Many more couples, however, experience involuntary childlessness for at least one year: estimates range from 12% to 28%. [4] Male infertility is responsible for 20–30% of infertility cases, while 20–35% are due to female infertility , and 25–40% are due to combined problems in both parts. [2] [5] In 10–20% of cases, no cause is found. [5] The most common cause of female infertility is ovulatory problems, which generally manifest themselves by sparse or absent menstrual periods. [6] The most frequent cause of infertility today in occidental population is the delay of maternity, because the quality of oocytes decreases dramatically with age, especially after 35 years. ... Affected individuals displayed more severe forms of infertility such as azoospermia and severe oligozoospermia . [27] Other causes [ edit ] Factors that can cause male as well as female infertility are: DNA damage DNA damage reduces fertility in female ovocytes, as caused by smoking, [28] other xenobiotic DNA damaging agents (such as radiation or chemotherapy) [29] or accumulation of the oxidative DNA damage 8-hydroxy-deoxyguanosine [30] DNA damage reduces fertility in male sperm, as caused by oxidative DNA damage, [31] smoking, [28] other xenobiotic DNA damaging agents (such as drugs or chemotherapy) [32] or other DNA damaging agents including reactive oxygen species, fever or high testicular temperature. [33] The damaged DNA related to infertility manifests itself by the increased susceptibility to denaturation inducible by heat or acid [34] or by the presence of double-strand breaks that can be detected by the TUNEL assay . [35] General factors Diabetes mellitus , [36] [37] thyroid disorders, [38] undiagnosed and untreated coeliac disease , [39] [40] [41] [42] adrenal disease [43] Hypothalamic-pituitary factors Hyperprolactinemia Hypopituitarism The presence of anti-thyroid antibodies is associated with an increased risk of unexplained subfertility with an odds ratio of 1.5 and 95% confidence interval of 1.1–2.0. [44] Environmental factors Toxins such as glues, volatile organic solvents or silicones , physical agents, chemical dusts, and pesticides . [45] [46] Tobacco smokers are 60% more likely to be infertile than non-smokers. [47] German scientists have reported that a virus called adeno-associated virus might have a role in male infertility, [48] though it is otherwise not harmful. [49] Other diseases such as chlamydia , and gonorrhea can also cause infertility, due to internal scarring ( fallopian tube obstruction ). [50] [51] [52] Alimentary habits [53] Obesity : Obesity can have a significant impact on male and female fertility. ... "Sperm DNA integrity assays: diagnostic and prognostic challenges and implications in management of infertility" . J. Assist. Reprod. Genet . 28 (11): 1073–85. doi : 10.1007/s10815-011-9631-8 .

Retrieved 15 October 2012 . ^ Coleman, E. (2011). "Chapter 28. Impulsive/compulsive sexual behavior: Assessment and treatment" . ... Contrary to Love: Helping the Sexual Addict . Hazelden Publishing . p. 28. ISBN 1568380593 . ^ Schaefer GA, Ahlers CJ (2017). "1.3, Sexual addiction: Terminology, definitions and conceptualisation" . ... "Compulsive Sexual Behavior Disorder in ICD-11" . Psychology Today . Retrieved 28 November 2018 . ^ Patrick Carnes; David Delmonico; Elizabeth Griffin (2001). ... Atsa.com . 16 November 2017 . Retrieved 28 December 2017 . ^ a b c d e f g h i j k l m n o p q r s t u v w Olsen CM (December 2011). ... S2CID 53418034 . ^ "Compulsive sexual behavior – Symptoms and causes – Mayo Clinic" . Mayoclinic.com . Retrieved 28 December 2017 . ^ a b Levine, M. P.; Troiden, R.

Enoxaparin is listed as Pregnancy Category B, meaning animal studies have failed to show harmful effects to the fetus and therefore are safe to use in pregnant women. [25] [27] However, pregnant women taking LMWH may not experience the full anticoagulant effect due to the nature of the medication compared to other anticoagulants (i.e. warfarin) and may be less favorable for users as it is an injectable medication. [28] Unfractionated Heparin (UFH) [ edit ] Unfractionated heparin is another type of anticoagulant that has been widely used. ... As many studies looking at DOACs exclude pregnant women, there is not enough evidence to demonstrate the safety and efficacy of DOACs in pregnant women. [28] Currently, rivaroxaban (Xarelto), dabigatran (Pradaxa), and edoxaban (Savaysa) are DOACs listed under Pregnancy Category C, and apixaban (Eliquis) is listed under Pregnancy Category B. [29] Antidiarrheal [ edit ] Diarrhea is not a common symptom of pregnancy; however, it can occur as a result of reduced gastric acidity and slowed intestinal motility. [30] Bismuth subsalicylate (Pepto-Bismol), loperamide (Imodium), and atropine/diphenoxylate (Lomotil) are antidiarrheal agents that can be used to treat diarrhea. ... National Institute on Drug Abuse . Retrieved 28 July 2020 . ^ a b "Gestational diabetes - Diagnosis and treatment - Mayo Clinic" . www.mayoclinic.org .

This characteristic typically manifests as an indifference to other people. [25] In contrast to introversion , a nonpathological dimension of human personality, social anhedonia represents a deficit in the ability to experience pleasure . [26] Additionally, social anhedonia differs from social anxiety in that social anhedonia is predominantly typified by diminished positive affect, while social anxiety is distinguished by both decreased positive affect and exaggerated negative affect . [27] This trait is currently seen as a central characteristic to, as well as a predictor of, schizophrenia spectrum disorders , [28] as it is seen as a potential evolution of most personality disorders, if the patient is above age 24, when prodromal schizophrenia may be excluded. [29] Signs and symptoms [ edit ] Decreased ability to experience interpersonal pleasure Social withdrawal/isolation Decreased capacity for social contact and interaction Lack of close friends and intimate relationships, and decreased quality of those relationships Poor social adjustment Decreased positive affect Flat affect Depressed mood State-related anxiety [28] [30] Background and early clinical observation [ edit ] The term anhedonia is derived from the Greek an- , "without" and hēdonē , "pleasure". [31] Interest in the nature of pleasure and its absence dates back to ancient Greek philosophers such as Epicurus . [3] The symptoms of anhedonia were introduced to the realm of psychopathology in 1809 by John Haslam , who characterized a patient suffering from schizophrenia as indifferent to "those objects and pursuits which formerly proved sources of delight and instruction". [32] The concept was formally coined by Théodule-Armand Ribot and later used by psychiatrists Paul Eugen Bleuler and Emil Kraepelin to describe a core symptom of schizophrenia. [3] In particular, Rado postulated that schizotypes, or individuals with the schizophrenic phenotype, have two key genetic deficits, one related to the ability to feel pleasure (anhedonia) and one related to proprioception . ... This dysfunctional stress reactivity may correlate with hedonic capacity, providing a potential explanation for the increased anxiety symptoms experienced in people with social anhedonia. [47] In an attempt to separate out social anhedonia from social anxiety, the Revised Social Anhedonia Scale [48] didn't include items that potentially targeted social anxiety. [28] However, more research must be conducted on the underlying mechanisms through which social anhedonia overlaps and interacts with social anxiety. ... Journal of Abnormal Psychology . 103 (4): 719–28. doi : 10.1037/0021-843x.103.4.719 .

One theory is resistance to digestion, the thinking being that when largely intact proteins reach the small intestine the white blood cells involved in immune reactions will be activated. [26] The heat of cooking structurally degrades protein molecules, potentially making them less allergenic. [27] Allergic responses can be divided into two phases: an acute response that occurs immediately after exposure to an allergen, which can then either subside or progress into a "late-phase reaction," prolonging the symptoms of a response and resulting in more tissue damage . [28] [29] In the early stages of acute allergic reaction, lymphocytes previously sensitized to a specific protein or protein fraction react by quickly producing a particular type of antibody known as secreted IgE (sIgE), which circulates in the blood and binds to IgE-specific receptors on the surface of other kinds of immune cells called mast cells and basophils . Both of these are involved in the acute inflammatory response. [28] Activated mast cells and basophils undergo a process called degranulation , during which they release histamine and other inflammatory chemical mediators ( cytokines , interleukins , leukotrienes , and prostaglandins ) into the surrounding tissue causing several systemic effects, such as vasodilation , mucous secretion, nerve stimulation, and smooth muscle contraction. ... Depending on the individual, the allergen, and the mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system, while eczema is localized to the skin. [28] After the chemical mediators of the acute response subside, late-phase responses can often occur due to the migration of other white blood cells such as neutrophils , lymphocytes , eosinophils , and macrophages to the initial reaction sites. ... Pediatric Allergy and Immunology . 28 (1): 6–17. doi : 10.1111/pai.12659 . ... Archived from the original on 2009-06-28. ^ a b Grimbaldeston MA, Metz M, Yu M, Tsai M, Galli SJ (December 2006).

Leukoplakia may be white, whitish yellow or grey. [27] The size can range from a small area to much larger lesions. [27] The most common sites affected are the buccal mucosa, the labial mucosa and the alveolar mucosa , [28] although any mucosal surface in the mouth may be involved. [2] The clinical appearance, including the surface texture and color, may be homogenous or non-homogenous (see: classification ). ... Mutation of p53 can disrupt its regulatory function and lead to uncontrolled cell growth. [27] Mutations of p53 have been demonstrated in the cells from areas of some leukoplakias, especially those with dysplasia and in individuals who smoke and drink heavily. [27] Diagnosis [ edit ] Definition [ edit ] Leukoplakia is a diagnosis of exclusion, meaning that which lesions are included depends upon what diagnoses are currently considered acceptable. [27] Accepted definitions of leukoplakia have changed over time and are still controversial. [28] It is possible that the definition will be further revised as new knowledge becomes available. [27] In 1984 an international symposium agreed upon the following definition: "a whitish patch or plaque, which cannot be characterized clinically or pathologically as any other disease, and is not associated with any physical or chemical agent except the use of tobacco." [27] There were, however, problems and confusion in applying this definition. [27] At a second international symposium held in 1994, it was argued that, whilst tobacco was a likely causative factor in the development of leukoplakia, some white patches could be linked directly to the local effects of tobacco by virtue of their disappearance following smoking cessation, suggesting that this kind of white patch represents a reactive lesion to local tissue irritation rather than a lesion caused by carcinogens in cigarette smoke, and could be better termed to reflect this etiology, e.g. smokers' keratosis. [27] The second international symposium therefore revised the definition of leukoplakia to: "a predominantly white lesion of the oral mucosa that cannot be characterized as any other definable lesion." In the mouth, the current definition of oral leukoplakia adopted by the World Health Organization is "white plaques of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer". [32] However, this definition is inconsistently applied in the medical literature, and some refer to any oral white patch as "leukoplakia". [3] The term has been incorrectly used for white patches of any cause (rather than specifically referring to idiopathic white patches) and also to refer only to white patches which have a risk of cancerous changes. [3] It has been suggested that leukoplakia is an unhelpful term since there is so much inconsistency surrounding its use, [3] and some clinicians now avoid using it at all. [28] Biopsy [ edit ] Microscopic examination of keratinocytes scraped from the buccal mucosa Tissue biopsy is usually indicated [5] to rule out other causes of white patches and also to enable a detailed histologic examination to grade the presence of any epithelial dysplasia. ... While the degree of dysplasia has been shown to be an important predictor of malignant change, [3] many have challenged its use due to the low predictive value from the lack of objectivity of grading dysplasia. [37] [38] [39] While 10% of leukoplakia lesions show dysplasia when biopsied, [8] as many as 18% of oral lesions undergo malignant change in the absence of dysplasia. [40] Leukoplakia located on the floor of the mouth, the posterior and lateral tongue, and the retromolar areas (the region behind the wisdom teeth) have higher risk, whereas white patches in areas such as the top surface of the tongue and the hard palate do not have significant risk. [3] Although these "high risk" sites are recognized, statistically, leukoplakia is more common on the buccal mucosa, alveolar mucosa, and the lower labial mucosa. [28] Leukoplakia of the floor of the mouth and tongue accounts for over 90% of leukoplakias showing dysplasia or carcinoma on biopsy. [2] This is thought to be due to pooling of saliva in the lower part of the mouth, exposing these areas to more carcinogens held in suspension. Red lesions (erythroplasia) and mixed red and white lesions (erythroleukoplakia/"speckled leukoplakia") have a higher risk of malignant change than homogenous leukoplakia. [14] Verrucous or nodular areas have a higher risk. [3] Although smoking increases risk of malignant transformation, smoking also causes many white patches with no dysplasia. [3] This means that statistically, white patches in non smokers have a higher risk. [2] Older people with white patches are at higher risk. [3] Larger white patches are more likely to undergo malignant transformation than smaller lesions. [3] White patches which have been present for a long period of time have higher risk. [3] Persons with a positive family history of cancer in the mouth. [3] Candida infection in the presence of dysplasia has a small increased risk. [3] A change in the appearance of the white patch, apart from a change in the color, has a higher risk. [3] Changes in the lesion such as becoming fixed to underlying tissues, ulceration , cervical lymphadenopathy (enlargement of lymph nodes in the neck), and bone destruction may herald the appearance of malignancy. [27] White patches present in combination with other conditions that carry a higher risk (e.g. oral submucous fibrosis ), are more likely to turn malignant. [3] Although overall, oral cancer is more common in males, females with white patches are at higher risk than men. [3] Epidemiology [ edit ] The prevalence of oral leukoplakia varies around the world, but generally speaking it is not an uncommon condition. [8] Reported prevalence estimates range from less than 1% to more than 5% in the general population. [8] Leukoplakia is therefore the most common premalignant lesion that occurs in the mouth. [36] Leukoplakia is more common in middle-aged and elderly males. [28] The prevalence increases with increasing age. [2] In areas of the world where smokeless tobacco use is common, there is a higher prevalence. [2] In the Middle East region, the prevalence of leukoplakia is less than 1% (0.48%). [41] Etymology [ edit ] The word leukoplakia means "white patch", [3] and is derived from the Greek words λευκός - "white" and πλάξ - "plate". [42] History [ edit ] The term leukoplakia was coined in 1861 by Karl Freiherr von Rokitansky, who used it to refer to white lesions of the urinary tract. [24] In 1877 Schwimmer first used the term for an oral white lesion. [28] It is now thought that this white lesion on the tongue represented syphilitic glossitis, [28] a condition not included in the modern definitions of oral leukoplakia.

In this sense, the goal of the label is not to identify particular objective facts that differentiate one medical condition from another; instead, the main goal is to validate the real suffering experienced by people living with an invisible illness and to provide social support for them as they cope with it. [28] Political actions [ edit ] While there is general agreement on the optimal treatment for Lyme disease, the existence of chronic Lyme is generally rejected because there is no evidence of its existence. [27] [29] [30] Even among those who believe in it, there is no consensus over its prevalence, symptoms, diagnostic criteria, or treatment. [27] [29] [30] The evidence-based perspective is exemplified by a 2007 review in The New England Journal of Medicine , which noted the diagnosis of chronic Lyme disease is used by a few physicians despite a lack of "reproducible or convincing scientific evidence", leading the authors to describe this diagnosis as "the latest in a series of syndromes that have been postulated in an attempt to attribute medically unexplained symptoms to particular infections." [1] Medical authorities agree with this viewpoint: the Infectious Diseases Society of America (IDSA), the American Academy of Neurology , the Centers for Disease Control and Prevention (CDC), and the National Institutes of Health (NIH), advise against long-term antibiotic treatment for people who identify as having chronic Lyme disease, given the lack of supporting evidence and the potential for harmful side-effects. [31] including toxicities. [10] [11] [12] A minority, primarily not medical practitioners, holds that chronic Lyme disease is responsible for a range of unexplained symptoms , sometimes in people without any evidence of past infection. [29] This viewpoint is promoted by many who have been told they have the condition by people who lack experience in science or medicine. [27] Groups, advocates, and the small number of physicians who support the concept of chronic Lyme disease have organized to lobby for recognition of this diagnosis, as well as to argue for insurance coverage of long-term antibiotic therapy, which most insurers deny, as it is at odds with the guidelines of major medical organizations. [29] [32] Paul G. ... The Providence Journal . Retrieved 28 July 2019 . ^ John Ferro (18 December 2014). ... The New York Times . Retrieved 2017-06-28 . ^ Gleiberman, Owen (20 November 2009).

Refractive errors in patients with FXS are also common. [19] Neurology [ edit ] Individuals with FXS are at a higher risk of developing seizures , with rates between 10% and 40% reported in the literature. [28] In larger study populations the frequency varies between 13% and 18%, [12] [28] consistent with a recent survey of caregivers which found that 14% of males and 6% of females experienced seizures. [28] The seizures tend to be partial , are generally not frequent, and are amenable to treatment with medication. ... "Circuit and plasticity defects in the developing somatosensory cortex of FMR1 knock-out mice" . The Journal of Neuroscience . 28 (20): 5178–88. doi : 10.1523/JNEUROSCI.1076-08.2008 .

Beckwith–Wiedemann syndrome , Sotos syndrome , Perlman syndrome , Simpson-Golabi-Behmel syndrome [23] ) are often characterized by macrosomia. [24] [25] Other risk factors [ edit ] Gestational age: pregnancies that go beyond 40 weeks increase incidence of an LGA infant [21] Fetal sex: male infants tend to weigh more than female infants [5] Obesity prior to pregnancy and maternal weight gain above recommended guidelines during pregnancy [26] [27] [28] Multiparity: giving birth to previous LGA infants vs. non-LGA infants [5] Frozen embryo transfer as fertility treatment, as compared with fresh embryo transfer or no artificial assistance [29] [30] Diagnosis [ edit ] Diagnosing fetal macrosomia cannot be performed until after birth, as evaluating a baby's weight in the womb may be inaccurate. [21] While ultrasound has been the primary method for diagnosing LGA, this form of fetal weight assessment remains imprecise, as the fetus is a highly variable structure in regards to density and weight— no matter the gestational age. [21] Ultrasonography involves an algorithm that incorporates biometric measurements of the fetus, such as biparietal diameter (BPD), head circumference (HC), abdominal circumference (AC), and femur length (FL), to calculate the estimated fetal weight (EFW). [31] Variability of fetal weight estimations has been linked to differences due to sensitivity and specificity of ultrasound algorithms as well as to the individual performing the ultrasound examination. [32] In addition to sonography, fetal weight can also be assessed using clinical and maternal methods. ... However, the American College of Obstetricians and Gynecologists recommends that cesarean delivery should only be considered if the fetus is an estimated weight of at least 5,000 grams in non-diabetic mothers and at least 4,500 grams in diabetic mothers. [35] A number needed to treat analysis determined that approximately 3,700 women with suspected fetal macrosomia would have to undergo an unnecessary cesarean section in order to prevent one incident of brachial plexus injuries secondary to shoulder dystocia. [5] Management of gestational diabetes through dietary modifications and anti-diabetic medications has been shown to decrease the incidence of LGA. [36] The use of metformin to control maternal blood glucose levels has shown to be more effective than using insulin alone in reducing the likelihood of fetal macrosomia. [37] There is a 20% lower chance of having an LGA baby when using metformin to manage diabetes compared to using insulin. [38] Modifiable risk factors that increase the incidence of LGA births, such as gestational weight gain above recommended BMI guidelines, can be managed with lifestyle modifications, including maintaining a balanced diet and exercising. [39] [40] Such interventions can help mothers achieve the recommended gestational weight and lower the incidence of fetal macrosomia in obese and overweight women. [39] [40] The World Health Organization also recommends that mothers aim for their recommended BMI prior to conception. [28] In general, obese mothers or women with excessive gestational weight gain may have higher risk of pregnancy complications (ranging from LGA, shoulder dystocia, etc.). [41] Epidemiology [ edit ] In healthy pregnancies without pre-term or post-term health complications, large for gestational age, or fetal macrosomia have been observed to affect around 12% of newborns. [7] By comparison, women with gestational diabetes are at an increased risk of giving birth to LGA babies, where ~15-45% of neonates may be affected. [7] In 2017, the National Center of Health Statistics found that 7.8% of live-born infants born in the United States meet the definition of macrosomia, where their birth weight surpasses the threshold of 4000 grams (above ~8.8 pounds). [7] Women in Europe and the United States tend to have higher pre-term body weight and have increased gestational weight during pregnancy compared to women in east Asia. [42] Thus, women in Europe and the United States, with higher gestational weight gain, tend to have higher associated risk of LGA infants, macrosomia and cesarean. [42] In European countries, the prevalence of births of newborns weighing between 4,000 g and 4,499 g is 8% to 21%, and in Asian countries the prevalence is between 1% and 8%. [43] In general, rates of LGA infants have increased 15-25% in many countries including the United States, Canada, Germany, Denmark, Scotland and more in the past 20-30 years, suggesting an increase in LGA births worldwide. [44] References [ edit ] ^ Henriksen T (2008). ... "The management of large and small for gestational age fetuses". Seminars in Perinatology . 28 (1): 59–66. doi : 10.1053/j.semperi.2003.10.013 .

In the midst of trauma, the brain may wander off and work to avoid the memory. [26] Court cases [ edit ] Sexual abuse cases [ edit ] The question of the accuracy and dependability of a repressed memory that someone has later recalled has contributed to some investigations and court cases, including cases of alleged sexual abuse or child sexual abuse (CSA). [27] [28] [29] The research of Elizabeth Loftus has been used to counter claims of recovered memory in court [22] and it has resulted in stricter requirements for the use of recovered memories being used in trials, as well as a greater requirement for corroborating evidence . ... S2CID 20874393 . Retrieved January 28, 2008 . ^ "Recovered Memory Lawsuit Sparks Litigation" . ... Instead, it asks, "Why? " " . Vox . Retrieved December 28, 2019 . External links [ edit ] False memory syndrome at Curlie Memory controversies at Curlie Memory Wars is a website with information from all sides of the issue.

These findings suggest that teachers that do not have a sufficient background in mathematics may struggle with the development of comprehensive lesson plans for their students. Similarly, Laturner's research [28] (2002) shows that teachers with certification in math are more likely to be passionate and committed about teaching math than those without certification. ... Since 1995, studies have shown that the gender gap favored males in most mathematical standardized testing as boys outperformed girls in 15 out of 28 countries. However, as of 2015 the gender gap has almost been reversed, showing an increase in female presence. ... Ask the Cognitive Scientist" . American Educator . 38 (2): 28–43. ISSN 0148-432X . ^ Blazer, C. (2011). ... British Educational Research Journal , 28, 689-704. ^ Laturner, R.J. (2002). ... Archived from the original on 2011-06-28 . Retrieved 2011-06-30 . ^ Arem, C. (2010).

Increased levels of CRP as measured by a CRP test or the more sensitive high serum CRP (hsCRP) test and elevated levels of I6 as measured by an IL6 ELISA are markers for the increased risk of silent stroke. [27] Diabetes mellitus : untreated or improperly managed diabetes mellitus is associated with an increased risk for silent stroke. [28] Hypertension : which affects up to 50 million people in the United States alone is the major treatable risk factor associated with silent strokes. [29] Homocysteine : elevated levels of total homocysteine (tHcy) an amino acid are an independent risk factor for silent stroke, even in healthy middle-aged adults. [30] [31] [32] Metabolic syndrome (MetS):Metabolic syndrome is a name for a group of risk factors that occur together and increase the risk for coronary artery disease, stroke, and type 2 diabetes. ... CHS Collaborative Research Group". Stroke . 28 (6): 1158–64. doi : 10.1161/01.STR.28.6.1158 . ... Stroke: A Journal of Cerebral Circulation . 28 (6): 1158–64. doi : 10.1161/01.STR.28.6.1158 .

., 2 vs. 5 and 4 vs. 7) based on the Weber's law has also been used to further support the structure of the ANS. [28] The numerical ratio effect is observed when individuals are less accurate and slower in comparing pairs of numbers that have a larger ratio (e.g., 8 and 9, ratio = 8/9) than a smaller ratio (2 and 3; ratio = 2/3). A larger numerical distance or ratio effect with comparison of sets of objects (i.e., non-symbolic) is thought to reflect a less precise ANS, and the ANS acuity has been found to correlate with math achievement in typically developing children [28] and also in adults. [29] More importantly, several behavioral studies [30] [31] have found that children with developmental dyscalculia show an attenuated distance/ratio effect than typically developing children. ... Proceedings of the National Academy of Sciences . 109 (28): 11116–11120. Bibcode : 2012PNAS..10911116H . doi : 10.1073/pnas.1200196109 .

Even aspirin , which is sometimes used to treat arthritis in cats, can be toxic and must be administered cautiously. [23] Similarly, application of minoxidil ( Rogaine ) to the skin of cats, either accidentally or by well-meaning owners attempting to counter loss of fur, has sometimes proved fatal. [24] [25] In addition to such obvious dangers as insecticides and weed killers , other common household substances that should be used with caution in areas where cats may be exposed include mothballs and other naphthalene products, [23] as well as phenol -based products often used for cleaning and disinfecting near cats' feeding areas or litter boxes, such as Pine-Sol , Dettol (Lysol), hexachlorophene , etc. [23] which, although they are widely used without problem, have been sometimes seen to be fatal. [26] Essential oils are toxic to cats and there have been reported cases of serious illnesses caused by tea tree oil and tea tree oil-based flea treatments and shampoos. [27] [28] [29] Many human foods are somewhat toxic to cats; theobromine in chocolate can cause theobromine poisoning , for instance, although few cats will eat chocolate. ... Retrieved 14 Feb 2015 . ^ Welcome to Healthypet.com! Archived 2007-09-28 at the Wayback Machine ^ Zoonotic Disease: What Can I Catch From My Cat? ... "Acute Pinesol toxicity in a domestic cat". Vet Hum Toxicol . 28 (4): 316–7. PMID 3750813 . ^ K. Bischoff; F.

A 1994 report found that of those who were in a vegetative state a month after a trauma, 54% had regained consciousness by a year after the trauma, whereas 28% had died and 18% were still in the vegetative state. ... Stimulation techniques include sensory stimulation, sensory regulation, music and musicokinetic therapy, social-tactile interaction, and cortical stimulation. [28] Zolpidem [ edit ] There is limited evidence that the hypnotic drug zolpidem has an effect. [29] The results of the few scientific studies that have been published so far on the effectiveness of zolpidem have been contradictory. [30] [31] Epidemiology [ edit ] In the United States , it is estimated that there may be between 15,000 and 40,000 patients who are in a persistent vegetative state, but due to poor nursing home records exact figures are hard to determine. [32] History [ edit ] The syndrome was first described in 1940 by Ernst Kretschmer who called it apallic syndrome . [33] The term persistent vegetative state was coined in 1972 by Scottish spinal surgeon Bryan Jennett and American neurologist Fred Plum to describe a syndrome that seemed to have been made possible by medicine 's increased capacities to keep patients' bodies alive. [11] [34] Society and culture [ edit ] Ethics and policy [ edit ] An ongoing debate exists as to how much care, if any, patients in a persistent vegetative state should receive in health systems plagued by limited resources. ... I suspect that, if such individuals are indeed trapped in their bodies, they may be living in great torment and will request to have their care terminated or even active euthanasia." [36] Notable cases [ edit ] Tony Bland – first patient in English legal history to be allowed to die Paul Brophy – first American to die after court-authorization Sunny von Bülow – lived almost 28 years in a persistent vegetative state until her death Gustavo Cerati – Argentine singer-songwriter, composer and producer who died after four years in a coma Prichard Colón – Puerto Rican former professional boxer and gold medal winner who spent years in a vegetative state after a bout Nancy Cruzan – American woman involved in a landmark United States Supreme Court case Gary Dockery – American police officer who entered, emerged and later reentered a persistent vegetative state Eluana Englaro – Italian woman from Lecco whose life was ended after a legal case after spending 17 years in a vegetative state Elaine Esposito – American woman who was a previous record holder for having spent 37 years in a coma Lia Lee – Hmong person who spent 26 years in a vegetative state and was the subject of a 1997 book by Anne Fadiman Haleigh Poutre Karen Ann Quinlan Terri Schiavo Aruna Shanbaug – Indian woman in persistent vegetative state for 42 years until her death.

IVIG and plasmapheresis together can reduce or eliminate the need for an IUT. [27] Plasmapheresis - Plasmapheresis aims to decrease the maternal titer by direct plasma replacement. [28] Plasmapheresis and IVIG together can even be used on women with previously hydropic fetuses and losses. [29] [30] Mid to late pregnancy [ edit ] IUT - Intrauterine Transfusion (IUT) is done either by intraperitoneal transfusion (IPT) or intravenous transfusion (IVT). [31] IVT is preferred over IPT. [18] IUTs are only done until 35 weeks. ... Anti-M also recommends antigen testing to rule out the presence of HDN. [28] Hgb - the infant's hemoglobin should be tested from cord blood. [2] Reticulocyte count - Reticulocytes are elevated when the infant is producing more blood to combat anemia. [2] A rise in the retic count can mean that an infant may not need additional transfusions. [37] Low retic is observed in infants treated with IUT and in those with HDN from anti-Kell [36] Neutrophils - as Neutropenia is one of the complications of HDN, the neutrophil count should be checked. [6] [7] Thrombocytes - as thrombocytopenia is one of the complications of HDN, the thrombocyte count should be checked. [6] Bilirubin should be tested from cord blood. [2] Ferritin - because most infants affected by HDN have iron overload, a ferritin must be run before giving the infant any additional iron. [8] Newborn Screening Tests - Transfusion with donor blood during pregnancy or shortly after birth can affect the results of the Newborn Screening Tests. ... Ultrasound in Obstetrics and Gynecology . 28 (6): 814–20. doi : 10.1002/uog.2837 .

Arthroscopy [ edit ] Arthroscopy is another useful tool to diagnose and assess injuries to the posterolateral corner. [28] Arthroscopy is useful in two ways. ... A drive through sign occurs when there is more than 1 cm of lateral joint opening when a varus stress is applied to the knee which allows the surgeon to easily pass the arthroscope between the lateral femoral condyle and tibia . [28] Second, arthroscopy allows the surgeon to visualize individual structures in the posterolateral knee. ... The incidence of isolated posterolateral corner injuries has been reported to be between 13% and 28%. Most PLC injuries accompany an ACL or PCL tear, and can contribute to ACL or PCL reconstruction graft failure if not recognized and treated. [46] [47] A study by LaPrade et al. in 2007 showed the incidence of posterolateral knee injuries in patients presenting with acute knee injuries and hemarthrosis (blood in the knee joint) was 9.1%.

Occipital spikes are common (cases 28 and 37) but these are not a prerequisite for diagnosis (cases 40, 43, 44). ... On another occasion, he was found in bed unresponsive, floppy, and pale for 5 minutes. The last seizure occurred at age 28 months in the nursery. He fell on the floor and remained unresponsive and flaccid for 20 minutes and then he rapidly recovered. ... There is no evidence of superiority of monotherapy with any particular common AED. [28] [29] Autonomic status epilepticus in the acute stage needs thorough evaluation for proper diagnosis and assessment of the neurologic/autonomic state of the child.

Progress of tuberculosis control in China, 1991–2005 Year Proportion (%) of new smear-positive TB cases successfully treated Estimated proportion (%) of all new smear-positive TB cases detected Proportion (%) of counties implementing the WHO-recommended DOTS strategy 1991 69 4 5 1992 75 7 7 1993 79 10 19 1994 88 14 48 1995 92 21 58 1996 94 25 60 1997 94 26 61 1998 93 27 62 1999 92 28 63 2000 92 30 63 2001 91 29 65 2002 91 26 64 2003 92 44 77 2004 90 63 89 2005 90 80 100 Focusing on vulnerable groups [ edit ] One group of special concern are work migrants , most often poor men, who leave the countryside to join the wage economy in towns and cities all over China. [6] [7] [8] [9] Some come from areas such as Henan Province where huge numbers of peasants were infected with HIV from scandalous plasma-donor practices in the 1990s. ... The central government will provide 28% of the needed funding, with the rest coming from governments at various levels. ... WHO estimates that a third of the world's cases of MDR tuberculosis are in China, even though the country has only 15% of the global burden of tuberculosis. [28] The recent expansion of DOTS should help to limit the development of MDR tuberculosis.

In rare cases, however, some Adrenal Adenomas may become activated, in that they begin to produce hormones in much larger quantities than what adrenal glands tend to produce leading to a number of health complications including Primary aldosteronism and Hyperandrogenism. [28] Arrhenoblastoma [ edit ] An arrhenoblastoma is an uncommon tumor of the ovary. ... The Journal of Clinical Endocrinology & Metabolism (published 28 April 2011). 89 (8): 3835–3840. doi : 10.1210/jc.2003-031737 . ... New England Journal of Medicine. N Engl J Med, 28 September 1995. Web. 14 November 2016. ^ "Polycystic Ovary Syndrome (PCOS)."