷﹔遠端選穴為風池、合穀、足臨泣、外關。在治療顳部頭痛中，量頁肌的激痛點與太陽穴相近。4 、激痛點治療額部頭痛主要針刺胸鎖乳突肌鎖骨部、胸鎖乳突肌胸骨部、頭半棘肌、額肌、顴大肌的激痛點。傳統針灸療法治療額部頭痛局部選穴為印堂、上星、陽白、頭維﹔遠端選穴為內庭、解溪、合谷、曲池、足三裡。兩者在陽白穴有位置的相近或重合，其中額大肌的激痛點與地倉相近，同屬陽明經。結論：激痛點和傳統針灸療法治療慢性頭痛既有相似之處，又存在差異。1 、兩者在理論基礎、治療方式、針刺後效應及治療病種方面皆存在不同。2 、同時，兩者在位置及取穴手段上又有一定的相似和重合。其中激痛點的選穴，與傳統針灸的局部選穴比較類似。但激痛點取穴不限於疼痛局部，還會在疼痛稍遠但與疼痛部位有直接或稍間接的聯繫處選穴針刺。而傳統針刺，常會配合四肢遠端取穴。關鍵字：激痛點取穴﹔頭痛﹔文獻綜述

Being knowledgeable about sensory processing disorders can help dental teams provide effective care and improve the oral health of this patient population.

Polymethyl methacry late-antibiotic implants for the local treatment of osteomyelitis have been used in hospitals in the U.S. since the 1970s. This treatment requires a second surgery for removal of t he depleted implant. The purpose of this study is to investigate a new biodegradable implant system based upon poly(ortho esters) (POE) which can release tobramycin sulfate (TS) over a 21-day period (the usual clinical treatment period) with simultaneous and subsequent degradation of polymer in the tissues to harmless constituents. The POE-TS disks without any excipients showed a similar drug release pattern regardless of TS loading ( 4%, 8%, 12%, w/ w) and thickness (148, 244, 433 pm): 20%-60% TS-release within the first 24 hours followed by less than 10% release during the following 20 days with less than 3% weight loss of the polymer. These formulations did not meet therapeutic requirements of either drug release or polymer degradation rate. POE d egradation is known to be acid sensitive. To achieve uniform and high TS release over 21 days, various concentrations of lactic acid (LA), sorbic acid (SA), oleic acid (OA) and palmitoleic acids (PA) were incorporated in the 244pm-disks of 8% TS. The disks with LA demonstrated a pseudo zero-order TS release. With SA, OA & PA, the TS release was multi-phasic and the rate of polymer degradation was found to be acid concentration dependent. The TS release from these disks could be attributed to burst effect, polymer erosion and diffusion. Among these formulations, disks with 0.2% LA and 0 .9% OA gave the best release rate of 2mg TS/ day/ g implant; they achieved desirable therapeutic level of TS release and POE degradation. No physical or chemical interactio ns were detected by DSC, NMR and JR. Comparisons of POE weight loss and molecular weight loss with different acid catalysts revealed extremely different kinetics of acid catalysis. Uniform distribution of the drug in the disks was concluded based on content uniformity studies. Aqueous and solid state stability of TS were found to be suitable for clinical usage.

The most exciting area in current cancer research is immuno-oncology, which aims to develop immunotherapy that activates the human immune system to attack cancers. However, we still lack broadly effective drugs and drug targets for this promising new cancer treatment modality. In an attempt to seek new immuno-oncology drugs that particularly target the antitumor innate immunity, our lab had previously screened traditional Chinese herbal medicine and found that water extract from a medicinal plant, Alocasia Cucullata (AC), has strong anticancer activity in mouse solid tumor models and acts partly by promoting antitumor, proinflammatory macrophages. However, the active components responsible for this exciting immuno-oncology activity and the corresponding immune targets are unknown. Therefore, the aim of my PhD study is to develop chemical biology strategies to isolate and purify the active components of AC from the crude water extract and identify the corresponding cellular targets and mechanisms. Results from my study identified two separable activities and active components, one smaller than 3K and the other larger than 100K, which work synergistically to simulate antitumor macrophages. Further analysis revealed the >100K active component is a large polysaccharide that binds to multiple Toll-like Receptors (TLRs) critical for activating proinflammatory M1-type macrophages. Identity of the Nonetheless, I was able to clean up this fraction by 50 fold and perform RNAseq to examine the innate immune targets of this intriguing drug lead and found it acts to differentiate monocytes to macrophages. Overall my PhD thesis has explored new chemical biology strategies to purify and characterize active components from traditional Chinese medicine towards new drug development and developed a variety of cell-based immune activity assays for identifying and characterizing novel innate immune drug targets and mechanisms

Background: ICG-001, an antagonist of CBP (CREB-binding protein), has been demonstrated to exert anti-tumor activity via the modulation of the Wnt signalling pathway. It has previously been demonstrated that miRNAs play an important role in ICG-001-mediated tumor suppression. In the present study, the role of miRNA-134 and 1-integrin in ICG-001-mediated anti-tumor activity in nasopharyngeal carcinoma (NPC) was examined. Methods: NPC cell lines including C666-1, HONE-1 and HK-1 were used in this study. RT-PCR and Western blot were used to study the expression of miRNA-134 and the protein expression of the target proteins, respectively. Confocal microscopy was used to analyse the subcellular localization of 1-integrin. In the functional studies, in vitro endothelial adhesion assay and in vivo nude mice model were used to evaluate the adhesion and migration of ICG-001-treated NPC cells in animals, respectively. Results: ICG-001 was found to up-regulate the expression of miRNA-134 and down-regulate 1-integrin in NPC cells. The effect was accompanied with the inhibition of the adhesion of NPC cells to lung endothelial cells. In addition, over-expression of miRNA-134 would down-regulate the expression of 1-integrin. Results from 1-integrin 3'UTR Renilla luciferase reporter assay confirmed that 1-integrin is a target of miRNA-134 in NPC cells. In the animal study, the ability of ICG-001-pretreated NPC cells or stable miRNA-134 expressing NPC cells to migrate to the mouse lung was greatly reduced. Conclusion: The CBP antagonist ICG-001 may further be developed as an anti-tumor agent for the treatment of nasopharyngeal carcinoma

Investigation of the adenosine A(2A) receptor on the enhanced rewarding effects of nicotine and dopamine D2 receptor signaling in a novel heritable model of drug abuse vulnerability Seth E. Turney, Loren D. Peeters, Olivia A. Jennings, Liza J. Wills, Russell W. Brown Many years ago, our laboratory along with a collaborator established that neonatal treatment of the dopamine (DA)D2-like receptor agonist quinpirole (NQ) to rats induces an increase in DAD2 receptor sensitivity throughout the animal’s lifetime, which has validity to schizophrenia (SZ) and a number of clinical conditions. These clinical conditions, which include SZ but also bipolar disorder, obsessive-compulsive disorder, panic disorder, and major depression all demonstrate increased drug abuse vulnerability, especially to cigarette smoking. Based on this permanent change in DAD2 sensitivity, we bred NQ-treated male and female rats with their NQ-treated or neonatal saline (NS)-treated counterparts. This F1 generation also demonstrated increases in DAD2 signaling, both behaviorally as well as through DAD2 signaling mechanisms. We have shown both d enhanced behavioral responding to nicotine on the conditioned place preference (CPP) and behavioral sensitization paradigms. These F1 offspring of NQ-treated rats also demonstrated increases of G-protein dependent and G-protein independent DAD2 signaling. Interestingly, the adenosine A(2A) receptor forms a mutual inhibitory heteromer with the DAD2 receptor. Adenosine is a known neuromodulator that can increase or decrease synaptic transmission in the brain, and there exists a hypothesis that adenosine dysfunction is the primary system which is disrupted in SZ which leads to changes in the dopamine and other neurotransmitter systems. The drug CGS 21680, an A(2A) agonist which stimulates the A(2A) receptor, is known to decrease DAD2 signaling and has been shown to block nicotine behavioral sensitization. A major focus in this project is on the adenosine A(2A) receptor as a novel pharmacological treatment target, since it is known that antipsychotic drugs which are often used to treat SZ and these other clinical conditions which have increased DAD2 signaling produce deleterious side effects, and novel medications are needed. Results here revealed that a 0.09 mg/kg dose of CGS 21680 was effective to block enhanced nicotine CPP and changes in DAD2 G-protein independent signaling in F1 generation rats. Interestingly, CGS 21680 did not affect G-protein dependent signaling in F1 generation animals, suggesting that the mechanism through which it is working may not be through the traditional DAD2 signaling mechanism. Future work is designed to analyze underlying mechanisms of this effect.