Poisoning by toxic plants in Hong Kong: a 15-year review.

INTRODUCTION: Hong Kong has a great diversity of plants, many of which are toxic to humans. The aim of this study was to identify the plant species most commonly involved in cases of plant poisoning in Hong Kong and to provide clinicians with a reference tool for the diagnosis and management of plant poisoning. METHODS: We retrospectively reviewed all plant poisoning cases referred to the Hospital Authority Toxicology Reference Laboratory from 1 January 2003 to 31 December 2017. Demographics, clinical presentation, laboratory findings, treatment and outcomes of patients, as well as morphological identification and analytical testing of the plant specimens, were investigated. RESULTS: A total of 62 cases involving 26 poisonous plant species were identified, among which Alocasia macrorrhizos (Giant Alocasia), Gelsemium elegans (Graceful Jessamine), and Rhododendron (Azalea) species were the three most commonly encountered. Gastrointestinal toxicity (n=30, 48%), neurological toxicity (n=22, 35%), and hepatotoxicity (n=6, 10%) were the three most common clinical problems. Forty-nine (79%) and eight (13%) patients had mild and moderate toxicity, respectively; they all recovered shortly with supportive treatment. The remaining five (8%) patients experienced severe toxicity requiring intensive care support. Most patients (n=61, 98%) used the plants intentionally: as a medicinal herb (n=31), as food (n=29), and for attempting suicide (n=1). Reasons for using the poisonous plants included misidentification (n=34, 55%), unawareness of the toxicity (n=20, 32%), and contamination (n=6, 10%). CONCLUSIONS: Although most plant exposure resulted in a self-limiting disease, severe poisonings were encountered. Epidemiology of plant poisonings is geographically specific. Clinicians should be aware of local poisonous plants and their toxicities.

Overexpression of Aurora-C interferes with the spindle checkpoint by promoting the degradation of Aurora-B.

The chromosomal passenger complex (CPC) plays a pivotal role in controlling accurate chromosome segregation and cytokinesis during cell division. Aurora-B, one of the chromosomal passenger proteins, is important for the mitotic spindle assembly checkpoint (SAC). Previous reports noted that Aurora-C is predominantly expressed in male germ cells and has the same subcellular localization as Aurora-B. Increasing evidence indicates that Aurora-C is overexpressed in many somatic cancers, although its function is uncertain. Our previous study showed that the aberrant expression of Aurora-C increases the tumorigenicity of cancer cells. Here, we demonstrate that overexpressed Aurora-C displaces the centromeric localization of CPCs, including INCENP, survivin, and Aurora-B. When cells were treated with nocodazole to turn on SAC, both the Aurora-B protein stability and kinase activity were affected by overexpressed Aurora-C. As a result, the activation of spindle checkpoint protein, BubR1, and phosphorylation of histone H3 and MCAK were also eliminated in Aurora-C-overexpressing cells. Thus, our results suggest that aberrantly expressed Aurora-C in somatic cancer cells may impair SAC by displacing the centromeric localization of CPCs.

Mechanisms of calcium oxalate crystal attachment to injured renal collecting duct cells.

BACKGROUND: Renal cell or tissue injury results in a loss of membrane lipid asymmetry and/or loss of cell polarity, and both events lead to changes on the surface of the cell membranes that enhance crystal attachment. We have proposed two distinct mechanisms of crystal attachment following membrane changes induced by various modes of injury. METHODS: Annexin V was used to determine whether phosphatidylserine (PS) exposure on the cell membrane surface plays a role in calcium oxalate monohydrate (COM) crystal attachment to cells that have lost their polarity as well as to cells that have lost their lipid asymmetry. We utilized two different experimental models of injury to renal epithelial cells in culture. The first model used calcium ionophore A23187 to induce a loss of lipid asymmetry, and the second model used EGTA to break down tight junctions and lose cell polarity. RESULTS: Inner medullary collecting duct cells that have lost lipid asymmetry demonstrated an increase in the number of cells that bound annexin V. However, when cells lost their polarity, they did not bind annexin V. In addition, the attachment of crystals to cells following a loss of cell polarity was not inhibited by annexin V. CONCLUSIONS: This study indicates that both individual cell injury (loss of lipid asymmetry) and generalized cell monolayer injury (loss of cell polarity) result in the presentation of different cell surfaces and that both forms of injury result in an increased affinity for crystal attachment. Both mechanisms could be important independently or collectively in the retention of microcrystals to renal collecting duct cells in urolithiasis.

Protein 4.1 R-135 interacts with a novel centrosomal protein (CPAP) which is associated with the gamma-tubulin complex.

Using a yeast two-hybrid system, we isolated a novel human centrosomal protein, CPAP (centrosomal P4.1-associated protein), which specifically interacts with the head domain of the 135-kDa protein 4.1R isoform (4.1R-135). Sequence analysis revealed that the carboxyl terminus of CPAP has 31.3% amino acid identity with human Tcp-10 (a t-complex responder gene product). Interestingly, most of the sequence identity is restricted to two conserved regions. One carries a leucine zipper, which may form a series of heptad repeats involved in coiled-coil formation; the other contains unusual glycine repeats with unknown function. Immunofluorescence analysis revealed that CPAP and gamma-tubulin are localized within the centrosome throughout the cell cycle. CPAP cosediments with gamma-tubulin in sucrose gradients and coimmunoprecipitates with gamma-tubulin, indicating that CPAP is a part of the gamma-tubulin complex. Furthermore, functional analysis revealed that CPAP is localized within the center of microtubule asters and may participate in microtubule nucleation. The formation of microtubule asters was significantly inhibited by anti-CPAP antibody. Together, these observations indicate that CPAP may play an important role in cell division and centrosome function.

Oxalate-induced exposure of phosphatidylserine on the surface of renal epithelial cells in culture.

A molecular mechanism of crystal attachment to renal cells after injury has been proposed in which the exposure of phosphatidylserine (PS) on the cell membrane surface following injury provides attachment sites for calcium-containing crystals. Annexin V was used to determine whether injury to kidney cells by oxalate in culture resulted in PS exposure on the cell surface. When continuous cultures of intermedullary collecting duct cells were exposed to various levels of oxalate, a dose-dependent increase in PS exposure was observed on the cell surfaces. Initially, only scattered cells expressed PS on the surface. However, as the level of oxalate increased, groups of cells began to express PS, suggesting that the injured cells may have an influence on neighboring cells. Exposure of PS on the cell membrane surface correlated with a corresponding increase in calcium oxalate monohydrate crystal attachment to the cells. This indicates that damage to kidney epithelial cells by elevated concentrations of urinary components, in this case oxalate, could result in exposure of PS on cells, which could provide a point of fixation or nucleation for calcium-containing crystals.

Clinical distinction between acute hemorrhagic and acute ischemic stroke by Siriraj stroke score.

BACKGROUND: The clinical distinction between hemorrhagic and ischemic stroke cannot be achieved by simple clinical evaluation, and it is impossible to submit all stroke patients to computed tomography. A simple, reliable, and safe diagnostic tool for acute stroke syndrome is needed. This study tested the Siriraj stroke score to verify its accuracy for distinguishing among the pathological subtypes of stroke. METHODS: This study included the one hundred and seventy-one patients with acute supratentorial stroke syndromes consecutively admitted to the Emergency Room of the Taichung Veterans General Hospital from April 1 to September 30, 1993. The Siriraj stroke score was calculated, then compared with results of computed tomography. The Siriraj stroke score was calculated as (2.5 x level of consciousness) + (2 x vomiting) + (2 x headache) + (0.1 x diastolic blood pressure) - (3 x atheroma markers) - 12. A score above 1 indicates supratentorial intracranial hemorrhage, while a score below -1 indicates infarction. The score between 1 and -1 represents an equivocal result needing further evaluation to verify diagnosis. RESULTS: The diagnostic sensitivities of the Siriraj stroke score for intracranial hemorrhage and infarction were 85% and 90% respectively, with an overall predictive accuracy of 88.5%. When three cases with subarachnoid hemorrhage whose scores were all above 1 were excluded, the sensitivities for cerebral hemorrhage and infarction were 83.8% and 90% respectively, with an overall predictive accuracy of 88.2%. CONCLUSIONS: The Siriraj stroke score can be used as a reliable bedside method for diagnosing acute stroke and for deciding which patients should have priority for computed tomography, it is also a valuable tool for epidemiology studies of stroke incidence and outcome.