In addition, subglottal pressure may increase during lip trills, and result in the generation greater vocal fold vibration. [24] Surgery [ edit ] After 9 months of observation, should the paralysis not resolve and the patient be dissatisfied with the outcomes of voice therapy, the next option is temporary injection medialization. [25] In this procedure, a variety of materials can be injected into the body of the vocal fold in order to bring it closer to the midline of the glottis. [25] Materials such as Teflon, autologous fat, collagens acellular dermis, fascia, hydroxyapatite and hyaluronates are available to be used in the procedure. [26] The choice of substance is dependent on several factors, taking into consideration the specific condition and preference of the patient as well as the clinical practice of the surgeon. [27] The materials serve the purpose of filling up the vocal folds and increasing their volume. [26] This allows the paralyzed vocal fold to make contact with the alternate fold, in order to more efficiently produce phonation. [25] While injection augmentation has been long considered best practice, neither technique nor materials used have been standardized across clinicians. [25] With this, results prove to be both safe and effective, but variable in their duration, lasting anywhere from 2 to 12 months. [23] For patients with significant paralysis at 12 months post-onset, medialization thyroplasty may be suggested. [25] This surgical procedure introduces a shim between the inner wall of the larynx and the soft tissue supporting the vocal fold. [28] As a result, the paralyzed vocal fold is supported in a position closer to the midline of the glottis, and retains its ability to vibrate and phonate efficiently. [28] In addition to medialization thyroplasty , arytenoid adduction can be performed to improve phonation results. [26] This medical procedure consists of pulling the vocal processes of the arytenoid medially while monitoring the voicing quality being produced by the patient. [26] When the best phonation appears to be achieved, the vocal processes are then maintained in place by a thread. [26] A further surgical intervention used to mitigate vocal fold paresis is laryngeal reinnervation. [29] This procedure restores nerve supply to the larynx and can be accomplished according to different techniques. [29] [30] [31] Depending on the specific condition (i.e. bilateral versus unilateral vocal fold paralysis), these techniques include reconnecting parts of the RLN, supplying the laryngeal muscles with a donor nerve like the ansa cervicalis , or connecting the RLN to a donor nerve. [29] [30] [31] Post-surgical outcomes [ edit ] In many cases, the surgical treatment options described above (temporary injection medialization, medialization thyroplasty, arytenoid adduction, and laryngeal reinnervation) have led to favourable outcomes as measured perceptually, acoustically, by laryngoscope, or via quality of life measures. [32] However, none of these surgical interventions has been shown to be significantly better than the others. [32] Voice therapy after surgery [ edit ] It is generally recommended that voice therapy start 1 to 2 months after surgery, when swelling has subsided. ... Journal of the Saudi Heart Association . 28 (4): 266–269. doi : 10.1016/j.jsha.2016.02.006 .

For example, the city of Eagle River, Vilas County, Wisconsin, which has an incidence rate of 101.3 per 100,000; the county as a whole has been shown in two successive studies to have an incidence of ca. 40 cases per 100,000. [26] An incidence of 277 per 100,000 was roughly calculated based on 9 cases seen in a Wisconsin aboriginal reservation during a time in which extensive excavation was done for new housing construction. [27] The new case rates are greater in northern states such as Wisconsin , where from 1986 to 1995 there were 1.4 cases per 100,000 people. [28] The study of outbreaks as well as trends in individual cases of blastomycosis has clarified a number of important matters. ... MMWR Morb. Mortal. Wkly. Rep . 45 (28): 601–3. PMID 8676851 . ^ DiSalvo, A.F. (1992). ... Seminars in Respiratory Infections . 12 (3): 219–28. PMID 9313293 . ^ Proctor, ME; Klein, BS; Jones, JM; Davis, JP (2002).

The UK's official assessment of the incident was supported by 28 other countries which responded similarly. ... At 14:20 they dined at Zizzi on Castle Street, leaving at 15:35. [28] At 16:15 an emergency services call reported that a man and woman, later identified as Sergei and Yulia, had been found unconscious on a public bench in the centre of Salisbury by the passing Chief Nursing Officer for the British Army and her daughter. ... The vehicles included TPz Fuchs operated by Falcon Squadron from the Royal Tank Regiment . [64] On 11 March, the UK government advised those present at either The Mill pub or the Zizzi restaurant in Salisbury on 4 and 5 March to wash or wipe their possessions, emphasising that the risk to the general public was low. [65] [66] Several days later, on 12 March, Prime Minister Theresa May said the agent had been identified as one of the Novichok family of agents , believed to have been developed in the 1980s by the Soviet Union . [67] [68] According to the Russian ambassador to the UK, Alexander Yakovenko , the British authorities identified the agent as A-234 , [69] derived from an earlier version known as A-232. [70] By 14 March, the investigation was focused on Skripal's home and car, a bench where the two fell unconscious, a restaurant in which they dined and a pub where they had drinks. [71] A recovery vehicle was removed by the military from Gillingham in Dorset on 14 March, in connection with the poisoning. [72] [73] Subsequently, there was speculation within the British media that the nerve agent had been planted in one of the personal items in Yulia Skripal's suitcase before she left Moscow for London, [74] and in US media that it had been planted in their car. [75] [76] Ahmet Üzümcü , Director-General of the Organisation for the Prohibition of Chemical Weapons (OPCW), said on 20 March that it will take "another two to three weeks to finalise the analysis" of samples taken from the poisoning of Skripal. [77] On 22 March, the Court of Protection gave permission for new blood samples to be obtained from Yulia and Sergei Skripal for use by the OPCW. [78] [79] By 28 March, the police investigation concluded that the Skripals were poisoned at Sergei's home, with the highest concentration being found on the handle of his front door. [80] On 12 April the OPCW confirmed the UK's analysis of the type of nerve agent and reported it was of a "high purity", stating that the "name and structure of the identified toxic chemical are contained in the full classified report of the Secretariat, available to States Parties." [81] [82] [83] A declassified letter from the UK's national security adviser , Sir Mark Sedwill , to NATO Secretary General Jens Stoltenberg , stated Russian military intelligence hacked Yulia Skripal's email account since at least 2013 and tested methods for delivering nerve agents including on door handles. [84] The Department for Environment confirmed the nerve agent was delivered "in a liquid form". ... Bulgaria, Luxembourg, Malta, Portugal, Slovakia, Slovenia and the European Union itself have not expelled any Russian diplomats but have recalled their ambassadors from Russia for consultations. [249] [250] [251] [252] [253] [254] Furthermore, Iceland decided to diplomatically boycott the 2018 FIFA World Cup held in Russia. [255] Country or organisation Diplomats expelled Date announced Response by Russia Date announced Albania 2 26 March 2 diplomats expelled by Russia. [256] 30 March Australia 2 27 March 2 diplomats expelled by Russia. [256] 30 March Belgium 1 27 March 1 diplomat expelled (the economic attaché ). [257] 4 April Canada 4 [a] [258] 26 March 4 diplomats expelled by Russia. [256] 30 March Croatia 1 26 March 1 diplomat based in Zagreb declared PNG . [259] 30 March Czech Republic 3 26 March 3 diplomats expelled by Russia. [256] 30 March Denmark 2 26 March 2 diplomats expelled by Russia. [256] 30 March Estonia 1 26 March 1 diplomat expelled by Russia. [256] 30 March Finland 1 26 March 1 diplomat expelled by Russia. [256] 30 March France 4 26 March 4 diplomats expelled by Russia. [256] 30 March Germany 4 26 March 4 diplomats expelled by Russia. [256] 30 March Georgia 1 [260] 30 March 1 diplomat expelled by Russia. [261] 13 April Hungary 1 26 March 1 diplomat expelled by Russia. [262] 4 April Ireland 1 27 March 1 diplomat expelled by Russia. [256] 30 March Italy 2 26 March 2 diplomats expelled by Russia. [256] 30 March Latvia 1 26 March 1 diplomat expelled by Russia. [256] 30 March Lithuania 3 26 March 3 diplomats expelled by Russia. [256] 30 March Macedonia 1 26 March 1 diplomat expelled by Russia. [256] 30 March Moldova 3 27 March 3 diplomats expelled by Russia. [256] 30 March Montenegro 1 [263] 28 March 1 diplomat expelled by Russia. [264] 2 April NATO 7 [b] [243] 27 March Netherlands 2 26 March 2 diplomats expelled by Russia. [256] 30 March Norway 1 26 March 1 diplomat expelled by Russia. [256] 30 March Poland 4 26 March 4 diplomats expelled by Russia. [256] 30 March Romania 1 26 March 1 diplomat expelled by Russia. [256] 30 March Spain 2 26 March 2 diplomats expelled by Russia. [256] 30 March Sweden 1 26 March 1 diplomat expelled by Russia. [256] 30 March Ukraine 13 26 March 13 diplomats expelled by Russia. [256] 30 March United Kingdom 23 14 March 23 UK diplomats expelled by Russia.

Endogenous factors involve fetal inability to adequately move, whereas exogenous factors refer to insufficient intrauterine space available for fetal movements. [15] Incidence of breech presentation among diseases and medical conditions with the incidence of breech presentation higher than occurs in the general population, shows that the probability of breech presentation is between 4% and 50%. [16] [17] [18] These data are related to: single series of medical entities collections of series for some particular medical entity data obtained from repeated observations under the same conditions series of two concomitant medical conditions Rates in various medical conditions [ edit ] Fetal entities: First twin 17–30%; Second twin 28–39%; Stillborn 26%; Prader–Willi syndrome 50%, Werdnig–Hoffman syndrome 10%; Smith–Lemli–Opitz syndrome 40%; Fetal alcohol syndrome 40%; Potter anomaly 36%; Zellweger syndrome 27%; Myotonic dystrophy 21%, 13 trisomy syndrome 12%; 18 trisomy syndrome 43%; 21 trisomy syndrome 5%; de Lange syndrome 10%; Anencephalus 6–18%, Spina bifida 20–30%; Congenital hydrocephalus 24–37%; Osteogenesis imperfecta 33.3%; Amyoplasia 33.3%; Achondrogenesis 33.3%; Amelia 50%; Craniosynostosis 8%; Sacral agenesis 30.4%; Arthrogriposis multiplex congenita 33.3; Congenital dislocation of the hip 33.3%; Hereditary sensory neuropathy type III 25%; Centronuclear myopathy 16.7%; Multiple pituitary hormone deficiency 50%; Isolated pituitary hormone deficiency 20%; Ectopic posterior pituitary gland 33.3%; Congenital bilateral perisilvian syndrome 33.3; Symmetric fetal growth restriction 40%; Asymmetric fetal growth restriction 40%; Nonimmune hydrops fetalis 15%; Atresia ani 18.2%; Microcephalus 15.4%; Omphalocele 12.5%; Prematurity 40% Placental and amniotic fluid entities: Amniotic sheet perpendicular to the placenta 50%; cornual–fundal implantation of the placenta 30%; Placenta previa 12.5%; Oligohydramnios 17%; Polyhydramnios 15.8% Maternal entities: Uterus arcuatus 22.6%; Uterus unicornuatus 33.3%; Uterus bicornuatus 34.8%; Uterus didelphys 30–41%; Uterus septus 45.8%; Leiomyoma uteri 9–20%; Spinal cord injury 10%; Carriers of Duchenne muscular dystrophy 17% Combination of two medical entities: First twin in uterus with two bodies 14.29%; Second twin in uterus with two bodies 18.52%. [18] Also, women with previous Caesarean deliveries have a risk of breech presentation at term twice that of women with previous vaginal deliveries. [19] The highest possible probability of breech presentation of 50% indicates that breech presentation is a consequence of random filling of the intrauterine space, with the same probability of breech and cephalic presentation in a longitudinally elongated uterus. [17] Types [ edit ] Types of breech depend on how the baby's legs are lying. [14] A frank breech (otherwise known as an extended breech) is where the baby's legs are up next to its abdomen, with its knees straight and its feet next to its ears. ... However, there is not enough research to show this and a quick delivery might cause more harm to the baby than a conservative approach to the birth. [28] Injury to the brain and skull may occur due to the rapid passage of the baby's head through the mother's pelvis . ... The World Health Organisation recommends that women should have a planned cesarean section only if an ECV has been tried and did not work. [4] Women who have an ECV when they are 36–40 weeks pregnant are more likely to have a vaginal delivery and less likely to have a cesarean section than those who do not have an ECV. [28] Turning the baby before this time makes a head first birth more likely but ECV before the due date can increase the risk of early or premature birth which can cause problems to the baby. [3] There are treatments that can be used which might affect the success of an ECV.

Malaria can also lead to seizures which may precede going into a comatose state. [28] In regions of high transmission, such as Africa, women experiencing PAM may exhibit normal symptoms of malaria, but may also be asymptomatic or present with more mild symptoms, including a lack of the characteristic fever. ... Centers for Disease Control and Prevention. 2019-01-28. ^ Perlmann P, Troye-Blomberg M (2000). ... Retrieved 2020-08-02 . ^ Worldwide Antimalarial Resistance Network (WWARN) (2016-01-28). "Malaria in Pregnancy Consortium" .

Its current spectrum is as following: Seropositive Devic's disease, according to the diagnostic criteria described above Limited forms of Devic's disease, such as single or recurrent events of longitudinally extensive myelitis , and bilateral simultaneous or recurrent optic neuritis Asian optic-spinal MS - this variant can present brain lesions like MS. [22] Longitudinally extensive myelitis or optic neuritis associated with systemic autoimmune disease Optic neuritis or myelitis associated with lesions in specific brain areas such as the hypothalamus , periventricular nucleus , and brainstem [23] Some cases of tumefactive multiple sclerosis [24] Anti-MOG spectrum [ edit ] See Anti-MOG associated encephalomyelitis Anti-MOG associated spectrum , often clinically presented as an anti- MOG autoimmune encephalomyelitis , [25] [26] but can also appear as negative NMO or atypical multiple sclerosis. [27] The presence of anti-MOG autoantibodies has been associated with the following conditions [28] Some cases of aquaporin-4-seronegative neuromyelitis optica: NMO derived from an antiMOG associated encephalomyelitis , [29] Some cases of acute disseminated encephalomyelitis, specially the recurrent ones (MDEM) [30] Some cases of McDonalds-positive multiple sclerosis [28] [31] [27] [32] isolated optic neuritis or transverse myelitis [28] Recurrent optic neuritis. ... Journal of Neuroimmunology . 180 (1–2): 17–28. doi : 10.1016/j.jneuroim.2006.07.006 .

In the case of “a child capable of being born alive” (usually taken to mean after 28 weeks of pregnancy), a termination may be subject to a separate crime of child destruction in some states and territories. ... Police believed graffiti saying "baby killers" on the building was related to the attack, however, the medical clinic did not actually offer abortion services. [25] [26] Since at least the 1990s, tactics used by anti-abortion campaigners outside abortion clinics included "verbal abuse, threats, impeding entry to clinics, displaying violent imagery and acts of 'disturbing theater' such as pushing a blood-splattered doll in a pram." [27] In response, states and territories began creating "safe access zones", which prevent protesting about abortion within a proscribed area surrounding a clinic. [27] Tasmania was the first state to do so in 2013; [28] as of November 2020, only Western Australia did not have such laws, though the state did have a bill pending to introduce them. [29] In April 2019, the High Court of Australia upheld these laws after they were challenged by two people arrested for violating them. ... Safe access zones of 150 metres provided around abortion clinics effective since 1 January 2021. [67] [68] Legislation in 1969 legalised abortion when necessary to protect the life or physical or mental health of the woman—taking into account the current and reasonably foreseeable future—or in cases when the child was likely to be born with serious handicaps. [69] Abortions must be performed before a time limit of 28 weeks of pregnancy. Abortions must be performed in a hospital and be approved by two physicians, and are also subject to a residency requirement (patient must be a resident of South Australia for at least two months). ... ABC News . 21 February 2006. Archived from the original on 28 October 2016. ^ Nicola Berkovic (9 August 2010).

IVIG and plasmapheresis together can reduce or eliminate the need for an IUT. [28] Plasmapheresis – Plasmapheresis aims to decrease the maternal titer by direct plasma replacement and physical removal of antibody. [23] Plasmapheresis and IVIG together can even be used on women with previously hydropic fetuses and fetal losses. [29] [30] Mid- to late- pregnancy IUT – Intrauterine Transfusion (IUT) is done either by intraperitoneal transfusion (IPT) or intravenous transfusion (IVT). [31] IVT is preferred over IPT. [32] IUTs are only done until 35 weeks. After that, the risk of an IUT is greater than the risk from post birth transfusion. [33] Steroids – Steroids are sometimes given to the mother before IUTs and early delivery to mature the fetal lungs. [33] [34] Phenobarbital – Phenobarbital is sometimes given to the mother to help mature the fetal liver and reduce hyperbilirubinemia. [34] [35] Early Delivery – Delivery can occur anytime after the age of viability. [32] Emergency delivery due to failed IUT is possible, along with induction of labor at 35–38 weeks. [33] [36] Rhesus-negative mothers who are pregnant with a rhesus-positive infant are offered Rho(D) immune globulin (RhIG, or RhoGam) at 28 weeks during pregnancy, at 34 weeks, and within 48 hours after delivery to prevent sensitization to the D antigen. ... Ultrasound in Obstetrics & Gynecology . 28 (6): 814–20. doi : 10.1002/uog.2837 .

The treatment options available for VPI include prosthesis and surgery. [23] [24] [26] [27] [28] Difficulties acquiring vocabulary and formulating spoken language ( expressive language deficits) at the onset of language development are also part of the speech and language profile associated with the 22q11.2 deletion. ... Receptive language , which is the ability to comprehend, retain, or process spoken language, can also be impaired, although not usually with the same severity as expressive language impairments. [24] [27] [28] [29] Articulation errors are commonly present in children with DiGeorge syndrome. ... NORD (National Organization for Rare Disorders) . 2017. Archived from the original on 28 January 2017 . Retrieved 10 July 2017 . ^ Burn J, Takao A, Wilson D, Cross I, Momma K, Wadey R, Scambler P, Goodship J (October 1993).

., Lyme is most common in the New England and Mid-Atlantic states and parts of Wisconsin and Minnesota . [25] The first sign of about 80% of Lyme infections, typically one or two weeks after a tick bite, is usually an expanding rash that may be accompanied by headaches, body aches, fatigue, or fever. [26] In up to 10–15% of Lyme infections, facial palsy appears several weeks later, and may be the first sign of infection that is noticed, as the Lyme rash typically does not itch and is not painful. [27] [28] The likelihood that the facial palsy is caused by Lyme disease should be estimated, based on recent history of outdoor activities in likely tick habitats during warmer months, recent history of rash or symptoms such as headache and fever, and whether the palsy affects both sides of the face (much more common in Lyme than in Bell's palsy). ... "Herpes simplex virus type 1 reactivation and antiviral therapy in patients with acute peripheral facial palsy". Auris, Nasus, Larynx . 28 Suppl (Suppl): S13–17. doi : 10.1016/S0385-8146(00)00105-X . ... The American Journal of Medicine . 128 (6): 617–28. doi : 10.1016/j.amjmed.2014.11.033 .

Some of these include keeping the feet dry, clipping toenails short; using a separate nail clipper for infected toenails; using socks made from well-ventilated cotton or synthetic moisture wicking materials (to soak moisture away from the skin to help keep it dry); avoiding tight-fitting footwear, changing socks frequently; and wearing sandals while walking through communal areas such as gym showers and locker rooms. [8] [13] [28] According to the Centers for Disease Control and Prevention , "Nails should be clipped short and kept clean. ... CS1 maint: extra text: authors list ( link ) ^ a b c d e The Merck Manual Professional Edition tinea pedis page Archived 28 January 2015 at the Wayback Machine . ... Archived from the original on 9 November 2013. ^ National Health Service's webpage on Athlete's Foot causes Archived 14 January 2015 at the Wayback Machine ^ a b Mayo Clinic website, Athlete's Foot Risk Factors Archived 7 February 2015 at the Wayback Machine ^ The Merck Manual Professional Edition. Tinea Pedis Archived 28 January 2015 at the Wayback Machine ^ del Palacio, Amalia; Margarita Garau; Alba Gonzalez-Escalada & Mª Teresa Calvo.

It is also normal within Qatari society to be obese. [12] Saudi Arabia [ edit ] Main article: Obesity in Saudi Arabia Across the whole population from 1995–2000, 36.9% were overweight and 35.6% were obese. [9] Rates were high amongst children aged 5–17, as 16.7% of boys and 19.4% of girls were overweight. [12] By 2006, 52% of men, 66% of women, 18% of teenagers, and 15% of preschoolers were overweight or obese. [28] In 2008, 17.99% of deaths were caused by cardiovascular disease. [29] During this year, 95% of the 424,968 total appointments to diabetics clinics were made for Saudi citizens. 55% of these diabetic citizens were women and 44% were men. [29] The latest national prevalence for childhood obesity (ages 5 to 18) in Saudi Arabia reported: 23.1% were overweight, 9.3% were obese and 2% were severely obese (2%) (El-Mouzan et al., 2010). [30] Part of the reason for the high rate of overweight and obesity within the population are urban residents that consume hypercaloric foods while maintaining a sedentary lifestyle. ... In schools, physical activity for girls is avoided because some fear that changing clothes outside of the home would cause girls to lose their shyness, an admirable moral quality. [28] United Arab Emirates [ edit ] In 1999, 24.8% of boys and 89.2% of girls age 4–18 were overweight. [12] This number increased to 25% in 2008. ... Listeners could also receive medical information via fax from the program. [28] United Arab Emirates [ edit ] The United Arab Emirates has launched an intense campaign to address the high rates of obesity. ... Archived from the original on 2014-04-02 . Retrieved 2010-10-28 . ^ a b c d Mokhtar, Najat; et al. (2001).

Birds were first artificially infected with rabies in 1884; however, infected birds are largely, if not wholly, asymptomatic, and recover. [26] Other bird species have been known to develop rabies antibodies , a sign of infection, after feeding on rabies-infected mammals. [27] [28] The virus has also adapted to grow in cells of cold-blooded vertebrates. [29] [30] Most animals can be infected by the virus and can transmit the disease to humans. ... Archived from the original on 1 April 2014 . Retrieved 28 February 2014 . ^ "Rabies - Symptoms and causes" . ... Archived from the original on 4 December 2014 . Retrieved 28 November 2014 . ^ a b c d e f g Giesen A, Gniel D, Malerczyk C (March 2015). "30 Years of rabies vaccination with Rabipur: a summary of clinical data and global experience" . ... Retrieved 23 May 2018 . ^ "Rabies: Differential Diagnoses & Workup" . eMedicine Infectious Diseases . 3 October 2008. Archived from the original on 28 November 2010 . Retrieved 30 January 2010 . ^ Taylor DH, Straw BE, Zimmerman JL, D'Allaire S (2006). ... ISBN 9780080919027 . Archived from the original on 28 April 2016 . Retrieved 8 January 2016 . ^ The Natural History of Rabies Archived 2 March 2016 at the Wayback Machine The first major epizootic in North America was reported in 1768, continuing until 1771 when foxes and dogs carried the disease to swine and domestic animals.

Control programs aimed at discouraging the consumption of raw and undercooked food have been successful at reducing the incidence of cholangiocarcinoma in some countries. [21] People with chronic liver disease, whether in the form of viral hepatitis (e.g. hepatitis B or hepatitis C ), [22] [23] [24] alcoholic liver disease , or cirrhosis of the liver due to other causes, are at significantly increased risk of cholangiocarcinoma. [25] [26] HIV infection was also identified in one study as a potential risk factor for cholangiocarcinoma, although it was unclear whether HIV itself or other correlated and confounding factors (e.g. hepatitis C infection) were responsible for the association. [25] Infection with the bacteria Helicobacter bilis and Helicobacter hepaticus species can cause biliary cancer. [27] Congenital liver abnormalities, such as Caroli's syndrome (a specific type of five recognized choledochal cysts ), have been associated with an approximately 15% lifetime risk of developing cholangiocarcinoma. [28] [29] The rare inherited disorders Lynch syndrome II and biliary papillomatosis have also been found to be associated with cholangiocarcinoma. [30] [31] The presence of gallstones ( cholelithiasis ) is not clearly associated with cholangiocarcinoma. ... "Risk of liver and other types of cancer in patients with cirrhosis: a nationwide cohort study in Denmark". Hepatology . 28 (4): 921–5. doi : 10.1002/hep.510280404 . ... "Thorotrast-induced cholangiocarcinoma: case report". Abdominal Imaging . 28 (1): 72–4. doi : 10.1007/s00261-001-0148-y . ... International Journal of Radiation Oncology, Biology, Physics . 28 (4): 945–51. doi : 10.1016/0360-3016(94)90115-5 .

A review of cocaine cardiovascular toxicity found benzodiazepines may not always reliably lower heart rate and blood pressure. [26] Nitric-oxide mediated vasodilators , such as nitroglycerin and nitroprusside , are effective at lowering blood pressure and reversing coronary arterial vasoconstriction, but not heart rate. [26] Nitroglycerin is useful for cocaine-induced chest pain, but the possibility of reflex tachycardia must be considered. [27] Alpha-blockers such as phentolamine have been recommended [25] and may be used to treat cocaine-induced hypertension and coronary arterial vasoconstriction, but these agents do not reduce heart rate. [26] [28] Furthermore, phentolamine is rarely used, not readily available in many emergency departments, and many present-day clinicians are unfamiliar with its use. ... "Cocaine intoxication". Critical Care Clinics . 28 (4): 517–526. doi : 10.1016/j.ccc.2012.07.003 . ... PMID 19401135 . ^ Hollander, Judd (December 28, 2011). "Update on Cocaine Myocardial Ischemia" .

In the late 19th and early 20th centuries, trachoma was the main reason for an immigrant coming through Ellis Island to be deported." [27] [28] In 1913, President Woodrow Wilson signed an act designating funds for the eradication of the disease. [29] [30] Immigrants who attempted to enter the U.S. through Ellis Island , New York, had to be checked for trachoma. [27] During this time, treatment for the disease was by topical application of copper sulfate. ... Australian Institute of Health and Welfare. 2008. Archived from the original on 28 October 2012 . Retrieved 11 April 2013 . ^ a b "Ghana eliminates trachoma, freeing millions from suffering and blindness" . ... "The Treatment of Trachoma with Sulfanilamide: A Report of 28 Cases" . Transactions of the American Ophthalmological Society . 37 : 395–403.

Supplementing folic acid during pregnancy reduces the prevalence of NTDs by not exposing this otherwise sub-clinical mutation to aggravating conditions. [27] Other potential causes can include folate antimetabolites (such as methotrexate ), mycotoxins in contaminated corn meal, arsenic , hyperthermia in early development, and radiation. [28] [29] [30] Maternal obesity has also been found to be a risk factor for NTDs. [31] Studies have shown that both maternal cigarette smoking and maternal exposure to secondhand smoke increased the risk for neural tube defects in offspring. [32] A mechanism by which maternal exposure to cigarette smoke could increase NTD risk in offspring is suggested by several studies that show an association between cigarette smoking and elevations of homocysteine levels. [ citation needed ] Cigarette smoke during pregnancy, including secondhand exposure, can increase the risk of neural tube defects. [33] All of the above may act by interference with some aspect of normal folic acid metabolism and folate linked methylation related cellular processes as there are multiple genes of this type associated with neural tube defects. [34] Other [ edit ] Folic acid supplementation reduces the prevalence of neural tube defects by approximately 70% of neural tube defects indicating that 30% are not folate-dependent and are due to some cause other than alterations of methylation patterns. [35] Multiple other genes related to neural tube defects exist which are candidates for folate insensitive neural tube defects. [34] There are also several syndromes such as Meckel syndrome , and Triploid Syndrome which are frequently accompanied by neural tube defects that are assumed to be unrelated to folate metabolism [36] Diagnosis [ edit ] Tests for neural tube defects include ultrasound examination and measurement of maternal serum alpha-fetoprotein ( MSAFP ). ... Other areas of research include tissue engineering and stem cell therapy but this research has not been used in humans. [48] Epidemiology [ edit ] Deaths from neural tube defects per million persons in 2012 0–0 1–1 2–3 4–6 7–10 11–15 16–20 21–28 29–69 Neural tube defects resulted in 71,000 deaths globally in 2010. [49] It is unclear how common the condition is in low income countries. [50] Prevalence rates of NTDs at birth used to be a reliable measure for the actual number of children affected by the diseases. [51] However, due to advances in technology and the ability to diagnose prenatally, the rates at birth are no longer reliable. [51] Measuring the number of cases at birth may be the most practical way, but the most accurate way would be to include stillbirths and live-births. [51] Most studies that calculate prevalence rates only include data from live-births and stillborn children and normally exclude the data from abortions and miscarriages. [51] Abortions are a huge contributing factor to the prevalence rates; one study found that in 1986 only a quarter of the pregnancies with an identified NTD were aborted, but that number had already doubled by 1999. [51] Through this data, it's clear that excluding data from abortions could greatly affect the prevalence rates. ... "Folic acid in pregnancy and fetal outcomes". J. Obstet. Gynaecol . 28 (1): 3–13. doi : 10.1080/01443610701814195 .

Viability is usually placed at about seven months (28 weeks, approx. 196 days) but may occur earlier, even at 24 weeks." ... Advancements in medical technology meant that a fetus might be considered viable, and thus have some basis of a right to life, at 22 or 23 weeks rather than at the 28 that was more common at the time Roe was decided. ... Des Moines Register . Retrieved 2020-03-28 . ^ Rodriguez, Barbara. "Governor's office says order suspending 'non-essential' surgery includes halting surgical abortions" . Des Moines Register . Retrieved 2020-03-28 . ^ News, U. S. "Kansas lawmakers pass sweeping anti-abortion legislation" . ... Retrieved February 7, 2019 . ^ MacIntyre, Krystal. " Mississippi abortion ban bill fails as legislators miss deadline for compromise ", Jurist News Archive (2006-03-28). Retrieved 2007-01-23. ^ Curry, Tom.

After cessation of drug use, there is a strong tendency to relapse." [6] Nicotine dependence leads to heavy smoking and causes severe withdrawal symptoms and relapse back to smoking. [6] Nicotine dependence develops over time as a person continues to use nicotine . [6] Teenagers do not have to be daily or long-term smokers to show withdrawal symptoms . [16] Relapse should not frustrate the nicotine user from trying to quit again. [13] A 2015 review found "Avoiding withdrawal symptoms is one of the causes of continued smoking or relapses during attempts at cessation, and the severity and duration of nicotine withdrawal symptoms predict relapse." [17] Symptoms of nicotine dependence include irritability, anger, impatience, and problems in concentrating. [18] Diagnosis [ edit ] There are different ways of measuring nicotine dependence. [3] The five common dependence assessment scales are the Fagerström Test for Nicotine Dependence , the Diagnostic and Statistical Manual of Mental Disorders , the Cigarette Dependence Scale, the Nicotine Dependence Syndrome Scale, and the Wisconsin Inventory of Smoking Dependence Motives. [3] The Fagerström Test for Nicotine Dependence focuses on measuring physical dependence which is defined "as a state produced by chronic drug administration, which is revealed by the occurrence of signs of physiological dysfunction when the drug is withdrawn; further, this dysfunction can be reversed by the administration of drug". [3] The long use of Fagerström Test for Nicotine Dependence is supported by the existence of significant preexisting research, and its conciseness. [3] The 4th edition of the American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorder (DSM-IV) had a nicotine dependence diagnosis which was defines as "...a cluster of cognitive, behavioral, and physiological symptoms..." [3] In the updated DSM-5 there is no nicotine dependence diagnosis, but rather Tobacco Use Disorder, which is defined as, "A problematic pattern of tobacco use leading to clinically significant impairment or distress, as manifested by at least 2 of the following [11 symptoms], occurring within a 12-month period." [19] The Cigarette Dependence Scale was developed "to index dependence outcomes and not dependence mechanisms". [3] The Nicotine Dependence Syndrome Scale, "a 19-item self-report measure, was developed as a multidimensional scale to assess nicotine dependence". [3] The Wisconsin Inventory of Smoking Dependence Motives "is a 68-item measure developed to assess dependence as a motivational state". [3] Mechanisms [ edit ] Traditional cigarettes are the most common delivery device for nicotine. [ citation needed ] However, electronic cigarettes are becoming more popular. [20] Nicotine can also be delivered via other tobacco products such as chewing tobacco, snus, pipe tobacco, hookah, all of which can produce nicotine dependence. [ citation needed ] Biomolecular [ edit ] Dopamine Pre-existing cognitive and mood disorders may influence the development and maintenance of nicotine dependence. [21] Nicotine is a parasympathomimetic stimulant [10] that binds to and activates nicotinic acetylcholine receptors in the brain, [11] which subsequently causes the release of dopamine and other neurotransmitters , such as norepinephrine , acetylcholine , serotonin , gamma-aminobutyric acid , glutamate , endorphins , [22] and several neuropeptides . [23] Repeated exposure to nicotine can cause an increase in the number of nicotinic receptors, which is believed to be a result of receptor desensitization and subsequent receptor upregulation . [22] This upregulation or increase in the number of nicotinic receptors significantly alters the functioning of the brain reward system . [24] With constant use of nicotine, tolerance occurs at least partially as a result of the development of new nicotinic acetylcholine receptors in the brain. [22] After several months of nicotine abstinence, the number of receptors go back to normal. [11] Nicotine also stimulates nicotinic acetylcholine receptors in the adrenal medulla , resulting in increased levels of adrenaline and beta-endorphin . [22] Its physiological effects stem from the stimulation of nicotinic acetylcholine receptors, which are located throughout the central and peripheral nervous systems . [25] Chronic nicotinic acetylcholine receptor activation from repeated nicotine exposure can induce strong effects on the brain, including changes in the brain's physiology, that result from the stimulation of regions of the brain associated with reward, pleasure, and anxiety. [26] These complex effects of nicotine on the brain are still not well understood. [26] When these receptors are not occupied by nicotine, they are believed to produce withdrawal symptoms. [27] These symptoms can include cravings for nicotine, anger, irritability, anxiety, depression, impatience, trouble sleeping, restlessness, hunger, weight gain, and difficulty concentrating. [28] Neuroplasticity within the brain's reward system occurs as a result of long-term nicotine use, leading to nicotine dependence. [1] There are genetic risk factors for developing dependence. [12] For instance, genetic markers for a specific type of nicotinic receptor (the α5-α3-β4 nicotine receptors) have been linked to increased risk for dependence. [12] [29] The most well-known hereditary influence related to nicotine dependence is a mutation at rs16969968 in the nicotinic acetylcholine receptor CHRNA5 , resulting in an amino acid alteration from aspartic acid to asparagine. [30] The single-nucleotide polymorphisms (SNPs) rs6474413 and rs10958726 in CHRNB3 are highly correlated with nicotine dependence. [31] Many other known variants within the CHRNB3–CHRNA6 nicotinic acetylcholine receptors are also correlated with nicotine dependence in certain ethnic groups. [31] There is a relationship between CHRNA5 - CHRNA3 - CHRNB4 nicotinic acetylcholine receptors and complete smoking cessation. [32] Increasing evidence indicates that the genetic variant CHRNA5 predicts the response to smoking cessation medicine. [32] Psychosocial [ edit ] In addition to the specific neurological changes in nicotinic receptors, there are other changes that occur as dependence develops. [ citation needed ] Through various conditioning mechanisms ( operant and cue/classical ), smoking comes to be associated with different mood and cognitive states as well as external contexts and cues. [24] Treatment [ edit ] There are treatments for nicotine dependence, although the majority of the evidence focuses on treatments for cigarette smokers rather than people who use other forms of tobacco (e.g., chew , snus , pipes , hookah , e-cigarettes). [ citation needed ] Evidence-based medicine can double or triple a smoker's chances of quitting successfully. [13] Medication [ edit ] There are eight major evidence-based medications for treating nicotine dependence: bupropion , cytisine (not approved for use in some countries, including the US), nicotine gum , nicotine inhaler , nicotine lozenge/mini-lozenge , nicotine nasal spray , nicotine patch , and varenicline . [33] These medications have been shown to significantly improve long-term (i.e., 6-months post-quit day) abstinence rates, especially when used in combination with psychosocial treatment. [13] The nicotine replacement treatments (i.e., patch, lozenge, gum) are dosed based on how dependent a smoker is—people who smoke more cigarettes or who smoke earlier in the morning use higher doses of nicotine replacement treatments. [ citation needed ] There is no consensus for remedies for tobacco use disorder among pregnant smokers who also use alcohol and stimulants. [4] Psychosocial [ edit ] Psychosocial interventions delivered in-person (individually or in a group) or over the phone (including mobile phone interventions) have been shown to effectively treat nicotine dependence. [33] These interventions focus on providing support for quitting and helping with smokers with problem-solving and developing healthy responses for coping with cravings, negative moods, and other situations that typically lead to relapse. [ citation needed ] The combination of pharmacotherapy and psychosocial interventions has been shown to be especially effective. [13] Epidemiology [ edit ] First-time nicotine users develop a dependence about 32% of the time. [34] There are approximately 976 million smokers in the world. [8] Estimates are that half of smokers (and one-third of former smokers) are dependent based on DSM criteria, regardless of age, gender or country of origin, but this could be higher if different definitions of dependence were used. [35] Recent data suggest that, in the United States, the rates of daily smoking and the number of cigarettes smoked per day are declining, suggesting a reduction in population-wide dependence among current smokers. [36] However, there are different groups of people who are more likely to smoke than the average population, such as those with low education or low socio-economic status and those with mental illness. [36] There is also evidence that among smokers, some subgroups may be more dependent than other groups. [ citation needed ] Men smoke at higher rates than do women and score higher on dependence indices; however, women may be less likely to be successful in quitting , suggesting that women may be more dependent by that criterion. [36] [37] There is an increased frequency of nicotine dependence in people with anxiety disorders. [9] 6% of smokers who want to quit smoking each year are successful at quitting. [7] Nicotine withdrawal is the main factor hindering smoking cessation. [38] A 2010 World Health Organization report states, "Greater nicotine dependence has been shown to be associated with lower motivation to quit, difficulty in trying to quit, and failure to quit, as well as with smoking the first cigarette earlier in the day and smoking more cigarettes per day." [39] E-cigarettes may result in starting nicotine dependence again. [40] Greater nicotine dependence may result from dual use of traditional cigarettes and e-cigarettes. [40] Like tobacco companies did in the last century, there is a possibility that e-cigarettes could result in a new form of dependency on nicotine across the world. [41] Concerns [ edit ] Play media Nicotine use and addiction. ... Current Topics in Behavioral Neurosciences. 28 . pp. 121–150. doi : 10.1007/7854_2015_5005 . ... Pediatric Allergy, Immunology, and Pulmonology . 28 (1): 2–6. doi : 10.1089/ped.2015.0490 .

As a result, different types of head restraints have been developed by various manufactures to protect their occupants from whiplash. [27] Below are definitions of different types of head restraints. [28] Head restraint — refers to a device designed to limit the rearward displacement of an adult occupant's head in relation to the torso in order to reduce the risk of injury to the cervical vertebrae in the event of a rear impact. ... B., Yoganandan, N., Pintar, A.F., and Rao D.R. (2006) ^ Medical Engineering And Physics, 28(6), 515-524. ^ Panjabi M.M.; Cholewicki J.; Nibu K.; Grauer N.J; Babat B.L.; Dvorack J. (1998). ... "Active intervention in patients with whiplash-associated disorders improves long-term prognosis: a randomized controlled clinical trial". Spine . 28 (22): 2491–8. doi : 10.1097/01.BRS.0000090822.96814.13 .