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Resources for Food Producers in Flooded Areas Due To Hurricane Michael
What's New
October 12, 2018
The FDA has added updated reconditioning request contact information to help farmers in other parts of the Southeast that may have been affected by Hurricane Michael. Information for FL, GA, and AL remains the same and can be found at the bottom of this update.
Reconditioning requests for contamination events that occur in North Carolina and South Carolina:
- Derek Price, 404-253-2277
Reconditioning requests for contamination events that occur in Virginia, Delaware, and Maryland:
- Randy Pack, 410-779-5417
Original Constituent Update
October 10, 2018
Among those in Hurricane Michael's path in the Southeast U.S. are farmers and their fields of crops grown for human consumption. The U.S. Food and Drug Administration's Center for Food Safety and Applied Nutrition has several resources to help growers who may be affected by the impacts to their crops from severe weather conditions.
The FDA's Guidance for Industry: Evaluating the Safety of Flood-affected Food Crops for Human Consumption provides the information that producers can use as they assess potential damage to their food crops. This guidance is an important resource for the growers who produce and market these crops, as they are responsible for assuring the safety of flood-affected food crops for human consumption.
The FDA reminds harvesters that generally, if the edible portion of a crop is exposed to contaminated flood waters, it is considered "adulterated" under the Federal, Food, Drug and Cosmetic Act and should not enter the human food supply. This applies to all food crops including underground crops (e.g., peanuts, potatoes). For crops (e.g., pecans) that were in or near flooded areas but where flood waters did NOT contact the edible portions of the crops, the growers should evaluate the safety of the crops for human consumption on a case-by-case basis for possible food safety concerns.
Sometimes, crops that have been harvested and then subsequently deemed unsuitable for human use can be salvaged for animal food. For more information please see CVM Update: Resources for Animal Food Producers in Flooded Areas.
Reconditioning requests for contamination events that occur in Georgia:
- Derek Price, 404-253-2277
Reconditioning requests for contamination events occurring in Alabama:
- Toniette Williams, 513-679-2700 ext. 2160
Reconditioning requests for contamination events occurring in Florida:
- Edwin Ramos, 787-729-8662
We encourage growers to work with state regulators and local FDA offices to assess their unique situations and to take into consideration all possible types and routes of contamination from flood waters in determining whether a particular crop is adulterated.
For more information:


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Ozark Farmers Market Opening -- Drive-Through Market
Where: Ozark Famers Market at Finley Farms
When: Thursdays from 3-7 PM
"OFM will open May 7th, 3:00-7:00 pm as a Drive-Thru and/or Pre-order Pick-Up shopping format. Customers will interact with vendors through their driver's side window as no customers will be permitted to exit their vehicles. OFM/Finley Farms staff will guide customers to vendors' booths, so come at your preferred time and we'll direct you to your favorite local foods. Maps and vendor lists will be provided upon arrival, and many vendors accept direct pre-orders to maximize your shopping efficiency. Tokens for cash purchases and SNAP/ebt will be available at the HUB tent. Come support locally grown and crafted foods at OFM."

subset: commoncrawl


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Perspective Free access | 10.1172/JCI17741
1Department of Neurology2 Department of Genetics and Development, Columbia University, New York, New York, USA 3 Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA
Address correspondence to: Eric A. Schon, Department of Neurology, P&S 4-431, Columbia University, 630 West 168th Street, New York, New York 10032, USA. Phone: (212) 305-1665; Fax: (212) 305-3986; E-mail: firstname.lastname@example.com.
Find articles by Schon, E. in: JCI | PubMed | Google Scholar
1Department of Neurology2 Department of Genetics and Development, Columbia University, New York, New York, USA 3 Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA
Address correspondence to: Eric A. Schon, Department of Neurology, P&S 4-431, Columbia University, 630 West 168th Street, New York, New York 10032, USA. Phone: (212) 305-1665; Fax: (212) 305-3986; E-mail: firstname.lastname@example.com.
Find articles by Manfredi, G. in: JCI | PubMed | Google Scholar
Published February 1, 2003 - More info
Over the last decade, the underlying genetic bases of several neurodegenerative disorders, including Huntington disease (HD), Friedreich ataxia, hereditary spastic paraplegia, and rare familial forms of Parkinson disease (PD), Alzheimer disease (AD), and amyotrophic lateral sclerosis (ALS), have been identified. However, the etiologies of sporadic AD, PD, and ALS, which are among the most common neurodegenerative diseases, are still unclear, as are the pathogenic mechanisms giving rise to the various, and often highly stereotypical, clinical features of these diseases. Despite the differential clinical features of the various neurodegenerative disorders, the fact that neurons are highly dependent on oxidative energy metabolism has suggested a unified pathogenetic mechanism of neurodegeneration, based on an underlying dysfunction in mitochondrial energy metabolism.
Mitochondria are the seat of a number of important cellular functions, including essential pathways of intermediate metabolism, amino acid biosynthesis, fatty acid oxidation, steroid metabolism, and apoptosis. Of key importance to our discussion here is the role of mitochondria in oxidative energy metabolism. Oxidative phosphorylation (OXPHOS) generates most of the cell's ATP, and any impairment of the organelle's ability to produce energy can have catastrophic consequences, not only due to the primary loss of ATP, but also due to indirect impairment of "downstream" functions, such as the maintenance of organellar and cellular calcium homeostasis. Moreover, deficient mitochondrial metabolism may generate reactive oxygen species (ROS) that can wreak havoc in the cell. It is for these reasons that mitochondrial dysfunction is such an attractive candidate for an "executioner's" role in neuronal degeneration.
The mitochondrion is the only organelle in the cell, aside from the nucleus, that contains its own genome and genetic machinery. The human mitochondrial genome (1) is a tiny 16.6-kb circle of double-stranded mitochondrial DNA (mtDNA) (Figure 1). It encodes 13 polypeptides, all of which are components of the respiratory chain/OXPHOS system, plus 24 genes, specifying two ribosomal RNAs (rRNAs) and 22 transfer RNAs (tRNAs), that are required to synthesize the 13 polypeptides. Obviously, an organelle as complex as a mitochondrion requires more than 37 gene products; in fact, about 850 polypeptides, all encoded by nuclear DNA (nDNA), are required to build and maintain a functioning organelle. These proteins are synthesized in the cytoplasm and are imported into the organelle, where they are partitioned into the mitochondrion's four main compartments — the outer mitochondrial membrane (OMM), the inner mitochondrial membrane (IMM), the intermembrane space (IMS), and the matrix, located in the interior (the organelle's "cytoplasm"). Of the 850 proteins, approximately 75 are structural components of the respiratory complexes (Figure 2) and at least another 20 are required to assemble and maintain them in working order. The five complexes of the respiratory chain/OXPHOS system — complexes I (NADH ubiquinone oxidoreductase), II (succinate ubiquinone oxidoreductase), III (ubiquinone–cytochrome c reductase), IV (cytochrome c oxidase), and V (ATP synthase) — are all located in the IMM. There are also two electron carriers, ubiquinone (also called coenzyme Q), located in the IMM, and cytochrome c, located in the IMS.
Map of the human mitochondrial genome (1). Polypeptide-coding genes (boldface) are outside the circle and specify seven subunits of NADH dehydrogenase–coenzyme Q oxidoreductase (ND), one subunit of coenzyme Q–cytochrome c oxidoreductase (Cyt b), three subunits of cytochrome c oxidase (CCO), and two subunits of ATP synthase (A) (see also Figure 2). Protein synthesis genes (12S and 16S rRNAs, and 22 tRNAs [one-letter code]) are inside the circle. Mutations in mtDNA associated with MELAS and MERRF, and mutations with features of neurodegenerative disorders, such as ataxia, chorea, dystonia, motor neuron disease (MND), and parkinsonism, are boxed. A complete list of pathogenic mtDNA mutations may be found in ref. 64.
Schematic representation of the mitochondrion with its electron transport chain (ETC). The ETC is the principal source of ROS in the cell. In addition to mutations in mtDNA- and nDNA-encoded components of the ETC, a number of mutant mitochondrial proteins that do not belong to the ETC have been associated with neurodegenerative disorders. The intramitochondrial localization and the clinical phenotypes associated with mutations of some of these proteins (in ovals) are indicated.
Besides the fact that it operates under dual genetic control, four other features unique to the behavior of this organelle are important in understanding mitochondrial function in neurodegeneration. First, as opposed to the nucleus, in which there are two sets of chromosomes, there are thousands of mtDNAs in each cell, with approximately five mtDNAs per organelle. Second, organellar division and mtDNA replication operate independently of the cell cycle, both in dividing cells (such as glia) and in postmitotic nondividing cells (such as neurons). Third, upon cell division, the mitochondria (and their mtDNAs) are partitioned randomly between the daughter cells (mitotic segregation). Finally, the number of organelles varies among cells, depending in large part on the metabolic requirements of that cell. Thus, skin fibroblasts contain a few hundred mitochondria, whereas neurons may contain thousands and cardiomyocytes tens of thousands of organelles. Taken together, these features highlight the fact that mitochondria obey the laws of population genetics, not mendelian genetics.
Mitochondria and their DNA are inherited exclusively from the mother. Thus, pathogenic mutations in mtDNA can cause maternally inherited syndromes. Since these mutations arise initially in only one mtDNA, the population of mtDNAs that was originally homoplasmic (i.e., only one mtDNA genotype) becomes heteroplasmic (two or more coexisting mtDNA genotypes). Obviously, the ratio of normal to mutated mtDNAs in a heteroplasmic population, and their spatial and temporal distributions, will be critical in determining whether and when a subpopulation of mutant mtDNAs will have overt phenotypic consequences. In this regard, it is important to note that most mitochondrial diseases due to maternally inherited mutations in mtDNA are recessive, that is, a very high amount of mutated mtDNA must be present (typically more than 70% of the total population of mtDNAs) in order to cause overt dysfunction. Since mtDNA encodes subunits of the respiratory complexes, pathogenic mutations in mtDNA cause diseases arising from problems in OXPHOS. On the other hand, mutations in nucleus-encoded proteins that are targeted to mitochondria, or that affect organellar function indirectly, can affect almost any aspect of cellular function, not just oxidative energy metabolism.
Diseases associated with mtDNA mutations are typically heterogeneous and are often multisystemic. Since heart, skeletal muscle, and brain are among the most energy-dependent tissues of the body, it is not surprising that many mitochondrial disorders are encephalo-cardiomyopathies. For example, mutations in the tRNALeu(UUR) gene cause mitochondrial encephalomyopathy with lactic acidosis and strokelike episodes (MELAS), mutations in tRNALys cause myoclonus epilepsy with ragged-red fibers (MERRF), and large-scale spontaneous deletions cause Kearns-Sayre syndrome (KSS) and progressive external ophthalmoplegia (PEO) (2). While these diseases are clinically distinct, they share a number of features found in many (but by no means all) mitochondrial diseases, including lactic acidosis, massive mitochondrial proliferation in muscle (resulting in ragged-red fibers [RRFs]), and cytochrome c oxidase (CCO) deficiency. In muscle biopsies, the mutated mtDNAs accumulate preferentially in the RRFs, and RRFs are typically negative for CCO activity.
On the other hand, there are some mtDNA mutations that tend to cause rather selective neuronal degeneration (Figure 1 and Table 1). This situation applies, for example, to mutations in the mtDNA genes coding for subunits of complexes I and V. Mutations in complex I subunits have been associated specifically with Leber hereditary optic neuropathy (LHON), a subacute degeneration of the optic nerve causing bilateral visual failure and blindness. Remarkably, LHON affects males far more than females. Equally remarkably, many patients are homoplasmic for the mutation (i.e., the mutation affects all mtDNAs), which is present in all tissues, and yet the disease is essentially confined to the optic nerve. Complex I activity in cells from these patients ranges from extremely mild to severe. Mutations in complex I genes are also associated with an "LHON-plus" syndrome, characterized pathologically by basal ganglia degeneration and dystonia, and with a maternally inherited form of levodopa-responsive parkinsonism.
Neurodegenerative disorders with mitochondrial involvement
Mutations in the mtDNA-encoded subunit 6 of complex V (ATPase 6) are associated with a syndrome characterized clinically by neuropathy, ataxia, and retinitis pigmentosa (NARP) at mutation loads of 70–90% in brain, and with a form of subacute necrotizing encephalomyelopathy known as Leigh syndrome (maternally inherited Leigh syndrome [MILS]) at mutation loads above 90%. These mutations cause varying degrees of impairment of mitochondrial ATP synthesis. Other mutations in mtDNA that cause Leigh syndrome (LS) have been found in ND5, tRNATrp, tRNAVal, and CCO III; patients with the latter two were atypical, in that the disease was of relatively late onset.
Mutations in a small but growing subset of the 850-odd nDNA-encoded gene products that are present in mitochondria have been implicated in neurodegenerative disease (Table 1). While some, such as LS, are essentially the mendelian counterpart of diseases previously associated with mutations in mtDNA, the others are sui generis and have highly diverse genetic origins.
LS is a fatal neurodegenerative condition pathologically characterized by subacute symmetrical necrotic lesions in the subcortical regions of the CNS, including thalamus, basal ganglia, brainstem, and spinal cord, accompanied by demyelination, gliosis, and vascular proliferation in affected areas. Onset is most frequently in infancy or early childhood but may sometimes be in adult life. Symptoms include motor and mental regression, dystonia, ataxia, and abnormal breathing. Death generally occurs within 2 years after onset. It is now clear that LS results from impaired mitochondrial energy metabolism, which can arise from a variety of causes. As noted above, LS can be caused by maternally inherited mutations, but inheritance of LS can also be autosomal-recessive or X-linked. In the latter group are mutations in subunits of the pyruvate dehydrogenase complex, mutations in nuclear-encoded respiratory chain subunits (mainly of complex I but sometimes also of complex II), and mutations in proteins involved in respiratory chain assembly.
CCO deficiency is one of the most common causes of autosomal-recessive LS, but interestingly, all the mutations described to date have been in genes that are required for CCO assembly. Only one sporadic mutation causing LS was found in a CCO structural subunit, in mtDNA-encoded CCO III. CCO-deficient LS is most commonly due to mutations in SURF1, a mitochondrially targeted CCO assembly protein of unknown function, and in SCO2, a mitochondrially targeted protein required for insertion of copper into the CCO holoprotein.
Friedreich ataxia (FRDA) is the most common of the hereditary ataxias. It is defined clinically by progressive limb and gait ataxia, axonal sensory neuropathy, absent tendon reflexes, and pyramidal signs. FRDA, which is autosomal-recessive, results from mutations in FRDA, which encodes frataxin, a mitochondrially targeted iron-storage protein (3, 4). Trinucleotide repeat (GAA) expansions in intron 1, sometimes in combination with point mutations on the other allele, reduce frataxin expression, resulting in decreased activities of holoproteins containing iron-sulfur groups, including complexes I, II, and III, and aconitase, a Krebs cycle enzyme. Notably, frataxin is particularly abundant in the cerebellum and spinal cord. Mitochondrial enzyme deficiencies and late-stage iron accumulation were also found in a frataxin knockout mouse (5). While the pathogenesis of FRDA is still unclear, one possibility is that the presence of unbound (free) reactive iron, via the Fenton reaction, generates free radicals within the mitochondria, leading to oxidative damage and inactivation of mitochondrial enzymes. For unknown reasons, mitochondrial superoxide dismutase (Mn-SOD), a key antioxidant protein, is deficient in cultured cells from FRDA patients, making them even more prone to oxidative damage. The role of oxidative damage in the pathogenesis of FRDA is also supported by the finding that idebenone, an antioxidant similar to ubiquinone, can reduce myocardial hypertrophy and also decrease markers of oxidative stress in FRDA patients (6, 7).
Hereditary spastic paraplegia is a progressive disorder resulting in paraparesis, with onset in childhood or early adulthood. Upper motor neurons are involved selectively, and ataxia and retinitis pigmentosa are also common. Autosomal-dominant, X-linked, and autosomal-recessive forms have been described. Patients with a recessive form of hereditary spastic paraplegia harbor mutations in SPG7, which encodes paraplegin (8), a mitochondrially targeted protein with strong similarity to yeast metalloproteases. Although the underlying pathogenic mechanism is still unclear, mutations in paraplegin cause OXPHOS dysfunction with CCO deficiency and mitochondrial proliferation (i.e., RRFs) in muscle (8). Recently, an autosomal-dominant form of hereditary spastic paraplegia (SPG13) has been attributed to mutations in the mitochondrial import chaperonin HSP60 (9).
Deafness-dystonia syndrome, also called Mohr-Tranebjaerg syndrome, is an X-linked recessive disorder characterized by progressive sensorineural deafness, dystonia, cortical blindness, and psychiatric illness. It results from mutations in TIMM8A, which encodes deafness/dystonia protein-1 (DDP1) (10), a component of the mitochondrial protein import machinery located in the IMS. In fibroblasts from patients, mitochondrial protein import is impaired (although not in a global fashion), probably because the DDP1 mutation impairs assembly of TIMM8A into a functional subcomplex of the import machinery (11).
Wilson disease is an early-onset autosomal-recessive disease characterized by movement disorders (e.g., parkinsonism and dystonia), psychiatric symptoms, and liver failure. The defect results from mutations in ATP7B, which encodes a copper-transporting P-type ATPase and results in copper accumulation in kidney, liver, and the basal ganglia of the brain. ATP7B exists in two isoforms, a 159-kDa form that localizes to the trans-Golgi network, and a 140-kDa form that localizes to mitochondria (12). The mitochondrial localization of the 140-kDa isoform (presumably it is in the inner membrane, but this has not yet been demonstrated) suggests that it might play a role in the functions of copper-dependent enzymes, such as CCO. In fact, mitochondria in affected tissues have morphological abnormalities, as well as deficiency of liver mitochondrial enzymes, especially complex I and aconitase. Thus, oxidative damage mediated by mitochondrial copper accumulation may play a role in the pathogenesis of Wilson disease. Since ATP7B is present in multiple subcellular compartments, the role of mitochondria in the pathogenesis of the disease may be secondary rather than primary, and the issue of mitochondrial involvement in Wilson disease remains controversial.
The most problematic and contentious connections between mitochondrial dysfunction and neurodegeneration involve those disorders that result either from primary mutations in gene products not targeted to mitochondria or from still unknown causes (Table 1). Because, in toto, these disorders account for the vast majority of neurodegenerative disease, the possibility of a unifying principle based on mitochondrial dysfunction as a primary cause of neuronal cell death (13) has become not only attractive, but even seductive. The key question, of course, is whether the data supporting this hypothesis are persuasive. We summarize here the evidence for and against such connections.
AD is the most common form of dementia in the elderly. Approximately 5% of AD cases are familial (FAD) with autosomal-dominant transmission; these result mainly from mutations in the amyloid β precursor protein (ABPP) or in the ABPP processing proteins presenilin-1 (PS1) and presenilin-2 (PS2). Most patients with AD have sporadic cases (SAD) without a known genetic defect. The neuropathology in both FAD and SAD is characterized by neuronal loss and by the presence of amyloid plaques and neurofibrillary tangles. Aggregated β-amyloid peptide (Aβ), a 40– to 42–amino acid subfragment of the much larger ABPP, is considered by many to be the principal culprit in the pathogenesis of AD, but the mechanism by which Aβ40-42 causes neurodegeneration is highly controversial. It is not clear whether plaques and tangles are a cause or an effect, and it has even been proposed that the accumulation of Aβ40-42 is a protective response to oxidative damage caused by mitochondrial dysfunction (14).
Although the findings of mutated forms of APP or presenilins in FAD point toward a pathogenetic role for Aβ40-42, the lack of a clear-cut mechanism for pathogenesis has caused hypotheses involving mitochondrial dysfunction to flourish. In fact, there are several disparate lines of evidence pointing to mitochondrial involvement in the disease. For example, it has long been known that patients with trisomy 21 (Down syndrome) develop the neuropathology of AD, presumably because of an increased dosage of the ABPP gene, which resides on chromosome 21. Not only did cultured astrocytes from Down syndrome patients show increased intracellular levels of Aβ42 associated with impaired mitochondrial membrane potential, but the converse was also true, namely, that impairment of mitochondrial OXPHOS in normal astrocytes resulted in alterations of ABPP processing and elevated levels of Aβ42 (15). These data are consistent with the finding that Aβ can inhibit respiration when added to isolated mitochondria (16).
Several groups have found either reduced CCO activity (17) or reduced levels of immunohistochemically detectable CCO polypeptides (18, 19) in AD brains. At this point, there is no conclusive evidence that mtDNA mutations are higher in AD patients than in normal elderly individuals, or that any particular mtDNA mutation is pathogenic in AD. Therefore, it is more likely that the respiratory chain defects observed in AD brains derive from nuclear gene defects or from acquired damage to respiratory chain components.
ALS is a neurodegenerative disorder affecting cortical motor neurons and the anterior horn cells of the spinal cord. The disease generally starts in the fourth or fifth decade of life and progresses rapidly, leading to paralysis and premature death. While most cases are sporadic and of unknown etiology, about 15–20% are familial (FALS); of these, about 10% are caused by dominant mutations in SOD1, encoding Cu,Zn-superoxide dismutase (Cu,Zn-SOD). Consistent with the dominant nature of the disorder, mutations in SOD1 do not decrease Cu,Zn-SOD activity significantly, implying that the mutations confer some as-yet unknown toxic "gain of function" on the protein.
Mutant mice carrying the common G93A mutation on a transgene develop severe motor neuron disease reminiscent of ALS, and in addition, the motor neurons develop massive mitochondrial degeneration. In SOD1G93A mice, the motor symptoms were preceded by a transient explosive increase in vacuoles derived from degenerating mitochondria in the motor neurons (20). These mice also had reduced respiratory chain function (21, 22), and, when fed creatine, a key component of the mitochondrial energy buffering and transfer system, their motor performance improved, as did survival (23).
Interestingly, some patients with sporadic ALS (SALS) accumulate abnormal mitochondria in anterior horn cells (24). Reductions in respiratory chain activity have been observed in spinal cords from SALS patients (25, 26), and this reduction appeared to correlate with a concomitant decline in total mtDNA in the tissue, implying that total numbers of organelles were reduced in the spinal cords of these patients (26).
It had long been thought that Cu,Zn-SOD was confined to the cytosol, and that only Mn-SOD (SOD2) was present in mitochondria. Recently, however, it has been determined that SOD1 is also located in the IMS of mitochondria. Thus, SOD activity in mitochondria is compartmentalized within the organelle itself, with SOD1 in the IMS and SOD2 in the matrix. This observation now provides a stronger rationale to explain some of the mitochondrion-related pathology in ALS, as mutant SOD1 could damage mitochondria directly. Transgenic mice expressing the G93A mutation in SOD1 show early activation of the mitochondrion-dependent apoptotic pathway (see below), with release of cytochrome c to the cytosol and translocation of the proapoptotic protein Bax to mitochondria, and similar effects have been observed in the spinal cords of SALS patients. Furthermore, mouse neuroblastoma cells expressing mutant SOD1 had impaired mitochondrial calcium buffering capacity, leading to elevated cytoplasmic calcium, a potential stimulus for apoptosis. Another proposed mitochondrion-related mechanism is based on the finding that cytosolic chaperones, such as HSP70, block the import of mutant SOD1, but not wild-type SOD1, into mitochondria (27). In this scenario, the mutant SOD1 forms aggregates with these HSPs and at the same time titrates them out of the cytosol, thereby killing the cell. Finally, mutant SOD1, but not wild-type SOD1, has been found to interact with at least four proteins, one of which — lysyl-tRNA synthetase — has an isoform that is targeted to mitochondria (28).
Taken together, these findings suggest that mitochondrial dysfunction might play a role in the pathogenesis of both sporadic and familial ALS (29). The mechanisms, however, appear to be complex and may very well involve not only OXPHOS deficiency, but also apoptosis and oxidative damage, as culprits. Notably, treatment of SOD1-mutant mice with the antibiotic minocycline, which inhibits mitochondrial permeability transition-mediated cytochrome c release, extended survival (30). Recent data, however, have failed to support the hypothesis that the gain of function of mutant Cu,Zn-SOD is an increase in copper-mediated free radical damage (31). Specifically, mice that lacked dismutase activity still developed the features of ALS, implying that the gain of function is not mediated by an increase in ROS that results from elevated or altered SOD1 activity.
HD is a chronic autosomal-dominant disease characterized by choreoathetotic movements and progressive cognitive and emotional disturbances. Pathologically, there is selective degeneration of striatal neurons, with marked atrophy of the putamen and caudate nucleus. HD is a trinucleotide repeat disorder, with expansions of a CAG repeat near the N-terminus of huntingtin, the product of the IT15 gene on chromosome 4. The mutated protein accumulates as nuclear inclusions in striatum and cortex.
Nevertheless, a defect in energy metabolism has been proposed as a potential pathogenic mechanism underlying HD, based on evidence obtained both in vivo and at autopsy. MRI spectroscopy in occipital cortex and basal ganglia of HD patients showed elevated lactate (32), as well as a reduced ratio of phosphocreatine to inorganic phosphate (PCr/Pi) in muscle (33). Animals treated with malonate, which inhibits respiratory chain complex II, develop pathological lesions in the striatum that closely resemble those of HD (34). Defects in complexes II and III, and in aconitase, have been described in postmortem HD brains, especially in the basal ganglia. In transgenic mouse models of HD, similar defects have been observed by some groups, but not by others. Lymphoblasts from HD patients showed increased cyanide-induced depolarization of mitochondria, as well as a greater vulnerability to staurosporin, an inducer of mitochondrion-mediated apoptosis. Recently, it was demonstrated by electron microscopy that mutant huntingtin localizes on neuronal mitochondrial membranes. Furthermore, it was shown that lymphoblast mitochondria from patients with HD have a lower membrane potential and a tendency to become depolarized at lower calcium levels than control mitochondria. Brain mitochondria from transgenic mice expressing mutant huntingtin showed similar mitochondrial defects (35).
Despite evidence in support of mitochondrial involvement in the pathogenesis of HD, the mechanism by which mutated huntingtin could cause bioenergetic dysfunction is still unknown, but some hypotheses have been formulated. Mutant huntingtin is known to bind to, and presumably downregulate, the activity of several polyglutamine-containing transcription factors that modulate nuclear gene transcription, such as Sp1, p53, TATA-binding protein, and cAMP-responsive element–binding (CREB) protein. These factors are thought to be involved in regulating the transcription of proteins involved in mitochondrial energy metabolism and in mitochondrion-initiated apoptosis. For example, mitochondrial dysfunction was shown to be associated with increased activated CREB in cultured cells (36). Therefore, by blocking the activity of critical transcription factors, mutant huntingtin might cause mitochondrial dysfunction. This hypothesis is partially weakened by the recent observation that, in a transgenic mouse model of HD, polyglutamine-containing transcription factors did not seem to be critically depleted in the nuclei of brain cells (37).
The issue of cause and effect has been highlighted by the recent finding that the expanded polyglutamine stretch in mutated huntingtin prevents it from binding to Hip-1 (huntingtin-interacting protein-1), as normal huntingtin does, thereby allowing free Hip-1 to bind to Hippi (Hip-1 protein interactor). Since Hip-1/Hippi heterodimers can recruit procaspase-8 (cysteine aspartic acid–specific protease 8) (see below), the weakened interaction between mutated huntingtin and Hip-1 is a proapoptotic event (38). As apoptosis, including that associated with caspase-8, can occur via both a mitochondrial (i.e., cytochrome c–induced) and a nonmitochondrial ("extrinsic") pathway, it is unclear at present whether the caspase-Hippi pathway is upstream or downstream of the known mitochondrial alterations in HD.
Nowhere is the role of mitochondrial respiratory chain dysfunction more persuasive, but also more contentious, than in the field of PD. PD is a neurodegenerative disorder characterized clinically by rigidity, tremor, and bradykinesia. The pathological hallmark of the disease is the loss of dopaminergic neurons in the substantia nigra pars compacta. As with ALS and AD, most PD cases are sporadic, but there are a few rare cases in which PD is inherited as a mendelian trait (familial PD [FPD]).
The mitochondrial connection to PD began almost 20 years ago, when it was discovered that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes parkinsonism in humans and in laboratory animals. MPTP inhibits complex I of the respiratory chain, but only indirectly, as it is the MPTP metabolite N-methyl-4-phenylpyridinium ion (MPP+), produced by the mitochondrial outer membrane protein monoamine oxidase B (MAO-B), that causes the damage. Soon thereafter, investigators found complex I deficiency and oxidative damage in the substantia nigra of PD patients, as well as reduced immunoreactivity for complex I subunits in affected neurons. Because complexes I and III are the principal sources of free radicals in the cell, altered complex I function in the substantia nigra pars compacta could be responsible for the increased DNA damage and lipid peroxidation found in PD brains (39).
Mutations in FPD have been found in the genes encoding α-synuclein and parkin, but the role of these polypeptides in neurodegeneration is unknown. It is noteworthy, however, that both α-synuclein and parkin, which are components of Lewy bodies (abnormal aggregates found in PD neurons), can bind to each other in vitro (40), that α-synuclein can bind to CCO (41), and that mitochondrial respiratory chain inhibitors can stimulate aggregation of α-synuclein into Lewy bodies in vitro (42, 43).
As with AD, the role of mtDNA mutations in the respiratory chain defects of PD is quite controversial: while some groups showed that cybrids containing mtDNA derived from PD platelets had reduced complex I activity, others could not replicate this finding. Only three mutations in mtDNA were associated specifically with parkinsonism, and they did not present as "classical" PD. Patients with a heteroplasmic mutation in the 12S rRNA gene had parkinsonism as part of a syndrome characterized by deafness and neuropathy, while a boy with a heteroplasmic microdeletion in the cytochrome b gene had an overlap syndrome of parkinsonism and MELAS. A parkinsonian syndrome was also associated with one of the LHON mutations in complex I. On the other hand, it was recently reported that about 10% of patients diagnosed with clinical, biochemical, and/or morphological features of mitochondrial disease had features of parkinsonism, and that these patients responded positively to anti-Parkinson medications (44). Unfortunately, however, none of the 76 patients studied were diagnosed at the genetic level.
Progressive supranuclear palsy (PSP) is a late-onset (age 50–70 years) neurological disorder with rapid progression, characterized by extrapyramidal symptoms, palsy of vertical gaze of supranuclear origin, and cognitive impairment. The pathological hallmark of PSP is the presence of neurofibrillary filaments containing hyperphosphorylated tau protein in the subcortical regions of the brain, with diffuse neuronal degeneration and gliosis. Genetic studies have linked an extended tau haplotype (H1) with the disease.
OXPHOS defects have been reported in muscle from PSP patients. Postmortem PSP brains had an increased content of malondialdehyde, a marker of lipid peroxidation, and reduced activity of α-ketoglutarate dehydrogenase, the rate-limiting enzyme of the Krebs cycle, but they also had normal respiratory chain activities (45, 46). While it is conceivable that a combination of mitochondrial dysfunction and oxidative stress could generate a vicious cycle leading to further oxidative damage and neuronal degeneration, at this point it is difficult to hypothesize a model consistent with both OXPHOS defects in muscle and normal complex I and IV activities in brain, or to explain why the Krebs cycle should be affected in particular.
In neurodegenerative diseases, specific populations of neurons die, but by what mechanism? Apoptotic cell death has been invoked as the underlying basis for neuronal loss, but the data are both conflicting and confusing. Apoptosis in mammalian cells is a highly regulated process that operates to sculpt cell populations during the normal course of embryonic and fetal development, but it can also operate during adult life to eliminate cells that are under various stresses. In broad view, apoptosis can operate via two pathways, one mitochondrion-mediated and the other receptor-mediated but mitochondrion-independent (Figure 3). In the mitochondrion-dependent pathway, an external insult — elevated cytosolic calcium, to cite but one example — acts to cause release of cytochrome c, which is located in the IMS. Cytosolic cytochrome c can then bind APAF-1 (apoptotic protease-activating factor 1), which then binds to the inactive form of caspase-9. This "initiator" caspase complex, or "apoptosome," can now activate a cascade of events, beginning with activation of downstream "effector" caspases, such as caspase-3, followed by activation of caspases further downstream, ultimately resulting in the hallmarks of apoptosis (condensation of nuclear and cytoplasmic contents, nDNA fragmentation, cell blebbing, and autophagy of membrane-bound bodies). Mitochondrion-mediated activation of caspase-9 can also occur via external (extracellular) receptor-mediated signals (e.g., TNF, growth factor deprivation, etc.) to target various ligands — e.g., Bad, Bax, Bik, Noxa — to the mitochondrion, thereby causing cytochrome c release and binding of APAF-1. Under other circumstances, a separate mitochondrion-independent pathway also operates (Figure 3).
A schematic view of the main pathways of apoptosis: mitochondrion-mediated and mitochondrion-independent. See text for details.
Among the numerous stresses known to participate in mitochondrion-mediated apoptosis, at least in vitro, bioenergetic failure and elevated ROS figure prominently (47). Thus, two key hypotheses immediately present themselves. First, one would expect a causal relationship between mitochondrial dysfunction and neurodegeneration via apoptosis, perhaps due, at least in part, to changes in ROS levels. Second, if neurodegeneration is related in any way to defects in respiratory chain function or in OXPHOS, then one would expect authentic mitochondrial diseases to show many, if not all, of the features of cell death that are postulated to occur in neurodegenerative diseases. So what do we know about apoptosis and ROS in mitochondrial disease and in neurodegeneration? Not unexpectedly, the literature is conflicting.
It is well known that muscle biopsies from patients with "classic" mitochondrial disorders, including those with RRFs, show little or no evidence of necrosis, fiber loss, elevated circulating creatine kinase, or inflammation. Nevertheless, markers of increased ROS have been found in muscle biopsies from patients with mitochondrial disease (48–50). It is clear that elevated ROS are injurious to mitochondria. For example, ablation of the mitochondrial SOD2 gene in mice caused rapid death via a fatal cardiomyopathy (51), and even loss of only one SOD2 allele was harmful (52). Encouragingly, pathology could be ameliorated, and lifespan extended, in SOD2–/– mice upon pharmacological intervention to reduce free radicals (53).
An analysis of muscle biopsies from patients with CCO deficiency due to various known pathogenic mutations in mtDNA (e.g., those causing MERRF, MELAS, KSS, and PEO) and in nucleus-encoded mitochondrially targeted proteins (e.g., those causing LS) showed features of apoptosis in CCO-negative RRFs — DNA fragmentation by terminal deoxynucleo-tidyl transferase–mediated dUTP nick end-labeling (TUNEL), condensed chromatin, and elevated immunostaining for caspase-1, caspase-3, and Fas ligand (54, 55). However, another group found no evidence for apoptosis (56). In a third study, some apoptotic markers (Bax, p53, Fas, and caspase-3) were not increased in CCO-negative RRFs, in spite of the fact that other apoptosis-related proteins (Bcl-2, Bcl-XL, DNase I) were increased, as was the amount of cytosolic cytochrome c (50). What little evidence there was for apoptosis in muscle seemed to be confined to a few RRFs (57).
If markers of elevated ROS and apoptosis can be found in these muscle biopsies, why do these muscle fibers not degenerate? This apparent paradox points out that a marker of apoptosis is merely that — a marker — and does not necessarily imply that apoptosis is actually occurring. In skeletal muscle, there are at least two reasons why apoptosis is not occurring in muscle. First, APAF-1 is either present at very low levels (58) or missing entirely (59) in skeletal muscle. In the absence of APAF-1, cytosolic cytochrome c has no partner with which to bind in order to activate caspase-9 and induce apoptosis (60) (although in some circumstances the absence of APAF-1 may trigger a "default pathway" of necrosis [ref. 61]). In other words, cytosolic cytochrome c in this situation is a marker of, but cannot induce, apoptosis. In support of this view, Nonaka's group could detect APAF-1 and released cytochrome c only in RRFs from patients with MERRF, MELAS, or PEO, but not in the far more abundant relatively normal muscle fibers (57). Second, an inhibitor of apoptosis called ARC (apoptotic repressor with caspase recruitment domain), which is expressed almost exclusively in skeletal and heart muscle (62), not only inhibits apoptosis in these tissues but can also protect mitochondria from free radical damage (63).
What about neuronal death in mitochondrial disease? There is neuronal loss in KSS, MERRF, and MELAS, and the regions that are affected differ in each disease, but no studies have been published regarding apoptosis in these cells. Intriguingly, TUNEL assays in postmortem brains from these patients showed little if any positive staining in neurons, but staining was observed in non-neuronal cells, such as microglia (E. Bonilla, personal communication). Moreover, there are regions of the brain — the choroid plexus in KSS, for example — that are nearly homoplasmic for mutated mtDNA and are devoid of CCO immunoreactivity, and yet are both morphologically intact and TUNEL-negative (E. Bonilla, personal communication). Therefore, it is still unclear how neurons die in mitochondrial disorders.
It is clear that impairment of mitochondrial energy metabolism is the key pathogenic factor in a number of neurodegenerative disorders (Table 1). This is most clearly seen in maternally inherited diseases that result from pathogenic mutations in mtDNA that interdict the normal functioning of the respiratory chain and OXPHOS. Examples of this group of diseases include LHON and maternally inherited LS. Similarly, mutations in nuclear genes that encode mitochondrially targeted proteins required for respiratory chain assembly and homeostasis can cause neurodegenerative disease. Examples in this class are autosomal-recessive LS, FRDA, hereditary spastic paraplegia, and Mohr-Tranebjaerg syndrome.
What is striking about both of these groups of neurodegenerative disorders is how diverse they are in their clinical manifestations, and how little they resemble the "classic" neurodegenerative disorders — AD, ALS, HD, PD, and PSP — that have no obvious connection to primary mitochondrial bioenergetic dysfunction. Put another way, it is remarkable that almost no pathogenic mutation in mtDNA causes the typical clinical manifestations associated with the most common neurodegenerative diseases. Of the more than 150 pathogenic mtDNA mutations that have been described to date (64), only one is associated with chorea and dementia; only three are associated with parkinsonism, but as part of a complex and atypical clinical picture; only three are associated with dystonia, but in the context of LHON or MELAS; only one is associated with spinocerebellar ataxia, but in the context of deafness, neuropathy, and dementia; and only one is associated with motor neuron disease, but in a syndrome with unusual secondary features. If respiratory chain dysfunction is a key factor in neurodegenerative diseases, why are there not more patients with "mitochondrial AD," "mitochondrial PD," or "mitochondrial ALS"? Conversely, why do so many mitochondrial diseases present as encephalopathies, myopathies, cardio-pathies, endocrinopathies, neuropathies, or combinations thereof, in which dementia and/or neurodegeneration is but one feature?
One response to these questions is that mitochondrial diseases that result from mtDNA mutations have features that are unique to the population genetics of mtDNA. In particular, the combination of heteroplasmy, mitotic segregation, and the threshold effect can conspire to mask features that might be more overt in disorders that obey the rules of mendelian genetics. In addition, it could be argued that many mitochondrial disorders strike early in life, thus precluding the features of dementia, chorea, and the like to evince themselves as they do in AD, ALS, or HD, which have later onset. While formally these are valid objections, they are not particularly convincing. There are many mitochondrial patients with extremely high levels of mutations in multiple tissues (and especially in the brain), and there are enough patients who live into their fourth and even fifth decades of life in whom the symptoms of AD, ALS, and PD should eventually be recapitulated.
This does not mean, however, that OXPHOS defects play no role in the late-onset neurodegenerative diseases. Rather, mitochondrial dysfunction probably plays an important, but secondary, role in these disorders. For example, it is clear that there is respiratory chain deficiency in hippocampal neurons in AD patients, as measured by biochemistry, histochemistry, and immunohistochemistry. It is likely, however, that these deficits are secondary to some underlying dysfunction, of which Aβ deposition is but one of many possible primary causes.
The failure to detect true cell death in muscle from patients with mitochondrial disease tells us little about neuronal cell death in these patients. It does, however, send a cautionary message regarding a too-eager willingness to equate cell death markers with the event itself. Conversely, the massive amounts of cell death in the neurodegenerative disorders mean that the very cells that are postulated to be dying due to mitochondrial dysfunction — e.g., motor neurons in ALS, striatal cells in HD, and, most pointedly, nigral cells in PD — are, in the final analysis, unavailable for examination, especially in the terminal stages of the disease and in autopsy tissue. Thus, many, if not all, studies that rely on patient material have, a fortiori, focused on the function, or lack of same, in a skewed population of surviving cells, such as glia, that are likely to be unrepresentative of the true pathogenetic course of events. Furthermore, studies of patient neuronal tissue or of model cells in vitro have their own limitations, not the least of which is the absence of the interactions among entire populations and subpopulations of cells that define the behavior of a vascularized tissue in vivo. These caveats point out the truly difficult nature of deducing pathogenesis in diseases as complex as neurodegenerative disorders. A mechanistic relationship between neurodegeneration and mitochondrial dysfunction still awaits a direct, clear, and unequivocal demonstration.
We thank Salvatore DiMauro, Michio Hirano, Michael T. Lin, and Serge Przedborski for insight and advice on the manuscript. This work was supported by grants from the NIH (NS-28828, NS-39854, and HD-32062, to E.A. Schon), from the Muscular Dystrophy Association (to E.A. Schon and G. Manfredi), and from the New York Academy of Medicine Speaker's Fund (to G. Manfredi).
Conflict of interest: The authors have declared that no conflict of interest exists.
Nonstandard abbreviations used: Huntington disease (HD); Parkinson disease (PD); familial Parkinson disease (FPD); Alzheimer disease (AD); familial Alzheimer disease (FAD); amyotrophic lateral sclerosis (ALS); sporadic amyotrophic lateral sclerosis (SALS); oxidative phosphorylation (OXPHOS); reactive oxygen species (ROS); mitochondrial DNA (mtDNA); ribosomal RNA (rRNA); transfer RNA (tRNA); nuclear DNA (nDNA); inner mitochondrial membrane (IMM); intermembrane space (IMS); mitochondrial encephalomyopathy with lactic acidosis and strokelike episodes (MELAS); myoclonus epilepsy with ragged-red fibers (MERRF); ragged-red fiber (RRF); Kearns-Sayre syndrome (KSS); progressive external ophthalmoplegia (PEO); cytochrome c oxidase (CCO); Leber hereditary optic neuropathy (LHON); Leigh syndrome (LS); Friedreich ataxia (FRDA); mitochondrial superoxide dismutase (Mn-SOD); Cu,Zn-superoxide dismutase (Cu,Zn-SOD); β-amyloid peptide (Aβ); progressive supranuclear palsy (PSP); terminal deoxynucleotidyl transferase–mediated dUTP nick end-labeling (TUNEL).
Series Introduction: Neurodegeneration: What is it and where are we?Serge Przedborski et al.
Alzheimer disease therapy: Can the amyloid cascade be halted?Todd E. Golde
Rare genetic mutations shed light on the pathogenesis of Parkinson diseaseTed M. Dawson et al.
Programmed cell death in amyotrophic lateral sclerosisChristelle Guégan et al.
Oxidative stress and nitration in neurodegeneration: Cause, effect, or association?Harry Ischiropoulos et al.
Neuronal degeneration and mitochondrial dysfunctionEric A. Schon et al.
Huntingtin in health and diseaseAnne B. Young
Malignancies and mitochondrial dysfunction.
Sergio Stagnaro


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Press Release
May 3, 2018
U.S. Gives Prestigious Emerging Young Leaders Award to LCC International Student
Zina Salim Hassan Hamu
On May 2, in Washington, D.C., the U.S. Department of State presented its Emerging Young Leaders Award to Zina Salim Hassan Hamu, a Yazidi woman currently studying at LCC International University in Klaipeda. Each year, the U.S. presents this award to only ten outstanding young leaders from around the world. The award recognizes Zina's extraordinary efforts to educate the world about the horrors faced by the Yazidi people after ISIS attacked their homes in Iraq and forced them into camps for displaced people. She tells this very personal story through photojournalism, a craft she plans to pursue professionally after completing her studies.
"Zina is doing exceptional work to promote tolerance and create positive change in the world. The intent of this award is to shine a light on people who do difficult things, and Zina is certainly one of them. We want more people to hear her voice so that they can understand the challenges faced by people in Iraq and in refugee camps all over the world," said U.S. Ambassador to Lithuania Anne Hall.
In 2014, Zina, now age 22, fled with her family as ISIS attacked her hometown of Shingal, Iraq. She lived in a camp for displaced people for two years before earning an opportunity to study English in Lithuania. Over the past three years, she has dedicated herself to telling the story of the Yazidi people through photojournalism. Having personally witnessed genocide as ISIS kidnapped or killed Yazidi girls, Zina has become a voice to carry their story to the international community.
While living in the Khanke camp in the Kurdistan region of Iraq, Zina volunteered as a child protector with ACTED, a UNICEF organization, and as a health guide with AMAR Foundation – a London-based organization. She also participated in health and vaccine awareness campaigns and street cleanups. In 2015, Zina took part in a project supported by UNICEF to teach photography to Yazidi girls as a means to empower them. There she found her passion and decided to become a photojournalist. Zina has shown her photos in Iraq, Italy, France and Lithuania to educate people who know little about the Yazidi people or their experiences.
LCC International University recruited Zina for its Middle East Scholars program while she was still living in the camp. After completing LCC's intensive English program, she intends to continue her studies in Canada.
The U.S. Department of State's Emerging Young Leaders Award and Exchange Program recognizes youth around the world for their efforts to create positive social change. U.S. embassies nominate outstanding young people and the State Department chooses ten to receive this prestigious award. This initiative goes beyond highlighting successful youth-led community projects: the award and exchange program set young leaders on a path for increased collaboration on global issues affecting youth by providing skills and tools for continued success.


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The FSCS guards UK savers against the risk of their bank or building society going under, currently offering coverage for up to £75k of losses. Peer-to-peer investments have to date sat outside of the scheme. A number of major platforms in the UK operate their own internal provision fund structure – which can make investors good in the instance of borrower default – but P2P has never enjoyed the security of a state-backed guarantee.
That now appears to be changing. The FSCS has published an update suggesting that it may be able to step in in order to compensate investors who receive "unsuitable advice" about the merits of investing in peer-to-peer lending and loan-based crowdfunding platforms. Depending on individual circumstances, the scheme may be able to provide compensation of up to £50k.
There are a number of caveats. Claims will need to relate to advice that has been received on or after 6 April 2016. The firm offering advice must be authorised. The firm must no longer have sufficient assets to meet compensation claims (it's somewhat unclear whether "firm" in this instance refers to the peer-to-peer lending company or the advisory firm). Most importantly, the FSCS has reiterated that it does not provide compensation in relation to losses incurred by poor investment performance. In other words, the scheme will not cover the risk of borrower default.
The advent of the Innovative Finance ISA (IFISA) – and the increased attention that financial advisers will likely pay to P2P products as a result – appears to have persuaded the FSCS to broaden its remit.
The IFISA – long billed as a game-changer for P2P – certainly seems to be living up to the billing. Yesterday we learnt that Octopus Investments would be entering into the peer-to-peer space with a new property backed offering. However, the "big three" peer-to-peer platforms (Zopa,RateSetter and Funding Circle) are as yet unable to offer IFISA investment, as they await full authorisation from the FCA. There are eight companies that have already received full authorisation, which were fast-tracked through the application process due to having launched after the closing of the interim permissions window.
Peer-to-peer lending has come under fire from incumbent lenders in the past for not being covered by the FSCS, and also for not making that lack of coverage clear. Yorkshire Building Society, for one, has issued several notes of caution about the sector's rapid rise to prominence.
RateSetter CEO Rhydian Lewis has long called for a retooling of the FSCS – stating in December 2014 that it was "no longer fit for purpose". Ceri Williams, senior commercial manager at RateSetter, offered his thoughts on today's news:
"This is a further sign that marketplace lending is an increasingly important part of the UK's financial landscape. Total investment with RateSetter made via advisers is significant, thanks to our IFA portal, and we expect this to continue to grow - this announcement is likely to give it a further boost. However, it is important to note that the FSCS will still not cover losses which arise from bad loan performance – our Provision Fund has protected our investors without fail for more than five years."


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The Dalai Lama: 'Sometimes I cry.'
At age 82, the Nobel peace laureate urges youth to take up his work of building peace.
In a conference room at his offices in northern India, the Dalai Lama sat among young civil society leaders trying to build peace in their homelands scarred by violent conflicts. These days, a question troubles him when he wakes from a night's sleep. "During that eight, nine hours, how many people [have been] killed in different parts of the world?" he asked. "And how many children died due to starvation?"
In this slideshow, USIP photographer Bill Fitz-Patrick captures this month's two-day meeting between the Dalai Lama and youth leaders struggling to build peace in homelands facing violent conflicts. Fitz-Patrick, a longtime White House photographer to four U.S. presidents, comments on the photos in the story—and in the full version of the slideshow, below.
The Dalai Lama sat stone-faced, thinking. His question hung like the sound of a tolling bell. "The room was dead silent. It's a cliché, but you could have heard a pin drop," said Bill Fitz-Patrick, who was covering the meetings as USIP's staff photographer.
For two days this month, the Tibetan Buddhist spiritual leader and Nobel Peace Prize laureate mentored the group of 25 youth leaders gathered by USIP. Fitz-Patrick watched and listened as he shot the photos above. He is a witness to a half-century of war and peacemaking, from Army tours in Vietnam and Berlin to 15 years as a White House photographer to four U.S. presidents.
"Not long after coming home from Vietnam, I was working in a camera store in Washington, and I wound up getting hired to the White House photo staff under President Nixon," Fitz-Patrick said. "I worked under Presidents Ford, Carter and Reagan. People had respect for these leaders partly because they had real, practical power. An American president can pick up the phone and give a directive that can change something. The Dalai Lama is a Buddhist monk who lives in exile. People respect him not for any practical power that he has, but for his spiritual power—the way that he touches people's hearts and conscience."
The Dalai Lama said he monitors global violence, from the assaults on Rohingya Muslims in Myanmar to the wars in the Middle East and Africa. On BBC and CNN, "I see too much … suffering. Sometimes I cry."
'Our Hope … Is on You'
At age 82, "since last year, I am feeling more tiredness," he said, and must restrict his travel and rely on others for the peacebuilding work he hopes to see achieved in the last years of his life. "Now, you young people, all of our hope and trust is on you," he told the group."
For two days, the Dalai Lama heard stories from the youth leaders—of being forced from home by warfare, or being arrested or beaten by authoritarian police forces. Others recounted government or traditional authorities telling them they were too young, or were ineligible as females, to have their voices heard in their communities.
The Dalai Lama, who saw his own homeland invaded as a child before being forced to flee into exile, empathized. "Now the question," he said, is "should we remain demoralized" in the face of violence and suffering? "Who created these problems? We human beings, ourselves! So then logically, if we make some effort, with vision, certainly we can reduce the suffering that we human beings created."
For Fitz-Patrick, watching the exchanges through his camera lens, "it was remarkable to see how the Dalai Lama makes connections with people, immediately and intensely," he said. They were "so fully engaged by him," said Fitz-Patrick. "When I was framing him up through the lens, I was, too."
USIP photographer Bill Fitz-Patrick took these photos of the two days of meetings between His Holiness the Dalai Lama and USIP's delegation of youth leaders from around the world. "It was remarkable to see how the Dalai Lama makes connections with people, immediately and intensely," said Fitz-Patrick. During the sessions, the Dalai Lama met briefly with many of the leaders individually—here with Tin, who promotes human rights and development in Myanmar.
"This is Lourd, who comes from the Iraq's Kurdistan region. Like the others, she was so fully engaged by him," said Fitz-Patrick. "When I was framing him up through the lens, I was, too." Lourd co-founded a non-government organization in Iraq that builds peace by bringing together people of different religious, ethnic, and political backgrounds.
Darine is a young Sudanese physician working with communities of people displaced by warfare in her country, including girls and women subjected to violence. Bill Fitz-Patrick recalled shooting this photo: "They spoke for a few moments, and then, as they connected emotionally, this happened. It was reverential."
From South Sudan, Ger Duany grew up during the Sudanese civil war. He was taken by the military and forced to fight as a child soldier until he escaped, walking hundreds of miles to become a refugee. Duany since has become a film actor and fashion model, and works with the U.N. refugee agency, UNHCR, to promote understanding of the problems facing millions of displaced people worldwide. In workshops with the young civic leaders, Duany discussed the ways that victims of war can turn traumatic experiences into personal growth. "During a break in the meetings, Duany came and knelt beside the Dalai Lama's chair to talk one-on-one," Fitz-Patrick said.
Jeremy Richman is an American specialist in neuroscience and pharmacology. He is the co-founder of the Avielle Foundation, which works to prevent violence and build compassion, and is named for Richman's six-year-old daughter, who was killed in the 2012 mass shooting at a school in Newtown, Connecticut. Early in the group's sessions with the Dalai Lama, the two spoke one-on-one.
The young leaders asked questions and explained problems they were facing. The Dalai Lama offered advice and empathy. Here Fatima, a women's development activist from Nigeria, asks a question. At home, she leads a mentoring program for Nigerian girls, including rescued victims of the Boko Haram extremist group.
"Look at their faces—how fully and happily they're engaged by him," said Fitz-Patrick. "These gatherings around him would happen each time we took a tea break. The group sessions each ran for several hours, and he would be speaking, and maybe in the middle of a sentence, suddenly, he would say, "Time for tea!" And his assistants would have prepared tea and cookies in the back of the room. And they would bring him his tea in his green mug. And he would start an informal conversation with one or two people, and pretty quickly, a group like this would gather."
"One of the youth leaders was Nagi, who has led peace movements in Sudan," said Fitz-Patrick. "Here, His Holiness pointed at Nagi's shaven head and told him, 'you could be a Buddhist monk!'"
During a tea break, the Dalai Lama talks with Adeng, a journalist and human rights from South Sudan, and examines how her hair is braided. "We are the same, human beings," the Dalai Lama told the group. "Different hairstyle, different color, different shape of nose, but basically, the same human beings."
The Dalai Lama and USIP President Nancy Lindborg co-led discussion sessions with the group of youth leaders. The Dalai Lama is known for his ready, mischievous sense of humor—and laughter was frequent in the room.
Height can be an advantage for a photographer who has to shoot amid crowds of people. USIP's staff photographer, Bill Fitz-Patrick, is six feet, six inches tall—and His Holiness has commented on Fitz-Patrick's size each time they have met. "I wish I could remember what I told him here that got such a big laugh from everyone," Fitz-Patrick said.
"To get just the picture you want of someone in a conversation, you have to anticipate a gesture or a facial expression, so that you're squeezing the shutter almost before you see it." Fitz-Patrick said. "So as I'm framing him, I'm listening to his voice, trying to sense when he's about to make a movement that I'll want to capture."
"Here is the full group gathered around His Holiness," said Fitz-Patrick. "Bright lights bother his eyes, so the room actually was dimly lit, and it would have been disruptive to use a flash. So I set the camera's ISO up to 2500, which was pushing the limit for getting good pictures without them getting grainy."


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Recent incidents, including a bridge collapse in Minneapolis and a steam tunnel explosion in New York City, have brought the nation's aging infrastructure into the spotlight. What are some of the country's major problem areas?
I-71, Columbus, OH: Years of poor maintenance have led to erosion and a rise in quicksand traps that swallow semitrucks whole
Four Corners Power Plant, Fruitland, NM: Aging gerbil no longer able to power Southwest
Water Treatment Facility, Missoula, MT: Constructed on Indian burial ground, ancient curse causing foundation to settle unevenly
Disney World Monorail, Orlando, FL: Once purported to run entirely on happy thoughts, the 36-year-old Disney monorail system has relied increasingly on regular electricity
Statue of Liberty, New York City: Lady Liberty is showing stress fractures and other structural damage following more than a century of being leaned on by huddled masses
Seven Mile Bridge, Key West, FL: Overburdened by discarded responsibilities
Levee system, metropolitan New Orleans: Actually, it's in perfect condition


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Legacy of Life Experiences continues with Bill Perry
Previous Life Experiences, Inc. employee Bill Perry is affectionately known as Mr. Bill. Life Experiences, Inc. is a better place because of the wonderful people that have worked in our many departments over the years and still today. Mr. Bill started with Life Experiences, Inc. when we opened in 1978. He worked in our Bakery, Sprouts and Laundry departments until 2006. After his retirement in 2006, Mr. Bill has continued to visit us as a monthly volunteer.
Mr. Bill was born in 1936 in Georgia, where he raised frogs and sold them as a youngster. He attended the academy for five years and then moved to Cary and has lived here for 35 years. As Mr. Bill turns 77 this year, he looks back and fondly remembers his time as an employee here at Life Experience, Inc. He laughs as he tells me about breaking eggs and spreading them over the cinnamon rolls while he worked in the bakery.
Mr. Bill has been a very busy man, throughout his career at Life Experiences, Inc. he worked in almost every department we have. He proudly explained that he was happy to have a job and receive pay. He was able to save his money and purchase haircuts, new suits, and go on trips.
When asked what he would say to a brand new employee Mr. Bill said, "Welcome to Life Experiences and I hope you enjoy it like I did. Continue working, when you get aggravated just settle down and work."
When asked what he would say to family members thinking about placing their loved one at Life Experiences, Inc. Mr. Bill said, "We enjoy working here. I was just sitting in a room when I first moved here. Then someone from Life Experiences interviewed me, and I was able to start working here."
Mr. Bill is now enjoying retirement by going out monthly with his fellow residents, volunteering monthly at Life Experiences, Inc., being an usher at First Baptist Church and visiting with his family (Betty Gibson, Pennie Gibson and Peggy Caroll). His next adventure will be flying back to Atlanta, Ga for the upcoming Braves game.


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Saturday, June 13, 2015
Pallet Top Sofa Table
9 comments:
I love love love this! You are so creative! You never cease to amaze me!!ReplyDelete
WOW. You are awesome. I saw the before on your FB actually and didn't get around to looking at it yet and then realized it's the same table you linked up to Trash 2 Treasure tonight! I didn't see that one coming - it looks amazing. Oh, and I voted for your dresser turned bench!! It's my fave!!ReplyDelete
So pretty! The table looks totally different!ReplyDelete
Brooke your sofa table turned out fabulous! I think it has so much character with the plank wood top than it would have with the glass. The seagull color milk paint is gorgeous with the plank wood. Very nice makeover!ReplyDelete
Marie@The Interior Frugalista
Love your table and the color! Great job! I love milk paint!ReplyDelete
Your table looks amazing! Love the finish and the pallet top. You breathed new life into it!ReplyDelete
hi how are you? Wow you are one busy gal with three kids under 6. Bravo to you for even blogging and finding time to do projects let alone beautiful furniture makeovers like this table. It's beautiful and I just love it and am featuring it this week at our Something to Talk About Link Party and will be sharing it on Social Media too. Hope you can stop by. Have a great day, Lisa at Concord CottageReplyDelete
I'm in love with this! Thank you for sharing this with us! Pinned and tweeted! I hope to see you at tonight's party. We are always so impressed with your creations and can't wait to see them! Lou Lou GirlsReplyDelete
Wow! What a wonderful transformation -- You'd never know that was the same piece. Great job!ReplyDelete


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Came across a Roisin McRoberts post that let us all know she was going to be hosting or having a CaseCAT tips session at 3 p.m. PST on June 9, 2019 on her Twitch channel, Burngirl. As far as I know, there are not CEUs offered, but it is a chance to learn new things. For people on the East Coast like me, we're looking at it being at 6 p.m. EST. For those that don't know, Twitch is primarily a video game streaming service and business, so if you tune in before that, you might just find someone playing some video games. All I can really say is thank you for taking the time to put together what you're putting together and I hope it makes every attendee just a little more knowledgeable.
I think this is a really interesting idea, and I would love to see our profession spread to more platforms and marketplaces, so it's a good time to mention that you too can join the streaming world. I believe Facebook and YouTube both provide simplified live streaming service. Last I checked it, Twitch required a streaming software like the free program, OBS, to work well, but perhaps that's changed. Regardless, if you are a trainer or teacher out there who wants to help people, there are free video edit softwares like Shotcut out there to help. There are free or low-cost screen capture softwares like OBS or Fraps. Additionally, remember that if you follow the continuing education program rules, you can also offer CEUs to your audience.
We are really at a point where we can use technology to spread our message and help a lot of people. I have had friends in the past use video gaming itself as a way to donate money to serious causes like cancer or children, and I can only imagine all the ways that these platforms could be used. We could see NCRF matching drives or other causes that support steno rise up and hit bigger audiences. It's a world of unlimited ideas, and every contribution is important.


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The Originators of Quick & Easy Cooking!
Bacon Corn Bread
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- 6
- 5 Min
- 30 Min
It doesn't matter when you get a craving for our Bacon Corn Bread, this fun twist on a Southern favorite is good anytime of the year! Serve it slathered in butter during the summer, or alongside steaming chili in the winter; start your day with a bacon-y breakfast bread, or end it with the perfect dinner side. This easy corn bread recipe is going to be a yummy part of any meal, anytime!
What You'll Need
- 1 cup sour cream
- 1 cup milk
- 1 egg
- 3 tablespoons butter, melted
- 1 1/2 cups yellow cornmeal
- 1/4 cup all-purpose flour
- 1/4 cup real bacon bits
- 2 tablespoons sugar
- 1 teaspoon baking powder
- 1/2 teaspoon baking soda
- 1/2 teaspoon salt
What to Do
- Preheat oven to 400 degrees F. Coat an 8-inch square baking dish with cooking spray.
- In a large bowl, whisk sour cream, milk, egg, and butter. Add remaining ingredients and whisk until mixed. Pour batter into baking dish.
- Bake 25 to 30 minutes or until a wooden toothpick inserted in center comes out clean. Let cool 15 minutes, then cut into squares and serve warm.
Check This Out!
- We can't get enough corn bread! If you loved this Bacon Corn Bread recipe, be sure to try our Corn Bread Pudding and our Crazy Corn Dog Muffins!
- If you're looking for dinner rolls that are sure to impress, check out our Homemade Pretzel Rolls, or our classic Better Buttermilk Biscuits.
- This Bacon Corn Bread recipe is the perfect side to our saucy Hillbilly Ribs or our Fire Station Chili!
If you love these recipes, then you'll love this FREE eCookbook!
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Nutritional InformationShow More
Servings Per Recipe: 6
- Amount Per Serving % Daily Value *
- Calories 374
- Calories from Fat 159
- Total Fat 18g 27 %
- Saturated Fat 9.4g 47 %
- Trans Fat 0.3g 0 %
- Protein 10g 20 %
- Amount Per Serving % Daily Value *
- Cholesterol 76mg 25 %
- Sodium 555mg 23 %
- Total Carbohydrates 45g 15 %
- Dietary Fiber 2.8g 11 %
- Sugars 7.8g 0 %
kleibrandt 4683221
Mar 06, 2019
And Mr. Food has done it again. Made this for the first time yesterday to go with homemade Chicken Noodle soup for dinner. This bacon Corn Bread is awesome. Nice and moist. The only change I will make is adding more bacon bits the next time I make it.
- WAS THIS HELPFUL? YesNo
robby6897 9217803
Feb 07, 2019
I made this tonight with a few changes. I used buttermilk instead of milk. I also added some shredded Parmesan cheese to the batter after pouring the batter into baking dish, I sprinkled fresh blueberries on top. Next time I make this, I'll probably leave out the cheese but the salty bacon with the sweet blueberries was really good to me.
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doloreseleeson 3927811
Jan 15, 2018
I think I will make this adding some heat with cayenne.
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1 Minute Cinnamon Bun
With our recipe for 1 Minute Cinnamon Bun you can enjoy a cinnamon bun for breakfast, dessert, or anytime you want! All you need is a microwave, some easy ingredients from your pantry, and your favorite mug. Before you know it, you'll be enjoying a cinnamon bun that's all your own.


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Nearly one-third of Germans back Martin Schulz's plans for a "United States of Europe," but support for his ideas varies greatly across the Continent, according to a poll released Thursday.
Schulz, a former European Parliament president and now leader of Germany's Social Democrats (SPD), proposed earlier this month drafting a constitutional treaty to turn the EU into a United States of Europe by 2025.
According to Thursday's YouGov survey, which was carried out before Christmas, 30 percent of German respondents said they favored the idea of a United States of Europe, making Germany the country that was most supportive of Schulz's plan among the seven European nations surveyed. French participants were also relatively supportive of the idea, with 28 percent endorsing Schulz's proposal.
The U.K., which is set to leave the EU in March 2019, was the least supportive country with just 10 percent of British participants saying they agreed with the plans.
Scandinavian respondents — from Denmark, Sweden, Finland and Norway — were similarly unenthusiastic, with between 12 percent and 13 percent in favor of the idea.
When Schulz announced his plans for a United States of Europe at an SPD party convention, he said that once a constitutional treaty was drafted, it would "be presented to the member states, and those who are against it will simply leave the EU."


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How To Start a Blog and Make Money Online
- Updated On 13/04/2021
- Author : Ram kumar
- Topic : Blogging
- Short URL : https://hellboundbloggers.com/?p=64786
People can find everything on the internet. This is the reason why the internet is very popular among the people of different ages. People look for various information, buy goods and simply amuse themselves using it. Some years ago, everybody understood that if they can spare money on the internet then it means that they also can earn there. The most enterprising of them created a webpage for their business and started earning on internet sales. Those who do not have their own business can start it in virtual reality and earn money there. One of the most popular ways of getting benefits of internet activity is to earn money from blogging.
After making the strong decision to start doing it you must find as much as possible information on topic how to create a blog and earn money. There are many sources of information from successful bloggers where you can find something like step-by-step instruction about the way of making interesting, amusing, useful, and, what is important, earning money blogs. To make your blog the best one it will not be superfluous to read all this information and make your own conclusions about making money online.
Choose a topic
Before creating your personal webpage the first thing you need to do is to choose the best theme for it. It must be interesting primarily for you because if it is not so then you cannot fill blog with useful and readable content. If you've decided what theme will be proper both for you and your followers then it's a high time to create new blog for free. There are a lot of free of charge domains where you can create your webpage. Usually, experienced bloggers advice to choose such domains as blogger.com or Livejournal.com to start with. Or you can get blogspot.com domain for free.
Add the content
Ok, you've created a new personal website: got your domain name, choose the theme for its content. Then it's a high time to fill it with articles and other video and photo materials. Of course, it will be better to write them by yourself but if you do not have time for it or simply do not want to spare your life on writing these content you can hire authors on the internet. Just make a request in any searching system: "write my essay for me" and find plenty of writers. Notice, that if you 're using for your account the articles created by others, not by yourself, then check each of it attentively before posting on your personal website.
Do not expect fast success in blogging. You'll need a lot of time to make your blog popular: from day to day it must be filled with qualitative content. Post articles for people, not for earnings.
Where's the profit?
After reading all this information you will ask: "When and how will I get my profit?" It is quite a fair question. This is the answer: You will earn money on personal website only after it is popular enough. It means that you need to have more than five hundreds of visitors daily on your website. It mostly takes from six months to one year to gain such number of daily visitors. It is the recipe for success for a blog that earns money. If you already have such number of followers every day, then start earning by placing different advertising on a webpage.
Be sure – if your blog is popular advertisers will find you. There are six main ways to earn money on advertising: Pay-Per-Click (paying for each click on advertising), Pay-Per-Impression (paying for opening the page with advertisement), Pay-Per-Action (paying for definite action with advertisement, for example for selling operation), Affiliate Adds (paying for placing advertisement in your blog), Direct Adds (buying advertising space in the blog), and Text-Link-Adds (or Text Link Brokers).
Now you know the most widespread ways of earning on having a personal website, so if you have not changed your mind then please be patient and start earning online!
Want to discuss your queries and interact with experts? You can connect with HellBound Bloggers (HBB) Facebook group for free!
Join HellBound Bloggers (HBB) and get Instant Updates. We'll also notify you with Great Deals, Discounts and other Interesting Tips. We won't SPAM or SHARE your Email Address with anyone.
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by Connor Morgan | CBS2 | Saturday, November 26th 2016 MARION, Iowa (CBS2/FOX28) — Black Friday is…
Marion library looks for new site to expand
By Makayla Tendall | The Gazette | Oct 22, 2016 at 4:00 pm
MARION — Abandoning an earlier idea of tearing down Marion's library and building a larger one there as part of a mixed-use project, the library board and developer now are hoping to secure some other land for the concept within 30 days.
The Marion Public Library Board, director and representative from developer Ryan Companies presented the modified plans to the Marion City Council last week.
Susan Kling, president of the library board, said once Ryan Companies is able to find a location and provide a cost estimate, the board plans to ask the City Council to schedule a public referendum on issuing bonds to pay for the project.
Kling said at this point she's unsure if the city would lease or buy the library space.
Board members have long said the community was outgrowing the 24,500-square-foot library building, but debate over what do about it has gone on for years.
In September 2014, the library board brought developer Ryan Companies on board to conceptualize a mixed-use facility that would house the library as well retail and apartment spaces.
Such a facility would provide more space for the library and bring more housing and retail to the core of Marion, said Lydia Brown, director of development for Ryan Companies.
"By creating that retail front, we will allow for the city to generate tax revenue, as well as the revenue that comes from the apartments above," Brown said. "When the space was created, it was not only to create a library, it was to create a revenue stream that would assist in paying for the upkeep and operational expenses of the library."
Elsworth Carman, the library director since March, said earlier plans for the facility included:
l Tearing down the current library at 1095 Sixth Ave, which was built in 1996, and building a two-story structure in the same location.
l Building a mixed-use facility with a skywalk across the street from the Sixth Avenue building.
Carman said that after hearing feedback from residents, the board and Ryan Companies modified their plans.
"We got a lot of community feedback that there was concern of taking down a building that was fairly new," Carman said. "It's definitely been outpaced by the community growth. The questions were: does it make sense to take down a building that could be reused if you widen your footprint a little bit and add to it. But the cost of building on could be as much or more than if you were to build a new building."
Carman also said residents didn't like a skywalk downtown.
At last week's City Council work session, Brown said the group no longer planned to build on the site of existing structure. It plans to secure another location soon in Uptown Marion, though Brown said she couldn't disclose the location yet because negotiations were underway.
Under the proposed library design Brown showed the council, the new space would be 40,000 to 45,000 square feet and budgeted at $12 million.
Carman said the library would be one story and have as open of a floor plan as possible so it could be restructured based on future needs.
"We will customize that space as the community grows and changes," he said. "From a library perspective, the square footage that we're talking about, that would allow us to have a very functional main library with as few fixed walls as possible."
Brown said Ryan Companies is partnering with Genesis Equities to create 80 market-rate apartments above the library, but Ryan Companies has not yet reached out to potential retailers.
Kling said she hopes to compile information for Marion voters as soon as the board has more information on costs.
Under a bond referendum, voters would have to agree to tax themselves extra to pay for the project.
Carman said he hopes the concept progress.
"It will be a symbiotic relationship where the library draws foot traffic from the retail, the retail draws foot traffic from the library," he said. "Everyone feeds off that additional energy and bodies.
"The library is perceived as wholesome learning organization. I think that's something people are drawn to, especially when we're talking about the core of Uptown."


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Friday, May 26, 2017
Notre Dame Grads Walk Out On Pence Speech
Last Sunday as Vice President Mike Pence came to the podium to give the commencement speech at Notre Dame University, a good number of graduates and their families stood and walked out.
Pence's speech encouraged the grads to keep their religious faith and value the freedom of speech---promising, "The future is yours."
Divisive? Hardly.
It wasn't his words. It was his personal beliefs and his associations. And the spirit of rebellion, self centeredness and deception that is pervasive in our "open minded" institutions of higher learning.
Is this what freedom looks like?
Did those whom we memorialize this Memorial Day weekend give their lives for this?
By all accounts, Vice President Mike Pence is both soft spoken and well spoken---someone who typically would not cause people to feel "unsafe"---a word often used in regard to conservatives on college campuses--by his mere presence or his scripted comments.
He was invited to speak at Notre Dame after students and faculty objected to a prospective invitation to President Trump, who would have been the 7th US President to give the commencement address.
Pence appeared unfazed by the walkout, proceeding to give his prepared speech.
He said, "This university (Notre Dame) is a vanguard of the freedom of expression and the free exchange of ideas at a time, sadly, when free speech and civility are waning on campuses across America."
The rest of his speech focused on faith and conservative principles like protecting Notre Dame and other groups from having to go against their religious beliefs to offer birth control coverage to employees under Obamacare, for example.
He said, "Just as Notre Dame has stood strong to protect religious liberty, I'm proud that this president just took steps to ensure that this university and the Little Sisters of the Poor could not be forced to violate their consciences to fully participate in American life."
"Notre Dame is exceptional," the Vice President said, "This university stands without apology for human freedom and the inherent dignity of every human person, and holds fast to the faith that gave it birth."
Isn't this what everyone in America wants---life, liberty and the pursuit of happiness---including religious liberty?
Isn't that what so many of those whom we remember this weekend gave their lives for?
Well, not exactly. Along with other values and virtues, freedom---freedom of religion and freedom of speech--- has been redefined by some in this enlightened generation.
Pence said, "While this institution has maintained an atmosphere of civility and open debate, far too many campuses across America have become characterized by speech codes, safe zones, tone policing, administration-sanctioned political correctness---all of which amounts to nothing less than suppression of the freedom of speech---These all-to-common practices are destructive of learning and the pursuit of knowledge, and they are wholly outside the American tradition."
This may be the point where some would begin to feel "unsafe" because "education" has more to do with so-called "social justice" than it does about actual learning.
The New York Times was quick to quote Luis Miranda who graduated from a master's program.
Miranda says, "Of course we welcome and support free speech on campus....", but Mr Pence's role in graduation was particularly unsavory for some students and their families---including gay people and immigrants---who have been hurt by the policies favored by the Trump administration.
Miranda, who was one of the walk out organizers, says, "If it was just five of us, we would have thought we were successful because we were doing the right thing. The fact that so many people showed up was mind blowing."
This walkout was not lost to the foreign press either.
Al Jazeera, the Muslim organization, said in their report after identifying Pence as a "religious social conservative", "The protest comes amid mounting controversy over what constitutes free speech at college campuses since the election of President Donald Trump in November, with students objecting to appearances by divisive conservative figures. Some schools have canceled events."
Luis Mirada's "mind blown joy" was not limited to his interview with the New York Times.
He and Aniela Tyksinski appeared on CNN Monday following the intrusion of Vice President Mike Pence.
Tyksinski explained to CNN's Brooke Baldwin, "The walkout was in response to the fact that members of our own community felt unwelcome, uncomfortable, and even unsafe."
Wow. No one should ever have to experience such hardships.
Miranda said he didn't know if campuses were too liberal---but he definitely supports free speech--"It's a very important thing and that we shouldn't be shutting it out."
He supports "free speech" despite being one of the organizers of the walkout on VP Pence's speech.
I'm not a fan of CNN, but to her credit, Baldwin asked this pair of freedom lovers "but how can you be welcoming if you are not respecting---despite the fact that you totally disagree with his views..."
George Washington once said, "Guard against the impostures of pretend patriotism."
Abraham Lincoln defined our culture in his time as a "House Divided"---drawing from Scripture to illustrate the importance of his point. The point being, a divided house will not remain divided, because one view will ultimately prevail over the other.
Those whom we remember this Memorial Day weekend---many of whom who gave their lives for a cause greater then themselves, most likely at some point in their fight to sustain freedom felt "unwelcome, uncomfortable and even unsafe."
Washington State's own Congressman Doc Hastings said a few years back, "137 years later, Memorial Day remains one of America's most cherished patriot observances. The spirit of this day has not changed--it remains a day to honor those who died defending our freedom and democracy."
My favorite poet, Henry Wadsworth Longfellow wrote these words as he looked out over the rolling green acres of grave markers: "You silent tents of green, We deck with fragrant flowers; Yours has the suffering been, The memory shall be ours."
Years later, in 1984, Lee Greenwood recorded the hit "God Bless The USA," repeating the sentiments of Longfellow: "And I'm proud to be an American, where at least I know I'm free. And I won't forget the men who died, who gave that right to me..."
Have a wonderful Memorial Day weekend---And keep the memories alive.
Be Free. Be Blessed.


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Major Maltese airline Air Malta has revamped its in-flight menu, adding brand new vegan options.
The new menu, which will be introduced on July 12 and change seasonally, will feature over 70 new food and beverage options, including a vegan wrap. "By listening to passenger feedback across various channels, it became evident that our guests prefer a choice of good quality snacks," Paul Sies, Air Malta's Chief Commerical Officer, said in a statement. "In line with how the airline business has developed, our guests want better quality and a wider selection."
The new vegan wrap, according to the Air Malta team, is expected to be the menu's most popular item based on feedback already received. It will include locally sourced ingredients, such as hummus and fresh spinach, as well as falafel, which according to Lovin Malta is the nation's current favorite food. "Falafel is having a moment in Malta right now," said the publication. "[It's] found in menus across the island, and now it's made it onto the national airline. This wrap is vegan, but more importantly, the falafel balls themselves are handmade daily on premises right next to the airport, to ensure maximum freshness."
The wait is over. This is the official launch of our brand new Sky Bar, redefining the in-flight experience for all guests in Economy Class. The new buy-on-board catering service will be introduced on flights as from Thursday 12 July 2018, with a selection of over 70 quality food and drink items available for purchase on board selected flights (excluding the shortest routes where a bar service is not offered). The menu can be viewed via @facebook (link in bio) and will change seasonally based on guest feedback. We invite you to see the launch video on our @youtube channel and look forward to everyone's input to keep improving your KM experience. On your next Air Malta flight … Treat yourself! #airmalta #morethanjustanairline #news #catering #inflight #buyonboard #skybar #menu #foodies #quality #choice #freshness #commitment #economyclass #service #fly
The wrap can be purchased on its own or as part of a meal deal, along with a snack and a drink for €10.
Air Malta is not the first airline to add more vegan options to its in-flight menu. In early July, Air New Zealand announced the addition of the vegan meat-like Impossible Burger to its Business Premier menu. For the next three months, guests traveling from Los Angeles to Auckland will be able to enjoy the plant-based 'bleeding' burger in the air. "We're confident vegetarians, flexitarians and dedicated meat lovers alike will enjoy the delicious taste of the Impossible Burger," said the airline's customer experience manager, Niki Chave.
Australia's Jetstar airlines also recently debuted a new vegan in-flight menu, featuring a lentil and tabbouleh salad with falafel and garden vegetable noodles. The airline received an award for its new onboard plant-based options from animal rights organization, PETA. "Cruelty-free culture has taken off in Australia and we applaud Jetstar for listening to its vegan customers," said PETA Australia.


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My 13 Favorite Christmas Carols
Songs or albums that get me feeling festive. I've been feeling a bit rushed and tense these last couple weeks, and I find I need to do some remembering of what makes Christmas fabulous.
1. Do you hear what I hear? -Third Day (Best Arrangement I've ever heard of this song, normally it ranks right up there with Little Drummer Boy in terms of suckiness, but not this one)
2. Little Drummer Boy/Peace on Earth -Bing Crosby and David Bowie (this doesn't stink either, and the little bits where they talk to each other just proves how Awesome Bing really was!)
3. Silent Night (When our church does this on Christmas Eve by candlelight, it is Awesome. This year, we're hoping that Eric can pull together a small bell choir ensemble to accompany, the bells arrived early, it would take a miracle, but hey, that's what God does best!)
4. O Holy Night (solo is the only way for this one, unless I'm accompanying in the car ;))
5. Dance of the Sugar Plum Fairy, ah heck, the whole Nutcracker Suite by Tchaikovsky (There's just something great about the Nutcracker at Christmas Time)
6. John Denver and Muppets Christmas Album (Flipping Awesome Album! I could never pick just one song!)
7. Feliz Navidad -Jose Feliciano (You can't be sad or stressed about Christmast time listening to this one)
8. White Christmas -Bing Crosby (Something is just right about the world when Bing sings it.)
9. White Christmas -Drifters (A completely different feel when they do it, not just for Home Alone, but just because it's fun!)
10. O Come O Come Emmanuel (This hymn was one of the most effective lullabies for Chris in the NICU, and remained his lullabye, still is. We sang to him a lot in the NICU, home of his 1st Christmas, and on Christmas, another mother came up and thanked us for singing, providing a little Christmas joy, her thanks made me cry.)
11. Carol of the Bells (When it's well done, not like fake bells, but with bells and voices, and all that, oh yeah!)
12. What child is this?
13. Disney's Merry Christmas Carols-sung by Mickey and the gang, and joined by Molly Ringwald and Larry Groce. (We used to listen to this record every year, even when my parents were [AH!] Married. Ma still has it, but we're never there to hear it. I wish I had it on CD, it's just not the same not listenting to it all the time during the holidays, but we have no record player.)
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