In this study, we re-evaluated the CP proteins by conducting a similar comprehensive CP proteome analysis comparing the mass spectrometry results of the axoneme sample prepared from Chlamydomonas strains with and without CP complex. We identified a similar set of CP protein candidates and additional new 11 CP protein candidates. Furthermore, by using Chlamydomonas strains lacking specific CP sub-structures, we present a more complete model of localization for these CP proteins. This work has established a new foundation for understanding the function of the CP complex in future studies.Coccidioidomycosis, a fungal infection caused by inhaling spores of Coccidioides immitis/posadasii, is endemic to the southwestern states of the United States, Northern Mexico and some parts of Central and South America. It is primarily a pulmonary infection with less than 0.5% of symptomatic cases showing dissemination. Skin, lymph nodes and bone are the commonest sites. Neurological involvement is rare and commonly presents as strokes, abscesses or meningoencephalitis. We present the case of a previously healthy 23-year-old African American male, presented with a four-month history of progressive right upper extremity weakness that initially started with right shoulder pain followed by worsening weakness and loss of muscle mass. Electromyography (EMG) demonstrated right brachial plexopathy with moderate-to-severe active denervation changes. MRI cervical spine revealed a 9-cm contrast enhancing extradural mass extending through the neural foramen from C4-T1 roots and forming a 4-cm right apical lung mass subsequently seen on MRI of the brachial plexus. All trunks, divisions and cords were thickened, hyperintense and showed contrast enhancement on MRI. Neuromuscular ultrasound (NUS) demonstrated enlargement of peripheral nerves. Differentials prior to biopsy of the mass ranged from neurofibromas to pancoast lung tumors. see more Coccidioidomycosis did not figure on the initial list of differentials. Patient underwent subsequent biopsy of the extradural and lung masses that showed coccidiodes. Serum coccidioides antibody titers were elevated. The patient was treated with high-dose intravenous fluconazole and aggressive mass debridement. His weakness improved on four months follow-up evaluation with significant resolution of EMG abnormalities and decreased swelling on NUS.A 62-year-old female presented to the emergency department (ED) with fatigue and generalized body weakness for the last three days. Upon arrival, initial ECG showed wide complex tachycardia with sine waves and a heart rate (HR) ranging between 100-170 bpm. She was otherwise vitally stable. The patient had a past medical history of hyperaldosteronism, type 2 diabetes mellitus (DM), chronic kidney disease (CKD) with microalbuminuria, and hypertension. She also had a history of cerebrovascular accident (CVA) and residual left-sided weakness more pronounced in the upper limb. Initial venous blood gas (VBG) analysis showed a potassium level of more than 10 mmol/L, chloride 114 mmol/L, bicarbonate 9 mmol/L, sodium 135 mmol/L, and pH of 7.1. Treatment for hyperkalemia was started immediately with calcium gluconate 1 gm that effectively narrowed her QRS complex and normalized her ECG. Salbutamol nebulization, glucose/insulin infusion, and calcium polystyrene syrup were given. Later, she was started on 100 mg sodium bicarbonate infusion, and Foley's catheter was inserted to follow urine output (UOP) strictly. However, she did not show a decrease in serum potassium levels. Then the patient underwent hemodialysis for two hours. Her first potassium reading after hemodialysis was 5.2 mmol/L. The purpose of this case report is to emphasize the importance of hemodialysis in patients with persistent severe life-threatening hyperkalemia.With the growing global rates of diabetes and hypertension, chronic kidney disease (CKD) appears to be a major contributor to morbidity and all-cause mortality. In recent years, there has been growing controversy regarding the optimal timing for the initiation of hemodialysis in this patient cohort. In this report, we present the case of a 52-year-old female with a 15-year history of CKD who was admitted to the hospital with clinical manifestations of uremia, volume overload, and symptomatic anemia. The patient presented with fatigue, nausea, progressive shortness of breath, and lightheadedness for two weeks, which had limited the activities of daily living. For the past eight years, her estimated glomerular filtration rate (GFR) had ranged from 5 to 15 mL/min/1.73 m2, consistent with kidney failure seen in stage 5 CKD. Prior to her recent admission, the patient had been grossly asymptomatic and had been responsive to medical therapy. After appropriate management with hemodialysis, a transfusion of packed red blood cells, and medication adjustment, the patient was scheduled for maintenance dialysis through an arteriovenous fistula. She had no further complaints and her laboratory abnormalities were found normalized at the six-month follow-up. This case report presents the survival and outcome of a patient with stage 5 CKD, who was only initiated on hemodialysis eight years after her diagnosis.Waardenburg syndrome (WS) is an interesting inherited audio-pigmentary disorder. The syndrome shows no gender, racial, or ethnic predilection. This unique disorder is characterized by pigmentary abnormalities, deafness, and neural crest-derived tissue defect. WS can be recognized by some specific clinical features that appear after birth; not all affected individuals possess all the clinical features. It has four clinical sub types based on the mutant gene and characteristic morphology. These morphological features are broad nasal root, white forelock, the difference in the colour of eyes, congenital leukoderma, and sensorineural deafness. We report an interesting case of WS in twin boys who fulfill the criteria of WS-II. Our cases have four major criteria (white forelock, heterochromia, sensorineural hearing loss, first degree relative with WS), and 1 minor criterion to establish the diagnosis of WS-II. Most clinical features of WS-II except sensorineural deafness are benign and do not need any intervention but severe deafness can be a serious problem.