Neuronal expression of c-Fos protein in the brain after intraperitoneal injection of leptin in Wistar rats

Leptin has been recognized to be an important neuroendocrine signal in the regulation of food intake and energy balance. We aimed to survey central neurons that might be activated after peripheral administration of leptin, by examining the distribution of neurons expressing c-Fos protein. Leptin dissolved at a dose of 500 μg/kg in physiological saline was intraperitoneally injected in Wistar rats. One and a half hours after the injection, rats were transcardially perfused with saline and fixed with fixatives. The brain was removed and sectioned at 40 μm in thickness. Every fourth section was treated with anti-c-Fos antiserum, and c-Fos protein was immunohistochemically stained using the avidin-biotin complex method. Control rats were injected with saline solution, and brain sections were processed similarly as described above. It was found that leptin injected intraperitoneally induced the neuronal expression of c-Fos protein in several nuclei throughout the brain. In the central nucleus amygdala, ventromedial nucleus of hypothalamus, periaqueductal gray matter, lateral parabrachial nucleus, and the solitary tract nucleus, numbers of neurons expressing c-Fos protein were much more in the test experiments than those in the control experiments. Intraperitoneally injected leptin was found to stimulate central neurons that may play some roles in the regulation of such as a food intake

ABO-Incompatible Kidney Transplantation

Previously, ABO-incompatible kidney transplantation (KTx) was believed to be a “taboo” for immunological reasons. In Japan, the Tokyo Women’s Medical University reported the first successful case of such transplantation, performed on January 19, 1989. Since then, we have been striving to improve the outcome of ABO-incompatible transplantation for a quarter of a century

Influence of Visual Stimulation-Induced Passive Reproduction of Motor Images in the Brain on Motor Paralysis After Stroke

Finger flexor spasticity, which is commonly observed among patients with stroke, disrupts finger extension movement, consequently influencing not only upper limb function in daily life but also the outcomes of upper limb therapeutic exercise. Kinesthetic illusion induced by visual stimulation (KINVIS) has been proposed as a potential treatment for spasticity in patients with stroke. However, it remains unclear whether KINVIS intervention alone could improve finger flexor spasticity and finger extension movements without other intervention modalities. Therefore, the current study investigated the effects of a single KINVIS session on finger flexor spasticity, including its underlying neurophysiological mechanisms, and finger extension movements. To this end, 14 patients who experienced their first episode of stroke participated in this study. A computer screen placed over the patient’s forearm displayed a pre-recorded mirror image video of the patient’s non-paretic hand performing flexion–extension movements during KINVIS. The position and size of the artificial hand were adjusted appropriately to create a perception that the artificial hand was the patient’s own. Before and after the 20-min intervention, Modified Ashworth Scale (MAS) scores and active range of finger extension movements of the paretic hand were determined. Accordingly, MAS scores and active metacarpophalangeal joint extension range of motion improved significantly after the intervention. Moreover, additional experimentation was performed using F-waves on eight patients whose spasticity was reduced by KINVIS to determine whether the same intervention also decreased spinal excitability. Our results showed no change in F-wave amplitude and persistence after the intervention. These results demonstrate the potential clinical significance of KINVIS as a novel intervention for improving finger flexor spasticity and extension movements, one of the most significant impairments among patients with stroke. The decrease in finger flexor spasticity following KINVIS may be attributed to neurophysiological changes not detectable by the F-wave, such as changes in presynaptic inhibition of Ia afferents. Further studies are certainly needed to determine the long-term effects of KINVIS on finger spasticity, as well as the neurophysiological mechanisms explaining the reduction in spasticity

Comprehensive investigation of areae gastricae pattern in gastric corpus using magnifying narrow band imaging endoscopy in patients with chronic atrophic fundic gastritis.

Background:  Barium radiographic studies have suggested the importance of evaluating areae gastricae pattern for the diagnosis of gastritis. Significance of endoscopic appearance of areae gastricae in the diagnosis of chronic atrophic fundic gastritis (CAFG) was investigated by image-enhanced endoscopy. Materials and Methods:  Endoscopic images of the corpus lesser curvature were studied in 50 patients with CAFG. Extent of CAFG was evaluated with autofluorescence imaging endoscopy. The areae gastricae pattern was evaluated with 0.2% indigo carmine chromoendoscopy. Micro-mucosal structure was examined with magnifying chromoendoscopy and narrow band imaging. Results:  In patients with small extent of CAFG, polygonal areae gastricae separated by a narrow intervening part of areae gastricae was observed, whereas in patients with wide extent of CAFG, the size of the areae gastricae decreased and the width of the intervening part of areae gastricae increased (p < 0.001). Most areae gastricae showed a foveola-type micro-mucosal structure (82.7%), while intervening part of areae gastricae had a groove-type structure (98.0%, p < 0.001). Groove-type mucosa had a higher grade of atrophy (p < 0.001) and intestinal metaplasia (p < 0.001) compared with foveola type. Conclusions:  As extent of CAFG widened, multifocal groove-type mucosa that had high-grade atrophy and intestinal metaplasia developed among areae gastricae and increased along the intervening part of areae gastricae. Our observations facilitate our understanding of the development and progression of CAFG

Long-term CMV monitoring and chronic rejection in renal transplant recipients

IntroductionCytomegalovirus (CMV) is well established to be an independent risk factor for graft loss after kidney transplantation (KTx). Monitoring for CMV in the chronic phase is not defined in the current guideline. The effects of CMV infection, including asymptomatic CMV viremia, in the chronic phase are unclear.MethodsWe performed a single-center retrospective study to investigate incidence of CMV infection in the chronic phase, defined as more than 1 year after KTx. We included 205 patients who received KTx between April 2004 and December 2017. The CMV pp65 antigenemia assays to detect CMV viremia were continuously performed every 1–3 months.ResultsThe median duration of the follow-up was 80.6 (13.1–172.1) months. Asymptomatic CMV infection and CMV disease were observed in 30.7% and 2.9% in the chronic phase, respectively. We found that 10–20% of patients had CMV infections in each year after KTx which did not change over 10 years. The history of CMV infection in the early phase (within 1 year after KTx) and chronic rejection were significantly associated with CMV viremia in the chronic phase. CMV viremia in the chronic phase was significantly associated with graft loss.DiscussionThis is the first study to examine the incidence of CMV viremia for 10 years post KTx. Preventing latent CMV infection may decrease chronic rejection and graft loss after KTx

Purinergic P2Y(6) receptors heterodimerize with angiotensin AT1 receptors to promote angiotensin II-induced hypertension

The angiotensin (Ang) type 1 receptor (AT1R) promotes functional and structural integrity of the arterial wall to contribute to vascular homeostasis, but this receptor also promotes hypertension. In our investigation of how Ang II signals are converted by the AT1R from physiological to pathological outputs, we found that the purinergic P2Y6 receptor (P2Y6R), an inflammation-inducible G protein (heterotrimeric guanine nucleotide–binding protein)–coupled receptor (GPCR), promoted Ang II–induced hypertension in mice. In mice, deletion of P2Y6R attenuated Ang II–induced increase in blood pressure, vascular remodeling, oxidative stress, and endothelial dysfunction. AT1R and P2Y6R formed stable heterodimers, which enhanced G protein–dependent vascular hypertrophy but reduced β-arrestin–dependent AT1R internalization. Pharmacological disruption of AT1R-P2Y6R heterodimers by the P2Y6R antagonist MRS2578 suppressed Ang II–induced hypertension in mice. Furthermore, P2Y6R abundance increased with age in vascular smooth muscle cells. The increased abundance of P2Y6R converted AT1R-stimulated signaling in vascular smooth muscle cells from β-arrestin–dependent proliferation to G protein–dependent hypertrophy. These results suggest that increased formation of AT1R-P2Y6R heterodimers with age may increase the likelihood of hypertension induced by Ang II

Plastic bronchitis associated with influenza B virus infection: A case report

Plastic bronchitis (PB) is a severe acute respiratory disease that develops as a result of the formation of branching mucus plugs in the bronchial tree. PB is known as a complication of influenza A virus infection, but some cases have been associated with influenza B virus infections. This patient was a 3-year-old boy with no history of allergic disease who developed PB requiring ventilator management after influenza B virus infection. He was hospitalized and managed with ventilator support because of acute respiratory failure. Influenza B virus infection was diagnosed via rapid antigen test and real-time reverse-transcription polymerase chain reaction (RT-PCR). A bronchoscopy performed after a chest X-ray and computed tomography confirmed the presence of extensive atelectasis in the right lung field and mucus plugs in the right bronchus. The patient's respiratory condition improved rapidly after removal of the plugs. Quantitative real-time RT-PCR performed with nasal and aspirated sputum samples obtained at hospitalization revealed a higher viral RNA load in the upper rather than in the lower respiratory tract. Viral replication in the lower respiratory was not found to be a major contributor toward mucus plug formation. The finding of increased serum IgE in the absence of a history of allergic disease suggests that an allergic reaction contributed to the formation of mucus plugs

Routine hypercapnic challenge after cervical spinal hemisection affects the size of phrenic motoneurons

Abstract After an individual experiences a cervical cord injury, the cell body's adaptation to the smaller size of phrenic motoneurons occurs within several weeks. It is not known whether a routine hypercapnic load can alter this adaptation of phrenic motoneurons. We investigated this question by using rats with high cervical cord hemisection. The rats were divided into four groups: control, hypercapnia, sham, and sham hypercapnia. Within 72 h post-hemisection, the hypercapnia groups began a hypercapnic challenge (20 min/day, 4 times/week for 3 weeks) with 7% CO2 under awake conditions. After the 3-week challenge, the phrenic motoneurons in all of the rats were retrogradely labeled with horseradish peroxidase, and the motoneuron sizes in each group were compared. The average diameter, cross-sectional area, and somal surface area of stained phrenic motoneurons as analyzed by software were significantly smaller in only the control group compared to the other groups. The histogram distribution was unimodal, with larger between-group size differences for motoneurons in the horizontal plane than in the transverse plane. Our findings indicate that a routine hypercapnic challenge may increase the input to phrenic motoneurons and alter the propensity for motoneuron adaptations