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J Assoc Physicians India. 2000 Jun;48(6):603-5.
Diabetic autonomic neuropathy causing gall bladder dysfunction.

Gaur C, Mathur A, Agarwal A, Verma K, Jain R, Swaroop A.

Department of Medicine, Jawahar Lal Nehru Hospital, Ajmer.

OBJECTIVE: The objective of the study was to study gall bladder volume in fasting and 45 minutes post-prandial, by real time ultrasound in healthy controls and diabetic patients with and without autonomic neuropathy and to compare them. METHOD: Age, Sex and body mass index (BMI) matched 50 healthy subjects and 10 patients with insulin dependent diabetes mellitus and 40 patients with noninsulin dependent diabetes mellitus were evaluated according to National diabetes Data Group of National Institute of Health (1979) criteria: 1. Fasting (overnight) venous plasma glucose concentration of > 140 mg/dl on two separate occasions. 2. Following ingestion of 75 gms of glucose, venous plasma glucose concentration of > 200 mg/dl at second hour and at one other occasion during two hour test. Autonomic neuropathy was assessed by the presence of symptoms like dysphagia, abdominal fullness, nausea, vomiting, diarrhea +/- nocturnal, faecal incontinence or constipation, dysuria, urinary incontinence, the gustatory sweating, impotence etc. and were confirmed by standing test for orthostatic hypotension, hand grip test, Valsalva test and deep breaths test. RESULT: The study showed that: 1. Patients of diabetes mellitus had statistically significant larger fasting gall bladder volumes and these values were highly significant amongst patients with autonomic neuropathy. 2. Patients of diabetes mellitus and statistically significant larger post fatty meal gall bladder volume and these values were highly significant in patients with autonomic neuropathy. CONCLUSIONS: We therefore conclude that impaired gall bladder contraction was found amongst patients of diabetes mellitus with autonomic neuropathy. The mechanism responsible for cholecystoparesis is attributed to vagal neuropathy. Incomplete

Gut. 2001 May;48(5):671-5.
Analysis of the RET, GDNF, EDN3, and EDNRB genes in patients with intestinal neuronal dysplasia and Hirschsprung disease.

Gath R, Goessling A, Keller KM, Koletzko S, Coerdt W, Muntefering H, Wirth S, Hofstra RM, Mulligan L, Eng C, von Deimling A.

Department of Neuropathology, University of Bonn Medical Centre, D-53105 Bonn, Germany.

BACKGROUND: Hirschsprung disease (HSCR) is a frequent congenital disorder with an incidence of 1 in 5000 live births, characterised by the absence of parasympathetic intramural ganglion cells in the hindgut resulting in intestinal obstruction in neonates and severe constipation in infants and adults. Intestinal neuronal dysplasia (IND) shares clinical features with HSCR but the submucosal parasympathetic plexus is affected. IND has been proposed as one of the most frequent causes of chronic constipation and is often associated with HSCR. METHODS: We examined 29 patients diagnosed with sporadic HSCR, 20 patients with IND, and 12 patients with mixed HSCR/IND for mutations in the coding regions of the RET, GDNF, EDNRB, and EDN3 genes. The entire coding regions were analysed by single strand conformational polymorphism and DNA sequencing. RESULTS: Only three RET mutations were detected in patients with HSCR. In patients with IND or a mixed HSCR/IND phenotype, no mutations in these genes were observed. While HSCR and HSCR/IND showed over representation of a specific RET polymorphism in exon 2, IND exhibited a significantly lower frequency comparable with that of controls. CONCLUSIONS: The mutation frequency found in our sporadic HSCR patients (10%) and the allelic distribution of RET polymorphisms are comparable with earlier published data. A significantly different allelic distribution in an established HSCR associated polymorphism argues against common genetic pathways for HSCR and IND.

Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11302967&dopt=Abstract constipation laxative colon cleansing

Pediatr Surg Int. 2001 Mar;17(2-3):140-3.
New pathogenetic aspects of gut dysmotility in aplastic and hypoplastic desmosis of early childhood.

Meier-Ruge WA, Holschneider AM, Scharli AF.

Institut fur Pathologie, Universitat Basel, Schonbeinstrasse 40, 4003 Basel, Switzerland.

The peristaltic movement of the gut is a function of the alternating contraction and relaxation of circular and longitudinal muscles. This movement is induced by a tendon-like connective-tissue net (TCTN) in the circular and longitudinal muscles, which are both rooted in a connective-tissue plexus layer (CTPL). In children with a therapy-resistant aperistaltic or hypoperistaltic syndrome who had normally-developed enteric innervation, a lack of the TCTN in the muscularis propria was observed. Over the last 2 years, 241 children with chronic constipation were investigated histopathologically; 46 children surgically treated by partial resection of the gut or diagnostically investigated by whole-mount biopsy. Fifteen children had a hypoperistalsis syndrome and 3 had an aperistalsis syndrome. All specimens were native and cut in a cryostat. Enteric innervation was examined by acetylcholinesterase and dehydrogenase reactions. The TCTN in the muscularis propria was stained with picric acid/sirius red. In the children with an aperistalsis syndrome, a complete lack of the TCTN in circular and longitudinal muscles was observed. A CTPL was not developed. The children with a hypoperistalsis syndrome had no CTPL, but had a partly-developed TCTN in the circular and longitudinal muscles, which gradually faded in the direction of the plexus layer. Independent of a well-developed enteric nervous system, a lack of the TCTN in longitudinal and circular muscles and a missing CTPL (aplastic desmosis) abolishes the coordinated peristaltic movement of the gut. An isolated lack of the CTPL in the myenteric plexus (hypoplastic desmosis) results in a hypoperistalsis syndrome. An anomaly of the TCTN in the muscularis propria disturbs gut-muscle m

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