Introduction: Most of the confirmed 2009 H1N1 pandemic cases showed mild influenza like illness similar to seasonal influenza. However, there were also severe and fatal cases. Knowledge of the risk factors associated with severe and fatal cases is important. This study assessed the risk factors for severe and fatal manifestations. Materials and Methods: Search of Medline/PubMed (search period unrestricted) using keywords ‘Pandemic’, ‘H1N1 influenza’, ‘risk factor’, ‘severe and/or fatal’ was performed. In addition, existing articles in our libraries concerning H1N1 influenza and environmental factors were used, without cross reference check on other search engines. Results: The incidence of severe and fatal cases ranged from 20 to 100% and from 0.7 to 39% respectively. Studies on the age as a factor showed mixed results but generally showed the younger age group to be at higher risk, different to that of seasonal influenza. Various co morbid conditions such as pregnancy, obesity, diabetes mellitus, chronic pulmonary and cardiac disease, being immune suppressed, nutritional status, and delay in treatment have been shown to important risk factors for severe disease. One study showed Streptococcus pneumoniae and Human respiratory syncytial virus A co-infection to have a role in the severity of the disease. Indirect racial study suggested that genetic factors are important. Other factors that may be important and required further research such as associated preexisting conditions such as arterial hypertension, active tuberculosis and neurological disease, in addition to over-responsive innate immune response, viral dose, alcohol consumption, and environmental factors. Conclusion: In the 2009 H1N1 influenza pandemic, risk factors for severe and fatal cases include preexisting medical conditions, obesity, underweight, pregnancy, and delay in antiviral treatment. Respiratory co-infection may be important.

The hallmark of Parkinson's disease is on-going degeneration of dopaminergic neurons in the substantia nigra, which may be due to various etiologies. Various approaches to alleviate symptoms are available, such as life-long pharmacological intervention, deep brain stimulation, and transplantation of dopaminergic neuron-containing fetal tissue. However, each of these approaches has a disadvantage. Several studies have shown that various kinds of stem cells, induced pluripotent stem cells, and other cells can differentiate into dopaminergic neurons and may be promising for treating Parkinson's disease in the future. Therefore, this review addresses those cells in terms of their prospects in cell therapy for Parkinson's disease. In addition, the need for safety and efficacy studies, various cell delivery modes and sites, and possible side effects will be discussed.
Deep Brain Stimulation ; Dopaminergic Neurons ; Fetus ; Induced Pluripotent Stem Cells ; Parkinson Disease ; Putamen ; Stem Cells ; Substantia Nigra ; Tissue Therapy ; Transplants

Transplantation of bone marrow derived stem cells (BMSCs) has been reported inhibits liver fibrosis. Several in vitro studies by co-culturing BMSCs and hepatic stellate cells (HSCs) indirectly or directly in 2D models showed inhibition of HSC as the key player in liver fibrosis. In this study, we investigated direct effect of BMSCs on HSCs by co-culturing BMSCs and HSCs in 3D model as it represents the liver microenvironment with intricate cell-cell and cell-matrix interactions. Primary isolated rat HSCs and BMSCs were directly co-cultured at 1:1 ratio with hanging drop method. The monoculture of rat HSCs served as positive control. Mono-culture and co-culture samples were harvested on day 3, 5 and 7 for histological analysis. The samples were analyzed for extracellular matrix deposition by Masson's Trichrome staining, tenascin-C immunocytochemistry, resting HSC's state as shown by positive Oil Red O stained cells. Our results indicated CD90+CD34− BMSCs anti-liver fibrosis potency as evidenced by higher proportion of Oil Red O-positive cells in the co-culture group compared to the monoculture group and the significant decrease in extracellular matrix deposition as well as the decrease in tenascin-C expression in the co-culture group (p<0.05) compared to the monoculture group. These findings demonstrate that BMSCs have a potential therapeutic effect against liver fibrotic process through their capacity to inhibit HSCs activation and their effect in minimizing extracellular matrix deposition.
Animals ; Bone Marrow* ; Coculture Techniques ; Extracellular Matrix* ; Fibrosis* ; Hepatic Stellate Cells* ; Immunohistochemistry ; In Vitro Techniques ; Liver ; Liver Cirrhosis ; Methods ; Rats ; Stem Cells* ; Tenascin