Peptic ulcer disease is one of the most prevalent gastrointestinal disorders that affect millions of people per year. The pathophysiology of peptic ulcer has centered on an imbalance between aggressive and protective factors in the stomach. Ulcer healing is a cumulative effect of several physiological and constitutive processes that occurs in tandem. A high degree of coordination and regulation during complex sequence of ulcer healing is carried out by different factors. Among them prostaglandins and growth factors have received much attention in recent years. Prostaglandin gets synthesized in the mucosal cells by cyclooxygenase (COX) enzyme. Therefore, induction of COX-2 expression leading to higher level of prostaglandin appears to be an important contributing factor in drug mediated ulcer healing apart from the respective mechanisms of different drugs.
risk of complications and socioeconomic impact (absenteeism, high cost of the explora- tions and treatments). Studies led in Australia and in Great Britain gave prevalence between 5.2% and 9.9% in the general population . In Black Africa, since the intro- duction of endoscopy (1980), more and more publications show that this disease occu- pies a significant place in the pathology of the black African. In Mali, Togo and Congo the prevalence of the Peptic Ulcer Disease (PUD) was respectively 10.88%, 15.53% and 30.42%   .
DOI: 10.4236/gep.2019.74017 268 Journal of Geoscience and Environment Protection expansion of the pathogens of the ulcer disease. However, in the spring of 2017, Langqi occurred two times of low-temperature and high-humidity weather, which occurred in the middle to late mid-March and The average daily temper- ature for continuous 14 days is 6.8˚C - 15.1˚C, the daily average relative humid- ity is 80% - 98%, and the average temperature for the 8th day in late April is 11.5˚C - 14.6˚C, and the daily average relative humidity is 82% - 100%. Weather (Figure 4(b1)); 2 times of low temperature and high humidity weather occurred in Pugu, respectively, in mid-March and averaged 9.6˚C to 14.2˚C for 5 consecu- tive days, daily average relative humidity of 82% to 94% and continuous in late April The average daily temperature of 6d is 13.3˚C - 16.1˚C, and the daily aver- age relative humidity is 83% - 88% (Figure 4(b2)). Rice bran also occurs twice in low temperature and high humidity, which appears in early March and is conti- nuous. The average daily temperature of 5 d is 7.7˚C - 11.2˚C, The average rela- tive humidity of 88% to 95% in late April and 8d consecutive daily average tem- perature of 13.0˚C - 16.3˚C, daily average relative humidity of 81% to 95% of the low-temperature and humid weather (Figure 4(b3)). It can be seen that the me- teorological conditions in winter cannot satisfy the proliferation and expansion of the pathogens of ulcer disease, but the tree body should be accompanied by ulcerative pathogens. Once the spring temperature and humidity conditions sa- tisfy the active pathogen of the ulcer disease, the leaves of the red heart kiwifruit can reflect the symptoms of ulcer disease.
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Moynihan, an Irish surgeon was the first to relate the clinical symptoms of peptic ulcer disease with the pathological findings. [69-70] It has been reported that small ulcers may not cause any symptoms and large ulcer can cause serious bleeding.  The most common symptom is burning pain, especially just below the breast bone.  Gastric ulcer pain may be less severe than duodenal ulcer pain and is noticeably higher in abdomen. Eating may increase pain in subjects rather than relieving pain. Other symptoms may include nausea, vomiting and weight loss. Vomiting might be related to partial or complete gastric outlet obstruction. Duodenal ulcer pain may awaken the patients from sleep and also involve burning or gnawing sensation in upper abdomen. Pain in back, lower abdomen or chest area may occasionally arise and occurs when the stomach is empty about two hours after a meal or during the night. Relief frequently occurs after eating.  Epigastric tenderness, melena resulting from acute or sub acute gastrointestinal bleeding and complete gastric outlet obstruction may also occur in ulcer disease. 
Peptic ulcer is a worldwide health problem because of its high morbidity, mortality and enormous financial implication. An estimated 15,000 deaths per year occur as a consequence of complicated PUD. A large number of drugs for peptic ulcer disease are available in mainstream medicine but they are associated with numerous side effects like arrhythmias, impotence, gynaecomastia and haematopoietic changes and the recurrence is also very common. In recent times, focus on plant research has increased all over the world and a large body of evidence has been collected to show immense potential of medicinal plants used in various traditional systems. Here, an attempt is made to summarise experimentally proved herbs used in PUD during last decade.
show geographic differences in Western and Eastern populations. The VacA protein represents one of the major secreted virulence factors of H. pylori. The toxin has two domains, p33 and p55, are cleaved after secretion from the bacteria. The p33 domain is responsible for pore formation rather than enzymatic activity, and the p55 domain is responsible for interaction with the host cell membrane. The VacA protein is capable of internalizing and inducing the formation of intracellular vacuoles due to the osmotic swelling of late endocytic compartments. A large variety of additional cytotoxic functions has been attributed to VacA in the recent years such as altering the endosomal function, inhibiting T-cell proliferation, internalizing and damaging mitochondria, and inducing apoptosis both in epithelial and immune cells. The vacA gene is present nearly in all H. pylori strains, including both toxin positive and negative isolates,but only 50% of strains induce toxic vacuolization in certain cell lines (6). Depending on the vacA gene,strains were further classified into three categories of high vacuolation (s1/i1/m1), low vacuolation (s1/i1/m2), and non- vacuolation (s2/i2/m2, s1/i2/m1, s1/i2/m2, and s2/i1/m2). The cagA gene contributes to the development of peptic ulcer disease, while the presence of the vacA gene is a risk factor for increased activity and gastritis severity (5).Based on the presence or absence of the cytotoxin- associated gene-pathogenicity island (cagPAI) and the vaculating cytotoxin (VacA), H. pylori strains were categorized as type I or typeII, respectively. The correlation between cagA gene and VacA protein expression is not yet clear. The researchers have shown functional antagonism between vacA and cagA gene in host cells in the processes of nuclear factor of activated T-cells (NFAT) and (2) epidermal growth factor (EGF) receptor signaling (2-4) that could cause morphological changes. Patients with peptic ulcer disease show an increase in Th1 and Th2 cellular responses. In contrast, the role of T-regulatory (Treg) cells appears as a protective factor against epithelial cell injury. Treg cells secrete IL10 is inversely correlated with IL-8 and NF-κB (nuclear factor kappa B) in Table 1. Demographic information of 130
Peptic ulcer disease is a common benign ulceration of the epithelial lining of the stomach (gastric ulcer) or duodenum (duodenal ulcer). Under normal conditions, a physiologic balance exists between peptic acid secretion and gastro duodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occurs when the balance between the aggressive factors and the defensive mechanisms is disrupted. Peptic ulcer disease has been a major threat to the world’s population over the past two centuries, with a high morbidity and substantial mortality 1 . It has been found that H. pylori is the
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experimented in rats at a dose of 2.5 g/kg. It was studied on various parameters of possible mechanism for treating ulcer. The main mechanism is to prevent acid- pepsin secretion. Neem did not show any effect on mucin secretion though it improved life span of mucosal cells as evidenced by a decrease in cell shedding in the gastric juice. Thus the ulcer protective activity is due to its anti-secretory and proton pump inhibitory activity rather than on defensive mucin secretion. Bark extract of Azadirachta indica inhibits H+-K+-ATPase activity in vitro. It stops oxidative damage of the gastric mucosa by blocking lipid peroxidation and by scavenging the endogenous hydroxyl radical (OH), the major causative factor for ulcer 11,12,13 .
Peptic ulcer development depends on age and gender; accordingly, all the selected patients were matched accurately in terms of their age and gender. Four biopsy speci- mens were taken from the antrum and gas- tric body of each patient for histological study. All the specimens were stained by hematoxylin and eosin stain (H&E) or Giemsa after having been fixed overnight in buffered formalin, embedded in paraffin, and cut in five µm thickness. The speci- mens were evaluated by a pathologist. If at least five bacilli in each microscopic field were found, H. pylori was considered posi- tive. Five milliliters of blood sample was taken from each patient and was sent to the Immunology Laboratory of Iran University of Medical Sciences for centrifuge and anti- cagA antibody measurement.
the functional parietal cell volume or secretory capacity in smokers. Smoking causes mucosal injury by increasing content of free oxygen radicals, PAF, pituitary vasopressin, gastric endothelin and pituitary vasopressin. Smoking and nicotine stimulate pepsinogen secretion also by increasing chief cell number or with an enhancement of their secretory capacity. Long-term nicotine treatment in rats also significantly decreases total mucus neck cell population and neck-cell mucus volume. Bile salt reflux rate and gastric bile salt concentration are increased thereby increasing duodenogastric reflux that raises the risk of gastric ulcer in smokers. Smoking and nicotine not only induce ulceration, but they also potentiate ulceration caused by H.pylori, alcohol, NSAID or cold restrain stress. Smoking also alter processes important in gastric and duodenal mucosal integrity or protection such as mucosal bicarbonate secretion, prostaglandin content, mucosal blood flow, or epidermal growth factor [95,96] .
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The rationality of such a treatment strategy is questionable. Some authors however favour the empirical treatment strategy for all patients with duodenal ulcer, even without confirmation of the infection 13, 14, 15, 16, 17, 18 . The argument saying that the cost of such confirmatory tests to determine H. pylori infection is high, and also that such results may be misleading in case of a false negative result. This justifies the empirical use of HP kits but the widespread use of antibiotics for H. pylori eradication may itself pose another public health problem in the form of antibiotic resistance.
Objectives. Investigating the nocturnal secretion of melatonin in patients with duodenal ulcer or ulcer−like dyspepsia. Material and Methods. The investigations were carried out in 34 patients with recent duodenal ulcer (DUD), 36 patients with functional ulcer−like dyspepsia (ULD, according to the Rome Criteria II), and in 30 healthy control sub− jects. Blood samples were taken for examination in a red−lit room at 10 p.m. and then at 2 and 6 a.m. The serum con− centration of melatonin was measured with ELISA before and after a six−week treatment with omeprazole (40 mg daily). Patients with H. pylori infection additionally took amoxicyllin (2.0 g) and clarithromycin (1.0 g) for seven days. Results. The average melatonin concentration in duodenal ulcer patients was lower than in the healthy subjects (25.50 ± 6.22 pg/ml and 34.71 ± 4.72 pg/ml, respectively; p < 0.05). The highest concentration of melatonin was found in patients with ulcer−like dyspepsia (42.42 ± 9.93 pg/ml, p < 0.05). After six weeks, the duodenal ulcers healed and dyspeptic symptoms improved in all patients, but nocturnal secretion had not changed significantly. Conclusions. The findings suggest that melatonin may play an important role in the pathogenesis of duodenal ulcer disease. In patients with ulcer−like dyspepsia, the influence of melatonin on nocturnal and fasting abdominal pains is also possible (Adv Clin Exp Med 2006, 15, 5, 811–815).
and clinical cure are not always the same. In other words, even though M ulcerans was successfully eliminated from the lesion site with antibiotic treat- ment (microbiological cure), this does not correspond to clini- cal cure if the patient has already manifested an ulcer. Moreover, in such ulcerated cases, methods used in wound care would also modify the healing process; this is another challenge in correctly evaluating antimicrobial treatment efficacy in people with Buruli ulcer. Selection of wound care methods is often dependent upon daily practice and resource availability. Velding 2014 documented that there was a wide diversity in local wound care methods prac- ticed by health practitioners/healthcare givers in Ghana and Benin. Due to these atypical clinical features and medical practices re- lated to the disease, it has been difficult to develop a clear case definition for cure. Many studies evaluating treatment efficacy in Buruli ulcer disease have used complete epithelialization, Chauty 2007; Sugawara 2015, or reduction in wound size, Etuaful 2005; BURULICO Study 2010; Sugawara 2015, as their definition of cure (clinical cure), while a few studies have also used microbio- logical cure as their case definition of cure, employing laboratory methods (Etuaful 2005; Sarfo 2010).
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More recently, proton pump inhibitors (PPIs) are replacing the H2-receptor antagonists in clinical practice, as a result of improved efficacy in the treatment of a number of gastrointestinal diseases with PPIs. Lifestyle modifications (weight loss, elevation of the head, avoiding late meals, avoiding specific foods, etc.) may also be helpful in the treatment of the gastrointestinal disorders. Recent guidelines for the treatment of GERD and esophageal disease (2008) recommend initial treatment with a PPI once to twice daily.  According to the guidelines, long- term treatment with the PPIs should be avoided and use should be limited to the lowest dose and shortest course possible to relieve symptoms. Some clinicians advocate PPI use on an as needed or “on demand” basis only or with a "stepdown" approach by either decreasing the dose of the PPI or switching to an H2 receptor antagonist. [5,6] For the treatment of peptic ulcer disease (PUD, gastric and duodenal ulcers), both PPIs and H2-receptor antagonists are effective; although, PPIs may relieve symptoms and promote healing more rapidly than H2 antagonists.8 Non-steroidal anti-inflammatory drugs (NSAID) use is frequently reported with peptic ulcers/bleeding and should be avoided in patients who are at increased risk of PUD. Intravenous PPI therapy is recommended in patients with acute bleeding ulcers. 
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Poor granulation formation, prolonged abscess presence and impaired wound healing are further complicating the diabetic foot ulcer. Once the skin has been breached, continued mobilization on a broken area impairs the healing process. Inevitably, direct contiguous spread of microbes on the skin follows on, with colonization and infection of superficial and then deeper tissues is likely if the process is allowed to proceed unchecked. Both the healing process and the response to infection are further compromised by vascular insufficiency, which is commonly present in patients burdened with complications of diabetes . The infection in diabetic foot is mainly by aerobic bacteria [88, 89, 102, 114, 123-125]. Anaerobic bacterial infection also plays a significant role in the infection of DFU but this has not been studied since the strict anaerobic culture techniques are not available at all the clinical laboratories. The impact of anaerobes was reported first by Louie et al.,  and subsequently by many researchers [88, 89, 123, 125, 127, 128]. There are only few reports available on the incidence of fungal pathogens in diabetic foot infections [129, 130-132]. DFU infection is usually polymicrobial in nature and this was first reported by Louie et al., , and subsequently by many [88, 89, 102, 114, 124, 125]. The unique anatomy of the foot is the main reason that infection is potentially serious in this location . The structure compartment, tendons, sheaths, and neurovascular bundles tend to favour the proximal spread of infection. The deep planter spaces were divided into medial, central, and lateral compartments. The infections may spread from one compartment to another at their calcaneal or by direct performation of septae, but lateral or dorsal spread is a late sign on infection .
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In this review, the concepts of biological rhythms, chronobiology, chronopharmacology, and chronotherapy for various diseases have been discussed. Chronopharmaceutical Drug Delivery Systems (ChrDDS) is novel system which provides a pattern of real‐time drug input at different release rates and it may be achieved by stimuli‐sensitive and pulsatile drug delivery systems. Drug pharmacokinetics can also be time dependent; therefore, variations both in a disease state and in drug plasma concentration need to be taken into consideration in developing drug delivery systems intended for the treatment of disease with adequate dose at appropriate time. A number of chronotherapeutic medications, aiming at synchronizing medications and the intrinsic biorhythms of disease have been developed by novel drug delivery technology.
The serum concentration of certain acute phase proteins significantly increases during various pathological conditions in cattle. The aim of this study was to determine the influence of claw disorders etiology on the concentrations of two major acute phase proteins in dairy cattle: haptoglobin (Hp) and serum amyloid protein A (SAA). Fifty dairy cows with claw pathology were included. Fourteen clinically healthy heifers served as controls. The animals were subdivided in 5 groups according to the pathological findings on their claws: 1. Heel horn erosion (HE), 2. Acute laminitis (AL), 3. Sole ulcer (SU), 4. Digital dermatitis (DD) and 5. White line separation (WLS). Hp and SAA concentrations were measured in serum samples using commercial ELISA kits. Higher concentrations of both Hp and SAA were found in the AL and SU groups (p<0.01) compared to the HE, DD and WLS and control groups. Dairy cows in the DD group had higher (p<0.05) Hp and SAA concentrations than the HE and WLS groups and the controls. The serum values between the HE, WLS and the control group did not differ significantly. The presented results indicate that the claw diseases are associated with a systemic acute phase response. Hp and SAA could be used as valuable biomarkers for early detection of claw diseases in dairy cows.
In the late 1800s, Sir Albert Cook described cases of chronic disﬁguring skin ulcers in Uganda (3). In 1948, MacCallum et al. linked these chronic skin ulcers to a myco- bacterium in six cases from rural Australia (5). These skin ulcers are known by many names (Buruli ulcer, Bairnsdale ulcer, Daintree ulcer, Mossman ulcer, Kumasi ulcer, or Searls ulcer), mostly depending on the geographic area where they are found (6). “Buruli ulcer,” the most frequently known name, refers to a Ugandan region in the southern bank of the Victoria Nile river (7). Until now, cases have been found in at least 33 countries in tropical, subtropical, and temperate climates in Asia (Malaysia, Papua New Guinea, and Sri Lanka), Western Paciﬁc regions (Australia), the Americas (Guyana, Mexico, and Peru), and Africa, where the highest concentrations of cases occur in Benin, Cameroon, Cote d’Ivoire, Democratic Republic of the Congo, and Ghana (1). In 2015, 13 countries reported a total of 2,037 new cases (1). However, not all countries have health care systems that can detect and diagnose BU, so underreporting of cases is likely. For example, the sharp increase in the number of BU cases in Japan around 2009 to 2010 was mostly secondary to increased physician awareness and availability of diagnostic techniques (8).
of ulcer into 2 groups; Group 1 being the high grade of ulcer (grade 3, 4, 5) and Group 2 the low grade of ulcer (grade 0, 1, 2). The duration of ulcer was recorded from the first pre- sentation (using medical record) to the date visited or re- ferred to our clinic. Glycosylated hemoglobin was measured at baseline and any follow-up period. The mean percentage of glycosylated hemoglobin values was derived from base- line and any follow-up period. Macrovascular complica- tions were defined as the presence of a history of angina pectoris or myocardial infarction, any positive cardiac stress test result, or pathologic signs on coronary angiogra- phy. 8,9 Microvascular complication was defined as retinopa-
sodium chloride solution or lactated Ringer's injection), 500 to 1,000 mL, should be given intravenously over 5 to 10 minutes, until mean arterial pressure and tissue perfusion are adequate (about 4 to 8 L total over 24 hours for the typical patient). Boluses of 250 mL are appropriate for patients who are elderly or who have heart disease or suspected pulmonary edema. Red blood cells should be reserved for patients with a hemoglobin value of less than 10 g/dL and either evidence of decreased oxygen delivery or significant risk from anemia (eg, coronary artery disease).
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