Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although it is known that malnutrition hinders early wound healing, it has not been determined whether this occurs because of formation of a poor scar or a slow rate of normal healing; the ultimate fate of the malnourished wound is unknown. Malnutrition was produced in rats by short gut syndrome. Elemental diet was compared to rat chow and silk was compared with polyglycolic acid suture. Nutritional deficiency was seen in short gut rats for two weeks postoperatively. Thereafter adaptation allowed partial recovery, but relative deficiency persisted. Morbidity and mortality of short gut rats doubled that of controls and all wound complications were limited to this group, occurring within the first two weeks. Malnourished animals surviving for 60 days had wound strength equal to the control rats as determined by gut anastomosis bursting strength, skin wound breaking strength and wound hydroxyproline content. Neither diet nor suture material altered ultimate wound strength. Improved nutrition allowed more animals and wound to survive, but ultimate healing survivors was indistinguishable from that of normal controls. Thus early weakness probably results from slow healing rather than formation of poor scar. Nutrition plays an important role in early strength and survival, but not in ultimate wound healing.
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PMID:Effect of nutrition, diet and suture material on long term wound healing. 121 97

An outbreak of Gnathostoma larva migrans occurred among guests of a New Year's party in Chachoengsao, Thailand. Nine people who consumed a raw fish dish called 'Hu-sae' contracted the disease. Five of them developed gastro-intestinal symptoms consisting of nausea, vomiting, abdominal cramps and diarrhea as early as within the first 24 hours, while in the other four, symptoms started on the following day. After the initial symptoms pertaining to the gut, malaise, chest discomfort, cough, myalgia, weakness, itching and migratory swellings were experienced. Eosinophilia was demonstrated in every patient with a mean (+/- SE) count of 5,516 +/- 1,010 cells/cu mm. Detection of antibody against aqueous extracts of G. spinigerum adult antigen using an enzyme-linked immunosorbent assay showed a titer of 1:1,600 or greater in every patients except one who had a titer of 1:400 (positive greater than or equal to 1:400). This outbreak illustrates the high attack rate when heavily infected fish are consumed.
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PMID:Gnathostoma larva migrans among guests of a New Year party. 182 91

Manometric, radiological and neurophysiological investigations were performed on 34 women, aged between 14 and 53, who suffered with chronic constipation refractory to treatment, and on 27 age-matched normal female control subjects. The constipated patients had more difficulty in evacuating simulated stools than control subjects and 13 out of 19 patients tested obstructed defaecation by contracting the external sphincter during straining. The constipated group required a greater degree of rectal distension than control subjects to induce rectal contractions, anal relaxation and a desire to defaecate. Other modalities of rectal sensation were normal in the constipated subjects. Compared with controls, constipated patients had significantly lower anal pressures, an abnormal degree of perineal descent on straining and an obtuse anorectal angulation at rest. These results were compatible with weakness of the pelvic floor and neuropathic damage to the external sphincter. Mouth to anus transit time was abnormally prolonged in 60% of constipated patients, but was within the normal range in the remainder. Anorectal function in patients with slow transit was not significantly different from that in patients with a normal transit time. The mouth to caecum transit time of a standard meal was prolonged in constipated patients irrespective of the duration of the whole gut transit. Gastric emptying was not significantly prolonged.
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PMID:Physiological studies in young women with chronic constipation. 361 44

There are large amounts of zinc in muscle and zinc ions can enhance the degree of muscle contraction in response to direct stimulation while at the same time inhibiting neuromuscular transmission. The opposites of these effects would lead to myotonia and muscle weakness. There are many parallels between the non-muscular features of myotonic dystrophy and those of zinc deficiency. The particular patterns of reproductive disturbance in both males and females, the abnormalities of metabolism, the defects in gut funcion, the defects in bone and the congenital abnormalities are very similar in the two conditions. However there are important differences between simply zinc deficiency states and myotonic dystrophy which mean that the latter is unlikely to be due to the former. Instead it is proposed that the fundamental defect in myotonic dystrophy is the presence of an abnormal zinc binding ligand which fails to deliver appropriate amounts of zinc ions to the tissues. The functioning of this ligand may, however, be affected by dietary zinc, perhaps accounting for the apparent variation in the expression of the dominant myotonic dystrophy gene due to some unknown environmental factor. Some of the effects of zinc may be due to lack of the zinc ion directly, while others are probably related to defects in essential fatty acid and prostaglandin metabolism. The hypothesis can be readily tested by the employment of nutritional measures designed to counteract the defects in zinc and essential fatty acid metabolism.
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PMID:Myotonic dystrophy: a disease caused by functional zinc deficiency due to an abnormal zinc-binding ligand? 699 20

Infant botulism is a rare disease caused by the release of toxin produced in the intestinal tract by Clostridium botulinum. The disease primarily affects infants under 1 year of age. We report a 3-year-old child with stage IV neuroblastoma who developed symptoms of progressive motor weakness, bulbar palsy and respiratory failure 42 days after autologous BMT. The diagnosis of infant botulism was established by identifying botulism toxin in the stool. Human botulism immune globulin (HBIG) was administered. Following the diagnosis, the patient made significant recovery over the next 7 weeks and was successfully extubated from mechanical ventilation. However, her neuroblastoma eventually recurred and she subsequently died of progressive disease. Although the etiology of the development of infant botulism in this case following autologous BMT still remains unclear, alteration of the intestinal microbial environment from gut sterilization and laminar airflow room isolation or, alternatively, immune suppression during pre- and post-autologous BMT and activation of endogenous spores may have contributed to the development of this disease. The use of HBIG in children with botulism over 1 year of age may be beneficial.
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PMID:Development of infant botulism in a 3-year-old female with neuroblastoma following autologous bone marrow transplantation: potential use of human botulism immune globulin. 819 79

Microbial and fermentation changes in the ingesta of the large intestine and their influence on the pathogenesis of acute lactic acidosis were studied in 4 cows fitted with permanent cannulas in the ileum and cecum. Feed mixture containing 65% of maize was infused into the cecum for several days in amounts of 2 and 4 kg per day. The daily amount was divided in 8 equal portions and given with 3 l of warm physiologic saline solution. During the period of ad libitum feeding of hay, the pH values in cecal digesta were 7.4 to 7.6 and the amount of total volatile fatty acids 40-60 mmol/kg with high molar percentage (87-90 mol%) of acetic acid. As to lactic acid only the L(+) lactic isomer was found in a concentration of about 0.4 mmol/kg. Infusion of low amounts of starch induced mild lactic acid fermentation in the cecum associated with a pronounced increase in the concentration of L(+) and D (-) lactic acid to peak levels of 80 +/- 10 mmol/kg and 7 +/- 1 mmol/kg, respectively. Lactic acid fermentation ceased within 2 to 3 days indicating that the gut microflora had adapted to the starch infusion. Slight decreases of blood pH and bicarbonates in blood as well as a moderate increase of netto acid-base excretion in urine indicated mild changes of acid-base balance, but clinically no pathological symptoms were observed. Higher amounts of infused starch caused pronounced lactic acid production in the large intestine which persisted throughout the experiment. Peak L(+) and D(-) lactic acid concentration in cecal digesta reached on the average 137 +/- 16 mmol/kg and 45 +/- 7 mmol/kg respectively. Significant decreases of blood pH values from 7.41 +/- 0.02 to 7.18 +/- 0.08 (P < 0.001), actual bicarbonate from 28.2 +/- 3.2 to 11.0 +/- 2.6 mmol/l (P < 0.001) and base excess from 3.9 +/- 3.6 to -15.2 +/- 3.8 mmol/l (P < 0.001) were observed. D (-) lactic acid concentration in blood increased to 3.2 +/- 0.4 mmol/l, but L(+) lactic acid values remained unchanged under 1 mmol/l. Clear clinical symptoms of indigestion and intoxication characterized by severe inappetence, ruminal stasis and general weakness were also observed. Typical clinical symptoms of disease as well as blood and urine changes in acid-base balance indicated that lactic acid fermentation in the large intestine contributes considerably to the pathogenesis of acute ruminant lactic acidosis.
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PMID:[Impact of lactic acid fermentation in the large intestine on acute lactic acidosis in cattle]. 1147 93

Botulinum toxin is the most potent toxin known to humans and as little as 100 ng can be lethal. The toxin blocks peripheral cholinergic neurotransmission at the neuromuscular junction and cholinergic autonomic nervous system by introducing an endopeptadase enzyme into the presynaptic side of the synapse. The endopeptadase cleaves acetylcholine vesicle docking proteins that are required for the synapse to release acetylcholine into the synaptic cleft. Botulism occurs from consumption or inhalation of preformed botulinum toxin or growth of Clostridium botulinum bacteria in the infant gastrointestinal tract or within a wound. Growth of C. botulinum in the immature gut or wound will release botulinum toxin that reaches the circulation. All forms of botulism cause progressive weakness, bulbar signs (blurred vision, diplopia, mydriasis, dysphagia, and dysarthria), and respiratory failure with normal sensation and mentation. Treatment is aimed at 1) maintaining respiration via intubation and mechanical ventilation, 2) stopping progression of weakness by administration of botulinum antitoxin (equine trivalent botulinum antitoxin for adults and botulism immune-globulin intravenous-human for infant botulism), and 3) preventing complications from weeks of paralysis with good supportive care. The source of the botulinum toxin should be identified to prevent additional cases. Patients can recover normal muscle strength within weeks to months, but usually complain of fatigue for years.
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PMID:Botulism. 1252 61

Metabolic bone disease and some of the disorders of the skeleton are associated with alterations in calcium and phosphorus homeostasis. For example, calcium salts are not freely soluble in body fluids and increases in either calcium or phosphate or both can lead to deposition of calcium salts in the soft tissues. In addition, because the crystalline material in bone is very tiny, there is a rapid and very active exchange system with the extracellular space so that disorders of calcium or phosphorus are reflected by a change in bone structure and, in fact, contribute to the ease with which fractures occur. Also, in many disorders, bone formation and destruction are equal in activity but opposite in sign; in some conditions such as osteoporosis, destruction exceeds production and lead to weakness of bone structure. Finally, the transfer of calcium across lumens such as the gut, kidney, or bone requires a system, which consists of parathyroid hormone and 1,25-dihydroxyvitamin D and a low phosphate level.
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PMID:Metabolic bone disease: an update. 1269 Sep 1

Cladistic analysis is a popular method for reconstructing evolutionary relationships on the human lineage. However, it has limitations and hidden assumptions that are often not considered by palaeoanthropologists. Some researchers who are opposed to its use regard cladistics as the preferred method for taxonomic "splitters" and claim it has lead to a revitalisation of typology. Typology remains a part of human evolutionary studies, regardless of the acceptance or use of cladistics. The assumption/preference for "splitting" over "lumping" in cladistics (alpha) taxonomy and the general failure to evaluate (post-hoc) such taxonomies have served to reinforce this assertion. Researchers have also adopted a number of practices that are logically untenable or introduce considerable error. The evolutionary trend of human encephalisation, apparently isometric with body size, and concurrent reduction in the gut and masticatory apparatus, suggests continuous cladistic characters are biased by problems of body size. The method suffers a logical weakness, or circularity, leading to bias when characters with multiple states are used. Coding of such characters can only be done using prior criteria, and this is usually done using an existing phylogenetic scheme. Another problem with coding character states is the handling of variation within species. While this form of variation is usually ignored by palaeoanthropologists, when characters are recognised as varying, their treatment as a separate state adds considerable error to cladograms. The genetic proximity of humans, chimpanzees and gorillas has important implications for cladistic analyses. It is argued that chimpanzees and gorillas should be treated as ingroup taxa and an alternative outgroup such as orangutans should be used, or an (hypothetical) ancestral body plan developed. Making chimpanzees and gorillas ingroup taxa would considerably enhance the biological utility of anthropological cladograms. All published human cladograms fail to meet standard quality criteria indicating that none of them may be considered reliable. The continuing uncertainty over the number and composition of fossil human species is the largest single source of error for cladistics and human phylogenetic reconstruction.
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PMID:Problems with the use of cladistic analysis in palaeoanthropology. 1273 96

We hypothesize that a yet-to-be-identified motor neuron toxin produced by a clostridial species causes sporadic amyotrophic lateral sclerosis (ALS) in susceptible individuals. This clostridial species would reside undetected in the gut and chronically produce a toxin that targets the motor system, like the tetanus and botulinum toxins. After gaining access to the lower motor neuron, the toxin would be transported back to the cell body, as occurs with the tetanus toxin, and destroy the lower motor neuron - the essential feature of ALS. Again like the tetanus toxin, some of the toxin would cross to neighboring cells and to the upper motor neuron and similarly destroy these motor neurons. Weakness would relentlessly progress until not enough motor neurons remained to sustain life. If this hypothesis were correct, treatment with appropriate antibiotics or antitoxins might slow or halt progression of disease, and immunization might prevent disease.
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PMID:Hypothesis: a motor neuron toxin produced by a clostridial species residing in gut causes ALS. 1623 60


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