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Limb girdle muscular dystrophy type 2D (LGMD2D, OMIM600119) is a genetic progressive myopathy that is caused by mutations in the human α-sarcoglycan gene (SGCA). Here, we have introduced in mice the most prevalent LGMD2D mutation, R77C. It should be noted that the natural murine residue at this position is a histidine. The model is, therefore, referred as SgcaH77C/H77C. Unexpectedly, we observed an absence of LGMD2D-like phenotype at histological or physiological level. Using a heterologous cellular model of the sarcoglycan complex formation, we showed that the R77C allele encodes a protein that fails to be delivered to its proper cellular localization in the plasma membrane, and consequently to the disappearance of a positively charged residue. Subsequently, we transferred an AAV vector coding for the human R77C protein in the muscle of Sgca-null mice and were able to pharmacologically rescue the R77C protein from endoplasmic reticulum-retention using proteasome or mannosidase I inhibitors. This suggests a therapeutic approach for LGMD2D patients carrying mutations that impair α-sarcoglycan trafficking.
α-Sarcoglycan is a 50 kDa sarcolemmal protein that forms, together with β, δ and γ sarcoglycans, a subcomplex participating in the dystrophin–glycoprotein complex (DGC), an important link between the actin cytoskeleton, the sarcolemma and the extracellular matrix (1). Genetic defects in any of the sarcoglycans lead to a recessive limb-girdle muscular dystrophy (LGMD2), respectively, LGMD2D, E, C and F for α, β, γ and δ-sarcoglycans (2). Immunohistochemistry studies indicated that dysfunction of one of the sarcoglycan destabilizes the whole sarcoglycan complex, leading to a partial or complete disappearance of the other sarcoglycans at the membrane (3–5). This particularity was shown to impair the structural integrity of the muscle fiber during contraction, explaining, at least partly, the pathophysiological mechanism by which muscle cells degenerate (6).
Patients with α-sarcoglycan deficiency (LGMD2D, OMIM600119) present a clinical phenotype with proximal muscle involvement and a highly elevated serum creatine kinase level (7,8). At the histological level, muscles show marked regeneration and degeneration pattern, inflammatory infiltrates, fibrosis and variation in fiber size. Age of onset is variable, although, in most cases, first symptoms appear around the 20s. The progression of muscle weakness is also variable and is often correlated to the level of residual α-sarcoglycan expression (9,10). No treatment is currently available for this devastating disease. The most frequently reported mutation in the α-sarcoglycan gene is a C to T transition at position 229 in exon 3, resulting in the substitution of an arginine in position 77 by a cysteine (R77C). This mutation accounts for up to one-third of all mutations in European populations except in Finland where it is found in every LGMD2D patients often in both alleles (10,11).
Here, we have introduced this mutation in the murine genome. Unexpectedly, no apparent LGMD2D-like phenotype was induced. As a first step to explain this difference in outcome between the human and murine species, we showed that the R77C protein fails to be delivered to its proper sarcolemmal localization, and consequently to the disappearance of a positively charged residue at the 77 position. Most importantly, following expression of the human R77C protein in Sgca-null mice, we were able to pharmacologically rescue the R77C protein from retention in the secretory pathway by blocking the protein quality control using proteasome or mannosidase I inhibitors in living mice without evidence of toxicity of the treatment.
A cysteine at position 77 in Sgca induces no phenotype in mice
To explore the pathophysiological mechanism of the R77C mutation, we introduced in the murine genome a 'knock-in' mutation that encodes a cysteine residue at the 77 position of the α-sarcoglycan protein (Fig. 1; Supplementary Material, Fig. S1). It should be noted that the natural murine residue at this position is a histidine in place of an arginine in the human protein.
Obtaining homozygous mice, denoted as SgcaH77C/H77C mice, was confirmed by PCR and sequencing (Supplementary Material, Fig. S1). RT–qPCR and western blot analyses performed on skeletal muscle did not detect any difference between WT and SgcaH77C/H77C regarding the relative amount of α-sarcoglycan mRNA or protein (Fig. 1). To investigate the subcellular localization of α-sarcoglycan in SgcaH77C/H77C mice, we performed immunohistochemistry analysis using an α-sarcoglycan-specific antibody. Sections from wild-type (WT) mice and from an Sgca-null model previously described by Duclos et al. (6) were used as positive and negative controls, respectively. Staining of α-sarcoglycan was clearly observed at the fiber membrane in SgcaH77C/H77C and WT mice, whereas it was totally absent in Sgca-null mice (Fig. 2A). To examine the localization of DGC components, immunohistochemistry analyses were performed on sections with β-, γ-sarcoglycan and dystrophin antibodies. Noticeably, staining for sarcoglycan proteins was equivalent to WT in SgcaH77C/H77C muscles, whereas it was greatly reduced in Sgca-null skeletal muscles (Fig. 2A). Thus, the mutated α-sarcoglycan was expressed, localized correctly at the membrane and did not perturb the DGC assemblage in mouse muscle, in contrast to the human situation where α-sarcoglycan was not detected at the membrane in biopsies from patients carrying the R77C mutation (data not shown).
Muscle histology on deltoid, psoas, gastrocnemius, gluteus, extensor digitorum longus and quadriceps removed from SgcaH77C/H77C mice at 3 and 9 months of age showed no dystrophic features (Fig. 2B and data not shown). We submitted Sgca77C/77C mice of the same two ages to an eccentric contraction exercise protocol followed by an intraperitoneal injection of Evans blue dye (EBD). No noticeable uptake of the dye was detected in any of the tested muscles, indicating the absence of plasma membrane disruption (Fig. 2C, right panel). In contrast, EBD uptake was always observed as clusters of skeletal muscles from Sgca-null mice with 13% of fibers being positive (Fig. 2C, left panel). Thus, inconsistent with the human clinical features but in accordance with the presence of the sarcoglycan complex at the membrane, SgcaH77C/H77C mice showed no histological dystrophic signs, not even after exercise. As Sgca-null mice present a severe dystrophic phenotype, we know that α-sarcoglycan is as essential in mice as in humans and that no compensatory mechanism takes place in mice (12,13).
The R77C mutant is retained in the secretory pathway in human, and consequently to the disappearance of a positively charged residue
To explore the underlying cause of the difference in outcome between the two species, we established a heterologous cellular model. A human cell line (HER911) was cotransfected with pcDNA3 vectors expressing β, γ and δ-sarcoglycans from human together with WT or mutated α-sarcoglycan. Whereas α-sarcoglycan WT co-transfected with other members allowed the formation of the complex (Fig. 3A, left panel), transfection with the R77C mutant did not show any labeling when non-permeabilized cells were used, indicating an absence of the complex at the membrane (Fig. 3A, right panel). Western blot analyses confirm that the absence of labeling was not due to the absence of expression of the mutated proteins (Fig. 3, insets). Thus, these observations indicate that this model recapitulates features observed in human patients. It would have been also interested to analyze the fate of H77C in cells as this protein was able to reach the surface in mouse. However, the available antibody directed against the extracellular domain of α-sarcoglycan does not recognize the murine protein by immunohistochemistry. In addition, using the galactosyltransferase–GFP fusion protein as reporter of endoplasmic reticulum (ER), we observed, in permeabilized cells labeled with anti-α-sarcoglycan, accumulation of the R77C protein in the secretory pathway (Fig. 3B).
The presence of the cysteine residue in R77C may have been responsible for an illegitimate interaction, possibly by disulfide bond formation, resulting in retention in the secretory pathway. Yet, no membrane associated-labeling was detected when a non-conservative mutant, R77G was co-expressed with the three other human sarcoglycans, demonstrating that the presence of cysteine was not the cause of the pathology (Fig. 3C). In contrast, when a mutant that conserves a positively charged residue at the 77 position was expressed (R77K), a clear labeling at the plasma membrane was observed (Fig. 3D). In conclusion, it appeared that the phenotype observed was the consequence of the disappearance of a positively charged residue instead of the presence of a cysteine.
In vitro rescue of the R77C mutant protein
In an attempt to genetically rescue the R77C protein, we expressed it in a context where its immediate partners were of a murine origin by co-transfecting the human mutant with all other murine sarcoglycans. No membrane labeling was observed (Fig. 4A). As a control for the complex formation between species, we co-transfected the human WT α-sarcoglycan with all other murine sarcoglycans. A membrane-associated fluorescence was observed (Fig. 4B). These data demonstrated that the murine sarcoglycans could not rescue the mutated human α-sarcoglycan.
In a second step, considering the observation presented in Figure 3B, we hypothesized that it could be possible to act at the level of ER retention. The fate of newly synthesized glycoproteins is determined by the protein quality control machinery that includes ER chaperones and glycosylation/deglycosylation enzymes (14,15). Folding attempts are eventually interrupted upon substrate demannosylation by mannosidase I (16,17). Terminally misfolded polypeptides are retrotranslocated into the cytosol and degraded by the ubiquitin–proteasome pathway, a mechanism known as ER-associated degradation (ERAD). To test whether the R77C mutant trapped in the secretory pathway was recognized by this system, we treated our model cells with MG 132, a proteasome inhibitor. The use of this non-specific inhibitor of the ERAD system increased the amount of α-sarcoglycan that could reach the membrane. A secondary restoration of sarcoglycan complex at the membrane was observed (Fig. 4C). To confirm that R77C is a substrate of the ubiquitin/proteasome system, we performed an immunoprecipitation experiment. Extracts of HER911 cells co-transfected with the β-, γ- and δ-sarcoglycans together with a plasmid coding for R77C in the absence or presence of MG132 were immunoprecipitated with an α-sarcoglycan antibody. We subsequently analyzed the ubiquitination of the proteins by western blot using an anti-ubiquitin antibody. Poly-ubiquitinated proteins were detected in immunoprecipitates of cells expressing the R77C mutant treated with MG132 (Fig. 4D).
Mannosidase I enzymatic activity leads to the irreversible exclusion of the defective polypeptide from the chaperone folding attempts and therefore consists of a late control quality check point upstream of the retrotranslocation and proteasomal degradation. To investigate the participation of this enzyme in the abnormal trafficking of the R77C mutant, we treated transfected cells with kifunensine or deoxymannojirimycine, two inhibitors of the mannosidase I activity. A restoration of α-sarcoglycan at the membrane was clearly seen (Fig. 4E and F). As a control, we also treated cells transfected with the WT α-sarcoglycan (Fig. 4G and H). Altogether, results obtained in our cellular model seem to indicate that R77C mutant was retained in the secretory pathway and that inhibition of ERAD allowed the R77C mutant to reach the plasma membrane.
In vivo rescue of the R77C mutant protein
Our next step was to investigate whether mannosidase inhibition was able to readdress the mutant to the membrane in vivo in the perspective of using this type of intervention as a treatment in humans. We constructed an adeno-associated virus (AAV) vector containing a sequence coding for the human mutant protein placed under the control of a muscle-specific promoter (Supplementary Material, Fig. S2) and injected 1010 viral genome (vg) in the tibialis anterior (TA) muscles of 4-week-old Sgca-null mice. A group of Sgca-null mice injected with the AAV-R77C vector were treated for 2 weeks with kifunensine starting 20 days after AAV injection. To evaluate the subcellular distribution of α-sarcoglycan with and without the kifunensine treatment, we labeled muscle sections with α-sarcoglycan and calreticulin, a marker of the ER. Muscle section from mice non-treated with kifunensine showed accumulation of α-sarcoglycan around the nucleus and co-localization with calreticulin, indicative of aggregation of the transgenic protein in the ER (Fig. 5A, upper panels). Muscle from mice treated with kifunensine showed a decrease in the number of fibers containing such accumulation (Fig. 5A, lower panels). This reduction in ER aggregation is associated with an increase in the intensity of labeling of α-sarcoglycan at the plasma membrane (mean fluorescence level associated at the plasma membrane: 2.32 U.A. for the non-treated muscles versus 13.26 U.A. for the kifunensine treated muscle. This 575% increase indicates that kifunensine allowed the R77C mutant to by-pass the ER associated quality control and reach the plasma membrane.
Kifunensine-mediated localization of the mutated α-sarcoglycan at the plasma membrane allowed the formation of the sarcoglycan complex as seen by the β-sarcoglycan staining at the surface and its perfect co-localization with α-sarcoglycan (Fig. 5B). We also analyzed the effect of kifunensine on Sgca-null mouse muscles that have not been transduced with AAV. As no labeling was observed with β-sarcoglycan, we excluded the possibility that kifunensine promote the trafficking of the residual sarcoglycan complex in the absence of α-sarcoglycan (Fig. 5C). The presence of the complex in turn ameliorated the histological phenotype of transduced Sgca-null muscle (Fig. 5D). Morphological analyses showed a decrease number of centrally located nuclei and a reduced dispersion in fiber cross-section area in kifunensine-treated muscle compared with the non-treated muscles [dispersion factor (DF): 1.39 µm compared with 1.71 µm] (Fig. 5E). This improvement in phenotype was also associated with a reduction in the membrane instability evaluated by EBD staining (data not shown). All these data indicated that the treatment with kifunensine has the capacity to redirect the human mutant protein to the plasma membrane, to ensure the stability of the sarcoglycan complex in this murine context and to ameliorate the phenotype. It is worth to note in regards to potential safety of this approach that muscles from WT mice injected with kifunensine did not display any histological abnormalities (data not shown).
A large proportion of patients suffering LGMD2D have been reported to carry the R77C missense mutation in the α-sarcoglycan gene. In this study, we report the identification of a new pharmacological strategy that could potentially treat such patients. Our starting point was the observation of a lack of phenotype in a knock-in murine model carrying an equivalent mutation. This unexpected finding was confirmed by another study in which a different construct introducing the same mutation was used (18). In this other model, the mutant α-sarcoglycan was also correctly localized at the membrane and failed to give any dystrophic signs over the lifetime of the H77C/H77C mouse.
As a means to identify the possible therapeutic options, we thought it would be of interest to identify the reason for the difference in the outcome between the human and murine species. We provide evidences that the disappearance of a positively charged residue at the 77 position of the human α-sarcoglycan protein seems to prevent the correct sarcolemmal targeting of the protein in human. Our observations are further supported by a previous study showing that the R77C mutation leads to a fundamental defect in α-sarcoglycan protein synthesis which blocks its exit from the ER (19).
Kobuke et al. (18) also performed adenovirus-mediated transfer of the human R77C protein in Sgca-null pups and observed restoration of the sarcoglycan complex. This observation is to some extent different from our own gene transfer experiments in which, even if α-sarcoglycan was observed at the membrane, its level was reduced. It is possible that this difference may be related to the age of the mice used (neonates versus 3–4 weeks of age), especially as the disease is already widespread in muscle in the older animals, the nature of the vector (adenovirus versus AAV) or the strength of the promoter (Rous sarcoma virus promoter versus the muscle-specific C5-12 promoter). Altogether, both studies are in favor of a difference in the processing of the mutant protein between human and murine species. The weaker α-sarcoglycan staining after AAV-mediated transfer of R77C suggests that the human version of the mutated protein is still not quantitatively fully considered as a normal protein in a murine context. Even though, considering the absence of a dystrophic phenotype of both models, the murine mutant seems to be processed normally, it is possible that the shorter lifespan of the mouse could prevent the apparition of deleterious effect resulting from a slightly imperfect processing. In addition, variability in the efficacy of the processing pathways may provide an explanation for the variability of phenotype in human patients and components of this pathway are, hence, potential disease-modifying factors.
Following this demonstration that the central defect in the R77C patients is a failure in the correct delivery of the protein at the sarcolemma, we hypothesized that a pharmacological intervention could be beneficial for these patients. The first obvious target for such intervention is the proteasome. Indeed, we showed that inhibition of the ubiquitine/proteasome system by the use of MG132 increased the sarcolemmal targeting of the R77C protein in transfected cells. However, because of the potential toxicity of such treatment in humans, we decided to intervene upstream in the ERAD system by inhibiting mannosidase I, an ER enzyme that ensures that terminally misfolded glycoproteins are preferentially targeted for degradation. The inhibitor that we used, kifunensine, is routinely used in vitro to manipulate the ERAD system but has not been used in living animals. Most importantly, we showed that the in vivo use of kifunensine could block the ERAD upstream of the proteasome and allowed the rerouting of mutated protein to the plasma membrane. Noticeably, this treatment did not present any overt pathological effect. The animals tolerated well the injection and we did not notice any pathological signs in normal injected muscles. Importantly, the mutated R77C human protein is correctly targeted at the membrane following transfer in a murine context and treatment with kifunensine and once at the membrane is able to stabilize the sarcoglycan complex, demonstrating therapeutic efficiency. Increasing the amount of a mutant protein to the membrane by pharmacological agents has been previously used in several diseases, exemplified in the case of the most common cystic fibrosis (CF) mutation, deltaF508. In this disease, amelioration of the folding, and hence the presence at the membrane, by chemical chaperones (e.g. TMAO) has been successful in vitro and in vivo (20). However, the dose used to obtain such efficiency is very close to the 50% lethality dose. Increased trafficking of mutant forms of the CF transmembrane conductance regulator protein has been achieved in vitro by reducing its degradation by the proteasome (21). Although one proteasome inhibitor has reached the clinic, this type of drug is highly toxic in vivo. Compared with those compounds, mannosidase inhibitors have the potential to have a similar efficiency at a lower toxicity level in vivo.
The data presented may open a new therapeutic approach of LGMD2D. It has been reported that other mutations in α-sarcoglycan or in other sarcoglycan proteins could also lead to an abnormal trafficking and absence of the whole complex at the membrane (22). Therefore, these mutants, as well as mutations in other pathologies linked to defect in trafficking of secreted or membrane proteins, would undoubtedly be candidate for mannosidase inhibition.
In conclusion, our results, in addition of being a concrete example of the interest to investigate the underlying reason of difference in phenotype between species, define a new therapeutic strategy that could be of significance for other disease apart from LGMD2D.
Cell culture, transient transfection and cell treatment
Human embryonic retinoblast HER911 cells were grown in Dulbecco's modified Eagle's medium supplemented with glutamine, antibiotic (Gentamycin), 10% fetal calf serum and MEM vitamin solution (100×, Sigma M6395). Cells were transfected using 6 µl of Fugene (ROCHE) for 1 µg of plasmid. Forty-three hours later, cells were treated for 5 h with a proteasome inhibitor (5 µm of MG132 dissolved in DMSO, Sigma C2211) or a mannosidase inhibitor (5 µm of kifunensine, VWR calb 422500-1). In six-well plates, 0.5 µg of each plasmid (α-sarcoglycan, α-sarcoglycan-R77C, α-sarcoglycan-R77G or α-sarcoglycan-R77K together with β-sarcoglycan, γ-sarcoglycan and δ1-sarcoglycan) was used. The Golgi compartment was labeled using pAcGFP1-Golgi vector which expressed the galactosyltransferase fused to EGFP (Clontech).
In vivo analysis
All experiments were performed in accordance with the European guidelines and regulations. Mice were submitted to a 30 min running session on a treadmill set to a 15° down slope at a speed of 10 m/min. At the end of the 3-day training period, the mice were injected intraperitoneally with EBD (1 mg/g of body weight, Sigma). The next day, mice were sacrificed and muscles were removed and quickly frozen in liquid nitrogen-cooled isopentane.
Female Sgca-deficient mice of 3 or 4 weeks of age were used throughout this study. Each rAAV2/1 viral preparation was injected (1010 vg in 30 µl in total) into the left TA muscle. At days 20, 21, 22, 25, 27, 29, 32 and 34, kifunensine (VWR, calb 422500-1) was injected directly into the same muscle. Initially, two quantities have been used (30 or 90 pmoles) with similar results. Subsequent experiments were performed only with the lowest dose. This mode of administration was chosen as no data exist about the bioavailability for oral or IV administration. Left and right TA muscles from untreated and treated Sgca-null mice were collected and quickly frozen in liquid nitrogen-cooled isopentane for further analysis.
The fiber diameter was analyzed by measuring the minimum cross-section area of more than 2000 individual fibers. The width of the confidence interval gives the dispersion in the size fibers. The equation used to calculate the DF was the following: DF=mean+(Z* (SD/square root (n)) − mean+(Z * (SD/square root (n)). The value for Z was defined as 1.96 for a confidence of 95%.
mRNA analysis
Muscle RNAs were extracted by the TRIZOL method after pulverization using a Fast-prep apparatus (Bio101). Synthesis of cDNA was performed from 1 µg of total RNA using the SuperScript II first-strand synthesis system for RT–PCR kit (Invitrogen) and random primers. PCR amplification of the α-sarcoglycan cDNA was done on this cDNA with the forward primer (mSgca.s: 5′-ACTGGCTAGGCCCCGGGCAA-3′) located just upstream of the ATG and the reverse primer (mSgca.as: 5′-GGCTGGGCTGTCAGTGCTGG-3′) located across the stop codon under the following conditions: 94°C for 3 min, then 30 cycles of 94°C for 30 s, 61°C for 40 s and 72°C for 1 min, then 3 min at 72°C. A 1195 bp product was obtained.
Western blot, immunohistology and immunoprecipitation
Western blot and immunohistology were performed as previously described (23) and briefly summarized in Supplementary Material and Materials and Methods.
Transfected HER911 cells were scraped from cell culture dishes. After centrifugation and washing with ice-cold PBS, the cell pellet was incubated 20 min with 200 µl of ice-cold lysis buffer [10 mm Tris (PH 7.4), 5 mm EDTA, 50 mm NaCl, 50 mm NaF, 1% (v/v) Triton X-100, 500 µm sodium orthovanadate, 1× Complete Mini protease inhibitor cocktail (Roche Biomedicals)]. After centrifugation, the lysate was incubated 2 h at 4°C with a monoclonal mouse antibody against α-sarcoglycan (1/100, Novocastra NVL-a-SARC) on rotating wheel. Lysates were mixed with protein A-sepharose (100 mg/ml) for 45 min at 4°C on rotating wheel. The beads were washed three times with lysis buffer. Immunoprecipitated proteins were eluted from the beads by incubating at 70°C in SDS–PAGE sample buffer for 10 min and processed for western blot analysis. Revelation was performed using anti-ubiquitin antibody (1/100, Santa Cruz Biotechnology Ub-P4D1).
Image analysis
Quantitation of confocal microscopy images of muscle sections from mice treated or not with kifunensine was performed using the Plot Profile tool of NIH ImageJ software. Appropriate linear slices were chosen to cross several fibers. The relative magnitude of fluorescence distribution along linear slices after background subtraction of the fiber was quantified. The average pixel intensity in 10–30 lines from n = 3 mice for each condition was determined. Histogram of the different conditions is presented and it reveals quantitative differences in plasma membrane localization. Values are presented as fluorescence arbitrary unit (AU) ± standard deviation (SD).
Supplementary Material is available at HMG Online.
This work was funded by the Association Française contre les Myopathies.
We acknowledge the excellent expertise of the In vivo Department of Généthon. We thank the Howard Hughes Medical Institute for providing us with Sgca-null mice (Iowa City, USA). We also thank Dr Serge Bouaziz for helpful discussion and Dr S. Cure for critical reading of the manuscript. The SgcaH77C/H77C mutant mice were developed with the support of the platform RIO-MNG with the technical help of Anne-Marie Mura and Mireille Richelme.
Conflict of Interest statement. A patent covering these results has been filled with IRi as an inventor.


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The BBC News website has published a blog post by professional photographer Matt Dunham, looking back at his year shooting for the Associated Press (AP) picture agency. Dunham was on-hand to capture a wide variety of events this year, from documenting the devastating Tsunami in Japan to capturing the British royal wedding. His post discusses everything from choosing the the moment to the kit he uses and is well worth a read. It comes amidst a week of fascinating guest blog posts looking at different aspects of photojournalism.
Click here to read Matt Dunham's blog on the BBC News website
Click here to read Agence France-Presse (AFP) staffer Leon Neal's post
Click here for freelance photographer Philip Wolmuth's post on the future of freelancing
Click here for university lecturer Max Houghton's discussion of the ethics of photojournalism
Dec 15, 2014
Dec 11, 2014
Dec 11, 2014
Dec 10, 2014
Interesting. First I read the exploits of Matt Dunham. The guy has a good eye and has the latest equipment. Can I make the assumption that AP pays for his kit? I'm going to, even if I'm wrong. He gets flown around the world on assignment, has to get the shot (or he wouldn't even have this job) but basically has a photography job as opposed to freelance.
Then I read the exploits of another photog in the same position as Matt. "Here's where we want you to be shooting this event" sort of job. Again, the guy is good.
Then I read about the exploits of a third photog, a "freelancer". Pays for his own gear, has to come up with what event he wants to attend (while paying his own expenses) and then tries to sell his stuff to whoever will buy it at a reduced price.
All three are photogs with skilz, two of them have paying jobs and the third, just as qualified, wonders where his next paycheck is coming from.
thanks for those links
Good link!
Thanks for the links!
This'll be good.
*brews coffee*
The one about ethics was good, too. Oddly the most interesting series of articles I remember reading about the grind of photojournalism was a blog by a chap who shot for the Daily Mirror. Possibly the only times I have ever looked at the Daily Mirror's website. Unfortunately they're gone now, but there's a glimpse at the typical pap kit circa 2009 here:

subset: commoncrawl


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Disney, one of the largest and most successful movie studios in the world and is known for making blockbusters, and they flop and bomb and just make terribly bad movies. WatchMojo presents the Worst Disney Movies that completely flopped at the box office. But what will take the top spot on our list? John Carter, The Black Cauldron, or Mars Needs Moms? Watch to find out!
Home >> Entertainment and Hobbies >> Top 10 Biggest Disney Movie Flops – WatchMojo


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Logged In: NO
I'd be interested in SimPE for OSX too. I used to have it on my laptop (before
it broke) and it was a very neat program. I'd love to be able to use it on my
Millie G.
Are there any plans to port SimPE to OSX??
If not I would be interested in doing that.
I am using OSX 10.3, XCode and G5 2Mhz dual proc.
SimPE looks like a good tool that I could really use on my mac.
Let me know....
Lon Giese
Alturas CA
Logged In: NO
I'd be interested in SimPE for OSX too. I used to have it on my laptop (before
it broke) and it was a very neat program. I'd love to be able to use it on my
Millie G.
Logged In: YES
I would really like this too. I have no access to a PC and I really want this for my
computer. I hope it's possible.
Logged In: YES
I am not planing to create a native port of SimPE, but
anyone who likes to do so, iw more than welcome.
However, I am contantly testing wether or not SimPE is
running on the Mac using Mono, an OpenSource alternative for
the .NET Framework. So far I only had limited succes (didn't
try for about two months), but I was able to start
WizardsOfSimPE, and list several Objects there.
Logged In: NO
FUSE has recently been ported over to the mac. http://googlemac.blogspot.com/2007/01/taming-mac-os-x-file-systems.html
I'd like to find more information about the file protocols inside the sims2 .package format.
I'm thinking it might be interesting to find someone with the skills to write a FUSE file system to open game files, initially package files, and display their contents as a directory. Then it could be up to anyone else to write the tools that access the files inside that directory.
I feel this would allow more development on multiple OS's by providing a protocol foundation. The SimFUSE filesystem could later be updated to implement interpretations of the data files contained in the package I.E. allowing access to the contents of a texture as directory holding a bitmap (imagine drag and drop texture replacement.) Further extensions would be implemented to facilitate access to meshes, behaviours, animations, essentially opening object creation to a broader base of users.
Perhaps utilizing xml to hold some of the information common between the elements of the package.
As a self professed jack of all trades (and admittedly master of none), this concept is presently way beyond my skills. I can, however, see the fertile seed this idea could be.
Although conceptual at this time, please consider that this idea is copyright, it and its derivations may be distributed under the terms of GNU GENERAL PUBLIC LICENSE.
Logged In: YES
Originator: NO
O.K. I just proved the master of none part. I REALLY should have created an account BEFORE posting the message about fuse. I'm sure weblogs somewhere will be able to successfully tie this message to the previous one.
Logged In: YES
Originator: NO
As this is a Win32 app and not Linux i think it's rather unprobable that anyone would care doing a SimPE to MacOSX even if EA GAMES has expanded to MacOSX
Log in to post a comment.


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Square officials have already hinted at the possibility of a sequel to their 2002 blockbuster title whose two versions have sold more than 1.2 million copies in Japan alone. Back then however, Square president and CEO Yoichi Wada noted, that a decision regarding a possible sequel had to be made by Disney, whereas his company was definitely interested in making a sequel.
In further Kingdom Hearts-related news, producer Shinji Hashimoto and director and character designer Tetsuya Nomura will receive the IGDA's Visual Art Award at the Game Developers Conference in San Jose, California.
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Marianne Williamson Quotes About GloryQuotes about: Glory
Abundance Acceptance Activism Addiction Age Angels Anxiety Art Atonement Attitude Awareness Babies Beauty Being Happy Belief Birth Blame Blessings Books Challenges Change Changing The World Chaos Children Choices Commitment Community Compassion Confidence Consciousness Courage Creation Creativity Culture Darkness Decisions Desire Discipline Drama Dying Earth Effort Ego Empowerment Enemies Energy Enlightenment Evolution Excuses Eyes Failing Fate Fear Feelings Fighting Flowers Focus Forgiveness Gardens Giving Giving Up Glory Goals God Grace Graduation Gratitude Greatness Grief Grieving Growth Guilt Habits Happiness Hate Hatred Healing Heart Heaven Hell Holy Spirit Home Honor Humanity Humility Hurt Illness Innocence Inspiration Inspirational Integrity Intimacy Jesus Journey Joy Judging Judgment Kindness Letting Go Life Life Is Beautiful Love Love And Fear Lying Magic Making Love Manifestation Mankind Marriage Maturity Meditation Mercy Miracles Mistakes Morning Mothers Motivational New Beginnings Nonviolence Opportunity Overcoming Pain Parents Passion Past Peace Perception Perfection Personality Perspective Positive Positive Thinking Positivity Praise Prayer Progress Purpose Reality Recovery Reflection Regret Responsibility Romance Running Sadness Self Confidence Self Esteem Self Love Separation Silence Slaves Songs Sorrow Soul Soulmates Spiritual Growth Spirituality Stress Struggle Success Suffering Surrender Talent Teaching Today Transformation Understanding Universe Values Violence Vision Waiting Wall War Weakness Well Being Winning Wisdom Worry Writing Yoga Youth
You are a child of God, small games do not work in this world. For those around us to feel peace, it is not example to make ourselves small. We were born to express the glory of God that lives in us. It is not in some of us, it is in all of us. While we allow our light to shine, we unconsciously give permission for others to do the same. When we liberate ourselves from our own fears, simply our presence may liberate others.
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A Dallas Man Was Sitting at a Park When He Was Kicked in the Face, Forced to Sing a Song
It was a really nice day yesterday, wasn't it? Not too windy, not too hot, not too humid. Perfect Sunday weather, all the better to sit in the park, feel the fresh air, and, with any luck, not have some asshole come along and kick you in the face.
See also: - Doggy-Door Gun Heist Ends in Federal Gun, Conspiracy Charges - More bizarre crime stories in Dallas
A 21-year-old Dallas man managed to achieve two out of three yesterday. The man, who we'll call John -- because, according the police report, that's his first name -- was sitting on a bench near Casa Linda Park, a few miles east of White Rock Lake. It was around one in the afternoon. He was alone, smoking a cigarette, when a man he didn't know sprinted up to him.
"What's your name?" the man asked. "Where do you live? What are you doing at the park?"
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John stood up. His questioner apparently didn't much care for that, because he promptly kicked him in the face.
"Don't move," the man told John. "Keep your hands on the bench."
Then things got weird. The man demanded that John sing him a song. Thinking fast, John sang an improvised number, according to the police report, "about wanting to go home."
After this impromptu yet deeply disturbing vocal recital, John's captor kept asking him questions about where he stayed. He also kept telling him not to get up. Once or twice, to drive the point home, he punched him in the face. Several times, he casually told John that he was going to kill him. John later told the cops that he didn't try to run because he assumed, sensibly enough, that the man would hurt him if he tried.
The whole thing lasted for about an hour. Finally, John's captor apparently got bored and walked off. The police report doesn't list any physical description of the suspect, and no arrests have been made.
John seems to have kept admirably calm, considering. We're also impressed that he didn't just opt to sing "Happy Birthday" or the Friends theme song, as so many of us would probably default to under similar circumstances. Or maybe "Twinkle Twinkle Little Star"? There's really no right answer here, is there?
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'Adele: Live in New York City,' is a concert recorded at Radio City Music Hall and broadcast on NBC as an hour-long special and you can watch the full video here and see a review roundup. Social media lit up with excitement and so too did music critics as the multi-Grammy winning superstar returned to the stage after a four-year absence.
The long awaited concert was recorded in November at Radio City Music Hall in New York City and now, after weeks of hearing about it second-hand from those lucky attendees, now the rest of world has joined in with what has become a celebration of musical excellence. Social media erupted in massive praise as the hashtag #AdeleLiveInNYC trended for hours on Twitter.
With an introduction from none other than Jimmy Fallon, concertgoers — and now the world — were in for a unique and powerful night of performances from the woman who arguably is the greatest living pop music star on the planet. After all, there are the staggering sales for her new album '25.'
And beyond that, there is the music itself. It's not the often overmanufactured, overproduced, over-the-top tunes we've become so accustomed to call pop music. And Adele herself is the antithesis of all of that. How wonderful that an artist can appear on the stage in a floor-length gown and a bouffant hairstyle and not have to go through a dozen costume changes and reveal more and more skin as the night goes on.
No, there weren't backup dancers and gyrating moves to upset parents' groups, but Adele being Adele, we have all come to expect that she is always unexpected with her stage banter which is peppered with a hefty helping of F-bombs. Yes, it's been four years and Adele is back. She began with her mega hit "Hello" and from there it was a mix of the new songs and the iconic hits — "Set Fire to the Rain" and "Someone Like You" notably — we've listened to over and over during these past few years that she's been absent from the stage. had the audience crying and by the end of it, see herself was crying.
Now the music critics are weighing in, and, let's say, they have become a cheering section just as has social media. Here's a roundup.
"…..Her special, Adele: Live in New York City, which aired on Monday night on NBC and was taped at Radio City Music Hall in November, fully expressed her extraordinary power; not just in the way she effortlessly commands the stage, but in the intensity of the emotions she can pull out of people – and even herself. ….." The Guardian
"….She halted Someone Like You mid-intro to explain: "I don't sing this from the same place anymore because of my man. He's here tonight and this is the first show of mine he's been to." Throughout the show, she wept, cackled and treated the crowd like intimates. She may have been teetering under the weight of a massive bouffant and been resplendent in a sparkly brown floor-length gown but Adele is the antithesis of a diva….." The Telegraph
"….The one-night-only concert marked the British singer's welcome return to the stage after four years and earned her rave reviews from fans. […] The only complaint seemed to be that the one-hour show wasn't long enough.
Adele kicked off the night with the blockbuster hit "Hello" from her new "25" album, and went on to warm up the crowd with "Someone Like You," "All I Ask" and "When We Were Young" — with a few F-bombs and unexpected jokes along the way……." The Wrap
"…. She ran through the old hits (sup, "Rolling in the Deep"), treated fans to new favorites ("When weeeeeee were youuuunnnnng"), and broke down in tears as she finished her first full concert in over four years. …." — Entertainment Weekly
"….In a tribute to her talent and that of director Beth McCarthy-Miller, the taping went smoothly from the audience's vantage point with no stops and starts. Nor did the star engage in costume changes or pyrotechnics beyond the visual imagery projected behind her on the stage.
Instead, Adele offered her own biographical annotation as she moved through her songbook. She introduced "Hometown Glory," from her 2007 album "19," as the first song she ever wrote. As the taping came just four days after the Nov. 13 Paris terror attacks, she dedicated it to the victims. "Tonight, this is about everyone's hometown," she said..…." — Variety
Thankfully, one does not have to just read about the mesmerizing performance. NBC has released the replay in full, Watch Adele: Live in New York City video below!
Pictures: PR Photos


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Dim Sum for Diabetes raises funds for Diabetes Awareness Month
The third Dim Sum for Diabetes took place Nov. 4 at Empire Garden. Continue reading
The third Dim Sum for Diabetes took place Nov. 4 at Empire Garden. Continue reading
The eighth annual Boston Asian American Film Festival opened on Oct. 20 with the premiere of "Tyrus" at the Brattle Theatre in Harvard Square. Continue reading
The Asian American Commission held the fifth annual Young Leaders Symposium on Oct. 15 at Hunneman Hall in Brookline's main library. Continue reading
The Acton Chinese American Civic Society held a forum on grassroots political organizations on Sept. 25 at the Bellows Farm Club House. Continue reading
Boston Mayor Marty Walsh announced the Boston Redevelopment Authority will be known as the Boston Planning and Development Agency on Sept. 27. Continue reading
Former Taiwanese vice president Wu Den-yih visited the Chinese Consolidated Benevolent Association of New England on Sept. 25. Continue reading


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NEW SYDNEY-U.S.A. AIRLINER RECORD SYDNEY, Monday.— A new- re cord. time for a flight to San Francisco and back w.es. estabr .ished by- the B.C.P.A. DC6 air liner Resolution last week in three days, seven hours.. Resolution left, Kingsford Smitii Airport at 11 a.m. on Wednesday and torched, down again, at 6.5, p.na. on Saturday.
HUGE FIRES RASE IN ALASKA FORESTS ANCHORAGE (Alaska), Mon day (A'.A.P.). — Huge,' uncontroll able forest fire? wore raging un checked in northern Yukon' and ?\laska, forest officials reported today. The vast fire menaced Fort Yukon, and only rainfall could halt -t,^they said. .''The fire was spread over 1,000,000 acres and had swept to within .25 miles of Fort Yukon, ihe officials added.
No Overtime By Sydney Gas Workers SYDNEY, Monday. — Sydney gas workers who held a 24-hour stoppage today, d^cidcd they wjli not work more than 40) b°W?s during any weefc. ' This means they will refuse to woik overtime, which may lead to. rationing of Sydney's gas supplies 4uvih? week-ends. Meanwhile. 20.00 members of the Gas Employees' Union who ceased wo;-k at 6 a.m. today \yill report for duty at 6 a.m,. tomorrow,. Dv^i-ing today's stoppage*' employees; of Sydney's two ' gas companies manned the gas plants, and maintained near nor «ial supplies. Toclay's stoppage was, called to, discuss- the. decision by the Federal ' '' Conciliation Conn?iis sto$e? (^r.. Blackbui-n) that, had' npt' the power to grant a %Vr. a wgek. wage, rise.
SYDNEY SOFTBALL TEAM ENTERTAINED BY ILLAWARRA The, representative fixture set dp,wn for the lliawarra District Women's Softball Association on Sunday was cancelled due to the inclement weather. However the Sydney team travelled. do\y$i tcon fbe city; and were met by officials of. the; Illawai'ra Association. After haying, lunch,. they-f we,r§ taken to the Coniston Hall and enter tained. ' A large crowd of softball and .baseball enthusiasts enjoyed community singing, and a few individual itenis were rendered by various players. The Sydney team, which in cluded five of last year's State representatives, and incidentally, t\vo Austr^aiy representatives in joyce King and . Dot Barker, expressed disappointment at not| being able to play. A return game has been arranged fori Sunday ,, August -20. The softball tijip which was to; take place to Camden next Sun-.| day has been cancelled, and the, lliawarra competition is to be. resumed. -? ;.' The draw js the'same as last; week with * Cbriis...
'Daily Mercury' Classified Advertisements RATES: Two shillings and threepence (2/3) for first two lines; ninepence for each subsequent Line. Casual advertisements 6/- per inch. LOtTC OPTICAL * SERVICE 134 CROWN STREET , WOLLONGONG (Near Gas Co.) Telephone Woll. 833 HOUSES AND LAND FOR SALE A RARE opportunity to com mence your home and secure a temporary dwelling within a vgry. short.time. at popular Lake ;iiej^Ktsr-'' VBiis, waier, 'light jand alt Vdeliyeries .atj^h^dpor.^ -Foe alDOuV £150 this ' opportunity . can. be yours. Tradesmen available to help you. Inquire immediate ly as sites are limited. J. N. King and Sons Pty. Ltd., . 343 Crown Street, Wollongong. T- ALGOWNIE : Home Site in convenient position. Gener ous dimensions. Inspect today. Only £225. Willmore & Randell, 57a Keira St. Phone Woll. 1198. /'^ORRIMAL: 3-bedroom Wea therboard Home — all elec tric. Floor coverings and blinds. £2,550. -Immediate V.P. Will more '& Randell, 57a Keira St. Phone Woll. 1198....
SWEDISH TENNIS WIN FOR AUSTRALIANS : STOCKHOLM, Mon. (A.A.P.). -rit Australians Adrian Quist ap:d Mrs. Thelpia Long yester day. won the Swedish mixed doubles tennis title, b, eating Sp.uth African Eric Sturgess an.d England's Miss Joan Curry 6/2' 6/4. ' Mrs. LOng also, won the women's singles -title, beating Sweden's Hiid'e Sterling 3/6 .6/2 6/4 in the final. ' '
PAKISTAN FREE OF POLITICAL UNREST (From Noel Buckley, Reuter's Correspondent at Karachi) Pakistan is virtually free of political un rest. In all the breadth of this land of 8.0-, 600,000' people there is no substantial oppo sition to the all-powerful Muslim League. Yet there is misery enough, and discontent. Maladministra tion is frequently and promin-. ently complained of in the area. I Corruption is so . widespread that special- -anii-corruption ser- 1 vices are maintained. . There is misery- and discontent on the pavements of Karachi where some 150,000 refugees live-, in rtiajceshii't lean-to. 'sijeltpjysJ -. ! An- other ' 200,000 live' in siianty 'towns about the city.'; \ ; H'he,re is misery , and discon tent in hundreds , of towns .and ' cities throughout West and'East Pakistan whepe uncounjted thou , sands of u'nrehahilitated - refu gees. stiU' live;- a . h^nd-r.9:-mduth existence in camps or -out' of camps. '? But the refugees have done no more than give'f resh edge to the a...
BlilLDER FINED ON DRIVING UNDER INFLUENCE CHARGE A ; 26-years-old builder was convicted in Wollongong Court of' Petty Sessions yesterday on a charge' of having driven a motor lorry ' 'while under the influence of. ihtoxicatlng liquor on July 21. He' was Bernard George Com erfdrd, who pleaded guilty to the charge. Police said Comerford was driving north in Wollongong Road, Port Kembla, and when approaching the .Tom Thumb Bridge, veered from side to side as another car was coming in the opposite direction. Although the other car drew over until its near side was off the bitumen Comerford's lorry swung oyer and collided with the front of the car. Botjx vehicles were damaged. The driver of the other car received a bruised hip, whilst his wife, Who was sitting alongside him, received a. bruised back and ri^ht shoulder, abrasions, to ,the head and contusions to both knees. After medical treatment she was allowed to go home. At the . timer. Comerford was most unsteady on his feet and his e...
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CLEM SANDS DRAWS IN N.Z. AFTER SOLID BOUT AUCKLAND, Monday (A.A.P. Reuter). — In a sensational fight In Auckland tonight, Australian Clem Sands (10.6J) floored Auck land's Jackie Jenkins (10.6) eight times in ten rounds in a welter weight contest but could still only draw with him. The final gong rang as Jen kins was knocked on to his back fr.om a -terrific ..right cross; ? * ????? Jenkins gained a - big' points lead in the early rounds.
SOUTH COAST ; RAINFALL - South Coast rainfall registra tions, for the '-48-hour period ended 9 a.m. Monday: Camden , 41, Picton .47,- Woliongdiig. 251, ^Robertson . 354;' . Bowral . 213, Moss . Vale . 245; . Sutton .''Forest 246/ Kiama ,'42i; Berry; 428, Nowra 293, - 'Crookhaven 285, Jervis Bay 185,- Milton 485, Ulla . clulla 4.79,, , Braid^tfo.pd - 1.26, , AxQr luen 98, 'Bateman's Bay 269, Moruya Heads 163, Port Kem bla 240, Bega 92, Candelo 63, Pambula 87, Eden 128.
Many Advance Subscriptions To Security Loan SYDNEY, Monday. — Excep tionally strong support through, advance subscriptions, has been given to the Commonwealth Government's £50,000,000 .Tenth Security Loan,' the. ' Common wealth Loans director (Mr. C. Banfield) said, today.' 'Mr. Banfield said that since th'e .loan was . announced' by the Treasurer * (Mr, . Fadden) in June,, the volume of 'advance subscriptions 'had ' increased greatly. Of the i50, 000,000 to be sought between August 1 and -August -15, !£37,0l00,p00. , was. represented by, f Commonwealth securities maturing on August 15 and the remainder .was required for war ' rehabilitation and the works programme of the Com monwealth, and the : -States.. Already, through advance subscriptions, 257 voluntary loan, coinmijttiees In'; the. 'various States have exceeded the quotas for new cash allotted to them.
Buffaloes Present £282 T o Charity At Annual Balll As a result of the Grand Order of Buffaloes' annual ball held in the Diggers' Hall, Wollongong, ihe IMawaraa Cottage Hospital, Coledale, received £72 and the Diggers' Rest Home, Mount Keira, £210. Approximately 450 attended the ball, the music for which was supplied by Charles Hayes and his 'orchestra} 'At -9 p.m. air. .'Howard r'Ca'riton, announced. , /..that . 'the. ' pfltcial opening ceremony A'Wduld ' take place. ? . .? r . 1 / ? To the , tune ' of 'Old ^Com rades','' 22. Buffaloes, ? .bearing swords;, executed, a neat march ing .manoeuvre, ?? culminating with the -formation of* an''arch of. steel, down the centre ? of which ' marched the ' .President of the Ball Committee, Mr. Roy. Tate, ? accompanied'.' ? by Mrs. Green and preceded, by eight year-old Robyn' Barrington who, dressed in, a period costvuiie' of pink and blue satin, . mad.e.'. a charming flo.wec girl.' Mrs.. Green wore an attractive dress of royal blue iaffeta.. wi...
PRAISE FOR AUSTRALIA IN MALAYA SINGAPORE, Mon. (A.A.P.). — The Chinese-owned English language newspaper, ''Singapore Standard', today began its edi torial: 'It's time somebody said 'thank you' to, Australia for tha help that country is giving Malaya in her struggle againscl elements of lawlessness.' After recalling the services of the Australian . Eighth Divi sion in 1942 and the recent ar rival of R.A.A.F. squadrons, the 'Standard'- - referred,- to . a statement by Labor Senator W. Morrow, of Tasmania, that Aus tralia's .intervention in Malaya was equivalent to strikebreaK ing.: y -V -? The .statement, 'declared the '(Standard',, 'reflects., an^' ap. .pauiing.' .'Jlack ? ..of .'kn6.\vl:e(:l;e about; ' the actual ' situation in Malaya''.' . ' The ' 'Standard' urged the Australian . Military Mission and the, '..Commissioners here tb ''t'ell Australia the truth', th,. ?whole- 'truth and nothing but tbe truth about : the ' ani.:. terrorist campaign'.
'Teen-Age Dance At Austinmer Despite the unfavourablie' Weather an enjoyable 'teen-age dance was held at the Austinmer School on;- Friday night. The dance was, conducted by the: Parehts and Citizens; : As sociation, -which hopes to intro. duce regular- dances of this type. The present 'flu epidemic 'pre vented many of the younger members from, being present. During the evening nbvelty dances were conducted. Among those, who won prizes were Mrs. 1 Foreman, Miss Marilyn James and Miss Dawn Jones. j The music, consisting of piano and drums, was supplied by Mr. and'Mrs^Leary. Mfc Atliol Dent, a member of the. P. and C., acted: as ,M.C. .
'VICTORY SOCIAL' FOR W'GONG PENNANT BOWLERS. Wojlongong bowl.e.rs held a 'Victory Smoko' in the club rooms on Friday night to pay tribute to their fellow' club mem bers who had won the Country i Pennant. . The Wollongong No. 1 Pen nant team, which had won the South Coast Pennant, was also runner-up , in the .State' final.. Wollpngong, club's'' Vice-presi- dent Mr. Babidge proposed the toast of the victorious' team. He complimented the players oja their great achievement. The So.uth Coast delegate, to the N.S.W.B.A., Mr. Sam. Blake n.ey; Northern Section delegate, Mr. Con Quilke'y; President of the Thirroul Club, Mr. Hugh Ross ; President of- the Corrimal r Club, Mr. George Hindmarsh I and President of the -.'Vyoonona Club, Mr. Syd. Dumbrell, sup ported the toast of Wollongong's top team. ' President of; the Wollongong Club, Mr. Phil Healey, acknow ledged the' words of praise. ' Mr. Healey. said the team's win had| brought great: honour to the club. ? ; He introduced' the members of ...
OBITUARY HENRY CHARLES HERD. The death occurred yester day in the Wollongong District Hospital of Henry Charles Herd, of. Kembla Street, .Wol longong. Mr. Herd, who, was ?born in Wollongong, was prominent in the Protestant Al liance 'Lodge over a great num ber of years and had held of fice on . several occasions. He had -resided with his 'sister at Kembla Street, Wollongong. He ?was a master painter, but had not -engaged in his occupation, for many years owing to indif ferent health. He. is to he buried privately at. the. Methodist Cemetery, Wollongong. The , Rev. Almond will officiate.
OWNER OFFERS SHIP FOR KOREAN WAR LONDON,. Monday. (A.A.P.).— Danish shipowner Kniid Laurit zen has placed ' the 3500 ton steamship Vilma Dan at' the dis posal of the United Nations for use in the Korean war. ' He made the offer in a cable which has ,be'en forwarded to Mr. Trygve ? Lie by the Danish Ministry of 'Foreign' -Affairs. '
MINISTER FOR NETHERLANDS RETIRES Members of the Diplomatic Corr for Brazil (left), M. G. Pa da retiring Minister for the Nethnd the Minister for the Philip Senor J. C. de Alencar, Ministesation during the function, vani, Ambassador for France, aps attended a farewell to the pines, Dr. R."Regala, in convererlgnds (Mr. P. E. Teppema).
U.S. Aid For French Forces SAIGON, Monday (A.A.P. Reuter). — The first two ship ments of United States' military aid for the French Union forces fighting the Russian recognised Vietnin Government guerillas in Indo-China arrived last week. The cargoes comprised equip ment for the ' State ' forces being formed by Indo-China's three Western-recognised States — Viet- nam, Cambodia and Laes. The shipment also' included aeroplane engines and _ other spares needed by the French Air Force which is supporting the French Union ground forces pro viding communication links with French outposts in difficult mountain country near the Com munist China border. The aid has been given by the United States against a. list of requirements supplied by the French authorities. , . It is expected,' inat aid, apart from military equipment, will also be sent to Indo-China.


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The basic difference between a visa and a green card is that a visa is a temporary pass to enter and remain in the U.S. for a designated period of time while a green card is a permit that does not expire and allows the holder to remain in the U.S. as long as he desires. Many visas can result in a green card; however, the majority of visas require a designated entry and exit from the U.S.
Nonimmigrant Visas
A nonimmigrant visa refers to all types of visas that are issued based on the applicant's intention to leave the United States after her task or visit has ended. In definition, a nonimmigrant visa cannot result in permanent residency, though there are channels and loops that the applicant can jump through to obtain permanent residency with a nonimmigrant visa. Nonimmigrant visas include tourist and business visitor visas, temporary work visas, student visas and exchange visitors. These visas expire and are all subject to an I-94 date issued upon entry to the U.S. that states when you must leave the country. Failure to leave by the I-94 date results in the visa holder being out of status, which results in penalty of deportation and a possible ban from returning to the U.S. for a set period of time.
Immigrant Visas
Immigrant visas are issued based on the intention of the applicant to remain as a permanent resident in the U.S. Once an immigrant visa is issued, the holder can enter the U.S. and apply for a green card. However, immigrant visas are more difficult to obtain than nonimmigrant visas and are petition based. All immigrant visas (excluding the Diversity Visa Lottery winners and refugee and asylee immigrants) must be petitioned for by a U.S. citizen. An applicant can be petitioned by a U.S. employer, family member or fiancée to receive a visa. The visa itself does not give the holder permanent residency; after entering the U.S. he must apply for a green card in order to remain in the country.
Permanent Residency
Legal permanent residents (LPR), or green card holders, are not visa holders as they are considered residents and are not subject to any time limit in the U.S. A green card does not expire unless the conditional rules are broken and the LPR is found guilty in immigration court. A green card can be considered a never-ending visa that expires only if the holder is convicted of a felony and found guilty in immigration court or if the holder abandons residence (the U.S.) for a period of one year or more.
Rights and Responsibilities
Visa holders, unless on a specific work visa, cannot work in the U.S. while green card holders are free to work in any occupation. A green card holder maintains all of the rights of a U.S. citizen except for the the right to vote, serve on a jury and obtain federal funding for college. Green card holders can own houses, open bank accounts, apply for a driver's license, apply for social security and are required to pay federal taxes. Depending on the type of visa, nonimmigrant visa holders can apply for a driver's license, bank account and social security if their visa type allows, such as an H1 visa. The majority of nonimmigrant visas, however, are not accompanied by the same rights as a green card is.


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The Ventures Vol.2, Walk Don't Run...plus Digipack
catalog number: CD3930294
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The Ventures: Vol.2, Walk Don't Run...plus Digipack(2003/Magic) 15 tracks! All recordings are from '64! Aufnahmen sind aus dem Jahre 1964! 24-Bit Remastered! 15 Titel!
Artikeleigenschaften von The Ventures: Vol.2, Walk Don't Run...plus Digipack
Interpret: The Ventures
Albumtitel: Vol.2, Walk Don't Run...plus Digipack
- Format CD
- Music Genre Rock 'n' Roll
- Music Style Instrumental Rock & Roll - Beat
- Music Sub-Genre 277 Instrumental R&R/Beat
- Title Vol.2, Walk Don't Run...plus Digipack
Label MAGIC
- weight in Kg 0.100
Artist description "Ventures, The"
The Ventures
Instrumental; group formed in 1958 by Nokie Edwards (lead guitar), Don Wilson (guitar), Bob Bogle (bass) and Howie Johnson (drums). They had a million-seller with 'Walk – Don't Run' on Dolton 25 in 1960 (initially released on Blue Horizon 101 in 1959), and although they didn't have many other big hit singles (the exception being 'Hawaii Five-O', a No.4 in 1969), they have sold more than a 100 million albums, which makes them the best-selling instrumental group ever.
It helps that they are also extremely popular in Japan! Johnson was replaced by Mel Taylor in 1961. Edwards was replaced by Gerry McGee in 1967, but returned to the group 1972-85, and again in late 1996. Taylor was replaced by Joe Barile 1973-78.
Taylor died in 1996 and Bogle in 2009.


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Re: Catherine Normile family
In reply to:
Re: The newest Normile
Ellen Visse 8/18/03
Hi Ellen
Here is information on your grandmother Catherine's brothers(4)James,Michael,Wilbert,Thomas and sisters(2)Agnes and Francis.All but your grandmother and Thomas lived their lives in Cleveland.Thomas went to Detroit and Catherine went to St.Louis.Nobody in Cleveland seem to know anything about a Anastasia or a Sr.Mary.
All the information I have points to the family coming from County Clare. Ray


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How's your mamandaddy? Saturday morning . . .
You may remember me telling you I was going to be the guest speaker at, "Saturday Morning With Friends" sponsored by the First United Methodist Church in Pensacola, Florida. Well, everything was perfectly organized, and went off like clock-work. Here I am with my darling Bob, who braved a room-full of mostly women to accompany me and be my assistant. The photo was snapped by my childhood friend, Gloria, who along with our other longtime friend, Cheree, came to hear me speak. I was also happy to see my good schoolteacher friend Pat, who helped me so much the first few years I taught school in Pensacola.
Chairwomen Julia Crowe and Connie Vance and their power-house committee did a stunning job of filling this entire room with gorgeous auction items. For the first hour, everyone strolled around and listened to beautiful live music and sipped on cranberry coolers and flavored coffee and said Southern Lady things like, "Oh honey, you look darlin'!"— "Oh, no sweetie, you're the one who looks precious!"— "How's your mamandaddy?" People who think Florida isn't Southern haven't been to Pensacola.
The funds raised from the auction and ticket sales went to support The United Methodist Children's Home in the North Florida, South Alabama Conference, and also to the Weiss Elementary After School Program — both causes dear to my heart.
Every single woman I spoke with was completely charming. I could have plopped down at any table and made plans to go shopping with them later in the day. That's high praise, because you can't go shopping with just anyone.
I spoke about how God shows His love for us by giving us gifts . . . that we need to use. Just like the ladies of this church used their gifts to raise funds for those in need. (If you loved someone enough to give them a gift and they didn't use or appreciate it, you wouldn't be in a hurry to give them anything else, would you? Hmmm).
The food was not only beautiful, but completely delicious. It always seems when you prepare food for a large crowd, the flavor suffers, but not this time. Whoever chaired the food committee, obviously knew her way around a kitchen! "Crystal and silver for 300? Why, sure honey! What did you expect, Chinette? Hahahaha!"
And this is why everyone really came . . . GRITS BAR! Oh, my goodness, they were creamy and tasty all by themselves, but with bacon, cheese, peppers, tomatoes . . . I can't even remember all the other toppings, but it was fabulous!
No one (not even Bob, my photographer husband) remembered to take a single picture of me speaking, but I snapped this one of Connie while she was making a few announcements. You'll see a story soon about how this deceivingly simple-looking stage caused me to reveal my secret identity . . . Klutz Girl. Oh well, I had them charmed for a while, until the ugly truth came out . . . I can't walk. Maybe it's a good thing no one had a camera ready.
The topic of my talk was, "Gayfers, Grits and God . . . Proof we are Loved." One of the church members, Mitzi Presley Holt, who served as the former art director for Gayfers, presented me with this autographed ad she created for the dearly departed department store. I am going to frame it and hang it in my office because I just adore it!
The hand painted ornament is gorgeous, and I used it on my Valentine's Day dinner table. And the hand-turned wood bowl . . . be still my heart. Mr. Bob Joseph, a member of FUMC who is 80 years old, created this stunning bowl from the root of a Pink Perfection Camellia bush. I KNOW! How perfect is that?!!! Such lovely, kind gifts from people with sweet, sweet spirits.
I may be getting a video of my actual speech later, and if I can figure out how to post it, I'll let you know. Thank you so much to the ladies of FUMC Pensacola for a wonderful experience.
Now, how can we all be like this group and get busy using our gifts?
Other Recent Posts
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The True Joy of Cooking
My brother, Robert Harrison — not to be confused with my son, Harrison Robert, or my husband Robert, threw a party dedicated to the well loved church casserole. Robert (the brother) is single, and he's always looking for a way to get women to bring him food without making any kind of commitment, so the […]
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The Fairhope Writer's Group has been busy promoting our book, "The Original Fairhope Guidebook." Above with me on the left, are co-authors, Jule Moon, Ron Meszaros and his wife Ellen Grigg — who is the wonderful artist for our book illustrations, Phyllis Pittman and Rosanne Gulisano. Those missing, or else running through the deli, are […]
Quilted car coat, perfect for travel
I've had four different readers ask about the coat I was wearing in my photos from Italy. It's often difficult to find a heavier coat around here, because we rarely need them. Even on cold mornings, it usually warms up by lunchtime and we can dash about in lightweight jackets or even heavy sweaters. […]
Is your dog royalty? Mystic Mutts of Revelry
This is Lois Lane's perfect man. The King of Mystic Mutts of Revelry 2016. And it gets better . . . he smells of Milk Bones. Ruff Ruff!! Ha-roooo! Does your special pup have what it takes to be Mardi Gras royalty? How about a loyal subject? How about a court jester? Ok then, how about […]
As we left the sneak-peek dress rehearsal, my husband said, "I think that's my favorite show I've ever seen at Theatre 98!" I had no idea what to expect before I saw Ripcord, a new play written by David Lindsay-Abaire and directed by Timothy Guy, and what I got was a hilarious, heartbreaking, breathtaking, […]
Saturday Morning With Friends
If you want to see a force that rivals a hurricane, just watch the power of, "the ladies of the church." Like most fundraisers, the project started with someone saying, "You know, we should do something to help." Julia Crow of Pensacola, saw a need and decided several local charities could use extra funding, […]
Greenery 2017
I know I'm a step behind, getting the new year off to a slow but wonderful start. Travel plus the flu have pushed my new year back a bit, but thankfully, this weekend I was finally able to get (most of ) the Christmas decorations put away. Here's my method; pile it all on the […]
Mama always said, "You can't judge a book by its cover"
All the buzz at the Curl Up and Dye Beauty Parlor hasn't been about the new president. They're over and done with that topic and like most people, have talked it to death. The real point of interest now is our new First Lady, Melania Trump and the woman who will have to suck in […]
Security abroad
We're home! Of course I was back for two full days before I came down with the flu, bronchitis and another lung infection. Go figure. Since we left for Italy the day after Christmas, I've returned to a house completely decorated for the season. The full tree is still up, stockings, advent calendar — the […]
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Greetings Guest!!Dismiss Notice
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On the second day of Christmas....
Discussion in 'UO Siege Perilous' started by Luka Melehan, Dec 12, 2008.


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Senior External Auditor jobs in Munich | Careers in Audit
Find your next Senior External Auditor job on CareersinAudit.com. Sign up for our jobs by email service to be notified of new External Audit Senior jobs in Munich as they are listed.
Found 4 jobs in this campaign
Audit Senior
Excellent Senior External Auditor job opportunity with UK Top 10 Accountancy Firm, Mazars.
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Audit Senior
Excellent Senior External Auditor job opportunity with UK Top 10 Accountancy Firm, Mazars.
Top job
Senior Internal Auditor- 3 Year Rotation in to the business.
SENIOR INTERNAL AUDITOR (Flat Structure) Location: Munich, Germany Travel: 65% (average per year- busy season Sep- March- Low travel from Apr-Aug) ...
Audit Senior, French or German speaking - Luxembourg
A world leading accountancy firms has an excellent opportunity for an to join its firm based in Luxembourg, working in Financial Services.
External Audit Big 4- Audit Manager- Lausanne, Switzerland (French Speaking)
Live and work in Switzerland, one of the most desirable locations on the planet, earning a wage in Swiss Francs - a preferred safe-haven currency.
External Audit Big 4- Audit Manager- Munich, Germany (German Speaking)
Live and work in Germany, one of the most prestigious markets in the world, earning a competitive salary whilst living in the beautiful city of Munich


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Under attack from senior Congress leader Digvijaya Singh for being "weak & ineffective", Special Investigation Team (SIT) chief Justice Chandresh Bhushan said the veteran leader should go beyond words and provide the SIT evidence to support his contention that excel sheet contained in the pen drive provided by him was original.
Bhushan said quashing FIR against governor was not a setback for him as the MP High Court has only restrained the STF from acting against the governor till he is in office, something which the investigative agency would not have done in any case following registration of FIR.
Three-member SIT has been created by the HC to monitor the Special Task Force (STF) probe into the Professional Examination Board (PEB) scam.
Bhushan told HT, "Digvijaya Singh has given us a mere pen drive and he claims it contains the original excel sheet. But, where is the evidence? He or whistleblower X from whom he has obtained the pen drive should at least explain where did they get the excel sheet from. STF has the clone of excel sheet and also the hard disk from which they have downloaded the relevant data. Both the clone and the original excel sheet as contained in the hard disk are the same."
"Digvijaya Singh has also given us clone of the excel sheet which he claims to be original but where is the source of that mirror image so that the data in the two could be tallied," said the retired judge of MP High Court, who has also been Up Lokayukta of MP.
When asked would Singh go to the extent of presenting a fake pen drive as original excel sheet seized from former principal system analyst Nitin Mahindra, Bhushan said, "I don't know. We have given our opinion, which the high court has endorsed. If he has any grievances, he could go to court and challenge our finding."


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Latest Journal Entry . . .
You are My Friend (so I gotta help us out here . . . )
Women have created quite a name for themselves lately. "I'm a vulva." "I'm angry." "I'm nasty." "I'm afraid." I'd like to refresh this conversation in ways we hope our daughters will mimic. Instead of clenching fists, maybe we can open our hands a little on what it really means to be a woman and offer a […]


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After suffering an abrupt fall that interrupted an impressive upward trajectory, shares of Fortuna Silver Mines
Without question, silver miners as a group are likewise trying to gain a foothold here in 2012 and stage the sort of climb that has typified this bull-market cycle for precious metals. Silver has only lost a sliver so far this year, while the performance of the Global X Silver Miners ETF suggests that miners on average have shed roughly 14% year to date. Endeavour Silver
Fortunately for Fortuna and its fortitudinous fold of faithful followers, the San Jose mine in Mexico continues to ramp up beautifully, providing a powerful counterpoint to the elevated costs at Caylloma. Even as the Caylloma cash cost rose sequentially to $7.21 per ounce, the company improved its consolidated mine operating margin substantially from 43% in the fourth quarter of 2011 to 52% in the first quarter of 2012. The San Jose operation is running three months ahead of schedule in pursuit of 1,400-ton-per-day throughput, and continues to achieve underground development milestones well in advance of planned production. That enviable condition lends substantial support to Fortuna's plan to deliver 6.4 million silver-equivalent ounces by 2014.
Although Aurcana (OTC: AUNFF.PK) retains the distinction of the silver industry's greatest growth story as production from its Shafter mine draws near, Fortuna's rapidly expanding production profile may have us all looking back at the current stock price as a powerful opportunity. I have purchased shares myself in recent weeks, and I fully expect to earn a tidy profit as San Jose matures. It may take a bit before my bullish CAPScall on the stock moves back into the green, but investing in this sector has turned me into a very patient Fool. In the meantime, stay in the loop by bookmarking my article list for ongoing coverage of silver and gold miners, or follow me on Twitter. Whatever path you choose, I hope you make a fortuna.
- Add Fortuna Silver Mines to My Watchlist.
- Add Endeavour Silver to My Watchlist.
- Add Pan American Silver to My Watchlist.
- Add Aurcana to My Watchlist.


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Pet Owner in Glenside
We live in Glenside, have 2 maine cats that require an in home pet sitter when we go on vacation. They are indoors but large and used to a routine. is there someone who can look after this pair? We need someone who can keep them indoors and visit at least once a day.
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Studio: Be Hairy
Cast: Yuliya
When you see her, you just want to spend the entire day(and maybe night too)plowing her. It's the magic her tight young body and her beautiful raven-haired bush work on you!Check out this stud boning her silly and creaming that bush.
Format: Windows Media
Duration: 15:16
Video: 1280x720, Windows Media Video 9, 5076kbps
Audio: 78kbps
File size: 578.9 MB