Thoracic outlet syndrome comprises a group of disorders that result in compression of the brachial plexus and subclavian vessels exiting the thoracic outlet. Symptoms include pain, paresthesia, pallor, and weakness depending upon the compromised structures. While consensus in diagnostic criteria has not yet been established, a thorough patient history, physical exam, and appropriate imaging studies are helpful in diagnosis. General first-line therapy for thoracic outlet syndrome is a conservative treatment, and may include physical therapy, lifestyle modifications, NSAIDs, and injection therapy of botulinum toxin A or steroids. Patients who have failed conservative therapy are considered for surgical decompression. This article aims to review the epidemiology, etiology, relevant anatomy, clinical presentations, diagnosis, and management of thoracic outlet syndrome.
Myocardial hypertrophy is an independent risk factor for heart failure (HF), yet the mechanisms underlying pathological cardiomyocyte growth are incompletely understood. The c-Jun NH2-terminal kinase (JNK) signaling cascade modulates cardiac hypertrophic remodeling, but the upstream factors regulating myocardial JNK activity remain unclear. In this study, we sought to identify JNK-activating molecules as novel regulators of cardiac remodeling in HF. We investigated mixed lineage kinase-3 (MLK3), a master regulator of upstream JNK-activating kinases, whose role in the remodeling process had not previously been studied. We observed increased MLK3 protein expression in myocardium from patients with nonischemic and hypertrophic cardiomyopathy and in hearts of mice subjected to transverse aortic constriction (TAC). Mice with genetic deletion of MLK3 (MLK3−/−) exhibited baseline cardiac hypertrophy with preserved cardiac function. MLK3−/− mice subjected to chronic left ventricular (LV) pressure overload (TAC, 4 wk) developed worsened cardiac dysfunction and increased LV chamber size compared with MLK3+/+ littermates ( n = 8). LV mass, pathological markers of hypertrophy ( Nppa, Nppb), and cardiomyocyte size were elevated in MLK3−/− TAC hearts. Phosphorylation of JNK, but not other MAPK pathways, was selectively impaired in MLK3−/− TAC hearts. In adult rat cardiomyocytes, pharmacological MLK3 kinase inhibition using URMC-099 blocked JNK phosphorylation induced by neurohormonal agents and oxidants. Sustained URMC-099 exposure induced cardiomyocyte hypertrophy. These data demonstrate that MLK3 prevents adverse cardiac remodeling in the setting of pressure overload. Mechanistically, MLK3 activates JNK, which in turn opposes cardiomyocyte hypertrophy. These results support modulation of MLK3 as a potential therapeutic approach in HF. NEW & NOTEWORTHY Here, we identified a role for mixed lineage kinase-3 (MLK3) as a novel antihypertrophic and antiremodeling molecule in response to cardiac pressure overload. MLK3 regulates phosphorylation of the stress-responsive JNK kinase in response to pressure overload and in cultured cardiomyocytes stimulated with hypertrophic agonists and oxidants. This study reveals MLK3-JNK signaling as a novel cardioprotective signaling axis in the setting of pressure overload.
Cubital Tunnel Syndrome (CuTS) is the compression of the ulnar nerve as it courses through the cubital tunnel near the elbow at the location colloquially referred to as the “funny bone”. CuTS is the most commonly diagnosed mononeuropathy after carpal tunnel syndrome. Cubital tunnel syndrome can manifest as numbness, tingling, or pain in the ring/small fingers and dorsoulnar hand. Repetitive pressure, stretching, flexion, or trauma of the elbow joint are known causes of CuTS. Chronic ulnar nerve compression and CuTS, when left untreated, can lead to atrophy of the first dorsal interosseus muscle and affect one’s quality of life to the point that they are no longer able to participate in daily activities involving fine motor function. It is estimated that up to 5.9% of the general population have had symptoms of CuTS. CuTS is underdiagnosed due to lack of seeking of treatment for symptoms. Compression or damage to the ulnar nerve is the main cause of symptoms experienced by an individual with CuTS. Repetitive elbow pressure or a history or elbow joint trauma or injury are additional known causes that can lead to CuTS. Common presentations of CuTS include paresthesia, clumsiness of the hand, hand atrophy and weakness. The earliest sign of CuTS is most commonly numbness and tingling of the ring and 5th finger. Older patients tend to present with motor symptoms of chronic onset; younger patients tend to have more acute symptoms. Pain and point tenderness at the medial elbow may also be seen. CuTS lacks universally agreed upon diagnostic and treatment algorithms. CuTS can be diagnosed by physical exam using Tinel’s sign, flexion-compression tests, palpating the ulnar nerve for thickening presence of local tenderness along the nerve. Ultrasound and nerve conduction studies may be used in combination with physical exam for diagnosis. Conservative treatment for CuTS is almost always pursued before surgical treatment and includes elbow splints, braces, and night-gliding exercises. Surgical treatment may be pursued in severe CuTS refractory to conservative treatment. Surgical options include open and endoscopic in-situ decompression, medial epicondylectomy, and anterior transposition of the ulnar nerve. CuTS is a prevalent disease that, if left untreated, can significantly alter an individual’s quality of life. Therefore, an accurate diagnosis and appropriate treatment is paramount in reducing further damage and preventing worsening or future symptoms.
Midwave infrared interband-cascade light-emitting devices (ICLEDs) have the potential to improve the selectivity, stability, and sensitivity of low-cost gas sensors. We demonstrate a broadband direct absorption CH4 sensor with an ICLED coupled to a plastic hollow-core fiber (1 m length, 1500 µm inner diameter). The sensor achieves a 1σ noise equivalent absorption of approximately 0.2 ppmv CH4 at 1 Hz, while operating at a low drive power of 0.5 mW. A low-cost sub-ppmv CH4 sensor would make monitoring emissions more affordable and more accessible for many relevant industries, such as the petroleum, agriculture, and waste industries.
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