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Police immediately organized a task force to conduct an investigation. About 0:00 on April 12, 2013, after the police determined that Lin was a suspect and summoned him, Lin then confessed that he had put N -nitrosodimethylamine in dorm 421's water dispenser. ... From intimate roommate to poison, it's not just education that needs to rethink." [ citation needed ] References [ edit ] ^ a b "权威发布 - 中华人民共和国最高人民法院" . www.court.gov.cn . ... Archived from the original on 2015-01-25. ^ "最高法复核复旦投毒案被告人死刑判决" . Ifeng.com . 2015-05-27. Archived from the original on 2018-11-05. ^ " " 复旦投毒案"续：最高法已核准林森浩死刑" . ... Archived from the original on 2017-11-15. ^ 于艳彬. "复旦投毒案：最高法死刑复核法官接见凶手父亲_中国新闻_南方网" . news.southcn.com . Retrieved 2017-11-06 . ^ "复旦投毒案嫌犯被核准死刑 律师将向最高检抗诉_新闻_腾讯网" . news.qq.com (in Chinese) .
2001 Japan Airlines mid-air incident 日本航空機駿河湾上空ニアミス事故 Accident Date January 31, 2001 ( 2001-01-31 ) Summary Near miss , ATC error Site near Yaizu, Shizuoka , Japan Total fatalities 0 Total injuries 100 (All on Japan Airlines Flight 907) Total survivors 677 (all) First aircraft JA8904, the aircraft involved seen in 2004. ... Type McDonnell Douglas DC-10-40 Operator Japan Airlines Registration JA8546 [1] Flight origin Gimhae International Airport , Busan , South Korea Destination Narita International Airport , Tokyo , Japan Occupants 250 Passengers 237 Crew 13 Fatalities 0 Injuries 0 Survivors 250 (all) On January 31, 2001, Japan Airlines Flight 907, a Boeing 747-400 en route from Haneda Airport , Japan , to Naha Airport , Okinawa , narrowly avoided a mid-air collision with Japan Airlines Flight 958, a McDonnell Douglas DC-10-40 en route from Gimhae International Airport , South Korea , to Narita International Airport , Japan . The event became known in Japan as the Japan Airlines near miss incident above Suruga Bay ( 日本航空機駿河湾上空ニアミス事故 , Nihonkōkūki surugawan jōkū niamisu jiko ) . ... Aftermath [ edit ] JAL907 injury chart By 18:00 on February 1, eight Flight 907 passengers remained hospitalized, while 22 injured passengers had been released. ... External links [ edit ] Aircraft and Railway Accidents Investigation Commission Aircraft Accident Investigation Report ( Archive ) (in Japanese) Aircraft Accident Investigation Report ( Archive ) Ministry of Land, Infrastructure and Transport " 日本航空９０７便事故に係る書類送検に関する航空局長コメント ." May 7, 2003 (15th year of Heisei ). ( Archive ) " 日本航空９０７便事故に係る民事調停成立に関する 航空局長コメントについて ."
Sun Wei Statement . Retrieved April 19, 2013 . ^ "我比任何人都想将真凶绳之于法" . Southern Metropolis Daily . ... One of the original Usenet posts asking for help] Sun Wei's first statement on Tianya Club (in Chinese, "孙维的声明－－驳斥朱令铊中毒案件引发的谣言") , December 30, 2005, retrieved on April 19, 2013 Sun Wei's second statement on Tianya Club (in Chinese, "声明:要求重新侦查，为"窃听器"错误向网友和公安道歉") , January 13, 2006, retrieved on April 19, 2013 The whole story about the Poisoning of Zhu Ling (in Chinese, "朱令被投毒事件始末", PDF file)
Retired husband syndrome ( 主人在宅ストレス症候群 , Shujin Zaitaku Sutoresu Shoukougun , literally "One's Husband Being at Home Stress Syndrome") [1] ( RHS ) is a psychosomatic stress -related illness which has been estimated to occur in 60% of Japan 's older female population. [2] It is a condition where a woman begins to exhibit signs of physical illness and depression as their husband reaches, or approaches, retirement. [2] Contents 1 Common symptoms 2 Theorized reason for RHS 3 Research 4 References Common symptoms [ edit ] The following are some of the common symptoms of RHS: [2] Depression Skin rash Asthma Ulcers High blood pressure Theorized reason for RHS [ edit ] This syndrome was identified and coined by Nobuo Kurokawa [2] and first appeared in a presentation of his to the Japanese Society of Psychosomatic Medicine in 1991. [3] Kurokawa has theorized that RHS is a result of the fact that many of Japan's citizens who are reaching retirement age, 60, [2] are members of the Baby Boomer generation of Japan. ... They may also ask their husbands to stay on at work past retirement age. [2] Many wives do not tell their husbands what is happening [2] and this can worsen the stress as their husbands may not understand or even realize their wives are RHS sufferers. [2] [3] Research [ edit ] Marco Bertoni and Giorgio Brunello of the University of Padova published a discussion paper in July 2014 based on empirical research in Japan. [5] References [ edit ] ^ "Retired husband syndrome あるいは「主人在宅ストレス症候群」 [医学・科学関連]" (in Japanese).
Field was a type of a protective energy shield, dubbed a "holy area no one can intrude upon" ( 何人にも侵されざる聖なる領域 ) and made a being using it impervious to attacks. ... A Billion Wicked Thoughts: What the World's Largest Experiment Reveals About Human Desire (性欲の科学: なぜ男は「素人」に興奮し、女は「男同士」に萌えるのか) . p. 32 . Retrieved 2013-03-16 . ^ ネット語研究委員会, ed. (2009).
Taijin kyofusho Specialty Psychology Taijin kyofusho ( Japanese : 対人恐怖症 , TKS , for taijin kyofusho symptoms ) is a Japanese culture-specific syndrome . ... New York: Springer. ISBN 978-1-4419-5659-0 . [ page needed ] ^ Fritscher, L. (2013, April 01).
While diarrhea is common in people with SARS, the fecal–oral route does not appear to be a common mode of transmission. [9] The basic reproduction number of SARS-CoV, R 0 , ranges from 2 to 4 depending on different analyses. ... As a result of quarantine procedures, some of the post-SARS patients have been documented as suffering from post-traumatic stress disorder (PTSD) and major depressive disorder . [31] [32] Epidemiology [ edit ] Main article: 2002–2004 SARS outbreak SARS was a relatively rare disease; at the end of the epidemic in June 2003, the incidence was 8,422 cases with a case fatality rate (CFR) of 11%. [4] The case fatality rate (CFR) ranges from 0% to 50% depending on the age group of the patient. [9] Patients under 24 were least likely to die (less than 1%); those 65 and older were most likely to die (over 55%). [33] As with MERS and COVID-19 , SARS resulted in significantly more deaths of males than females. 2003 Probable cases of SARS – worldwide Probable cases of SARS by country or region, 1 November 2002 – 31 July 2003 [34] Country or region Cases Deaths Fatality (%) China [a] 5,327 349 6.6 Hong Kong 1,755 299 17.0 Taiwan [b] 346 73 [35] [36] 21.1 Canada 251 43 17.1 Singapore 238 33 13.9 Vietnam 63 5 7.9 United States 27 00 Philippines 14 2 14.3 Thailand 9 2 22.2 Germany 9 00 Mongolia 9 00 France 7 1 14.3 Australia 6 00 Malaysia 5 2 40.0 Sweden 5 00 United Kingdom 4 00 Italy 4 00 Brazil 3 00 India 3 00 South Korea 3 00 Indonesia 2 00 South Africa 1 1 100.0 Colombia 1 00 Kuwait 1 00 Ireland 1 00 Macao 1 00 New Zealand 1 00 Romania 1 00 Russia 1 00 Spain 1 00 Switzerland 1 00 Total excluding China [a] 2,769 454 16.4 Total (29 territories) 8,096 774 9.6 ^ a b Figures for China exclude Hong Kong and Macau, which are reported separately by the WHO . ^ After 11 July 2003, 325 Taiwanese cases were 'discarded'. ... For a more detailed news coverage in Chinese, see: "石正丽团队两年前已发现蝙蝠冠状病毒感染人现象" . The Beijing News [ 新京报 ]. 26 February 2020. ^ a b c Chan-Yeung M, Xu RH (November 2003). ... Retrieved 4 February 2020 . ^ "衛生署針對報載SARS死亡人數有極大差異乙事提出說明" (in Chinese). 台灣衛生福利部疾病管制署. 16 June 2003. ... Retrieved 19 February 2020 . ^ "十年前SARS流行 346人感染73死亡" (in Chinese). 公視. 24 April 2013.
A rare pulmonary disease induced by SARS-CoV coronavirus infection, with a reported incubation period varying from 2 to 7 days. Patients present flu-like symptoms, including fever, malaise, myalgia, headache, diarrhoea, and rigors. Dry, nonproductive, cough and dyspnea are frequently reported. Severe cases evolve rapidly, progressing to respiratory distress and failure, requiring intensive care. Mortality rate is 10%. The disease appeared in 2002 in southern China, subsequently spreading in 2003 to 26 countries. Reported human-to-human transmission occurred in Toronto (Canada), Hong Kong Special Administrative Region of China, Chinese Taipei, Singapore, and Hanoi (Viet Nam).
"Functional magnetic resonance imaging of brain of college students with internet addiction" 网络成瘾大学生脑功能性磁共振成像特点 [Functional magnetic resonance imaging of brain of college students with internet addiction] (PDF) .
A number sign (#) is used with this entry because of evidence that pachyonychia congenita-2 (PC2) is caused by heterozygous mutation in the KRT17 gene (148069) on chromosome 17q21. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
Pachyonychia congenita (PC) is a rare genodermatosis predominantly featuring painful palmoplantar keratoderma, thickened nails, cysts and whitish oral mucosa. Epidemiology The prevalence is not known but approximately 1000 patients have been registered to date worldwide. Clinical description PC presents clinically as a spectrum of conditions. PC onset is variable with most cases manifesting soon after birth, others becoming clinically apparent only in late childhood and rarely in adulthood. The first signs of the disease usually are thickened nails or neonatal teeth.
For a phenotypic description and a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Inheritance Chong-Hai and Rajagopalan (1977) suggested autosomal recessive inheritance of pachyonychia congenita in a 4-year-old Malaysian girl with first-cousin parents, although they recognized new dominant mutation as a possibility. See also Sivasundram et al. (1985). INHERITANCE - Autosomal recessive HEAD & NECK Mouth - No oral leukoplakia SKIN, NAILS, & HAIR Skin - Horny papules (face, leg, buttocks) - No palmoplantar hyperkeratosis - No hyperhidrosis Nails - Episodic inflammatory swelling of nail bed - Recurrent shedding of nails - Hard,thickened nails (pachyonychia) - Subungual hyperkeratosis MISCELLANEOUS - See also pachyonychia congenita, type 3 (PC1, 167200 ) ▲ Close
A number sign (#) is used with this entry because pachyonychia congenita-3 (PC3) is caused by heterozygous mutation in the keratin-6a gene (KRT6A; 148041) on chromosome 12q13. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
A number sign (#) is used with this entry because pachyonychia congenita-4 (PC4) is caused by heterozygous mutation in the KRT6B gene (148042) on chromosome 12q13. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
Pachyonychia congenita (PC) is a rare inherited condition that primarily affects the nails and skin. The fingernails and toenails may be thickened and abnormally shaped . Affected people can also develop painful calluses and blisters on the soles of their feet and less frequently on the palms of their hands ( palmoplantar keratoderma ). Additional features include white patches on the tongue and inside of the mouth (leukokeratosis); bumps around the elbows, knees, and waistline (follicular hyperkeratosis); and cysts of various types including steatocystoma. Features may vary among affected people depending on their specific mutation.
A number sign (#) is used with this entry because pachyonychia congenita-1 (PC1) is caused by heterozygous mutation in the keratin-16 gene (KRT16; 148067) on chromosome 17q21. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita. PC type 1, the Jadassohn-Lewandowsky type, shows oral leukokeratosis.
Most common are the person's conviction that he or she emits a foul odor from the skin, mouth, rectum or vagina." [5] In the fifth edition (DSM-5), ORS again does not appear as a distinct diagnosis, but it is mentioned in relation to taijin kyōfushō (対人恐怖症, "disorder of fear of personal interaction"). [12] The variants of taijin kyōfushō (shubo-kyofu "the phobia of a deformed body" and jikoshu-kyofu "fear of foul body odor") are listed under 300.3 (F42) "other specified obsessive compulsive and related disorders", [12] and is about someone's fear that his or her body, or its functions, is offensive to other people. [4] There are four subtypes of taijin kyōfushō. [13] 17% of these individuals suffer from "the phobia of having foul body odor", the subtype termed jikoshu-kyofu. [5] [13] Although taijin kyōfushō has been described as a culture-bound syndrome confined to east Asia (e.g. ... Cambridge: Cambridge University Press. pp. 334–353. ISBN 978-0-521-84922-7 . Archived from the original (PDF) on 2014-01-08. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az Begum, M; McKenna, PJ (Mar 2011). ... Incorporated. 2013. pp. 263–264, 837 . ISBN 978-0-89042-554-1 . ^ a b Sajatovic M, Loue S, eds. (2012-02-29). ... New York: Springer. ISBN 978-1-4419-5659-0 . ^ Robles, DT; Romm, S; Combs, H; Olson, J; Kirby, P (Jun 15, 2008).
The influential Tang physician and alchemist Sun Simiao 's c. 640 alchemical Taiqing zhenren dadan 太清真人大丹 (Great Purity Essentials of Elixir Manuals for Oral Transmission) recommends 14 elixir formulas he found successful, most of which seem poisonous, containing mercury and lead, if not arsenic, as ingredients (Needham et al. 1976: 133). ... For instance, the 8th-century Zhang zhenren jinshi lingsha lun 張真人金石靈沙論 (The Adept Zhang's Discourse on Metals, Minerals, and Cinnabar) emphasized the poisonous nature of gold, silver, lead, mercury, and arsenic, and described witnessing many cases of premature death brought about by consuming cinnabar.
On 11 July 2007, the AIDS Prevention and Control Act was renamed the HIV Infection Control and Patient Rights Protection Act ( Chinese : 人類免疫缺乏病毒傳染防治及感染者權益保障條例 ). [1] As of March 2016, there are 31,620 reported cases of Taiwanese testing positive, and 1,020 foreigners testing positive. [2] Until January 2015, the original HIV Infection Control and Patient Rights Protection Act required foreigners who tested positive to be deported, therefore most of the reported foreigners are no longer in Taiwan. ... The AIDS Prevention and Control Act was renamed the HIV Infection Control and Patient Rights Protection Act (人類免疫缺乏病毒傳染防治及感染者權益保障條例) on July 11, 2007, [1] and will be referred to as such hereafter.
Human African Trypanosomiasis (HAT), also called sleeping sickness, is a vector-borne parasitic disease caused by a protozoa of the Trypanosoma genus transmitted by the bite of a tsetse fly (genus Glossina ), that is found under its chronic form (average duration of 3 years) in western and central Africa (in case of the T. brucei gambiense sub-species), and under its acute form (lasting from few weeks to 6 months) in eastern and southern Africa (in case of the T. brucei rhodesiense sub-species). HAT comprises an initial hemo-lymphatic stage characterized by fever, weakness, musculoskeletal pain, anemia, and lymphadenopathy, along with dermatologic, cardiac and endocrine complications or hepatosplenomegaly, followed by a meningo-encephalitic stage characterized by neurologic involvement (sleep disturbances, psychiatric disorders, seizures) that progresses, in the absence of treatment, towards a fatal meningoencephalitis.
Glycogen storage disease type 0 (also known as GSD 0) is a condition caused by the body's inability to form a complex sugar called glycogen, which is a major source of stored energy in the body. GSD 0 has two types: in muscle GSD 0, glycogen formation in the muscles is impaired, and in liver GSD 0, glycogen formation in the liver is impaired. The signs and symptoms of muscle GSD 0 typically begin in early childhood. ... Because some people with muscle GSD 0 die from sudden cardiac arrest early in life before a diagnosis is made and many with liver GSD 0 have mild signs and symptoms, it is thought that GSD 0 may be underdiagnosed. Causes Mutations in the GYS1 gene cause muscle GSD 0, and mutations in the GYS2 gene cause liver GSD 0.
A number sign (#) is used with this entry because of evidence that liver glycogen storage disease-0 (GSD0A) is caused by homozygous or compound heterozygous mutation in the GYS2 gene (138571), which encodes glycogen synthase-2, on chromosome 12p12. ... Mapping Orho et al. (1998) established linkage of glycogen storage disease 0 to intragenic and flanking polymorphic markers of the GYS2 gene on chromosome 12p12.2. Molecular Genetics In affected members of 5 families with liver glycogen storage disease 0, Orho et al. (1998) identified homozygous or compound heterozygous mutations in the GYS2 gene (138571.0001-138571.0008) Inheritance - Autosomal recessive Neuro - Seizures Lab - Glycogen synthetase deficiency Metabolic - Neonatal hypoglycemia - Fasting hypoglycemia - Fasting hyperketonemia - Hyperglycemia and hyperlactatemia with feeding ▲ Close
Glycogen storage disease type 0, liver (liver GSD 0), a form of glycogen storage disease (GSD), is a rare abnormality of glycogen metabolism (how the body uses and stores glycogen, the storage form of glucose). Unlike other types of GSD, liver GSD 0 does not involve excessive or abnormal glycogen storage, and causes moderately decreased glycogen stores in the liver. ... This condition differs from another form of GSD 0 which chiefly affects the muscles and heart ( Glycogen storage disease type 0, muscle ) and is thought to be caused by mutations in the GYS1 gene.
A genetically inherited anomaly of glycogen metabolism and a form of glycogen storage disease (GSD) characterized by fasting hypoglycemia. This is not a glycogenosis, strictly speaking, as the enzyme deficiency decreases glycogen reserves. Epidemiology It is an extremely rare disease; about 20 cases have been reported in the literature so far. Clinical description It commonly appears in infancy or in early childhood. Patients present with morning fatigue and fasting hypoglycemia (without hepatomegaly) associated with hyperketonemia but without hyperalaninemia or hyperlactacidemia.
Glycogen storage disease type 0 Glycogen storage disease type 0 has defect in glycogen synthase Specialty Medical genetics Glycogen storage disease type 0 is a disease characterized by a deficiency in the glycogen synthase enzyme (GSY). ... Serum electrolytes calculate the anion gap to determine presence of metabolic acidosis ; typically, patients with glycogen-storage disease type 0 (GSD-0) have an anion gap in the reference range and no acidosis. ... In patients with glycogen-storage disease type 0, hyperlipidemia is absent or mild and proportional to the degree of fasting. ... In patients with glycogen-storage disease type 0, urine ketones findings are positive, and urine-reducing substance findings are negative. ... The identification of asymptomatic and oligosymptomatic siblings in several glycogen-storage disease type 0 families has suggested that glycogen-storage disease type 0 is underdiagnosed. [2] Mortality/Morbidity [ edit ] The major morbidity is a risk of fasting hypoglycemia, which can vary in severity and frequency.
Affluenza: How to Be Successful and Stay Sane . Vermilion . ISBN 978-0-09-190011-3 . ^ James, Oliver (2008). The Selfish Capitalist . Vermilion . ISBN 978-0-09-192381-5 . ^ James, Oliver (2007). ... London: Vermilion. p. 344 . ISBN 978-0-09-190010-6 . 1. The mean prevalence of emotional distress for the six English-speaking nations combined was 21.6%. ... (Archive is the same work, but on a different website) Further reading [ edit ] The Circle of Simplicity , Cecile Andrews, ISBN 0-06-092872-7 The Golden Ghetto: The Psychology of Affluence , Jessie H. O'Neill, ISBN 978-0-9678554-0-0 Voluntary Simplicity , Duane Elgin, ISBN 0-688-12119-5 Voluntary Simplicity , Daniel Doherty & Amitai Etzioni, ISBN 0-7425-2066-8 How Much Is Too Much?
Jaypee Brothers Publishers. 2007. pp. 347–. ISBN 978-81-8061-996-0 . ^ Leonard J. Deftos (1 January 1998). ... Rowman & Littlefield Publishers. pp. 73–. ISBN 978-0-7591-2332-8 . ^ Vasan; R.S. (1 January 1998). ... Biochemistry and Function of Sterols . CRC Press. pp. 26–27. ISBN 978-0-8493-7674-0 . ^ Michael Crocetti; Michael A. ... Lippincott Williams & Wilkins. pp. 564–. ISBN 978-0-7817-3770-8 . ^ W. Steven Pray (2006). ... Elsevier Health Sciences. pp. 1281–. ISBN 978-0-323-08678-3 . ^ Guy I. Benrubi (28 March 2012).
Neonatal Skin: Structure and Function . CRC Press. pp. 67–. ISBN 978-0-8247-0887-0 . ^ Mariagrazia Stracquadanio; Lilliana Ciotta (20 April 2015). ... A Woman Doctor's Guide to Skin Care: Essential Facts and Information on Keeping Skin Healthy . Hyperion. ISBN 978-0-7868-8100-0 . ^ Sarah Bekaert (2007). ... CUP Archive. pp. 321–. ISBN 978-0-521-22673-8 . ^ Raphael Rubin; David S. ... Lippincott Williams & Wilkins. pp. 816–. ISBN 978-0-7817-9516-6 . ^ Andrea Dunaif; R. ... Academic Press. 3 October 1994. pp. 1994–. ISBN 978-0-08-058373-0 . Further reading [ edit ] Shukla, G.
