Hospitalized pain patients have recently doubled: a retrospective case series study in Shenzhen Nanshan People's Hospital of China.

AIM: To study the characteristics of hospitalized pain patients in Shenzhen with the aim of identifying some of the social, economic and therapeutic aspects of pain management in China. METHODS: A retrospective study was designed to collect the information of 3061 hospitalized pain patients in 2003, 2007 and 2011. Their demographic characteristics, diagnoses of pain types, hospitalization, therapeutic effect, economic cost and payment types were analyzed. RESULTS: The number of female patients significantly increased with time. The patient's average age increased from 41.3 in 2003 to 49.7 years old in 2011. The most common diagnosis of pain was lumbar intervertebral disc herniation. The total hospitalization days of each patient per year significantly decreased from 15.7 days in 2003 to 10.4 days in 2011. However, the hospitalization cost for each patient was almost doubled. CONCLUSION: The hospitalized pain patients and their economic burdens have almost been doubled in the recent four years.

Propidium iodide (PI) stains Nissl bodies and may serve as a quick marker for total neuronal cell count.

Propidium iodide (PI) reacts with both DNA and RNA and is a commonly used fluorescent reagent for nucleic acid staining. The aim of the study was to compare the cellular staining patterns of PI with that of Nissl staining in rat nervous tissues and to report a modified staining method that selectively labels Nissl bodies in neurons. Cryosections and paraffin sections of different tissues of normal Sprague-Dawley rats, including trigeminal ganglia, dorsal root ganglia, spinal cord, liver, and small intestine, were stained by either PI or the hematoxylin and eosin method. Some sections were treated with RNase or DNase before the above staining, and some were double stained with PI and a Nissl stain. The sections were observed by light, fluorescence or confocal microscopy. Results showed strong PI signals detected as patterns of granules in the neuronal cytoplasm of all nervous tissues, whereas the staining of neuronal nuclei was weaker. In contrast, nuclei of neuroglial cells were strongly stained by PI, while the cytoplasm was not obviously stained. Pretreatment of the neural tissue with RNase abolished the PI signals. Furthermore, the PI positive granules in neuronal cytoplasm co-localized with Nissl bodies stained by the fluorescent Nissl stain. When the tissue was pretreated with DNase, PI only stained the cytoplasmic granules of neurons, but not that of glial cells. Our results show that PI stains Nissl bodies and may serve as an economical and convenient neuron marker for neuronal cell counting when specific neural markers such as antibodies are not readily available.

Hepatocyte growth factor promotes long-term survival and axonal regeneration of retinal ganglion cells after optic nerve injury: comparison with CNTF and BDNF.

AIMS: Different trophic factors are known to promote retinal ganglion cell survival and regeneration, but each had their own limitations. We report that hepatocyte growth factor (HGF) confers distinct advantages in supporting ganglion cell survival and axonal regeneration, when compared to two well-established trophic factors ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF). METHODS: Ganglion cells in adult hamster were injured by cutting the optic nerve. HGF, CNTF, or BDNF was injected at different dosages intravitreally after injury. Ganglion cell survival was quantified at 7, 14, or 28 days postinjury. Peripheral nerve (PN) grafting to the cut optic nerve of the growth factor-injected eye was performed either immediately after injury or delayed until 7 days post-injury. Expression of heat-shock protein 27 and changes in microglia numbers were quantified in different growth factor groups. The cellular distribution of c-Met in the retina was examined by anti-c-Met immunostaining. RESULTS: Hepatocyte Growth Factor (HGF) was equally potent as BDNF in promoting short-term survival (up to 14 days post-injury) and also supported survival at 28 days post-injury when ganglion cells treated by CNTF or BDNF failed to be sustained. When grafting was performed without delay, HGF stimulated twice the number of axons to regenerate compared with control but was less potent than CNTF. However, in PN grafting delayed for 7 days after optic nerve injury, HGF maintained a better propensity of ganglion cells to regenerate than CNTF. Unlike CNTF, HGF application did not increase HSP27 expression in ganglion cells. Microglia proliferation was prolonged in HGF-treated retinas compared with CNTF or BDNF. C-Met was localized to both ganglion cells and Muller cells, suggesting HGF could be neuroprotective via interacting with both neurons and glia. CONCLUSION: Compared with CNTF or BDNF, HGF is advantageous in sustaining long-term ganglion cell survival and their propensity to respond to favorable stimuli.

Anti-tumor action of trichosanthin, a type 1 ribosome-inactivating protein, employed in traditional Chinese medicine: a mini review.

Trichosanthin (TCS) as a midterm abortifacient medicine has been used clinically in traditional Chinese medicine for centuries. Additionally, TCS manifests a host of pharmacological properties, for instance, anti-HIV and anti-tumor activities. TCS has been reported to inhibit cell growth of a diversity of cancers, including cervical cancer, choriocarcinoma, and leukemia/lymphoma, etc. This article purported to review the various anti-tumor activities of TCS and the mechanism of apoptosis it induced in these tumor cells. These research progresses provide an insight into cancer research and treatment as well as disclose new pharmacological properties of the ancient but popular Chinese medicine.

Mechanism of the specific neuronal toxicity of a type I ribosome-inactivating protein, trichosanthin.

The aim was to study the mechanism of neuronal toxicity, the cellular pathway, and the glial cell reactions induced by trichosanthin (TCS), a type I ribosome-inactivating protein (RIP). Ricin A chain (RTA) was included for comparison. TCS, RTA, and fluorescein isothiocyanate (FITC)-labeled TCS and RTA were separately injected into rat eyes. Saline or pure FITC was used as the control. Electron microscopy, confocal microscopy, and lectin and immunohistochemical staining were used to study the neurotoxic mechanism. TCS mainly induced apoptosis by causing degeneration of the mitochondria. TCS was able to enter the Müller and pigment cells. It caused a change in cell number of the following types of glial cells: a decrease in Müller cells, an increase in astrocytes, and little change in microglia. In contrast, RTA mainly induced necrosis and entered vascular endothelial cells. Astrocyte and microglia reactions were stronger in the RTA-treated retinas than those in the TCS-treated retinas. In conclusion, TCS appears to selectively enter and destroy Müller and pigment epithelia cells, which subsequently induce the death of photoreceptors. Degeneration of mitochondria is involved in the pathways of apoptosis of the photoreceptors caused by TCS. In sharp contrast, RTA can enter vascular endothelial cells and damage the vascular endothelium, resulting in retinitis and necrosis.