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Elevation of ALP is an abnormal feature in TAFRO syndrome, but the cause is unknown. This article is the first report that histologically showed intrahepatic cholangitis may be the cause of ALP elevation in TAFRO syndrome. [ABSTRACT FROM AUTHOR]

• Ceftriaxone can cause encephalopathy in patients with end-stage renal disease. • Ceftriaxone-associated encephalopathy (CAE) can develop even at a dose of 1 g/day. • A high blood and cerebrospinal fluid ceftriaxone level may be CAE-related. • Estimation of ceftriaxone level may contribute to an accurate diagnosis. Neurotoxicity is a rare and intolerable adverse effect of ceftriaxone therapy. In most cases, it has been diagnosed on the basis of medical history rather than quantitative blood and cerebrospinal fluid testing. We report the case of a woman aged 78 years with ceftriaxone-associated encephalopathy. She regularly underwent hemodialysis. The patient received intravenous ceftriaxone at a dose of 1 g/day for 10 days for a urinary tract infection, and her consciousness level began to deteriorate during the therapy. Five days after ceftriaxone discontinuation, her symptoms rapidly improved. Thus, ceftriaxone-associated encephalopathy was suspected. Ceftriaxone levels in the blood and cerebrospinal fluid were high while the patient had disturbed consciousness. This case showed that ceftriaxone levels were related to ceftriaxone-associated encephalopathy. Therefore, the estimation of ceftriaxone levels may facilitate an accurate diagnosis. [ABSTRACT FROM AUTHOR]

Wernicke encephalopathy is caused by vitamin B1 deficiency. It presents as a triad consisting of altered mental status, oculomotor dysfunction, and gait ataxia. Early vitamin B1 administration alleviates symptoms. We present a video of gaze‐evoked nystagmus in an elderly patient with Wernicke encephalopathy. It is often difficult to evaluate the mental and ambulatory states of frail elderly patients with dementia. In such cases, nystagmus is the only useful physical finding in the diagnosis of Wernicke encephalopathy. [ABSTRACT FROM AUTHOR]

Rapidly destructive coxarthrosis is a rare entity of unknown etiology that is characterized by rapid hip joint destruction. Blood tests are thought to be non‐specific. However, we herein show a patient with rapidly destructive coxarthrosis, which was accompanied by fluctuating C‐reactive protein level. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Negative myoclonus may present in the early stages of cefepime neurotoxicity. Cefepime neurotoxicity typically presents as reduced consciousness, myoclonus, and seizures; however, negative myoclonus is uncommon. This video shows an older woman with cefepime neurotoxicity that presented as a negative myoclonus of the upper limbs. [ABSTRACT FROM AUTHOR]

Background: We experienced a pseudo-outbreak of aspergillosis in a newly constructed COVID-19 ward. Within the first 3 months from the commencement of the ward, six intubated patients of COVID-19 developed probable or possible pulmonary aspergillosis. We suspected an outbreak of pulmonary aspergillosis associated with ward construction and launched air sampling for the investigation of the relationship between these. Methods: The samples were collected at 13 locations in the prefabricated ward and three in the general wards, not under construction, as a control. Results: The results from samples revealed different species of Aspergillus from those detected by the patients. Aspergillus sp. was detected not only from the air samples in the prefabricated ward but also in the general ward. Discussion: In this investigation, we could not find evidence of the outbreak that links the construction of the prefabricated ward with the occurrence of pulmonary aspergillosis. It might suggest that this series of aspergillosis was more likely occurred from fungi that inherently colonized patients, and was associated with patient factors such as severe COVID-19 rather than environmental factors. Once an outbreak originating from building construction is suspected, it is important to conduct an environmental investigation including an air sampling. [ABSTRACT FROM AUTHOR]

A 56-year-old man presenting with massive melena and loss of consciousness was diagnosed with an infected thoracoabdominal aneurysm, an aortoduodenal fistula, and Leriche syndrome following an evaluation by computed tomography. Emergency surgery for uncontrolled infection included the reconstruction of the superior mesenteric and bilateral renal arteries using a four-branched graft. The aortoduodenal fistula was resected after omental filling, and an enterostomy was performed for feeding. Intestinal reconstruction was performed in two stages. The patient was discharged on postoperative day 48 and was without evidence of recurrence at 23 months postoperatively. [ABSTRACT FROM AUTHOR]

• Adenosine deaminase (ADA) in the cerebrospinal fluid (CSF) is not specific for diagnosing tuberculous meningitis in HIV infected patients. • Retroviral rebound syndrome can cause meningitis and can also cause ADA elevation in the CSF. • We have to be aware of retroviral rebound syndrome as a cause of ADA elevation in CSF, to avoid unnecessary anti-tuberculous treatment. Adenosine deaminase (ADA) in cerebrospinal fluid (CSF) is considered to be a useful biomarker in differentiating tuberculous meningitis (TBM) from other meningitis in non-HIV patients. However, its specificity decreases in patients with HIV, and other diseases such as cytomegalovirus encephalitis, toxoplasmosis or meningeal lymphomatosis can also elevate ADA in CSF. We here report a rare case of retroviral rebound syndrome in a HIV patient, whose ADA in CSF was elevated. [ABSTRACT FROM AUTHOR]

Platelets store self. agonists such as ADP and serotonin in dense core granules. Although exocytosis of these granules is crucial for hemostasis and thrombosis, the underlying mechanism is not fully understood. Here, we show that incubation of permeabilized platelets with unprenylated active mutant Rab27A-Q78L, wild type Rab27A, and Rab27B inhibited the secretion, whereas inactive mutant Rab27A-T23N and other GTPases had no effects. Furthermore, we affinity-purified a GTPRab27A-binding protein in platelets and identified it as Munc13-4, a homologue of Munc13-1 known as a priming factor for neurotransmitter release. Recombinant Munc13-4 directly bound to GTP-Rab27A and -Rab27B in vitro, but not other GTPases, and enhanced secretion in an in vitro assay. The inhibition of secretion by unprenylated Rab27A was rescued by the addition of Munc13-4, suggesting that Munc13-4 mediates the function of GTP-Rab27. Thus, Rab27 regulates the dense core granule secretion in platelets by employing its binding protein, Munc13-4. [ABSTRACT FROM AUTHOR]

Platelets play critical roles in hemostasis and thrombosis through their aggregation following activation of integrin α[sub IIb]β[sub 3]. However, the molecular mechanism of the integrin activation inside platelets remains largely unknown. Pharmacological experiments have demonstrated that protein kinase C (PKC) plays an important role in platelet aggregation. Because PKC inhibitors can have multiple substrates and given that non-PKC-phorbol ester-binding signaling molecules have been demonstrated to play important roles, the precise involvement of PKC in cellular functions requires re-evaluation. Here, we have established an assay for analyzing the Ca[sup 2+]-induced aggregation of permeabilized platelets. The aggregation of platelets was inhibited by the addition of the arginine-glycine-aspartate-serine peptide, an integrin-binding peptide inhibitor of α[sub IIb]β[sub 3], suggesting that the aggregation was mediated by the integrin. The aggregation was also dependent on exogenous ATP and platelet cytosol, indicating the existence of essential cytosolic factors required for the aggregation. To examine the role of PKC in the aggregation assay, we immunodepleted PKCα and β from the cytosol. The PKC-depleted cytosol lost the aggregation-supporting activity, which was recovered by the addition of purified PKCα. Furthermore, the addition of purified PKCα in the absence of cytosol did not support the aggregation, whereas the cytosol containing less PKC supported it efficiently, suggesting that additional factors besides PKC would also be required. Thus, we directly demonstrated that PKCα is involved in the regulation of Ca[sup 2+]-induced platelet aggregation. [ABSTRACT FROM AUTHOR]