Such environmental degradation, coupled with the growth in world population, is major causes behind the rapid
increase in human diseases.
Not exact matches
But we have dramatically reduced poverty, shown ways to build institutions that respect
human rights and liberties, virtually eliminated famines, found ways to prevent and remedy
diseases, dramatically
increased the longevity of people everywhere, and come to include more and more persons
in the «circle of exchange.»
Disease and early mortality, which were understandably judged to be evil, nonetheless kept
in check the natural
increase in human population.
For amid all the advantages of contemporary life, where fewer people suffer
disease, hunger, or lack of opportunity than
in years past, there still is probably no
increase in the sum total of
human happiness and very slight advantage, if any,
in the main business of making sense of one's life.»
These include the infant with galactosemia, 53,54 the infant whose mother uses illegal drugs, 55 the infant whose mother has untreated active tuberculosis, and the infant
in the United States whose mother has been infected with the human immunodeficiency virus.56, 57 In countries with populations at increased risk for other infectious diseases and nutritional deficiencies resulting in infant death, the mortality risks associated with not breastfeeding may outweigh the possible risks of acquiring human immunodeficiency virus infection.58 Although most prescribed and over-the-counter medications are safe for the breastfed infant, there are a few medications that mothers may need to take that may make it necessary to interrupt breastfeeding temporaril
in the United States whose mother has been infected with the
human immunodeficiency virus.56, 57
In countries with populations at increased risk for other infectious diseases and nutritional deficiencies resulting in infant death, the mortality risks associated with not breastfeeding may outweigh the possible risks of acquiring human immunodeficiency virus infection.58 Although most prescribed and over-the-counter medications are safe for the breastfed infant, there are a few medications that mothers may need to take that may make it necessary to interrupt breastfeeding temporaril
In countries with populations at
increased risk for other infectious
diseases and nutritional deficiencies resulting
in infant death, the mortality risks associated with not breastfeeding may outweigh the possible risks of acquiring human immunodeficiency virus infection.58 Although most prescribed and over-the-counter medications are safe for the breastfed infant, there are a few medications that mothers may need to take that may make it necessary to interrupt breastfeeding temporaril
in infant death, the mortality risks associated with not breastfeeding may outweigh the possible risks of acquiring
human immunodeficiency virus infection.58 Although most prescribed and over-the-counter medications are safe for the breastfed infant, there are a few medications that mothers may need to take that may make it necessary to interrupt breastfeeding temporarily.
Physiologic sleep studies have found that breastfed infants are more easily aroused from sleep than their formula - fed counterparts.247, 248
In addition, breastfeeding results in a decreased incidence of diarrhea, upper and lower respiratory infections, and other infectious diseases249 that are associated with an increased vulnerability to SIDS and provides overall immune system benefits from maternal antibodies and micronutrients in human milk.250, 251 Exclusive breastfeeding for 6 months has been found to be more protective against infectious diseases compared with exclusive breastfeeding to 4 months of age and partial breastfeeding thereafter.2
In addition, breastfeeding results
in a decreased incidence of diarrhea, upper and lower respiratory infections, and other infectious diseases249 that are associated with an increased vulnerability to SIDS and provides overall immune system benefits from maternal antibodies and micronutrients in human milk.250, 251 Exclusive breastfeeding for 6 months has been found to be more protective against infectious diseases compared with exclusive breastfeeding to 4 months of age and partial breastfeeding thereafter.2
in a decreased incidence of diarrhea, upper and lower respiratory infections, and other infectious
diseases249 that are associated with an
increased vulnerability to SIDS and provides overall immune system benefits from maternal antibodies and micronutrients
in human milk.250, 251 Exclusive breastfeeding for 6 months has been found to be more protective against infectious diseases compared with exclusive breastfeeding to 4 months of age and partial breastfeeding thereafter.2
in human milk.250, 251 Exclusive breastfeeding for 6 months has been found to be more protective against infectious
diseases compared with exclusive breastfeeding to 4 months of age and partial breastfeeding thereafter.249
«Now, using genomic methods that were not available 10 years ago, it appears that components made by the virus interact with
human DNA
in the places where the genetic risk of
disease is
increased,» Harley says.
«But
in this case, when this virus infects cells, the virus makes its own transcription factors, and those sit on the
human genome at lupus risk variants (and at the variants for other
diseases) and that's what we suspect is
increasing risk for the
disease.»
«Much like the spread of
human disease in populated areas, urban centers can foster
increases in multiple
disease types
in wild animals,» said McGraw, senior author of the study.
IN A rare instance of
humans beating one of the impacts of climate change, measures to combat malaria appear to be neutralising the expected global
increase of the
disease driven by rising temperatures.
With global
increase in obesity and diet - related metabolic
diseases, interest has intensified
in ancestral or «Palaeolithic» diets, not least because — to a first order of approximation —
human physiology should be optimized for the nutritional profiles we have experienced during our evolution.
Buttke is interested
in using public interest
in personal health as a way to
increase support for public green space, and enhancing public understanding of how
human actions can drive infectious
disease spread through a variety of avenues including school programs, websites, and smart phone apps.
To maintain its foothold
in large - scale, world - class research, Japan has launched its own Brain Mapping by Integrated Neurotechnologies for
Disease Studies (Brain / MINDS) project,
in line with the
increasing interest
in brain - mapping projects around the world, such as the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative project
in the United States and the
Human Brain Project (HBP)
in Europe.
«The next step
in understanding sleep apnea
in the future will be to dissect different subtypes of sleep apnea, likely defined by distinct pathophysiological mechanisms which may underlie different outcomes and predisposition to comorbidities,» Cavadas says, «As
human life expectancy
increases, delaying the onset of age - related
diseases becomes critical to our society.»
«If lowering of LDL cholesterol affects atherosclerosis
in humans in the same way, our observations mean that clinically advanced plaques could be prevented if cholesterol - lowering treatments are administered early enough
in individuals with
increased risk of cardiovascular
disease.
The findings indicate that not only might Oprl1 become dysregulated
in humans following the development of PTSD, but inherited variants of the
disease could
increase the likelihood of someone developing the disorder to begin with.
When mice with the
disease were given
increased amounts of the protein PGC -1-alpha, which is naturally present
in both mice and
humans, the neural decay was dramatically reduced.
He analyzed data on 6,000 American women collected by the Centers for
Disease Control and Prevention and found that concentrations of mercury
in the
human population had
increased over time.
So far there have been no reports of Parkinson's
disease in human survivors of the H5N1 flu, Smeyne says, but because only a few years have passed since the first cases were reported, it's too early to know whether those infected are at
increased risk.
And
in tracking
human disease patterns, she's established a clear link between such low - dose chronic exposure and
increases in high blood pressure and heart
disease.
Since 1996, major changes
in infectious
diseases have occurred, such as the introduction of
human immunodeficiency virus (HIV) / AIDS and West Nile virus into the United States, advances
in HIV / AIDS treatment, changes
in vaccine perceptions, and
increased concern over drug - resistant pathogens.
As the
human population
in West Africa has grown, people have
increasing contact with wildlife, which has aided the spread of zoonotic
diseases.
Acute sleep loss
in humans is associated with
increased appetite and insulin insensitivity, while chronically sleep - deprived individuals are more likely to develop obesity, metabolic syndrome, type 2 diabetes, and cardiovascular
disease.
Humans are considered uniquely susceptible to Alzheimer's
disease, potentially due to genetic differences, changes
in brain structure and function during evolution, and an
increased lifespan.
In recent years, interest in this fifth DNA base has increased by showing that alterations in the methyl - cytosine contribute to the development of many human diseases, including cance
In recent years, interest
in this fifth DNA base has increased by showing that alterations in the methyl - cytosine contribute to the development of many human diseases, including cance
in this fifth DNA base has
increased by showing that alterations
in the methyl - cytosine contribute to the development of many human diseases, including cance
in the methyl - cytosine contribute to the development of many
human diseases, including cancer.
Animals with gene mutations that significantly alter their circadian rhythms have shorter life spans, and circadian rhythm sleep disorders
in humans can have profoundly negative effects, including
increased risk for obesity, depression, cardiovascular
disease and cancer.
The new NIST
human genome RMs
increase the ability of DNA sequencing laboratories to be more confident
in their reporting of true positives, false positives, true negatives and false negatives, and therefore, significantly improve genetic tests used for
disease risk prediction, diagnosis, and progression tracking.
«The dramatic
increase in these
diseases has occurred amidst constant
human genetics, suggesting a pivotal role for an environmental factor,» said Chassaing, assistant professor
in the Institute for Biomedical Sciences.
Research has shown that giving TMAO to rodents promotes atherosclerosis and that
humans with higher concentrations of TMAO
in the bloodstream are at
increased risk of developing heart
disease.
«Recent
increases in chronic
diseases like childhood asthma and autism can not be due to major shifts
in the
human gene pool,» says physician and geneticist Francis Collins, former director of the National Human Genome Research Insti
human gene pool,» says physician and geneticist Francis Collins, former director of the National
Human Genome Research Insti
Human Genome Research Institute.
«We want to see how much variability there is
in this phenomenon
in the healthy
human population, to evaluate if there is a correlation between retrotransposition frequency and brain tumor formation, and to see whether it is
increased or reduced
in Alzheimer's
disease.»
The selective loss of large herbivores, for instance, is known to cause relatively systematic
increases in abundance of rodents [71], which are thought to be particularly effective at hosting and transmitting
human - borne zoonoses, thus driving landscape - level
increases in rodent - borne
disease [72].
Climate change effects on the geographical distribution and incidence of vector - borne
diseases in other countries where these
diseases are already found can also affect North Americans, especially as a result of
increasing trade with, and travel to, tropical and subtropical areas.63, 197 Whether climate change
in the U.S. will
increase the chances of domestically acquiring
diseases such as dengue fever is uncertain, due to vector - control efforts and lifestyle factors, such as time spent indoors, that reduce
human - insect contact.
As researchers team up with computer scientists to develop powerful algorithms and machine learning tools, they are
increasing their capacity to identify patterns
in huge datasets of biological information and reveal unknown connections to
human disease.
Although of course there are a number of caveats since mice can be cured from cancer at higher rates, they don't suffer from some of our
diseases, they are sensitive to being handled (if grabbing them can shorten their lifespan through stress, the mouse version of standard
human medical care may do the same), so I guess that
increases in maximum lifespan are indeed the only reliable indicator that an intervention is impacting age - related mortality.
In other words, do
human impacts on biodiversity
increase the prevalence of
diseases by eroding natural «checks and balances» on transmission or decrease prevalence when they remove the free - living biodiversity on which
disease agents depend?
Bethesda, Md. (January 24, 2018)-- A review of more than 80 studies reveals that changes
in the immune cells of people with
human immunodeficiency virus (HIV) infection may
increase their risk of cardiovascular
disease (CVD).
Health improvement (allowing to post - pone / escape the
diseases and thus live, healthier /
disease - free longer, but not above
human MLSP of around 122 years; thus these therapies do not affect epigenetic aging whatsoever, they are degenerative aging problems not regular healthy aging problem (except OncoSENS - only when you Already Have Cancer - which cancer
increases epigenetic aging, but cancer removal thus does not change anything / makes no difference about what happens
in the other cells / about what happens
in the normal epigenetic «aging» course
in Normal non-cancerous healthy cells) Although there is not such thing as «healthy aging» all aging
in «unhealthy» (as seen from elders who are «healthy enough» who show much damage), it's just «tolerable / liveable» enough (
in terms of damage accumulating) that it does not affect their quality of life (enough yet), that is «healthy aging»: ApoptoSENS - Clearing Senescent Cells (this will have great impact to reduce
diseases, the largest one, since it's all inflammation fueled by the inflammation secretory phenotype (SASP) of these senescent cells) AmyloSENS - Dissolving the Plaques (this will allow
humans to evade Alzheimer's, Parkinsons and general brain degenerescence, allowing quite a boost; making people much more easily reach the big 100 - since the brain is causal to how long we live; keeping brain amyloid - free and keeping our memories / neuron sharp / means longer LongTerm Potentiation - means longer brain function means longer heavy brain mass (gray matter / white matter retention seen
in «sharp - witted» Centenarians who show are younger brain for their age), and both are correlated to MLSP).
Our
increased understanding
in areas such as stem - cell biology,
human immune systems, and identification of
disease - specific biomarkers all have contributed significantly to that progress.
10/29/2008 Eating Red Meat Sets Up Target for
Disease - Causing Bacteria Non-human molecules absorbed by eating red meat
increase risk of food poisoning
in humans Offering another reason why eating red meat could be bad for you, an international research team, including University of California, San Diego School of Medic... More...
In the article describing the work in Molecular Therapy, co-authors Charis Himeda, Takako Jones and Peter Jones highlight the important implications for similar types of genetic diseases: «With increasing evidence that the repeat genome (comprising nearly half the human genome) plays important roles in gene regulation, additional diseases will likely be found associated with aberrant repetitive genomic sequences,» they writ
In the article describing the work
in Molecular Therapy, co-authors Charis Himeda, Takako Jones and Peter Jones highlight the important implications for similar types of genetic diseases: «With increasing evidence that the repeat genome (comprising nearly half the human genome) plays important roles in gene regulation, additional diseases will likely be found associated with aberrant repetitive genomic sequences,» they writ
in Molecular Therapy, co-authors Charis Himeda, Takako Jones and Peter Jones highlight the important implications for similar types of genetic
diseases: «With
increasing evidence that the repeat genome (comprising nearly half the
human genome) plays important roles
in gene regulation, additional diseases will likely be found associated with aberrant repetitive genomic sequences,» they writ
in gene regulation, additional
diseases will likely be found associated with aberrant repetitive genomic sequences,» they write.
In light of the widespread role of oxidative stress in the pathology of diverse human diseases and the ability of the Nrf2 - dependent antioxidant response gene network to protect against oxidative stress, considerable effort has been directed towards discovering compounds that can increase the activity of Nrf
In light of the widespread role of oxidative stress
in the pathology of diverse human diseases and the ability of the Nrf2 - dependent antioxidant response gene network to protect against oxidative stress, considerable effort has been directed towards discovering compounds that can increase the activity of Nrf
in the pathology of diverse
human diseases and the ability of the Nrf2 - dependent antioxidant response gene network to protect against oxidative stress, considerable effort has been directed towards discovering compounds that can
increase the activity of Nrf2.
Potential projects include identifying common pathways that modify retinal degenerative
disease from a large collection of actively maintained mouse models; determining molecular networks implicated
in pathological disruption of the retinal pigment epithelium; identifying molecular pathways that regulate postnatal ocular growth; and using mouse models to assess the pathogenic role of gene variants that
increase the risk of age - related macular degeneration as identified by
human genome - wide association studies.
One of the goals of this research is to
increase our understanding of
human mitochondrial
diseases caused by translation defects
in this organelle.
Infected patients are at - risk for long - term joint stiffness and pain, which
increases the need to better understand the sequence diversity of these viruses and how any viral mutations affect the severity of
disease in the
human host.
Major problems
in high TB
disease burden countries are
human and environmental factors that contribute to a weakened immune system and can
increase susceptibility to Mtb infection, recurrence of latent infection and high morbidity and mortality.
Analyzes whole genome and detailed clinical data from nearly 300,000 Icelanders Finds several novel variations
in the sequence of the
human genome modulating cholesterol levels Five variants are also causally linked to
increased risk of coronary artery
disease Shows...
Only
in the last 10 years, with
increasing knowledge of the senescent phenotype and the ability to detect senescent cells
in human tissues, have biologists been able to investigate the relationship between cellular senescence and
disease.
Translational medicine is the integrated application of innovative pharmacology tools, biomarkers, clinical methods, clinical technologies and study designs to improve
disease understanding, confidence
in human drug targets and
increase confidence
in drug candidates, understand the therapeutic index
in humans, enhance cost - effective decision making
in exploratory development and
increase phase II success.
Three recent experimental studies focused on low consumption / exposure.949596
In one study, 29 smokers each consumed a single cigarette, immediately after which they had a significant decrease in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.
In one study, 29 smokers each consumed a single cigarette, immediately after which they had a significant decrease
in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.
in blood vessel output power and significant
increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.
in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94
In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.
In another study,
human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role
in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.
in the development of heart
disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.96