An inguinal hernia is a protrusion of abdominal-cavity contents through the inguinal canal. Symptoms are present in about 66% of affected people. This may include pain or discomfort especially with coughing, exercise, or bowel movements. Often it gets worse throughout the day and improves when lying down. A bulging area may occur that becomes larger when bearing down. Inguinal hernias occur more often on the right than left side. The main concern is strangulation, where the blood supply to part of the bowel is blocked. This usually produces severe pain and tenderness of the area.
Risk factors for the development of a hernia include: smoking, chronic obstructive pulmonary disease, obesity, pregnancy, peritoneal dialysis, collagen vascular disease, and previous open appendectomy, among others. Hernias are partly genetic and occur more often in certain families. It is unclear if inguinal hernias are associated with heavy lifting. Hernias can often be diagnosed based on signs and symptoms. Occasionally medical imaging is used to confirm the diagnosis or rule out other possible causes.
Groin hernias that do not cause symptoms in males do not need to be repaired. Repair, however, is generally recommended in females due to the higher rate of femoral hernias which have more complications. If strangulation occurs immediate surgery is required. Repair may be done by open surgery or by laparoscopic surgery. Open surgery has the benefit of possibly being done under local anesthesia rather than general anesthesia. Laparoscopic surgery generally has less pain following the procedure.
The incidence of inguinal hernia in Nigeria is not new. About 27% of males and 3% of females develop a groin hernia at some time in their life. Groin hernias occur most often before the age of one and after the age of fifty. Inguinal, femoral and abdominal hernias resulted in 51,000 deaths in 2013 and 55,000 in 1990.
An inguinal hernia occurs when tissue pushes through a weak spot in your groin muscle. This causes a bulge in the groin or scrotum. The bulge may hurt or burn.
Most inguinal hernias happen because an opening in the muscle wall does not close as it should before birth. That leaves a weak area in the belly muscle. Pressure on that area can cause tissue to push through and bulge out. A hernia can occur soon after birth or much later in life. You are more likely to get a hernia if you are overweight or you do a lot of lifting, coughing, or straining. Hernias are more common in men. A woman may get a hernia while she is pregnant because of the pressure on her belly wall.
The main symptom of an inguinal hernia is a bulge in the groin or scrotum. It often feels like a round lump. The bulge may form over a period of weeks or months. Or it may appear all of a sudden after you have been lifting heavy weights, coughing, bending, straining, or laughing. The hernia may be painful, but some hernias cause a bulge without pain.
A hernia also may cause swelling and a feeling of heaviness, tugging, or burning in the area of the hernia. These symptoms may get better when you lie down.
Sudden pain, nausea, and vomiting are signs that a part of your intestine may have become trapped in the hernia. Call your doctor if you have a hernia and have these symptoms.
Signs and symptoms

Frontal view of an inguinal hernia (right).
Hernias present as bulges in the groin area that can become more prominent when coughing, straining, or standing up. They are rarely painful, and the bulge commonly disappears on lying down. The inability to “reduce”, or place the bulge back into the abdomen usually means the hernia is ‘incarcerated’ which requires emergency surgery.
Significant pain is suggestive of strangulated bowel (an incarcerated indirect inguinal hernia).
As the hernia progresses, contents of the abdominal cavity, such as the intestines, liver, can descend into the hernia and run the risk of being pinched within the hernia, causing an intestinal obstruction. If the blood supply of the portion of the intestine caught in the hernia is compromised, the hernia is deemed “strangulated” and gut ischemia and gangrene can result, with potentially fatal consequences. The timing of complications is not predictable. Emergency surgery for incarceration and strangulation carry much higher risk than planned, “elective” procedures. However, the risk of incarceration is low, evaluated at 0.2% per year.[5] On the other hand, surgical intervention has a significant risk of causing inguinodynia, and this is why minimally symptomatic patients are advised to watchful waiting.

An incarcerated inguinal hernia as seen on cross sectional CT scan

A frontal view of an incarcerated inguinal hernia (on the patient’s left side) with dilated loops of bowel above.
There are two types of inguinal hernia, direct and indirect, which are defined by their relationship to the inferior epigastric vessels. Direct inguinal hernias occur medial to the inferior epigastric vessels when abdominal contents herniate through a weak spot in the fascia of the posterior wall of the inguinal canal, which is formed by the transversalis fascia. Indirect inguinal hernias occur when abdominal contents protrude through the deep inguinal ring, lateral to the inferior epigastric vessels; this may be caused by failure of embryonic closure of the processus vaginalis.
In the case of the female, the opening of the superficial inguinal ring is smaller than that of the male. As a result, the possibility for hernias through the inguinal canal in males is much greater because they have a larger opening and therefore a much weaker wall through which the intestines may protrude.
In men, indirect hernias follow the same route as the descending testes, which migrate from the abdomen into the scrotum during the development of the urinary and reproductive organs. The larger size of their inguinal canal, which transmitted the testicle and accommodates the structures of the spermatic cord, might be one reason why men are 25 times more likely to have an inguinal hernia than women. Although several mechanisms such as strength of the posterior wall of the inguinal canal and shutter mechanisms compensating for raised intra-abdominal pressure prevent hernia formation in normal individuals, the exact importance of each factor is still under debate. The physiological school of thought thinks that the risk of hernia is due to a physiological difference between patients who suffer hernia and those who do not, namely the presence of aponeurotic extensions from the transversus abdominis aponeurotic arch

Worldwide, inguinal hernia remains a common problem presenting to surgeons. At many hospitals in developing countries, the waiting period for admission is often long owing to long list of patients, limited bed spaces and inadequate qualified manpower. Day-case surgery for inguinal hernia is therefore the panacea to these many challenges.

1. Royal College of Surgeons of England. Guidelines for Day-case surgery. 1992; RCSE: 10.
2. Badoe EA. Hernia. In: Badoe EA, Archampong EQ, Jaja MOA. (Ed) Principles and practice of surgery. Tema: Ghana Publishing Corporation, 1994: 461-71.
3. Keith WM, Daniel JD. The Management of Hernia – Considerations in cost-effectiveness. Surgical Clinics of North America 1996; 76: 105-15.
4. Lau H, Lee F. An audit of the early outcomes of ambulatory inguinal hernia repair at a surgical day-case centre. Hong Kong Med. J. 2000; 6 (2): 218-20.
5. Adejuyigbe O, Abubakar AM, Sowande OA, Olasinde AA. Day-case surgery in children in Ile-Ife, Nigeria: An audit. Nigerian Journal of Surgery.1998; 5(2):60-3
6. Awojobi OA, Sagua AG, Ladipo JK. Outpatient management of external hernia: A district hospital experience. West Afr. J. Med. 1987; 6: 201-4.
7. McHugh GA, Thomas GMM. The Management of Pain following day-case surgery. Anaesthesia. 2002; 57: 270-5.
8. Rai S, Chandra S, Smile SR. A Study of the risk of strangulation and obstruction in groin hernias. A N Z J Surg 1998; 88:650-4.
9. Ibrahim NA, Ugburo AO, Atoyebi OA. Early outcome of day surgery for inguinal hernia in sub-urban general hospital in Lagos, Nigeria Medical Journal. 2005; 46 (2): 33-5.
10. Adeyemi SD, da Rocha-Afodu JT, Olayiwola B. Outpatient herniotomy with ketamine: A prospective study of 50 herniotomized children and review of 219 herniotomies with ketamine. West Afr. J. Med 1985; 4: 151-61.


Malaria is a mosquito-borne infectious disease of humans and other animals caused by parasitic protozoans (a group of single-celled microorganism) belonging to the genus Plasmodium.[1] Malaria causes symptoms that typically include fever, fatigue, vomiting, and headaches. In severe cases it can cause yellow skin, seizures, coma or death.[2] The disease is transmitted by the biting of mosquitos, and the symptoms usually begin ten to fifteen days after being bitten. If not appropriately treated, people may have recurrences of the disease months later. In those who have recently survived an infection, re-infection typically causes milder symptoms. This partial resistance disappears over months to years if the person has no continuing exposure to malaria.
The disease is transmitted most commonly by an infected female Anopheles mosquito. The mosquito bite introduces the parasites from the mosquito’s saliva into a person’s blood. The parasites travel to the liver where they mature and reproduce. Five species of Plasmodium can infect and be spread by humans. Most deaths are caused by P. falciparum because P. vivax, P. ovale, and P. malariae generally cause a milder form of malaria. The species P. knowlesi rarely causes disease in humans. Malaria is typically diagnosed by the microscopic examination of blood using blood films, or with antigen-based rapid diagnostic tests
Malaria is endemic throughout most of the tropics. Of the approximately 3.4 billion people worldwide who are exposed annually, 1.2 billion are at high risk; the World Health Organization (WHO) states that there were 198 million cases of symptomatic malaria in 2013.
Between 2000 and 2010, the number of annual malaria cases reported by the WHO in 34 malaria-eliminating countries decreased by 85 percent from 1.5 million to 232,000 cases. Most of these are attributable to P. falciparum, but P. vivax and P. knowlesi can also cause severe disease. Malaria deaths peaked at 1.82 million in 2004 and fell to 1.24 million in 2010 (714,000 children <5 years and 524,000 individuals ≥5 years); over 80 percent of the deaths occur in sub-Saharan Africa. The WHO’s estimates of deaths from malaria (627,000 in 2012; uncertainty range 473,000 to 789,000) are approximately half the more reliable estimates above.
Important components for reducing the burden of malaria morbidity and mortality include more sensitive diagnostic tools, effective use of antimalarial drugs, and improved personal and community protection and mosquito control. The approach to elimination or control of malaria includes these basics, along with improvements in tracking of human illness and parasite surveillance, and effective resource delivery.
Issues related to epidemiology of malaria, including definitions and strategies for control, will be reviewed. Other related topics are discussed in detail separately.
Overview — Malaria is transmitted via the bite of a female Anopheles spp mosquito, which occurs mainly between dusk and dawn. Other comparatively rare mechanisms for transmission include congenitally acquired disease, blood transfusion, sharing of contaminated needles, and organ transplantation
The epidemiology of malaria in adults who live in malaria endemic areas is a neglected area of research. Malaria control strategies have focussed on children under the age of 5 years and pregnant women, as the majority of malaria-related sickness and death is seen in these two groups. However, early studies in West Africa showed that clinical attacks of malaria also occur in adults living in areas of high endemicity and a recent report points out the considerable contribution of malaria as a cause of death in adults.
The risk of malaria attacks in residents of malaria endemic areas falls as they become older, suggesting that protection is a function of age. This protective immunity is sequentially being reflected first by a reduction of life-threatening disease, then by a fall in the incidence of mild malaria and finally by a reduction in parasite prevalence. The means by which acquired immunity develops is still a matter of contention. It is likely that cumulative exposure to the enormous repertoire of antigenic variants of blood stage malaria parasites plays an important part. However, there is evidence which suggests that protection can be established after a relatively brief period of exposure and lasts for many years. Indeed, passive transfer of naturally acquired immunity and malariotherapy of syphilitic patients have suggested that there is a strong component of non-variant specific immunity involved in the protection against malaria which may be age-dependent.
The immune mechanisms that deal with a malarial infection probably change with age, as suggested by the age-dependency of malariometric indices, the pyrogenic threshold of parasitaemia, the speed with which infections are controlled, the incidence of clinical episodes and the parasitological complexity of individual infections. It is generally accepted that protective immunity effectively prevents the severe clinical manifestations of Plasmodium falciparum infections and substantially reduces parasite loads, but does not prevent infection. The consequence of this process is that the presence of blood-stage parasites in a semi-immune host is not synonymous with disease. This, together with the non-specificity of the malaria signs and symptoms in adults, make the individual diagnosis of clinical malaria in adults difficult in highly endemic areas.
Studies of malaria in semi-immune adults of Africa are scarce. More attention to the natural history of malaria affecting adults is needed to understand the dynamics of malaria infection and its interaction with the immune system. The present study was undertaken to investigate the clinical, parasitological and haematological status of adults living in a region in Mozambique where malaria is endemic, and to characterize parasites in these individuals who progressively acquire protective immunity.
Malaria is a life threatening parasitic disease transmitted by female anopheles mosquitoes. There are four types of human parasites; Plasmodium vivax, P. malariae, P ovale and P. falciparum. P. falciparum and P. vivax are the most common and P. falciparum, the most deadly type of infection, is most common in sub-Saharan Africa. A large number of environmental factors affect the distribution, seasonality and transmission intensity of malaria. Rainfall provides breeding sites for mosquitoes and increases the humidity, which enhances their survival. While malaria is largely endemic in Africa, varying proportion of countries in the continent are at risk of endemic malaria. Today, approximately 40% of the world population, mostly those living in the world's poorest countries, is at risk of malaria. This is mostly in the tropical and sub-tropical regions of the world. There are at least 300 million acute cases of malaria each year globally resulting in more than a million deaths, around 90% of these occur in Africa, mostly young children. In areas of stable malaria transmission, very young children and pregnant women are the population at highest risk for malaria morbidity and mortality. The populations most at risk of epidemics are those living in highlands, arid and desert-fringe zones and those living in areas where successful control measures have not been consolidated or maintained.
Malaria has been recognised as a severe and life-threatening illness for thousands of years. It still is one of the most common diseases affecting humans worldwide. The major impact of the disease is almost entirely on the developing countries, with the heaviest burden in Africa. Almost half of the total world population is exposed to the risk of contracting malaria.
Along with direct health cost there is a severe economic burden of the disease in terms of lost days of work. In fact malaria is thought to take off 1.3% from the economic growth of some African countries. In some of the most severely affected countries, it accounts for 40% of public health expenditure, 30-50% of inpatient admissions, and 50% of outpatient visits. It affects developing countries in more ways than one including determent of tourism.
There were an estimated 219 million cases of malaria (154–289 million) and 660 000 deaths (range 610 000–971 000) in 2010. Of total numbers 80% of estimated malaria deaths occur in just 14 countries and approximately 80% of estimated cases occur in 17 countries.
The Democratic Republic of the Congo and Nigeria account for over 40% of the estimated total of malaria deaths globally. The Democratic Republic of the Congo, India and Nigeria account for 40% of estimated malaria cases.
Estimated malaria mortality rates are highest in countries with a lower GNI per capita. Countries with higher proportions of their population living in poverty (less than US$ 1.25 per person per day) have higher mortality rates from malaria.
Of the deaths a large proportion was young children in sub-Saharan Africa. This is the most vulnerable group affected with the condition. In areas with high transmission, the most vulnerable groups are young children. These children are vulnerable because they have not developed immunity to malaria yet. Pregnant women are also at risk because their immunity has been decreased by pregnancy.
Malaria affects mainly poor tropical and subtropical areas of the world. Where the disease is endemic it is the leading cause of illness and death.
Africa has several factors that make it high risk for malaria. Some of these include very efficient mosquito (Anopheles gambiae) responsible for transmission, predominant parasite species is Plasmodium falciparum that leads to more severe malaria, warm and humid climate that allows transmission to occur year round as well as lack of resources and poor socio-economic conditions that prevents malaria control efforts. Other areas that are at risk include some countries in South America and South Asia.

To summarize, malaria is the leading cause of death and disease in many developing countries. According to the World Health Organization’s World Malaria Report 2011 and the Global Malaria Action Plan, 3.3 billion people worldwide live in areas at risk of malaria transmission in 106 countries and territories.
In 2012 malaria led to 216 million clinical episodes, and 655,000 deaths. An estimated 91% of deaths in 2010 were in the African Region, followed by 6% in the South-East Asian Region and 3% in the Eastern Mediterranean Region (3%). 86% of all deaths worldwide are children.

• WHO. World Malaria Report 2014. Geneva, Switzerland http://www.who.int/malaria/publications/world_malaria_report_2014/report/en/ (Accessed on December 18, 2014).
• WHO. World malaria report 2011. Geneva: World Health Organization, 2011.
• Murray CJ, Rosenfeld LC, Lim SS, et al. Global malaria mortality between 1980 and 2010: a systematic analysis. Lancet 2012; 379:413.
• Filler S, Causer LM, Newman RD, et al. Malaria surveillance–United States, 2001. MMWR Surveill Summ 2003; 52:1.
• Owusu-Ofori AK, Betson M, Parry CM, et al. Transfusion-transmitted malaria in Ghana. Clin Infect Dis 2013; 56:1735.
• Guerra CA, Gikandi PW, Tatem AJ, et al. The limits and intensity of Plasmodium falciparum transmission: implications for malaria control and elimination worldwide. PLoS Med 2008; 5:e38.
• Snow RW, Guerra CA, Noor AM, et al. The global distribution of clinical episodes of Plasmodium falciparum malaria. Nature 2005; 434:214.
• Price RN, Tjitra E, Guerra CA, et al. Vivax malaria: neglected and not benign. Am J Trop Med Hyg 2007; 77:79.
• Breman JG. Eradicating malaria. Sci Prog 2009; 92:1.
• White NJ. Plasmodium knowlesi: the fifth human malaria parasite. Clin Infect Dis 2008; 46:172.
• Smith T, Maire N, Dietz K, et al. Relationship between the entomologic inoculation rate and the force of infection for Plasmodium falciparum malaria. Am J Trop Med Hyg 2006; 75:11.
• Kiszewski AE, Teklehaimanot A. A review of the clinical and epidemiologic burdens of epidemic malaria. Am J Trop Med Hyg 2004; 71:128.
• WHO Global Malaria Control and Elimination: report of a technical review 17-18 January 2008. Geneva, pp. 1-47.
• Bruce Chwatt LJ. Essential Malariology, Wiley Medical, 1985. p.193.
• Laufer MK, Takala-Harrison S, Dzinjalamala FK, et al. Return of chloroquine-susceptible falciparum malaria in Malawi was a reexpansion of diverse susceptible parasites. J Infect Dis 2010; 202:801.


Encopresis also known as paradoxical diarrhea, is voluntary or involuntary fecal soiling in children who have usually already been toilet trained. Persons with encopresis often leak stool into their undergarments. Encopresis (or fecal incontinence) is a disorder which affects children worldwide. It is even more stigmatized than enuresis and urinary incontinence and is associated with high levels of distress for both children and parents. Also, the rate of comorbid emotional disorders is higher, affecting 30%-50% of all children with encopresis (von Gontard et al, 2011).
Two major forms of encopresis can be differentiated: encopresis with and without constipation. The specific differentiation into these two subtypes is of utmost importance as they differ according to pathophysiology, clinical features and, especially, treatment (i.e., the former does not respond to laxatives, while in the latter they are essential in treatment). The aim of this chapter is to give an overview and practical approaches to assessment and treatment of these two subtypes of encopresis.
This term is usually applied to children, and where the symptom is present in adults, it is more commonly known as fecal leakage (FL), fecal soiling or fecal seepage.

Encopresis is a common disorder affecting 1% to 3% of children older than four years (the definitional age). Three different trajectories can be defined (Heronet al, 2008):
• Children with chronic encopresis over many years
• Those with relapses, and
• A group with a tendency to remit spontaneously.
In a Dutch study, 4.1 % of 5-6 year olds and 1.6 % of 11-12 year olds were affected (van der Wal et al., 2005). Prevalence depends on the definition used; for example, 5.4 % of 7-year old children soiled, but only 1.4 % once or more per week (Joinson et al, 2006). Encopresis can persist into adolescence and even young adulthood. Without constipation (i.e., non-retentive fecal incontinence), 49% of
children soiled at the age of 12 years, and 15% at 18 years in a long-term follow up (Bongers et al, 2007). The prognosis of constipation is less favorable: only 80 % had a good outcome by the age of 16 years, and 75% to 80% at 16-27 years (Bongers et al, 2010). Three to four times more boys are affected by encopresis than girls (Bellman, 1966). Encopresis occurs almost always during the day (Bellman, 1966). Nocturnal encopresis is more often associated with organic causes and requires a more detailed somatic assessment.
Most children from the age of four years onwards have one bowel movement a day – with great individual variability (Bloom et al, 1993). Chronic constipation is a more common disorder than encopresis. According to a large meta-analysis, the median prevalence was 9% world-wide with different definitions used (vanden Berg et al, 2006). This meta-analysis included studies from countries such as Italy, US, Hong Kong, Japan, Finland, Turkey, Brazil, Saudi Arabia, among others.

As the differentiation of the two subtypes – constipation and non-retentive fecal incontinence − is decisive for treatment, it is important to know the basic signs and symptoms of each. Children with encopresis with constipation (or functional constipation) have
a reduced number of bowel movements with large stools of altered consistency (too soft or too hard). They often experience pain during defecation. Abdominal pain and reduced appetite are typical. The colon transit time is increased, abdominal and rectal masses are palpable. In sonography, the rectal diameter is increased (> 25mm). Often, daytime urinary incontinence and even enuresis co-exists. Additional emotional and behavioral disorders are found in 30%-50% of them and, finally, laxative therapy is helpful.
Encopresis is commonly caused by constipation, by reflexive withholding of stool, by various physiological, psychological, or neurological disorders, or from surgery (a somewhat rare occurrence).
The colon normally removes excess water from feces. If the feces or stool remains in the colon too long due to conditioned withholding or incidental constipation, so much water is removed that the stool becomes hard, and becomes painful for the child to expel in an ordinary bowel movement. A vicious cycle can develop, where the child may avoid moving his/her bowels in order to avoid the “expected” painful toilet episode. This cycle can result in so deeply conditioning the holding response that the rectal anal inhibitory response (RAIR) or anismus results. The RAIR has been shown to occur even under anesthesia and when voluntary control is lost. The hardened stool continues to build up and stretches the colon or rectum to the point where the normal sensations associated with impending bowel movements do not occur. Eventually, softer stool leaks around the blockage and cannot be withheld by the anus, resulting in soiling. The child typically has no control over these leakage accidents, and may not be able to feel that they have occurred or are about to occur due to the loss of sensation in the rectum and the RAIR. Strong emotional reactions typically result from failed and repeated attempts to control this highly aversive bodily product. These reactions then in turn may complicate conventional treatments using stool softeners, sitting demands, and behavioral strategies.
The onset of encopresis is most often benign. The usual onset is associated with toilet training, demands that the child sit for long periods of time, and intense negative parental reactions to feces. Beginning school or preschool is another major environmental trigger with shared bathrooms. Feuding parents, siblings, moving, and divorce can also inhibit toileting behaviors and promote constipation. An initiating cause may become less relevant as chronic stimuli predominate.
The psychiatric (DSM-IV) diagnostic criteria for encopresis are:
1. Repeated passage of feces into inappropriate places (e.g., clothing or floor) whether voluntary or unintentional
2. At least one such event a month for at least 3 months
3. Chronological age of at least 4 years (or equivalent developmental level)
4. The behavior is not exclusively due to a physiological effect of a substance (e.g., laxatives) or a general medical condition, except through a mechanism involving constipation.
The DSM-IV recognizes two subtypes: with constipation and overflow incontinence, and without constipation and overflow incontinence. In the subtype with constipation, the feces are usually poorly formed and leakage is continuous, and this occurs both during sleep and waking hours. In the type without constipation, the feces are usually well-formed, soiling is intermittent, and feces are usually deposited in a prominent location. This form may be associated with oppositional defiant disorder (ODD) or conduct disorder, or may be the consequence of large anal insertions, or more likely due to chronic encopresis that has radically desensitized the colon and anus.
Following assessment, children and parents are given detailed information on the subtype of encopresis (psychoeducation). As in the treatment of enuresis, unspecific factors such as enhancing motivation and building a good therapeutic relationship are helpful. Feelings of guilt, dysfunctional parental attributions (“my child is doing this on purpose”) and frustration can be verbalized. Ineffective parental interventions such as punishment or non-indicated medication can be discussed with parents. If the child’s food intake is restricted to low fiber foods, a change in the child’s diet can be useful. Also, the amount of fluids should be increased, as many children do not drink enough during the day.

Encopresis is a common condition that is often associated with psychosocial health disorders but only a small proportion of the children with encopresis are taken to a general practitioner to discuss their problem. It is also called stool holding or soiling, occurs when your child resists having bowel movements, causing impacted stool to collect in the colon and rectum. When your child’s colon is full of impacted stool, liquid stool can leak around the impacted stool and out of the anus, staining your child’s underwear.
Encopresis usually occurs after age 4, when your child has already learned to use a toilet. In most cases, encopresis is a symptom of chronic constipation. Less frequently, it may be the result of developmental or emotional issues. Doctors categorize encopresis as primary or secondary. Primary encopresis happens in a child who has never been successfully toilet trained. In secondary encopresis, a child develops the condition after having been successfully toilet trained. Encopresis can be frustrating for you — and embarrassing for your child. However, with patience and positive reinforcement, treatment for encopresis is usually successful.

Achenbach TM (1991). Manual for the child behavior checklist /4-18
and 1991 profile. Burlington: University of Vermont.
American Psychiatric Association. Diagnostic and Statistical Manual
of Mental Disorders, 4th edition, text revision. Washington, DC: American Psychiatric Association.
Bakwin H, Davidson MD (1971). Constipation in twins. American
Journal of Disease in Children, 121:179-181.
Bekkali N, van den Berg M, Dijkgraaf MGW et al (2009). Rectal fecal
impaction treatment in childhood constipation: enemas versus high doses oral PEG. Pediatrics, 124:e1108-e1115.
Bellman M (1966). Studies on encopresis. Acta Paediatrica
Scandinavica, 170 (sup):1-151.
Bennigna MA, Buller HA, Heymans HS et al (1994). Is encopresis
always the result of constipation? Archives of Disease in Childhood, 71:186–193.
Bennigna MA, Voskuijl WP, Akkerhuis GW et al (2004). Colonic
transit times and behaviour profiles in children with defecation disorders. Archives of Disease in Childhood, 89:13-16.
Bloom DA, Seeley WW, Ritchey ML et al (1993). Toilet habits and
continence in children: an opportunity sampling in search of normal parameters. Journal of Urology,149:1087-1090.
Bongers MEJ, Tabbers MM, Benninga M (2007). Functional
nonretentive fecal incontinence in children. Journal of Pediatric Gastroenterology and Nutrition, 44:5-13.
Bongers MEJ, van Wijk MP, Reitsma JB et al (2010). Longterm
prognosis for childhood constipation: clinical outcomes in adulthood. Pediatrics,126:e156-e162.
Candy D, Belsey J (2009). Macrogol (polyethylene glycol) laxatives in
children with functioanl constipation and faecal impaction: a systematic review. Archives of Disease in Childhood, 94:156-160.


Encephalopathy means disorder or disease of the brain. In modern usage, encephalopathy does not refer to a single disease, but rather to a syndrome of overall brain dysfunction; this syndrome can have many different organic and inorganic causes.
The following are some major types of encephalopathy, along with their causes:
Type Cause
chronic traumatic encephalopathy occurs when there are multiple traumas or injuries to the brain
glycine encephalopathy a genetic condition where there are abnormally high levels of glycine (an amino acid) in the brain
Hashimoto’s encephalopathy a rare effect of an autoimmune disease that attacks the thyroid gland
hepatic encephalopathy a result of liver disease
hypertensive encephalopathy a result of very high blood pressure
hypoxic encephalopathy when the brain does not get enough oxygen
Lyme encephalopathy a result of Lyme disease. Infected ticks transmit this bacterial disease
static encephalopathy permanent brain damage or dysfunction. A lack of oxygen to the brain, such as when a fetus is exposed to alcohol in the womb, is one of many causes of this type
toxic-metabolic encephalopathy a result of infections, toxins, or organ failure
transmissible spongiform encephalopathies a result of prion diseases. Prion proteins occur normally in the body. But they can also mutate, causing disease. Prion diseases include chronic wasting disease, fatal familial insomnia, kuru, and Creutzfeldt-Jakob disease
uremic encephalopath a result of kidney failure
Wernicke encephalopathy a result of a vitamin B1 deficiency. Long-term alcoholism and poor food absorption can cause a vitamin B1 deficiency

What Are the Symptoms of Encephalopathy?
Your symptoms will depend on the cause and severity of your encephalopathy.
Mental Changes
You may have difficulty focusing or suffer from memory loss. Also, you may have trouble with problem-solving skills.
Other people may notice symptoms in you before you do. A changing personality is one such symptom. For example, you may be more outgoing than you were before the encephalopathy. You may be more or less calm than you were before the disease.
You could also be lethargic and drowsy.
Neurological Changes
• Possible neurological symptoms include:muscle weakness in one area, poor decision-making or concentration
• involuntary twitching
• trembling
• difficulty speaking or swallowing
• seizures

Encephalopathy is a broad term used to describe abnormal brain function or brain structure. (Encephalo= brain + pathy= disorder). The abnormality may be transient, recurrent, or permanent. The loss of brain function may be reversible, static and stable, or progressive with increasing loss of brain activity over time.
Normal brain function
Brain cells are linked together with neurons, called axons and dendrites, covered in myelin sheaths. The electrical impulses work together with chemical receptors to allow brain activity to translate into thought and action. Different locations in the brain are associated with specialized function, for example, vision function is located in the occipital lobes, speech production in Broca’s area in the lower part of the frontal lobe, speech recognition is located in Wernicke’s area of the temporal lobe, and the motor strip in the parietal lobes of each hemisphere.
The brain also requires blood flow to provide oxygen and glucose to function. Other chemicals, nutrients, and vitamins are needed for normal function both immediately and in the long term.
Abnormalities and conditions that affect brain function
• The brain develops quickly in the fetus as it grows in a mother’s uterus; and any disruption in this growth and development may lead to encephalopathy.
• Abnormalities in anatomic structure, electrical, and chemical function may lead to altered mental function and encephalopathy.
• Poisoning of brain tissue and cells may also affect function. This poison may be produced within the body, for example from liver or kidney failure, or it may be ingested intentionally or unintentionally. Examples of intentional ingestion include alcohol intoxication or drug abuse. Examples of unintentional ingestion include carbon monoxide poisoning, medications, or toxic substances such as lead paint.
• Encephalopathy may be due to a birth defect (a genetic abnormality causing abnormal brain structure or chemical activity with symptoms being found at birth), or it may be evident towards the end of life due to disease, such as dementia or Alzheimer’s disease.
In some contexts, it refers to permanent (or degenerative) brain injury, and in others it is reversible. It can be due to direct injury to the brain, or illness remote from the brain. In medical terms it can refer to a wide variety of brain disorders with very different etiologies, prognoses and implications. For example, prion diseases, all of which cause transmissible spongiform encephalopathies, are invariably fatal, but other encephalopathies are reversible and can have a number of causes including nutritional deficiencies and toxins.
Signs and symptoms
The hallmark of encephalopathy is an altered mental state. Depending on the type and severity of encephalopathy, common neurological symptoms are loss of cognitive function, subtle personality changes, inability to concentrate, lethargy, and depressed consciousness. Other neurological signs may include myoclonus (involuntary twitching of a muscle or group of muscles), asterixis (abrupt loss of muscle tone, quickly restored), nystagmus (rapid, involuntary eye movement), tremor, seizures, jactitation (restless picking at things characteristic of severe infection), and respiratory abnormalities such as Cheyne-Stokes respiration (cyclic waxing and waning of tidal volume), apneustic respirations and post-hypercapnic apnea.
Blood tests, cerebrospinal fluid examination by lumbar puncture (also known as spinal tap), brain imaging studies, electroencephalograms and similar diagnostic studies may be used to differentiate the various causes of encephalopathy.
Diagnosis is frequently clinical. That is, no set of tests give the diagnosis, but the entire presentation of the illness with nonspecific test results informs the experienced clinician of the diagnosis.
Treatment varies according to the type and severity of the encephalopathy. Anticonvulsants may be prescribed to reduce or halt any seizures. Changes to diet and nutritional supplements may help some patients. In severe cases, dialysis or organ replacement surgery may be needed.
Treating the underlying cause of the disorder may improve or reverse symptoms. However, in some cases, the encephalopathy may cause permanent structural changes and irreversible damage to the brain. These permanent deficits can be considered a form of stable dementia. Some encephalopathies can be fatal.
How Is Encephalopathy Treated?
The treatment for encephalopathy varies according to the cause. Treatment may consist of medications to treat your symptoms and medications or surgery to treat the underlying cause. Your doctor may recommend nutritional supplements to slow the damage to your brain, and/or a special diet to treat underlying causes. In some cases of the disease, such as when the brain does not receive enough oxygen, you may slip into a coma. In severe cases like this, your doctor may put you on life support to keep you alive.
Is Encephalopathy Preventable?
Some types of encephalopathy—like hereditary types—are not preventable. However, some types are preventable.
In general, living a healthy lifestyle can reduce your risk factors for brain disease. Making the following changes can lessen the risk of many underlying causes of encephalopathy:
• avoiding excess alcohol
• reducing exposure to toxic substances like drugs
• eating a healthy diet
• seeing your doctor regularly

Encephalopathy is a general term describing a disease that affects the function or structure of your brain. There are many types of encephalopathy and brain disease. Some types are permanent and some are temporary. Some types are present from birth and never change, while others are acquired after birth and may get progressively worse. Depending upon the cause, encephalopathy may occur at any age. Symptoms may present as a form of altered mental status including confusion and loss of memory because the impairment affects the thought process locations in the brain, or symptoms may present with a physical impairment like weakness or numbness of a body part, or uncoordinated movements because it affects the motor or sensory parts of the brain. Global involvement may present as seizure, or any combination of thought, motor, or sensory symptoms. The symptoms depend on what part of the brain is being affected and how much or how little it continues to function.

“eMedicine/Stedman Medical Dictionary Lookup!”. Retrieved 2008-11-30.
“encephalopathy” at Dorland’s Medical Dictionary

Müller M, Baumeier A, Ringelstein E, Husstedt I (2008). “Long-term tracking of neurological complications of encephalopathy and myopathy in a patient with nephropathic cystinosis: a case report and review of the literature”. J Med Case Reports 2: 235. doi:10.1186/1752-1947-2-235. PMC 2491650. PMID 18644104.


Silicosis (particularly the acute form) is characterized by shortness of breath, cough, fever, and cyanosis (bluish skin). It may often be misdiagnosed as pulmonary edema (fluid in the lungs), pneumonia, or tuberculosis
Silicosis (previously miner’s phthisis, grinder’s asthma, potter’s rot and other occupation-related names) is a form of occupational lung disease caused by inhalation of crystalline silica dust, and is marked by inflammation and scarring in the form of nodular lesions in the upper lobes of the lungs. It is a type of pneumoconiosis.
Silicosis is a long-term lung disease caused by inhaling large amounts of crystalline silica dust, usually over many years. Silica is a substance naturally found in certain types of stone, rock, sand and clay. Working with these materials can create a very fine dust that can be easily inhaled. Once inside the lungs, the dust particles are attacked by the immune system. This causes inflammation (swelling) and gradually leads to areas of hardened and scarred lung tissue (fibrosis). Lung tissue that’s scarred in this way does not function properly.
People who work in the following industries are particularly at risk:
• stone masonry and stone cutting – especially with sandstone
• construction and demolition – because of exposure to concrete and
• paving materials
• pottery, ceramics and glass manufacturing
• mining and quarrying
• sand blasting
Classification of silicosis is made according to the disease’s severity (including radiographic pattern), onset, and rapidity of progression. These include:
• Chronic simple silicosis
Usually resulting from long-term exposure (10 years or more) to relatively low concentrations of silica dust and usually appearing 10–30 years after first exposure. This is the most common type of silicosis. Patients with this type of silicosis, especially early on, may not have obvious signs or symptoms of disease, but abnormalities may be detected by x-ray. Chronic cough and exertional dyspnea are common findings. Radiographically, chronic simple silicosis reveals a profusion of small (<10 mm in diameter) opacities, typically rounded, and predominating in the upper lung zones.

• Accelerated silicosis
Silicosis that develops 5–10 years after first exposure to higher concentrations of silica dust. Symptoms and x-ray findings are similar to chronic simple silicosis, but occur earlier and tend to progress more rapidly. Patients with accelerated silicosis are at greater risk for complicated disease, including progressive massive fibrosis (PMF).
• Complicated silicosis
Silicosis can become "complicated" by the development of severe scarring (progressive massive fibrosis, or also known as conglomerate silicosis), where the small nodules gradually become confluent, reaching a size of 1 cm or greater. PMF is associated with more severe symptoms and respiratory impairment than simple disease. Silicosis can also be complicated by other lung disease, such as tuberculosis, non-tuberculous mycobacterial infection, and fungal infection, certain autoimmune diseases, and lung cancer. Complicated silicosis is more common with accelerated silicosis than with the chronic variety.
• Acute silicosis
Silicosis that develops a few weeks to 5 years after exposure to high concentrations of respirable silica dust. This is also known as silicoproteinosis. Symptoms of acute silicosis include more rapid onset of severe disabling shortness of breath, cough, weakness, and weight loss, often leading to death. The x-ray usually reveals a diffuse alveolar filling with air bronchograms, described as a ground-glass appearance, and similar to pneumonia, pulmonary edema, alveolar hemorrhage, and alveolar cell lung cancer.
The symptoms of silicosis usually take many years to develop and you may not notice any problems until after you've stopped working with silica dust. The symptoms can also continue to get worse, even if you're no longer exposed.
In most cases, exposure for at least 10-20 years is required to cause the condition, although in a few cases it can develop after 5-10 years of exposure or, in rare cases, after only a few months of very heavy exposure.
Factory, mine, and masonry workers are at the greatest risk for silicosis because they deal with silica in their work. Silica is a highly common mineral found in sand, rock, and quartz. People who work in the following industries are at greatest risk:
• asphalt manufacturing
• concrete production
• crushing or drilling rock and concrete
• demolition work
• glass manufacturing
• masonry
• mining
• quarrying
• sandblasting
• tunneling
Workers and their employers must take steps to protect themselves from silica exposure.
The main symptoms of silicosis are:
• a persistent cough
• persistent shortness of breath
• weakness and tiredness
If the condition continues to get worse, these symptoms may become more severe. Some people may eventually find simple activities such as walking or climbing stairs very difficult and may be largely confined to their house or bed. The condition can ultimately be fatal if the lungs stop working properly (respiratory failure) or serious complications develop (see below), but this is rare in the UK.
Silicosis can also increase your risk of other serious and potentially life-threatening conditions, including:
• tuberculosis (TB) and other chest infections
• pulmonary hypertension
• heart failure
• arthritis
• kidney disease
• chronic obstructive pulmonary disease (COPD)
• lung cancer
The links above will take you to more information on these conditions, including their treatment.
People who suspect that they have silicosis should seek medical attention. The physician will ask questions about when or how the patient may have been exposed to silica. They can test lung function with pulmonary function tests.
A chest X-ray can test for scar tissue. On X-rays, silica scars appear as small, white spots.
A bronchoscopy may also be conducted. This procedure involves passing a thin, flexible tube down the throat. A camera attached to the tube allows the physician to view the lung tissue. Tissue and fluid samples can also be taken during a bronchoscopy.
Silicosis does not have a specific medical treatment. The aim of treatment is to reduce symptoms. Cough medicine can help with cough symptoms, while antibiotics can help to treat respiratory infections. Inhalers can be used to open up the airways. Some patients wear oxygen masks to increase the amount of oxygen in the blood.
Patients with silicosis should avoid further silica exposure. Because smoking damages lung tissue, quitting smoking can help. Because silicosis patients are at higher risk for tuberculosis (TB), they should be tested regularly for the condition. A physician can prescribe medications to treat TB. Patients with severe silicosis may require a lung transplant.
Silicosis has become less common over time, thanks to increased work safety rules (MedlinePlus, 2013). However, silicosis can still occur. There is no cure for silicosis. After diagnosis, a person may live a few months to several years (American Lung Association, 2013). The prognosis depends on how severe the condition is. Intense lung scarring can develop in both accelerated and chronic silicosis. Scarring destroys healthy lung tissue, reducing the amount of oxygen the lungs can transmit to the blood.
Workers can wear special masks called respirators to keep from inhaling silica. These masks may be marked for “abrasive blasting” use. Silicosis can be prevented by avoiding prolonged exposure to silica dust. Water sprays and wet cutting methods reduce the risk for silica exposure. Work spaces should meet Occupational Safety and Health Administration (OSHA) standards. This includes proper ventilation. Employers can monitor air quality at worksites, to ensure that excess silica is not in the air. Employers must report all diagnosed incidents of silicosis.
Workers should eat, drink, and smoke away from silica dust. They should also wash their hands before doing any of these activities to reduce silica dust on the hands.
There's no cure for silicosis, as the lung damage cannot be reversed. Treatment aims to relieve symptoms and improve quality of life. The condition may continue to get worse, leading to further lung damage and serious disability, although this may happen very slowly over many years.
The following steps may limit the risk of complications:
• ensure you're not exposed to any more silica
• stop smoking (if you smoke)
• have regular test to check for TB, if advised by your doctor
• have the annual flu jab and the pneumococcal vaccination
You may be offered long-term oxygen therapy if you're having difficulty breathing and have low levels of oxygen in your blood. Bronchodilator medicines may also be prescribed to widen your airways and make breathing easier.
You'll be given a course of antibiotics if you develop a bacterial chest infection.
In very severe cases, a lung transplant may be an option, although there are strict health requirements to meet before this will be considered.

Silicosis is a lung disease caused by breathing in tiny bits of silica, a mineral that is part of sand, rock, and mineral ores such as quartz. It mostly affects workers exposed to silica dust in occupations such mining, glass manufacturing, and foundry work. Over time, exposure to silica particles causes scarring in the lungs, which can harm your ability to breathe.
Silicosis has been a human scourge since antiquity. In 1705, Ramazzini cited Diembrock's description of the lungs of stonecutters "in whom he found heaps of sand that in running the knife through the pulmonary vesicles he thought he was cutting through some sandy body." In 1870, Visconti introduced the term silicosis, derived from Latin silex, or flint. Although silicosis has been recognized for many centuries, its prevalence increased markedly with the introduction of mechanized mining. The prevalence has declined markedly in developed countries in recent decades because of effective industrial hygiene measures


Jane A. Plant; Nick Voulvoulis; K. Vala Ragnarsdottir (13 March 2012). Pollutants, Human Health and the Environment: A Risk Based Approach. John Wiley & Sons. p. 273. ISBN 978-0-470-74261-7. Retrieved 24 August 2012.

Derived from Gr. πνεῦμα pneúm|a (lung) + buffer vowel -o- + κόνις kóni|s (dust) + Eng. scient. suff. -osis (like in asbestosis and silicosis, see ref. 10).
GBD 2013 Mortality and Causes of Death, Collaborators (17 December 2014). "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013.". Lancet. doi:10.1016/S0140-6736(14)61682-2. PMID 25530442.
United States Bureau of Mines, "Bulletin: Volumes 476-478", U.S. G.P.O., (1995), p 63.
Rosen G: The History of Miners' Diseases: A Medical and Social Interpretation. New York, Schuman, 1943, pp.459-476.

Dioscorea bulbifera,

Dioscorea bulbifera, the air potato, is a species of true yam in the yam family, Dioscoreaceae. It is known as varahi in Sanskrit, kaachil in Malayalam and dukkar kand in Marathi. It is native to Africa, southern Asia (India, China, Japan, Philippines, Indonesia, etc.) and northern Australia. It is widely cultivated and has escaped to become naturalized in many regions (Latin America, the West Indies, the southeastern United States, and various oceanic islands.
Air Potato has a winter dormant period when the stems die back to the ground. After dormancy, the underground tubers give rise to stems which quickly grow, often reaching up to 70 feet long by the end of the growing season.
The vine’s stem is herbaceous, not woody and round. The large leaves are up to 8 inches long and are heart-shaped (cordate). The leaf blade’s basal lobes are rounded. Leaf veins radiate from a single point. The leaves have long stems (petioles), and are alternate on the stem. Air Potato flowers are small, greenish and fragrant, hanging in relatively long clusters (panicles and spikes) up to 4 inches long. The fruit is a capsule of seeds. Air potato plants produce “aerial tubers” that are attached closely to the stems where leaves attach to the stem (axil). These air potatoes are grayish and somewhat irregular. Tubers also grow underground where they may be larger.
The scope of study is necessitated by the need to investigate the effect of discora bulbiferia on albino whister rats
The work is limited by lack of availability of space, time and lack of research material on the above topic.
The aim of study is to investigate the antidyslipidemic effect of dioscora bulbiferia on albino wistar rats, thus other objectives includes;
1. To find the effect of disocora bulbieria on albino wistar rats
2. To find the feeding habits of albino wistar rats
3. to find out the effect of antidyslipidemic on albino wistar rats,
3. to profer solutions to the effects of disocora bulbifera on albino rats.

AIR POTATOES Dioscorea bulbifera

Florida is foster home to another invasive non-native Dioscorea, the water yam (= winged yam) Dioscorea alata. D. bulbifera and D. alata are superficially similar in appearance but distinguishing the two is straightforward. D. alata has a stem that is squarish in cross-section with wide ridges or wings, whereas the D. bulbifera stem is round in cross-section. Leaves are opposite in D. alata and alternate in D. bulbifera. The underground tubers of D. alata are also enormous, some weighing more than 45 kg, whereas the undergroind tubers D. bulbifera are small and may even be absent altogether (Langeland and Burks 1998).
Non-native Dioscorea species in Florida may also be mistaken for either of two native wild yams, D. floridana and D. quarternata. The native plants are only infrequently encountered in north and west Florida hammocks and floodplains. Where overlap with the exotic species occurs, the lack of aerial tubers in the native species can aid in identification (Langeland and Burks 1998).
Dioscorea bulbifera can propagate through both sexual and asexual means, In Florida, flowering is rare and sexual reproduction is therefore only a minor contributor to propagation of the species.
Dioscorea species are dioecious, with male and female flowers occurring in separate plants. Flowering is uncommon in the Florida populations but the flowering that does occur takes place in summer. Pollination is dependent on insects, commonly thrips, and the seeds are wind dispersed (Langeland and Burks 1998, Hammer 1998).
The chief means of reproduction in D. bulbifera is asexual and is dependant on vegetative growth from underground tubers and above-ground bulbils. Tubers and bulbils generally sprout in the spring and the new shoots often climb the dead stems of the previous year to reach the tree canopy. In the summer (June-July), a large number of new bulbils are produced which fall to the ground in late August. By the time seasonal stem die-back begins around October, a single vine may have put out as many as 200 bulbils (swww.killerplants.com 2004).
In areas where they are produced, Dioscorea bulbifera seeds are wind-dispersed (Hammer, 1998). Even where flowering occurs more regularly, sexual reproduction via seed is still likely of secondary importance. Seeds of D. bulbifera and other members of the genus are believed to undergo an obligate dormancy period of several months before they germinate. This strategy is probbably an evolutionary adaptation to ensure the presence of viable seeds in the seed bank when breaks in forest canopy cover occur. A laboratory germination regime for viable, non-dormant D. bulbifera seeds indicates that germination occurs in approximately 21 days at 30°C (Ellis et al. 1985).
Bulbils can last a year or more on the ground and still sprout, and soil contact in not necessary for sprouting. They also float and may be dispersed by flood waters and appear to be little impacted by feeding from raccoons, feral pigs, and other animals (Coursey 1967, Morisawa, 1999).
Air potato is one such non-native, invasive plant. This vine can grow eight inches a day and produces large numbers of potato-like growths that sprout new plants.

Aerial yam (Discoreabulbifera) belongs to Discoreae species, in Nigeria the aerial yam plants are predominantly noticed in some parts of the country which include Ibadan, oyo, Ogbomosho, Ile Ife, Ile Oluji, Ikire and Akure. It grows in a wide range of soils and most varieties require long rainy seasons. The Planting procedure include planting the bulbils or tubers either whole or small pieces, the tubers produced by the plants grown from bulbils are usually very small in the first year and often used as sets for planting the following year to produce edible tubers of a reasonable size. The tubers are occasionally used for the production of flour, they are also used has food in times of scarcity, but detoxification is necessary and this is done by soaking in water or prolong boiling before they are safe to consume and are very useful medicinally.
Wild yam(Discoreavillosa) is a plant native to North America, Mexico and Asia. In Nigeria the wild yam plants are predominantly seen in western part of the country like Owo, Oyo, Ogbomosho, Ikire Ile -Ife. It is believed to bea wonderful, natural hormone regulator. The herb
contains compound that are similar to female hormones which are helpful for female disorders. It contains natural steroid called dehydro-epiandrosterone(DHEA) that is said to rejuvenate and give vigor to love making. It is also considered to be a liver cleaner,it is has sometimes been called one of the best natural relievers of jaundice, and nausea.
There are many species of the genus discoreaa and lot of research work has been done on them but wild yam(Discorea villosa) and aerial yam(Discorea bulbifera) have not been investigated for their Rheological properties. The essence of the study is to carry out the rheological properties of the two varieties of the yam, wild yam(Discoreavillosa) and aerial yam(Discoreabulbifera).

Material used for the study includes;
-animal cage
-Albino wistar rat
-weighing balance
-Dioscorea bulbifera
-masking tape
-animal feed (Rat feed)
-animal fats (high fat diet)
-saw dust
-tables, etc

Air potato is a member of the yam family (Dioscoreaceae). Yams are cultivated for their edible underground tubers in western Africa, where they are important commodities. However, uncultivated species—such as air potato—are generally bitter and even poisonous. Air potato is a vigorously twining herbaceous vine, often arising from an underground tuber. Freely branching stems grow to 60 ft. in length. Stems are round or slightly angled in cross section and twine to the left (counter-clockwise). Aerial tubers (bulbils) freely form in leaf axils. Bulbils are usually roundish with mostly smooth surfaces, and grow up to 5 in. x 4 in. Leaves are long petioled (stalked), alternate; blades to 8 in. or more long, broadly heart shaped, with basal lobes usually rounded and with arching veins all originating from one point. Flowers are rare (in Florida), small, and fragrant, with male and female arising from leaf axils on separate plants (i.e., a dioecious species) in panicles or spikes to 4 in. long. Fruit is a capsule; seeds are partially winged.

Coursey, D.G. 1967. Yams: an account of the nature, origins, cultivation, and
utilization of the useful members of Dioscoraceae. London: Longmans,
Green and Co. Ltd. 230 pp.
Ellis R.H, Hong T.D., and E.H. Roberts. 1985. Handbook of seed technology for
genebanks – Volume II. Compendium of specific germination information and test recommendations. International Board for Plant Genetic Resources, Rome. Available online.
Hammer, R.L. 1998. Diagnosis: Dioscorea. Wildland Weeds:8-10.

Horvitz C.C., Pascarella J.B., McMann S., Freedman A., and R.H. Hofstetter.
1998. Functional roles of invasive non-indigenous plants in hurricane-
affected subtropical hardwood forests. Ecological Applications. 8:947-974.

Langeland K.A. 2001. Natural Area Weeds: Air Potato (Dioscorea bulbifera).
UF/IFAS Document SS AGR 164. 4 pp. Available online.

Langeland K.A. and K. Craddock Burks. 1998. Identification and Biology of
Non-Native Plants in Florida’s Natural Areas, IFAS Publication SP 257. University of Florida, Gainesville. 165 pp.

Morisawa T.L. 1999. Weed Notes: Dioscorea bulbifera, D. alata, D.
sansibarensis. The Nature Conservancy. Wildland Invasive Species Program.


Use any of these method below to link your BVN to your other bank account;
1. Link Your BVN to your other account using ATM machine
To link your BVN Link via ATMs;
• visit any ATM machine close to you
• Insert bank ATM Card
• Select BVN Link on the transaction menu screen
• Enter your 11-Digit BVN (gotten by dialling *565*0#)
• Confirm your BVN details
• Submit your BVN
2. BVN linking online
For GTBank customers
• Log on to GTBank Internet Banking
• Select BVN Linker from the left-hand panel
• Click on New Request
• From the drop down menu, insert your Bank Verification Number
• Select the Nigerian Bank where your BVN was Issued
• Answer your Secret Question and continue
For FCMB customer
BVN Linking online
if you are registered for e-banking, go to your profile under ‘NO BVN LINK HERE’ and link
BVN Linking by email
send an email to customerservice@fcmb.com
1. Account name
2. Account number
3. BVN number
4. bank you initially registered and got your BVN number from
For SKYEBANK Customers
BVN Linking online
if you are registered for e-banking, go to your profile and link it from there,
BVN Linking by email
Send an email to. yescenter@skyebankng.com
1. Account name
2. Account number
3. BVN number
4. bank you initially registered and got your BVN number from
For Zenith bank customers
BVN Linking online
if you are registered for e-banking, go to your profile and link it from there,
BVN Linking by email
request for bvn update form from their twitter team @ZenithBank , fill and email to zenithdirect@zenithbank.com.
3. Link your BVN via Gtbank Verification Number Portal For Gtbank Customers
• Enter Nuban (GTBank account number)
• Select bank account you wish to link to.
• Enter your BVN
• Type the text for Captcha
• Hit submit
4. Link your BVN via text code
For Fidelity Bank customers
• Send your BVN to 09035090000 to link to your other bank accounts
For ACCESS BANK customers
BVN Linking by Text Message
With the Access BVN short code, you can link your BVN to your Access Bank Account. To do this, simply text BVN, your account number and BVN number to 20121. E.g: BVN 0123456189 78956834758 to 2021
For UBA customers
BVN Linking by Text Message
All a customer has to do is to send his or her valid BVN from the telephone number that was used to open their account to the short code number and it will become automatically linked,


An educational psychologist is a psychologist whose differentiating functions may include diagnostic and psycho-educational assessment, psychological counseling in educational communities (students, teachers, parents and academic authorities), community-type psycho-educational intervention, and mediation, coordination, and referral to other professionals, at all levels of the educational system. Many countries use this term to signify those who provide services to students, their teachers, and families while other countries use this term to signify academic training in the discipline of educational psychology, with no intention of preparing persons to provide services.
An educational psychologist is concerned with helping children or young people who are experiencing problems within an educational setting with the aim of enhancing their learning.
Challenges may include social or emotional problems or learning difficulties. Work is with individual clients or groups, advising:
• teachers
• parents;
• social workers;
• other professionals.
Client work involves an assessment of the child using observation, interviews and test materials. Educational psychologists offer a wide range of appropriate interventions, such as learning programmes and collaborative work with teachers or parents.
They also provide in-service training for teachers and other professionals on issues such as behaviour and stress management. Thus Educational psychology is the branch of psychology concerned with the scientific study of human learning. The study of learning processes, from both cognitive and behavioral perspectives, allows researchers to understand individual differences in intelligence, cognitive development, affect, motivation, self-regulation, and self-concept, as well as their role in learning. The field of educational psychology relies heavily on quantitative methods, including testing and measurement, to enhance educational activities related to instructional design, classroom management, and assessment, which serve to facilitate learning processes in various educational settings across the lifespan
Entrepreneurship is a multidimensional process.
A look at the vast array of research on entrepreneurs indicates that there is still no standard universally accepted definition of an entrepreneur. The definition used in a particular study is dependent on what one’s intent is, or what one hopes to accomplish. For the purpose of this study as an educational psychologist, entrepreneurs are defined as individuals who pursue opportunities with a long-term focus in mind (Miner, 1997; Begley, 1995). This definition recognizes that tendencies such as internal locus of control, achievement orientation, risk taking propensity and work values, are important in analyzing the psychology of entrepreneurs.
Although entrepreneurship is mostly associated with the fields of administration, management and economy, in fact it is an interdisciplinary subject. Entrepreneurship and enterprise as being a broad subject and conceptual field was studied within the field of
psychology, at least at the beginning, more than the fields of economy, administration and management. The studies of psychology over entrepreneurship have played an important role for a detailed consideration of the concept and in giving the concept the broader meaning that is used now. One of the first studies of psychology over entrepreneurship was conducted by Mc Clelland, Atkinson and Feather in the second half of twentieth century.
According to them, the motivation of individual and society is one of the most important factors that explain entrepreneurship and individual’s becoming an entrepreneur depends on the highest possibility of achievement (Korpysa, N.d). In other words, when the
possibility of achievement gets higher, entrepreneurial propensity rate increases. Studies in the field of psychology have focused on the details of the factors that play a role in entrepreneurship’s achievement (Baron, 2000).These studies stated that entrepreneurial ability of individual is connected with societies’ perception of success and to what extent individuals are affected by this perception. However, even if it was stated that culture influence entrepreneurship, it was observed that individual differences have important effects on entrepreneurship despite cultural commonality.
Psychology’s extensive interest for the subject matter of entrepreneurship at the beginning is closely associated with periodic interest to understand psychological dynamics of human
Entrepreneurship – Born, Made and Educated behaviors. Studies that were focused over people’s relationships with enterprises and
organizations realized that not only enterprises affect individuals, but also individuals affect enterprises. Therefore, when the characteristics of individuals were studied, it was wondered whether individuals with entrepreneurial characteristics affect enterprises more strongly so they looked for an answer for the question of “Who is the entrepreneur?” In this process, the data about entrepreneurship that psychology obtained became popular and the relationship between entrepreneurship and the characteristics like risk-taking, uncertainty avoidance, power distance, need for achievement and risk-management has been studied.
However, although psychology was in the first place in the development of entrepreneurship research, later using the findings of psychology in understanding entrepreneurship was abandoned. The fact that research that has been carried out in psychology field is often limited by character approaches and over-emphasis of the effects of personality over the consequences played a role in this divergence. However, in later years the picture changed again and empirical studies that put forward the importance of psychological variables increased. From then on studies over the characteristics of individual with entrepreneurial qualities and entrepreneurship culture have become widespread and research over entrepreneurship in the field of psychology has become the focus of interest again. When we consider it in general, it is possible to analyze the studies over entrepreneurship that psychology carried out and emphasized individual traits in two groups. One group of
these studies has looked for a connection between entrepreneurship and personal characteristics and proved that individuals with entrepreneurial qualities are self-controlled, self-confident and competitive people. They also have a great imagination and they do not avoid risks. Another group of study examined motivation resources of entrepreneurial individual and has discovered that entrepreneurship is nurtured by sources such as motivation for achievement, power distance and willingness for taking risks. Besides, the studies that focused on entrepreneurship’s relationship with culture try to uncover cultural resources that nurture and weaken entrepreneurship; therefore, entrepreneurship is also studied as an issue that draws socio-psychology’s attention. Nowadays, entrepreneurship research continues by making associations with psychological variables like cognitions, emotions, perceptions, behaviors and motivation and the effects of psychological variables over entrepreneurship cannot be ignored. Even if different countries seem to have different development policies, especially since 1980s, entrepreneurship has become more important due to competitive development program that countries have to apply because of neo liberal development policies. The fact that societies have to increase their share in international markets or maintain their own national markets depends on the existence of human resources who have entrepreneurial characteristics to a certain extent.

Entrepreneurship psychology indicates many intersection points between industrial/organizational psychology and entrepreneurship. First of all, organizations which are the central phenomenon of organizational psychology exist by means of entrepreneurship and entrepreneurs. Organizations have to renovate themselves regularly so as to continue their own existence and in order not to be destroyed by their competitors who aimed at the same targets in tough market conditions. Providing this renovation is only possible by watching over the possibilities and opportunities in the market. Therefore, some of the individuals in every organization must have entrepreneurial skills such as innovative thinking, creative, risk-taking, and powerful future design; they also have to be bold and self-confident. One of the main elements in this kind of organization is entrepreneurship.
This process leads industrial/organizational psychology researchers to study entrepreneurship process.

• Cameron, R. J. (2006). Educational psychology: The distinctive contribution. Educational Psychology in Practice, 22, 289-304.
• • Fagan, T. K., & Wise, P. S. (Eds.). (2007). School psychology: Past, present and future (3rd ed.). Bethesda, MD: National Association of School Psychologists. ISBN 978-0-932955-71-5.
• • Jimerson, S. R., Oakland, T. D., & Farrel, P. T. (Eds.).(2007). The handbook of international school psychology. Thousand Oaks, CA: Sage. ISBN 978-1-4129-2669-0.
• • Mayer, R., & Alexander, P. A. (Eds.) . (2010). Handbook of research on learning and instruction. New York: Routledge. ISBN 978-0-415-80461-5.
• • Reynolds, W. M., & Miller, G. J. (Eds.).(2003). Handbook of psychology. Vol. 7: Educational Psychology. New Jersey: Wiley. ISBN 978-0-471-38406-9.
• • Wittrock, M. C. (1992). «An empowering conception of educational psychology». Educational Psychologist, 27, 129-141.
• • Zimmerman, B. J., & Schunk, D. H. (Eds.). (2003). Educational psychology: A century of contributions. Mahwah, NJ: Erlbaum. ISBN 978-0-8058-3682-0.
• • Bonfenbrenner, U. (1979). The ecology of human development: Experiments by nature and design. Cambridge, MA: Harvard University Press. ISBN 0-674-22457-4.
• • Watkins, M. W., Crosby, E. G., & Pearson, J. L. (2001). Role of the school psychologist: Perceptions of school staff. School Psychology International, 22, 64-73.
• Fernández, J. (2008). Assessment of teaching quality: A circular model of evaluation. Madrid: Editorial Complutense. ISBN 978-84-7491-943-1.


Emergency services and rescue services are organizations which ensure public safety and health by addressing different emergencies. Some of these agencies exist solely for addressing certain types of emergencies whilst others deal with ad hoc emergencies as part of their normal responsibilities. Many of these agencies engage in community awareness and prevention programs to help the public avoid, detect, and report emergencies effectively. The availability of emergency services depends very heavily on location, and may in some cases also rely on the recipient giving payment or holding suitable insurance or other surety for receiving the service.
There are three main emergency service functions:
• Police — providing community safety and acting to reduce crime against persons and property
• Fire department (fire and rescue service) — providing firefighters to deal with fire and rescue operations, and may also deal with some secondary emergency service duties
• Emergency medical services (EMS) — providing ambulances and staff to deal with medical emergencies
In some countries such as the UK, these three functions are performed by three separate organizations in a given area. However, there are also many countries where fire, rescue and ambulance functions are all performed by a single organization.
Emergency services have one or more dedicated emergency telephone numbers reserved for critical emergency calls. In some countries, one number is used for all the emergency services (e.g. 911 in the U.S., 999 in the UK). In some countries, each emergency service has its own emergency number.
These services can be provided by one of the core services or by a separate government or private body.
• Military — to provide specialist services, such as bomb disposal or to supplement emergency services at times of major disaster, civil dispute or high demand.
• Coastguard — Provide coastal patrols with a security function at sea, as well as involvement in search and rescue operations
• Lifeboat — Dedicated providers of rescue lifeboat services, usually at sea (such as by the RNLI in the United Kingdom).
• Mountain rescue — to provide search and rescue in mountainous areas, and sometimes in other wilderness environments.
• Cave rescue — to rescue people injured, trapped, or lost during caving explorations.
• Mine rescue — specially trained and equipped to rescue miners trapped by fires, explosions, cave-ins, toxic gas, flooding, etc.
• Technical rescue — other types of technical or heavy rescue, but usually specific to a discipline (such as swift water).
• Search and rescue — can be discipline-specific, such as urban, wildland, maritime, etc.
• Wildland fire suppression — to suppress, detect and control fires in forests and other wildland areas.
• Bomb disposal — to render safe hazardous explosive ordnance, such as terrorist devices or unexploded wartime bombs.
• Blood/organ transplant supply — to provide organs or blood on an emergency basis, such as the National Blood Service of the United Kingdom.
• Emergency management — to provide and coordinate resources during large-scale emergencies.
• Amateur radio emergency communications — to provide communications support to other emergency services, such as RAYNET in the UK
• Hazmat — removal of hazardous materials
• Air search providing aerial spotting for the emergency services, such as conducted by the Civil Air Patrol in the US, or Sky Watch in the UK.

These groups and organizations respond to emergencies and provide other safety-related services either as a part of their on-the-job duties, as part of the main mission of their business or concern, or as part of their hobbies.
• Public utilities — safeguarding gas, electricity and water, which are all potentially hazardous if infrastructure fails
• Emergency road service — provide repair or recovery for disabled or crashed vehicles
• Civilian Traffic Officers — such as operated by the Highways Agency in the UK to facilitate clearup and traffic flow at road traffic collisions
• Emergency social services
• Community emergency response teams — help organize facilities such as rest centers during large emergencies
• Disaster relief — such as services provided by the Red Cross and Salvation Army
• Famine relief teams
• Amateur radio communications groups — provide communications support during emergencies
• Poison Control — providing specialist support for poisoning
• Animal control — can assist or lead response to emergencies involving animals
• Forest Service
• St. John Ambulance / Red Cross / Order of Malta Ambulance Corps — Medical & First Aid Support
The Rivers State Police Command is the state branch of the Nigerian Police Force in Rivers State. It is responsible for maintaining public order and safety, enforcing the law, and preventing crime. The Rivers State police has 3 area commands with 52 divisional police headquarters, 25 police stations and 23 police outposts. It is headed by a Commissioner of Police and has a staff strength of about 17,207.Its Headquarters is at Moscow Road, Port-Harcourt, Rivers State, Nigeria.
Tel: 07059171776, 07059171818, 08094504256
Email: info@npf.rv.gov.ng
Website: http://www.npf.rv.gov.ng

The Rivers State Fire Service is the state-owned firefighting body in Rivers State, primarily tasked with providing fire protection, emergency response and safety services to the state, its residents and visitors. The Fire Service has stations located at Borokiri, Port Harcourt, Degema, Ahoada and Rumuodomaya with HQ at Aba Road, Mile Park, Port Harcourt. Its activities are overseen by the Rivers State Ministry of Special Duties.07031522199
Address: 51, Ikwerre Road, Mile 1, Diobu, Port Harcourt, Rivers
Phone: 0803 340 1017

Federal Road Safety Corps is the government agency with statutory responsibilities for road safety administration in Nigeria. Founded in 1988, the Federal Road Safety Corps (FRSC) operates in all Nigerian states as well as the Federal Capital Territory. The Federal Road Safety Commission (FRSC) Nigeria. Established in 1988, the FRSC is the lead agency in Nigeria on road safety administration and management. The statutory functions include: Making the highways safe for motorists and other road users, recommending works and infrastructures to eliminate or minimize accidents on the highways and educating motorists and members of the public on the importance of road discipline on the highways. The FRSC is currently headed by Boboye O Oyeyemi, MFR, mni whose title is the Corps Marshal and Chief Executive (COMACE) the highest rank in the Corps ranking system.
The FRSC rivers command is a branch of the federal body.
frsc emergency text message number 0807 – 7690 – 362. frsc emergency contact number 0700 – 2255 – 3772.
Effective emergency service management requires agencies from many different services to work closely together and to have open lines of communication. Most services do, or should, have procedures and liaisons in place to ensure this, although absence of these can be severely detrimental to good working. There can sometimes be tension between services for a number of other reasons, including professional versus voluntary crew members, or simply based on area or division. To aid effective communications, different services may share common practices and protocol for certain large-scale emergencies.
Lastly, the government has established a short code (112) to provide a platform for Nigerians to call for help irrespective of the location and the circumstance and get help.



The relationship between Paul the Apostle and women is an important element in the theological debate about Christianity and women because Paul was the first writer to give ecclesiastical directives about the role of women in the Church. However, there are arguments that some of these writings are post-Pauline interpolation.
By the time Paul began his missionary movement, women were important agents within the different cities. Letters generally accepted as Paul’s are Romans, 1 and 2 Corinthians, Galatians, Philippians, 1 Thessalonians and Philemon. His casual greetings to acquaintances offer solid information about many Jewish and Gentile women who were prominent in the movement. His letters provide vivid clues about the kind of activities in which women engaged more generally.
In several of his letters (epistles), Paul sends greetings to a number of people and specifically mentions the following as being important in ministry:
• Priscilla (Prisca) and her husband Aquila. She and her husband are mentioned seven times in the New Testament as being missionary partners with the Apostle Paul.
• Mary and “the beloved Persis” are commended for their hard work.
• He greets Julia, and Nereus’ sister, who worked and traveled as missionaries in pairs with their husbands or brothers.
• He commends to their hospitality, Phoebe, a leader from the church at Cenchreae, a port city near Corinth
• Junia is also mentioned. According to Bart Ehrman, Paul praises Junia as a prominent apostle who had been imprisoned for her labor.
• Chloe, was a prominent woman of Corinth. It was from “Chloe’s people” that Paul, then at Ephesus learned of the divisions in the congregation of Corinth.
• In Philippians he expresses appreciation for Euodia and Syntyche his fellow-workers in the gospel.
According to Karen King, these biblical reports seem to provide credible evidence of women apostles active in the earliest work of spreading the Christian gospel.
In Galatians 3:28, Paul wrote that there is “neither male nor female” for all are one in Christ.
The discussion of head coverings for women in 1 Corinthians 11:2–16 clearly implies and assumes that women, as well as men, engage in prayer and prophecy (1 Corinthians 11:5). The participation in prophecy is the “highest” gift in the Church because it is the means of edification, encourage-ment, and comfort in the Church (1 Corinthians 14:3). Such edification is the purpose of the Church’s life together and constitutes, under the Holy Spirit, the exercise of authority and teaching in the Church. Thus, Paul concludes the first part of his discussion on head coverings (1 Corinthians 11:2–10) by stating that women ought to have authority on their heads. First Corinthians 11:10 is rarely translated accurately in English (most often one finds “a sign of authority” or “veil”), but Paul asserts that women have authority, using his normal word, which always means the active exercise of authority (and never the passive reception of it).

Galatians 3:28, like Acts 2, has been cited for hundreds of years as a basis for women in ministry. Detractors of women in ministry often argue that Galatians 3:28 refers only to the spiritual reality of equal access to God through faith in Christ Jesus. The text does refer to this, but it clearly encompasses other realities as well. There are three traditional pairings, and they reflect the three basic social divides of hostility within the first century AD in the Roman Empire. Paul’s declaration would have had no less actual social impact than an American preacher’s statement in the 1950s that “in Christ Jesus there is neither Black nor White” would have had.

• Odell-Scott, D.W. “Editorial dilemma: the interpolation of 1 Cor 14:34–35 in the western manuscripts of D, G and 88.” Web: 15 Jul 2010.
• • Ingrid Maisch (1998). Mary Magdalene: the image of a woman through the centuries. Liturgical Press. ISBN 978-0-8146-2471-5.
• • Margaret MacDonald, “Reading Real Women Through Undisputed Letters of Paul” in Women and Christian Origins, ed. by Ross Sheppard Kraemer and Mary Rose D’Angelo (Oxford: University Press, 1999), p. 204
• • Elisabeth Schüssler Fiorenza (1994). In Memory of Her: A Feminist Theological Reconstruction of Christian Origins. The Crossroad Publishing Co. ISBN 978-0-8245-1357-3.
• • Leonhard O.S.F., Barbara. “St. Paul and Women: A Mixed Record”, St. Anthony Messenger, Franciscan Media
• Frontline: from jesus to christ – the first christians: paul’s mission and letters. PBS. Retrieved on 2011-02-13.