text:
Q: javascript for loop to generate forms currently have working code that requires the following where we increment the number 2 all the way up to 250
const form2 = document.forms['submit-to-google-sheet2']
   form2.addEventListener('submit', e => {
    e.preventDefault()
    fetch(scriptURL, { method: 'POST', body: new FormData(form2)})
     .then(response => console.log('Success!', response), alert('Successfully Submitted!'))
     .catch(error => console.error('Error!', error.message))
   })

I would like to do this with a for loop or other non brute force technique but so far my attempts have failed
for (i = 0; i < 251; i++) {
    const form[i] = document.forms['submit-to-google-sheet',[i],']
    form[i].addEventListener('submit', e => {
    e.preventDefault()
    fetch(scriptURL, { method: 'POST', body: new FormData(form[i])})
    .then(response => console.log('Success!', response), alert('Successfully Submitted!'))
    .catch(error => console.error('Error!', error.message))
    })
   }

A: In your code, you're trying to set the nth member of the list in form, but you don't seem to initialize form as an empty list. One way to fix this problem is to just redefine form as you pass through the list of integers (this avoids storing the whole list of forms in main memory):
for (let i=2; i<251; i++) {
  let form = document.forms['submit-to-google-sheet' + i];
  form.addEventListener('submit', e => {
    e.preventDefault()
    fetch(scriptURL, {method: 'POST', body: new FormData(form)})
      .then(response => console.log('Success!', response))
      .catch(error => console.error('Error!', error.message))
  })
}

Note also that if you want to start counting at 2, and want to continue counting until 251, you can use the loop above to achieve this effect. I hope that helps!

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No topic is more controversial in religious circles than the evolution of man. Evolution is controversial enough by itself, but when we start saying that man himself evolved from lower animals … well, look out!
I hope that this quote by C.S. Lewis and some of my own explanation will help those of you with doctrinal difficulties with human evolution. Remember, I'm a Christian! I believe in the fall of man!
The evidence for the evolution of man is more than fossils and missing links. There is an amazing pattern to the fossils that have been found, and I hope to bring that out in this section.
From the human evolution timeline we can pull an amazing lineage. That this series is some sort of accident—by a stroke of luck as numerous errors fell together into a continuous series of dates, events, and locations—is rather hard to believe, don't you think?
Pierolapithecus catalaunicus – This 11.9 million-year-old fossil may represent what the public considers "the missing link," though that term is inaccurate. Scientists are hoping that this is the last common ancestor of apes and humans. As you can see below, the chain of human evolution has many links that are not missing, and they give clues to links, plural, that are missing.
Ardipithecus ramidus – (All new information as of 10/2/2009!) This forest dweller had the brain-size of a chimp (400 cc), small canines, and was bipedal! It changed some ideas about the evolution of man! It was found in Ethiopia, not far from Chad in central Africa.
Australopithecus anamensis – This creature also had an unknown cranial capacity. It lived about 4 mya, and it had thick enamel on its teeth, one of the marks of human lineage. It was found in Kenya, just south of Ethiopia.
Australopithecus afarensis – Many fossils of this link—no longer missing—in the evolution of man have been found. It lived from 3.9 to 2.9 mya. Its cranial capacity was up to 500 cc. It's teeth are more human-like than the previous creatures, and its jaw is beginning to have the human parabolic shape. Its fossils, as well as footprints—fully establishing its bipedality—have been found in Ethiopia, Cameroon, and Tanzania.
Australopithecus africanus – Similar to afarensis in brain size, its jaw has a fully human shape. It was found in South Africa and dates from 2 to 3 mya. This line almost certainly died out.
Homo habilis – Homo habilis lived from 2.4 to 1.5 mya and had a primitive-looking, flat face with a sloping brow and no chin, like the australopithecines, but its teeth are smaller and more human-like. Its brain was shaped like a human brain and averaged 650 cc in size. It, like robustus and boisei has been found in Kenya and Tanzania.
Homo floresiensis – Dubbed "hobbits" because of their dimunitive size, these fossils were found on the island of Flores in Indonesia. Studies of brain size make it seem these are descendants of habilis, georgicus, or an unknown species, and they possibly emigrated from Africa. That would be stunning with their chimpanzee-sized brains. They've probably been in Indonesia for at least 1 million years and only went extinct 17,000 years ago.
Homo erectus – This is the species that first left Africa. It lived from 1.8 mya to 300,000 years ago. In early fossils, its brain size averages 900 cc. A million years later, the skulls have an average cranial capacity of 1100 cc. It had a small forehead and still no chin, but it probably walked better than we do. We have larger pelvises to accomodate the birth of large-brained babies.
Homo ergaster and heidelbergensis – These are likely just the African and European races of Homo erectus. They vary like human races vary, only in height and robustness, though later fossils of heidelbergensis are difficult to distinguish from early Homo sapiens.
Denisovans – Denisovans are known only from DNA extracted from a finger bone and a molar found in Denisova cave in Siberia. Thus, all there are no morphological data on the Denisovans. Humans carry DNA from denisova, thus indicating that they will not be classified as a separate species, but simply a population of archaic humans. Their DNA is primarily found in Melanesians, indicating a possible ancestral mix in southeast Asia. Their role in the evolution of man is much debated. Work is still being done in the Denisova cave, and progress in news of this find has been rapid.
Homo neandethalensis – Neanderthals (now usually Neandertals) have been found only in Europe and the Middle East. They are a side branch in the evolution of man and died out about 30,000 years ago. They were shorter than Homo sapiens with bigger brains (1450 cc) and much stronger bodies. Scientists say their adaptations are typical for cold weather. Recent DNA studies have established that Neanderthals intermingled with humans. Many humans carry Neandertal DNA, especially outside of Africa.
Homo sapiens – This is us. Our average cranial capacity is about 1300 cc, and we have much more upright foreheads and pronounced chins than Homo erectus (except some of the later European versions).
I hope you can see how hard it is to ignore this series of evolution of man fossils, most of them very well attested.
We begin 6 to 7 million years ago in central Africa with a creature much like a chimpanzee, except that its canines are smaller. From there we find progressive adaptations in teeth moving closer and closer to humans, while cranial capacity increases smoothly. The knees, tibia, feet, and toes become more and more adapted to walking and less and less adapted to climbing.
The recent release of the results of the study of Ardipithecus ramidus fossils has shed much light on the evolution of man. Habitual bipedality is now driven back to 4.4 million years ago, and knuckle walking was not a halfway measure between walking on four legs and walking on two. Instead, it evolved separately on the ape line.
The ape line, by the way, is a separate line of primates, not ape to human evolution.
Then, somewhere around 1.5 million years ago some Homo erecti left Africa. They spread throughout Europe and Asia, growing larger in brain capacity, and their faces becoming more and more human until about 195,000 years ago the first fully anatomical humans appear.
Finally around 35,000 or 40,000 years ago, these humans began to show behavior typical of modern humans, making art, burying their dead, and performing ceremonies.
Even over the last 20,000 years, we still find that human teeth size and bone structure is still becoming progressively smaller.
It's hard to ignore this progression or to pretend like it is not evolution of man from some primate that was the ancestor of both apes and man.
For Christians that struggle with the idea of the evolution of man, I have two comments to help. One, even evolutionary history suggests that there was a time that God breathed a living soul into primitive man.
For the second comment I turn to C.S. Lewis, famed author of The Chronicles of Narnia and Mere Christianity and one of the most respected Christian thinkers of the 20th century.
For long centuries, God perfected the animal form which was to become the vehicle of humanity and the image of Himself. He gave it hands whose thumbs could be applied to each of the fingers, and jaws and teeth and throat capable of articulation, and a brain sufficiently complex to execute all of the material motions whereby rational thought is incarnated.
The creature may have existed in this stage for ages before it became man: it may have even been clever enough to make things which a clever archaeologist would accept as proof of its humanity. But it was only an animal because all its physical and psychical processes where directed to purely material and natural ends.


NOTE: Philaster, or Love Lies a-Bleeding was produced about 1609 and first printed in an imperfect quarto in 1620. It is now a public domain work and may be performed without royalties.
Scorched them even to the roots and dried them there.
Your children, mighty king; and I have done.


text:
Psychology & Neuroscience (School of)
Psychology & Neuroscience Theses
Development of a neurophysiological sensory gating model in the rat to aid in the preclinical identification of possible treatments of sensory flooding in schizophrenia
AndrewBloomfieldMPhilThesis.pdf (803.0Kb)
Bloomfield, Andrew
Bowman, Eric MacDonald
Objective: It has been widely hypothesized that a failure to properly filter, or 'gate', incoming auditory information occurs in schizophrenic patients. This can be observed in a reduced event-related potential response to the second of a pair of clicks, and this is referred to as P50 suppression after the name of the component that is attenuated to the second click. Our aim was to develop a model of gating failure in rats by measuring event-related potentials at different intervals between the clicks to validate that apparent gating in rats looks like P50 suppression in humans. We also sought to determine the relationship between two of the most commonly used assays of auditory gating: the mismatch negativity (an event-related potential evoked when a series of standard tones is followed by a deviant or oddball tone) and neurophysiological suppression in the double-click paradigm. Methods: Male outbred Lister Hooded rats (N=8) were tested using electrophysiology to record P50-like event-related potentials (ERPs) to assess the overall competence of the rats' sensory gating. The rat N40 potential, thought to be equivalent to the human P50 potential, was measured after each of two 85-dBZ paired (conditioning and test) 0.1msec duration clicks separated by inter-stimulus intervals of 250msec, 500msec, 1000msec, and 2000msec presented at 10second inter-trial intervals. If the N40 potentials are similar to the human P50, then the magnitude of the potential of the second click should be attenuated (a measure of gating of the repetitive stimulus). Additionally, we were interested in whether the suppression of the rat N40 to the second click was similar to the suppression of the human P50 in being vulnerable to disruption by amphetamine. We measured N40 suppression in four conditions: pre-drug, after saline injection, after 6 dextroamphetamine injection, and post-drug. Finally, we correlated the N40suppression with another neurophysiological measure of gating, the mismatch negativity. Results: We determined that as the inter-stimulus interval increased in duration, the degree of N40 suppression decreased linearly. The administration of d-amphetamine had a non-significant effect, although our results indicate that further testing with a slightly larger sample size would be relevant. Finally, the relationship between the MMN and N40 suppression was weak, which is similar to the relationship between the human P50 suppression and mismatch negativity. Conclusions: These data are a relevant initial step towards a neurophysiological sensory gating model to aid in preclinical identification of possible treatments of sensory flooding in schizophrenia. The characteristics of the rat N40 suppression match those of the human P50 suppression with the apparent exception of vulnerability to disruption by amphetamine.
Thesis, MPhil Master of Philosophy

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Copyright © 2013 Julio Beltrame Daleprane and Dulcinéia Saes Abdalla. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Propolis has attracted attention in recent years due to its beneficial effects, which make it a potential preventive and therapeutic agent as well as a useful additive in food and cosmetics. The aim of this review is to discuss the growing evidence that propolis may, via a diverse array of biological actions, assist in the prevention of some inflammation-mediated pathologies including cardiovascular disease. The active components of propolis that have been identified so far include polyphenols and flavonoids. These compounds have cardioprotective, vasoprotective, antioxidant, antiatherosclerotic, anti-inflammatory and antiangiogenic actions. Many studies have been undertaken to elucidate the mechanism(s) by which propolis acts, which involve cellular signaling targets and interactions at the genomic level. This review will highlight the effects of propolis that may assist in the prevention of chronic degenerative diseases, such as cardiovascular disease.
The growing market for natural products and alternative medicines has renewed interest in bee products, such as honey, royal jelly, pollen, and propolis [1, 2]. Propolis is the generic name for a complex resinous mixture collected by honey bees from the buds and exudates of various plants. Once collected, this material is enriched with saliva and enzyme-containing secretions and used in the construction, adaptation, and protection of hives [3, 4].
In recent years, many studies of the chemistry of propolis have been published, which reveal that its highly variable composition is influenced by the local flora at the collection site [5–7]. Although many biological activities of propolis are consistently observed, the components responsible vary between geographic and climatic zones .
There is considerable evidence on various chemical and biological aspects of propolis, but the therapeutic application and utilization by the pharmaceutical industry are still limited. This is mainly due to the variability of its chemical composition with geographical origin because bees utilize different plants in different ecosystems. Identification of the major compounds in propolis samples is essential; reports of the biological properties of propolis should include a detailed investigation of its composition and botanical sources [7, 8].
The constituents of propolis include polyphenols (flavonoids, phenolic acids, and esters), terpenoids, steroids, and amino acids . There has been extensive research into the composition and biological activities of propolis from various countries [10–13]. Propolis samples from Europe, South America, and Asia have different compositions and therefore different biological activities [12, 14, 15]. However, propolis samples generally show great similarity in their overall composition, regardless of botanical source . Brazilian red propolis has been found in two reports to contain high concentrations of phenolic compounds, 232 mg/g  and 257.98 mg/g, respectively . Brazilian propolis also contained higher concentrations of total phenols than samples from other countries: China, mg/g  and mg/g ; Korea, mg/g ; Argentina, 187 mg/g ; India, mg/g ; Portugal, mg/g ; Cyprus, mg/g ; and Thailand, mg/g .
Studies indicate that propolis from Europe and China contains many flavonoids and phenolic acids; tropical propolis generally contains low concentrations of flavonoids [21, 24, 25].
Studies of propolis demonstrate the complexity of its composition and pharmacology; some compounds act independently, while others act synergistically. The therapeutic potential of propolis and its constituents has been the subject of many studies, which have established many pharmacological actions in preclinical testing.
In particular, propolis shows therapeutic potential and may have applications in the pharmaceutical and food processing industries [25–27]. Propolis reportedly has a range of biological activities, including immunomodulatory [28, 29], antibacterial , fungicidal [31, 32], anti-inflammatory, healing , analgesic/anesthetic [34, 35], and anticarcinogenic effects .
The relationship between oxidative stress, cardiovascular disease, and angiogenesis is well established. Events related to the pathophysiology of angiogenesis and associated cytokines and growth factors can lead to a poor prognosis in many diseases. In fact, chronic cardiovascular disease, oxidative stress, and angiogenesis are strongly associated with one another. In this review, we will present evidence that propolis extracts and their bioactive compounds have antioxidant, cardioprotective, and antiangiogenic activities (Figure 1).
Figure 1: Schematic representation of the relationship between oxidative stress, cardiovascular disease, and angiogenesis, and the effects of propolis on these integrated systems. Propolis influences multiples biochemical signaling pathways, including protective mechanisms reducing events related to chronic inflammatory diseases.
It is well established that cellular metabolism generates reactive oxygen species (ROS), such as hydrogen peroxide (H2O2), the superoxide anion ( ), and the highly reactive hydroxyl ion ( ), as well as reactive nitrogen species (RNS), especially nitric oxide (NO). ROS and RNS are ideal signaling molecules because they are locally generated, are highly and rapidly diffusible, and can be neutralized by cellular antioxidants [37, 38]. ROS are usually detoxified by intracellular enzymes, such as glutathione, superoxide dismutase, and catalase . However, unbalanced production and degradation of ROS and RNS can result in accumulation of these reactive species, commonly referred to as oxidative stress. Exposure of macromolecules (lipid, proteins, DNA, etc.) to reactive species results in oxidative modifications with deleterious effects [40, 41].
The antioxidant capacity of propolis may be related to some of its biological effects, including chemoprevention. The flavonoids in propolis are powerful antioxidants, capable of scavenging free radicals and thereby protecting the cell membrane against lipid peroxidation . Moreover, ROS and RNS, together with other factors, are involved in cellular ageing and death in conditions, such as cardiovascular disease, arthritis, cancer, diabetes, Parkinson's disease, and Alzheimer's disease [43–47]. Propolis can reduce cellular levels of H2O2 and NO, which may be involved in its anti-inflammatory effects .
Diverse compounds from propolis have been described as potent inhibitors of oxidative stress. It is well known that the composition of propolis is variable; however, one of its major components, caffeic acid phenethyl ester (CAPE), blocks ROS production in several systems . CAPE has also been identified as one of the major cancer chemopreventive and anti-inflammatory compounds in propolis. In vitro, propolis inhibits peroxidation of LDL and nitration of proteins. Moreover, in bovine aortic endothelial cells, propolis was reported to increase eNOS expression and inhibit NADPH oxidase (NOX) . In vivo, propolis can increase antioxidant capacity in animals  and humans , leading to decreased lipid peroxidation, which is strongly associated with the risk of cardiovascular disease [53, 54]. Turkish propolis inhibited hydrogen peroxide (H2O2-) induced damage to DNA in cultured fibroblasts . The antioxidant activity of phenolic components of the Turkish propolis may reduce damage to DNA induced by H2O2, which may be related to its chemopreventive activity. Red propolis from Cuba has shown protective effects in models of alcohol-induced liver damage, most likely due to its antioxidant properties . Propolis inhibited macrophage apoptosis via effects on glutathione (GSH) and the tumor necrosis factors/nuclear factor kappa B (TNF/NF-κB) pathway [57, 58]. Moreover, Brazilian propolis from Baccharis dracunculifolia modulated 1,2-dimethlyhydrazine (DMH-) induced DNA damage in colon cells .
Isla et al.  described the protective effect of the Argentinian propolis from different sources against copper-mediated oxidative modification of lipids in unfractionated serum. Five types of Argentinian propolis, collected in different regions, inhibited lipid oxidation during the initiation and propagation phases. All five types of propolis diminished the maximal rate and extent of diene production, indicating that flavonoids can scavenge free radicals, such as superoxide [61, 62], protecting serum lipids from oxidation . Jasprica et al.  showed that daily intake of powdered propolis for 15 days decreased the plasma malondialdehyde concentration in men. The extract (0.65 g), available in Croatian community pharmacies, contained 2.5% total flavonoids, equivalent to 16.25 mg of galangin. After 30 days of treatment, an increase in superoxide dismutase activity and changes in red blood cell parameters were detected, including cell count, hemoglobin and mean corpuscular volume, and cell distribution.
The antioxidant effect of Brazilian red propolis has been attributed to chalcones and isoflavonoids (including 7-O-methylvestitol, medicarpin, and 3,4,2′,3′-tetrahydrochalcone) that act as electron donors . Furthermore, total flavonoid content in Brazilian red propolis is correlated with antioxidant activity, suggesting that all the phenolic and flavonoid compounds present contribute to this activity . Chinese red propolis had a higher antioxidant activity than propolis from other sources, which was attributed predominantly to CAPE . Chilean propolis also has antioxidant properties, which are correlated with its chemical composition . Additionally, the antioxidant and free-radical-scavenging properties of propolis may be due to its phenylpropanoid content . Thus, the available data indicate that propolis of different origins and distinct compositions consistently exhibit antioxidant actions. In addition to this antioxidant effect, bioactive compounds in propolis influence a large number of biochemical signaling pathways, and therefore physiological and pathological processes. Antioxidant capacity is one of the most important properties of propolis. Although there are several studies corroborating the potential antioxidant activity of propolis, there is no robust data on the safe dose in humans. Thus, there is need for clinical studies using propolis and its biologically active compounds, including studies of safety and bioavailability.
The modulation of cardiovascular disease markers by propolis has been shown in several studies. In vitro and in vivo assays have been developed to elucidate the molecular mechanisms of this beneficial effect: regulation of glucose and lipoprotein metabolism; modulation of gene expression; decrease of the activity of scavenger receptors, inflammatory cytokines, and oxidative stress; improvement of endothelial function; and inhibition of platelet aggregation.
Atherosclerosis is a complex process involving the accumulation and modification of plasma lipoproteins in the arterial wall as well as the recruitment and proliferation of immune cells. This process advances through a series of stages beginning with the appearance of a fatty streak lesion, composed largely of foam cells, which are lipid-engulfed macrophages. The fatty streak evolves into a complex atherosclerotic plaque consisting of a lipid core covered by a fibrous cap, with some areas that are rich in inflammatory cells [68–70]. Several authors have postulated that dietary polyphenols reduce the risk of cardiovascular disorders and prevent the development of atheromatous plaques [71–73]. Thus, as a rich source of polyphenols, propolis represents a potential alternative strategy for the prevention of cardiovascular disorders.
Propolis has been shown to modulate lipid and lipoprotein metabolism. Propolis administration diminished liver cholesterol and triglyceride content and decreased the rate of hepatic triglyceride synthesis in rats [74, 75]. In LDL receptor knockout mice (LDLr−/−), treatment with Brazilian red propolis (250 mg/kg/day) decreased levels of triacylglycerol (TAG), total cholesterol (TC), and non-high-density lipoprotein cholesterol (non-HDL-C) . LDLr−/− mice treated with Brazilian green propolis, which is rich in Artepillin C, pinocembrin, kaempferol, or with Chilean brown propolis, which is rich in pinocembrin, CAPE, quercetin, and galangin, also presented low levels of non-HDL-C. Moreover, mice treated with Brazilian red propolis showed significantly reduced TAG and TC, and increased HDL-C, compared to untreated mice. Furthermore, Turkish propolis, which is rich in flavonoids (mainly galangin, quercetin, kaempferol, apigenin, pinobanksin, pinocembrin, and pinostrobin) prevented alcohol-induced acute liver damage and lipid accumulation and induced beneficial changes in the serum lipid profile. HDL levels were high, and LDL levels were low, in mice treated with propolis and alcohol compared to alcohol only . Moreover, propolis also positively affected HDL and LDL levels in rats. Treatment of diabetic rats with propolis of poplar origin diminished levels of total cholesterol, LDL-cholesterol, VLDL-cholesterol, and triglycerides, reinforcing the case that propolis modulates lipid metabolism and may be helpful in syndromes caused by blood lipid abnormalities .
In a recent study, the authors hypothesized that propolis may aid in the prevention rather than treatment of atherosclerosis. LDLr−/− mice were treated with distinct polyphenol-rich propolis extracts (250 mg polyphenols/mL/Kg) . Brazilian green, Brazilian red, and Chilean brown propolis reduced the area of atherosclerotic lesions when administered preventively. The strongest inhibitory effect was observed for Brazilian red propolis, which also induced regression of atherosclerotic lesions . Polyphenols from propolis inhibited the progression of atherosclerosis in LDLr−/− mice by improving the lipid profile and by downregulating proinflammatory cytokines, chemokines, and angiogenic factors. Propolis downregulated the mRNA expression of key genes involved in the atherosclerotic process, such as MCP-1, INFg, IL6, CD36, and TGFβ .
It is well known that the modification of the lipid profile is strongly associated with cardiovascular disease [76, 77]. Propolis diminished total cholesterol and elevated HDL-cholesterol in mice. One proposed mechanism of the hypocholesterolemic action of propolis involves the ABCA1 receptor. Many types of propolis upregulate ABCA1 gene expression, which is associated with increased HDL levels; thus, ABCA1 up-regulation may be one mechanism by which propolis improves the lipid profile .
An ethanolic extract of Brazilian red propolis (EERP) enhanced ABCA1 promoter activity in THP-1 macrophages . Additionally, cholesterol efflux from macrophages to ApoA-I was significantly increased in a dose-dependent manner by EERP treatment. Thus, EERP significantly enhanced ApoA-I-mediated cholesterol efflux in THP-1 macrophages, which was accompanied by a marked up-regulation of the ABCA1 gene. The effect of EERP on ABCA1-dependent cholesterol efflux may be due to the activation of PPARγ and LXRα . In HepG2 and Raw 264.7 cell lines, EEP promoted cholesterol efflux and increased the expression of ABCA1 and ABCG1. Accordingly, C57BL/6 mice treated with 50 mg/kg EEP once a day for 4 weeks by oral gavage showed increased plasma HDL-cholesterol but unchanged LDL-cholesterol . Thus, in vitro and in vivo data suggest that the beneficial effects of propolis on lipid profile may be one of the mechanisms involved in its atheroprotective effects. This finding suggests that polyphenols from propolis may be useful for the prevention of atherosclerosis.
Platelet aggregation is a major contributor to the atherosclerotic process. Propolis components have shown important effects on platelet aggregation. CAPE (15 and 25 μM) markedly inhibited collagen-stimulated platelet aggregation. As CAPE is involved in various inhibitory pathways influencing platelet aggregation, it may be an important contributor to the potent antiplatelet actions of propolis .
NO is an important vasoactive mediator, with vasodilatory and antiaggregative actions that protect blood vessels when released from endothelial cells at low concentrations. However, when NO is produced in high concentrations by inflammatory cells, it may react with other nitrogen and oxygen species, inducing oxidative and/or nitrosative stress. Following the treatment of diabetic mice with poplar propolis, the levels of NO and nitric oxide synthase (NOS) decreased compared to nondiabetic mice . Propolis decreases NO level by decreasing NOS activity, thus protecting blood vessel endothelial cells and reducing neuronal toxicity. Additionally, propolis exerts pharmacological effects by decreasing the actions of NO and PGE2 as well as by reducing the activation of protein kinase in diabetes [75, 80]. Moreover, ethanolic extracts of propolis (EEP) inhibit NO production by decreasing iNOS expression in Raw 264.7 macrophages and by directly inhibiting the catalytic activity of iNOS. The inhibitory effect of EEP on LPS plus IFN-g-induced NO production is mediated either by inhibition of iNOS gene transcription via an action on NF-κB sites in the iNOS promoter or by direct inhibition of the catalytic activity of iNOS . As excess NO production has been implicated in the cardiovascular inflammatory process, the anti-inflammatory activities of EEP may also be mediated by modulation of NO levels.
It is well established that proliferation of vascular smooth muscle cells (VSMCs) is involved in the onset of atherosclerosis. Roos et al.  evaluated the antiproliferative activity of CAFE, one of the major components of propolis and honey-derived products, in primary rat aortic VSMCs stimulated by platelet-derived growth factor (PDGF). CAFE inhibited proliferation of VSMCs upon exposure to PDGF in a dose-dependent manner, by interfering with cell cycle progression from the G0/1- to the S-phase. This study indicates that the inhibition of smooth muscle cell proliferation may also be involved in the atheroprotective action of propolis.
Angiogenesis is the multistep process by which blood vessels are formed. This tightly regulated process involves the migration, proliferation, and differentiation of endothelial cells . Regulation of angiogenesis is absent or aberrant in several diseases characterized by persistent, inappropriate blood vessel development. Inappropriate angiogenesis occurs in more than 80 diseases, particularly in many types of cancer and inflammatory diseases as atherosclerosis [84, 85].
According to Keshavarz et al. , green propolis extracts containing artepillin C and CAPE significantly reduced the number of new vessels formed and the expression of metalloproteinases (MMPs) and production of vascular endothelial growth factor (VEGF) from endothelial cells . Different steps of angiogenesis can be affected by propolis and its components. Brazilian propolis and its major component, artepillin C, can inhibit proliferation of human umbilical vein endothelial cells (HUVEC), as well as endothelial cell migration and capillary tube formation, in a dose-dependent manner. Moreover, artepillin C can suppress angiogenesis in both in vivo and in vitro models, while CAPE inhibits MMP-2, MMP-9, and VEGF activity [87–90].
The effects of Brazilian propolis on HUVEC apoptosis were investigated by Xuan et al. . At a low concentration (12.5 μg/mL), the polyphenols in ethanol extracts of Brazilian propolis decreased the expression of integrin b4 and p53 and the production of ROS. The opposite effects were observed at high polyphenol concentrations (25 and 50 μg/mL), along with depression of mitochondrial membrane potential. Thus, high doses of polyphenols from Brazilian propolis may induce HUVEC apoptosis by acting on the integrin b4 and p53 signaling pathway, resulting in disturbance of mitochondrial membrane potential and increased ROS generation.
Daleprane et al.  investigated the actions of polyphenols from Brazilian red propolis on models of angiogenesis. Brazilian red propolis is rich in 1,2,3-trimethoxy-5-(2-propenyl)-benzene, methoxyeugenol, homopterocarpin, medicarpin, 2,4,6-trimethylphenol, 49,7-dimethoxy-29-isoflavonol, 7,49-dihydroxyisoflavone, and 2H-1-benzopyran-7-ol . Brazilian red propolis (10 mg/L) reduced the migration and sprouting of endothelial cells, attenuated the formation of new blood vessels, and decreased the differentiation of embryonic stem cells into CD31-positive cells. Moreover, Brazilian red propolis inhibited hypoxia- or dimethyloxalylglycine-induced mRNA and protein expression of the crucial angiogenesis promoter, vascular endothelial growth factor (VEGF), in a time-dependent manner .
Hypoxia is implicated in many inflammatory diseases. The proposal that hypoxia can induce inflammation has gained general acceptance from studies of the hypoxia signaling pathway . Brazilian red propolis decreases accumulation of hypoxia-inducible factor 1 alpha (HIF1α) under hypoxic conditions, which in turn attenuates VEGF gene expression . Reduced HIF1α protein half-life was associated with increased von Hippel-Lindau (pVHL-) dependent proteasomal degradation of HIF1α and reduced Cdc42 protein expression .
Brazilian green propolis extract, which is rich in artepillin C, was evaluated by Hattori et al. for its effects on cellular responses to hypoxia . Five compounds that modulated HIF-1 activity were identified. Hydroxycinnamic acid derivatives from Brazilian green propolis inhibited not only HIF-1 transcriptional activity but also hypoxia-induced expression of HIF-1α protein and downstream target genes, such as Glucose transporter 1, Hexokinase 2, and vascular endothelial growth factor A. Furthermore, the HIF-1 inhibitors also inhibited angiogenesis. Daleprane et al.  investigated the effect of polyphenols from Brazilian propolis on angiogenic gene expression in atherosclerotic lesions of LDLr−/− mice, finding that angiopoietin I, angiopoietin II, VEGF, fibroblast growth factor, metalloproteinases 2 and 9, platelet-derived growth factor, and platelet endothelial cell adhesion molecule were downregulated by polyphenols from Brazilian red and green propolis.
It has been reported that the propolis extracts show antiproliferative activity and that both extracts induced cell death by necrosis . The latter result indicates that certain compounds contained in propolis possess cytocidal activity based on necrosis rather than apoptosis. On the other hand, polyphenols, which are tumor necrosis factor-related, apoptosis inducing ligands, preferentially induce apoptosis in cancer cells and are not toxic to normal cells . These results are therefore not consistent with each other. The inconsistency of propolis activity may be due to the presence of numerous compounds in varying levels, depending on their geographical origin. Generally, biological activity has been assessed by independent groups, making a direct comparison of their work difficult. Propolis-based medicines are often prepared from ethanol extracts of honey hive, as the extracts are generally water insoluble. Further studies are required to establish the quantity and safety control criteria for propolis to allow it to be used safely, and to gain the maximum benefit from its biological activities.
In vitro and in vivo studies are uncovering antiangiogenic activity in many natural health products, including propolis extracts and their constituents. Further preclinical research is required to determine whether individual compounds or complex mixtures will be optimal for clinical trials. A potential advantage of phytochemicals and other compounds from propolis is that they may act through multiple cellular signaling pathways, acting in different pathophysiological conditions, while also inhibiting angiogenesis and reducing inflammation. Overall, propolis constituents may be helpful as auxiliary therapies for diseases in which angiogenesis must be controlled, such as cancer and cardiovascular disease.
Propolis contains a broad spectrum of compounds that have many biological activities. It is considered a useful product and is already used in alternative medicine. Recently, there has been a growing interest in its utilization by the food processing, cosmetic, and pharmaceutical industries. Considering this, further studies on the bioactive constituents of propolis are necessary to identify interactions mediating their biological effects. Further studies are also required on their bioavailability, stability in different preparations, and safe and effective doses for prevention or treatment of disease in animals and humans.


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Stuart Christopher John Broad,  (born 24 June 1986) is an English cricketer who plays Test cricket for the England cricket team and a former One Day and Twenty 20 International captain.

A right-arm seam bowler and left-handed batsman, Broad began his professional career at Leicestershire; in 2008 he transferred to Nottinghamshire, the county of his birth and the team for which his father played. In August 2006 he was voted the Cricket Writers' Club Young Cricketer of the Year. In the fourth Test of the 2015 Ashes series Broad took career-best figures of 8–15 in the Australian first innings as they were dismissed for just 60. This performance was named as Wisden's Men's Test spell of the decade.

Broad was awarded the Man of the Match in the fifth Test of the 2009 Ashes series at the Oval, after figures of 5/37 in the afternoon session of the second day. On 30 July 2011, at the Nottingham Test match against India, he achieved a Test match hat-trick in the process gaining his then best Test figures of 6–46.  As a batsman, he holds the second-highest ever Test score made by a number 9, having scored 169 against Pakistan in August 2010. At the start of the summer in 2012 Broad, returning from injury, produced figures of 7 for 72 in a match haul of 11 wickets against the West Indies. He is England's second highest wicket taker in Test cricket.

During the 2020 series against the West Indies, Broad became the seventh bowler to take 500 wickets in Test cricket, after dismissing Kraigg Brathwaite. Broad was the fourth fast bowler, and second bowler for England to reach the milestone after James Anderson, who achieved it against the same batsman. In December 2021, in the second match of the 2021–22 Ashes series, Broad played in his 150th Test match.

Early life
Broad was born 12 weeks prematurely and his life was saved by a doctor called John, after whom he was (middle) named when he survived. Broad originally started his cricketing career as an opening batsman, following in the footsteps of his father, the former England opener and current ICC match referee Chris Broad. It was not until he was 17 and had a growth spurt that he started to consider being a fast bowler. Broad had been associated with Leicestershire since he was 8 years old, having represented them at Under-9 level, and played for Melton Mowbray club Egerton Park, which also produced England seamer Tim Munton. Broad played for Egerton Park from the ages of 9 to 19; in his final two seasons he opened the batting with fellow Leicestershire player Matthew Boyce and spearheaded the attack. He was awarded the Leicestershire Young Cricketers Batsman Award in 1996.

At the age of 16, he considered himself better at field hockey and played as a goalkeeper, for Leicestershire and the Midlands, and had a trial with an England underage team. At the age of 17, he had a growth spurt and converted from a batsman to a seam bowler.

Education
Broad was educated at Brooke Priory School and Oakham School, a co-educational independent school in the market town of Oakham in Rutland, where he was in the same year as England Rugby back-row Tom Croft. Broad finished his school career with three B grades at A-level, and was given the choice of a place at Durham University or a contract with Leicestershire County Cricket Club.

Domestic career
Broad played his first game for Leicestershire 2nd XI in 2004 just before his 18th birthday and impressed enough to be given a full contract for the following season. Broad continued to impress Director of Cricket James Whitaker and made his first-class debut early in the 2005 season against Durham University Centre of Cricketing Excellence. He returned credible figures of 1/40 from 15 overs. His maiden first-class wicket was that of Nick Lamb. Broad followed this appearance with his first County Championship appearance against Somerset at the familiar location of Oakham.

In the 2006 season Broad took his first 5 wicket haul against championship favourites Surrey and scored his first championship 50 against Derbyshire. His most eye-catching performances were in the Twenty20 Cup, where his economy of 4.50 was the second-best of the season of bowlers with more than 15 overs bowled. In the County Championship Broad played twelve of Leicestershire's 13 matches until called up for England, and his 44 wickets at an average of 31.38 meant he led his county both in terms of wickets and bowling average. On 23 August 2007 it was announced that Broad would be leaving Leicestershire at the end of the season to join Nottinghamshire, after choosing not to renew his contract and to return to his home county.
In the 2013 season, Broad played in the final of the Yorkshire Bank 40 tournament. He was out for a duck and got three wickets in his last over wrapping up the game against Glamorgan.
Broad was a part of the Nottinghamshire side that beat Surrey in the final of the Royal London One Day Cup in 2017 played at Lords.

International career

Development
Broad played for the England Under-19 squad in 2005, facing the Sri Lankan Under-19 squad, and took five for seventeen in the first 'Test' at Shenley. He was named in the ECB National Academy squad for the winter of 2005–06 and was then called up to the England 'A' squad touring the West Indies, as a replacement for James Anderson, who had been drafted into the Test side touring India. In April 2006, Broad was again called up to the England A squad, facing the touring Sri Lankan team.

Broad was also included in the ECB's 25-man development squad for the 2006 season. David Graveney, the chairman of selectors, said, "The squad essentially enables the England Head Coach (Duncan Fletcher), working with his support staff and the National Academy staff, to monitor more closely the development of international players and better prepare them for the demands of the international game."

2006-07: Pakistan, West Indies, India, T20 World Cup and Sri Lanka

On 23 August 2006, Broad was included in the England one-day squad for the one-day internationals against Pakistan, and a couple of days later was named Young Cricketer of the Year by the Cricket Writers' Club. On 28 August, Broad made his first England appearance, in the Twenty20 International against Pakistan. Broad bowled four overs for 35 runs, and took two wickets in two balls, Shoaib Malik and Younis Khan, and narrowly missed out on a hat-trick, after a lofted shot from Shahid Afridi fell just short of Kevin Pietersen. On 30 August, he made his ODI debut, taking a wicket in his first over, as well as being involved in a last-wicket partnership of 29 with Darren Gough. In the third ODI on 5 September 2006, Broad once again found himself on a hat-trick with the wickets of Abdul Razzaq and Kamran Akmal, but again missed out on the third. He bowled ten overs and ended with figures of three for 57 with one maiden.

Broad was left out of the squad for the 2006 ICC Champions Trophy and the 2006-07 Commonwealth Bank Series. However, he was called up for the finals in the latter following injuries to Jon Lewis and Chris Tremlett. He was also called into England's squad as a replacement partway through the 2007 World Cup. He finished the tournament by scoring the winning runs in England's final match against the West Indies.

Broad also featured in the ODI squad at the end of the West Indies tour of England in summer 2007, taking three for twenty in the first match to take England to a 1–0 lead in the ODI series. In the second ODI he took 2–49 but England lost the match by 61 runs. Broad was expensive in the final match of the series, conceding 71 runs for no wickets.

He took his first wicket against India in the ODI against them in the second match at Bristol. On 30 August, he took career-best bowling figures of four for 51 as England bowled out India for 212 in the fourth match of the summer's ODI series. Broad also hit an unbeaten 45 to take his first ODI Man of the Match award. The definitive unbeaten partnership of 99 runs he shared with Ravi Bopara is a record eighth-wicket stand for England in ODIs. He bowled poorly in the next match, taking 1–84 as India won by 38 runs. He took 2–46 at the Oval but India narrowly won the match by 2 runs.

Broad took 1–29 in the opening match of the 2007 world T20 against Zimbabwe. He followed this up by taking 0–23 against Australia as England lost by eight wickets. He took 3–37 against South Africa but England suffered another defeat, this time by 19 runs. He took 1–35 against New Zealand but could not prevent another defeat for England.

On 19 September 2007, Indian batsman Yuvraj Singh hit six sixes from one Broad over in a group match at Kingsmead Cricket Ground in Durban, South Africa, during 2007's ICC World Twenty20. The 36 runs from the Broad over helped Yuvraj Singh make the quickest 50 in international cricket, off just 12 balls. Referring to this rare occurrence as "Yuvraj's magic moment", Phil Long of BBC's Test Match Special blogged: "Every so often you have to take off your England sunhat, sit back and enjoy a once-in-lifetime 'I was there' moment." This was the fourth time the feat had been performed in senior cricket and the first time in Twenty20 cricket. The performance was not repeated in any form of international cricket against a Test-playing nation until Kieron Pollard did the same against Sri Lanka in a T20 International in 2021.

Broad enjoyed a hugely successful ODI series in Sri Lanka in October 2007, taking eleven wickets in the series at an average of 19.27. He took figures of 2–54 in the first match and followed this up with 2–42 in the second match. In the third match of the series Broad made an unbeaten 20 with the bat and took another two wickets. In the final match of the series he took 3–36 and although England lost the match by over 100 runs, they won the series three-two to record its first ever ODI series win in Sri Lanka. This resulted in Broad making his Test debut against Sri Lanka; in a high scoring game, he took a single wicket, conceding 95 runs in the process as the match ended in a draw.

2008: New Zealand, South Africa and India
Broad went on to have an equally successful ODI series against New Zealand. Although England fell to a three-one defeat, Broad was the leading wicket taker and held the highest batting average, 52, in the England team. During the tour of New Zealand in 2008, Broad, along with Alastair Cook and James Anderson, posed naked for the Cosmopolitan paper with just a cricket bat for cover. England won the first Test against New Zealand by 121 runs, with Broad taking figures of 3–54 to help England win the game.

In the first Test against New Zealand on home soil, Broad took three wickets in the match. England won the second match by six wickets, although Broad picked up no wickets in the match. On 6 June 2008, Broad scored his maiden Test fifty, against New Zealand at Trent Bridge, making 64 before being bowled by Chris Martin. In the first ODI against New Zealand Broad took 2–14, before taking another two wickets in the final match of the series, conceding fifty runs in the process.

He made his second Test fifty in July 2008, in the Test series against South Africa, scoring a new best of 76. In the Second Test at Headingley, Broad contributed seventeen runs in the first innings, as England was bowled out on the first day for 203. In the second innings, with the match already lost, Broad top-scored with 67 in an innings that included some impressive drives through midwicket and cover, giving further evidence of his batsmanship. After this, his Test batting average briefly rose above 40. His performances with the bat at the time led pundits to suggest that he may become a genuine all rounder, with Geoffrey Boycott comparing him to Garfield Sobers: "He's a wonderful player. There's a little bit of Sobers in him". Broad was surprisingly dropped for the following Test at Edgbaston, making way for the returning Paul Collingwood. England captain Michael Vaughan said he was left out because of his bowling, but the decision has been criticised: Collingwood was no better a bowler than Broad, and Broad's batsmanship quite encouraging. Broad duly took seven wickets for Nottinghamshire against Durham while the Test was being played.

On 26 August 2008, he recorded the first five-wicket haul in his international career with best figures of five for 23 against South Africa at his home ground in the second ODI of the series, with England winning the series 4–0 with Broad taking 8 wickets within the series at an average of 18.4 and shooting up to 4th in the ICC ODI world rankings, the highest in his career and the best by any English bowler since Andrew Flintoff in 2003.

In the second ODI against India Broad performed well, taking figures of 4–55. He took 1–36 in the next match as England lost by 18 runs. In the final match of the series he took 1–54, but England lost again, this time by six wickets. In the second Test against India, Broad was ineffectual with the ball. He took 1–84 in an India's first innings before taking 1–50 in India's second innings as the match ended in a draw.

2009: West Indies, Ashes, ICC Champions Trophy and T20 World Cup
On 26 May 2009, Broad was named Man of the Series (one-day) against the West Indies in England. He took a total of six wickets, and England won the series two-nil after the first ODI was rained out. In the adjacent Test series, in which the home side fairly routed its opponents, Broad's wickets came at an average of just eighteen – "further evidence," reckoned journalist Nick Hoult, "of the top class international cricketer that lurks within. His bowling, particularly the variety he has added to his game, makes him a potential Ashes star [...]."

On 5 June 2009, Netherlands defeated England by four wickets in the first match of the ICC World Twenty20. The Netherlands needed seven to win from the final over with Broad bowling. He spurned two run-out opportunities from the first two balls, and dropped a catch off the third. The Dutch needed two runs from the final ball to win, and got them after Broad picked up the ball in his follow through and, attempting to win the match, overthrew, missing his third run-out opportunity of the over and allowing the batsmen to come back for the match-clinching second run. in the next match against Pakistan, he took 3–17 to help England win by 48 runs. England also beat India by 3 runs. Although Broad failed to take a wicket, he bowled his four overs for just 21 runs to help England secure a narrow victory. England lost their final game of the tournament against the West Indies, with Broad taking 1–20.

In July 2009, Broad was named in The Ashes squad to face Australia for the first Test at the SWALEC Stadium, Cardiff – his maiden Ashes Test. He scored a 22-ball 19 in England's first-innings total of 435, but in 32 overs he took just one wicket (that of Michael Clarke, caught behind for 83) as Australia amassed 674 for 6 declared, with four centurions. Nonetheless, his final-day 14 proved crucial, keeping the Australians at bay alongside Paul Collingwood for a minute over an hour before James Anderson and Monty Panesar blocked out the final 11 overs to salvage an unlikely draw.

The second Test at Lord's saw Broad take three wickets, including the important wicket of Australian skipper Ricky Ponting, bowled off an inside-edged cut for 38 as England pursued victory, and took a diving outfield catch to remove the opener Simon Katich in the first innings, as England took a 1–0 lead in the series.

Though he took no wickets in the first innings of the third Test at Edgbaston, Broad hit a 64-ball 55 to extend England's first-innings lead to 114. On the final day, Broad took two of the three wickets to fall: Mike Hussey for 64 and, late in the day, Marcus North for 96. Nonetheless, Australia drew the match with ease.

In the fourth Test at Headingley, Broad took his place in an England first-innings collapse, clipping Stuart Clark to square leg for 3 as Australia's seam attack bowled England out for 102. As Australia scored 445, Broad took six wickets for 91 in Australia's only innings, at that time his best first-class innings return, and in the second innings contributed a rapid 61 from 48 balls, though he could not avert an innings defeat.

England therefore started the fifth Test at the Oval with the series level at 1–1, with a victory required to secure the Ashes. He took 5 for 37 in the afternoon session of the second day, taking five of the first seven wickets to fall to take the Australian innings from 73/0 to 111/7 and eventually 160 all out. He also contributed 37 and 29 with the bat, and on the final day took the wicket of Shane Watson lbw for 40, the second wicket to fall in consecutive overs to start Australia's collapse, winning the Man of the Match award as England won by 197 runs to regain the Ashes 2–1.

He finished the tour with an aggregate of 234 runs and 18 wickets, leading England's bowling figures both in wickets taken and in bowling average (30.22). Though three Australian bowlers took more wickets, Broad was the only bowler from either side to claim two five-wicket innings hauls during the series.

This was a good tournament for Broad. He was the second highest wicket taker overall throughout the tournament with 10 wickets in 3 matches, only behind Wayne Parnell who took 11 in the same number of matches. In the first match of the tournament against Sri Lanka he took 3–49 in a winning effort. He followed it up with a 3–67 vs South Africa, putting England through to the semi finals. He then took 4–39 vs New Zealand in a losing effort after England had already been bowled out for 146, with New Zealand making the runs in just 27.1 overs. This was his last game in the tournament with Broad picking up an injury that kept him out of the semi finals, which England lost to Australia.

2009–10: South Africa, Bangladesh, T20 World Cup, Australia and Pakistan
Broad's injuries continued through to the tour of South Africa, keeping him out of the two twenty20 matches, which both ended up being abandoned. The weather affected the 1st One Day International which was probably an advantage for Broad and the England team with Broad being fit for the 3rd ODI, with England winning the second ODI by 7 wickets after Paul Collingwood and Jonathan Trott had a partnership of 162 with Collingwood getting 105.

When Broad returned he instantly made an impact with numerous wickets but turned out to be very expensive. With his first game getting figures of 4–71, England suffered defeat by 112 runs. Broad improved on his economy rate in the 4th ODI with figures of 2–30 from 9.5 overs. This backed up James Anderson who took 5–23. The final game was rained off before a ball was bowled to leave England with a 2–1 victory and only the second team to win a one-day series vs South Africa in South Africa.

Broad struggled in the First test in Centurion with only taking 1–74 in the first innings and 2–54 in the second. His batting was unsuccessful, getting only 17 and a duck. The duck was during a dramatic collapse where England went from 205–4 to 218–9 with Graham Onions batting out the final over to save the test.

In the second test Broad showed good form with the ball with 2–44 in the first innings but then taking 4–43 in the second dismissing Jacques Kallis, AB de Villiers and JP Duminy all within 3 overs. He took the wicket of Mark Boucher the next day to leave Graeme Swann to dismiss the rest of the South African line up. This gave England an innings and 98 run victory. After this test Broad went up to 7th in the ICC Test bowling rankings, the highest in his career. During this tour he declined to play in the IPL with James Anderson on the grounds he wanted to focus on his Test cricket first, and feared injury in the IPL.

After South Africa, England toured Bangladesh, playing three ODIs and two Test matches. Injuries to Anderson, Onions and Sidebottom meant that Broad was the leader of a relatively inexperienced pace attack. However, an injury before the Test series meant that he wasn't fully fit and was outbowled by Tim Bresnan and debutant Steven Finn.

England then travelled to the West Indies for the 2010 ICC World Twenty20. England won the tournament, beating Australia in the final. Broad won the man of the match award against Sri Lanka in the semi-final, and overall took 8 wickets at an average of 17.50.

Back in England, Broad was rested for the home series against Bangladesh before returning to the side for a 5-match ODI series against Australia. England won the first three games to take the series, with Broad named man of the match in the second game after bowling figures of 4–44. England lost the last two games, though Broad did achieve another four-wicket haul in the fifth game to finish the series with an average of 19.83. The ODIs against Bangladesh were less note-worthy – England won 2–1 with Broad taking 4 wickets.

In the home series against Pakistan, Broad was involved in a disciplinary incident in the second Test. After Pakistani batsman Zulqarnain Haider defended a ball bowled by Broad down the pitch, Broad picked the ball up and threw it at Haider, striking him on the hand. Broad was fined 50% of his match fee.

In the final Test of the series, Broad reached his maiden Test century at Lord's. Coming to the crease at 102–7, he scored 169 and put on a 332-run partnership with fellow centurion Jonathan Trott; a world record for an eighth-wicket partnership. It was his first century in all forms of cricket since an under-19's match for Leicestershire and saw his name go on the Lord's batting honours board, a feat that his father never achieved. He also surpassed his father's Test best of 162, and they became the first father and son both to score centuries for England in Test match cricket. His efforts both with the bat and with the ball (he also took three wickets during the match and made a direct-hit run out) earned him the man of the match award.

2010–11: Ashes series

Broad had an indifferent tour of Australia, which was cut short due to injury. He started with a half-century in a warm-up game, and overall took 6 wickets over the two games against Western Australia and South Australia. In the first Test at the Gabba, Brisbane, he fell for a golden duck in England's innings, the final victim of Peter Siddle's hat-trick. Wicketless in Australia's first innings, he had Simon Katich caught in the second as the Test was drawn. In the second Test at Adelaide, he finished Australia's first innings off with the wicket of Brad Haddin, but a stomach muscle injury limited his participation in the second where England won by an innings. That injury was revealed to be a muscle tear, and it ruled Broad out of the remaining three Tests and the one-day series that followed. He was not missed for the rest of the Test series but he was for the ODIs because England were plagued by injuries throughout the 6–1 series defeat.

2011–12: India, Pakistan and Sri Lanka
After a difficult series against Sri Lanka there was much pressure on the England selectors to drop him for the upcoming series against India.  However, Broad was named in the side for the first Test at Lord's and ended with match figures of 7–94, as well as scoring an unbeaten 74 in the second innings, as England won by 196 runs. His good form with both bat and ball continued in the second test. Top scoring with an aggressive 64 in the first innings, he helped England recover from 124–8 to 221 all out before achieving his career best figures of 6–46 in India's first innings. This included a hat-trick, taking the wickets of Mahendra Singh Dhoni, Harbhajan Singh and Praveen Kumar. Broad took five wickets from his final 16 balls of the innings, without conceding a single run. With a positive second innings contribution with both bat and ball (44 runs with the bat and then two wickets, including the final wicket of the match) Broad was named Man of the Match. In the Third Test at Edgbaston, Broad took four wickets along with Tim Bresnan to bowl India out cheaply. In England's innings he was not needed as Alistair Cook scored 294 to pass 700. Broad took two wickets in the second innings to beat India and for England to become World number 1 in Test Cricket. Broad made a lesser impact in the fourth Test, taking two wickets in each of India's innings, and did not bat, due to an early declaration.

In the first Test against Pakistan Broad took 3–84 in the first innings. However, England suffered a ten wicket defeat as the batsmen struggled to acclimatise to sub continent conditions. Broad took 4–47 in the next match as well as an unbeaten fifty in England's 1st innings (he'd only score 1 test fifty in 5 years after scoring this 50) but another batting collapse saw England lose the match again (bowled out for 72 chasing 145) to go 2–0 down in the three match series. In the final match Broad took 4–36 in the first innings to help bowl out Pakistan for 99. However, Pakistan made over 300 in their second innings to build up a lead. England were unable to chase down their target and went on to lose the series 3–0. England lost their fourth straight match, this time against Sri Lanka as the batsmen continued to struggle. Broad took just two wickets in the match, although he made 33 runs with the bat in the match, and was not out in the second innings.

2012: West Indies and South Africa
Broad started off his summer with his best international innings yet, of 7–72, against the West Indies, at Lord's, the first test match of the series, was started with a bang as he was able to get a five wicket haul at the home of cricket, Lord's, becoming only the 8th player to join an elite club of all-rounders to be on both honours boards, after his maiden test century of 169 against Pakistan in 2010.

He soon followed this up by taking 4 more wickets in the next innings, missing a possible hat trick however, to get Test best figures of 11 for 165, being the first to take a 10 wicket haul at Lord's since Ian Botham in 1978. He had to wait until after Lunch on the 4th day to take the last 3 wickets he needed for the haul. He was named Man of the Match the next day after England won by 5 wickets, in a chase of 191.

Broad followed the performance by taking four wickets in the second test. which England also won. He was rested for the last Test match against the West Indies along with James Anderson. However the game was heavily disrupted by rain and the game ended as a draw. England won the following One Day series 2–0 with the third game being abandoned because of rain. On Broad's 26th birthday, he captained the team to a comfortable victory with Notts teammate Alex Hales scoring 99. He was then named in the squad to play Australia in a five match ODI series. Broad's bowling was overshadowed by Finn who took 11 wickets in four games compared to Broad's 5.

Broad was picked in the first Test against South Africa but failed to take a wicket. He added 16 with the bat in England's first innings of 386. Broad and the England bowlers struggled in South Africa's innings of 637–2 with Hashim Amla scoring a triple century (the first South African to do so) with Jacques Kallis and Graeme Smith also scoring centuries. In the second innings Broad was out for a duck as England lost by an innings and 12 runs. In the second Test, South Africa scored 419 in the first innings with Broad taking 3–96. He then scored 1 run in England's innings of 425. Broad then had a burst of wickets on the last day with the wickets of AB de Villiers and JP Duminy in successive deliveries. He finished with figures of 5–69 as England couldn't reach the target and the game ended in a draw. In the following Test, Broad was pushed up the order to number 8 after Tim Bresnan was left out. Broad only managed one wicket in South Africa's first innings of 309. He then added 16 in England's first innings of 315. Broad, who had been down on pace all summer struggled as he took 2–76 as South Africa set England 346 to win. England lost by 51 runs, Broad adding 37 runs.

2013: New Zealand and Ashes series

On the fifth day of the 3rd Test against New Zealand, Broad set a new record for the longest time spent at the crease without scoring a run, with 103 minutes out in the middle, facing 62 balls. The previous record was 101 minutes set by New Zealander Geoff Allott against South Africa in 1999.

On 19 May, in the First Test against New Zealand at Lord's, Broad took career best figures of 7/44 in the second innings of the match. In England's second innings, he also contributed 26 runs to their total of 213.

In the first Test of the 2013 Ashes held at Trent Bridge, Broad stood his ground after being given not out when edging an Ashton Agar delivery which deflected off wicket-keeper Brad Haddin's gloves and was caught by Australia captain Michael Clarke at first slip; the Umpire Decision Review System was in use during the series, but Australia had used all of its challenges when the incident occurred. Although neither the rules nor common practice required Broad to walk, he drew heavy criticism from many observers who thought his edge was too thick to have reasonably stood his ground. Broad was on 37 at the time of the incident and went to make 65, sharing a partnership of 138 with Ian Bell. England went on to win the match by 14 runs with Broad taking the wickets of Shane Watson and Clarke in Australia's second innings. Australia coach Darren Lehmann was later fined 20% of his match fee for calling Broad a cheat on Australian radio, and in doing so inciting Australian crowds to boo Broad in future English tours of Australia.

On 2 August 2013, Broad took his 200th Test wicket, bowling Clarke in the first innings of the drawn third Ashes Test at Old Trafford.

In the fourth Test, at the Riverside Ground in Chester-le-Street, Broad took eleven wickets with two five-wicket hauls and was named man of the match as England ensured a series win. In the first innings, he took 5–71, including a spell of 3–12 in the morning session of day 2 where he removed David Warner, Usman Khawaja and Clarke to reduce Australia to 49–3. In their second innings, chasing 299 to win, Australia had made 174–3 when Broad took the wicket Clarke for the fifth time in the series, with the first delivery after a drinks break. In this spell he took 6–20 from 45 balls, including the final Australian wicket, to bowl Australia out for 224 and win the match by 74 runs. Broad ended the match with his best test bowling match figures of 11–121.

2013–14: Ashes series
Broad was England's leading wicket taker in the first Test of the 2013–14 Ashes series at the Gabba in Brisbane, taking 6–81 in the first innings and ending with match figures of 8–136, in the match that England lost in four days by 381 runs. In the second Test Broad took 3–98 in Australia's first innings, but as England struggled he only bowled six overs in the second innings as Australia romped to victory. Broad took 3–100 in the third Test but was then injured by a delivery from Mitchell Johnson, which dismissed him for just 5. The injury prevented him from bowling in the second innings, as England went on to lose the game and the series. Broad was declared fit for the fourth Test and took 3–45 in the Australian first innings, but struggled in the second, bowling 10 wicketless overs for 58 runs. In the final Test, Broad batted well, making an unbeaten 30 in the first innings and then 42 in the second. England went on to lose the game and the series 5–0, leading to the England team being heavily criticised. Despite this, Broad was one of the few members of the team to come out of the series with any credibility.

2014: West Indies, T20 World Cup, Sri Lanka and India
Broad continued as captain for the tour of the West Indies. This included three ODIs and three T20Is. In the ODI series England won 2–1, with Broad bringing England home in the 2nd game with a knock of 28 not out. In the third game he took 2–58 as England won by 25 runs. He only played in the first T20I, as England lost by 27 runs, taking figures of 0–26.

Broad was named captain of the England cricket team for the 2014 ICC World Twenty20 in Bangladesh. He did not take a wicket in the first two games, as England lost to New Zealand and beat Sri Lanka. In the third game, against South Africa, Broad took 1–33 but England lost the match to end their hopes of qualifying for the next stage. He took 3–24 against the Netherlands, but he was unable to prevent an embarrassing defeat for England.

In the first Test of the series against Sri Lanka, Broad took one wicket in the first innings and three in the second, as England came close to winning the match. In the second Test at Headingley, he became only the fourth player, and the first Englishman, to take two Test hat-tricks, although he needed to be informed of this by the PA system as he was unaware. England went on to lose the game after James Anderson was dismissed off the penultimate ball of the match, meaning England lost the series 1–0.

Broad bowled well on a good batting pitch in the first game of the series against India, taking four wickets in the match. However, in the second game he was accused of bowling badly in the first innings, as India won the match to go 1–0 up in the series. Broad's form improved in the next game, as he took 3–66 in the first innings to help England win the game and level the series. He took figures of 6–25 in India's first innings of the next game to help dismiss them for 152. Broad was badly injured while batting and it was later revealed he had broken his nose. Broad was later named man of the match. Despite being an injury doubt, he took part in the final Test, taking 3 wickets in the match and scoring 37 to help England secure a 3–1 series win.

2015: Tri-Series, World Cup, West Indies and New Zealand
Following an injury which had kept him out of the one-day tour of Sri Lanka, Broad returned for the Tri-Series against Australia and India. In the first match of the series he was wicket less as England lost to Australia. In the next match against India, Broad finished with figures of 0–33. His worst performance of the series came in the following match against Australia, where he finished with figures of 0–61. However, he played well in the must win game against India, taking figures of 2–56 to help England qualify for the final. In the final match against Australia he took figures of 3–55 and made 24 with the bat, but it was not enough to prevent an England defeat as they went on to finish the tournament as runners-up.

Broad took figures of 2–66 in England's opening game loss to Australia. In the following game against New Zealand, he was unimpressive as England suffered a humiliating eight wicket defeat. He failed to take a wicket against Scotland as England won their first match of the tournament, and also finished wicket less as England suffered a nine wicket defeat against Sri Lanka, meaning he had failed to take a wicket in his past three matches. He finished with 1–52 in England's must win game against Bangladesh, but was dismissed for 9 as England lost the game to bow out of the tournament at the group stage. He finished with figures of 1–18 against Afghanistan in a rain affected as England won their final match of the tournament by nine wickets.

The first match against the West Indies, Broad took 2–67 in their first innings to help restrict them to 295. However, in the second innings he could only manage to take one wicket as the West Indies held on for a draw. In the second Test ok 4–61 in West Indies first innings to help out England in a strong position. He took another wicket in the second innings as England forced a result to go 1–0 up in the series. In the first Test Broad took 1–31 in West Indies first innings to help England into a lead. However, England collapsed in their second innings and Broad himself was out for a duck. He took 1–29 in the West Indies second innings but it wasn't enough to prevent a five wicket defeat as the West Indies levelled the series at 1–1.

In the two match series against New Zealand, Broad took 3–77 in New Zealand's first innings. With New Zealand chasing a big score to win the match, Broad took 3–50 in New Zealand's second innings to help England win by 124 runs and go 1–0 up in the series. Broad took 5–109 in New Zealand's first innings of the next Test, although he went at an economy rate of over six an over. He made 46 with the bat to help England level the scores after the first innings. He took 2–94 in the second innings but was again expensive, and New Zealand went on to win the match and tie the series 1–1.

2015: Ashes series
In Australia's first innings of the first Test, Broad took figures of 2–60 and followed this up by taking 3–39 in their second innings as England won the match to take the lead in the series. Broad took 4–83 in Australia's first innings of the second Test but they built a large first innings score of 566. Broad did not take a wicket in the Australians second innings as they won by 405 runs. In the third Test Broad took 2–44 in Australia's first innings and also took a wicket in their second as England won the game to regain the lead. In the fourth Test Broad took career best figures of 8–15 in the Australian first innings as they were dismissed for just 60. England went on to win the match convincingly and regain the Ashes. In the final Test Broad did not take a wicket as Australia won by an innings and 48 runs, although England won the series 3–2.

2015–16: Pakistan and South Africa

Broad played in the first Test against Pakistan, which was played in the UAE. While Broad only took one wicket in the match, he bowled economically, including bowling eight overs for just eight runs in the second innings. England came to close to forcing a result, but the match ended in a draw. In the second Test Broad again only managed to take one wicket as Pakistan enjoyed a convincing win to go 1–0 up in the three-match series. In the third Test, Broad continued to bowl economically, taking figures of 2–13 from 13 overs in Pakistan's first innings, as they were dismissed for 234. In the second innings, he took 3–44 but England struggled in their second innings and Pakistan went on to win the game to win the series 2–0.

In the first test in South Africa, Broad took figures of 4–25 and 1–29 and hit an unbeaten 32 from just 33 balls as England won by 241 runs. The second game ended in a high scoring draw, with Broad taking 2–94 in South Africa's first innings. In the third Test, Broad took 2–82 in South Africa's first innings in a game which looked to be finely poised. However, in South Africa's second innings, he ripped through their top order, finishing with figures of 6–17. Included in his six wickets were the prized wickets of AB de Villiers and Hashim Amla. England went on to win the game by seven wickets, with the result giving them an unassailable 2–0 series lead. England performed poorly in the final game, with Broad taking three wickets in the match as South Africa secured a victory by a margin of 280 runs, meaning the series finished 2–1 to England. As a result of his performances, Broad became the number one ranked Test bowler in the world.

After not playing for England in limited overs cricket since their poor showing at the 2015 World Cup, Broad was included in the squad for the ODI series against South Africa. He played in the fourth ODI, although he returned expensive figures, finishing up with 1–55 in seven overs, as England lost the game. He was selected in the side for the final game, which proved to be the decider, and although he bowled economically, he did not pick up a wicket and England went on to lose the game and the series 3–2.

2016: Sri Lanka, Pakistan, Bangladesh and India
Broad took figures of 4–21 in Sri Lanka's first innings of the first Test as they were dismissed for just 91. In the second innings he took 1–57 as England won by an innings and 88 runs. In the second match, Broad took 4–40 in Sri Lanka's first innings, but was less effective in their second, finishing with just one wicket, as England won the match by nine wickets. In the final rain affected match of the series, Broad took 2–79 as Sri Lanka were dismissed for 288, but the match ended in a draw due to the bad weather.

Broad took figures of 3–71 in Pakistan's first innings of the first Test, and took 3–38 in their second innings, although Pakistan did enough to secure a 75 run victory. In the second Test Broad took 1–20 in Pakistan's first innings as they were dismissed for 198 and England secured a 330 run victory. In the third Test, Broad took 3–83 in Pakistan's first innings as they reached 400, and then took 2–24 in their second innings to help England secure an unlikely victory after dismissing them for 201. In the final match of the series, Broad was less effective, taking just one wicket in the match, as England lost by 10 wickets.

In the first innings of the first Test against Bangladesh, Broad did not take a wicket in the first innings, although he bowled economically. In the second innings he took figures of 2–31 to help England win by 21 runs. He was rested for the second Test, which England lost

Broad played in the first Test against India, taking figures of 1–78 in the first innings, before taking 0–8 in the second innings as the match ended in a draw. In the second Test he took 1–49 as India made 455 in their first innings. He took 4–33 in the second innings to restrict India to 204 runs, although India won the match by 246 runs. Broad missed the next two Tests through injury, but returned in the fifth Test. He took figures of 2–80 as India scored 759/7 and went on to win the match by an inning and 75 runs to win the series 4–0.

2018 and beyond
On 22 March 2018, In the first Test against New Zealand, Broad took his 400th wicket in Tests and became the youngest fast bowler to do so.

In the first Test of the 2019 Ashes series, Broad took his 100th wicket in The Ashes in the first innings of the match. In the second innings of the match, he took his 450th wicket in Test cricket, dismissing David Warner.

On 29 May 2020, Broad was named in a 55-man group of players to begin training ahead of international fixtures starting in England following the COVID-19 pandemic. On 17 June 2020, Broad was included in England's 30-man squad to start training behind closed doors for the Test series against the West Indies. On 4 July 2020, Broad was named in England's thirteen-man squad for the first Test match of the series. Broad was not selected for the first test, a match that England subsequently lost, and publicly vented his frustration. Broad took 6 wickets after being recalled for the second match of the series, an England win. On 28 July 2020, Broad took his 500th wicket in Test cricket, dismissing Kraigg Brathwaite (who was also James Anderson's 500th wicket) along with scoring 62 runs and taking 10 wickets in the match including the final wicket, to win the final Wisden Trophy 2–1. For his efforts Broad was named man of the match and man of the series.

Following his dismissal for 0 by Trent Boult in the second test against New Zealand in June 2021, Broad moved to second in the all-time list of test match ducks (37), second only to the West Indian fast bowler Courtney Walsh (43).

In the fifth Test of the 2022 India tour of England at Edgbaston, Broad conceded 35 runs in an over, the most in Test cricket history.

Achievements and honours

 On 17 September 2015, NET tram 237 was named in honour of Broad.
  He was appointed a Member of the Order of the British Empire (MBE) in the 2016 Birthday Honours for services to cricket.
 At the conclusion of the 5th Test in India's tour of the United Kingdom in 2018, Broad and Anderson had tallied 850 wickets playing together across 111 Tests, third all-time on the list of bowling pairs in Tests, behind only Glenn McGrath and Shane Warne (1,001 wickets in 104 Tests together) and Chaminda Vaas and Muttiah Muralitharan (895 wickets in 95 Tests together). They have subsequently gone on to pass Warne and McGrath as the top bowling pair, , with a combined 1,009 wickets in 133 Tests played together.
 On the morning of the fifth and final day of the third Test of the 2020 series against the West Indies, Broad became the seventh bowler to take 500 wickets in Test cricket, after dismissing Kraigg Brathwaite. Broad was the fourth fast bowler, and second bowler for England to reach the milesteone after James Anderson, who achieved it against the same batsman.

Personal life
Broad's father, Chris Broad, played Test cricket for England from 1984 to 1989, and his sister Gemma worked for the England team as a team analyst.  His stepmother Michelle "Miche" Broad died by suicide in July 2010. She was suffering with motor neurone disease.

Broad supports Nottingham Forest F.C. and Leicester Tigers. During the 2017-18 Premier League season, Broad won Manager of the Week in Round 37 in the official fantasy game.

Broad is in a relationship with The Saturdays singer and BBC Radio 1 presenter Mollie King, and they became engaged in January 2021. The pair reside in London, and announced in June 2022 that they were expecting their first child. In November 2022 King gave birth to their first child, a daughter Anabella Broad.

References

External links

Nottinghamshire County Cricket Club Profile

England Test cricketers
England One Day International cricketers
England Twenty20 International cricketers
English cricketers of the 21st century
Leicestershire cricketers
People educated at Oakham School
Sportspeople from Melton Mowbray
Cricketers from Leicestershire
1986 births
Living people
Nottinghamshire cricketers
Cricketers from Nottingham
English cricketers
Wisden Cricketers of the Year
Cricketers at the 2007 Cricket World Cup
Cricketers at the 2011 Cricket World Cup
Cricketers at the 2015 Cricket World Cup
Test cricket hat-trick takers
English cricket captains
Punjab Kings cricketers
Members of the Order of the British Empire
Hobart Hurricanes cricketers
Marylebone Cricket Club cricketers

redpajama_set_name: RedPajamaWikipedia


It is for certain that the future of a modern healthcare lies with artificial intelligence (for short AI) and machine learning. Integrated in the hospital infrastructure and even in a small private clinic AI can help doctors and medical specialists to help patients faster, to make a more accurate diagnosis and to prescribe a more efficient treatment. In some cases, it can even overtake minor doctors work and help medical specialists to concentrate on a more important matter. The AI can read and interpret words through natural language processing, thus understanding patients and doctors better.
So, for example identifying skin cancer. Everyone has moles they are suspicious of and only doctors after an inspection can say if any of those are dangerous and possess a potential cancer risks. Imagine that you don't need to spend hours in a waiting room to get examined and its every time you get suspicious marks after the sunburn. All you will have to do is to take a photo of it with your phone camera and send it over for AI to analyze. It is much easier and certainly less time consuming. Scientists at Sandford University have managed to teach a computer program to recognize and spot "carcinoma" and "melanoma", two of the most common skin cancer types. Melanoma is especially dangerous type of a cancer, that can lead to the death of a patient.
Scientist of Sandford University have used an AI software that was originally created by Google with purpose to spot the difference between images of cats and dogs. After some adjustments, AI started to learn, during this training process it looked through more than 120 000 photos of different cancer types and was told what type of cancer it was looking at, it learned how to recognize the differences. The AI has shown some incredible results when tested against 21, trained skin cancer specialists, reaching nearly the same results as the doctors.
Of course, AI cannot completely replace a real doctor, as in some cases it is not enough to just look at the spot, a more detailed tissues analysis needed to be done, to identify some cancer types. But, with a correct training, it still has a very high potential, to become a professional doctor's assistant in the future.
The renowned IBM's AI — Watson has also showed some incredible results in cancer treatment. The university of North Carolina has tested Watson abilities in 1000 cancer cases, in 99 percent of the cases, it has suggested the same treatment method as a trained oncologist. In some cases (around 30%) it has also suggested some other options that the doctors have missed. All thanks to the ability of an AI to processes and learn from many more papers and medical cases than any human doctor can manage.
Now IBM is working with a medical lab company Quest Diagnostics to provide a cloud service for oncologists, combing the gene sequencing with Watson analytic abilities.


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Sonali Kar Biography, Age, Height, Family, Husband, Boyfriend, Super Dancer 4, Choreographer, Net Worth & More
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This article covers a detailed story about the Indian dancer & Choreographer Sonali Kar. It Covers more details about Sonali Kar's Biography, Wikipedia, Choreographer, Wiki, Early Life, Age, Date of Birth, birthday, Height, Height in Feet, Body measurement, Career, Caste, Affairs, Marital Status, Married, Father, Mother, Parents, Siblings, Family, Kids, Husband name, boyfriend, Son, Daughter, Child, Super Dancer 4, Dance India Dance, India's Best Dancer 2, Machi, Photos, About, Facebook, Instagram, Twitter, Net Worth, Salary, Income, Facts, Occupation, Profession, Education, Education Qualification, Achievements, Awards, Photos, Videos, Gossips, News, Career & more.
Sonali Kar is a popular Indian Dancer and Choreographer who is known for her choreography in Sony TV's dance reality show Super Dancer Chapter 4. Sonali was born on 5 September 1989 in Kolkata, West Bengal. Since childhood, she started dancing with the dream of making a career in dance
After completing her childhood studies in Kolkata, she moved to Mumbai to pursue a career in dance. Coming to Mumbai, she took training in dance and worked hard after that auditioned for different dance reality shows.
She first got a chance to participate in Zee TV's dance reality show Dance India Dance (DID Doubles). She made her debut in the television industry with this television dance reality show. After that, she appeared as a contestant in many television dance shows.
In the year 2017, she participated in Sony TV's popular dance reality show Super Dancer Chapter 2 as a choreographer. In this show, Sonali danced and choreographed for Super Dancer Contestant Abir Ahmed.
In the year 2021, she participated in Sony TV's dance reality show Super Dancer Chapter 4 as a contestant where she choreographed dance for the show's contestant Esha Mishra.
Now she is participating as a contestant in another dance reality show India's Best Dancer Season 2 of Sony TV in 2021. She is a choreographing dance for Zamrrudh, the contestant in the dance show in the show.
Read Also: Tushar Shetty Biography, Wiki, Birthday, Age, Height, Religion, Parents, Wife, Gf, Choreographer, Lifestyle, Net Worth & More.
Real Name Sonali Kar
Nick Name Sonali
Profession Dancer & Choreographer
Popular for Her dance & Choreography
Date Of Birth 5 September 1989
Day Tuesday
Birthplace Kolkata, India
Hometown Kolkata, India
Dance Training Not Known
Educational Qualification Not Known
Language Known Hindi, English, Marathi
Zodiac Sign/Star Sign Virgo ♍
Debut as Dance Contestant in Tv Zee Tv: Dance India Dance Doubles (DID Doubles)
Debut as Choreographer in Tv Sony Tv: Super Dancer Chapter 4 (2021)
Sonali Kar's age is 32 years in the year 2022. She is a great dancer and choreographer who is known for her physical looks. She is a very beautiful dancer, whose look is amazing.
She takes special care of her body, for which she resorts to exercise. Her dancing moves are so tremendous that her body gets exercised from it.
Dancing is very hard work that requires a lot of energy, and to maintain this energy, she also pays special attention to her food. She consumes green vegetables, and fresh fruits in her daily diet so that her body can remain healthy and her dance performance can be maintained.
Sonali Kar's height is 5 feet 3 inches, which is 160 cm. Her body weight is 50 kg and Sonali's body measurement is 32-26-32. Her eye color is Black and her hair color is Black.
Read Also: Chandni Srivastava Biography, Wiki, Dancer, Age, Height, Father, Family, Husband, Boyfriend, Movies, IBD2, Net Worth & More
Sonali was born in a middle-class Hindu family. His entire family believes in Hinduism and also worships Hindu deities. Sonali Kar's father's name is not known and her mother's name is also not known.
Talking about Sonali's marital status is Unmarried. Her husband's name is not known.
Parents Father: Name Not Known
Mother: Name Not Known
Siblings Brother: Not Known
Martial Status Unmarried
Marriage Date Not Known
Talking about the total net worth of Sonali Kar, her total net worth is around ₹25 lakh rupees. She charges ₹25k to ₹40k per episode. Apart from this, she earns a decent amount of money by promoting brands on her Instagram page.
Read Also: Vaibhav Ghuge Biography, Wiki, Dancer, Choreographer, Age, Height, Father, Family, Child, Wife, Son Name, Salary, Net Worth & More.
Salary ₹25 – ₹40k per Episode
Total Net Worth Approx ₹25 lac (As in 2021)
Sonali's account is present on all social media platforms where she keeps sharing her latest photos with her fan. Her account is also present on Instagram where she is followed by more than 105k people and the number of her posts is more than 2k. She is not available on Facebook & Twitter till now.
Wikipedia has not given him a place on her page yet, so the link to her Wikipedia page does not exist yet. In the table below, we have shared with you the links of all their social media platforms, by clicking on which you will be able to access their profile page directly.
Facebook Not Available
Instagram @karsonali
Wikipedia Not Available
Sonali Kar is an Indian dancer and Choreographer.
She grew up in a middle-class Hindu family.
She also drinks wine occasionally but she does not smoke.
Sonali Kar drinks alcohol occasionally
She primarily belongs to Kolkata, India.
She is very foody.
Sonali is also a devotee of Lord Shri Ganesha.
Sonali is also an animal lover and has a pet dog named Piku.
Sonali Kar with her pet dog named Piku
When she came to Mumbai then she decided to audition for tv shows.
Sonali successfully cracked the audition for the Zee tv dance show DID Doubles and takes part as a contestant in the show.
She also made her debut as a choreographer for the Sony tv show Super Dancer Chapter 2 & Chapter 4, where she choreographed the dance for Abir Rahman and Esha Mishra.
She has also choreographed a music video Honthon Pe Bas.
Her dance performance is excellent in all the dance reality shows. She has an extreme level of dance talent.
In 2021, Sonali also choreographed the dance for India's Best Dancer contestant Zamruddh in the Sony tv show India's Best Dancer Season 2.
Sonali Kar with India's Best Dancer contestant Zamruddh
Q. Who is Sonali Kar?
Ans. Sonali is a famous dancer and choreographer from Mumbai.
Q. Who is his boyfriend of Sonali Kar?
Ans. Sonali Kar is not dating anyone
Q. What is the age of Sonali?
Ans. As of September 5, 1989, she is 32 years old in 2021.
Q. Where is from Sonali Kar?
Ans. Sonali Kar belongs from Kolkata, India but now she lives in Mumbai.
Q. Is Sonali Kar a choreographer?
Ans. Yes, Sonali is a choreographer and she choreographed the dance for some contestants in the tv show India's best dancer season 2.
Disclaimer: All images are available on Sonali Kar's official Instagram Account. Images can be taken from her official Instagram account for educational purposes. Image Credit goes to the respective owners of the Image Creator.
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Jay-Z Enters Wildly Growing Cannabis Industry As Brand Strategist
(Photo by Frank Micelotta/Getty Images)
Lauryn Overhultz Columnist
July 10, 2019 11:45 AM ET
Billionaire rapper Jay-Z announced a partnership with a cannabis company in California.
Jay-Z, 49, has joined the wildly growing cannabis industry as a brand strategist with a California weed dispensary, according to a report published Tuesday by Bloomberg.
July 9, 2019 Caliva's new Chief Brand Strategist, Mr. Shawn "JAY-Z" Carter ????????
A post shared by Carter V Fan Page (@jayoncecarteriv) on Jul 9, 2019 at 12:57pm PDT
Caliva, a San Jose-based company, made the announcement on its website.
"[Jay-Z] will play a crucial role driving creative direction, outreach efforts and strategy for the brand," Caliva said in the announcement. (RELATED: Jay-Z: America's First Hip-Hop Artist Turned Billionaire)
"Mr. Carter will focus on and work to increase the economic participation of citizens returning from incarceration – many of who are not seeing the monetary benefits of legalization – through advocacy, job training, and overall employee and workforce development," Caliva added.
"We want to create something amazing, have fun in the process, do good and bring people along the way," Jay-Z said in a statement about the partnership.
JAY-Z's empire just keeps on growing—now he's entering the weed industry: https://t.co/dNea4aghnh pic.twitter.com/5A1hawLHvk
— Complex Music (@ComplexMusic) July 9, 2019
The rapper's newest business venture comes a month after Forbes named him the first hip-hop artist to reach billionaire status. Jay-Z's businesses span many industries including alcohol, real estate, arts, sports, music and now marijuana.
He joins Snoop Dogg as the latest to join the growing industry. Snoop owns his own brand called Leafs by Snoop.
Tags : california cannabis jay z
Lauryn Overhultz
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The Family Medicine Residency Program based at Lake Charles Memorial Hospital is a community-based program that began in January 1995. In January 1996 our program was granted provisional accreditation by the Accreditation Council for Graduate Medical Education and in January 2002 our program was awarded full accreditation.
The mission of our residency program is to promote and provide the highest quality physician education through patient care - utilizing the most up to date educational methods and information systems.
Our residents provide patient care that is continuous, comprehensive, and in the context of the entire family.
Our residents are prepared to practice medicine in a full range of practice settings and in a continuously evolving professional environment.
Our graduates demonstrate competence and compassion in providing the highest quality and comprehensive care to all members of the family.
Our graduates display leadership skills and good citizenship in the medical society and communities in which they practice their specialty of Family Medicine.
Since the inception of our program, we are proud and honored to have a total of 66 medical- school graduates select our residency program as their residency-training site. Our current residents and incoming residents understand the importance and impact that our program has on the community it serves.
The contributions that our residents and graduates make to Lake Charles, southwest Louisiana, the state of Louisiana and nationally are significant!