1) Should ethical treatment surrounding larger invertebrates be applied as a rule to smaller and less studied invertebrates or should

1) Should ethical treatment surrounding larger invertebrates be applied as a rule to smaller and less studied invertebrates or should they be assumed and treated as more basal?Q2) Should invertebrates that have the capacity for cognition, sentience, emotion, but not the experience of pain to be considered for animal ethics?Q3) Should ethical considerations for invertebrates be applied to pesticide research? Ex. Fast killing neurotoxin research vs the commonly used slow killing pesticidesQ4 ) Which criteria should matter for ethical consideration of invertebrates? -cognition? -sentience? -emotion? -self-awareness? -higher learning capabilities? -the experience of pain?

Please summarize and paraphrase this excerpt: Given the role of Sp1 in a multitude of cellular pathways and processes, it
Please summarize and paraphrase this excerpt: Given the role of Sp1 in a multitude of cellular pathways and processes, it is unsurprising that it is associated with the pathogenesis of a number of diseases, with perhaps the best studied being cancer. Sp1 overexpression is seen in a host of cancer cell types, where levels of Sp1 also correlate with tumor stage and a poor prognosis [12]. Knockdown of Sp1 in cancer cell lines (including breast, kidney, pancreatic, lung, and colon cancers) led to decreased survival and the inhibition of cell growth and migration. Similarly, tumor formation and metastasis was reduced in mouse xenograft models with Sp1 knockdown. Furthermore, the changes in gene expression following knockdown correlated with the observed phenotypic changes of the cells [106]. Indeed, several anticancer agents in clinical use act by inhibiting Sp1 action [107]. Mithramycin A (and its analogues) can alter the binding of Sp1 to DNA and downregulate Sp1-mediated transcription [108,109]. Tolfenomic acid increases the ubiquitination and degradation of Sp1 [110], while anthracyclines, one of the most effective anticancer treatments, bind DNA at GC-rich sequences, preventing Sp1 binding [111,112], though this may not be its sole mechanism of action. Other drugs can act on Sp1 indirectly, such as curcumin, which increases reactive oxygen species in the cell, causing activation of ZBTB4/10 proteins that displace Sp1 from GC-rich sites and decreased Sp1 expression [113].The role of Sp1 in cancer stems from its regulation of genes that are involved in all of the hallmarks of cancer: growth factor-independent proliferation, immortality, evasion of apoptosis, angiogenesis, tissue invasion and metastasis [72,114]. Sp1 is involved in the regulation of genes required for the progression of the cell cycle and entry into S-phase, such as cyclins and MYC, as well as in growth factor signaling pathways e.g. IGF1R has up to eight Sp sites at its promoter and IGF signaling is commonly used by cancer cells to maintain proliferation [115,116]. However, it also regulates the transcription of cell cycle inhibitor genes, for example, synergizing with p53 under conditions of cell stress to activate transcription of p21 [65]. Sp1 regulates the expression of telomerase subunits involved in the maintenance of telomeres and cell immortality. It can bind to five Sp sites present at the hTERT promoter to activate gene expression [117], or conversely, interact with HDACs to repress hTERT expression [57]. Sp1 is involved in the control of both pro- and anti-apoptotic factors, which have a direct role in cancer development. Survivin is a protein that promotes cell survival by inhibiting apoptosis and is essential in many tumors: its overexpression is directly associated with an increase in levels of Sp1 [118]. The pro-angiogenic factor VEGF has Sp1 binding sites at its promoter: estrogen signaling in breast cancer can result in interaction of Sp1 with ERα and subsequent upregulation of the VEGF gene [119]. Sp1 is also involved in maintaining genome stability via regulation of DNA damage factors and inflammatory signaling to drive oncogenesis [72].While the deregulation of signaling pathways and transcription factor networks has been well studied, the impact of aberrantly expressed miRNAs in cancer is a newly developing field. Specific miRNAs have been found to be downregulated in certain cancers, such as miRNA223 in gastric cancer [120]. In this example, Sp1 protein levels were also found to increase, but with no change in mRNA levels, suggesting post-transcriptional regulation. miRNA223 was found to bind to the 3′ untranslated region of Sp1 mRNA and inhibit its translation. The increase in Sp1 led to enhanced epithelial-mesenchymal transition (EMT), involved in promoting cell migration and invasion in tumorigenesis, whereas overexpression of miRNA-223 in a gastric cancer model caused decreased EMT and proliferation, and induced apoptosis [120]. A similar action was discovered for miRNA-324-5p in Hepatocellular carcinoma (HCC) [121] and miRNA-23b in multiple myeloma [122]. Additionally, Sp1 has been found to regulate the expression of miRNAs. miRNA-195 promotes cell apoptosis and suppresses cancer cell proliferation/metastasis; its expression is frequently reduced in various cancers. Characterization of its promoter region found an Sp1 site required for miRNA-195 expression, but in HCC cells, Sp1 interacted with HDAC3 at the promoter to repress transcription [123]. The miRNA-23a-27a-24-2 cluster is deregulated in many cancers. The promoter, containing 2 Sp1 sites, was found to be demethylated in Hep2 cells, compared to control HEK293 cells, leading to upregulation of the cluster and promotion of proliferation and cell survival of cancer cells [124]. Furthermore, Sp1 was found to be involved in a regulatory network with another transcription factor (NFκB), an epigenetic regulator (HDAC) and a miRNA (miRNA-29b) to modulate KIT expression in a subset of acute myeloid leukemia (AML) [125]. miRNA-29b acts to post-transcriptionally inhibit Sp1. Conversely, Sp1, along with NFκB, binds to the miRNA-29b enhancer and interacts with HDAC1/3 to form a repressive complex and inhibit miRNA-29b expression. Aberrant activation of KIT in AML cells leads to upregulation of MYC, which in turn results in downregulation of miRNA-29b and an increase in Sp1 expression. Sp1, along with NFκB, activates KIT transcription, thus completing the regulatory loop and contributing to the disease state [125].Sp1 can be linked to the changes in DNA methylation often observed in cancer cells. Sp1 can be involved in the protection of regulatory regions of genes (especially housekeeping genes) from methylation [55,56] and when methylation spreads to Sp1 sites, binding is inhibited, contributing to gene silencing [126]. Sp1 mediates transcription of the tumor suppressor RASSF1A, whose promoter has four Sp sites. In cancer, a change in histone modifications (H3 deacetylation and K9 trimethylation) causes a reduction in Sp1 binding, followed by methylation of the promoter and gene silencing [127]. This suggests that the increase in Sp1 levels in cancer cells is not sufficient to overcome the silencing of its target genes through DNA methylation. However, Sp1 can also interact with DNMT1 to promote methylation at specific sites [53,54], suggesting a role for Sp1 in establishing the epigenetic state of both normal and cancer cells. More studies are needed to completely understand its mechanism in transcription activation and epigenetics. The ability of Sp1 to regulate oncogenes and tumor suppressors, pro-survival and pro-apoptotic genes, highlights the need to fully understand Sp1’s activity at different promoters and in different cell conditions to develop a therapy that can specifically target Sp1 in cancer.Sp1 has been implicated in Huntington’s disease, a dominantly inherited neurodegenerative disorder caused by expansion of a polyglutamine tract in the Huntingtin (Htt) protein. Htt was found to bind to Sp1 and TAFII130 and inhibit DNA binding, while overexpression of both factors in striatal cells from a mouse model of Huntington’s led to an improvement of symptoms and reversed inhibition of the dopamine D2 receptor gene, known to be a marker of the disease [128]. Further studies suggested the protective role of Sp1 overexpression involved activation of cystathione γ-lyase gene expression, the biosynthetic enzyme for cysteine, which is depleted in disease tissues [129]. However, this issue is still disputed, as other studies have found Sp1 contributes to the pathology in Huntington’s disease. Sp1 was found to be overexpressed in the brains of mouse models and in model cell lines: inhibition or knockout of Sp1 led to amelioration of toxicity caused by mutant Htt and the mice survived longer, possibly due to Sp1 negatively regulating the Dopamine D2 gene. This suggests Sp1 is a potential therapeutic target in Huntington’s disease [130].A positive role of Sp1 has been found in Alzheimer’s disease, where inhibition of Sp1 with mithramycin A in transgenic mouse models led to further memory impairment and an increase in the levels of Amyloidβ peptides (a major hallmark of the disease) [131]. A polymorphism in an Sp1 binding site of the COL1A1 gene, encoding collagenα1, a major protein in bone, is associated with a predisposition to osteoporosis by altering the ratio of collagen α1 to α2 chains, causing reduced biomechanic strength in the bones [132]. In contrast, there was a negative correlation between the same polymorphism and hip osteoarthritis, suggesting there is a reduced risk of the disease [133]. Furthermore, Sp1 has been implicated in the development of multiple sclerosis (MS). Polymorphisms in the IRF5 and CD24 genes, factors involved in MS, can lead to increased Sp1 binding at these genes and an increased risk of MS [134,135]. Gene expression analysis in MS patients suggested the involvement of Sp1 in gender-specific gene signatures and inhibition of Sp1 transcription reduced the incidence and severity of experimental autoimmune encephalomyelitis in mice (the model of MS), highlighting Sp1 as a potential therapeutic target in MS [136].

-Typically xylem and phloem are found next to each other in plants (hence the name, vascular bundles). By including
-Typically xylem and phloem are found next to each other in plants (hence the name, vascular bundles). By including vascular bundles in your answer, what are the 4 steps in translocation of photosynthates in phloem from source (example, a leaf) to sink (example, a tuber). -Mention one structural feature that is typically found in a mature xylem cell? What function of xylem cell is facilitated by this structural feature and how ? -As part of its maturation, xylem undergoes programmed cell death. However, prior to this cell death, the xylem cell undergoes secondary cell wall thickening. Why didn’t the xylem cell wait to undergo such a thickening at the end of cell death process?

For the Musculoskeletal System this week I have picked websites for you to research. Please pick a website and locate
For the Musculoskeletal System this week I have picked websites for you to research. Please pick a website and locate an article or item that interests you. Please place the topic of your post in the subject line and ask 10 questions regarding the material to your classmates. Please introduce your questions by writing a paragraph about the topic and what you learned from the article (not long, just about

16- Which of the following is true about evolution today? EvolutionGroup of answer choices :a) is only one theory about
Biology Assignment Writing Service16- Which of the following is true about evolution today? EvolutionGroup of answer choices :a) is only one theory about how life on Earth began. Another scientifically proven theory is: creationism.b) is only a theory, so there is no way to prove that any part of it has ever occurred.c) stopped occurring on Earth once humans arose.d) no longer occurs on Earth today.e) is highly supported by observing genetic relationships, fossil records, radiometric dating, and morphology.17- Microevolution, through natural or artificial selection (selected breeding by humans), can be observed on Earth today. This is exampled by:Group of answer choicesa) changes in insects from the use of pesticides in the farming industry.b) antibiotic overuse or misuse, which often creates super-strains of bacteria.c) various breeds of livestock and produce that have been selectively bred for best outcome – over many generations.d) All of these are examples.e) None of these are examples – there is no such thing as evolution!18- The change in allele frequencies in a relatively short time is called _____________; whereas the observed rise of completely new species over long periods of time is called _____________.Group of answer choicesa) Hardy-Weinberg Principle… genetic driftb) gene flow…genetic driftc) adaptation…natural selectiond) microevolution…macroevolution19- The smallest unit that can be considered a ‘unit of evolution’ (the smallest unit of life that can “evolve”) is a(n):Group of answer choicesa) individual organism.b) population.c) gamete.d) phylum.e) society.20- According to the Hardy-Weinberg principal:Group of answer choicesa) traits in a population will be found more frequently if the alleles are dominant.b) traits in a population will be found more frequently if the alleles are heterozygous.c) the allele frequency of any trait will remain stable unless acted on by specific forces.d) nothing in nature can change an allele frequency in a population, except human intervention.e) Who’s Hardy-Weinberg?21- The migration of alleles into a new population is an example of ________; whereas, a shift in the frequency of various alleles (traits) within a population is said to be _________.Group of answer choicesa) gene flow…genetic driftb) bottle neck…founder effectc) artificial selection…natural selectiond) microevolution…macroevolution22- Which of the following is NOT considered an agent of change factor – that can have a direct effect on allele frequencies in a gene pool?Group of answer choicesa) mutationb) sexual

43- Which, if anynoamniotic eggsa) reptilesb) birdsc) mammalsd) They ALL have amniotic eggs within their class. , of the following
43- Which, if anynoamniotic eggsa) reptilesb) birdsc) mammalsd) They ALL have amniotic eggs within their class. , of the following Chordate Classes have members within its Class that lay ?Group of answer choices44- Which of the following is true about animal evolution in general?Group of answer choicesa) Amphibians were the first to lay amniotic eggs – eggs enclosed in a shell containing a “artificial pond/sea”.b) Reptiles were the first animals to have legs and walk on land.c) Fish and Amphibians tend to have more porous skin, spawn (release large numbers of sperm and egg into the water) and have gills at some stage of their development.d) Bird were the direct link to mammal evolution, as their feathers evolved into hair.e) All mammals develop their fetuses in a placenta, they are the only group to no longer lay eggs at any level.45- Mammals that give live birth to embryonic/fetal babies (not fully developed at birth), and the babies develop/mature in a pouch, belong to which group? Group of answer choicesa) Monotremesb) Marsupialsc) Placentalsd) Echinoderms46- Mammals that nourish their young with milk, have fur, but lay eggs. belong to which group? Group of answer choicesa) Monotremesb) Marsupialsc) Placentalsd) Echinoderms47- Mammals that develop their embryo/fetuses in a ‘uterus’, with a supporting structure of blood vessels and tissue belong to which group?Group of answer choicesa) Monotremesb) Marsupialsc) Placentalsd) Echinoderms48- Which of the following is true about Homo sapiens? Homo sapiens are thought to have:Group of answer choicesa) been the first hominin species to travel out of Africa.b) died out as a species in Asia.c) directly evolved from the Neanderthals.d) first evolved in Africa, and migrated further north than the first hominin migration.e) None of these are true.49- Both fossil records and mitochondrial DNA indicate that the ancestors of modern humans probably originated in:Group of answer choicesa) Australia.b) the Arabian peninsula.c) eastern central Africa.d) northwestern Asia.

Waterweed grows near the surface of the water in lakes and ponds. It often grows in dense clumps. It has
Waterweed grows near the surface of the water in lakes and ponds. It often grows in dense clumps. It has been observed that the chloroplasts in this plant move around inside the cell. How might this be an advantage and a disadvantage to the plant? Keep in mind the function of the chloroplast

Access this page from the Learn Genetics Website: https://learn.genetics.utah.edu/content/basics/observable/ Choose one of the traits listed.Draw a pedigree of your family
Access this page from the Learn Genetics Website: https://learn.genetics.utah.edu/content/basics/observable/ Choose one of the traits listed.Draw a pedigree of your family for the trait.Upload your drawing as a picture file.Specific instructions for drawing the pedigree:Include three generations in your pedigree.Start drawing your pedigree by just drawing the relationships among people (don’t note the trait just yet). Include all four grandparents, all of their children, all of their children’s children.Males are squares, females are circles, and unknown is a triangle.Use the picture below to be sure you are connecting marriages and siblings correctly.Apply slashes to anyone who is decreased.Color in the circles or squares of people you know are affected with the trait.

1.If the cells in alignment 1 were sperm (from a male), and the cells from alignment 2 were eggs (from
1.If the cells in alignment 1 were sperm (from a male), and the cells from alignment 2 were eggs (from a female) when the sperm gets together with the egg to make a new individual this new individual would havea. 1 y gene and 2 s genes totalb. 1 y gene and 1 s gene totalc. 2 y genes and 2 s genes totald. 2 y genes and 1 s gene total2.According to the diagram below, if the cells in the top row in alignment 1 were sperm (from a male), and the cells from the top row in alignment 2 were eggs (from a female) when the sperm gets together with the egg to make a new individual this new individual would have a. ssyy phenotypeb. ssYy phenotypec. ssYy genotyped. SSYY genotype3.According to the diagram below, if the cells in the top row in alignment 1 were sperm (from a male), and the cells from the top row in alignment 2 were eggs (from a female) when the sperm gets together with the egg to make a new individual this new individual would have a. SY phenotypeb. sy phenotypec. sY phenotype

1) Ginger Williams has pain in her heel caused by a calcium deposit. This calcium deposit is known as a…….2)
1) Ginger Williams has pain in her heel caused by a calcium deposit. This calcium deposit is known as a…….2) Clue: abnormally increased muscle function or activity HYPER-HYPO-DYS-Item 1 KINES/ITONKINESItem 2 3)Torticollis is commonly also known as hiccups. a. True b. False4)A diagnostic test involving recording the electrical activity within muscle fibers in response to nerve stimulation is known as .5)Inflammation of the sheath surrounding a tendon is known as ……6) Plantar flexion bends the foot upward at the ankle. a. True b. False7) A/An ….. blocker is a drug that causes temporary paralysis by blocking the transmission of nerve stimuli to the muscles.8)Chronic fatigue syndrome results from repeated motions performed in the course of normal work and daily activities. a. True b. False9)Which term means the paralysis of all four extremitiesa. quadriplegia b. hemiplegia c. hemiparesis d. paraplegia10)Which term means a disease characterized by the simultaneous inflammation of voluntary muscles in many parts of the body?a. myasthenia gravis b. quadriplegia c. polymyositis d. myalgia11)Sarcopenia is a band of fibrous tissue that holds structures together abnormally. a. True b. False12)Muscular dystrophy is a group of genetic diseases characterized by progressive weakness and degeneration of the skeletal muscles. a. True b. False13)A chronic pain disorder that affects muscles and fascia throughout the body is called …….