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1750_34 | The high-resolution machines (PC-98XA, XL and PC-H98) offered an 1120 × 750 display mode and aimed for tasks such as CAD and word processing.
The PC-9801U (optional) and VM introduced a custom chipset GRCG (GRaphic CharGer) to access several planar memory in parallel. The PC-9801VX introduced a blitter chip called the EGC (Enhanced Graphic Charger). It had raster operations and bit shifting.
In 1993, NEC introduced a 2D Windows accelerator card for PC-98, called the Window Accelerator Board, which employed a S3 86C928. Video cards for C-bus, local bus and PCI are also available from other manufacturers. DirectX 7.0a is the last official supported version for PC-98.
Sound |
1750_35 | The first generation of PC-9801s (the E, F and M models) only have an internal buzzer. PC-9801U2 and later models can change the sound frequency by controlling the programmable interval timer, like the PC speaker. The PC-8801mkIISR home computer, introduced in 1985, has a Yamaha YM2203 FM synthesis, an Atari joystick port and BASIC sound commands. The optional PC-9801-26 sound card is based around these features, although in some PC-9801 models it is integrated with the motherboard. It was replaced by the PC-9801-26K to support the 80286 CPU. This became the most common sound card for playing in-game music on the PC-98. |
1750_36 | The PC-9801-26K was succeeded by the PC-9801-73 (1991) and PC-9801-86 (1993) sound card, which employs the YM2608 FM synthesis and adds support for CD-quality PCM playback. The latter has a reasonable price and fully backward compatibility with the 26K sound card, so it gained strong support in PC games. Due to lack of DMA support and poor sound drivers, it often has issues in Windows and created popping and clicking sounds. Late PC-9821 models use the Crystal Semiconductor's Windows Sound System audio codec to resolve this, but the newer sound chip is not compatible with the older conventional sound cards. The PC-9801-118 (1995) sound card has both the YMF297 (hybrid of YM2608 and YMF262) and the WSS audio, but its PCM playback is not compatible with the 86 sound card.
Roland released a music production starter kit for PC-98, which combines the MT-32 synthesizer module, a MIDI interface card and a MIDI editing software. Creative Labs developed a C-bus variant of Sound Blaster 16. |
1750_37 | Keyboard
The first PC-9801 model has the same keyboard layout as the PC-8801's except it adds conversion key XFER and 5 function keys. Later models have some minor changes: NFER, 15 function keys, LED status indicators, and replacing CAPS and alternate action switches.
Mouse
The bus mouse and interface card kit was introduced for PC-98 in 1983. The PC-9801F3 and later models have a mouse interface. Although the PS/2 port became popular among IBM PC clones in the 1990s, the bus mouse was used until the end of PC-98.
Epson clones
Seiko Epson manufactured PC-9801 clones between 1987 and 1995, as well as compatible peripherals. |
1750_38 | In the 1980s, Epson's clones preceded NEC's in terms of its features such as performance and portability. In the early 1990s, Epson concentrated a line of low-priced computer which had low profit margins, but it did not sell well. This made resellers negative. Also, NEC had strong sales in the enterprise market, but Epson did not. Manufacturers of DOS/V computers began to get sales channels, and they became competitors for the PC-98 and its Epson clones. Nikkei Personal Computing magazine reported in 1992 that "NEC has various opinions inside the company about the future PC-98, and it is doubtful whether the PC-98 will continue to be the domestic standard. The decline of the 98 compatible machine business may lead to the decline of the PC-98 itself". |
1750_39 | In May 1992, Epson released a high performance machine, the PC-486GR. It has a 32-bit local bus for graphic processing and an Intel 486SX CPU running at 20 MHz, which was faster than NEC's flagship PC-9801FA, which had a 486SX running at 16 MHz. In January 1993, NEC released the 98MATE to compete with Epson's clones and DOS/V computers.
From 1992 to 1994, Epson sold about 200,000 units of PC-98 clones every year. As of 1994, Epson expected only 40% growth in their PC sales despite they expected 100% growth in their peripherals sales by 1995. However, Nikkei Personal Computer magazine expected that Epson would continue manufacturing PC-98 clones for a while because NEC had kept a 50% share of the Japanese PC market.
AST Research Japan released the DualStation 386 SX/16 in 1990 which was both PC-9801 and IBM PC compatible, but it failed because of poor marketing. |
1750_40 | Sharp, Sanyo and Seikosha each worked on PC-98 clones, but all gave up. An executive of Sanyo said, "NEC paid far more attention to its copyright than we had imagined. We decided that the loss of our corporate image would be greater than its profit, and cancelled the 98 compatible machine business."
Software |
1750_41 | The PC-98 was primarily used for businesses and industry in Japan from 1980s to mid-1990s. As of September 1992, out of 16,000 PC-98 software applications, 60% of them were corporate business software applications (including CAD), 10% of them were operating systems and development tools, 10% of them were educational software applications, with the rest being a mix of graphic design, networking, word processing and games. The Nikkei Personal Computing magazine reported in 1993 that most home users purchased PCs to complete office work at home. The publisher sent a questionnaire to 2000 readers, and out of 1227 readers who answered, 82% of users used it for word processing, 72% for spreadsheets, 47% as a database, and 43% for games. |
1750_42 | Ichitaro, a Japanese word processor for the PC-98 and considered one of its killer applications, was released in 1985 and ported to other machines in 1987. A Japanese version of Lotus 1-2-3 was also ported to PC-98 first in 1986. 1 million copies of all Ichitaro versions and 500,000 copies of Lotus 1-2-3 were shipped by 1991.
PC-98 software generally ran from program and data disks (Disk 0 & 1 or A & B). For example, Ichitaro's system disk contained a runtime version of MS-DOS, main programs, an input method editor (ATOK) and its dictionary file. It used the entire space of an 1.2 MB floppy disk. In 1980s, most machines only had two floppy drives because HDDs were an expensive additional feature.
NEC provided a variety of operating systems including CP/M-86, Concurrent CP/M, MS-DOS, PC-UX, OS/2 and Windows (discontinued after Windows 2000). Localized versions of NetWare and FreeBSD were also available. |
1750_43 | The PC-98 had many game titles designed for it, many of which made creative use of the system's limitations (as it was originally designed as a business machine) to great commercial success. Despite having hardware specifications inferior to the FM Towns and the X68000, the massive install base and steady flow of game titles (in particular "dōjin" style dating sims and RPGs, as well as games such as Policenauts, YU-NO: A Girl Who Chants Love at the Bound of this World, Koutetsu no Kishi, Mayonaka no Tantei Nightwalker, MechWarrior, Rusty, Hiōden: Mamono-tachi tono Chikai, Shūjin e no Pert-em-Hru, Corpse Party, Slayers, J.B. Harold Murder Club and Touhou Project) kept it as the favored platform for PC game developers in Japan until the rise of the DOS/V clones.
Models
Partial list of PC-98 models sold in the Japanese market (no 1992-2000 models, no notebook models, etc.).
Timeline of PC-9801 models
Reception |
1750_44 | Marketing
A journalist explained in 1988 how NEC established the nation of Japanese personal computers:
NEC responded quickly to the new demand for business personal computers.
NEC succeeded in attracting many third-party suppliers and dominated software production and distribution.
NEC adopted Microsoft's MS-DOS as an operating system for the PC-98. |
1750_45 | Western computers lacked Japanese support due to its display resolution and memory, so they could not get into the Japanese PC market until the DOS/V and faster computers came out; for example, IBM Japan sold the IBM 5550 instead of the IBM PC. Yoshihiko Hyodo, a programmer who developed the text editor VZ Editor, said two advantages that the PC-98 had were its kanji character memory and non-interlaced monitor. Both provided users with a more comfortable Japanese environment. A senior vice president of Otsuka Shokai (a computer distributor for enterprises) recalled that "early users such as Kao already had office automation with the PC-8000, but it lacked speed and kanji support. Then, the PC-9800 was released, and it was perfect, so distributors and users immediately switched to it.". |
1750_46 | Shunzo Hamada of NEC thought the biggest reason for the success of PC-98 was that NEC could get software companies to cooperate. He said, "Third-party suppliers of Japanese PCs had already grown up to a certain extent. However, it was not because they were organized. They were born by themselves, and hardware manufacturers didn't touch them. When we developed the PC-9800 series, we changed our method to make a conscious effort to grow them up". PC-98's large software library assured buyers that the machine could be used for all purposes, although most users actually purchased only a few major softwares. |
1750_47 | Ichiran Kou, a computer consultant, pointed out that IBM influenced NEC's strategy. Since 1982, NEC had four personal computer lines, and they covered a wide price range, similar to IBM's mainframe business. However, NEC's computers had poor backward compatibility and as such was criticized by users and software developers. After reforming personal computer lines in 1983, NEC began expanding the PC-9801 series and its number of models exceeded its competitors.
NEC encouraged third-party developers as IBM did for the IBM PC. The basic hardware of PC-98 was also similar to the IBM PC, though it was not IBM compatible. Kou guessed that NEC avoided releasing an IBM compatible PC because the company was proud of developing an original mainframe. |
1750_48 | Yasuhiro Uchida, a literature professor, wrote an essay titled "Users chose the most playable PC". He felt the PC-98 was an "ordinary" 16-bit personal computer, but it had plenty of games because it did not deny the playability. He theorized that Fujitsu did not consider the 16-bit personal computer as a game platform, and considered IBM JX handling games to be of minor importance, which made personal computers less attractive. He concluded that the actual value of personal computers must be found by not sellers but consumers. |
1750_49 | Legacy
A writer of the ASCII magazine wrote that the Japanese input method and the Japanese video game industry were significantly developed in the PC-98 era. Because the PC-98 had a kanji character ROM, Japanese applications were developed for it, which influenced Japanese input methods being developed for them; the two built off of each other. Software companies that developed games for the PC-98 immediately expanded the video game business on the Famicom platform. He believed most programmers learned computer programming on the PC-98 at that time. |
1750_50 | Criticism
In the late 1980s, competitors accused NEC of monopolizing the Japanese computer market. Takayoshi Shina, a founder of Sord, said, "The Japanese PC market is suffocating because of one company's dominance. There is no freedom. This is why its prices are 3-4 times as expensive as America's. To fulfil the same international price as America's, we really need the era of clone computers.". A software company also complained that "although there are few excellent engineers in Japan, the more incompatible machines appear, the more development resources are divided.". |
1750_51 | Contrary to the IBM PC and the Apple II, every Japanese personal computer had a short lifespan; NEC released a new model of the PC-98 every year. When the PC-9801VX01/21/41 models brought a new BASIC interpreter which supported the Enhanced Graphic Charger (EGC) chipset, most commercial software did not use it as they were written in C. Many developers did not follow it because they wanted to make their software less dependent on the specific platform. A software developer said, "Using the special one (EGC) goes against the trend. I don't want to use it if new machines come out so frequently.".
See also
PC game
PC-8800 series
X68000
TurboGrafx-16
Commodore 64
FM-7
FM Towns
MSX
References
Further reading
Joel West and Jason Dedrick, "Innovation and Control in Standards Architectures: The Rise and Fall of Japan's PC-98", Information Systems Research, Vol. 11, No. 2, June 2000, pp. 197–216
External links |
1750_52 | Intro to NEC PC-9800 World
PC 9801, the first model of the series
Info about NEC PC-9801M with uPD8086D-2
Neko Project II, a PC-98 emulator for Windows and Mac OS X
PC-9801
8086-based home computers
Home video game consoles
Computer-related introductions in 1982
1982 establishments in Japan |
1751_0 | Pattern hair loss is hair loss that primarily affects the top and front of the scalp. In male-pattern hair loss (MPHL), the hair loss typically presents itself as either a receding front hairline, loss of hair on the crown (vertex) of the scalp, or a combination of both. Female-pattern hair loss (FPHL) typically presents as a diffuse thinning of the hair across the entire scalp.
Male pattern hair loss seems to be due to a combination of genetics and circulating androgens, particularly dihydrotestosterone (DHT). The cause in female pattern hair loss remains unclear.
Management may include simply accepting the condition or shaving one's head to improve the aesthetic aspect of the condition. Otherwise, common medical treatments include minoxidil, finasteride, dutasteride, or hair transplant surgery. Use of finasteride and dutasteride in women is not well-studied and may result in birth defects if taken during pregnancy. |
1751_1 | Pattern hair loss by the age of 50 affects about half of males and a quarter of females. It is the most common cause of hair loss.
Signs and symptoms
Classic male-pattern hair loss begins above the temples and at the vertex (calvaria) of the scalp. As it progresses, a rim of hair at the sides and rear of the head remains. This has been referred to as a 'Hippocratic wreath', and rarely progresses to complete baldness. Pattern hair loss is classified as a form of non-scarring hair loss.
Female-pattern hair loss more often causes diffuse thinning without hairline recession; similar to its male counterpart, female androgenic alopecia rarely leads to total hair loss. The Ludwig scale grades severity of female-pattern hair loss. These include Grades 1, 2, 3 of balding in women based on their scalp showing in the front due to thinning of hair.
In most cases, receding hairline is the first starting point; the hairline starts moving backwards from the front of the head and the sides. |
1751_2 | Causes
Hormones and genes
KRT37 is the only keratin that is regulated by androgens. This sensitivity to androgens was acquired by Homo sapiens and is not shared with their great ape cousins. Although Winter et al. found that KRT37 is expressed in all the hair follices of chimpanzees, it was not detected in the head hair of modern humans. As androgens are known to grow hair on the body, but decrease it on the scalp, this lack of scalp KRT37 may help explain the paradoxical nature of Androgenic alopecia as well as the fact that head hair anagen cycles are extremely long. |
1751_3 | Research indicates that the initial programming of pilosebaceous units of hair follicles begins in utero. The physiology is primarily androgenic, with dihydrotestosterone (DHT) being the major contributor at the dermal papillae. Men with premature androgenic alopecia tend to have lower than normal values of sex hormone-binding globulin (SHBG), follicle stimulating hormone (FSH), testosterone, and epitestosterone when compared to men without pattern hair loss. Although hair follicles were previously thought to be permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown the scalp contains the stem cell progenitor cells from which the follicles arose. |
1751_4 | Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor (IGF) at the dermal papillae, which is affected by DHT. Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands, apocrine hair growth, and libido. With increasing age, androgens stimulate hair growth on the face, but can suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'. |
1751_5 | Men with androgenic alopecia typically have higher 5α-reductase, higher total testosterone, higher unbound/free testosterone, and higher free androgens, including DHT. 5-alpha-reductase converts free testosterone into DHT, and is highest in the scalp and prostate gland. DHT is most commonly formed at the tissue level by 5α-reduction of testosterone. The genetic corollary that codes for this enzyme has been discovered. Prolactin has also been suggested to have different effects on the hair follicle across gender.
Also, crosstalk occurs between androgens and the Wnt-beta-catenin signaling pathway that leads to hair loss. At the level of the somatic stem cell, androgens promote differentiation of facial hair dermal papillae, but inhibit it at the scalp. Other research suggests the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles as contributive. |
1751_6 | These observations have led to study at the level of the mesenchymal dermal papillae. Types 1 and 2 5α reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles. They catalyze formation of the androgens testosterone and DHT, which in turn regulate hair growth. Androgens have different effects at different follicles: they stimulate IGF-1 at facial hair, leading to growth, but can also stimulate TGF β1, TGF β2, dickkopf1, and IL-6 at the scalp, leading to catagenic miniaturization. Hair follicles in anaphase express four different caspases. Significant levels of inflammatory infiltrate have been found in transitional hair follicles. Interleukin 1 is suspected to be a cytokine mediator that promotes hair loss. |
1751_7 | The fact that hair loss is cumulative with age while androgen levels fall as well as the fact that finasteride does not reverse advanced stages of androgenetic alopecia remains a mystery, but some possible explanations have been put forward: Higher conversion of testosterone to DHT locally with age as higher levels of 5-alpha reductase are noted in balding scalp, and higher levels of DNA damage in the dermal papilla as well as senescence of the dermal papilla due to androgen receptor activation and environmental stress. The mechanism by which the androgen receptor triggers dermal papilla permanent senescence is not known, but may involve IL6, TGFB-1 and oxidative stress. Senescence of the dermal papilla is measured by lack of mobility, different size and shape, lower replication and altered output of molecules and different expression of markers. The dermal papilla is the primary location of androgen action and its migration towards the hair bulge and subsequent signaling and size |
1751_8 | increase are required to maintain the hair follicle so senescence via the androgen receptor explains much of the physiology. |
1751_9 | Diagnosis
The diagnosis of androgenic alopecia can be usually established based on clinical presentation in men. In women, the diagnosis usually requires more complex diagnostic evaluation. Further evaluation of the differential requires exclusion of other causes of hair loss, and assessing for the typical progressive hair loss pattern of androgenic alopecia. Trichoscopy can be used for further evaluation. Biopsy may be needed to exclude other causes of hair loss, and histology would demonstrate perifollicular fibrosis. The Hamilton–Norwood scale has been developed to grade androgenic alopecia in males by severity.
Treatment |
1751_10 | Androgen-dependent
Finasteride is a medication of the 5α-reductase inhibitors (5-ARIs) class. By inhibiting type II 5-AR, finasteride prevents the conversion of testosterone to dihydrotestosterone in various tissues including the scalp. Increased hair on the scalp can be seen within three months of starting finasteride treatment and longer-term studies have demonstrated increased hair on the scalp at 24 and 48 months with continued use. Treatment with finasteride more effectively treats male-pattern hair loss at the crown than male-pattern hair loss at the front of the head and temples.
Dutasteride is a medication in the same class as finasteride but inhibits both type I and type II 5-alpha reductase. Dutasteride is approved for the treatment of male-pattern hair loss in Korea and Japan, but not in the United States. However, it is commonly used off-label to treat male-pattern hair loss. |
1751_11 | Androgen-independent
Minoxidil dilates small blood vessels; it is not clear how this causes hair to grow. Other treatments include tretinoin combined with minoxidil, ketoconazole shampoo, dermarolling (Collagen induction therapy), spironolactone, alfatradiol, and topilutamide (fluridil).
Female pattern
There is evidence supporting the use of minoxidil as a safe and effective treatment for female pattern hair loss, and there is no significant difference in efficiency between 2% and 5% formulations. Finasteride was shown to be no more effective than placebo based on low-quality studies. The effectiveness of laser-based therapies is unclear. Bicalutamide, an antiandrogen, is another option for the treatment of female pattern hair loss. |
1751_12 | Procedures
More advanced cases may be resistant or unresponsive to medical therapy and require hair transplantation. Naturally occurring units of one to four hairs, called follicular units, are excised and moved to areas of hair restoration. These follicular units are surgically implanted in the scalp in close proximity and in large numbers. The grafts are obtained from either follicular unit transplantation (FUT) or follicular unit extraction (FUE). In the former, a strip of skin with follicular units is extracted and dissected into individual follicular unit grafts, and in the latter individual hairs are extracted manually or robotically. The surgeon then implants the grafts into small incisions, called recipient sites. Cosmetic scalp tattoos can also mimic the appearance of a short, buzzed haircut. |
1751_13 | Alternative therapies
Many people use unproven treatments. Regarding female pattern alopecia, there is no evidence for vitamins, minerals, or other dietary supplements. As of 2008, there is little evidence to support the use of lasers to treat male-pattern hair loss. The same applies to special lights. Dietary supplements are not typically recommended. A 2015 review found a growing number of papers in which plant extracts were studied but only one randomized controlled clinical trial, namely a study in 10 people of saw palmetto extract.
Prognosis
Psychological
Androgenic alopecia is typically experienced as a "moderately stressful condition that diminishes body image satisfaction". However, although most men regard baldness as an unwanted and distressing experience, they usually are able to cope and retain integrity of personality. |
1751_14 | Although baldness is not as common in women as in men, the psychological effects of hair loss tend to be much greater. Typically, the frontal hairline is preserved, but the density of hair is decreased on all areas of the scalp. Previously, it was believed to be caused by testosterone just as in male baldness, but most women who lose hair have normal testosterone levels.
Epidemiology
Female androgenic alopecia has become a growing problem that, according to the American Academy of Dermatology, affects around 30 million women in the United States. Although hair loss in females normally occurs after the age of 50 or even later when it does not follow events like pregnancy, chronic illness, crash diets, and stress among others, it is now occurring at earlier ages with reported cases in women as young as 15 or 16.
Society and culture |
1751_15 | Studies have been inconsistent across cultures regarding how balding men rate on the attraction scale. While a 2001 South Korean study showed that most people rated balding men as less attractive, a 2002 survey of Welsh women found that they rated bald and gray-haired men quite desirable. One of the proposed social theories for male pattern hair loss is that men who embraced complete baldness by shaving their heads subsequently signaled dominance, high social status, and/or longevity.
Biologists have hypothesized the larger sunlight-exposed area would allow more vitamin D to be synthesized, which might have been a "finely tuned mechanism to prevent prostate cancer" as the malignancy itself is also associated with higher levels of DHT.
Myths
Many myths exist regarding the possible causes of baldness and its relationship with one's virility, intelligence, ethnicity, job, social class, wealth, and many other characteristics. |
1751_16 | Weight training and other types of physical activity cause baldness
Because it increases testosterone levels, many Internet forums have put forward the idea that weight training and other forms of exercise increase hair loss in predisposed individuals. Although scientific studies do support a correlation between exercise and testosterone, no direct study has found a link between exercise and baldness. However, a few have found a relationship between a sedentary life and baldness, suggesting exercise is causally relevant. The type or quantity of exercise may influence hair loss.
Testosterone levels are not a good marker of baldness, and many studies actually show paradoxical low testosterone in balding persons, although research on the implications is limited. |
1751_17 | Baldness can be caused by emotional stress, sleep deprivation, etc.
Emotional stress has been shown to accelerate baldness in genetically susceptible individuals.
Stress due to sleep deprivation in military recruits lowered testosterone levels, but is not noted to have affected SHBG. Thus, stress due to sleep deprivation in fit males is unlikely to elevate DHT, which is one cause of male pattern baldness. Whether sleep deprivation can cause hair loss by some other mechanism is not clear. |
1751_18 | Bald men are more 'virile' or sexually active than others
Levels of free testosterone are strongly linked to libido and DHT levels, but unless free testosterone is virtually nonexistent, levels have not been shown to affect virility. Men with androgenic alopecia are more likely to have a higher baseline of free androgens. However, sexual activity is multifactoral, and androgenic profile is not the only determining factor in baldness. Additionally, because hair loss is progressive and free testosterone declines with age, a male's hairline may be more indicative of his past than his present disposition. |
1751_19 | Frequent ejaculation causes baldness
Many misconceptions exist about what can help prevent hair loss, one of these being that lack of sexual activity will automatically prevent hair loss. While a proven direct correlation exists between increased frequency of ejaculation and increased levels of DHT, as shown in a recent study by Harvard Medical School, the study suggests that ejaculation frequency may be a sign, rather than a cause, of higher DHT levels. Another study shows that although sexual arousal and masturbation-induced orgasm increase testosterone concentration around orgasm, they reduce testosterone concentration on average, and because about 5% of testosterone is converted to DHT, ejaculation does not elevate DHT levels. |
1751_20 | The only published study to test correlation between ejaculation frequency and baldness was probably large enough to detect an association (1390 subjects) and found no correlation, although persons with only vertex androgenetic alopecia had fewer female sexual partners than those of other androgenetic alopecia categories (such as frontal or both frontal and vertex). One study may not be enough, especially in baldness, where there is a complex with age.
Names
Male pattern hair loss is also known as androgenic alopecia, androgenetic alopecia (AGA), alopecia androgenetica, and male pattern baldness (MPB).
Other animals
Animal models of androgenic alopecia occur naturally and have been developed in transgenic mice; chimpanzees (Pan troglodytes); bald uakaris (Cacajao rubicundus); and stump-tailed macaques (Macaca speciosa and M. arctoides). Of these, macaques have demonstrated the greatest incidence and most prominent degrees of hair loss. |
1751_21 | Baldness is not a trait unique to human beings. One possible case study is about a maneless male lion in the Tsavo area. The Tsavo lion prides are unique in that they frequently have only a single male lion with usually seven or eight adult females, as opposed to four females in other lion prides. Male lions may have heightened levels of testosterone, which could explain their reputation for aggression and dominance, indicating that lack of mane may at one time have had an alpha correlation.
Although primates do not go bald, their hairlines do undergo recession. In infancy the hairline starts at the top of the supraorbital ridge, but slowly recedes after puberty to create the appearance of a small forehead.
References
External links
NLM- Genetics Home Reference
Conditions of the skin appendages
Genetic disorders with no OMIM
Hair diseases
Human hair
Testosterone |
1752_0 | Bank of New South Wales Building is a former heritage-listed bank at 101-111 Flinders Street, Townsville CBD, City of Townsville, Queensland, Australia. It was built in 1887 by Denis Kelleher. It is also known as Australian Meat Industry Employees Union (Queensland Branch). It was added to the Queensland Heritage Register on 21 October 1992.
History
The former Bank of New South Wales Building was built for the Bank of New South Wales in 1887. It was third building which the bank had constructed. Built by Townsville builder Denis Kelleher at a cost of , the building was probably designed by Sydney architect John Smedley, with construction supervised by architect WM Eyre of the Townsville firm of Eyre and Munro and Brisbane architect FDG Stanley.
The Bank of New South Wales was the second banking company to be established in Townsville. The Australian Joint Stock Bank opened on 19 February 1866 and the Bank of New South Wales on 20 March 1866. |
1752_1 | The Bank of New South Wales was founded in 1817 in Sydney, New South Wales. In 1851 Robert Towns, a Sydney businessman, became a shareholder. During the early 1860s Towns formed a business partnership with John Melton Black in his North Queensland properties and investment speculations, including the establishment of a port on Cleveland Bay. Keen to protect his investment in the new settlement at the port and to encourage the expansion of the Bank of New South Wales into North Queensland, Towns facilitated the establishment of a branch of the bank in Townsville within a year of settlement. |
1752_2 | The first branch building, leased from Towns and Black, was located in Flinders Street East near the site of the present building, but the managers and staff soon complained that the building was hot and plagued by mosquitoes from Ross Creek. A decision was made to move after Queensland Bank Inspector, Alexander Archer, reported that the bank and its records were unsafe located amongst a group of wooden buildings.
The second bank building and a manager's residence were constructed in 1869 on the corner of Wickham Street and The Strand on the present Townsville Customs House site. While these premises were well placed for the sea breezes, the building was again deemed unsuitable because of the distance from the centre of town and the difficulty of access via Wickham Street. |
1752_3 | By August 1875 the Bank of New South Wales had purchased a new site closer to the centre of town while still taking advantage of the sea breezes. However, the block on the corner of Flinders and Wickham Streets remained undeveloped for a further twelve years, despite Brisbane architect James Cowlishaw calling tenders on 8 January 1883 for the erection of banking premises at Townsville for the Bank of New South Wales.
During the 1860s, Cowlishaw had supervised the construction of the Brisbane branch of the Bank of NSW for Sydney architect GA Mansfield, and was also involved in the construction of branches in Bowen and Rockhampton. It is not certain whether the 1883 tender for a new bank building in Townsville was for a building designed by Cowlishaw, or another design by Mansfield to be supervised by Cowlishaw. However, newspaper reports of 1887 suggest that, either way, the 1883 design for a Bank of New South Wales in Townsville was not constructed. |
1752_4 | By October 1887 however, the Townsville Herald noted that FDG Stanley, architect for three buildings being erected in Townsville including the Bank of NSW, inspected these with his local representative Mr WM Eyre who was supervising their construction. Three months later on 24 December 1887, the same newspaper congratulated the architect Mr Smedley of Sydney for his design of the newly completed Bank of New South Wales building. This suggests Smedley was Mansfield's successor as the bank's design architect in Sydney, and Eyre was the local supervising architect with Stanley his senior partner.
The new premises included the banking chamber, manager and accountant's offices, strong rooms and ablution facilities. The manager's residence included nine private rooms, kitchen, bathroom linen press and pantry. Included in the complex were stables, a coach house and a messenger's room. |
1752_5 | In 1925 Townsville architect Walter Hunt supervised alterations to the building including the installation of the pressed metal ceiling in the banking chamber. The work was carried out by contractor J Hillman.
On 17 November 1931 the Bank of Commerce amalgamated with the Bank of New South Wales. In Townsville the combined businesses operated from the Flinders St/Wickham Street offices until 12 January 1935 when the main office of the bank moved to new premises at the corner of Flinders and Stokes Streets.
The former premises became known as the East Flinders Street Branch of the Bank of New South Wales, with the branch operating from the building until it was sold. Historical Services Section of the Westpac Banking Corporation provided information that the property was sold in 1940 for but titles information indicates that the building was not sold until 26 February 1941 when the Queensland branch of the Australian Meat Industry Employees Union (AMIEU) purchased it. |
1752_6 | With the threat of invasion of Australia by Japan during the early years of WWII, Townsville was selected as the supply base for the allied forces in the south west Pacific. By 1941 many buildings in the city had been requisitioned including the former Bank of New South Wales from the AMIEU. |
1752_7 | A detachment of Area Signals personnel established a telegraph, switchboard and dispatch rider service in the building prior to February 1942. For a short time after the attack on Pearl Harbour, Col North, Commander of the Townsville area, established his headquarters in the building along with the Signals Corp. During this period PMG style switchboards were installed and the communication centre connected to service units being established throughout the region. Telegraph facilities in the building were linked to Charters Towers and to units further west as well as to Victoria Barracks, Brisbane. Part of the first floor was also used as living quarters for the Area Signals Officer and Operations Officer.
During this period, a concrete bunker was constructed at the rear of the property to house a cypher group who worked to decode Japanese messages. Pigeon lofts were also built in the yard to supply ships and aircraft with carrier pigeons. |
1752_8 | Towards the end of 1942 or early 1943, the switch installation became a security monitor of all telephone calls, both civil and military, emanating from North Queensland. About twenty AWAs manned the switch which was connected to the Security Monitoring Centre at Stuart, south of Townsville. The monitoring unit remained in the building until the end of the war.
The AMIEU, located in Denham Street during the war, did not move into this building until about 1948. For the next three decades the AMIEU building became a bastion of the Labor movement in Townsville and North Queensland, with the building and surrounding area becoming a focus for workers seeking permits to work at the Ross River Meatworks, seeking social security in the Queensland Building diagonally opposite, and visiting the Tattersalls Hotel, across Wickham Street which was a favourite recreation venue for all those who lived and worked in the area. |
1752_9 | From the late 1940s until the early 1970s, the building was a hive of activity and the centre of labour issues for North Queensland. During this period. apart from the AMIEU, the Trades and Labour Council and the Seamen's Union operated at various times from offices on the first floor, and later the Communist Party had an office on the Wickham Street verandah. |
1752_10 | The Seamen's Union, miners unions, the Trades and Labour Council and affiliated unions, and particularly the Communist Party were involved in the 1948 Railway Strike; a strike which highlighted the conflict between the unions and the Labor Party and a conflict which was to split the party a few years later. The Seamen's Union and various mining and craft unions played active roles in this conflict with the Queensland Government and the industrial court over wage fixing measures introduced by the court in 1939. This conflict was to raise questions of fundamental importance to a democratic society, such as the extent of civil liberties, the use of violence, and the distortion of truth. |
1752_11 | The labour organisations in this building were also involved in the Mount Isa Strike of 1964/65 when the Qld Trades and Labour Council, representing unionists at the mine, came into conflict with Mount Isa Mines management over bonus payments. The Communist Party was also involved to a lesser degree through union officials and members who were members of the Communist Party.
From 1 January 1954 Remington Rand Charters Pty Ltd leased most of the ground floor and part of the first floor of the building. They had a showroom of typewriters and business machines in the banking chamber, a workshop at the rear, and accounting branch offices upstairs connected by a stairs to the banking chamber. A partition in the corridor divided them from the other tenants. Remington Rand vacated the building early in the 1970s, then for several years ex-employees continued to work from the building. The ground floor has remained vacant since these workshops closed in the late 1970s. |
1752_12 | About 1962-3, the toilets on the first floor were altered to divide the single male toilet into male and female toilets. This became necessary after the introduction of a Federal award which, after some 60 years, again allowed women to work at the meatworks, and so women would be coming to the union offices in the building for their work tickets.
There were also apparently substantial wrought iron gates in the Flinders Street fence and at the Wickham Street entrance, which have all been removed.
In 1995, Townsville celebrate VP50 (the 50th anniversary of victory in the Pacific). A small ceremony was held in the building and a plaque presented recognising the service of the men and women of the Royal Australian Corps of Signals here during WWII.
The building has housed Flynns Irish Bar since 2001. |
1752_13 | Description
The former Bank of New South Wales building is a two-storeyed stuccoed masonry structure on the corner of Flinders Street East and Wickham Street, Townsville. With the Tattersalls Hotel, the Queensland Building and the Burns Philp Building, it forms a group of late-19th century commercial buildings on the four corners of this intersection. Flinders Street East also retains many other late-19th century commercial masonry buildings.
The principle facades of the Bank of NSW building are set on the street alignments of Flinders and Wickham Streets, and joined by a curved bay at the street corner. The facades are asymmetrical, and are divided by pilasters and by a horizontal moulded string course between the levels. In each bay are sets of windows, mostly double hung but some louvres and fixed lights to the curved bay at the corner, all with external moulded architraves. |
1752_14 | The simple squared parapet has a moulded and bracketed cornice above the windows, and a higher decorative parapet with "Bank of NSW" in relief above the main Flinders Street entrance. This entrance is emphasised by moulded pilasters to either side, decorative plasterwork and a segmented arch over the doorway.
Behind the parapet is a hipped roof with moulded chimneys and ventilators. The facades not facing the street have little decoration, apart from the two-storeyed verandah to the north-eastern end of the building. The upper level of the verandah, now enclosed with louvres and fibro, has segmental arched openings and cast iron balustrade, and the lower level has moulded semi-circular archways infilled with timber and masonry. |
1752_15 | Through the Flinders Street entry doors is a decorative timber vestibule, with timber and glass panelled walls and doors, which leads to the former banking chamber. The former chamber features highly decorative pressed metal ceilings, moulded architraves and dados, and two central decorative cast iron columns. It also has a concrete safe which retains its safe door and some timber shelving, and a curious window opening to the stair landing reputedly for managers to supervise their staff from above.
From Wickham Street is a second entrance lobby, and vestibule with tessellated tiles. The timber stair features substantial newels, twisted balusters, and boarding to the underside. From the mid landing is the window opening to the former chamber, and a doorway to a small room and stair to the exterior. |
1752_16 | The remainder of the ground floor includes several former offices between the chamber and the stair, and a series of small service rooms to the rear. Projecting from the north-western corner of the building is a single-storey wing, with three small former services rooms opening onto a common verandah. This wing has details consistent with the two-storey part of the building.
The First Floor has a central corridor with rooms opening to either side. The corridor is divided by a pedimented and panelled partition with a pair of glazed French doors, and by an adjacent fibro partition. The first floor interior features moulded timber skirtings and architraves, some panelled doors with toplights, some double hung windows, and decorative metal ceilings and cornices. |
1752_17 | At the top of the main stair is a hall, divided by a square arch with panelled architraves, and by a fibro partition with a small hatch. To the north-eastern end of this level is a verandah enclosed with louvres and fibro sheet, but with the cast iron balustrade still visible from the exterior.
At the north-western corner of the site is a rectangular concrete building, mostly covered with vines and other vegetation. It is a single room, with access from a covered entrance porch.
To the western end of the site is the garage, reputedly the former stables, which is constructed of brick with a corrugated iron skillion roof, double-hung windows and boarded doors. Access to the western yard is through a rendered masonry fence on the Flinders Street alignment. Along the north-eastern boundary is a face brick fence, with a curved coping, engaged piers and recessed panels. |
1752_18 | Heritage listing
The former Bank of New South Wales building was listed on the Queensland Heritage Register on 21 October 1992 having satisfied the following criteria.
The place is important in demonstrating the evolution or pattern of Queensland's history.
Built and occupied by the Bank of New South Wales from 1887-1935, the building is associated with the establishment of the presence of the bank in Townsville and the growth of Townsville as a major port in North Queensland.
The place is important in demonstrating the principal characteristics of a particular class of cultural places. |
1752_19 | It is typical of bank buildings of the nineteenth and early twentieth centuries, with a ground floor plan banking chamber and a second floor residence for the manager.
The interior of the building is substantially unaltered since WWII. It is of extremely high quality in its design, detailing and finishes. It is one of the few intact ground floor commercial interiors of all the historical buildings of Flinders Street East. The upper level retains its layout as a manager's residence, and includes a white marble fireplace and timber joinery. The building was probably designed by Sydney architect John Smedley, and constructed by Townsville builder Denis Kelleher under the supervision of Townsville architect WM Eyre and his partner FDG Stanley of Brisbane. Eyre's firm, Eyre and Munro, were later responsible for other Bank of NSW branches including Georgetown, Winton, Cairns and Charters Towers.
The place is important because of its aesthetic significance. |
1752_20 | The exterior of the Former Bank of New South Wales remains remarkably intact. The street facades form a major contribution to the streetscape of the Flinders Street East area, which retains many historical commercial buildings. The facade of the building along Wickham Street also contributes to the linking of this area with the historical government precinct of lower Melton Hill. The intersection of Flinders and Wickham Street has a prominent historical building on each of its four corners.
The place has a special association with the life or work of a particular person, group or organisation of importance in Queensland's history. |
1752_21 | The building is associated with the Royal Australian Corps of Signals who occupied it between 1941-1948. The announcement of the end of WWII first reached North Queensland through this facility. Purchased by the AMIEU in 1941, and occupied by them in 1948, the building is significant for its long association with the Union, over 50 years, and the substantial role that the Union played, in connection with other organisations such as the Ross River Meatworks, in the social and economic framework of Townsville. The building is associated with a number of other Unions, with offices being occupied at various times by the Seamen's Union, the Communist Party and the Queensland Trades and Labour Council (Townsville Branch). Whilst in this building, these organisations were involved in several industrial disputes, including the Mount Isa Mines Strike of 1964-5, in which the Trades and Labour Council played a key role.
References
Attribution
External links |
1752_22 | Queensland Heritage Register
Townsville CBD
Former bank buildings in Queensland
Articles incorporating text from the Queensland Heritage Register
Trades halls in Australia
Bank of New South Wales
Queensland Heritage Register sites located in Townsville |
1753_0 | Health issues in American football comprise a large number of health risks associated with participating in the sport. Injuries are relatively common in American football, due to its nature as a full-contact game. Injuries occur during both practice and games. Several factors can affect the frequency of injuries: epidemiological studies have shown older players can be at a greater risk, while equipment and experienced coaches can reduce the risk of injury. Common injuries include strains, sprains, fractures, dislocations, and concussions. Concussions have become a concern, as they increase the risk of mental illnesses like dementia and chronic traumatic encephalopathy (CTE). In individual leagues like the National Football League (NFL) and National Collegiate Athletic Association (NCAA), a public injury report is published containing all injured players on a team, their injury and the game-day status of each player. |
1753_1 | Catastrophic injuries—defined as serious injury to the spine, spinal cord, or brain—and fatalities are uncommon in football; both have become less common since the 1970s, although a small number of them still occur each year. Both concussions and catastrophic injuries can be caused by helmet-to-helmet collisions as well as impact against the ground or other players' knees; in other cases, they can be caused by players who have sustained a head injury returning to play, which can place the player at risk of sustaining a severe injury. Despite the decrease in catastrophic injuries, a greater number of NFL players have reported major injuries and shortened careers since the 1970s, in part due to the increasing size and speed of players and the use of artificial turf. |
1753_2 | In many cases, injuries sustained while playing can cause long-term damage. In addition to neurological damage caused by hits to the head, injuries to the mid and lower body can force players to retire or lead to nagging ailments in later life. Various methods have been used to reduce injuries in football, including rule changes such as the abolition of large wedge formations; a sharp decline in cervical spine injuries since the 1970s has been attributed to rule changes that altered blocking and tackling techniques. More recently, rule changes to protect players from head injuries have been instituted. Equipment like the football helmet and pads are used to give players a level of protection from injuries, while other factors such as cleat size are used to minimize the risk of injuries due to field condition.
Injuries |
1753_3 | Because American football is a full-contact sport, head injuries are relatively common. According to the San Francisco Spine Institute at Seton Medical Center in Daly City, California, up to 1.5 million young men participate in football annually, and there are an estimated 1.2 million football-related injuries per year. An estimated 51% of injuries occur during training sessions, while 49% occur elsewhere. Injuries are nearly 5 times more likely to happen during contact training sessions than in controlled, non-contact sessions. Older players are at the most risk for injuries, while teams with experienced coaches and more assistant coaches are less likely to experience injuries. 50% of injuries occur in the lower extremities (with knee injuries alone counting for roughly 36% of all injuries) and 30% occur in the upper extremities. |
1753_4 | The most common types of injuries are strains, sprains, bruises, fractures, dislocations, and concussions. According to the NFL Physicians Society, the most common injuries in football are "concussions, blunt injuries to the chest such as cardiac contusions, pulmonary contusions, broken ribs, abdominal injuries, splenic lacerations and kidney injuries." Orthopedic injuries to the knee, foot, ankle, shoulder, neck and back are also common, as are muscle strains to the hamstrings, quads, calves and the abdomen. |
1753_5 | Concussions are particularly concerning, as repeated concussions may increase a person's risk in later life for chronic traumatic encephalopathy (CTE) and mental health issues such as dementia, Parkinson's disease, and depression. Concussions are often caused by helmet-to-helmet collisions, impact against the ground or other players' knees, and upper-body contact between opposing players. However, helmets have prevented more serious injuries such as skull fractures. Cervical spine injuries can be catastrophic, but have sharply declined since the mid-1970s due to rule changes and improved workout regimes, equipment, and coaching. |
1753_6 | Performance-enhancing drugs (PEDs) are an issue in both high-school and professional-level football. Steroid use has been linked to an increased risk for musculoskeletal injuries among players. Human growth hormone (HGH) is used by some players to improve performance, recover from injuries, decrease aging, and to lose weight. Although none of these uses are scientifically proven or legal, HGH places users at risk for adverse side effects such as onset of diabetes and negatively impacting joints and organs such as the heart. However, there have been no studies of HGH use or the baseline levels of the hormone in NFL athletes. NFL players are routinely subject to drug tests in accordance with the NFL's two substance policies. Players found using performance-enhancing drugs, including anabolic steroids, can face suspension and other penalties. As of 2014, the league does not test for HGH use among players. |
1753_7 | National Football League |
1753_8 | An injury report section is common in the sports sections of American newspapers, detailing injuries for each team and the amount of time each injured player is expected to be out. The injury report was created to prevent gamblers from gaining inside information about injuries from players, and as a result, NFL teams must report on the status of injured players on a set schedule during the season. The standard severity descriptions are "out" (will not play in the upcoming game); "doubtful" (25% chance of playing); "questionable" (50% chance of playing); or "probable" (75% chance of playing). Teams have been known to downplay, exaggerate or overly detail their teams' injuries in an attempt to confuse or mislead upcoming opponents. Injured players may be placed on one of several injured lists, including the Physically Unable to Perform (PUP) list. If a player is injured in an event outside of a game or team practice, or during collegiate practice prior to being drafted, he is eligible |
1753_9 | for the Nonfootball Injury list. Players who have sustained major injuries and are not expected to play for the rest of the season may be placed on the Injured Reserve (IR) list. These players do not count towards the teams' roster limit. |
1753_10 | Aside from concussions, orthopedic injuries are among the most common in the National Football League. These injuries consist of trauma such as tears in the achilles, anterior cruciate ligament (ACL), and patellar tendon. A study was done but the Feinberg School of Medicine and Northwestern University, where they studied the "return to play rate" (RTP) for given orthopedic procedures done based on a given injury. They found that out of 559 NFL players, the most difficult injuries for NFL players to return to play in were patellar tendon tears (50.0 %) and achilles tears (72.5%). |
1753_11 | College and high school football
According to the College Football Assistance Fund, over 20,000 injuries occur from college football each year. The National Collegiate Athletic Association (NCAA) maintains an injury list similar to that used by the NFL – injured players are listed as "Out", "Doubtful", "Questionable", or "Probable", but suspended players are also included on the list. College players are limited to four years of eligibility, but can receive a medical redshirt that lets them play another year if they have suffered a season-ending injury and have not played in more than 30% of the season's games.
Brain injury |
1753_12 | In 1994, the NFL established the Mild Traumatic Brain Injury Committee (MTBI), which was later replaced by the Head, Neck and Spine Committee, to study concussions and brain injuries in professional football players. The committee and its leadership, including Ira Casson and Elliot Pellman, were criticized by former players for stating that there is not enough research to determine if concussions lead to permanent brain injury. Pellman, who served as chairman of the committee from 1994 to 2007, received a large amount of criticism because he did not have a background in neurology and the research he published on brain injuries disagreed with the findings of independent scientists. In 2009, an NFL-commissioned report showed increased incidence of diagnosis of memory loss and dementia among retired professional football players when compared to the general population. The study also indicated that these symptoms were related to the effects of concussions. However, the NFL and the |
1753_13 | report's own researchers questioned the reliability of some of the data-gathering methods employed by the study, including the fact that the study was conducted by phone. The same year, the committee acknowledged for the first time that concussions can lead to long-term brain injuries. A Congressional hearing in October 2009, as well as pressure from the National Football League Players Association (NFLPA), led to an overhaul of the concussion policy in November and December of that year. |
1753_14 | NFL commissioner Roger Goodell addressed the issue of head injuries in professional football during a talk held on November 15, 2012, at the Harvard School of Public Health. In the talk, he highlighted the NFL's efforts to reduce head injuries by enacting measures such as penalizing hits to the head, better assessing concussions on the sideline, and removing players from the game after they have been diagnosed or suspected of having sustained a concussion. He also discussed the need for increased research on brain injuries and long-term disorders, and called for a culture change in the league, saying that players need to be more willing to acknowledge their injuries to medical staff. In September 2012 the league pledged a $30 million donation to the National Institutes of Health to research the connection between brain injuries and long-term mental health issues. Beginning in 2012 the NFL was the subject of several lawsuits initiated by former players who alleged that the league |
1753_15 | withheld information and misled players about the potential long-term impacts of head injuries. Six of the lawsuits were approved to be tried together. In August 2013 the NFL reached a settlement with more than 4,500 former players, agreeing to pay $765 million to be used to pay for medical examinations for former NFL players and for research and education purposes. Additionally, the funds will also be used to compensate former players who are determined to have significant cognitive impairment. |
1753_16 | Concussions are also an issue outside of professional football. In a 2010 study by Purdue University and Indiana University, an estimated 43,000 to 67,000 football players suffer a concussion every season. However, because many injuries go unreported, the true number may exceed 100,000. The study, "Detected Cognitive Impairment in High School Football Players Without Clinically Diagnosed Concussion", was published in 2013 in the Journal of Neurotrauma and observed 21 high school players throughout a season; it determined that even players who would not be diagnosed with a concussion based on their symptoms can display notable impairments via MRIs and verbal or cognitive testing, indicating that the current tests used on the sideline to assess concussions may not be adequate. A 2013 study by the National Academy of Sciences found that concussion rates in college football exceed those in any other sport, and that high school players have twice the risk of sustaining a concussion as |
1753_17 | collegiate players. The study found that, as reported by athletic trainers, college football players sustain 6.3 concussions for every 10,000 athletic exposures (meaning an individual practice or game), and the rate for high school football players is 11.2. The high school concussion figure is nearly double that of the next-highest sport, lacrosse. The study, funded by a $75,000 donation from the NFL to the Centers for Disease Control Foundation, also found that there is no evidence that newer helmet technology decreases the risk for concussions. |
1753_18 | According to 2017 study on brains of deceased gridiron football players, 99% of tested brains of NFL players, 88% of CFL players, 64% of semi-professional players, 91% of college football players, and 21% of high school football players had various stages of CTE.
Catastrophic injuries and fatalities |
1753_19 | Catastrophic injuries are not common in American football. According to the National Center for Catastrophic Sport Injury Research, there were 468 non-fatal injuries resulting in permanent neurological damage across all high school sports in the United States from 1982 to 2011. In football, catastrophic injuries are rare but are devastating when they occur. The rate of catastrophic head injuries has remained low since the introduction of the modern football helmet in the 1970s, but rates of injury are much higher at the high school level than the college level. A 2007 study found that, in high school and college football, there are an average of 7.23 catastrophic head injuries per year: there were 0.67 injuries per 100,000 high school players and 0.21 injuries per 100,000 college players. Over a 13-year period from September 1989 to June 2002, there were 94 players who sustained catastrophic head injuries—8 of these players died as a result of the injury, 46 sustained permanent |
1753_20 | neurological damage, and 36 made a full recovery. 56% of these players had a history of head injuries, 71% of them occurring in the same season as their catastrophic injury, and most of the catastrophic injuries resulted from being tackled or making a tackle. The study recommended that players exhibiting neurological symptoms should be strongly discouraged from returning to play. |
1753_21 | The medical costs for catastrophic injuries can be extremely high—a 2011 estimate from the National Spinal Cord Injury Statistical Center notes that first-year costs of someone who has high tetraplegia, an injury that causes partial or full loss of use in all limbs, is USD $1,044,097, with subsequent years costing $181,328. Many high schools across the United States require students to have an insurance policy, while others offer supplementary insurance to help offset the cost; some schools also request that boosters help families pay for these policies. |
1753_22 | Catastrophic injuries have been on a steady decline since the 1960s, due in part to rules banning dangerous forms of contact such as spearing, face tackling and butt blocking. However, catastrophic injuries are still caused by helmet-to-helmet collisions, as well when players hit their heads against an opposing player's knee or the ground. Returning to play after sustaining a head injury earlier in the game also places players at risk for an even more severe injury. Many states are requiring teams to prevent players who have shown any signs of a concussion from returning to a game, while other steps such as more aggressive enforcement of safety rules and better condition of the neck muscles have been suggested. Additionally, coaches are being urged to train players to block with their shoulders instead of their heads. |
1753_23 | Fatalities in football are rare. A 2013 study of high school and college football players split fatalities into two types: direct fatalities, defined as those caused by "trauma from participation in a sport resulting in a brain injury, cervical fracture, or intra-abdominal injury" and indirect fatalities, defined as those resulting from external factors such as "cardiac failure, heat illness, sickle cell trait [SCT], asthma, or pulmonary embolism". The study found that, on average, there are 4 direct fatalities and 8.2 indirect fatalities among high school and college players per year, making indirect fatalities more than twice as common as direct fatalities.
Effects on post-career life |
1753_24 | In addition to immediate health effects, some injuries sustained during a player's career can have effects that extend to their post-career life. A cohort mortality study by researchers at the National Institute for Occupational Safety and Health (NIOSH) examined 3,349 NFL players who played at least five full seasons from 1959 to 1988. The findings from this study suggest that, in comparison to the typical American male, NFL players live longer on average but have around three times the risk of death associated with neurodegenerative disorders. In particular, the risk of death from Alzheimer's disease and Amyotrophic lateral sclerosis (ALS) was roughly four times higher among former players than the average American male. The study also compared mortality risks from speed players (quarterbacks, running backs, fullbacks, wide receivers, tight ends, linebackers, cornerbacks, and safeties) and nonspeed players (offensive and defensive linemen), with findings indicating that a greater |
1753_25 | number of deaths were attributable to neurodegenerative disorders in speed players than nonspeed players. This may be due to the increased momentum of collisions from speed players. |
1753_26 | Outside of neurodegenerative disorders, physical injuries sustained during a career can have an adverse effect on post-career life. A 1990 survey conducted jointly between the NFLPA and Ball State University found that 65% of surveyed players had suffered a major injury (defined as one that caused them to miss at least eight games): among players that played before 1959 this number was 42%, but it jumps to 72% among those who played in the 1980s. Additionally, roughly 50% of players who had played in the 1970s and 1980s reported that they retired due to injury, compared to only 32% among those who played prior to 1959. Two-thirds of players reported that injuries they had sustained limited their ability to engage in recreational activity and sports in retirement, while half said their injuries decreased their ability to perform manual labor. A follow-up survey in 1994 found that 47% of recipients reported having arthritis. These reports have been attributed to several factors, |
1753_27 | including the increase in the use of artificial turf as well as the increasing size and speed of players. Dr. James Andrews, a noted orthopedic surgeon, said that "athletes are bigger, stronger and running faster, and they're tearing up knees from cutting, changing direction on a dime". Andrews also noted the increase in the number of non-contact anterior cruciate ligament (ACL) injuries, which he attributed to the size of modern players. |
1753_28 | Prevention |
1753_29 | Injuries have always been a part of football, and various methods have been used historically and in modern times to prevent or minimize them. One method that has been used to prevent injuries is changing the rules of the sport. An early example of this was the elimination of mass formations like the flying wedge in the early 1900s, due to the large number of severe injuries the formations caused. Smaller wedges consisting of three, four, or five players were frequently used on kickoff returns before wedges were limited to two or fewer players in 2009 by the NFL; a similar rule was adopted by the NCAA a year later. The sharp decrease in the number of catastrophic cervical spine injuries since the mid-1970s has been partially credited to rule changes that modified tackling and blocking techniques. With the increasing awareness of the long-term effects of concussions, the NFL has passed rules prohibiting the targeting of "defenseless" players over-the-shoulder, requiring plays to be |
1753_30 | blown dead when the runner loses his helmet, and placing more stringent limits to the ability of players who have sustained a concussion to return to play. |
1753_31 | Similarly, modern equipment was developed to reduce injuries. The football helmet, although a scapegoat for concussions, serves as effective protection against more dangerous injuries like skull fractures. The modern helmet traces its roots back to the leather helmets used by football players in the early 1900s to protect themselves from head injuries. Helmets later evolved to be made of hard plastic, and a facemask was added to protect players from sustaining facial injuries. Many players also wear mouthguards to prevent injuries to their teeth and tongues; at some levels, such as the NCAA, the use of a mouthguard is mandatory. Football players wear a number of pads to protect themselves – shoulder pads are the most important pads, protecting the shoulder and sternum, but thigh pads, hip pads, tail pads, and knee pads are also used. Many quarterbacks wear flak jackets to protect their ribcage. Cleats come in a number of lengths, with players choosing which cleat to use based on the |
1753_32 | playing field – players prefer a shorter cleat when playing on artificial turf to prevent their feet from digging into the ground and risking injury, while longer cleats are generally used on fields that are wet or slippery to provide better traction. Athletic cups are not typically used at the professional level because athletic cups tend to make it harder to move and there is an unwritten code among players not to target the groin area. Additionally, studies have shown that proper conditioning techniques, fitness routines and exercise routines, as well as high-quality equipment and coaching, can reduce the risk of injury among players. |
1753_33 | See also
Concussions in American football
List of sportspeople who died during their careers
References
American football controversies
Health in the United States
Sports injuries |
1754_0 | The Winged Victory of Samothrace, or the Nike of Samothrace, is a votive monument originally found on the island of Samothrace, north of the Aegean Sea. It is a masterpiece of Greek sculpture from the Hellenistic era, dating from the beginning of the 2nd century BCE. It is composed of a statue representing the goddess Niké (Victory), whose head and arms are missing, and its base in the shape of a ship's bow.
The total height of the monument is 5.57 meters including the socle; the statue alone measures 2.75 meters. The sculpture is one of a small number of major Hellenistic statues surviving in the original, rather than Roman copies. Winged Victory has been exhibited at the Louvre Museum in Paris, at the top of the main staircase, since 1884.
Discovery and restorations
In the 19th century |
1754_1 | In 1863, Charles Champoiseau (1830-1909), acting in charge of the Consulate of France in Adrianopolis (now Edirne in Turkey), undertook from March 6 to May 7 the exploration of the ruins of the sanctuary of the Great Gods on the island of Samothrace. On April 13, 1863, he discovered part of the bust and the body of a large female statue in white marble accompanied by numerous fragments of drapery and feathers. He recognised this as the goddess Niké, Victory, traditionally represented in Greek antiquity as a winged woman. In the same place was a jumble about fifteen large grey marble blocks whose form or function was unclear: he concluded it was a funerary monument. He decided to send the statue and fragments to the Louvre Museum, and to leave the large blocks of grey marble on site. Departing Samothrace at the beginning of May 1863, the statue arrived in Toulon at the end of August and in Paris on May 11, 1864. |
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