Is left upper lobectomy for lung cancer a risk factor for cerebral infarction?

Purpose

Cerebral infarction is a rare complication of lung resection that can result in severe sequelae. Our aim was to investigate the characteristics of patients who suffer from cerebral infarction after surgery for lung cancer.

Methods

We retrospectively reviewed all patients who underwent resection of at least a single lobe for lung cancer at our institution between January 2008 and October 2013. We compared the patients who presented with cerebral infarction with those patients who did not within 30 days of surgery.

Results

A total of 562 patients underwent surgery, with five males and one female subsequently experiencing cerebral infarction. Five patients underwent left upper lobectomy and one underwent left lower lobectomy. Patient age, sex, body mass index, smoking index, and operative time were not significantly different between the six patients with postoperative cerebral infarction and the other 556 patients; only the type of operative procedure was significantly different (p < 0.001). Contrast-enhanced computed tomography revealed thrombosis in the stump of the left superior pulmonary vein in patients with postoperative cerebral infarction.

Conclusions

Cerebral infarction occurs at a high frequency in patients who undergo left upper lobectomy for lung cancer. Thrombosis in the left superior pulmonary-vein stump might cause cerebral infarction.

     

Prenatal diagnosis of Gaucher disease using next‐generation sequencing

In the prenatal diagnosis of Gaucher disease (GD), glucocerebrosidase (GBA) activity is measured with fetal cells, and gene analysis is performed when pathogenic mutations in GBA are identified in advance. Herein is described prenatal diagnosis in a family in which two children had GD. Although prior genetic information for this GD family was not obtained, next‐generation sequencing (NGS) was carried out for this family because immediate prenatal diagnosis was necessary. Three mutations were identified in this GD family. The father had one mutation in intron 3 (IVS2 + 1), the mother had two mutations in exons 3 (I[‐20]V) and 5 (M85T), and child 1 had all three of these mutations; child 3 had none of these mutations. On NGS the present fetus (child 3) was not a carrier of GD‐related mutations. NGS may facilitate early detection and treatment before disease onset.     

Safety of warfarin therapy in chronic hemodialysis patients: a prospective cohort study

Background

We conducted a multicenter prospective cohort study to assess the safety of warfarin therapy in Japanese hemodialysis (HD) patients.

Methods

Chronic HD patients on warfarin therapy (warfarin users) were recruited from 111 HD centers in Japan. Two dialysis-vintage-matched warfarin non-users (non-users) were selected from the same HD center as each warfarin user. Clinical data were collected upon registration and every 12 months thereafter for up to 36 months.

Results

The final cohort consisted of 365 warfarin users and 692 non-users and was followed for an average of 27.7 months. The mean age of warfarin users (68.8 ± 10.6 years) was significantly higher than that of non-users (66.9 ± 11.0 years, p < 0.001). The analyses by multivariate Cox proportional-hazard models showed that the age [hazard ratio (HR) = 1.07 for each 1-year increase, 95 % confidence interval (CI) 1.05–1.08, p < 0.001] was significantly associated with the death from any cause, but warfarin use (1.08, CI 0.75–1.57, p = 0.68) was not when being adjusted for sex, diabetes mellitus, antiplatelet use, and atrial fibrillation. The risk of composite events, which included death from any cause, stroke, cardiovascular disease, and peripheral arterial disease, was also associated with age but was not associated with warfarin use.

Conclusion

The results of this study suggested that warfarin use by HD patients might not be harmful in chronic state, while the safety for the initiation of warfarin therapy in HD patients remained to be determined.

     

Clinical features of patients with pars defects identified in adulthood

Purpose

Lumbar spondylolysis is considered a stress fracture of the pars interarticularis that occurs during growth. However, it is sometimes insidious and identified in adults as pseudoarthrosis, the terminal-stage of spondylolysis. The purpose of this study was to identify the clinical features of patients with terminal-stage spondylolysis that first manifested during adulthood.

Patients and methods

Thirty-six patients (21 men, 15 women; mean age 55.8 years; age range 25–77 years) with low back pain (LBP) were studied. In all patients, lumbar spondylolysis had not been diagnosed until the first visit to our hospital. Patient data collected were history of athletic activity and LBP during their growth period and radiological findings, such as spinal level, displacement, and spina bifida occulta (SBO).

Results

Among the 36 patients, including a patient with multi-level spondylolysis (L4 and L5), a total of 37 vertebrae with terminal-stage spondylolysis were identified. Twenty-three (89.2 %) of the 37 vertebrae had L5 spondylolysis. Sixteen patients (44.4 %) had no history of athletic activity, 26 (72.2 %) had no experience of LBP during their growth period, and 14 (38.9 %) had neither. Twenty of the 37 vertebrae (70.4 %) involved displacement (grade 1 = 14; grade 2 = 6). In nine patients (25.0 %; eight men, one woman), SBO of the sacrum was accompanied by L5 spondylolysis.

Conclusions

Approximately 90 % of patients with terminal-stage spondylolysis that was first diagnosed in adulthood involved the L5. Also, about 40 % had no history of athletic activity or experience of LBP during their growth period. In addition, only some patients with L5 spondylolysis had SBO, and all but one of these patients was male. This suggests that male patients with L5 spondylolysis may have some congenital predisposition.

     

Angiotensin II type 2 receptors facilitate reinnervation of phenol-lesioned vascular calcitonin gene-related peptide-containing nerves in rat mesenteric arteries

The present study was designed to investigate involvement of angiotensin II (Ang II) type 2 receptors (AT2 receptors) in restoration of perivascular nerve innervation injured by topical phenol treatment. Male Wistar rats underwent in vivo topical application of 10% phenol around the superior mesenteric artery. After phenol treatment, animals were subjected to immunohistochemistry of the third branch of small arteries, Western blot analysis of AT2 receptor protein expression in dorsal root ganglia (DRG) and studies of mesenteric neurogenic vasoresponsiveness. Ang II (750 ng/kg/day), nerve growth factor (NGF; 20 microg/kg/day) and PD123,319 (AT2 receptor antagonist; 10 mg/kg/day) were intraperitoneally administered for 7 days using osmotic mini-pumps immediately after topical phenol treatment. Losartan (AT1 receptor antagonist) was administered in drinking water (0.025%). Phenol treatment markedly reduced densities of both calcitonin gene-related peptide (CGRP)-like immunoreactivity (LI) and neuropeptide Y (NPY)-LI-containing fibers. NGF restored densities of both nerve fibers to the sham control level. Coadministration of Ang II and losartan significantly increased the density of CGRP-LI-fibers but not NPY-LI-fibers compared with saline control. The increase of the density of CGRP-LI-fibers by coadministration of Ang II and losartan was suppressed by adding PD123,319. Coadministration of Ang II and losartan ameliorated reduction of CGRP nerve-mediated vasodilation of perfused mesenteric arteries caused by phenol treatment. The AT2 receptor protein expression detected in DRG was markedly increased by NGF. These results suggest that selective stimulation of AT2 receptors by Ang II facilitates reinnervation of mesenteric perivascular CGRP-containing nerves injured by topical phenol application in the rat.     

Phosphorylation of neuronal nitric oxide synthase at Ser847 in the nucleus intermediolateralis after spinal cord injury in mice

We previously demonstrated that Ca2+/calmodulin (CaM)-dependent protein kinase IIalpha (CaM-KIIalpha) can phosphorylate neuronal nitric oxide synthase (nNOS) at Ser847 and attenuate NOS activity in neuronal cells. In the present study we focused on chronological alteration in levels and cellular location of nNOS, phosphorylated (p)-Ser847-nNOS (NP847), CaM-KII and p-Thr286-CaM-KIIalpha following spinal cord injury (SCI) in mice. Western blot analysis showed nNOS to be significantly phosphorylated at Ser847 from 3 h after SCI, peaking at 24 h and gradually decreasing thereafter, and CaM-KII to be colocalized with nNOS after SCI. Immunohistochemical analysis revealed that SCI causes an increase in both NP847 and p-Thr286-CaM-KIIalpha in the nucleus intermediolateralis. These findings suggest that SCI induces p-Thr286-CaM-KIIalpha, which phosphorylates the nNOS at Ser847 in the nucleus intermediolateralis where NO is thought to play a role as a neurotransmitter in autonomic preganglionic neurons. Thus, the NP847 signaling pathway might be involved in the autonomic failure which occurs immediately after SCI.