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At least 955 records · Page 53Linked to original sources
PubMed2006

Cholesterol and 24S-hydroxycholesterol trafficking in Alzheimer's disease.

Cholesterol and the cholesterol oxide 24S-hydroxycholesterol (24S-HC) are highly enriched in the human CNS. Clinical, genetic, neurochemical and epidemiological evidence continue to support dysfunctional cholesterol metabolism as an important contributing factor driving the development and/or progression of Alzheimer's disease (AD) neuropathology. Cholesterol overabundance in the brain plasma membrane lipid- raft domains, appears to be fundamental to the generation of the more neurotoxic forms of amyloid-beta (Abeta) peptide from beta-amyloid holoprotein precursor. 24S-HC may have a pivotal role in promoting altered inflammatory signaling, apoptotic genetic responses and AD-type change. In clinical studies, cholesterol-lowering statins, nonsteroidal anti-inflammatory drugs, cholesterol absorption/transport inhibitors and related modulators of cholesterol trafficking have demonstrated some pharmacological benefit for the treatment of AD, but overall their efficacy at slowing the cognitive decline and the progression of AD remains controversial and open to question.

Alzheimer Disease↗
PubMed2004

Emphysematous cystitis with severe hemorrhagic anemia resulting from diabetes mellitus type 2.

A 48-year-old woman suffering from hematuria was admitted to our hospital due to conscious disturbance. She had lower abdominal phantom tumor, anemia, renal dysfunction, hyperglycemia, metabolic acidosis and electrolyte abnormalities. Because of pelvocaliceal dilatation noted on abdominal ultrasonography, we first diagnosed her as having postrenal failure. With massive blood clots and gas emission from her urethra upon attempting cystoscopy, the remarkable expansion of the urinary bladder and a three-layered structure of gas, urine and complex of blood and debris inside her urinary bladder noted on abdominal CT scan, as well as the increased white blood cell count, we finally concluded our diagnosis as emphysematous cystitis.

Anemia↗
PubMed1986

Platelet dysfunction and alteration of prostaglandin metabolism after chronic alcohol consumption.

To study the effects of chronic alcohol consumption on platelet functions, the rate of arachidonate-induced platelet aggregation, the production of malondialdehyde in platelets, and plasma levels of prostaglandin endoperoxide metabolites were examined in 88 chronic alcoholics and 24 healthy controls. The rate of platelet aggregation and the production of malondialdehyde in platelets were greater in chronic alcoholics both on admission and 1 week after. However, these alterations returned to the level of healthy controls within 4 weeks of abstinence from alcohol and were independent of the number of circulating platelets. Furthermore, on admission, plasma levels of thromboxane B2 were significantly increased in chronic alcoholics when compared with those of healthy controls (400.8 +/- 36.5 versus 241.7 +/- 28.9 pg/ml plasma; p less than 0.025) and were also significantly correlated with malondialdehyde production in washed platelet debris (r = 0.6049; p less than 0.001). In contrast, plasma levels of 6-keto prostaglandin F1 alpha and prostaglandin E were not altered after chronic alcohol consumption. As a result, the ratio of 6-keto prostaglandin F1 alpha to thromboxane B2 was markedly decreased in chronic alcoholics (0.31 +/- 0.03 versus 0.62 +/- 0.13; p less than 0.001). These results strongly suggest that the imbalance in prostaglandin endoperoxide metabolites is produced by chronic alcohol ingestion. Moreover, a significant correlation was observed between platelet aggregation rate and malondialdehyde production during platelet aggregation (r = 0.559; p less than 0.005). Thus, we conclude that chronic alcohol consumption alters platelet thromboxane metabolism, which is likely associated with the increased ability of platelets to aggregate.

Adult↗
PubMed1991

Taiwan National Poison Center survey of glyphosate--surfactant herbicide ingestions.

Between January, 1986 and September, 1988, the Taiwan National Poison Center recorded 97 telephone consultations (49 male, 48 female) on cases of ingestion of glyphosate-surfactant herbicide concentrate containing the isopropylamine salt of glyphosate (N-phosphonomethyl glycine, CAS 1071-83-6) and a non-ionic tallow amine surfactant. Eleven of the cases resulted in fatalities, all among those attempting suicide. The average amount ingested by survivors was 120 +/- 112 mL and by nonsurvivors was 263 +/- 100 mL (p less than or equal to 0.0001). The average age of survivors was 35 +/- 15 years compared to 54 +/- 11 years for fatalities (p less than or equal to 0.0002). Irritation of the oral mucous membrane and gastrointestinal tract was the most frequently reported effect. Other effects recorded were pulmonary dysfunction, oliguria, metabolic acidosis, hypotension, leukocytosis and fever. Fourteen patients received either atropine or pralidoxime plus atropine despite the fact that glyphosate does not inhibit acetylcholinesterase. Thirteen percent of patients received a urine test for paraquat or treatment customarily used for paraquat ingestion, possibly reflecting similar initial presentations following ingestion of these two herbicides. Laboratory differentiation is essential if any doubt exists about which herbicide was ingested. Patients ingesting large volumes of concentrated glyphosate-surfactant herbicide formulations require close observation and supportive treatment.

Accidents↗
PubMed2026

Multi-Target HCC Blood Test Demonstrates Consistent Performance Across Subgroups of Patients with Chronic Liver Disease.

BACKGROUND: Early detection of hepatocellular carcinoma (HCC) is critical for improving patient outcomes; however, ultrasound-based surveillance has limited sensitivity and variable performance across patient populations. We evaluated the performance of a multitarget HCC blood test (mt-HBT), incorporating methylated DNA markers, alpha-fetoprotein (AFP), and patient sex, across clinically relevant subgroups. METHODS: We performed a subgroup analysis of a multicenter, prospective case-control study that included 159 patients with early-stage HCC (Barcelona Clinic Liver Cancer Stage 0/A) and 649 control patients with cirrhosis or chronic hepatitis B without HCC. The mt-HBT combined methylated HOXA1, TSPYL5, and B3GALT6 markers with AFP and sex. Sensitivity and specificity were evaluated overall and according to age, sex, obesity, liver disease etiology, Child Pugh class, and tumor size. Performance was compared with AFP and GALAD. RESULTS: Overall sensitivity and specificity of mt-HBT for early-stage HCC detection were 76.7% (95% CI, 69.6-82.6) and 87.5% (95% CI, 84.8-89.8), respectively. Sensitivity was significantly higher than that of AFP (35.2%, p < 0.001) and comparable to that of GALAD (78.6%, p = 0.56), whereas specificity was lower than that of AFP (98.5%, p < 0.001) but higher than that of GALAD (76.9%, p < 0.001). Sensitivity was maintained across key subgroups, including patients with obesity (68.9%), Child Pugh B cirrhosis (75.0%), hepatitis C (80.0%), hepatitis B (72.2%), alcohol-associated liver disease (80.5%), and metabolic dysfunction-associated steatotic disease (69.0%) (all p > 0.05 between subgroups). Specificity exceeded 80% in all examined populations and was significantly higher in women than in men (92.5% vs. 83.9%, p < 0.001). Sensitivity increased with tumor size, ranging from 60.0% for tumors < 2 cm to 100% for tumors > 5 cm. CONCLUSIONS: The mt-HBT demonstrated robust, consistent performance for early-stage HCC detection across diverse patient populations, including subgroups in which ultrasound surveillance commonly underperforms. These findings support the prospective validation of mt-HBT as a blood-based surveillance strategy for HCC.

liver cancer↗
PubMed2026

Hepatocyte-Specific Deficiency of Endoplasmic Reticulum-Associated Degradation Induces Coordinated Innate-Adaptive Immune Responses.

Hepatic inflammation is a defining feature of Metabolic Dysfunction-Associated Steatohepatitis (MASH), yet the specific contributions of individual immune cell populations and their reciprocal interactions remain incompletely understood. In this study, we combined flow cytometry with single-cell transcriptomic profiling to characterize the hepatic immune landscape in a novel model of spontaneous MASH caused by hepatocyte-specific deficiency of endoplasmic reticulum-associated degradation (ERAD). Hepatic ERAD deficiency led to the expansion of multiple immune cell populations in the liver, including CD8+ T cells, macrophages, monocytes, and dendritic cells, accompanied by extensive functional reprogramming of both innate and adaptive immune compartments. Myeloid cells exhibited enhanced phagocytic activity and increased antigen processing and presentation, whereas CD8+ T cells displayed elevated proliferation capacity, DNA repair activity and cytotoxicity. Notably, two functionally distinct triggering receptor expressed on myeloid cells 2 (TREM2)-expressing macrophage subsets emerged during the progression of ERAD deficiency-induced MASH. Depletion of CD8+ T cells increased monocyte infiltration and aggravated liver injury, suggesting that CD8+ T cells exert a previously unrecognized protective role by restraining monocyte recruitment. Collectively, these findings reveal highly coordinated interactions between innate and adaptive cells during MASH progression and identify CD8+ T cells as potential regulators of monocyte infiltration and hepatic injury.

Animals↗
PubMed1992

Diarrheal disease as a cause of malnutrition.

Although long associated with infectious diseases, malnutrition is recognized as a major effect of specific infections, especially those of the gastrointestinal tract. Synergistic exacerbation of infections and nutritional deficiency commonly begin with weaning, where the impact of repeated infections and possible monocyte mediator release may have an even greater effect on malnutrition of young children than that of deficient diets in many areas. Reviewed here are the detailed host alterations seen with specific enteric infections that lead to malnutrition. These include mucosal dysfunction, systemic metabolic responses, impaired intake, digestion and absorption, nutrient losses, altered immune responses, and ultimately, impaired growth, development, and nutrition. The tremendous health impact of diarrhea on both morbidity and mortality in many developing areas must be recognized and controlled along with correction of food shortages in order to improve the nutrition, growth, and survival of impoverished children.

Anorexia↗
PubMed1999

[Anesthesiologic aspects in patients with HIV infections].

A review of anaesthesia for patients with HIV-infection is given. The use of new antiretroviral drug combinations to treat HIV-infection may result in longer survival, and therefore more cases of HIV-positive patients who undergo surgery and require anaesthetic services. Clinical manifestations of the HIV infection in humans can be seen in almost every organ. The anaesthetist must have an understanding of the many manifestations of the syndrome. Physical examination and preoperative preparation is essential. Considerations for the anaesthetist include: the effects of medications and possible drug interactions, organ dysfunction, altered metabolism and choice of anaesthetic technique for the HIV-positive patient. Anaesthetists and other health care professionals must know about the manifestations of HIV-infection in order to provide competent and compassionate care.

Anesthesia↗
PubMed2002

[Respiratory and renal dysfunctions due to lipid storage metabolic myopathy: case report].

We report a case of a 26-years old male patient with rhabdomyolisis with myoglobinuria associated with acute renal and respiratory failure, that occurred three days after upper airway infection. In the clinical and laboratory investigation of the patient, including electromyography and muscular biopsy, the diagnostic lead to a metabolic myopathy due to an enzymatic deficiency related to a disorder of lipid metabolism. The patient improved successfully with institution of advanced life support, including ventilatory assistance, dialysis, dietary adjust and L-carnitine reposition.

Adult↗
PubMed1992

Neurotransmitter-mediated mechanisms of traumatic brain injury: acetylcholine and excitatory amino acids.

Research into traumatic brain injury (TBI), focusing on changes in energy metabolism, cerebrovascular dysfunction, and brain parenchymal morphology, has not produced complete descriptions of mechanisms mediating the pathophysiology of TBI. New studies indicate that neurochemical alterations mediate important components of brain physiology associated with TBI, and these alterations may be responsive to pharmacologic therapy. We discuss rodent models of TBI, review current experimental evidence of muscarinic cholinergic and excitatory amino acid (EAA) receptor involvement in its pathophysiology, and address issues relevant to the interpretation of these data.

Acetylcholine↗
PubMed2003

[Keloid and hypertrophic scars].

BACKGROUND: Keloid and hypertrophic scars develop most frequently in wounds with high skin tension and especially on the upper truncus. Both are characterized by an excessive dysfunctional collagen metabolism. MATERIAL AND METHODS: The article presents data from research in current literature and discuss the treatment of keloid and hypertrophic scars. RESULTS AND INTERPRETATION: Patients that are undergoing elective surgery should be handled with surgical techniques that reduce wound closing tension. Patients who are at high-risk or show excessive scar development should follow standard treatment. First-line therapy is silicone sheeting and/or pressure. In case of minimal response, steroid injections should be started after two months. The patient must be re-evaluated for a surgical approach combined with conservative treatment if the result is unsatisfactory after 12 months.

Cicatrix, Hypertrophic↗
PubMed2003

[Impairment of cardiovascular function in subclinical hypothyroidism].

Subclinical hypothyroidism (SH) is the most frequent thyroid disease, but administration of replacement L-thyroxin in it is not obvious. SH may present both with general nonspecific symptoms and disturbance of lipid metabolism, myocardial dysfunction. Many physicians think it valid to restore euthyroid condition, as it may improve general condition of the patients, diastolic and systolic myocardial function, prognosis in ischemic heart disease. However, there are no definite indications to starting L-thyroxin in SH.

Age Factors↗
PubMed2004

[Hepatic failure after liver resection in patients with cirrhosis].

Despite improvements in the preoperative assessment of liver function and advances in surgical techniques, liver resection for hepatocellular carcinoma still holds a risk for postoperative hepatic failure, especially in patients with cirrhosis. Physiologic characteristics in patients with cirrhosis include hyperdynamic state of the systemic circulation, decrease in hepatic blood flow, portal hypertension, metabolic disorders, dysfunction of the reticuloendothelial system, and thrombocytopenia. Surgical stress including massive bleeding, disturbance of hepatic circulation, and infection are risk factors for postoperative hepatic failure. The risk of hepatic failure also correlates with the severity of active hepatitis and the degree of hepatic fibrosis. To prevent postoperative hepatic failure, dopamine, prostaglandin, and hydrocortisone have been used. Although various treatments including plasma exchange have been tried in hepatic failure, the results have often been unsatisfactory. Careful preoperative evaluation of the hepatic functional reserve and the severity of active hepatitis, and adequate selection of surgical method are important to prevent postoperative hepatic failure.

Alprostadil↗
PubMed2001

[The role of hyperphosphatemia in the pathogenesis of secondary hyperparathyroidism].

Renal phosphate handling plays key role in phosphate metabolism. Kidney dysfunction induced hyperphosphatemia. The phosphatemia with renal insufficiency, especially uremia, indirectly progresses into secondary hyperparathyroidism via suppression of vitamin D/Ca system. This indirect effect on parathyroid is called "Trade-off theory". Recently, the direct effect of hyperphosphatemia on parathyroid has been reported independent of vitamin D/Ca system in renal failure. The control of serum phosphate is certainly important by restriction of phosphate intake in renal failure patients.

English Abstract↗
PubMedDate not supplied

Effects of supplementary parenteral nutrition on thyroid hormone patterns in surgical patients with liver cirrhosis.

The relationship between nutritional intervention and circulating thyroid hormones and rapid-turnover proteins was investigated in surgical patients with liver cirrhosis. Fourteen patients with well-compensated liver cirrhosis who were subjected to operations for esophageal varices or hepatoma were divided into two groups. The oral group was offered an oral diet containing 2200 kcal/day before surgery and conventional intravenous infusions of 5% glucose after the operation (500-600 kcal/day). The supplementary parenteral nutrition (SPN) group was offered the same oral diet as the oral group, combined with intravenous 50% glucose, fat emulsion, and branched-chain enriched amino acid solution, 600-1000 kcal and 7.32 g nitrogen/day during the 10 days before surgery and 800-1800 kcal and 7.32-9.76 g nitrogen/day during the first 2 wk postoperative. Plasma triiodothyronine (T3) was higher in the SPN group (1.26 +/- 0.09 ng/ml) than in the oral group (0.91 +/- 0.08 ng/ml) (P less than 0.001), and reverse T3 (rT3) was lower in the SPN group (297 +/- 33 pg/ml) than in the oral group (351 +/- 29 pg/ml (P less than 0.01) on the day of surgery. In addition, SPN significantly attenuated the low T3 and high rT3 levels found in the oral group throughout the 2 postoperative wk. In addition, attenuation of decreases in rapid-turnover proteins was achieved in the SPN group. It is likely that the SPN contributed to the partial correction of liver dysfunction and metabolic imbalance in traumatized cirrhotic patients.

Adult↗
PubMed1987

Carcinoma of the urinary bladder associated with schistosomiasis in Egypt: the possible causal relationship.

Carcinoma of the urinary bladder is the most common malignancy in Egyptians. At the National Cancer Institute in Cairo, it accounts for 27.6% of all cancers--38.5% of cancers in the male and 11.3% in the female. This very high frequency is attributed to underlying schistosomiasis. The infection can lead to malignancy through local tissue damage, mechanical irritation, bilharzial toxins or through secondary bacterial infection. Bacterial products include nitrate reductase capable of synthesizing nitrosoamines and beta glucuronidase enzymes, active at pH 7. Through liver involvement and dysfunction, tryptophan metabolism is disturbed, with the excretion of carcinogenic metabolites. Vitamin A deficiency is responsible for the squamous metaplasia and the high frequency of squamous cell carcinoma observed in the bladder. The characteristic clinico-pathological features of cancer of the urinary bladder are outlined, mainly the occurrence at a young age, the male predominance, especially farmers, and the high association with schistosomiasis. The tumors are often first seen in an advanced stage, arising from the posterior bladder wall and vault. The trigone is only affected in 8.5% of the cases. Histologically, squamous cell carcinomas of low grade are the most frequent cell type. Lymph node involvement is low in spite of the advanced stage of the tumor. Therefore, the results of radical surgery are encouraging. The results of a special study correlating the above parameters with the intensity of ova deposition are presented. Patients with heavy infection at a slightly earlier age but other tumor parameters the same are similar to those of egg-negative cases. This study indicates that other factors also play a role in the induction of tumors that are enhanced by the schistosomal infection. In Fayoum Province, schistosomiasis is decreasing while bladder cancer is increasing. Urine cytology as a screening tool is effective in detecting early bladder cancer. Studies are now in progress to detect tumor associated antigens in sera and urine of patients.

Adult↗