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  • ISSN: 2373-9819
    Volume 10, Issue 1
    Case Report
    Rachelle Sanjuan Chavez*, Sussannah Walsh, and Woojin Chong
    We present a case of a 24-year-old gravida 2, para 1 woman at an unknown gestational age with an omental ectopic pregnancy. She had started bleeding three weeks prior and she assumed that was her last menstrual period. Initial working diagnosis was an aborted tubal pregnancy after the first diagnostic laparoscopy. It was then subsequently discovered to be omental in location during a second diagnostic laparoscopic procedure searching for its location, in the setting of persistently rising quantitative bHCG levels. We encourage diligent exploration of the abdominal cavity in the setting of pregnancy of unknown location, even when bilateral adnexa and the pelvis appear normal during surgical exploration.
    Kenneth R. Cohen*
    Fluoroquinolone antibiotics are known to cause spontaneous tendinopathy and tendon rupture. Fluoroquinolones are not widely appreciated to cause neuropathy. Presented is a case of isolated motor neuropathy with prominent weakness and fasciculations caused by fluroquinalone use. Recovery was incomplete at 18 months. Central nervous system (CNS) toxicity is well documented with fluroquinalone use. Peripheral sensory neuropathy has been infrequently described; however, no well-documented case of isolated motor neuropathy appears in the literature. The mechanism is likely to be a direct axonal toxicity. With the increasing use of fluoroquinalones across all medical specialties, the recognition of potential neurotoxicity is important.
    Maha Alotaibi* and Shaza M Aloulou
    Background: A protein kinase domain, a Rhodanase-like domain, and the Tre-2/Bub2/Cdc16 (TBC) domain are all encoded by the TBCK gene. By modulating the mammalian target of rapamycin (mTOR) signaling pathway, the encoded protein is hypothesized to play a role in actin organization, cell growth, and cell proliferation. Has a role in the organization of the actin cytoskeleton. This protein may also play a role in the transcriptional control of mTOR complex components. And it’s found practically everywhere, including the kidneys, intestines, and other organs.
    Methods: The genetic etiology of facial dysmorphic disorder was investigated using whole exome sequencing (WES). Which was requested for two related cousin’s probands have developmental delays and hypotonia?
    Results: Splice site variants were found in both patients with an apparently homozygous for splice variants in the TBCK gene, according to WES.
    Conclusion: TBC1 domain-containing kinase (TBCK) homozygous mutation is closely linked to a severe global developmental delay. Hypotonia and seizure disorder, as well as a distinctive facial appearance and early death, we present two cousins patients with developmental delay, facial dysmorphism, and hypotonia as a result of TBCK.
    Matthew J. Rose*
    Blindness following facial trauma is a rare but serious complication. Traumatic optic neuropathy (TON) is a condition in which vision loss is due to direct or indirect trauma to the optic nerve. Here we present a case of a 30-year-old female that was struck by a car while riding her bicycle that immediately lost vision in her right eye. The current treatment options for TON are surgical optic nerve decompression and corticosteroids. Neither treatment has been shown to be overtly effective for traumatically induced visual deficiencies. There is a need for novel research looking for new treatment modalities for TON.
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