Publications by authors named "Michael A Malone"

11 Publications

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Infectious Disease Topics for Primary Care.

Authors:
Michael A Malone

Prim Care 2018 09;45(3):xv-xvi

Tidelands Health/ MUSC Family Medicine Residency Program, Murrells Inlet, SC 29576, USA; 4320 Holmestown Road, Myrtle Beach, SC 29588, USA. Electronic address:

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http://dx.doi.org/10.1016/j.pop.2018.07.001DOI Listing
September 2018

Skin Infections.

Prim Care 2018 Sep;45(3):433-454

Department of Family Medicine, Tidelands Health MUSC Family Medicine Residency Program, 4320 Holmestown Road, Myrtle Beach, SC 29588, USA.

The primary care provider will commonly see skin and soft tissue infections in the outpatient setting. Skin and soft tissue infections range from the uncomplicated impetigo to the potentially lethal necrotizing fasciitis. This article reviews these infections based on their underlying etiology: bacterial, fungal, and viral causes. This article discusses the etiology, presentation, evaluation, and management of impetigo, bullous impetigo, erysipelas, cellulitis, periorbital cellulitis, orbital cellulitis, folliculitis, furuncles, carbuncles, abscess, necrotizing fasciitis, sporotrichosis, tinea corporis, tinea pedis, tinea capitis, Herpes Simplex Virus, zoster, molluscum contagiosum, and warts.
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http://dx.doi.org/10.1016/j.pop.2018.05.004DOI Listing
September 2018

Allergy Primer for Primary Care.

Authors:
Michael A Malone

Prim Care 2016 Sep 14;43(3):xv. Epub 2016 Jul 14.

Department of Family and Community Medicine, Penn State College of Medicine, Hershey, PA 17033, USA; 2643 Westhampton Terrace, Elizabethtown, PA 17022, USA. Electronic address:

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http://dx.doi.org/10.1016/j.pop.2016.04.014DOI Listing
September 2016

Mastocytosis.

Prim Care 2016 Sep;43(3):505-18

Department of Family and Community Medicine, Penn State Milton S. Hershey Medical Center, 500 University Drive, Hershey, PA 17033, USA.

Mastocytosis is a rare disease caused by excessive production of mast cells. Clinical presentation is variable, often based on the type of mastocytosis, but in all types of mastocytosis there seems to be an increase in the risk of anaphylaxis. Systemic mastocytosis is diagnosed based on bone marrow biopsy. Treatment is variable based on the type of mastocytosis, but trigger avoidance and anaphylaxis treatment are mainstays. There are no therapies that change the natural course of mastocytosis. For cutaneous mastocytosis, treatment is conservative and aimed at symptom relief.
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http://dx.doi.org/10.1016/j.pop.2016.04.007DOI Listing
September 2016

Complementary and alternative treatments in sports medicine.

Prim Care 2013 Dec 26;40(4):945-68, ix. Epub 2013 Sep 26.

Department of Family and Community Medicine, Penn State Milton S. Hershey Medical Center, 500 University Drive, Hershey, PA 17033, USA. Electronic address:

Many patients suffering from pain and dysfunction attributable to musculoskeletal conditions will use some form of complementary and alternative medicine (CAM). Unfortunately, there is a paucity of both the quantity and quality of CAM treatments for specific musculoskeletal conditions. Many CAM treatments are used for a variety of musculoskeletal conditions, but may be more commonly used for specific conditions. This article addresses the use of CAM for specific musculoskeletal conditions, followed by a review of other CAM treatments and their potential indications for a multitude of conditions, based on the current medical literature and traditional use.
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http://dx.doi.org/10.1016/j.pop.2013.08.010DOI Listing
December 2013

Urinary tract infections.

Prim Care 2013 Sep 12;40(3):687-706. Epub 2013 Jul 12.

Penn State Department of Family and Community Medicine, Hershey, PA, USA.

Clinical presentation helps differentiate between upper and lower urinary tract infections (UTIs). UTIs are classified as either complicated or uncomplicated. A complicated UTI is associated with an underlying condition that increases the risk of failing therapy. Primary laboratory tests for UTIs consist of urinalysis and urine culture. The most common pathogen for uncomplicated cystitis and pyelonephritis is Escherichia coli. Nitrofurantoin, fosfomycin, and trimethoprim-sulfamethoxazole are first-line therapies for acute uncomplicated cystitis. Decisions regarding antibiotic agents should be individualized based on patients' allergies, tolerability, community resistance rates, cost, and availability.
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http://dx.doi.org/10.1016/j.pop.2013.06.005DOI Listing
September 2013

Irritable bowel syndrome.

Authors:
Michael A Malone

Prim Care 2011 Sep;38(3):433-47; viii

Department of Family Medicine, Penn State College of Medicine, 845 Fishburn Road, Hershey, PA 17033, USA.

Irritable bowel syndrome (IBS) is a common gastrointestinal disorder that leads to crampy pain, gassiness, bloating, and changes in bowel habits in the absence of any currently identifiable organic disorder. Patients with IBS may be classified by their predominant bowel habit: diarrhea-predominant, constipation-predominant, or IBS with alternating bowel movements. IBS is often associated with stress or anxiety. Although IBS can be frustrating and concerning to patients with this disorder, it does not cause permanent harm to the intestines and does not lead to a serious disease such as cancer. Although treatments exist for its symptoms, there is no known cure.
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http://dx.doi.org/10.1016/j.pop.2011.05.003DOI Listing
September 2011

Diabetes-induced bradycardia is an intrinsic metabolic defect reversed by carnitine.

Metabolism 2007 Aug;56(8):1118-23

Julia Parrish Diabetes Research Institute, University of South Florida College of Medicine, Tampa, FL 33612-4742, USA.

Rats with streptozotocin-induced diabetes (STZ-D) have reduced serum carnitine levels and bradycardia. Heart rates (HRs) of 24nondiabetic rats (NRs) and 24 STZ-D rats were compared. L-carnitine (C) was added to the drinking water of rats (12 STZ-D+C) to raise their serum carnitine level. The intrinsic HR for each animal was determined after parasympathetic and sympathetic blockade. The HRs of STZ-D rats (278+/-15 beats per minute) were less than those of NRs (348+/-8 beats per minute) (P<.01). STZ-D rats had low serum carnitine compared with control and STZ-D+C rats. The difference in HR of STZ-D rats and NRs continued after blockade, indicating that the bradycardia ofdiabetes is intrinsic to the heart. The metabolic milieu reflected in the rats' urinary organic acid profiles differed between the control and STZ-D rats. The HR of STZ-D+C rats (326+/-5 beats per minute) did not differ from those of NRs. Increasing either the insulin dose or the serum free carnitine reduced urinary organic acids, but normal HRs were associated only with elevated serum carnitine levels. When glucose is compromised as a myocardial energy source (diabetes mellitus), we propose that elevated levels of serum carnitine may increase myocardial fatty acid metabolism sufficiently to correct the bradycardia of STZ-D rats.
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http://dx.doi.org/10.1016/j.metabol.2007.04.005DOI Listing
August 2007

Cardio-protective effects of carnitine in streptozotocin-induced diabetic rats.

Cardiovasc Diabetol 2006 Jan 19;5. Epub 2006 Jan 19.

The Department of Pediatrics, University of South Florida, College of Medicine, Tampa, FL 33612, USA.

Background: Streptozotocin-induced diabetes (STZ-D) in rats has been associated with carnitine deficiency, bradycardia and left ventricular enlargement.

Aim: The purpose of this study was to determine whether oral carnitine supplementation would normalize carnitine levels and cardiac function in STZ-D rats.

Methods: Wistar rats (48) were made hyperglycemic by STZ at 26 weeks of age. Same age normal Wistar rats (24) were used for comparison. Echocardiograms were performed at baseline 2, 6, 10, and 18 weeks after STZ administration in all animals. HbA1c, serum carnitine and free fatty acids (FFA) were measured at the same times. Since STZ-D rats become carnitine deficient, 15 STZ-D rats received supplemental oral carnitine for 16 weeks.

Results: The heart rates for the STZ-D rats (290 +/- 19 bpm) were less than control rats (324 +/- 20 bpm) (p < 0.05). After 4 weeks of oral carnitine supplementation, the serum carnitine and heart rates of the STZ-D rats returned to normal. Dobutamine stress increased the heart rates of all study animals, but the increase in STZ-D rats (141 +/- 8 bpm) was greater than controls (79 +/- 8 bpm) (p < 0.05). The heart rates of STZ-D rats given oral carnitine, however, were no different than controls (94 +/- 9 bpm). The left ventricular mass/body weight ratio (LVM/BW) in the diabetic animals (2.7 +/- 0.5) was greater than control animals (2.2 +/- 0.3) (p < 0.05) after 18 weeks of diabetes. In contrast, the LVM/BW (2.3 +/- .2) of the STZ-D animals receiving supplemental carnitine was the same as the control animals at 18 weeks.

Conclusion: Thus, supplemental oral carnitine in STZ-D rats normalized serum carnitine, heart rate regulation and left ventricular size. These findings suggest a metabolic mechanism for the cardiac dysfunction noted in this diabetic animal model.
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http://dx.doi.org/10.1186/1475-2840-5-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1363717PMC
January 2006

Multiple mechanisms of rhabdom shedding in the lateral eye of Limulus polyphemus.

J Comp Neurol 2002 Jul;449(1):26-42

Department of Bioengineering and Neuroscience, Institute for Sensory Research, Syracuse University, Syracuse, NY 13244-5290, USA.

Rhabdom shedding in horseshoe crab lateral eye photoreceptors was studied with anti-opsin and anti-arrestin immunocytochemistry. Two, possibly three, distinct shedding mechanisms were revealed in animals maintained in natural lighting. Transient rhabdom shedding, triggered by dawn, is a brief, synchronous event that removes up to 10% of the rhabdom membrane. Whorls of rhabdomeral membrane break into vesicles and form compact multivesicular bodies. These debris particles are immunoreactive for opsin and are of a relatively uniform size, averaging approximately 2 microm(2) in area. Transient shedding requires that input from circadian efferent fibers to the retina precedes the light trigger, and cutting the optic nerve blocks efferent input and transient shedding. Light-driven rhabdom shedding is a progressive process. Rhabdomeral membrane is removed by coated vesicles that accumulate into loosely packed multivesicular bodies. These debris particles label with antibodies directed against opsin, arrestin, and adaptin, and they have a large distribution of sizes, averaging almost 6 microm(2) in area and ranging up to 25 microm(2) or more. The amount of rhabdomeral membrane removed by light-driven shedding has seasonal variation and depends on latitude. Light-driven shedding does not require circadian efferent input. A possible third shedding mechanism, light-independent shedding, is observed when transient shedding is blocked either by 48 hours of darkness or by cutting the optic nerve. Small particles, averaging 1.8 microm(2) in area, exhibiting opsin but not arrestin immunoreactivity can then be found in the cytoplasm surrounding the rhabdom. The nature of light-independent shedding is not yet clear.
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http://dx.doi.org/10.1002/cne.10263DOI Listing
July 2002