Facial Venous Tumour Thrombus from Submandibular Gland Mucoepidermoid Carcinoma: An Atypical Tumour Spread in Head and Neck Cancer.

Background: Tumour thrombus of the facial vein is an exceedingly rare complication arising from mucoepidermoid carcinoma of the salivary glands. Early detection is pivotal for appropriate management, as delays can lead to metastatic disease, worsening the prognosis. Case description: We present a case involving a 76-year-old male with a history of mucoepidermoid carcinoma of the right submandibular gland, previously treated with surgical resection and radiotherapy. The patient, a long-term worker in a rubber factory, presented with a painless, firm swelling in the right cheek, persisting for three months. Contrast-enhanced computed tomography (CECT) showed distended facial vein with enhancing thrombus confirmed by sonographic correlation demonstrating intralesional vascularity. Cannon ball pulmonary nodules were also noted. Radiological findings led to a core biopsy, confirming tumor thrombosis of the facial vein due to mucoepidermoid carcinoma. However, the patient declined a biopsy of the pulmonary nodules, and has been referred to oncology for further management. Conclusions: This case highlights the critical importance of considering venous tumour thrombus in patients with previous salivary gland malignancies presenting with new or persistent facial swellings. It emphasises the role of advanced imaging techniques in the early identification of this rare entity. Additionally, it stresses the need for healthcare providers to engage in thorough discussions with patients about the potential consequences of forgoing recommended treatments, reinforcing the need for vigilance in monitoring such patients. LEARNING POINTS: Tumours of head and neck may cause thrombosis of veins by direct invasion resulting in a tumour thrombus, or indirectly by exerting a mass effect and vein compression.These can be distinguished by contrast-enhanced computed tomography (CECT) or magnetic resonance imaging (MRI).Doppler ultrasound may show patchy neovascularisation in a tumour thrombus, which would be absent if thrombosis was caused by compression.

Harmaline toxicity on dorsal striatal neurons and its role in tremor.

Harmaline is one of the ß-carboline derivative compounds that is widely distributed in the food chain and human tissues. Harmine, a dehydrogenated form of harmaline, appeared to have a higher concentration in the brain, and appeared to be elevated in essential tremor (ET) and Parkinson's disease. Exogenous harmaline exposure in high concentration has myriad consequences, including inducing tremor, and causing neurodegeneration of Purkinje cells in the cerebellum. Harmaline-induced tremor is an established animal model for human ET, but its underlying mechanism is still controversial. One hypothesis posits that the inferior olive-cerebellum pathway is involved, and CaV3.1 T-type Ca2+ channel is a critical target of action. However, accumulating evidence indicates that tremor can be generated without disturbing T-type channels. This implies that additional neural circuits or molecular targets are involved. Using in vitro slice Ca2+-imaging and patch clamping, we demonstrated that harmaline reduced intracellular Ca2+ and suppressed depolarization-induced spiking activity of medium spiny striatal neurons (MSN), and this effect of harmaline can be partially attenuated by sulpiride (5 µM). In addition, the frequencies of spontaneous excitatory post-synaptic currents (sEPSCs) on MSNs were also significantly attenuated. Furthermore, the induced tremor in C57BL/6 J mice by harmaline injections (i.p. 12.5-18 mg/kg) was also shown to be attenuated by sulpiride (20 mg/kg). This series of experiments suggests that the dorsal striatum is a site of harmaline toxic action and might contribute to tremor generation. The findings also provide evidence that D2 signaling might be a part of the mechanism underlying essential tremor.

Interrelated Oncogenic Viruses and Breast Cancer.

Breast Cancer is a multifactorial disease and recent evidence that viruses have a greater role in its aetiology and pathophysiology than previously hypothesized, has garnered a lot of attention in the past couple of years. After the role of Mouse Mammary Tumour Virus (MMTV) in the oncogenesis of breast cancer has been proved in mice, search for similar viruses found quite a plausible relation of Human Papilloma Virus (HPV), Epstein-Barr virus (EBV), and Bovine Leukaemia Virus (BLV) with breast cancer. However, despite practical efforts to provide some clarity in this issue, the evidence that viruses cause breast cancer still remains inconclusive. Therefore, this article aims to clarify some ambiguity and elucidate the correlation of breast cancer and those particular viruses which are found to bring about the development of tumorigenesis by a previous infection or by their own oncogenic ability to manipulate the molecular mechanisms and bypass the immune system of the human body. Although many studies have reported, both, the individual and co-existing presence of HPV, EBV, MMTV, and BLV in patient sample tissues, particularly in Western women, and proposed oncogenic mechanisms, majority of the collective survey of literature fails to provide a delineated and strong conclusive evidence that viruses do, in fact, cause breast cancer. Measures to prevent these viral infections may curb breast cancer cases, especially in the West. More studies are needed to provide a definite conclusion.