Equatorial Kelvin waves (KWs) are fundamental components of the tropical climate system. In this study, we investigate Kelvin waves (KWs) during the Hai-Tang typhoon of 2005 using Empirical Mode ...Decomposition (EMD) of regional precipitation, zonal and meridional winds. For the analysis, we use daily precipitation datasets from the Global Precipitation Climatology Project (GPCP) and wind datasets from the European Centre for Medium-Range Weather Forecasts (ECMWF) Interim Re-analysis (ERA-Interim). As an additional measurement, we use in-situ precipitation datasets from rain-gauges over the Taiwan region. The maximum accumulated precipitation was approximately 2400 mm during the period July 17–21, 2005 over the southwestern region of Taiwan. The spectral analysis using the wind speed at 950 hPa found in the 2nd, 3rd, and 4th intrinsic mode functions (IMFs) reveals prevailing Kelvin wave periods of ∼3 days, ∼4–6 days, and ∼6–10 days, respectively. From our analysis of precipitation datasets, we found the Kelvin waves oscillated with periods between ∼8 and 20 days.
•The accumulated precipitation was approximately ∼2400 mm during Hai-Tang period.•Planetary wave characteristics are investigated using daily wind and precipitation datasets.•The planetary waves are extracted using Empirical Mode Decomposition and it is highly adaptive decomposition technique.•An upward propagating 2–20 day planetary wave was present during the typhoon period.
Peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) transcriptional coactivators are key regulators of energy metabolism-related genes and are expressed in energy-demanding ...tissues. There are several PGC-1α variants with different biological functions in different tissues. The brain is one of the tissues where the role of PGC-1α isoforms remains less explored. Here, we used a toxin-based mouse model of Parkinson's disease (PD) and observed that the expression levels of variants PGC-1α2 and PGC-1α3 in the nigrostriatal pathway increases at the onset of dopaminergic cell degeneration. This increase occurs concomitant with an increase in glial fibrillary acidic protein levels. Since PGC-1α coactivators regulate cellular adaptive responses, we hypothesized that they could be involved in the modulation of astrogliosis induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Therefore, we analysed the transcriptome of astrocytes transduced with expression vectors encoding PGC-1α1 to 1α4 by massively parallel sequencing (RNA-seq) and identified the main cellular pathways controlled by these isoforms. Interestingly, in reactive astrocytes the inflammatory and antioxidant responses, adhesion, migration, and viability were altered by PGC-1α2 and PGC-1α3, showing that sustained expression of these isoforms induces astrocyte dysfunction and degeneration. This work highlights PGC-1α isoforms as modulators of astrocyte reactivity and as potential therapeutic targets for the treatment of PD and other neurodegenerative disorders.
•PGC-1α2 and α3 expression increases in the nigrostriatal pathway of mice exposed to the MPTP model of Parkinson's disease.•PGC-1α variants control the expression of different gene sets in astrocytes in culture.•Expressing PGC-1α2 and α3 in reactive astrocytes changes inflammatory and antioxidant responses, cell motility, and viability.
Disruption of brain cholesterol homeostasis has been implicated in neurodegeneration. Nevertheless, the role of cholesterol in Parkinson's Disease (PD) remains unclear. We have used N2a mouse ...neuroblastoma cells and primary cultures of mouse neurons and 1-methyl-4-phenylpyridinium (MPP
), a known mitochondrial complex I inhibitor and the toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), known to trigger a cascade of events associated with PD neuropathological features. Simultaneously, we utilized other mitochondrial toxins, including antimycin A, oligomycin, and carbonyl cyanide chlorophenylhydrazone. MPP
treatment resulted in elevated levels of total cholesterol and in a Niemann Pick type C1 (NPC1)-like phenotype characterized by accumulation of cholesterol in lysosomes. Interestingly, NPC1 mRNA levels were specifically reduced by MPP
. The decrease in NPC1 levels was also seen in midbrain and striatum from MPTP-treated mice and in primary cultures of neurons treated with MPP
. Together with the MPP
-dependent increase in intracellular cholesterol levels in N2a cells, we observed an increase in 5' adenosine monophosphate-activated protein kinase (AMPK) phosphorylation and a concomitant increase in the phosphorylated levels of mammalian target of rapamycin (mTOR). NPC1 knockout delayed cell death induced by acute mitochondrial damage, suggesting that transient cholesterol accumulation in lysosomes could be a protective mechanism against MPTP/MPP
insult. Interestingly, we observed a negative correlation between NPC1 protein levels and disease stage, in human PD brain samples. In summary, MPP
decreases NPC1 levels, elevates lysosomal cholesterol accumulation and alters mTOR signaling, adding to the existing notion that PD may rise from alterations in mitochondrial-lysosomal communication.
The pathogenesis of post-transplantation erythrocytosis (PTE) is not well understood and appears to be multifactorial. Our hypothesis in this study was that several factors, including toxicity of ...calcineurin inhibitor, immunologic factors, and chronic allograft nephropathy, can trigger local tissue hypoxia in peritubular interstitium, which is where production of erythropoietin (EPO) takes place. This local interstitial tissue hypoxia can cause an increase in renal EPO production, which induces the development of PTE.
This cross-sectional study included 15 renal transplant recipients, in whom polycythemia developed after kidney transplantation, with elevated hematocrit level to >51%. Forty-eight age- and gender-matched renal transplant recipients with normal hematocrit level were included as the renal transplant control group. In addition, 13 age- and gender-matched healthy subjects were also included as the healthy control group. We used urine hypoxia-inducible factor-2 alpha (HIF-2α) levels to evaluate whether there is local tissue hypoxia in renal allograft. HIF-2α levels were measured by double antibody sandwich enzyme-linked immunosorbent assay (ELISA). Serum EPO and insulin-like growth factor-1 (IGF-1) levels were also measured.
HIF-2α levels were significantly lower in the polycythemia group than the other two groups, but there was no significant difference between the healthy control group and the renal transplant control group with regard to HIF-2α levels. There was no significant difference among the 3 study groups in terms of levels of serum EPO and IGF-1.
Local tissue hypoxia in renal allograft does not seem to play an important role in the development of PTE.
•The pathogenesis of PTE is not well understood and appears to be multifactorial.•Local tissue hypoxia in peritubular interstitium, which is the place of production of EPO, can induce the development of PTE by increasing renal erythrocytosis production.•HIF-α subunits are oxygen sensitive and increase in hypoxic conditions.•HIF-2α levels did not increase in renal transplant recipients with PTE.•Local tissue hypoxia in renal allograft does not seem to play an important role in the development of PTE.
Herein we report the case of hepatic amoebic abscesses in an HIV-positive Italian seaman with a history of promiscuous heterosexual intercourse. In October 2004, the patient was hospitalized because ...of fever and recurring abdominal pain. Abdominal ultrasonography revealed six hepatic hypoechoid oval lesions with hyperechoid margins. Stool samples were negative for parasites and bacteria, and serology for Entamoeba histolytica was also negative. Therapy with meropenem plus levofloxacin was initiated. After a partial resolution of clinical symptoms and reduction of three hepatic lesions, the patient was again hospitalized in December 2004, because of recurring intense pain at the right hypochondrium and fever. At this time, one hepatic lesion at the sixth segment was enlarged, two lesions were unchanged, and the remaining three smaller abscesses were resolved. Serum antibodies for E. histolytica and amoebic antigens on the largest abscess drainage were positive; moreover, E. histolytica was also identified on drainage fluid with polymerase chain reaction (PCR). Therapy with metronidazole followed by paromomycin improved both symptoms and radiographic images. This case report suggests that in HIV-infected patients, invasive amoebiasis should be considered and atypical aspects, such as multiple hepatic lesions, delayed positivity of serology for E. histolytica, and possible bacterial superinfection should be evaluated.
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