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Japan's best- known author of S& M fiction, Flower and Snake was the first of Nikkatsu’s Roman Porno films to deal with an S& M theme. Together with the later Wife to be Sacrificed (also directed by Konuma in 1. S& M Roman Porno series which helped save Nikkatsu from collapse during the 1. Background[edit]In a very successful effort to avoid bankruptcy, Nikkatsu, Japan's oldest major film studio, had entered the pink film, or soft- core pornography, genre three years earlier, in 1. Roman Porno series.[2] However 1. Since the late 1. Naomi Tani had been known as the "Queen of Pink," the most popular actress in the low- budget, independent "pink films" which dominated Japan's domestic cinematic market. Nikkatsu had been trying to recruit Tani into their Roman Porno series for years, but she had always refused since the studio had been reluctant to enter the S& M genre, which was Tani's specialty.[4] Tani finally agreed to join the studio on the condition that her first film be based on the Oniroku Dan S& M novel Flower and Snake.[5] Tani had already starred in a pink film version of Dan's novel entitled Flower and Snake: Rearing the Flesh(花と蛇より 肉の飼育), released by Yamabe Pro.[6][7]Nikkatsu agreed to Tani's conditions, but there remained the problem of convincing Oniroku Dan to allow the studio to film his novel. After lengthy, inconclusive negotiations, Dan invited director Masaru Konuma and scriptwriter Yozo Tanaka to his home for "further discussions." In the middle of the meeting, the electrical power suddenly went out, and Dan called for someone to light a candle. At this point, Naomi Tani, in traditional Japanese kimono, appeared in the room with a lantern. Konuma later said, "This was Dan's theatrical sense - his way of saying yes."[8]Director Konuma and script- writer Tanaka both agreed that Dan's novel was unfilmable, and made significant changes to the story. Dan and Naomi Tani both objected to this, and there was considerable friction between the two sides over the story during the writing of the script. Konuma later commented about Naomi Tani's role in this matter, "while we worked on the final script, she was very argumentative. However, I was impressed with her change in attitude after the company's final decision. During the shoot, she never gave us a problem. Instead- she was committed. I admire her professionalism."[8]After the film became a huge hit for Nikkatsu, the studio wanted to follow it with a sequel. Oniroku Dan remained bitter and did not agree to participate in the next film, Wife to be Sacrificed (1. Dan did reconcile with the studio however, and continued to have a strong professional relationship with both Nikkatsu and Naomi Tani.[9]Synopsis[edit]Makoto Katagiri (Yasunori Ishizu) is a 3. Miyo (Hiroko Fuji), who operates a pornographic photography business specializing in sadomasochistic content out of her combined home and adult toy store. As a child, Makoto shot and killed a black American soldier whom he found having sex with his mother. The incident left Makoto psychologically stunted as well as impotent, and as such his mother and her staff treat Makoto much as a child. Despite this, Makoto has developed a strong interest in BDSM, though he has no outlet for his interests. Senzô Tôyama (Nagatoshi Sakamoto) is the elderly owner of the company Makoto works for, and also has an interest in BDSM. However, his new wife Shizuko (Naomi Tani) refuses to let Senzô tie her up or even watch her bathe; instead he vents his frustrations and needs on their housemaid Haru (Hijiri Abe), forcing her to indulge in his need for S& M. After finding some bondage pornography in Makoto's desk, Senzô summons Makoto to his home, where he first asks, then orders Makoto to kidnap and "train" his wife in order to break her pride so that she will submit to his desires. After some hesitation, Makoto agrees. While in town, Senzô drugs Shizuko's tea with sleeping pills, allowing Makoto to leave with her in his vehicle. On the way home Makoto stops in a field and attempts to rape the semi- conscious Shizuko, but his arousal brings on a hallucination of the black soldier he killed, forcing him to stop. At home, Shizuko awakes to find herself tied up and calls for help, attracting the attention of Miyo. Rather than helping the woman, Miyo seems pleased at her son's actions, and encourages him to rape Shizuko. When he says he can't because she is too beautiful, Miyo suggests Makoto give Shizuko an enema to overcome that impression. He does, and after watching her expel it finds he is able to become aroused without issue. He rapes Shizuko while his mother listens outside his room. Makoto reports his progress to Senzô regularly, providing tapes and even physical evidence of his wife's continued training. However, he also finds himself becoming attached to Shizuko. Makoto returns home one day to find his mother and her staff have been torturing Shizuko while he was at work. He orders them off of her angrily, telling them not to touch her unless he is present. Shizuko finds herself becoming more at ease with her situation and Makoto, and later asks him if he will protect her; he says yes, going on to say he wants to spend the rest of his life with her. He tells his mother this, and when she objects he responds angrily, calling her an old hag. One day Makoto returns home to find Shizuko tied up and being used by the black soldier from his dreams. He recoils in horror when the man rises to attack him. His mother then steps in, paying the man, revealing that she staged the scene with a look- alike to render Makoto impotent once more. Makoto tries to have sex with Shizuko again, despairing when he finds that his impotence has returned. Despite this, he keeps training her, even taking her outside for a walk. Taking a chance, he unties her so that she might use the restroom; after a long, worrying delay, Shizuko returns, to the delight of Makoto. Later the two go to watch a pornographic film, which features a black man who resembles the soldier from Makoto's dreams. Uncomfortable at first, Makoto starts to remember his childhood incident in detail, eventually remembering that it was his mother who shot the man, not him. Overjoyed, Makoto calls his mother from a public phone booth to tell her he has remembered the truth, letting her listen as he has sex with Shizuko during the call. Finally, Senzô arrives to reclaim his wife. Makoto is surprised when Shizuko moves to her husband's side eagerly. He asks her to divorce him so that they might marry, but she refuses, saying that she is now happy since Makoto made her a "total slut" just as her husband wanted. However, she offers to let him come with the two of them, and though hesitant, Makoto agrees. Miyo begs her son not to go, but the three pile into Senzô's vehicle and leave, a distraught Miyo running after the vehicle in vain. The film ends with Shizuko bound, being ravaged simultaneously by Senzô and Makoto while Haru watches in shock. Naomi Tani[1. 0] - Shizuko Tôyama. Nagatoshi Sakamoto - Senzô Tôyama. Yasunori Ishizu - Makoto Katagiri. Hiroko Fuji - Miyo Katagiri. Akira Takahashi. Hijiri Abe - Haru. Critical appraisal[edit]Flower and Snake is considered important more from a historical standpoint than for its artistic merits. The later Wife to be Sacrificed is more highly regarded by the critics. Where to watch - Filmigos. Amazon Prime is a new service of the company Jeff Bezos, which among other advantages, provides the option to purchase and rent movies, with viewing through streaming. The biggest advantage of Amazon Prime, no doubt, is the ability to watch your movies in offline mode, you buy / rent, download and can watch it anywhere, and you also get free movies to subscribe to the service, the Amazon Video, responsible platform for playback of media. Just like Net. Flix, Amazon is investing too heavy to have its own productions and internal programs. It works on all popular platforms and video game consoles, such as Android, i. OS, PS4, Xbox, Kindle Fire. His films can reach 1. HD) and more recently 4k! Natural Products as Promising Drug Candidates for the Treatment of Alzheimer’s Disease: Molecular Mechanism Aspect. ![]() Natural Products as Promising Drug Candidates for the Treatment of Alzheimer’s Disease: Molecular Mechanism Aspect. Abstract. Alzheimer’s disease (AD) is the most common neurodegenerative disorder to date, with no curative or preventive therapy. Histopathological hallmarks of AD include deposition of β- amyloid plaques and formation of neurofibrillary tangles. Figure 2 Clinical Benefit of Pembrolizumab Treatment According to Mismatch-Repair Status. Kaplan–Meier curves are shown for progression-free survival in the cohorts. Myanmar song lyrics and VCD collections. Wine Su Khine Thein - Khar Cha Nay Ya Tal. Statistical Techniques | Statistical Mechanics. ![]() Extent studies on pathology of the disease have made important discoveries regarding mechanism of disease and potential therapeutic targets. Many cellular changes including oxidative stress, disruption of Ca. AD. Despite intensive research, only five approved drugs are available for the management of AD. Hence, there is a need to look at alternative therapies. Use of natural products and culinary herbs in medicine has gained popularity in recent years. Several natural substances with neuroprotective effects have been widely studied. Most of these compounds have remarkable antioxidant properties and act mainly by scavenging free radical species. Some of them increase cell survival and improve cognition by directly affecting amyloidogenesis and programmed cell death pathways. Further studies on these natural products and their mechanism of action, parallel with the use of novel pharmaceutical drug design and delivery techniques, enable us to offer an addition to conventional medicine. This review discussed some natural products with potential neuroprotective properties against Aβ with respect to their mechanism of action. Keyword: Alzheimer’s disease, Amyloid β, Apoptosis, Natural products, Neuroprotection, Tau protein. INTRODUCTIONAlzheimer’s disease (AD) is a progressive neuro- degenerative disorder that is characterized by the loss of memory and cognitive impairments [1]. Many biochemical changes within cell have been identified to induce neuronal cell death. Oxidative stress, disruption of Ca. AD [2]. Histopathological hallmarks of AD include deposition of β- amyloid (Aβ) plaques and formation of neurofibrillary tangles [3]. Indeed, AD is a protein mis- folding disease, called “proteopathy”. Senile plaques are made of insoluble Aβ peptides that are formed by proteolytic fragmentation of amyloid precursor protein (APP), a trans- membrane protein that penetrates through the neuronal membranes [4]. Neurofibrillary tangles are made of aggregates of hyperphosphorylated tau, a microtubule- associated protein [5]. Most of the researches in AD during past two decades have focused on “amyloid hypothesis”. This hypothesis postulates that Aβ deposition is the initial event in neuronal dysfunction in AD. The support given for this hypothesis is the dementia of patient with Down’s syndrome (trisomy 2. As APP genes locate in chromosome 2. APP cleavage by β- secretase at extracellular domain, and by γ- secretase at the trans- membrane region, leads to formation of Aβ proteins [7]. Gamma- secretase complex consists of at least four proteins, including Presenilin (PS). PS, an aspartyl protease, is the catalytic subunit of the enzyme and its mutation causes alterations in APP processing and increases the amount of toxic Aβ [8]. Although amyloid plaques are the major characteristic of AD pathology, their presence does not necessarily mean the increased amyloid production. Decrease of clearance could also lead to this accumulation. It has been also reported that some soluble species of Aβ are more toxic than Aβ aggregates [9]. Thus, the main focus has been made on preventing the formation of Aβ from its precursor. Although several compounds have been proposed to decrease neurodegeneration in AD models, limited approved drugs are available for the management of AD patients. A major part of today’s pharmaceutical market is the use of natural products. The use of drug substances derived from natural sources has a long tradition in medicine [1. This review article describes the mechanism of AD, current medications for AD and existed problems in developing new medications. We also summarize the potential of some natural products for inhibiting Aβ- induced cell death and recent findings on their mechanisms of action. Although Aβ is not the only factor capable of causing cognitive decline in AD, due to extent of compounds and experimental models, in this paper we focused on the active substances reported to inhibit Aβ- induced cognitive impairment or cell death. MECHANISM OF NEURONAL CELL DEATH IN ADOxidative stress is the imbalance between prooxidants and antioxidant factors that lead to accumulation of reactive oxygen species (ROS) [1. This reactive species can lead to cell membrane lipid destruction, DNA cleavage, oxidation of proteins, and finally apoptosis [1. Apoptosis is the predominant type of neuronal cell loss observed in AD [1. Apoptotic cell death signaling can be divided into two major pathways; intrinsic (or mitochondrial) pathway and extrinsic (or death receptor- mediated) pathways [1. Apoptosis in mammalian cells regulates by a large number of proteins (Fig. In the intrinsic pathway, stimuli acts directly or indirectly on mitochondria and affects mainly Bcl- 2 family and caspase [1. Mechanism of apoptotic pathways and ER stress. Bcl. 2 superfamily consists of both pro- apoptotic (such as Bax, Bad, and Bak) and anti- apoptotic (such as Bcl- 2 and Bcl- x. L) proteins. Decrease of anti- apoptotic protein and/or increase of pro- apoptotic factors results in disruption of mitochondria membrane potential, swelling of mitochondrial membrane, and release of cytochrome c to cytoplasm [1. In cytoplasm, cytochrome c forms a multi- molecular holoenzyme complex with apoptotic protease activating factor 1 (Apaf. Active caspase- 9 then cleaves procaspase- 3 and initiates the caspase cascades [1. Extrinsic pathway of apoptosis involves the interaction of death signals, for example tumor necrosis factor (TNF- α) with death receptors, such as tumor necrosis factor receptors 1 (TNFR1), and formation of death- inducible signaling complex that activates caspase- 8, which could also cleave procaspase- 3 to its active form [1. Activated caspase- 3, in both intrinsic and extrinsic pathways, activates poly (ADP- ribose) polymerase (PARP) and other death substrates, such as APP, PS1 and PS2 proteins [2. Stress conditions also affect the folding of proteins in endoplasmic reticulum (ER) lumen [2. Three main ER pathways involved in folding include inositol- requiring enzyme 1 (IRE1), protein kinase RNA- like ER kinase (PERK), and activating transcription factor 6 (ATF6) [2. ER stress response is mediated via three different signaling pathways: unfold protein response (UPR), which increases the level of chaperones; ER- associated protein degradation (ERAD) that degrades the misfolded proteins by activating ubiquitin/proteosomal pathway; and ER overload response (EOR) which is induced when ER is overload with proteins that are not transported to Golgi complex [2. Under ER stress conditions, glucose- regulated protein 7. GRP7. 8) which is an ER chaperone, dissociates from ATF6, PERK, and IRE1 and binds to malfolded proteins to facilitate their folding [2. C/EBP homologous protein (CHOP) together with caspase- 1. ER resident caspases, and calpain mediate ER stress- induced apoptosis by affecting executioner caspases, such as caspase- 3 [2. While accumulation of unfolded proteins in ER provokes these pathways, accumulation of misfolded proteins in the cytosol leads to increased expression of heat shock proteins (HSPs) which act as molecular chaperons [2. HSPs expression is induced by several stimuli including heat shock, ischemia damage, infection, and heavy metals [2. HSPs may protect cells by mechanisms unrelated to their chaperone function through inhibition of apoptosis [2. Stress- inducible Hsp. In addition to mitochondria- and ER- resident proteins, many stress- sensing transcription factors are also activated in AD. NF- E2 related factor 2 (Nrf. II detoxifying enzymes via antioxidant response element (ARE) [3. Release of Nrf. 2 from its cytoplasmic inhibitor, Kelch- like ECH- associated protein 1 (Keap. Nrf. 2 and its translocation to nucleus, where it activates transcription of ARE- driven genes, such as Hsp. GCS) [3. 2]. Nuclear factor- κB (NF- κB) is another transcription factor that is activated by TNF- α, interleukin 1β (IL- 1β) and lipopolysaccharide (LPS) (canonical pathway) or by LTα/β, CD4. In unstimulated cells, NF- κB is sequestered inactive in cytoplasm by binding to IκBs (Inhibitor of κB). |
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