ABSTRACT
A pilot mental health and wellness clinic was developed and implemented on the campus of Paul Quinn College, a small Historically Black College and University (HBCU) in Dallas, TX, to address mental health disparities in an African-American student population. Additionally, a series of student engagement activities was developed and implemented to address stigma and enhance linkage to the clinic. The student engagement activities were well attended. In all, 14 students requested a total of 97 appointments during the spring 2016 semester, but attended only 41 appointments. Students sought treatment of a variety of psychiatric disorders, most commonly major depressive disorder and adjustment disorder. A model based on this program could conceivably be extended to serve students more broadly in other HBCUs as well as in community colleges.
Subject(s)
Black or African American/psychology , Health Services Accessibility/organization & administration , Mental Disorders , Female , Healthcare Disparities , Humans , Male , Mental Disorders/diagnosis , Mental Disorders/ethnology , Mental Disorders/psychology , Mental Disorders/therapy , Pilot Projects , Program Development , School Health Services/organization & administration , Social Stigma , Students , Texas , UniversitiesABSTRACT
OBJECTIVES: The aim of the study was to determine the acute and long-term outcomes of preterm infants treated with an intravenous fish oil-based lipid emulsion (FishLE) for parenteral nutrition-associated liver disease (PNALD). METHODS: Preterm infants 14 days to 24 months of age with anatomic short gut or severe intestinal dysmotility, serum direct bilirubin ≥4 mg/dL, and requiring >60% calories from parenteral nutrition were eligible. Enrolled infants received 1 gâ·âkgâ·âday of FishLE until resolution of direct hyperbilirubinemia or return of enteral nutrition. Acute clinical effects and biochemical markers of liver function were monitored. Growth and developmental scores at 6 and 12 months postmenstrual age (PMA) were assessed and compared with controls matched by gestational age (GA). RESULTS: Thirteen patients with mean GA of 28â±â4 weeks were treated and compared with 119 GA-matched controls. Their mean direct bilirubin was 9.8â±â6.4 mg/dL at enrollment. All infants had resolution of cholestasis after study completion. There were no acute adverse events, deaths, or liver/intestinal transplants. Weight and head circumference were similar between FishLE-treated patients and controls at 6- and 12-month PMA. Cognitive and motor scores were decreased at 6 and 12 months PMA in FishLE-treated infants. Logistic regression analysis showed that prolonged hospitalization was detrimental to cognitive and motor development, whereas treatment was not. CONCLUSIONS: The use of intravenous FishLEs in premature infants appears to be safe and reverses PNALD despite significant liver disease and intestinal failure. This therapy should be used in preterm infants with PNALD and followed long term to evaluate development.
Subject(s)
Fat Emulsions, Intravenous/therapeutic use , Fish Oils/therapeutic use , Infant, Premature, Diseases/therapy , Liver Diseases/therapy , Parenteral Nutrition/adverse effects , Female , Follow-Up Studies , Humans , Infant, Newborn , Infant, Premature , Infant, Premature, Diseases/etiology , Liver Diseases/etiology , Logistic Models , Male , Prospective Studies , Treatment OutcomeABSTRACT
OBJECTIVE/BACKGROUND: To review the existing literature and describe a standardized methodology by expert consensus for the performance of trigger point injections (TPIs) in the treatment of headache disorders. Despite their widespread use, the efficacy, safety, and methodology of TPIs have not been reviewed specifically for headache disorders by expert consensus. METHODS: The Peripheral Nerve Blocks and Other Interventional Procedures Special Interest Section of the American Headache Society over a series of meetings reached a consensus for nomenclature, indications, contraindications, precautions, procedural details, outcomes, and adverse effects for the use of TPIs for headache disorders. A subcommittee of the Section also reviewed the literature. RESULTS: Indications for TPIs may include many types of episodic and chronic primary and secondary headache disorders, with the presence of active trigger points (TPs) on physical examination. Contraindications may include infection, a local open skull defect, or an anesthetic allergy, and precautions are necessary in the setting of anticoagulant use, pregnancy, and obesity with unclear anatomical landmarks. The most common muscles selected for TPIs include the trapezius, sternocleidomastoid, and temporalis, with bupivacaine and lidocaine the agents used most frequently. Adverse effects are typically mild with careful patient and procedural selection, though pneumothorax and other serious adverse events have been infrequently reported. CONCLUSIONS: When performed in the appropriate setting and with the proper expertise, TPIs seem to have a role in the adjunctive treatment of the most common headache disorders. We hope our effort to characterize the methodology of TPIs by expert opinion in the context of published data motivates the performance of evidence-based and standardized treatment protocols.
Subject(s)
Anesthetics, Local/administration & dosage , Headache Disorders/drug therapy , Nerve Block/methods , Nerve Block/standards , Trigger Points , Consensus , Humans , Injections, IntramuscularSubject(s)
Antiviral Agents/therapeutic use , Hepatitis B/therapy , Adult , Antiviral Agents/adverse effects , Biomedical Research , Carcinoma, Hepatocellular/virology , Global Health , Hepatitis B/epidemiology , Hepatitis B/physiopathology , Humans , Liver Cirrhosis/virology , Liver Neoplasms/virology , Prevalence , Risk Assessment , Treatment OutcomeABSTRACT
Hepatitis C is one of the most common indications for liver transplantation in the United States, accounting for approximately 40%-45% of all liver transplants. Unfortunately, recurrent disease is universal in patients who are viremic before transplantation. This can lead to cirrhosis in at least 25% of patients 5 years after liver transplantation, and recurrent hepatitis C is now emerging as an important but occasionally contentious indication for retransplantation. Several attempts have been undertaken to identify patients at high risk for severe recurrent disease who may benefit from treatment, but unfortunately antiviral therapy frequently is ineffective and often is associated with numerous side effects. Although we have made significant strides in understanding the natural history of this disease in nontransplant patients, this does not hold true for the transplant population in which several uncertainties covering virtually the entire spectrum of liver transplantation persist. Despite these concerns, on a more practical level, it is usually only in the postoperative setting that clinicians truly can assess the impact of their interventions on the natural history of recurrent hepatitis C, for example, by adjusting immunosuppression or prescribing antiviral therapy. Preoperative and perioperative (including donor) factors often are outside the control of hepatologists and transplant surgeons. This review is not an inclusive review of the literature but summarizes what we believe are the more controversial topics of this disease.
Subject(s)
Hepatitis C/surgery , Liver Transplantation , Antiviral Agents/therapeutic use , Health Status , Hepatitis C/drug therapy , Hepatitis C/etiology , Humans , Immunosuppression Therapy , Recurrence , Risk Factors , Treatment OutcomeABSTRACT
Acute and chronic liver disease contributes significantly to morbidity and mortality following hematopoietic cell transplantation (HCT). The best prognostic indicator for the development of severe liver dysfunction is an early rise in liver function test results after HCT. The leading causes soon after HCT are acute graft-versus-host disease (GVHD), sinusoidal obstruction syndrome, drug and total parenteral nutrition hepatotoxicity, sepsis, and viral infection. Hepatic herpesvirus and fungal infections after HCT, though uncommon, can be life-threatening and warrant immediate diagnosis and treatment. Hepatitis B, hepatitis C virus, iron overload, and chronic GVHD are among the most common causes for chronic liver disease after HCT. Because treatments are directed at the underlying etiology of liver disease, prompt diagnosis by means of laboratory tests, hepatic imaging, and often liver biopsy is required after HCT.
Subject(s)
Hematopoietic Stem Cell Transplantation/adverse effects , Liver Diseases/etiology , Biliary Tract Diseases , Drug-Related Side Effects and Adverse Reactions , Graft vs Host Disease , Hepatic Veno-Occlusive Disease , Hepatitis, Viral, Human , Humans , Iron Overload , Liver Diseases/diagnosis , Liver Diseases/epidemiology , Mycoses , Parenteral Nutrition, Total , Risk Factors , SepsisABSTRACT
BACKGROUND/AIMS: Protein-L-isoaspartyl methyltransferase (PIMT) is a methyltransferase that plays a crucial role in the repair of damaged proteins. In this study, we investigated whether ethanol exposure causes an accumulation of modified proteins bearing atypical isoaspartyl residues that may be related to impaired PIMT activity. We further sought to determine whether betaine administration could prevent the accumulation of these types of damaged proteins. METHODS: Livers of male Wistar rats, fed the Lieber DeCarli control, ethanol or 1% betaine-supplemented diets for 4 weeks, were processed for PIMT-related analyses. RESULTS: We observed a significant increase in the accumulation of modified proteins bearing isoaspartyl residues, i.e. the substrates for PIMT, in homogenate samples and various subcellular fractions of livers from ethanol-fed rats. Betaine supplementation prevented this accumulation of damaged proteins. In contrast, ethanol exposure induced no changes in the PIMT enzyme activity levels as compared to controls. The accumulation of damaged proteins negatively correlated with hepatic S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) ratios. CONCLUSIONS: Ethanol consumption results in the accumulation of modified proteins bearing atypical isoaspartyl residues via impaired in vivo PIMT activity. Betaine administration prevents the ethanol-induced accumulation of isoaspartyl-containing proteins by restoring the PIMT-catalyzed protein repair reaction through normalizing the hepatocellular SAM:SAH ratios.
Subject(s)
Alcohols/toxicity , Betaine/pharmacology , Liver/drug effects , Protein D-Aspartate-L-Isoaspartate Methyltransferase/physiology , Animals , Catalysis , Diet , Ethanol/toxicity , Male , Microsomes/metabolism , Protein D-Aspartate-L-Isoaspartate Methyltransferase/metabolism , Rats , Rats, Wistar , S-Adenosylhomocysteine/chemistry , S-Adenosylmethionine/chemistry , Subcellular FractionsABSTRACT
BACKGROUND/AIMS: Previous studies in our laboratory implicated ethanol-induced decreases in hepatocellular S-adenosylmethionine to S-adenosylhomocysteine (SAM:SAH) ratios in lowering the activity of phosphatidylethanolamine methyltransferase (PEMT), which is associated with the generation of steatosis. Further in vitro studies showed that betaine supplementation could correct these alterations in the ratio as well as attenuate alcoholic steatosis. Therefore, we sought to determine whether the protective effect of betaine is via its effect on PEMT activity. METHODS: Male Wistar rats were fed the Lieber DeCarli control or ethanol diet with or without 1% betaine supplementation for 4 weeks. RESULTS: We observed that ethanol feeding resulted in decreased phosphatidylcholine (PC) production by a PEMT-catalyzed reaction. Betaine supplementation corrected the ethanol-induced decrease in hepatic SAM:SAH ratios and by normalizing PC production via the PEMT-mediated pathway, significantly reduced fatty infiltration associated with ethanol consumption. This restoration of hepatocellular SAM:SAH ratio by betaine supplementation was associated with increases in the activity, enzyme mass and gene expression of the enzyme, betaine homocysteine methyltransferase (BHMT), that remethylates homocysteine. CONCLUSIONS: Betaine, by virtue of promoting an alternate remethylation pathway, restores SAM:SAH ratios that, in turn, correct the defective cellular methylation reaction catalyzed by PEMT resulting in protection against the generation of alcoholic steatosis.
Subject(s)
Betaine/administration & dosage , Fatty Liver, Alcoholic/prevention & control , Lipotropic Agents/administration & dosage , Phosphatidylcholines/metabolism , Phosphatidylethanolamine N-Methyltransferase/metabolism , Animals , Diet , Ethanol/toxicity , Fatty Liver, Alcoholic/enzymology , Liver/drug effects , Liver/enzymology , Liver/metabolism , Male , Phosphatidylethanolamine N-Methyltransferase/analysis , Rats , Rats, Wistar , S-Adenosylhomocysteine/analysis , S-Adenosylmethionine/analysis , Triglycerides/analysisABSTRACT
The field of noninvasive markers for the assessment of hepatic fibrosis has seen tremendous growth in the last two decades. Surrogate markers are gradually being substituted for biomarkers that reflect the complex balance between synthesis and degradation of the extracellular matrix. Coupled with these promising tests are artificial intelligence networks devised by sophisticated statistical instruments that incorporate a battery of laboratory tests and biomarkers with imaging modalities. Recently, gene identification and protein analysis have shown promise in identifying selected patients with mild or advanced fibrosis. Despite such progress, an important limitation of these tests is the frequent inability to detect mild fibrosis although patients at the end of the histological spectrum (i.e., advanced fibrosis or cirrhosis) are readily identified. With time, it is anticipated a combination of serological and radiological tests together with genetic and proteomic investigations will provide accurate assessment of fibrosis in a cost-effective and timely manner.
Subject(s)
Biomarkers/analysis , Liver Cirrhosis/diagnosis , Diagnostic Imaging , HumansABSTRACT
Patients and physicians are frequently unaware that pain coming from the muscles of the head and neck is probably the cause of the most frequent forms of migraine. Identifying the extracranial origins of the patient's headache by physical examination should reassure patient and examiner that the headache is benign and treatable. The results of the examination should lead to physical treatment, reducing headache frequency and severity. This paper describes techniques of the physical examination to identify the extracranial causes of migraine headache.
Subject(s)
Migraine Disorders/diagnosis , Physical Examination , Emergency Medical Services , Humans , Neurologic ExaminationABSTRACT
BACKGROUND: The effects of chronic ethanol feeding on rat hepatocytes have been shown to include impaired cell-extracellular matrix (ECM) adhesion events, such as decreased attachment and spreading as well as increased integrin-actin cytoskeleton association. These results, observed previously by this laboratory, are highly suggestive of impaired actin cytoskeleton reorganization, an event mediated by differential activation of the Rho family GTPases Rac, Cdc42, and RhoA. Therefore, the purpose of this study was to examine the effects of chronic ethanol administration on these GTPases. METHODS: Male Wistar rats were pair-fed 4 to 5 weeks with a liquid diet containing either ethanol (as 36% of total calories) or isocaloric carbohydrate. Hepatocytes were isolated and plated on collagen IV up to 24 hours. At specific times, the hepatocytes were lysed and these lysates were analyzed for RhoA, Cdc42, and Rac activation. RESULTS: In freshly isolated hepatocytes from ethanol-fed rats, the GTP-bound (active) forms of Rac and Cdc42 were significantly decreased compared with pair-fed control rats, while the GTP-bound form of RhoA was not significantly altered. These ethanol-induced impairments in Rac and Cdc42 activation persisted even after plating the hepatocytes on collagen IV. Additionally, chronic ethanol treatment did not directly affect GTP binding of Cdc42 and Rac, as incorporation of GTPgammaS was not affected. CONCLUSIONS: Chronic ethanol administration selectively impairs Rac and Cdc42 activation in rat hepatocytes. As activation of these 2 GTPases is crucial for efficient cell attachment and spreading on ECM substrates, the results from this study suggest that the ethanol-induced impairments in Rac and Cdc42 activation are responsible for the impaired hepatocyte-ECM adhesion events observed previously by our laboratory. Furthermore, these results raise the intriguing possibility that these GTPases are involved in other ethanol-induced functional impairments, such as protein trafficking and receptor-mediated endocytosis.